IS SCINTIGRAPHY STILL RELEVANT? PAGE 3 INCORPORATING MRI DIAGNOSTICS INTO YOUR PRACTICE PAGE 17 DIAGNOSIS AND MANAGEMENT OF SELECTED HINDLIMB LAMENESS ISSUES AND THOUGHTS PAGE 25 INJURIES OF THE SAGITTAL GROVE OF THE PROXIMAL PHALANX – A DIAGNOSTIC DILEMMA PAGE 34 DIAGNOSIS AND MANAGEMENT OF SUSPENSORY BRANCH DESMOPATHY IN SPORT HORSES PAGE 39 WHY IS IT IMPORTANT TO SEE SPORTS HORSES RIDDEN? PAGE 50 SACROILIAC JOINT REGION PAIN IN SPORTS HORSES: A GROWING PROBLEM?

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HINDLIMB PROXIMAL SUSPENSORY DESMOPATHY: WHY IS IT SUCH A MANAGEMENT CHALLENGE?

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MY HORSE WON’T BEND - CERVICAL STIFFNESS AND DYSFUNCTION PAGE 69 UNDERSTANDING BACK PAIN, THORACOLUMBAR FASCIA AND THE MIDDLE COMPARTMENT PAGE 79 BISPHOSPHONATES IN EQUINE PRACTICE PAGE 89

2 IS SCINTIGRAPHY STILL RELEVANT?

Michael W. Ross, D.V.M., Diplomate, ACVS Professor of Surgery University of Pennsylvania -- Kennett Square, Pennsylvania, USA [email protected]

Synopsis: In this day-and-age of standing and recumbent computed tomography and widespread use of magnetic resonance imaging, many may question the relevance of using nuclear scintigraphy as a diagnostic tool. Far from being over-the-hill the modality continues to be a workhorse for lameness diagnosis and one of the best ways of assessing current activity and relevance of bony abnormalities. I will tell you why using clinical cases.

+NO, a nuclear scintigraphic examination is neither a substitute for a detailed clinical lameness examination nor for diagnostic analgesia. Scintigraphy is HUGELY IMPORTANT in evaluating racehorses with poor performance but can be frustrating in sport horses (SHs). Scintigraphy is an enormously useful tool, is cost-effective when used with reasonable expectations and with proper case selection. Scintigraphy is an important ancillary imaging modality; it should not be viewed as an "answer machine." Often clients expect a straight-forward answer to a chronic, complex, and multifaceted performance problem with a single pass of the gamma camera. Scintigraphy cannot give an answer to every lameness problem but provides useful and interesting clinical information. Negative scintigraphic examination can in itself provide a clinical direction by ruling out active bony remodeling. A dressage horse has a chronic obscure performance problem and a negative whole- body bone scan would ensure a training intensity change could be done without exacerbating an existing bony lesion. Alternatively, a negative bone scan can implicate a soft-tissue abnormality (see below).

We have been through many generations of equipment, hardware, software and just recently upgraded our equipment to include a custom-made, 91 hex-photomultiplier rectangular LFOV camera, a Segami Oasis nuclear medicine workstation (custom designed to output images according to our specifications), and a modified overhead gantry with upgraded motion (can now rotate the camera on its axis).* If asked if I thought scintigraphy was still “in vogue” my answer would be a resounding, yes indeed! During this lecture and during presentation of case studies at this meeting I will share my thoughts regarding the continuing value of scintigraphy in lameness diagnosis despite advancements in other imaging modalities and why it remains the imaging modality of choice

3 for difficult lameness answers. My thoughts regarding scintigraphy can be found either in various publications or textbooks.1,2

Scintigraphy is a very sensitive modality, but lacks specificity, simply because resolution can be poor and focal areas of increased uptake can represent anything from abnormal bony remodeling to fracture. Resolution can be improved by reducing camera-to-limb distance and to some degree by upgrading imaging equipment. To improve overall accuracy multiple images should be used. For instance, to determine the position of a focal area of increased radiopharmaceutical uptake (IRU) in the fetlock joint, it is important to have lateral, dorsal (plantar), and flexed lateral images. With this information, rather than report a finding of a “hot spot in the fetlock joint,” the clinician can say, “there is a focal area of IRU involving the distal, plantarolateral aspect of MtIII” a much more accurate description of the area of abnormal bony activity. Flexed lateral images of the hock, flexed dorsal images of the carpus and solar or palmar images of the foot are important. To diagnose medial femorotibial joint disease, a caudal image of the stifle is mandatory. A minimum of 2 images should be taken when possible. For instance, after a peroneal and tibial nerve block, focal IRU is often seen in delayed images over the cranial tibial cortex. Without the caudal image showing uptake is clearly in soft-tissues, inadvertent diagnosis of a tibial stress fracture could be made (of course, tibial stress fracture involving the cranial cortex is unusual). Two images also allow a determination of cortical or medullary IRU in long bones, and differentiation of stress fractures from enostosis-like lesions (a.k.a. bone islands). Focal IRU is more important than diffuse IRU, regardless of intensity. Bone IRU early in the flow or pool phases usually indicates active periosteal proliferation, seen in stress fractures, cortical trauma, or osteomyelitis.

Most false negative scans result from problems with limb or camera positioning, body part-to-camera distance, shielding by overlying soft-tissues or bone, background (bladder) and physeal activity. Careful interpretation of caudal images of the stifle helps diagnose osseous cyst-like lesions. Authentic negatives are useful in horses in which an increase in exercise is planned, but care must be taken in racehorses. Negative delayed-phase supports pain is likely originating from soft tissues. In horses with hindlimb lameness, negative scan ﬁndings often lead me to suspect the stiﬂe because delayed images lack sensitivity. Findings in horses with chronic proximal suspensory desmitis (PSD) also are often negative. Remember it is called a bone scan for a reason; sensitivity for soft tissue injury, chronic problems such as PSD is poor. DO NOT expect the bone scan to be positive in a horse with PSD.

Case selection - racehorses are ideal since they undergo high-impact exercise and are prone to stress- related cortical or subchondral trauma. Older SHs, particularly Warmbloods are much less than ideal. Low-impact exercise coupled with advanced age decrease the possibility of an answer. Scintigraphic examination may provide disappointing information regarding chronic osteoarthritis, particularly of the fetlock joint. In racehorses IRU of the palmar/plantar aspect of the fetlock joint (Mc/MtIII most common) is often pronounced, whereas in sport horses focal, mild IRU, most often seen associated

4 with the dorsomedial aspect of the joint can be subtle and is often under-appreciated or interpreted incorrectly. It is sometimes difficult to find correlation between scintigraphic and radiological changes in the distal hock joint. In SHs, scintigraphic examination is useful with pain associated with the foot, fetlock, proximal metacarpus/metatarsus, stifle, and the back. But, two important factors determining the usefulness of the bone scan include, the horse is clinically lame at the time of the scan and lameness has been localized. Scintigraphy provides a "functional evaluation" of osteoblastic activity (modeling) at the time of the scan. If a horse with chronic lameness is rested for several months before evaluation, the chances of seeing IRU are greatly diminished. In a known area of clinical lameness, diagnostic accuracy can be increased, since a differentiation can be made between soft-tissue and bony problems, and radiographs can be more carefully evaluated considering scintigraphic findings. Scintigraphy is least likely to yield a diagnosis in SHs with nebulous histories of gait abnormalities and poor performance and with problems that can be perceived only by the rider. These horses usually are not lame, may have equivocal or negative manipulative test results, and may be difﬁcult individuals with which to work. Diagnostic analgesia may be difﬁcult to perform or interpret but selective analgesic techniques may improve the feel of the horse. Blocking one limb in a horse suspected of having bilateral nearly symmetric pain may produce obvious contralateral signs.

Scintigraphic examination has been used as part of a comprehensive purchase examination, but results must be carefully interpreted and clinical relevance established. Although unusual, this adjunct imaging procedure usually is requested in high-proﬁle, expensive, upper-level sport horses and results can often be confusing. Finding an upper-level horse of any type without any scintigraphic changes would be unusual, mirroring radiological ﬁndings in these horses. Scintigraphy was useful in establishing clinical relevance of mineralization of the cartilages of the foot and when present, intense IRU was associated with radiological changes that could be differentiated (wider and more irregular) from unimportant areas of mineralization or separate centers of ossification.3-5 A possible benefit to clinicians performing examinations before purchase was proposed.3

5 Focal or diffuse areas of IRU are found in the thoracolumbar dorsal spinous processes and may account for clinical signs of back pain, poor performance, or gait restriction but occur only in horses that are ridden. A wide spectrum of scintigraphic and radiological changes in the thoracolumbar spine in horses without back pain led to the conclusion that IRU of the dorsal spinous processes should be interpreted carefully and in light of other clinical signs; only 7 of 33 horses without back pain had no radiographic or scintigraphic abnormalities and in some horses IRU was pronounced.6 We have not identiﬁed areas of IRU in the thoracolumbar spine in the STB racehorse, but these are common in young TB in race training and in most are incidental scintigraphic findings. However in SHs scintigraphy may be helpful in the assessment of the clinical significance of radiological evidence of osteoarthritis of the thoracolumbar facet joints7 or spondylosis. 8 Blocking is the single most important procedure in horses suspected of having back pain, such as those that develop nappy behavior, resistance and signs such as bucking. Resistance to saddling or poor performance could be explained by fracture, anomaly or injury of ribs.9 WHAT WORKS BEST, A BONE SCAN OR MRI? WHAT ABOUT A COMBINED APPROACH? #

Advances in Equine Imaging – a perspective In 1981, the year I graduated from veterinary school, imaging was defined by the acquisition of plain radiographic images. There was no ultrasonographic imaging, digital imaging of any sort, magnetic resonance imaging (MRI), or computed tomography. Nuclear scintigraphy was in its infancy. To me ultrasonography became available over the next few years, and shortly I was able to use xeroradiography, but scintigraphy did not become available until late 1993. This gave me 12 years of experience with basic equine lameness examination, sharpening my skills as a lameness detective without the benefit of advanced imaging. At that point, combined imaging simply meant, use of radiography and ultrasonographic examination, referring horses to other centers equipped with scintigraphic imaging, or doing follow-up radiographic studies. I believe this was a hugely important time in my career, and this experience reinforced the importance of careful clinical examination and the use of diagnostic analgesia. I believe the most important aspect of the lameness examination is to determine the authentic source of pain causing lameness, whenever possible and safe to do so. Advanced imaging, scintigraphic imaging has been critical to my ability to answer difficult lameness questions, but clinical relevance, established using diagnostic analgesia, remains fundamental. A combined imaging approach, in a step-wise fashion is often the most successful imaging strategy to follow. Simply put, though, if asked if I had to choose between scintigraphy and MRI, what would I do? I would choose scintigraphy of course, but equivocate and say, “I’d really like both!”

Combined imaging – what can I learn?

6 Life as a lameness detective can be challenging when charged with finding “the answer” to difficult lameness questions, thus making paramount the opportunity to perform combined imaging in many horses. In practice economics or other practical considerations may dictate what and how many imaging modalities are used to determine a management plan. It is perfectly reasonable to localize pain, use radiography, ultrasonographic evaluation or both, and to initiate a management plan, when a definitive answer is not known. For instance, in horses in which pain is localized to the foot and radiographs are negative, an initial management plan may not differ if pain is originating from the suspensory ligament of the navicular bone or the bone itself (see below). Today, major medical insurance drives many investigations in our practice, and often insurance companies willingly pay for comprehensive imaging procedures and then, surgical management if necessary. To a certain extent, though, I still feel a reasonable approach involves step-wise acquisition of information to arrive at a lameness answer, rather than simply looking with every modality possible. I have a great respect for the value of scintigraphic examination to help answer difficult lameness questions and to help me assign relevance to clinical findings, but I realize the limitations of the imaging modality. Lessons learned from this important modality have been many.10-12

A positive bone scan means there is active bone modeling, bone formation, at the time of the scintigraphic examination, a finding that helps determine relevance to positive or negative radiological findings. There is nothing like a positive bone scan to pique your interest and prompt thorough investigation of current images or to acquire special images to highlight a particular area. I have been interested in investigating racehorses with mal or non-adaptive bone remodeling of several areas (repetitive osseous stress syndrome, ROSS), but a most important area is the distal aspect of the third metacarpal and metatarsal bones (Mc/MtIII).10,11 To make this diagnosis early in the disease process a bone scan is required. However, finding focal areas of increased radiopharmaceutical uptake (IRU) in the distal, plantarolateral aspect of MtIII lead me to investigate this region radiographically and discover, in some horses, the presence of radiolucent defects, which had not previously been identified (Fig 1).10,11 Combined imaging in this instance allows the clinician to “see” the areas of diseased subchondral bone and assign prognosis. Focal areas of IRU in the lateral condyle of MtIII could represent early subchondral bone injury with no obvious radiological changes, advanced subchondral bone injury as depicted in Fig 1., or the presence of a lateral condylar fracture; remember, scintigraphy is sensitive but not specific.

Horses with lameness abolished with palmar digital analgesia (PDA) are perfect candidates for a combined imaging approach. A common scenario is as follows: you examine a horse for the first time, localize lameness to the foot/lower pastern region using PDA, and obtain radiographs, which are negative or equivocal for bony changes. You recommend shoeing changes, a short period of rest with rehabilitation and non-steroidal anti-inflammatory drugs and the horse improves, only to go lame again. This horse is a perfect candidate for advanced imaging, such as pool and delayed phase scintigraphic examination, and potentially magnetic resonance imaging (MRI). In a step-wise fashion, lameness examination, radiographic examination and treatment have been performed, but an answer has not been given and the horse is lame once again. Horses with acute onset lameness can

7 be even more perplexing (Fig 2). I remain steadfast in recommending a bone scan for horses undergoing MRI examination for pain abolished with PDA. I find I can still answer many questions and make a diagnosis using scintigraphy, rather than proceeding to MRI examination. The ideal candidate for MRI examination is the horse with pain abolished with PDA, radiographs are negative, equivocal or show mild bony abnormalities in numerous locations, the pool phase scintigraphic examination is “suspicious” or positive, and delayed phase scintigraphic images are negative or equivocal (see Fig 2). In this case, a diagnosis of a primary soft tissue lesion lead to similar treatment recommendations as if the horse had navicular bone pathology but there were a number of differences including length of rest (4-6months) without turn out exercise, degree of heel elevation, and prognosis (better than if navicular bone involved). Neurectomy was specifically contraindicated.

Proximal suspensory desmitis in the forelimb and hindlimb can be difficult and challenging and requires comprehensive, combine imaging for proper diagnosis. Horses with hindlimb proximal suspensory desmitis, particularly in Warmblood jumpers or dressage horses with straight hindlimb conformation and recurrent desmitis, have a guarded to poor prognosis at best for return to previous level of competition and it is imperative to learn if pain is the result of soft tissue, bone or a combination of the 2 tissues. Prognosis is best if only bone is involved and worse if both soft tissue and bone are affected (Fig 3). I find ultrasonographic examination confusing particularly in horses in which swelling is minimal and cross-sectional area measurements of the suspensory ligament reveal only mild enlargement. In horses with recurrent desmitis ultrasonographic and radiographic evaluation are critical, but scintigraphic examination can reveal involvement of bone in horses without obvious radiographic abnormalities. There are numerous examples highlighting the value of combined imaging. In some horses information is simply redundant; in others it is critical for comprehensive understanding of the problem.

Figure Legends:

Fig 1: Lateral and plantar delayed phase scintigraphic images (a) and dorsolateral plantaromedial digital radiographic image of the metatarsophalangeal joint (b) taken with the conventional horizontal radiographic beam and a dorsolateral 25-30° proximal plantaromedial (down-angle) oblique digital radiographic image (c). Focal areas of increased radiopharmaceutical uptake in the plantarolateral aspect of the third metatarsal bone (MtIII) are one of the most important causes of lameness in racehorses. In horses with advanced subchondral injury, radiolucent defects develop. With a horizontal radiographic beam, the lateral proximal sesamoid bone overlaps a lesion involving the distal aspect of MtIII whereas with the down-angled radiographic beam the space between the PSBs and the proximal phalanx

8 is opened-up to allow evaluation of radiolucent and sclerotic changes (b, white arrows) associated with mal or non-adaptive bone remodeling of the distal medial aspect of MtIII. A small osteochondral (OCD) fragment involving the medial plantar process of the proximal phalanx can be seen (a, black arrow). (From Ross MW. Diagnosis of osteoarthritis and traumatic joint disease. In: Linder A: Management of lameness causes in sport horses, Wageningen Academic Publishers, Wageningen, The Netherlands, 2006;85-108.) Fig 1a

Fig 1b

9 Fig 1c

Fig 2: Images of an 8-year-old American Quarter Horse mare used for western performance competition. Acute RF lameness (3/5) developed and the referring veterinarian localized pain using palmar digital analgesia (PDA); radiographs revealed mild changes associated with the navicular bone but prominent changes commensurate with degree of lameness were not seen and the horse was referred for advanced imaging (a). Importantly pronounced lameness occurred acutely and the horse did not switch to LF lameness after PDA. Pool phase scintigraphic images (b, RF to the right) revealed mild pooling of radiopharmaceutical in the region of the navicular bone but in a somewhat linear fashion (arrows) consistent with increased radiopharmaceutical uptake (IRU) in the deep digital flexor tendon (DDFT). Delayed phase images (c and d) revealed mild IRU of the central portion of the navicular bone (arrows) but IRU was not commensurate with degree of lameness. A tentative diagnosis of a soft tissue injury, likely, DDF tendonitis was made. Magnetic resonance imaging (STIR image shown, e) revealed a large lesion of the DDFT (increased signal intensity in medial lobe of DDFT – arrows) between the navicular bone and the insertion on the distal phalanx. A diagnosis of DDFT tendonitis was made and the horse was managed with rest, elevation of the heel and NSAIDs. At 3 months the horse was improved, and follow-up MRI examination revealed the lesion to be smaller and less obvious, but still present.

10 Fig 2a

Fig 2b

Fig 2c

Fig 2d

Fig 2e

12 Fig 3: Images of an 11-year-old TB cross low-level jumper with LH lameness. The horse was referred because of poor performance and hindlimb gait deficit. Mild left hindlimb lameness (1- 2/5) was abolished with high plantar analgesia. Pool phase (not shown – early bone uptake of radiopharmaceutical was seen) and delayed phase scintigraphic images (a, lateral image showing a triangular area (arrow) of increased radiopharmaceutical uptake [IRU], typically seen in horses with avulsion injury of the third metatarsal bone [MtIII]) showed IRU of MtIII. Triangular areas of IRU are consistent with sclerosis or avulsion fracture of MtIII and radiographs are essential. Dorsoplantar radiographic projection showing the presence of sclerosis indication chronic modeling of MtIII (b, sclerosis is shown by arrows). Ultrasonographic examination revealed enlargement and poor fiber pattern of the proximal suspensory ligament (c, arrows). A guarded to poor prognosis was given.

Fig 3a

13 Fig 3b

Fig 3c

14 Footnotes:

+From Ross MW. Principles, usefulness and limitations of scintigraphy n the orthopedic work- up. Proceedings, Equine advanced imaging and lameness for practitioners, Vet PD Course, Elgin, IL, November 4-5, 2016.

*Rapid Scan HD, Diagnostic Services, Inc., Middlesex, NJ 08846.

#From Ross MW. Magnetic resonance imaging or a bone scan? Proceedings, West Indies Veterinary Conference, St. Kitts, West Indies, November 10-11, 2017. References:

1. Ross MW. Nuclear Medicine, in: Diagnosis and Management of Lameness in the Horse. 2nd edition. Ross MW, Dyson SJ, Eds. Elsevier (Saunders), St. Louis, 2011. 2. Ross MW: The Standardbred, in: Dyson SJ, Martinelli MJ, Pilsworth RC, Twardock AR: Equine Scintigraphy. Newmarket, UK, Equine Veterinary Journal 2003, pp 153-189. 3. Ruohoniemi M, Mäkelä O, Eskonen T. (2004) Clinical significance of ossification of the cartilages of the front feet based on nuclear bone scintigraphy, radiography and lameness examinations in 21 Finnhorses, Equine Vet J. 36,143. 4. Nagy, A., Dyson, S., Murray, R. (2007) Scintigraphic examination of the cartilages of the foot. Equine vet. J. 39, 250. 5. Nagy, A.,Dyson, S., Murray, R. (2008) Radiographic, scintigraphic and magnetic resonance imaging findings in the palmar processes of the distal phalanx. Equine vet. J. 40, 57.

6. Erichsen C, Eksell P, Holm KR, et al. (2004) Relationship between scintigraphic and radiographic evaluations of spinous processes in the thoracolumbar spine in riding horses without clinical signs of back problems, Equine Vet J. 36,458.

7. Gillen, A., Dyson, S., Murray, R. (2009) Nuclear scintigraphic assessment of the thoracolumbar synovial intervertebral articulations. Equine vet J. 41, 534-539.

8. Meehan, L., Dyson, S., Murray, R. (2009) Radiographic and scintigraphic evaluation of spondylosis in the equine thoracolumbar spine Equine vet J. 41, 800-807.

9. Dahlberg J, Ross MW. (2011) Clinical relevance of abnormal scintigraphic findings of adult equine ribs. Vet Radiol Ultrasound.52,573-9.

15 10. Ross MW. Bone Scintigraphy: Lessons Learned from 5000 Horses. Proceedings, 51st Annual Convention, American Association of Equine Practitioners, 2005;6-20. 11. Ross MW. Scintigraphic and clinical findings in the Standardbred metatarsophalangeal joint: 114 cases (1993-1995). Equine Vet J 1998;30:131. 12. Ross MW. Observations in horses with lameness abolished by palmar digital analgesia. Proc Am Assoc Equine Practnr 1998;230.

16 INCORPORATING MRI DIAGNOSTICS INTO YOUR PRACTICE

Richard D. Mitchell, DVM, MRCVS, Dipl. ACVSMR Fairfield Equine Associates, P. C. Newtown, CT, USA

Introduction Identification of lameness and its probable source is a daily challenge for the equine practitioner. Physical examination and careful observation can lead to a logical differential diagnosis, but a specific diagnosis often involves further investigation involving diagnostic anesthesia and imaging. While the principles of perineural and intra-articular anesthesia have long allowed veterinarians to localize the region of lameness related paini, the determination of the specific cause has often proven elusive. Modern imaging techniques of digital radiography, nuclear scintigraphy, and ultrasound have further enhanced the ability of the examiner to identify the cause of lameness. Magnetic Resonance Imaging (MRI) has proven to be a valuable tool for identifying specific pathology in the equine limb and many of these lesions have been corroborated with anatomical and histopathological studies.ii Familiarity with some basic MRI principles can make MRI reporting more meaningful and could facilitate a review of the images by the practitioner. As MRI technology has advanced in human clinical medicine, many imaging devices have become available for use in the horse. Closed and open magnets, low field and high field type, are now available and affordable for use in equine clinical practice. Most MRI systems require the horse to be anesthetized to fit within the field of the magnet and this presents some obstacles for certain horses and many clients. A low field standing MRI has been developed and is in widespread use in Europe and the USA. Motion can have a significant effect on image quality, and while general anesthesia may eliminate much motion artifact, adequate sedation techniques and motion correction software are now available to accommodate for these issues in the standing horse. The necessary equipment and specific concerns of general anesthesia and recovery are eliminated by using a standing scanning device. However, the field of view is larger, and the resolution of images is greater in high field magnets that require general anesthesia. Basic MRI Principles All materials are composed of atoms, and the atoms are composed of protons, neutrons and electrons. The protons and neutrons are condensed together to form a nucleus at the core, and the nucleus is surrounded by a cloud of electrons. Magnetic resonance imaging depends on the way that nucleus interacts with external magnetic fields.iii Hydrogen atoms (protons) are the primary target for study of the effects of magnetic fields in biological tissue. Hydrogen (and H+) is the most abundant element in the body, largely in water. A moving (spinning) charged particle (H+) generates its own little magnetic field. Spinning particles with mass have angular momentum as well. In a static magnetic field, the protons align along the axis of the field, and then when perturbed by an electrical pulse from a radiofrequency coil, the protons will change position toward the axis of the pulsed field. When the pulse stops, the protons return to the alignment of

17 the original axis of the static magnetic field and release energy as they do. This energy is measured by the coil and transmitted to a software program that translates this signal into an image. The various sequences that are used in the imaging process are weighted based on the duration of the radiofrequency pulse and the intervals of time when the radiofrequency is released and detected.iv

So why MRI? While newer techniques of digital radiography, ultrasound and nuclear scintigraphy have enhanced our ability to “see” pathology, there is much that escapes these modalities.v MRI helps to fill the gaps. Not only is MRI a modality for detecting anatomical variations, but it is also helpful in detecting physiological changes in tissue before any sort of real structural alteration can be detected with other imaging tools. In this respect, it can be useful in a manner that nuclear scintigraphy can be for detecting physiological changes in musculoskeletal tissues but it is more specific. Localization of the region of the issue is a prerequisite. A common MRI protocol, known as spin-echo imaging, includes three types of imaging sequences: T1-weighted (T1-wt), proton density (PD), and T2-weighted (T2-wt) images. All or some combination of sequences are usually acquired in each anatomic plane as each sequence provides different diagnostic information. Sagittal, transverse and frontal plane sections are normally used. The T1-wt images highlight the structural characteristics of tissues and are useful in evaluating the anatomy of bone and some soft tissues. T1-wt sequences are also used for the visualization of MRI paramagnetic contrast agents such as gadolinium. PD images offer excellent tissue contrast and are used for evaluating both osseous and soft tissues structures. T2-wt images emphasize fluid characteristics of tissues and are sensitive for detecting synovial effusions, cystic lesions and areas of inflammation or edema in orthopedic injuries.vi Other sequences are often utilized, in addition to spin-echo protocols, for orthopedic imaging. Sequences that suppress the normal high signal from fat will identify edema and inflammation that is present such as in trabecular bone edema and inflammation associated with microfractures that can occur in various early bone disease conditions. Subchondral bone contusions can go unrecognized unless fat-suppression images are utilized. An example of this kind of sequence is short-tau inversion recovery (STIR) where tau refers to the inversion time relating to a special pulse sequence. This causes suppression of the fat signal making it black instead of white. Other imaging protocols, such as gradient echo imaging (GE) can be used when there is a need for thinner slices. Spin-echo images are thicker slices and contiguous slices may be 3-10 mm thick. With GE images, slices may be as thin a 1-2mm but take longer to obtain.5 When describing most MRI sequences, the term intensity is often used to describe the various shades of gray that appear in tissues and fluid. High intensity signals are white, intermediate are gray and low intensity signals are black. These terms are often further modified to describe findings in a relative sense comparing to other tissues as hyperintense, isointense and

18 hypointense. Variations in fluid and fat content of soft tissues compared to bone, tendon and ligaments will demonstrate various levels of intensity. MRI Sequences in More Detail In describing images for purposes of this paper, the author will be using images from the Hallmarq Standing MRI scanner, but high field findings will be very similar. The more commonly used sequences will be discussed and information on how to interpret various findings will be presented. T1-weighted images are most often thought of as the most accurate representation of the anatomical structure. They are thought to be useful for musculoskeletal evaluations. In these sequences, fluids will have lower intensity, tendons and ligaments are often intermediate and fat (and the major portion of bones except for cortical bone) will have high intensity signals. T2 weighted sequences are included in all MRI protocols. Without modification the dominant sequences demonstrate fluid as hyperintense, tendon and ligament as low intensity, fat as hyperintense and cortical bone as low intensity. With the Hallmarq system, T2-weighted FSE images may more accurately reflect fluid content in some newer tendon and ligament lesions while T2* weighted images may reflect tissue content changes that are older and less acute. T2* weighted images in the Hallmarq system demonstrate a “phase cancellation artifact” where fat and significant fluid cancel out one another and the affected area is hypointense. This is often seen in cases of significant subchondral contusion and microfractures.

Fig. 1: T1-weighted 3D sagittal image (left) demonstrating fluid in the dorsal aspect of the coffin joint as dark gray as well as fluid within the body the navicular bone (gray). A T2*-weighted image(right) demonstrates hyperintense signal in the dorsal aspect of the coffin joint as well as some in the cystic area indicative of a mix of fluid and tissue. Low signal within the navicular body is fluid and fat tissue resulting in phase cancellation artifact which was also confirmed by the presence of a generalized hyperintense signal within the body of the navicular bone on STIR images (tbd).

Fig 2&3: T2-weighted FSE image and T2*-weighted images demonstrating different intensity of fluid signal in a deep digital flexor tendon within the navicular bursa. Lesion may be in a chronic phase.

Fig. 4&5: T2-weighted FSE on left and T1weighted GRE on right demonstrating the same area of bone edema (fluid) in P2 identified by arrows, hyperintense in T2-weighted FSE and hypointense in T1-weighted GRE. STIR images are of significant help for musculoskeletal imaging. Most cases of subchondral contusion and bone bruising were only speculation ante mortem prior to the use of MRI. STIR images are excellent at identifying the presence of fluid and inflammation in soft tissue and bone. The presence of osseous fluid and tissue edema will be evident as hyperintense signal. One study cites the resolution of STIR lesions in tendon and ligaments is associated with improved lameness status in horses, however this relationship did not exist in that study with bone marrow lesions.vii

Fig. 6&7: STIR FSE images demonstrating an area of hyperintense signal indicative of subchondral edema and contusion.

Fig.8&9: T2*weighted images demonstrating a zone of phase cancellation artifact and subchondral bone fluid in the presence of fat (in bone) similar to the previous images

Study sequence combinations Combinations of images in different sequences are utilized for a final MRI diagnosis. This may allow for “aging” some lesions as they will have different characteristics on the different series of images that vary with the age of the lesion, especially with soft tissue. Some different sequences will demonstrate lesions similarly, and it will take combinations of images to determine the true nature of the lesions. Images acquired in different planes are required to verify the existence of a lesion for certain. The following series of images demonstrate some of the different characteristics seen in the various sequences that comprise a study.

Fig. 10& 11: T1-weighted (left) and T2*-weighted appearance of the same lesion in the deep digital flexor tendon.

Fig. 12&13: These two T2-weighted FSE images demonstrate hyperintense signal in one lobe of the deep digital flexor tendon but are not so relatively intense as the previous images of the same lesion, emphasizing the different appearance of structural alterations compared with inflammation and fluid accumulation in differenct sequences. This lesion is relatively recent but chronic changes within the navicular bursa were likely there before severe disruption occurred. As previously stated, MRI can be of significant benefit in identifying the true nature of pathology in lameness issues that can be localized but not specifically identified. Another example below in Fig. 14&15 illustrates an example of a chronic lameness that was transiently responsive to intra- articular therapy but would soon become lame again. Diagnostic blocks had localized the lameness to the foot and likely the distal interphalangeal joint. Radiographic evaluation had been inconclusive. Further sequences clearly defined the nature of the problem.

Fig. 14&15: Chronic lameness with palmar foot pain demonstrating subchondral osseous cyst- like lesion that communicates with the joint space not readily apparent on radiographs.

Fig.16 &17: T2*-weighted image on the left demonstrates a hyperintense area (cyst) in P3 surrounded by hypointense signal that may be phase cancellation artifact or sclerosis. The STIR image on the right demonstrates an area of hyperintense signal within P3 surrounded by hypointense signal confirming that it is sclerosis and not fluid and phase cancellation artifact. Summary Basic knowledge of MRI principles and an understanding of the relative significance of lesions noted in the MRI report can contribute greatly to developing a therapeutic plan and prognosis for the patient and client. Comfort with MRI basics and what can be seen may make the practitioner somewhat more willing to refer earlier on to expedite a positive diagnostic process. Although there is expense involved, the ultimate cost of a more direct process may prove to be a savings for the client and reduce unnecessary treatment of the patient. References

23 1. Bassage LH and Ross MW. Diagnostic analgesia. In: Ross MW and Dyson SJ, ed. Diagnosis and Management of Lameness in the Horse, St. Louis: Saunders 2003;93-124 2. Murray RC, Blunden TS. Schramme MC, Dyson SJ. How does magnetic resonance imaging represent histologic findings in the equine digit? Vet Radiol Ultrasound 2006;47;17-31 3. Bolas N. Basic MRI principles, In: Equine MRI, Ed. Murray RC, Wiley-Blackwell, West Sussex, 2011 pp 3-37 4. Gold SJ. How to interpret a distal limb magnetic resonance imaging report, Proc. AAEP, 2015 pp. 360-368 5. Quiney LE, Ireland JL, Dyson SJ. Evaluation of the diagnostic accuracy of skeletal scintigraphy in lame and poorly performing sports horses. Vet Radiol Ultrasound. 2018;59:477–489 6. Tucker RL. Equine Musculoskeletal MRI, MR Imaging of the Equine Musculoskeletal System, WSU, Coeur d’Alene, Idaho, USA, Jan. 2004 7. Holowinski M, Judy C, Saveraid T. Maranda L. Resolution of lesions on STIR images is associated with improved lameness status in horses, Vet Radiol Ultrasound, 2010;51; 479-484

24 DIAGNOSIS AND MANAGEMENT OF SELECTED HINDLIMB LAMENESS ISSUES AND THOUGHTS

Michael W. Ross, D.V.M., Diplomate, ACVS Professor of Surgery University of Pennsylvania -- Kennett Square, Pennsylvania, USA [email protected]

Synopsis: Hindlimb lameness continues to be a mystery in some horses given the lack of obvious clinical signs and similar gait deficits seen in horses with disparate sources of pain causing lameness. Gait deficits, clinical characteristics, definitive diagnosis using the hallmark of relevance, diagnostic analgesia, and management of lameness issues from the common to the obscure will be highlighted.

Overview and Perspective* In my referral practice at the University of Pennsylvania’s New Bolton Center I saw between 300- 400 horses each year for various lameness problems. A majority were young performers, young racehorses in various stages of training/racing, including both Standardbred (STB) and Thoroughbred (TB) racehorses. I evaluated Sport Horses (SHs), hunters, jumpers, dressage and event horses, and saw many horses each year for poor performance. A common complaint in SHs and in some racehorses is the suspicion of an upper limb problem (usually hindlimb/pelvic issue is suspected), “something up high”, feels like the problem is “up high” or in the back. In fact, many horses with hindlimb lameness are often suspected of having back pain as a primary complaint, whereas the authentic problem lies elsewhere. Back pain specifically, and axial skeletal pain in general, are common complaints, yet I usually find at least one and usually numerous additional sources of pain. In my practice, authentic back pain as a sole cause of gait deficits or poor performance is rare. Even in SHs suspected of having back pain because of failure to round properly over fences, failure to bend properly while turning and other common clinical signs associated with back pain, I find other sources of hindlimb lameness. Careful clinical examination and advanced imaging are critical for accurate diagnosis. I approach examination of horses suspected of having back pain or suspected of having hindlimb lameness from the ground up – first eliminating the traditional sources of pain manifested from both hindlimb and forelimb lameness issues. It is important to note that forelimb and hindlimb lameness can often be confused and careful clinical examination is necessary. Information gained from quizzing the rider/trainer is often erroneous when it comes to identifying the authentic source of pain causing lameness. In most horses suspected of having back pain, or axial skeletal pain in general,

25 an additional source of hindlimb or forelimb lameness is commonly found, and the horses gait improved even before investigating the axial skeleton for a source of pain. Most of these horses have been through weeks-to-months of various therapeutic regimens including massage therapy, chiropractic manipulation and other forms of treatments aimed at suspected back or neck pain. Many horses I examine have back and neck pain as a compensatory/co-existent issue secondary to chronic hindlimb lameness.

Back Pain is Most Obvious in Horses While Ridden Horses suspected of having back pain are best evaluated while ridden. In SHs the difference in gait between what is seen while examining the horse in hand or while on a lunge line, even when saddled, and that seen while ridden, can be quite striking. Bucking and other signs of “nappy behavior” can be quite prominent when horses are ridden yet be unseen when examined in hand or while being lunged. Be aware, however, that hindlimb lameness can be much more obvious in horses while ridden when compared to what is seen at a trot-in-hand. Careful use of diagnostic analgesia is critical to differentiate horses with back pain from those with hindlimb lameness. Middle-aged to older horses used over fences appear to be most at risk of developing authentic back pain.

Hindlimb Diagnostic Analgesia in Horses Evaluated at a Trot-in-Hand Whenever possible I use perineural techniques working from a distal-to-proximal direction. I use a slightly different strategy in racehorses in the distal limb. Since fetlock region pain is quite prevalent, I avoid using the basisesamoidean or abaxial sesamoidean techniques (see notes Unravelling the Mystery of Diagnostic Analgesia). I use plantar digital analgesia, followed by a dorsally directed subcutaneous ring block, and then use the low-plantar technique (low 4-point). If I suspect the horse has subchondral bone pain I will use a modified approach (separately block the lateral and medial plantar metatarsal nerves). I will then proceed to a subtarsal block (I prefer conventional high plantar technique), peroneal (fibular)/tibial (P/T) and then intra-articular (IA) stifle analgesia. Be aware the peroneal/tibia can take 30-45 minutes for full effect and do not move to IA analgesia of the stifle too quickly. Occasionally horses will knuckle from extensor muscle blockade with this block; thus, I do not usually perform this block in horses ridden. In racehorses, IA analgesia of the coxofemoral joint, sacroiliac joint, and local analgesia of the dorsal spinous processes or other axial skeletal blocks are usually not necessary. In SHs, I will use the abaxial sesamoidean block in place of the dorsally directed ring block, since fetlock region pain is less prevalent. The rest of the limb is identical to the racehorse.

Hindlimb Diagnostic Analgesia in Horse Ridden It is extremely important to have an experienced rider working with you when evaluating horses ridden. Much information about how the horse feels on the diagonals at trot, bending, propulsion

26 and willingness to go forward can be obtained. Experienced riders can, however, make gait look better and more collected than inexperienced riders, so beware. Because of concerns about loss of proprioception with perineural analgesia in general, and knuckling from the P/T block, specifically, I change strategies in horses ridden as compared to those blocked while evaluated in hand. I use IA analgesia for joints and deep injection of the origin of the suspensory ligament (sub-tarsal) rather than completing the conventional high-plantar (high 4-point) technique. I avoid use of the P/T block if possible.

Diagnostic Analgesia of the Axial Skeleton I see very few horses in which I employ axial skeleton diagnostic analgesic techniques. If suspicious of pain from dorsal spinous processes or if areas of increased radiopharmaceutical uptake are identified I will use local infiltration (5-10 ml of mepivacaine at each site at the summit and along each side of the involved dorsal spinous processes). I use a technique like that described by Dyson to block the sacroiliac joints.1,2 I use ultrasonographic guided injection of the cervical facet joints for diagnosis and management of cervical pain from OA of these joints.

Scintigraphic Examination of the Spine and Upper Limbs The upper limbs and spine are often incriminated as the source of pain in the lame horse but when diagnostic analgesic techniques are used the authentic source of pain is most often localized to the lower forelimbs or hindlimbs. Riders, trainers and veterinary colleagues often comment that the horse looks like an “upper limb lameness” based on gait deficits or how the horse “feels” while ridden. There are few pathognomonic signs of upper limb lameness and in fact, many horses with primary or secondary pain associated with the thoracolumbar spine or sacroiliac region are often examined for poor performance rather than overt lameness. Since in many horses radiography of the upper limbs (hindlimb in particular) is difficult to obtain in the standing patient scintigraphy has been very useful to comprehensively evaluate these regions. There are many important considerations. Flow phase imaging can be used to evaluate the terminal aorta and branches in horses suspected of having thromboembolism. Pool (soft tissue) phase images of the upper limbs and spine are of little value (poor sensitivity) since retention of radiopharmaceutical in the large vessels, early uptake in the urinary tract and early bone uptake complicate interpretation. Delayed (bone) phase images are of tremendous value but several factors are important. In the upper limbs additional views such as medial, flexed lateral and cranial images are difficult or impossible to obtain. When possible, cranial views of the elbow, humerus and shoulder regions and caudal views of the stifle, femur and pelvis should be performed. Pelvic images should include right and left hemipelvic, cranial and caudal transverse pelvic, oblique (improves geometry of images of the ilial wing in horses suspected of having stress fractures), and caudal pelvic views. For the thoracolumbar and cervical spine both right and left lateral images should be taken to improve image resolution and to avoid missing unilateral lesions. Dorsal images of the thoracolumbar (TL) spine can be taken. Kidney uptake (right > left) is always present. Motion is a considerable problem because of body sway and motion correction software is useful (not mandatory). Assistants to steady the horse for pelvic images and a stationary

27 stand on which to rest the head can help minimize motion. Furosemide and bladder catheterization can reduce background radiation. Subtraction and masking techniques after image acquisition can be performed. Profile analysis and other quantitative techniques have been used in people for many years to evaluate areas of increased radiopharmaceutical uptake (IRU) of the pelvis, in particular, the sacroiliac region and recently have been validated in the horse.1,2 Abnormal areas of IRU include pelvic stress fractures, IRU of the sacroiliac/tuber sacrale, sacral and caudal vertebral fractures, enthesopathy or fracture of the tubera ischii and third trochanter, coxofemoral OA, articular and non-articular fractures, and fractures of the tubera coxae.3 Relevant and incidental areas of IRU of the dorsal spinous processes, vertebral body fracture (TL and cervical spine) and dorsal articular facet IRU (OA) can be seen. Localized or widespread IRU of skeletal muscle is seen in delayed images.

Detection of hindlimb lamaness4 Historically there has been confusion in the descriptions of hindlimb lameness. An important principle in the recognition of hindlimb lameness is the concept of the pelvic hike or asymmetrical movement of the pelvis. This has also been termed “hip hike” but I prefer the term pelvic hike because it accurately describes how the pelvis is moving in a horse with unilateral hindlimb lameness. The entire pelvis appears to be undergoing elevation, not just the lame side of the pelvis. Since there are 2 “hips” and only 1 pelvis, the term pelvic hike seems preferable. Pelvic hike is the vertical elevation of the pelvis when the lame limb is weight bearing. In other words the pelvis “hikes” upwards when the lame limb hits the ground and moves downwards when the sound limb hits the ground. “… the haunch settles downward when the sound leg touches the ground…”5. Some clinicians find it easier to see the downward movement of the pelvis, on the side of the lame limb, rather than the pelvic hike.8 It may be simpler to determine on which side there is most movement, rather than looking for either a hike or a drop.8 The observer must keep in mind that the pelvic hike is the clinical impression of the change in height of the pelvis, not the absolute or measured height. It is the shifting of weight or load that occurs as the horse tries to reduce weight bearing in the lame limb and transfer weight to the sound limb. Another explanation for asymmetrical movement of the pelvis involves one of the protective or compensatory mechanisms used by the horse to assist in break-over and minimize load on the lame limb. Many horses with hindlimb lameness drift away from the lame limb towards the sound limb. Drifting may decrease the magnitude of the observed pelvic hike but more importantly, makes the lame side look lower than the sound side. Therefore, it is important to watch the entire pelvis as a unit rather than the individual sides of the “hips.” In most horses with hindlimb lameness, in those without a substantial tendency to drift away from the lame limb, the elevation of the pelvis (pelvic hike up) when the lame limb hits the ground surpasses that when the sound limb is weight bearing. This can be seen readily when evaluating videotape both in real time and slow motion but may not be as obvious during clinical examination. It is helpful to observe horses with hindlimb lameness from the front as the horse is trotting towards you. This allows the pelvic hike to be seen clearly using the horse’s top line as a frame of reference.

28 Subtle pelvic elevation is best seen from this perspective. The use of markers on a fixed part of the pelvis can help to identify asymmetry. Stride length characteristics, height of foot flight, sound, and fetlock drop are also helpful. Horses with bilateral hindlimb lameness may have a short, choppy gait, lacking impulsion, but there may be no pelvic hike. Other methods to exacerbate the baseline lameness need to be performed, such as circling the horse at a trot in hand or while on a lunge line. Lameness may be accentuated when the lame or lamer limb is on the inside or outside of the circle (see below).

How and When Can Hindlimb Lameness Be Confused with Forelimb Lameness? It is important to understand how a horse with unilateral hindlimb lameness modifies its gait so that hindlimb lameness can mimic forelimb lameness at the trot. When the lame limb hits the ground, the horse shifts its weight cranially to transfer load away from the lame limb. This causes the head and neck to shift forward and nod down at the same time. The contralateral forelimb bears weight simultaneously with the lame hindlimb and the head nod coincides, thus mimicking lameness in the forelimb ipsilateral to the lame hindlimb. Head and neck movement in horses with hindlimb lameness is not always observed. In order to see compensatory head and neck movement horses must generally have prominent (>3 out of 5, see below) hindlimb lameness. At the pace, a lateral gait, LH lameness mimics RF lameness and RH lameness mimics LF lameness. Horses can have a head and neck nod from singular forelimb lameness, from singular ipsilateral hindlimb lameness, or concurrent forelimb and ipsilateral hindlimb lameness. A prominent head nod is seen in horses with simultaneous LF and LH lameness. The examiner must first determine whether both limbs are affected. Problems arise since a horse with only LF lameness may shorten the LH stride at the trot, leading the examiner to question whether or not LH lameness also exists. Horses with only LH lameness can have a rather pronounced head nod, so the examiner may question the existence of LF lameness. Although a horse with LF lameness may have a compensatory shortened stride of the LH, in the absence of lameness there should not be a marked pelvic hike. A head nod seen consistent with a LF lameness may be inappropriately severe to be caused by mild LH lameness. If a horse has simultaneous LF and LH lameness it is essential to nerve block the hindlimb first, because moderate to severe hindlimb lameness produces head and neck nod that will not be abolished unless the hindlimb lameness is resolved. With resolution of the hindlimb lameness you expect to see resolution of the pelvic hike and reduction in the head nod. Simultaneous lameness of a diagonal pair of limbs is less common than simultaneous ipsilateral lameness, except in trotters, since many horses perform at gaits that induce compensatory lameness either in the contralateral or ipsilateral limb. With simultaneous LH and RF lameness the head nod reflects the forelimb component, a mandatory clinical sign for perception of RF lameness. The horse may drift away from the LH and have a shortening of the cranial phase of the stride. The horse may have a short, choppy stride, both in the forelimbs and hindlimbs. The horse may

29 have a rocking gait. It cannot shift weight or compensate from stride-to-stride in the usual fashion, so it tends to rock back and forth from the hindlimbs to the forelimbs. In general, there is reasonable agreement between clinical recognition of hindlimb lameness and that found experimentally. Using markers placed on each tuber coxae of 13 horses with unilateral hindlimb lameness, there was a consistent increase in vertical displacement of the pelvis during early weight bearing of the lame limb.6 While the rise and fall of the pelvis was readily apparent and occurred consistently with weight bearing of the lame and sound limbs, respectively, the absolute height of the pelvis on the lame side did not rise above that of the lame limb.6 These findings are consistent with my clinical impressions. A head nod down when the diagonal forelimb was weight bearing, further confirmed clinical observations that hindlimb lameness can mimic lameness of the ipsilateral forelimb.7 In a kinematic study using a 3 dimensional optoelectronic locomotion system hip acceleration quotient increased in horses with hindlimb lameness.7 Vertical displacement corresponded to the pelvic hike up on the lame leg, with a simultaneous forward movement of the head and neck during the stance phase of the lame limb.7 GRF has been measured in normal horses and those with forelimb and hindlimb lameness.8-11 There is a reduction of GRF in the lame forelimb or hindlimb with compensation by the other limbs. With unilateral forelimb lameness, decreased horizontal GRF in the lame limb is compensated by increased GRF in the contralateral forelimb and ipsilateral hindlimb.12 Decreased vertical GRF in the lame limb is compensated by increased vertical GRF in the contralateral forelimb during the swing phase of the lame limb, and increased vertical GRF in both the ipsilateral and contralateral hindlimbs during the stance phase of the lame limb.12 During unilateral hindlimb lameness, the decreased GRF in the lame limb is compensated by increased GRF in the contralateral hindlimb, and in both the contralateral and ipsilateral forelimbs.9 This experimental data supports the clinical impression that a lame horse adapts by shifting load to the contralateral limb, or by shifting load in a caudal direction for forelimb lameness and in a cranial direction for hindlimb lameness. Using the optoelectronic Selspot II system and expert vision analysis high speed video system for motion analysis, it has been confirmed that horses with hindlimb lameness show false lameness in the ipsilateral forelimb.13 However, contrary to my clinical observations, 6 of 10 horses with severe forelimb lameness showed “false” lameness of the diagonal (contralateral) hindlimb.13 Review of videotape of lame horses reveals false lameness in the diagonal or ipsilateral hindlimb depending on several factors. Horses with pronounced forelimb lameness may look lame in the diagonal hindlimb. Horses with marked shortening of the cranial phase of the stride may appear lame in the ipsilateral hindlimb. Horses with forelimb lameness being circled with the lame limb on the inside may look lame in the ipsilateral hindlimb. Thus, analysis of lameness can be complex and determination of the lame limbs may not become clear until diagnostic analgesia is performed.

30 Hindlimb and Forelimb Lameness Can Be Differentiated Using the Key Clinical Observations

The Key Clinical Observations to Lameness Recognition

Head and neck nod (undulation, movement, HNN) – the head and neck will elevate (rise) to unload a lame (the lamest) forelimb and settle back to baseline (nod down) during weight-bearing of a sound (or less lame) forelimb. Differences between clinicians exist regarding which portion of the undulation is most easily recognized (I see nod DOWN). A HNN can be a result of forelimb pain, ipsilateral hindlimb pain (a horse with > 3 out of 5-degree hindlimb lameness will manifest a HNN mimicking ipsilateral forelimb pain) or coexistent ipsilateral forelimb and hindlimb pain.

Pelvic hike (rise and settling, PH) – the pelvis will rise (hike up) during protraction (advancement) of a lame hindlimb to unload weight and drop (settle) during weight-bearing to load the sound (or less lame) hindlimb. The pelvis is a single unit and PH is observed by evaluating a fixed point rather than comparing movement of right and left. Differences between clinicians exist regarding which portion of the PH is most easily recognized (I see hike UP). A HNN without PH is forelimb lameness; a HNN with PH is either ipsilateral hindlimb lameness or both forelimb and hindlimb lameness.

Shortening of the cranial phase of the stride (SCPS) – a hugely important observation is a measure of the horse’s willingness to put a limb in front of the contralateral limb during protraction. A horse will shorten the cranial phase of the stride in the lame limb and the diagonal limb (a stride-to-stride adjustment the horse must make to maintain balance during trot). SCPS in a diagonal limb occurs with singular forelimb or hindlimb lameness,but may represent authentic coexistent diagonal lameness. Diagnostic analgesia begins in a forelimb in horses with HNN or in a hindlimb if a PH is observed. Resolution of an abnormal SCPS of both the principal and diagonal limbs represents a key observation when blocking.

Fetlock drop (FD) – unless a horse has severe suspensory desmitis in which there is a substantial loss of fetlock support, the horse will hyperextend (dorsi-flex, drop) the fetlock that is receiving more load (the less lame limb) when compared to the lame limb. During real time this observation takes practice but can easily be seen using slow-motion video. For example, a horse with LF lameness will drop the RF fetlock more than the LF fetlock during trot (a SCPS LF/RH and HNN will be observed as well).

31 Drifting – a horse will drift away from a lame hindlimb if lameness is pronounced ( > 3 out of 5 degrees). For example, a horse with substantial LH lameness will drift to the right, have a SCPS in the LH/RF, a PH during LH protraction and may have a HNN consistent with LF lameness. Drifting in horses with forelimb lameness is rare but can occur with carpal pain where horses appear to be pushing away to the contralateral side.

Bonus observations include the use of sound, observation of a toe drag, and recognition of a short, choppy gait. Sound can be useful - if unshod horse’s hoof strike may be difficult to hear and fairness dictates if horses are shod they must be shod symmetrically. The principle is a horse will manifest a softer hoof strike on the “lame diagonal” (if the horse is lame in a LF, the lame diagonal is the LF/RH) and land harder/louder on the “sound” diagonal. Horses with asymmetrical front feet (large, platter-like foot compared to a small, upright foot) may lead you astray. Hindlimb toe drag is common but is sometimes subtle and can best be seen during slow motion replay of lameness examination video segments. I have seen toe drag most commonly in horses with stifle pain and in those with proximal suspensory desmitis, but it can be observed with any source of pain. Often after diagnostic analgesia a toe drag may persist even in horses in which PH abates. The short, choppy gait is common in horses with bilateral or quadrilateral lameness in which pain is symmetrical. In racehorses, subchondral bone pain originating from the distal aspects of the third metacarpal and metatarsal bones is the most common reason for this gait (not foot pain) whereas in non-racehorses such as western performance horses this gait is typical of bilateral foot or distal hock joint pain.

These observations are made when trotting horses in a straight line on a hard surface. Observations made during walk and comparing gaits at walk and trot are valuable lameness tools. Some horses with upper forelimb pain (elbow, shoulder regions) may manifest a HNN, which is more prominent (magnitude of the undulation) at a walk than at a trot. A horse with severe hindlimb lameness and SCPS when trotting, which has a decreased caudal phase of the stride when walking commonly have pain originating from the digit or the pelvis. There are numerous classic gait deficits easily recognized during movement. A simple, highly productive test for the effect of turning on the magnitude of baseline lameness is to circle a horse. Circling will often reveal pronounced lameness not see at a trot in a straight line particularly in horses with bilateral, nearly symmetrical lameness in which a short, choppy gait is not apparent.

References 1. Dyson S, Murray R, Branch M, et al. The sacroiliac joints: evaluation using nuclear scintigraphy. Part 1: The normal horse. Equine Vet J 2003;35:226. 2. Dyson S, Murray R, Branch M, et al. The sacroiliac joints: evaluation using nuclear scintigraphy. Part 2: Lame horses. Equine Vet J 2003;35:233. 3. Davenport-Goodall CLM, Ross MW. Scintigraphic abnormalities of the pelvic region in horses examined because or lameness or poor performance. 128 cases (1993-2000). J Am Vet Med Assoc 2004;224:88. 4. Modified from: Ross MW. Movement. In Ross MW, Dyson SD (eds): Diagnosis and Management of Lameness in the Horse. Philadelphia, Saunders, 2002, pp60-73. 5. Liautard A. Lameness of Horses. New York, William R Jenkins Press, 1888, p16. 6. May SA, Wyn-Jones G. Identification of hindleg lameness. Eq Vet J 1987;19:185-188. 7. Buchner HHF, Kastner J, Girtler D, et al. Quantification of hindlimb lameness in the horse. Acta Anat 1993;146:196-199. 8. Gingerich DA, Newcomb DM. Biomechanics in lameness. J Eq Med Surg 1979;3:251- 252. 9. Gingerich DA, Auer JA, Fackelman GE. Force plate studies on the effect of exogenous hyaluronic acid on joint function in equine arthritis. J Vet Pharmacol Therap 1979;2:291- 298. 10. Gingerich DA, Auer JA, Fackelman GE. Effect of exogenous hyaluronic acid on joint function in experimentally induced equine osteoarthritis: dosage titration studies. Res Vet Sci 1981;30:192-197. 11. Schamhardt HC, Merkens HW. Quantification of equine ground reaction force patterns. J Biomech 1987;20:443-446. 12. Merkens HW, Schamhardt HC. Evaluation of equine locomotion during different degrees of experimentally induced lameness II: Distribution of ground reaction force patterns of the concurrently loaded limbs. Eq Vet J Suppl 1988;6:107-112. 13. Uhlir C, Licka T, Kubber P, et al. Compensatory movements of horses with a stance phase lameness. Eq Vet J Suppl 1997;23:102-105. * Modified from Proceedings, Belgian International Congress of Equine Veterinarians and Farriers, 2009 and, Proceedings, South African Equine Veterinary Association Meeting, 2010

33 INJURIES OF THE SAGITTAL GROVE OF THE PROXIMAL PHALANX – A DIAGNOSTIC DILEMMA

Michael W. Ross, D.V.M., Diplomate, ACVS Professor of Surgery University of Pennsylvania -- Kennett Square, Pennsylvania, USA [email protected]

Synopsis: Mid-sagittal fractures are a classic form of severe injury of the proximal phalanx (PI) and while they most commonly occur in the race horse, these fractures represent the most common long-bone fracture in the non-racehorse. Horses with injuries such as traumatic collapse of the articular surface resulting in subchondral cyst-like lesions can be problematic. Important clinical characteristics of lameness associated with these injuries, why they can be a challenge in diagnosis and management will be highlighted.

Overview and Other Thoughts on Diagnosis

Unlike my other lectures where I am speaking on broad, general topics, in this lecture, the discussion focuses on a specific area, the sagittal grove of the PI. Why are injuries in this area a dilemma? Well, it depends on the type of horse you are evaluating, the age, discipline and degree of lameness. In racehorses, the most common injury by far is the mid-sagittal fracture. While fractures are unusual in sports horses (SHs), sagittal fracture of the PI is likely the most common fracture that occurs this sporting discipline. The proximal aspect of PI has a few radiological peculiarities, such as a small “notch” that occurs normally, which can easily be misinterpreted as a fracture (see below). The notch can be seen only on a dorsoplantar/palmar (DP) radiographic image and is most common in the hindlimb. While it may be present in 5-10% of horses, it is often bilateral and taking an image of the contralateral hindlimb is always a good approach for further information. Rarely, there will be a small radiolucent line or notch not involving the sagittal groove, seen on the DP image, which I have seen most commonly in young Thoroughbred (TB) racehorses in the forelimbs. Neither of these incongruities should be misinterpreted as fracture.

Horses with authentic fracture of the PI will often have pain on palpation of the dorsal cortex. Of course, this will depend greatly on whether the fracture involves the dorsal cortex. Most do, but some do not. Horses with incomplete fracture often do not have effusion; effusion is more likely in horses with longer fracture or those with subchondral erosive or traumatic lesions of PI (see below) and those with lesions associated with ongoing, progressive osteoarthritis (OA). Horses

34 with authentic fracture will often exhibit profound lameness while turning (hence some describe these as “screw driver” fractures – it with torsion, pain increases from fracture movement?).

Clinicians should be aware that the proximal phalanx is by far the most common bone to fracture after diagnostic analgesia. I say this not to dissuade clinicians from pursuing diagnostic analgesia, arguably the most useful clinical procedure to determine clinical relevance and localize the source of pain causing lameness. But, if the clinician feels likely a horse has a fracture of PI it behooves them to consider another approach to diagnosis – scintigraphic or MRI examination, or waiting to see the results of follow-up radiological examination before blocking. If my memory serves me correctly, I can recall only one horse that “shattered” a bone, or perhaps less dramatically developed further propagation of a fracture during/after diagnostic analgesia that was not a fracture of PI; and, that horse developed a displaced fracture of the middle phalanx after palmar digital analgesia. The bottom line - beware of blocking a horse suspected of having a PI fracture.

The proximal aspect of PI is not a common site for the occurrence of subchondral bone cysts developed because of osteochondrosis (OC). I have seen numerous older horses with bone cysts involving the distal aspect of PI, the proximal aspect of the middle phalanx and the distal phalanx, with rather sudden onset of lameness, and initial radiological examination reveals the presence of a “mature” bone cyst. In other words, the cyst was there long before the onset of clinical signs. I have no easy explanation. Horses that develop “cyst-like” lesions of proximal PI likely suffer from some form of acute trauma and radiological signs often are subtle but become more obvious over time. These “cyst-like” lesions are the result of trauma. Speaking of “cyst-like” lesions, I do not like the term “cyst” to describe radiolucent defects simply because the connotation is that they developed because of OC, since that is a common pathogenesis in the horse. The lesions to which I am referring are acute, traumatic lesions of the PI, not those that are true subchondral bone cysts because of OC.

Specific Conditions

Fractures - can be short, long-incomplete, long-complete and displaced and usually are relatively straight-forward to diagnose. A fracture of the PI MUST be differentiated from a small variable- in-length “notch” that occurs in the sagittal grove of the PI (much more common in the hindlimb). Many horses are diagnosed with fractures that are a variation of normal (the notch is normal) and it may be useful to obtain a digital radiographic image of the opposite PI with which to compare. Alternatively, an imaging modality that includes the ability to differentiate bone activity such as scintigraphy or magnetic resonance imaging (MRI) can be extremely useful; in the “old days” we would wait 12-14 days from the original radiographic study and obtain an additional set of images and look for changes in length and character of the defect seen in the dorsoplantar/palmar (DP) image and for signs of proliferative changes along the dorsal, proximal aspect of PI. Incidentally,

35 mid-sagittal fractures of PI are single-event injuries rather than repetitive stress injuries, at least in my opinion. This is not the case for dorsal plane fractures of PI.

Horses with authentic sagittal fractures of the proximal phalanx can be managed successfully with conservative or surgical management. The recommendation is based on fracture length, experience, owner financial commitment and of course other factors. Authentic fractures of any bone heal with time, but debate often revolves around quality of articular healing, speed of fracture healing, and recurrence. Horses with short, incomplete fractures heal equally well with screw fixation or conservative management.1 In general a surgeon should question the efficacy of a screw if it does not cross the fracture line; if this is the case the fracture must extend at least 10 mm distal to the sagittal groove in order to safely insert a screw (inserting the screw closer than 5 mm from the articular surface my result in subchondral bone pain?). Without computed tomography (CT) in horses with incomplete fracture (incomplete from a perspective that the fracture does not traverse from dorsal to plantar/palmar aspect of PI) a surgeon does not know a screw traverses the fracture line either, making putting in a screw in horses with short fractures questionable. However, experience suggests putting in a bone screw does make some sense and may augment healing without traversing the fracture line (bone-screw interaction?). In horses with longer fractures, those with gaps in the fracture line, or in those with displacement, surgery is mandatory. In these horses I use a “stacked repair” proximally, placing 2 screws across the proximal aspect of PI rather than using a conventional single-screw approach. I do not attempt to place screws in the distal most aspect of an incomplete fracture since without CT (and even in some horses with CT) a surgeon cannot be sure the distal-most screw will not act as a stress concentrator. I always recover horses from general anesthesia with a fiberglass cast incorporating the foot for hindlimb fractures and at a minimum a cast/bandage or cast for forelimb fractures.

Traumatic radiolucent defects in the sagittal groove of PI (TRDSGPI)– These defects in the sagittal grove of PI occur most commonly in SHs, and in the hindlimbs more than the forelimbs at least in my experience. Often, the size and shape of the radiolucent defect changes from the initial radiographic examination, starting from barely visible to obvious “cyst-like” lesions (see above). These lesions often develop in horses with preexisting OA making it compelling to describe the pathogenesis as a lesion that results from chronic, repetitive stress injuries (like subchondral lucency of the third carpal bone) – table-surface collapse of the cartilage and bone in the sagittal groove. A similar lesion develops on the distal, dorsal surface of the medial Mt/McIII condyle in SHs as well, usually in those with pre-existing OA; I believe the pathogenesis is similar. Management however in those horses is curettage and the prognosis is guarded at best.

I recommend surgical management of horses with TRDSGPI and have taken lessons learned from managing subchondral bone cysts from the medial femoral or other areas such as those involving the distal aspect of PI, the middle phalanx, distal phalanx and proximal, medial aspect of the radius. However, please keep in mind in those locations radiolucent defects most often result from OC

36 whereas TRDSGPI are traumatic in origin. The best way to surgically manage these horses is to use pre-operative CT to plan screw placement, since in many horses the lesion cannot be seen in a lateromedial (LM) radiographic image, so understanding where to put a screw in the PI in the dorsal-to-plantar/palmar direction is difficult. If the lesion is visible on both the DP and LM images, markers can be used to position a screw and CT is not necessary. Incidentally, CT will often reveal the lesion to look like fractures, but with increased radiopacity surrounding the radiolucent defect, documenting the chronic nature of the subchondral bone changers. While the radiolucent lesions can be drilled, I currently recommend cortex screw placement, and I put the screw in lag fashion. Transcondylar screw placement has been advanced as a new technique to manage medial femoral condylar cysts. 2,3 Lameness was eliminated in approximately 75% of horses when this technique was used, a result that compares quite favourably to other surgical methods to manage these lesions;2 experimental data supports the concept that a transcondylar screw alters the load placed on the proximal aspect of the tibial plateau in an ex vivo model to create subchondral bone cysts in the medial femoral condyle in equine cadaver limbs.3 I believe using a screw stabilized subchondral bone using compression, but importantly there is a bone/screw interaction that helps to heal the defect. It does not work in all horses (I will present a few cases). Four to 6 months of rest is recommended. In most horses the radiolucent defects heal but in some, lameness persists, and the radiolucent defect may enlarge. Of course, often prognosis depends on the degree of pre-existing OA.

TRDSGPI because of infection – lesions of the sagittal groove of PI or for that matter the distal aspect of Mc/MtIII or the proximal sesamoid bones can develop as a sequela of infectious arthritis. While unusual, erosion of articular surface and involvement of subchondral bone can be a complication of infectious arthritis. I recall a Standardbred racehorse with LF fetlock infectious arthritis that developed persistent severe lameness, in which a radiolucent defect developed in the sagittal groove of PI. Scintigraphy was useful to identify the lesion early in the process. Scintigraphy can be useful to identify subchondral bone involvement in such horses, and usefulness of this modality is not limited to the fetlock joint. Management of this horse was in the days before CT, but I drilled 2, 2.5 mm holes from lateral-to-medial and in fact cultured a Staphylococcus sp. from the drill filings. This horse was managed successfully using IA and intra- osseous (through drill holes) infusion of antibiotics. Decompression and access to infected bone was accomplished by drilling. Today, regional limb perfusion would be used as adjunctive therapy as well.

References

1. Tetens J, Ross MW, Lloyd JW. Comparison of racing performance before and after treatment of incomplete midsagittal fractures of the first phalanx in Standardbreds: 49 cases (1986-1992) J Am Vet Med Assoc 1997;210:82. 2. Santschi EM, Williams JM, Morgan JW, et al. Preliminary investigation of the treatment

37 of equine medial femoral condylar subchondral cystic lesions with a transcondylar screw. Vet Surg 2015;44:281. 3. Bonilla AG, Williams JM, Litsky AS, et al. Ex vivo equine medial tibial plateau contact pressure with an intact medial femoral condyle, with a medial femoral condylar defect and after placement of a transcondylar screw through the defect. Vet Surg 2015;44:289.

38 DIAGNOSIS AND MANAGEMENT OF SUSPENSORY BRANCH DESMOPATHY IN SPORT HORSES R. D. Mitchell, DVM, MRCVS, Dipl. ACVSMR Fairfield Equine Associates, Newtown, CT, USA

Introduction The most common site for lameness issues in the sport horse is the distal limb. The source of lameness can often be soft tissues involved in the suspensory apparatus. High-level show jumping, dressage and western performance horses often take several years to train to peak performance, and injuries or illness can substantially affect the time to produce a winning horse. Owners and trainers are concerned that these horses receive the best possible care without excess expense and down time. The veterinary care of such horses should take an aggressive approach to lameness diagnosis and rehabilitation of the horse in training, not simply attend to lameness after the horse is no longer able to train. Recognition of early problems involving the suspensory branches may prevent significant loss of training and competition time as well as extending the horse’s career. Additionally, accurate diagnosis allows for a more efficient and successful rehabilitation program. Risk Factors The distal limb plays a significant role for adaptation to footing and shock absorption during locomotion. In addition to the corium parietis acting as a ligament within the hoof and the digital cushion functioning in shock absorption,viiiixx the suspensory apparatus is crucial in absorbing the stress of impact and ground force reaction. Foot balance, both medial to lateral and dorsal to palmar can have a profound effect on the excursion of joints and the stress on soft tissues of the distal limb.xi Severely out of balance feet (medial to lateral) may therefore result in increased stresses on the suspensory branches. An extremely high heel structure may result in excessive fetlock drop which in turn stretches the suspensory ligament. Significantly toed-in or toed-out structure may abnormally stress one suspensory branch over the other, and an over in the knee structure can have some potential effect for increased suspensory ligament strain. Footing surfaces that are very hard, excessively soft or unstable can result in aberrant motion and stress that may result in injury. The demands of high-level sport result in more concussion as well as greater extension and flexion than casual exercise. Fatigue may not be as significant a factor in injuries of the sport horse (with exception perhaps for some endurance and combined training horses) compared to racing horses, but chronic repetitive trauma is thought to be a factor. Peruvian Paso horses often have what is believed to be a genetic predisposition for degenerative suspensory ligament disease (DSLD) and some Warmblood horses demonstrate a similar condition. Studies of DSLD in Peruvian Paso horses demonstrated that abnormally elevated levels of ligament proteoglycans (PGs) and aggrecans result from disruption of the normal homeostatic turnover process. Horses with degenerative suspensory ligament disease had changes in the collagen matrix similar to the characteristics of a non-healing wound with the

39 accumulation of aggrecans and enzymes responsible for their degradation. It has been proposed that ligament failure in DSLD results from a process involving tissue inflammation and the complexation of ADAMTS5, an aggrecanase.xii It is plausible that a similar process may occur at a lesser level in otherwise normal suspensory ligaments repeatedly subjected to stress and overload. This is yet to be proven in otherwise normal horses and is disputed to be the cause of DSLD by some investigators. It is interesting to note that many apparently asymptomatic horses often have thickened suspensory branches and periligamentous fibrosis by the time lameness is recognized and an ultrasound examination is performed.xiii This would suggest some chronic reactive process rather than sudden structural failure. Research has yet to clearly define this process. Certainly, the level of physical activity in which the horse is engaged also has an effect as certain disciplines demonstrate tendencies for specific regions of injury.6 Tendon and ligament stiffness increases with age and may be a factor in adapting to load changes which may be a factor in desmopathies of older horses. History and Clinical Signs Horses most often present with a unilateral lameness of varying degrees (0-4/5), especially if circled or ridden which will be discussed later. Some lameness may be very subtle and will require special efforts to make it more apparent for an objective diagnosis. Many horses vary in their degree of lameness, improving profoundly with a few days’ rest. Such mild lameness issues may be best re-examined after a day or two of exercise. Suspensory branch lameness may present in an acute fashion with significant lameness, local edema and pain to palpation, but more often signs may be subtle with the horse having a mild to moderate lameness that changes somewhat with work. Fore limb lameness may initially present with a mild shortness of stride that “warms out” with on-going exercise. Fore limb lameness may be more evident working in a circle with the affected limb on the outside. Hind limb issues may mimic more commonly thought of conditions such as distal tarsitis or proximal suspensory desmopathy in that the horse is “weak” behind and “warms out” of the lameness. Some heat or swelling may be perceived in the suspensory branch region, but often this is not the case. Deep palpation of the suspensory branches and forced flexion of the fetlock often produces a painful response. Distal limb flexion most often enhances or produces lameness. Frequently, increased effusion is apparent in the fetlock joint and the examiner may be tempted to assume it is a fetlock synovitis or OA of primary origin. It should be kept in mind that the distal suspensory branch makes up part of the margin of the fetlock joint and intrasynovial injury may cause synovitis.xiv The current competitive environment in North America often allows for NSAID use in competing horses; medicated horses with mild suspensory branch pain can compete comfortably. However, when Tuesday morning rolls around and the effects of the NSAID are gone, the horse may suddenly be more uncomfortable than prior to the event, often with filling and easily identifiable morphological change. This presents a good opportunity to investigate the case. Physical Examination This author believes it is essential to have periodic veterinary inspections of the training sport horse to identify subtle lameness and performance problems before they become serious clinical

40 issues. Although many trainers and owners are very adept at catching subtle soundness and health related issues, many things may be overlooked by the individual that sees the horse every day.xv Periodic veterinary inspection should include a general health check and a thorough lameness evaluation. The frequency of these exams will be somewhat dependent upon the age and activity of the horse, but two to four times yearly should be a minimum for the competitive horse. Horses with successfully managed orthopedic disease may need to be checked more often. A typical lameness examination should first include a thorough visual exam of the horse taking notice of body symmetry and muscle structure. Observing the horse in its stall may give the examiner some clues regarding the horse’s level of comfort. Watching the horse step out of its stall may give big clues about chronic lameness issues, taking note of shortened or quick steps. After the visual inspection, a palpation examination should be performed. The author uses a modification of an “acupuncture” examination that allows for complete palpation of the horse while eliciting responses from potentially painful areas. Careful inspection of the feet for balance and symmetry should be performed. Flexion manipulations can then be performed in a “passive” sense (not asking the horse to walk or jog away) while noting any resistance or painful responses. More chronic suspensory desmopathy may be readily apparent on palpation of the limb and passive flexion may produce discomfort. It may be appropriate to use hoof testers at this point before starting any exercise. Next the horse can be moved in hand at a walk and trot taking note of any obvious lameness or unusual foot flight or limb motion. This is best performed on hard footing if available. It is useful to see the horse walk in circles as well as on a straight line. Likewise, jogging the horse in circles as well as in a straight line may provide much more insight related to the horse’s level of comfort. If the horse is too fractious to lunge in circles, jogging in hand on circles may provide an acceptable alternative. The author frequently gives a small dose of sedative (detomidine hydrochloride, 1.5mg total dose)1 to evaluate lameness if the horse is not well behaved. Watching the horse move in straight lines and circles on both hard and soft footing can be immensely valuable in detecting lameness. The next step is to perform flexion tests of all limbs with the horse then walking or trotting away. These may give clues to soreness that is not otherwise evident. Keep in mind that a positive distal limb flexion may indicate a problem in any number of places, from the distal interphalangeal joint (DIPJ) to even a proximal suspensory ligament issue. It’s a tool for regionalization and augmentation for observation purposes. Often suspensory branch problems yield positive distal limb flexion responses. Care should be taken to not over exert the very lame horse (>3/5) until one has a good sense of the nature of the problem. A detailed record of observations should be maintained for each examination. Following flexion tests, it is advisable to observe the horse work on a lunge line and under saddle. Some horses are difficult to lunge and may pose hazard for injury to horse and handler. These horses should be lightly sedated or simply watched under tack. Many lameness conditions are not otherwise apparent until a rider is aboard, and/or the horse is asked to do more work.xv

1 Dormosedan®, Pfizer Animal Health, Exton, PA, USA 19341

41 The riding examination may give the veterinarian a great deal of information not otherwise apparent during the in-hand exam. Rider weight may change the balance of the horse in such a way as to augment lameness. Weight on the back may be the source of discomfort and may be demonstrated by a change in the shape of the back, height of head carriage, shortening of stride, or disobedience. The horse should be asked to perform the various gaits while under saddle and carefully observed for changes in the level of lameness with each gait, transitions from one gait to another and at directional changes. Distal limb lameness is often exacerbated by circling especially on hard footing.xvi Directional changes may enhance this effect, and most significantly at the initiation of the change in direction. Suspensory branch issues of a mild nature may be much more obvious under saddle. Obvious lameness in the under-saddle examination may then enable the examiner to perform diagnostic anesthesia. Diagnostic anesthesia is the author’s next diagnostic procedure of choice following the physical examination if they are deemed safe relative to the severity of the lameness. If the degree of lameness suggests further damage may be incurred by exercise or exercise with regions desensitized, the author will go straight to radiography, or ultrasound in select cases.xvii Various nerve block techniques have been previously discussed in referenced literature.xviii Many lameness conditions look alike and flex alike, however they are not of the same origin. If the lameness is of sufficient grade to produce a clear contrast and has not been reduced by exercise, i.e. warming up, the examiner would be wise to pursue the lameness with diagnostic nerve blocks. Once localized, further physical examination, radiographs and diagnostic ultrasound may further help elucidate the nature of the problem. In some cases, physical examination and diagnostic imaging may be sufficient to clearly define the diagnosis, and in such cases nerve blocks may not be required, allowing the veterinarian to proceed with appropriate therapy.xix Most often suspensory branch issues will block to a low four point palmar/plantar nerve block, however occasionally some will response to abaxial sesamoid blocks and intra-synovial fetlock anesthesia. Occasionally, hsoundness can be achieved with a diagnostic block (1/2 of a 4 point block for example) just over the presumed affected suspensory branch. Keep in mind that going straight to a proximal suspensory block will affect the branches as well. Subtle suspensory ligament branch issues may require a combination of diagnostic anesthesia, radiography, ultrasound and perhaps MRI to fully assess the extent of injury to provide a better prognosis. Imaging Radiography may be very helpful in the assessment of the fetlock region and suspensory branch issues. Lesions of the proximal sesamoids (sesamoiditis) related to the areas of insertion of the suspensory branches may give the examiner a significant clue for the next step in the diagnostic plan. Lesions such as lysis and fragmentation may indicate significant enthesopathies of the suspensory branchesxx and dystrophic mineralization may indicate chronicity. Ultrasound examination is the next step in evaluating problems of the fetlock and distal metacarpal region. Good knowledge of the anatomy and understanding of mild pathological changes is required to properly evaluate the structures, but the suspensory ligament branches can be readily imaged in detail. Lesions occur in various locations along the course of the suspensory branch but injuries in the middle to distal one third of the branch are more common in this

42 author’s experience. Lesions may be general diffuse enlargement and hypoechoic character with no discrete “core lesion,” or focal anechoic marginal or centralized core lesions. Many lesions have a linear character and extend along the course of the branch frequently extending from the surface of the sesamoid proximally. Surface irregularities of the proximal sesamoids are common reflecting osteolytic lesions of the enthesis. Periligamentous fibrosis and dystrophic mineralization is often seen in more chronic lesions.

Fig. 1: Demonstrates periligamentous fibrosis and edema within the suspensory branch indicative of chronic active desmopathy Occasionally, nuclear scintigraphy can be useful in further regionalizing the source of the lameness. Areas of increased radiopharmaceutical uptake (IRU) are characteristic to some structures in working horses and knowledge of this is requiredxxi, but this imaging modality can be extremely helpful in evaluating the significance of the findings of other modalities such as radiography and ultrasound. A suspicious looking proximal sesamoid on radiography that demonstrates dramatic IRU on scintigraphy is thought to have more clinical significance and could reflect a significant suspensory branch enthesopathy. In recent years MRI has become more available to many equine practitioners for imaging lameness cases. While high field magnets may produce a more detailed image, they currently require general anesthesia for imaging. The standing units are low field magnets and image resolution is not as high, but they are nonetheless capable of providing diagnostic images in many, if not most cases. A specific region should be identified prior to the MRI as the ability to image multiple regions is limited. MRI provides increased detail of the anatomy and pathology of the fetlock and distal metacarpal region over other modalities currently used clinically.xxii Soft tissue issues not otherwise apparent may be readily visible with MRI. Changes in specific sequence signals related to processes such as bone inflammation, are often evident with MRI

43 before any appreciable radiographic changes are evident. The advantage in this is that detection of bone or ligament trauma and inflammation at an earlier stage may allow for more specific treatment modalities and exercise management. The previously discussed imaging modalities are those most often used by this author. Choosing appropriately from this combination of modalities should give the practitioner specific information that increases the significance of physical exam findings and local anesthetic blocks that lead to a reasonable diagnosis. This author prefers to revisit any MRI lesions identified in the suspensory branches with ultrasound in hopes of identifying such for future monitoring.

Fig. 2 & 3: A hyperintense lesion is present in the STIR FSE images in the lateral suspensory branch indicative of fiber pattern disruption and fluid infiltration. Treatment and Rehabilitation Techniques Acute presentations with heat, swelling and significant palpation discomfort should be initially treated with anti-inflammatory medications and physical therapies such as ice, poultice and support to cool out the initial injury. This often facilitates a better objective assessment of the nature of the injury. Initial fluid and hemorrhage that may be present in an acute injury/exacerbation can be misleading as to the extent and exact nature of the damage. Giving things a few days to stabilize may change the appearance and appreciation of the extent of injury. Therapeutic management and rehabilitation for suspensory ligament injuries branch injuries should start with assessment of the foot and shoeing status of the horse. Shoeing techniques can reduce suspensory ligament loading on initial weight bearing. A wider web at the toe and narrowed bearing surface in the heel region, which allows the heel to settle a bit more and the toe to “float,” allows the DDFT to accept relatively more load. A somewhat wider web of the shoe on the side of the affected suspensory branch is appropriate unless both branches are significantly affected. Medial to lateral “balance” should be assessed and modified for an even hoof strike if possible.

44 Intralesional and perilesional injections of PRP, stem cell preparations, bone marrow aspirate or extracellular matrix (ECM) may be very helpful to encourage healing with good organization. Intralesional injection of PRP followed by controlled exercise was reported in improve prognosis in a study of mid-body suspensory lesions in standardbred racehorses.xxiii Another study in yearling thoroughbreds treated for suspensory branch injuries with PRP suggested they were more likely to start as 2-year-olds but no more so as 3 or 4-year-olds, leaving the authors with the conclusion that such treatment was no more valuable for racing performance than saline injection.xxiv A report of the use of ultrasound-guided autologous bone marrow transfer used to treat suspensory body and branch core lesions in 30 racehorses indicated a likelihood of good prognosis for return to racing.xxv Intra-articular Autologous Protein Solution2 has been very useful in the treatment of concurrent fetlock synovitisxxvi and suspensory branch injuries that appear to have an articular component, in the author’s experience, in conjunction with supportive physical therapy (tbd). The author has also used this modified PRP product in suspensory branches, as well, with reliable results. Intralesional and perilesional treatment with urinary bladder matrix (UBM) has been an effective horse-side means for the management of suspensory branch injuries with similar outcomes to other more involved processes.xxvii Regenerative therapy with various agents has proven useful in more severe injuries of suspensory branches in the author’s experience and prompt treatment results in a better prognosis. Application of Class IV laser therapy or ESWT can encourage resolution of edema and generation of fibroplasia. Recently, shockwave therapy has been suggested to possibly improve healing response if used immediately post treatment with PRP in enhancing the release of growth factors, TGF-β₁ and PDGF-ββ.xxviii Shockwave therapy would then normally continue for a series of 3-4 treatments every 10-14 days. Class IV laser treatment is normally accomplished with an extended series of 15-30 treatments depended upon the nature of the injury. Healing responses have been very encouraging with this modality in this author’s experience. Suspensory branch healing is generally slow and requires a slow rehabilitation program over 4-6 months at a minimum. Additional stimulation with therapeutic ultrasound every other day for 3-4 weeks can be of benefit in minimizing edema and stimulating circulatory flow in the affected tissue following the use of previously suggested modalities.

2 ProStride APS, Owl Manor Veterinary, Warsaw, IN 46581-1217

Figure 4: Examples of a front foot (on left) and hind foot (on right) suspenory branch shoe

Fig. 5: Sound™ Portable RLT laser may prove helpful for management of tendon and ligament injuries

46 Recently a supportive apparatus for suspensory ligament injury from Horsepower Technologies Inc. has been introduced that is similar to knee braces made for human orthopedic use. This device has received extensive treadmill testing on horses at Tufts University exercising at a walk, trot and canter for extended trials, and thus far it has been well tolerated. This device functionally controls fetlock hyperextension and may prove useful in managing suspensory disease.

Return to activity There is no “cook book” recipe for rehabilitation of suspensory branch injuries of the sport horse.xxix Controlled studies of injuries coupled with rehabilitative plans simply have not been done that allow for blanket recommendations. A significant commitment from the owner, trainer and rider are necessary for successful outcomes. Regardless of the nature of the injury, time plays a big part in the rehabilitative process. It must be understood that, while truly unfortunate, some horses will not return to their previous level of performance. The nature of the tissue injury will dictate much of the rehabilitative process. Early passive mobilization of joints may minimize capsular fibrosis and joint stiffness, and limited activity may improve comfort in weight bearing. Significant injuries involving the suspensory branches

47 will require one to three months before any significant activity can begin, and it can be a challenge to regulate the horse’s activity during this phase. Some low-level activity following suspensory injury may be beneficial for healing and may help in managing the behavior of the horse. Walking exercise in a water treadmill after the first two months for more serious injuries has been beneficial in this author’s experience. This can then be then followed by a slow return to walk/trot exercise under saddle gradually increasing to 10 minutes trot work over eight to ten weeks. Once trotting ten minutes, canter work may be resumed. Concurrent use of the Horsepower brace may be beneficial in progressive exercise. Ancillary therapies to help maintain overall condition during “lay-up” must not be overlooked. Daily use of carrot stretch exercises in multiple planes may prove useful for maintaining flexibility of the neck and muscle tone of the back and abdomen. Application of functional electrostimulation (FES) may reduce loss of topline muscle and reduce stiffness, and there is evidence of the value of FES in the horse for increasing mitochondrial concentration in the muscle cells. Mobilization and stretching exercises of the limbs may help to minimize joint stiffness as previously mentioned. Daily activity and simply moving around and not being “stall bound” have significant effects on the physiology and well-being of the horse.

References: 1. Denoix JM. In: Course notes: Module 1, Series 2 The foot and pastern, The International Society of Locomotor Pathology (2008), Middleburg, Va 2. Denoix J-M, Houliez D. Déformations du pied à l'appui. In Proceedings 'Congrès de Podologie Vétérinaires-Maréchaux-Ferrants'. Cluses (France) 1997, pp 54-61 3. Nomina Anatomica Veterinaria (Fifth edition) (2012) International Committee on Veterinary Gross Anatomical Nomenclature. Integumentum commune, p. 156-158 4. Lawson SEM, et al. Effect of toe and heel elevation on calculated tendon strains in the horse and the influence of the proximal interphalangeal joint, J. Anat (2007) 210: pp. 583-591 5. Plaas, A et al. Biochemical identification and immunolocalizaton of aggrecan, ADAMTS5 and inter-alpha-trypsin–inhibitor in equine degenerative suspensory ligament desmitis, Journal of Orthopaedic Research, Vol 29, Issue 6, June 2016 pp. 900-906 6. Dyson S. Is degenerative change within hindlimb suspensory ligaments a prelude to all types of injury? Equine Vet. Educ. (2010) 22(6) pp 277-274 7. Minshall, GJ and Wright, IM. Arthroscopic diagnosis and treatment of intra-articular insertional injuries of the suspensory ligament branches in 18 horses, Equine vet. J (2006) 38 (1) pp10-14 8. Dyson S, Greve L. Subjective gait assessment of 57 sports horses in normal work: a comparison of the response to flexion tests, movement in hand, on the lunge and ridden; JEVS 38 (2016) pp 1-7 9. Ross M. Lameness in horses: Basic facts before starting. In: Diagnosis and Management of Lameness in the Horse, Eds, Ross M and Dyson SJ, Saunders, Philadelphia, 2003: pp3- 8

48 10. Boswell RP, Mitchell RD, Dyson SJ. Lameness in the Show Hunter and Show Jumper. In: Diagnosis and Management of Lameness in the Horse, Eds, Ross M and Dyson SJ, Saunders, Philadelphia, 2003: pp 951-975 11. Mitchell RD. Distal limb lameness in the sport horse-a clinical approach to diagnosis, Proceedings Ocala Equine Conference, Jan 2016 12. Dyson SJ. The swollen limb. In: Diagnosis and Management of Lameness in the Horse, Eds, Ross M and Dyson SJ, Saunders, Philadelphia, 2003: pp 150-151 13. McLellan J, Plevin S. Do radiographic signs of sesamoiditis yearling Thoroughbreds predispose the development of suspensory ligament branch injury? Equine Vet. J (2013) Vol 46, issue 4,Oct 2014, pp 446-450 14. Dyson SJ, Martinelli MJ. Image description and interpretation in musculoskeletal scintigraphy. In: Equine Scintigraphy, Eds: SJ Dyson, RC Pilsworth, AR Twardock, M Martinelli,(2003) Newmarket, Suffolk, pp.89-91 15. Greet T, Foreword. In: Equine MRI, Ed. Murray RC, Wiley-Blackwell, West Sussex, UK, 2011: pp. xi-xi 16. Waslau M, Sutter W, Genovese R, Bertone A. Intralesional injection of platelet-rich plasma followed by controlled exercise for treatment of midbody suspensory ligament desmitis in Standardbred racehorses, JAVMA (2008) Vol.232 (10) pp 1515-1520 17. Garrett K, Bramlage L, Spike-Pierce D, Cohen N. Injection of platelet-rich plasma at the junction of the proximal sesamoid bone and the suspensory ligament for treatment of yearling Thoroughbreds with proximal sesamoid bone inflammation and associated suspensory ligament branch desmitis, JAVMA (2013) Vol 243 (1): pp 120-125 18. Hall MS, Vasey JR, Russell JW, Russell T. Use of ultrasound-guided autologous bone marrow transfer for treatment of suspensory ligament desmitis in 30 race horses (2003- 2010) Austral. Vet. Jour., Vol 91, Issue 3, pp 102-107 19. Bertone A. Evaluation of a single intra-articular injection of autologous protein solution for treatment of osteoarthritis in horses, JAVR (2014) 75: 141-151 20. Mitchell RD. Treatment of tendon and ligament injuries with UBM powder (ACell-Vet). Proc. 14th Am Coll Vet Surg Symp: 190-193, 2004 21. Seabaugh, KA, Thoresen, M, Giguere. Extracorporeal shockwave therapy increases growth factor release from platelet-rich plasma in vitro, Frontiers in Veterinary Science, Dec 2017, Vol. 4, article 205 22. Peters, D. Tendon and ligament injury with an eye on rehabilitation. In: Proceedings FAEP, October 2014, Hilton Head Island, SC

49 WHY IS IT IMPORTANT TO SEE SPORT HORSES RIDDEN? Sue Dyson, Centre for Equine Studies, Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk, CB8 7UU, UK.

Many riders experience performance-related problems during ridden exercise. It is vital to recognise the problems that the rider is experiencing when they ride the horse. Ridden exercise is crucial, because there are some lamenesses, both forelimb and hindlimb, that are only apparent ridden [1]. A baseline lameness seen in hand or on the lunge may have no relevance to the horse’s performance when ridden.

Ideally the horse should be assessed ridden by its normal rider in its usual tack. The fit of the tack should be assessed. The skill and balance of the rider and their size relative to the horse should be noted. It is important to recognise that a rider can potentially induce lameness by overly restricting the horse via the reins and failing to ask the horse to go forwards with sufficiently strong seat and leg aids. A rider who is poorly balanced, has poor core strength, or moves out of synchrony with the horse’s gait can create irregularities of the horse’s gait. A rider who is both large for a horse and out of balance can inhibit the movement of the horse’s thoracolumbar region with secondary changes in limb flight. A rider who is constantly moving their hands may induce movement of the horse’s head and neck, which sometimes may mimic lameness. A good rider can mask problems by making subtle readjustments to the horse’s balance and by riding the horse forward strongly. A horse which only experiences problems when doing advanced collected work, especially lateral work, may not show its problems unless ridden by a rider capable of producing that level of collection.

The horse should work through the movements which it would normally do in training and competition. This should include walk, trot and canter, upwards and downward transitions and lateral movements depending on the horse’s level of training. Working, collected, medium and extended trot and canter should be assessed. If the horse has experienced problems when jumping (e.g., jumping to the right, failing to land with the left forelimb leading) it should be assessed jumping.

With any horse it can be helpful to see the horse ridden in 10 m diameter circles at the trot, and circular figures of eight i.e., linking 10 m circles to the left and to the right alternately. The circle diameter is crucial because larger circles are too easy. It is quite remarkable how a horse may maintain a normal posture and rhythm in a circle of 12 m diameter, but look very different on a circle of 10 m diameter. Loss of rhythm, becoming overbent or more overbent, going above the bit, leaning in, crossing the inside hindlimb under the trunk during protraction, being more difficult to turn in one direction compared with the other may also reflect an adaptation to pain.

The horse and rider should be viewed coming toward and going away from the examiner, and from the side. This means that the horse is best assessed from two corners of the arena. If the saddle continually slips to one side on one rein this is usually a reflection of hindlimb lameness [2,3]. However, it could be the result of an ill-fitting or asymmetrically flocked saddle, asymmetry of

50 the thoracolumbar musculature or rider crookedness. Bear in mind that saddle slip secondary to hindlimb lameness may induce rider crookedness.

Pay attention to the diagonal on which the rider sits during rising trot. It is convention that the rider should sit when the inside hindlimb and outside forelimb are bearing weight. With hindlimb lameness a horse usually appears lamer when the rider sits on the diagonal of the lame limb. Some horses may alter their gait and hop to try to displace the rider to sit on the diagonal of the none- lame or less lame hindlimb.

Compare the horse’s posture and rhythm in rising trot and sitting trot. A horse with thoracolumbosacral pain may reduce the range of motion of the vertebral column i.e., stiffen its back, in sitting trot, and become slightly above the bit. Ask the rider if they feel any differences in the gait between rising and sitting trot. Consider the relative quality of the trot and the canter. The quality of canter in horses with sacroiliac joint region pain is usually worse than trot [4]. The clinical features of sacroiliac joint region pain are usually dramatically worse in a ridden horse than under other circumstances.

In some horses the quality of canter may be consistently worse on one rein (e.g., left rein) compared with the other (e.g., right rein) which may reflect asymmetrical pain. The rider may feel jarred by the horse (i.e., there is a high impact transmitted through the rider’s seat and back), or may feel that their pelvis is being rotated. The horse may reduce the range of motion of the thoracolumbosacral region as an adaptation to lameness, so that the rider will comment that the horse feels ‘solid behind the saddle’ [5]. Flying changes are physically more demanding for the hindlimbs than maintaining canter on the same lead, and difficulties in performing changes correctly may highlight the presence of pain.

With collected paces the horse has to engage the hindlimbs more than in working trot, with the centre of gravity moved caudally and more weight being carried by the hindlimbs. Obviously this is more demanding than working trot and may be the only occasion when resistances are recognised. Lateral work requires collection and increases the rotational forces on the trunk and limbs

How should a horse work correctly?

Based on the principles of training, an event horse or a dressage horse should ideally work ‘on the bit’ [6,7]. The cranial aspect of the head should be in a vertical position, with the neck flexed at the poll i.e., flexion of the cranial cervical vertebrae. The horse should accept the bit, taking an even contact via the reins on the rider’s hands (i.e. equal rein tension), keeping the mouth shut and producing saliva. The horse should be pushing energetically with the hindlimbs, tracking up, with the hindlimbs following the tracks of the forelimbs (i.e., on two tracks). There should be flexion at the lumbosacral joint, and fluid movement through the horse’s thoracolumbosacral region [8]. The horse’s trunk should be more or less vertical in both straight lines and circles, with the trunk curved to follow the radius of curvature of a circle [9, 10]. The horse should be in balance with proportionate weight distribution between the forelimbs and hindlimbs. The horse should move willingly forward, being responsive to the rider’s aids. The best showjumping riders work their

51 horses similarly, however at lower levels there is much less attention paid to correct balance and bend. A horse which has undergone correct basic training should be able to work correctly.

Horses’ responses to musculoskeletal pain

Resentment of being tacked up, manifest as the horse moving to the back of the stable as a rider enters with the tack, or laying the ears back, swishing the tail and attempting to bite or kick as the girth is tightened, may reflect discomfort induced by the tack, anticipation of pain associated with being ridden or gastric ulcer syndrome. Many musculoskeletal problems causing poor performance are slow and insidious in onset. How pain is manifest when ridden depends on the temperament of the horse and its tolerance of pain. Unwillingness to go forward freely (not because of lack of fitness, or cardiovascular or respiratory problems, or other systemic illness), so-called laziness and lack of power are typical findings. However there is a group of horses in which pain is manifest as tension, ‘buzziness’, hurrying or wanting to run away, sometimes with disproportionate sweating relative to the work done and the horse’s fitness. The horse may become less compliant and responsive to the aids, become spooky (shying repeatedly) and evade the aids (cues given by the rider) by putting the tongue over the bit or putting the head up (going above the bit), or twisting the head and neck. A horse may start to buck or rear [11-15].

Pain often causes a generalised restriction of movement, with reduced range of motion of the cervical and/or thoracolumbosacral regions and shortened steps. The horse may fail to track up. The horse may become more difficult to turn in one direction, especially in small (10m diameter) circles. A horse which had been similar to ride on both the left and right reins may have a deterioration in performance on one rein. A horse which formerly took a good quality, even contact with the bit may change by leaning on one side of the bit so giving a stronger pull (hanging) on the rein in the rider’s hand, and avoiding taking a proper contact via the other rein. Alternatively a horse which is on the forehand because of inadequate hindlimb impulsion may lean on both reins and be very heavy in the rider’s hands. Many horses evade by becoming overbent or behind the bit, often reducing the weight of the contact in the rider’s hands. Other horses evade by becoming above the bit. The tongue may loll out of the horse’s mouth, or the horse may constantly hold its mouth open or repeatedly chomp the teeth, or tooth grind. The mouth may be dry, lacking salivation. Pinning the ears back, flaring the nostrils and constant swishing of the tail are often signs of pain [11-15]. Application of a Ridden Horse ethogram has shown that the presence of ≥8/24 behavioural markers is likely to reflect the presence of musculoskeletal pain [13,15]. Abolition of musculoskeletal pain by diagnostic analgesia ± alteration of tack results in significant reduction in the behaviour score to < 8 [15].

A low-grade forelimb lameness may result in the horse taking slightly lame steps on turns, sometimes only in one direction. If bilateral, the horse may take symmetrically short steps with both forelimbs in all paces. A horse with hindlimb lameness may fail to push properly with the hindlimbs in upward transitions from walk to trot or from trot to canter and may therefore appear to ‘jump’ in the transition. The horse may be reluctant to flex the lumbosacral joint and engage the hindlimbs in downward transitions so the horse may become more on the forehand, be croup high and fall abruptly from canter to trot or from trot to walk, taking short steps with the hindlimbs. With hindlimb lameness it is typical that there are difficulties in movements requiring more collection e.g., lateral movements (shoulder-in, travers, half pass, walk or canter pirouettes). With

52 either forelimb or hindlimb lameness irregularities in the rhythm or asymmetries in limb flight may become apparent in medium and/or extended trot. For example, one forelimb may be elevated less than the other during protraction.

Although lameness cannot be detected in canter a change in the quality of the canter may be a reflection of pain e.g., lack of a suspension phase, a so-called four time canter; stiff and stilted canter ± close temporal and/or spatial placement of the hindlimbs; cantering crookedly, with the hindlimbs not following the same tracks as the forelimbs (usually with the hindquarters displaced to the inside of the track if working in an arena). The canter may become disunited or the horse may repeatedly change limbs behind (also referred to as changing leads behind). The horse may be reluctant to canter with one forelimb leading. This usually reflects hindlimb pain: with right hindlimb pain the horse may be reluctant to canter with the left forelimb leading, because left lead canter is initiated by the horse weight bearing on the right hindlimb alone. Less commonly unwillingness to lead with one forelimb is a manifestation of forelimb pain. The horse may show difficulties with flying changes from left to right or right to left or both, seen as reluctance to change, being croup high in the changes, leaping into the changes, or being crooked with the horse swinging excessively from side to side. These abnormalities usually reflect hindlimb pain. With forelimb pain the horse may have reduced height of the arc of the foot flight of the forelimbs in canter and paradoxically appear to land more heavily on the forelimbs than a normal horse. The forelimb gait can also change as a reflection of primary hindlimb pain.

Specific problems may be seen when a horse is jumping. The horse may fail to land with the correct limb leading i.e., the leading limb should be on the same side as the direction to which the horse is turning. On landing there is greater ground reaction force in the trailing forelimb compared with the leading forelimb. So with right forelimb pain the horse may repeatedly land with the right forelimb leading even when turning to the left if the biggest component of pain relates to impact. However if pain is associated with extension of the right fetlock and increased load on the suspensory apparatus the horse may prefer to always land with the left forelimb leading. Uncharacteristic stopping at fences or running out may relate to either forelimb or hindlimb pain. Horses with forelimb pain may be reluctant to jump going downhill. They may also show reluctance to gallop downhill. Lack of power and difficulties in making distances in combination fences usually reflect hindlimb pain. If a horse jumps crookedly across a fence, for example jumping from left to right, this usually reflects pain in the hindlimb on the same side to which the horse is jumping, because the horse creates less propulsion from the lame(r) limb. Having rails down uncharacteristically may reflect forelimb or hindlimb pain.

In conclusion, failure to see sports horses ridden may result in completely erroneous conclusions. It is crucial to understand the way in which ridden horses may adapt their gait and behaviour in the face of musculoskeletal pain.

53 1. Dyson, S., Greve, L. Subjective gait assessment of 57 sports horses in normal work: a comparison of the response to flexion tests, movement in hand, on the lunge and ridden. J Equine Vet Sci 2016; 38: 1-7.

2. Greve, L., Dyson, S. An investigation of the relationship between hindlimb lameness and saddle slip. Equine Vet J 2013; 45: 570-577.

3. Greve, L., Dyson, S. The interrelationship of lameness, saddle slip and back shape in the general sports horse population. Equine Vet J 2014; 46: 687-694.

4. Barstow, A., Dyson, S. Clinical features and diagnosis of sacroiliac joint region pain in 296 horses: 2004 – 2014. Equine Vet Educ 2015; 27: 637-647.

5. Greve, L., Dyson, S., Pfau, T. Alterations in thoracolumbosacral movement when pain causing lameness has been improved by diagnostic analgesia The Vet J 2017; doi:10.1016/j.tvjl.2017.03.009

6. Dyson, S. Evaluation of poor performance in competition horses: a musculoskeletal perspective. Part 1 Clinical assessment. Equine Vet Educ 2016; 28:284-293.

7. Dyson, S. Equine performance and equitation science: clinical issues. J Appl Anim Behav Sci 2017; 190: 5-17.

8. Greve, L., Pfau, T., Dyson, S. Thoracolumbar movement in sound horses trotting in straight lines in hand and on the lunge. The Vet J 2017; 220: 95-104.

9. Greve, L., Dyson, S. Body lean angle in sound dressage horses trotting in hand, on the lunge and ridden. The Vet J 2016; 217: 52-57.

10. Greve, L., Pfau, T., Dyson, S. Alterations in body lean angle in lame horses before and after diagnostic analgesia in straight lines in hand and on the lunge. The Vet J 2018; doi.org/10.1016/j.tvjl.2018.07.006

11. Mullard, J., Berger, J., Ellis, A., Dyson, S. Development of an ethogram to describe facial expressions in ridden horses (FEReq). J Vet Behav: Clin Appl Res 2017; 18:7-12.

12. Dyson, S., Berger, J., Ellis, A., Mullard, J. Can the presence of musculoskeletal pain be determined from the facial expressions of ridden horses (FEReq)? J Vet Behav: Clin Appl Res 2017; 19:78-89.

13. Dyson, S., Berger, J., Ellis, A., Mullard, J. Development of an ethogram for a pain scoring system in ridden horses and its application to determine the presence of musculoskeletal pain. J Vet Behav: Clin Appl Res 2017; doi:10.1016/j.jveb.2017.10.008

14. Dyson, S., Ellis, A., Mullard, J., Berger, J. Response to Gleerup: understanding signals that indicate pain in ridden horses. J Vet Behav: Clin Appl Res 2018, 23: 87-90.

15. Dyson, S., Berger, J., Ellis, A., Mullard, J. Behavioural observations and comparisons of non- lame horses and lame horses before and after resolution of lameness by diagnostic analgesia. J. Vet. Behav.: Clin. Appl. Res. 2018, 26: 64-70.

55 SACROILIAC JOINT REGION PAIN IN SPORTS HORSES: A GROWING PROBLEM?

Sue Dyson Centre for Equine Studies, Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk CB8 7UU, UK.

The following data relates to a study of 296 horses with sacroiliac joint region pain (43 with primary sacroiliac joint region pain [Group 1] and 253 with concurrent hindlimb lameness [Group 2]) [1] and additional clinical observations. For inclusion horses had to demonstrate substantial improvement in clinical signs when ridden (or on the lunge if unsafe to ride) after infiltration of local anaesthetic solution around the sacroiliac joints.

A subcutaneous bleb of local anaesthetic solution was placed axial to the cranial margin of each tuber sacrale through which a 15 cm 18 gauge spinal needle was inserted and directed caudoventrally toward the caudal aspect of the contralateral sacroiliac joint. The precise angle was dictated by the space between the tubera sacrale which varied among horses, and the orientation of the spinous processes of the sixth lumbar vertebra and sacrum. The needle was advanced 12-15 cm before injection of mepivacaine (up to 10ml per side). Horses were walked for 15 minutes and reassessed ridden or occasionally on the lunge if ridden exercise was not possible.

Clinical features

In Group 1, 14% of horses had a history of being difficult to shoe behind and 9% were reluctant to pick up a hindlimb and stand on the contralateral limb. There was increased tension in the longissimus dorsi muscles in 40% of horses and pain on palpation of the caudal thoracic and lumbar epaxial muscles of 12%. There was limited flexibility of the thoracolumbar region in 44% horses, with extension and lateral bending being principally affected; 19% became agitated when stimulated to flex and extend the thoracolumbar region. The thoracolumbar region was poorly muscled in 28%, especially in the lumbar region resulting in prominence of the summits of the lumbar spinous processes. The tubera sacrale were higher than the withers in 9%. During exercise 61% of horses demonstrated reduced range of motion of the thoracolumbosacral region. Twenty- one percent of horses moved closely or plaited behind at walk and trot, but a base-wide gait was seen in a minority. In hand 29 % of horses moved with poor hindlimb impulsion compared to 31% of horses on the lunge and 54% of horses when ridden.

When ridden, 65% of horses had a poor-quality contact with the bit, tending to be above the bit. The quality of canter was worse than trot in the majority (81%). The canter was often stiff and stilted when ridden (27%); 16% of horses refused to go forwards and 16% would spontaneously come to an abrupt stop. 14% of horses bucked in trot; 27% bucked in canter and 22%) kicked out behind. One horse (3%) struggled with flying changes; 14% stiffened and lost rhythm during lateral work; 8% resented being ridden in sitting trot and 5% broke from trot to canter instead of increasing hindlimb engagement. There was a general reluctance to go forwards in 46% of horses, however 11% of horses were excessively strong and tense. Unilateral hindlimb lameness (range 1-4/8; median 2) was observed in 12% of horses, which was abolished by infiltration of mepivacaine around the sacroiliac joint.

A greater proportion of horses in Group 1 had an exaggerated response to vertical pressure applied to the tubera sacrale, demonstrated a bunny hop-like hindlimb gait in canter when ridden, or were not ridden because of potentially dangerous behaviour compared with horses in Group 2.

In Group 2 concurrent problems included: hindlimb lameness (38%), forelimb and hindlimb lameness (24%), thoracolumbar pain and forelimb and/ or hindlimb lameness (21%) thoracolumbar pain (11%), forelimb lameness (5%), and ataxia (0.4%). Significantly more horses had SI pain in association with hindlimb lameness compared with SI joint region pain in association with: thoracolumbar pain (p<0.0001), thoracolumbar pain and lameness (p=0.0002), forelimb lameness (p<0.0001), and forelimb and hindlimb lameness (p=0.0006). Concurrent lameness was present in 89% of horses. Hindlimb lameness was observed in 80% of horses (90% bilateral; 10% unilateral). Proximal suspensory desmopathy was identified in 89% (94% bilateral; 6% unilateral) of horses with hindlimb lameness. Forelimb lameness was observed in 40% of all horses (49% bilateral; 51% unilateral). Pain localised to the digit contributed to forelimb lameness in 77% of horses with forelimb lameness.

Of 224 lame horses, 24% also had thoracolumbar region pain. A significantly greater proportion of horses had SI joint region pain, concurrent thoracolumbar pain and lameness compared with SI joint region pain and concurrent thoracolumbar pain (p=0.002). Significantly more horses had SI joint region pain and a concurrent hindlimb and forelimb lameness than SI joint region pain and concurrent thoracolumbar pain (p=0.0002).

In the majority of horses with concurrent pain contributing to lameness there was substantial improvement in the quality of the trot when ridden when the lameness was improved. Low-grade residual lameness was abolished by infiltration of mepivacaine around the sacroiliac joints. However, in some horses despite improvement in lameness, some aspects of the gait deteriorated especially in canter, presumably related to an alteration of the source and /or type of pain.

Diagnostic imaging

Nuclear scintigraphy was performed in 61% of horses. Abnormal radiopharmaceutical uptake (RU) in the region of the SI joints was present in only 47% of these horses. There was no significant difference in the proportion of horses having abnormal RU in Groups 1 and 2.

Ultrasonographic examination of the lumbosacral and sacroiliac joint regions was performed per rectum in 44% horses in which abnormalities were detected in 32%, including periarticular modelling of the sacroiliac joints, degenerative changes of the lumbosacral intervertebral disc ± disc protrusion, sacralisation of the lumbosacral joint and degenerative changes of the lumbar 5-6 intervertebral disc. There was no significant difference in presence of ultrasonographic abnormalities between Groups 1 and 2.

Discussion

Clinical signs may be more prevalent at the canter because of the three-beat asymmetrical gait resulting in one hindlimb weightbearing alone for a portion of the stride cycle [2]. This may

57 increase pain compared with walk and trot, both symmetrical gaits. There is also maximal flexion/ extension motion in the lumbosacral region in canter compared with walk and trot [33] which may exacerbate pain. These clinical signs were dramatically improved by sacroiliac joint region block, supporting their association with sacroiliac joint region pain. In some horses the quality of canter was consistently worse on one rein (e.g., left rein) compared with the other (e.g., right rein) which may reflect asymmetrical pain. Horses were less likely to change their hindlimbs and become disunited in ridden canter compared with on the lunge, perhaps because the rider is able to balance the horse better and maintain the correct canter lead. Although not analysed in the current study, some horses with sacroiliac joint region pain intermittently, transiently scoot forwards at any gait, as if experiencing sharp pain. This behaviour is abolished by sacroiliac joint block.

In Group 1, unilateral hindlimb lameness was present in five ridden horses which subsequently resolved following sacroiliac joint block. Fourteen horses in Group 2 had residual lameness after distal limb nerve blocks which was eliminated by the sacroiliac block. This indicates that occasionally unilateral lameness may be associated with sacroiliac joint region pain alone and sacroiliac joint region diagnostic analgesia may be indicated in horses in which distal limb nerve blocks fail to resolve lameness.

Poor hindlimb impulsion, back stiffness and a tendency to be above the bit were common non- specific features which were resolved by local analgesia of the sacroiliac joint region. Distinguishing primary thoracolumbar pain can be challenging because, as shown in this study, many horses with sacroiliac joint region pain have atrophy of the epaxial muscles (usually symmetrical), especially in the lumbar region (longissimus dorsi and middle gluteal muscles), pain on palpation of the caudal thoracic and lumbar epaxial muscles ± fascia (symmetrical or asymmetrical, depending on the presence of factors such as left–right symmetry of sacroiliac joint region pain, lameness, saddle fit and rider crookedness/ straightness) and thoracolumbar-sacral stiffness. The latter is manifest particularly as limited induced extension and lateral bending at rest, especially in the caudal thoracic and lumbar regions, and reduced lumbosacral flexion during dynamic examination, especially when ridden. Moreover, pain associated with impinging spinous processes or osteoarthritis of the thoracolumbar articular process joints may coexist. In some horses with sacroiliac joint region pain the development of epaxial muscle atrophy has been recognised to occur quickly, over 2 weeks to a month. This rapid lumbar muscle atrophy may be the result of changes in muscle recruitment due to sacroiliac joint region pain, as is evident in humans [4].

Approximately 10% of horses had abnormal static conformation with the tubera sacrale higher than the withers, thus these horse were out of balance [5] and likely to have difficulties in engaging the hindlimbs. Whether such conformation predisposes to the development of sacroiliac joint region pain or develops secondary to pain deserves further investigation. Approximately 9% of horses were reluctant to stand on one hindlimb with the other hindlimb flexed. We believe that this probably reflects rotation of the pelvis and asymmetric loading of the sacroiliac joints and supporting ligaments inducing joint torque, altered shear forces and pain. Asymmetric force distribution may also be the reason for lateral work exacerbating pain when ridden. A very small proportion of horses with sacroiliac joint region pain experience difficulties in getting down to roll or to lie down; they go down on their carpi with the hindlimbs semiflexed and quivering, before flopping on to one side.

The majority of horses in the current study had sacroiliac joint region pain and hindlimb lameness, a high proportion of which had hindlimb proximal suspensory desmopathy, as previously documented [6,7]. Although clear improvement in baseline lameness in hand was seen in some horses after perineural analgesia of the deep branch of the lateral plantar nerve, ridden exercise highlighted the presence of a significant component of residual pain, sometimes paradoxically worse after abolition of the baseline lameness. This emphasises the crucial importance of ridden exercise in both trot and canter when assessing lameness and poor performance. The biomechanical function of the sacroiliac joints in the horse is poorly understood; hindlimb lameness is presumed to alter loading of the joints but the mechanisms whereby this occurs are currently unknown [8].

The technique used to infiltrate local anaesthetic solution around the sacroiliac joints was well- tolerated, safe and effective, as previously demonstrated [6]. Two horses experienced transient ataxia following sacroiliac block in addition to two other horse in the study period which were excluded because the block could not be interpreted and scintigraphy was negative or not performed. A post mortem study demonstrated that haemorrhage is not associated with needle placement periarticular to the sacroiliac joint [9]. Ultrasound-guided injection of the sacroiliac joint region has been described [10], however the cranial approach is effectively blind once the needle has passed under the ilial wing. However, it was shown to be reliable in a cadaver study [11]. The caudal approach risks damage to neurovascular structures [12,13] and sciatic nerve paralysis. The dramatic clinical improvements following sacroiliac block demonstrate the high level of discomfort experienced by many horses with sacroiliac joint region pain. The technique described is a periarticular technique and not specific for the sacroiliac joint; other local structures may be affected. Methylene blue injected in the sacroiliac joint region tracked forward to the lumbosacral joint [6]. Since many horses with chronic pain respond poorly to local medication of the sacroiliac joints [14], the response to local analgesia is of far more value diagnostically than assessing the response to treatment. However, occasionally there are false negative responses to a sacroiliac joint region block. During the study period one horse with clinical signs typical of sacroiliac joint region pain did not respond to local analgesia, but at post mortem examination had extensive degenerative pathological abnormalities of the sacroiliac joints, in addition to asymmetry and slight malalignment of the lumbar articular process joints. Only 47% of horses which had a positive response to sacroiliac block and underwent scintigraphy had abnormal RU. Thus scintigraphy alone is unreliable for the diagnosis of sacroiliac joint region pain.

Ultrasonographic examination of normal [15] and abnormal [16] sacroiliac joint regions has been described. In our study population the frequency of occurrence of abnormalities of the sacroiliac joints was small. Abnormalities of the lumbosacral joint and the L5-6 intercentral joint were identified that may contribute to pain.

In conclusion, clinical signs of sacroiliac joint region pain are worse when horses are ridden and canter is generally more affected than trot. Sacroiliac joint region diagnostic analgesia is a useful, safe but non-specific block. Ultrasonography and scintigraphy can provide additional information in some horses, but negative results do not preclude sacroiliac joint region pain.

59 References

1. Barstow, A., Dyson, S. Clinical features and diagnosis of sacroiliac joint region pain in 296 horses: 2004 – 2014. Equine Vet Educ 2015; 27: 637-647.

2. Back W, Schamhardt H, Barneveld A. Kinematic comparison of the leading and trailing fore- and hindlimbs at the canter. Equine Vet J 1997; 29 (Suppl 23): 80-83.

3. Faber M, Johnston C, Schamhardt H, et al. Equine Vet J 2001; 33 (Suppl 33): 145-149.

4. Hungerford B, Gilleard W, Hodges, P. Evidence of altered lumbopelvic muscle recruitment in the presence of sacroiliac joint pain. Spine 2003; 28: 1593-1600.

5. Ross M. Conformation and lameness. In: Ross M, Dyson S. eds. Diagnosis and Management of Lameness in the Horse, 2nd edn., St. Louis: Elsevier, 2010; 15-32.

6. Dyson S, Murray R. Pain associated with the sacroiliac joint region: a clinical study of 74 horses. Equine Vet J 2003; 35: 240-245.

7. Dyson S, Murray R. Management of hindlimb proximal suspensory desmopathy by neurectomy of the deep branch of the lateral planter nerve and planter fasciotomy: 155 horses (2003-2008). Equine Vet J 2012; 44: 361-367.

8. Goff L, Jeffcott L, Jasiewicz J, et al. Structural and biomechanical aspects of equine sacroiliac joint function and their relationship to clinical disease. The Vet J 2008; 176: 281- 293.

9. Engeli E, Haussler K, Erb H. Development and validation of a periarticular injection technique of the sacroiliac joint in horses. Equine Vet J 2004; 36: 324-330.

10. Denoix J, Jacquet S. Ultrasound-guided injections of the sacroiliac area in horses. Equine Vet Educ 2008; 20: 203-207

11. Cousty, M., Rossier, Y., David, F. Ultrasound-guided periarticular injections of the sacroiliac region in horses: A cadaveric study. Equine Vet J 2008; 40: 160-166.

12. Engeli E, Haussler K. Review of injection techniques targeting the sacroiliac region in horses. Equine Vet Educ 2012; 24: 529-541.

13. Dyson S, Murray R, Branch M, et al.. The sacroiliac joints: evaluation using nuclear scintigraphy. Part 2: lame horses. Equine Vet J 2003; 35: 233-239.

14. Dyson S. Clinical features of pain associated with the sacroiliac joint region. Pratique Vétérinaire Équine 2008; 40: 123 – 128.

60 15. Tallaj, A., Coudry, V., Denoix, J.-M. Transrectal ultrasonographic examination of the sacroiliac joints of the horse: Technique and normal images. Equine Vet Educ 2017; doi: 10.1111/eve.12845

16. Tallaj, A., Coudry, V., Denoix, J.-M. Transrectal ultrasonographic examination of the sacroiliac joints of the horse: abnormal findings and lesions. Equine Vet Educ 2017; doi: 10.1111/eve.12858

61 HINDLIMB PROXIMAL SUSPENSORY DESMOPATHY: WHY IS IT SUCH A MANAGEMENT CHALLENGE?

Sue Dyson, Centre for Equine Studies, Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk, CB8 7UU, UK.

Proximal suspensory desmopathy (PSD) in hindlimbs is a degenerative condition on which repetitive strain injury may be superimposed. It can occur in all ages of all types of sports horses. Lameness may be insidious in onset and slowly progressive and in the earlier stages may only be apparent ridden and sometimes only under specialised circumstances. There may be coexistent sacroiliac joint region pain which may be overlooked unless the horse is evaluated in trot and canter, both before and after nerve blocks.

Clinical features

There are frequently no localising clinical signs. Lameness is variably accentuated by either proximal or distal limb flexion. Low-grade radiological subclinical abnormalities of the distal hock joints consistent with osteoarthritis may coexist and may never become symptomatic. Intraarticular analgesia of the tarsometatarsal joint has the potential to improve pain associated with the proximal aspect of the suspensory ligament if >3ml mepivacaine is used, due to plantarodistal diffusion.

Diagnostic analgesia

Perineural analgesia of the deep branch of the lateral plantar nerve is not a suspensory ligament block [1-6]. There is the potential to remove pain from the central and third tarsal bones, the centrodistal and tarsometatarsal joints, the third metatarsal bone, the interosseous ligaments of between the second and third and fourth and third metatarsal bones, the deep digital flexor tendon and its accessory ligament. It is important to image the hock and proximal metatarsal regions in a systematic way (using radiography and ultrasonography) and to compare the response to intra- articular analgesia of the tarsometatarsal joint. In horses with obvious bilateral hindlimb lameness then perineural analgesia of the deep branch of the lateral plantar nerve of one hindlimb will usually resolve lameness in that limb and lameness in the contralateral limb may become more obvious. However, in horses with lack of hindlimb impulsion and engagement it may be difficult to perceive a change in gait after blocking a single limb, however a big change may be observed after perineural analgesia of the deep branch of the lateral plantar nerve lack of both hindlimbs. In some horses with adhesion formation between the suspensory ligament and either the adjacent soft tissues or the third metatarsal bone, lameness will only be abolished by a tibial nerve block [7]. A negative response to perineural analgesia of the plantar (proximal to the digital flexor tendon sheath) and plantar metatarsal nerves (‘low 4-point block’) or exacerbation of lameness does not preclude the coexistence of suspensory branch pathology. When performing an ultrasonographic examination the entire tarsal and metatarsal region should be examined bilaterally. Occasionally horses present with unilateral lameness, but there is often suspensory ligament pathology bilaterally. Lesions of the accessory ligament of the deep digital flexor tendon or of the accessory ligament of the suspensory ligament may co-exist with PSD [3,7].

62 Radiography and ultrasonography

Many normal horses have mild increased opacity of the proximoplantar aspect of the third metatarsal bone in a dorsoplantar image and this is not necessarily synonymous with proximal suspensory desmopathy. More focal discrete areas of increased opacity may reflect entheseophyte formation. Computed tomography may be more accurate in detection of entheseophytes [8]. The presence of endosteal new bone seen in a lateromedial images is indicative of chronicity of proximal suspensory desmopathy. The shape of the proximoplantaromedial aspect of the metatarsal region influences the ease with which excellent quality ultrasonographic images can be acquired. Ideally structural abnormalities of the suspensory ligament should be able to be verified in both transverse and longitudinal images. There is good correlation between the presence of ultrasonographic abnormalities and the presence of histological abnormalities of the suspensory ligament [7], verifying that ultrasonography is a potentially reliable tool, contrary to previous suggestions [9]. Identification of adhesions is challenging but may be important prognostically.

A retrospective study was performed to compare ultrasonography with gross and histopathological post-mortem examination in horses with PSD diagnosed based on ultrasonography and control horses [7]. In Part 1 19 horses with hindlimb PSD and 10 control horses were humanely destroyed. All horses with PSD had multiple problems contributing to pain and poor performance and were humanely destroyed for reasons unrelated to the study. Twenty control limbs and 37 lame limbs were examined grossly and 40 suspensory ligaments (SLs) were examined histologically at predetermined anatomical sites and graded blindly.

Most of the horses exhibited mild to moderate lameness, in many horses only seen when ridden. Ultrasonographic lesions were graded moderate in 31/38 (81.6%) and severe in 7/38 (18.4%) lame limbs; in 4/37 (10.8%) limbs adhesion formation between the proximal aspect of the SL and the accessory ligament of the deep digital flexor tendon was predicted. Gross post-mortem and histological examinations of control limbs revealed no abnormalities. Gross post-mortem examination revealed substantial adhesions between the proximal aspect of the SL and adjacent soft tissues in 10/37 (27.0%) lame limbs; in 10/37 (27.0%) limbs there were adhesions between the body of the SL and the mid plantar aspect of the third metatarsal bone, extending distally in 6 (16.2%) limbs. Histology revealed abnormalities (grades 1-3) of the collagenous tissue in 25/36 (69.4%) limbs; muscle was abnormal (grades 1-3) in 35/36 (97.2%) limbs and adipose tissue (grades 1-3) in 16/36 (44.4%) limbs. In one lame limb no histological abnormalities were identified, but there were extensive adhesions between the SL and adjacent structures at gross post- mortem examination. It was concluded that ultrasonography was reliable for the detection of SL pathology based on histology as the gold standard.

In Part 2 of the study three horses with recurrent lameness after surgical management of PSD and four with PSD were assessed ultrasonographically and post mortem. Adhesions between the SL and adjacent soft tissues were predicted ultrasonographically and confirmed post mortem. The presence of such adhesions may explain why some horses fail to respond adequately to surgical treatment.

The use of off-incidence imaging in a non-loaded limb may give additional information [10,11], but is not essential for all horses. Low-field MRI is not reliable for identification of suspensory

63 pathology but can be helpful to identify osseous causes of pain and lameness. High-field MRI is more reliable for detection of both collagen and muscle tissue pathology of the suspensory ligament [12]. Knowledge of normal anatomy is an essential prerequisite for accurate interpretation [13].

Nuclear scintigraphy

The presence of increased radiopharmaceutical uptake in the proximoplantar aspect of the third metatarsal bone reflects entheseous reaction and may be a poor prognostic indicator in some horses. Its presence should alert the clinician to a careful appraisal of the horse’s hindlimb conformation. Large tarsal angles (≥165⁰) can be associated with progressive degeneration and loss of function of the suspensory apparatus [14]. There was increased radiopharmaceutical uptake in the proximoplantar aspect of the third metatarsal bone in six of 10 limbs (60.0%) of five horses with tarsal angles (≥165⁰), compared with 9.6% of 270 limbs of horses with smaller hock angles, suggestive of mechanical stress at the bone-ligament interface [14]. In a previous study, IRU was seen in 9% of hindlimbs of 82 horses with hindlimb PSD [15]. However, there was no significant difference in outcome for horses with primary PSD with or without IRU treated by neurectomy of the deep branch of the lateral plantar nerve and plantar fasciotomy [14], but this may reflect the small number of horses with IRU; 69% of horses with IRU had a successful outcome compared with 78% of all horses (excluding those which developed unrelated problems).

Conformation as a risk factor

In a study of 193 horses with proximal suspensory desmopathy and control horses, horses with PSD had larger tarsal angles than controls (p=0.003) [16]. The proportions of Warmblood-type horses and dressage horses with PSD were different to those of other breeds and work-disciplines (p=0.001, p=0.02, respectively). A final logistic regression model demonstrated a significant effect of tarsal angle on outcome when work-discipline and breed were accounted for. There was an 11% increase in the odds of PSD for every degree increase in tarsal angle (CI 1.004-1.220, p=0.04). There was no association between PSD or suspensory branch injury and metatarsophalangeal joint angle. A longitudinal study would be required to determine what is cause and effect. However, purchase of a horse with tarsal angles ≥165⁰ is not recommended. Surgical management of PSD by neurectomy of the deep branch of the lateral plantar nerve and plantar fasciotomy in a horse with tarsal angles ≥165⁰ may be associated with progressive degeneration of the suspensory ligament and persistent lameness or deterioration in lameness [14].

Work discipline

Although PSD occurs in horses of all types and uses, dressage horses may be particularly susceptible [17]. This may relate to repetitive overuse on single surfaces, selection for advanced diagonal placement [18], overload of the hindlimbs in specific movements [19,20]. The high prevalence of PSD in dressage horses may also reflect greater rider recognition of a compromised hindlimb gait compared with horse from other disciplines in which quality of the gaits is potentially of less importance.

Extension versus collection

In a study of 20 clinically sound horses in active dressage training were used: 1) ten young (≤ 6 years) were assessed at collected and medium trot; 2) ten mature (≥9 years) were assessed at collected and extended trot [21]. All horses were assessed on two different surfaces. High-speed motion capture (240Hz) was used to determine kinematic variables. Descriptive statistics and mixed effect multilevel regression analyses were performed. Hock angle and distal metatarsal coronary band ratio were outcome variables. Speed and stride length were reduced and stride duration increased at collected compared with medium and extended trot. Medium/extended trot was associated with increased fetlock extension in the hindlimbs. Hock angle was not significantly influence by pace. Medium or extended trot increase extension of the hindlimb fetlock joint compared with collected trot in both young and mature dressage horses, respectively. The risk of repetitive strain injuries of the suspensory apparatus or fetlock may be reduced by avoiding too frequent use of extended trot and excessively long periods of extended trot.

Work surfaces

We have previously observed clusters of horses with PSD based at specific yards and have speculated that arena surface may be a risk factor for injury. All 20 horses were assessed on two different surfaces: surface A - waxed sand and fibre, which had been rolled; surface B - unwaxed sand and rubber, which had been harrowed. No effect of arena surface type was observed in the final multivariable models. This may be due to the effect of small sample size, horses accustomed to being worked on these types of surfaces, or that we only determined kinematic values at midstance. At midstance the limb is being fully loaded and the base of the surface influences a lot of the characteristics that the horse experiences [22]. Characteristics such as cushioning, grip and dampening will have more influence at impact and push-off [22] and these may influence the kinematics of the horse at this point of the stride. The surfaces we evaluated did have differences in surface characteristics (unpublished data), but these differences were more likely to affect the top of the surface and the horse’s interaction with it at impact and push-off. Epidemiological and clinical data suggests that injury risk is linked to arena surface characteristics such as unevenness and poor maintenance [23,24]. Further investigation is required to evaluate the effect of surface on kinematics at different points of the stride.

Treatment options and prognosis

The reports of success of conservative management are variable [25,26], but in our clinical population is usually unsuccessful. Radial pressure wave therapy or extracorporeal shock wave therapy can be successfully used to manage pain associated with mild lesions [27,28]. Injection of biological preparations (platelet rich plasma, mesenchymal stem cells) has yielded poor results.

Neurectomy of the deep branch of the lateral plantar nerve and plantar fasciotomy continues to be a highly successful method of management of chronic hindlimb proximal suspensory desmopathy, with careful patient selection i.e., resolution of lameness after perineural analgesia of the deep branch of the lateral plantar nerve (or identification of another treatable source of pain), definitive evidence of proximal suspensory desmopathy and no predisposing conformational abnormalities [14, 29]. Pre-existing straight hindlimb conformation (hock angle > 165°) is a risk factor for progressive degenerative change of the ligament and failure of surgery.

In horses with acceptable hindlimb conformation, appropriate post-operative rehabilitation is helpful for best results. This should ideally include intensive physiotherapy and exercises designed to enhance core muscle strength and the strength and fitness of the muscles that stabilise the hindlimbs.

Recognition of concurrent sacroiliac joint region pain [30] sometimes only evident in ridden canter, is important to identify preoperatively, because this has a large influence on successful management [14].

A small proportion of horses develop low-grade lameness after resumption of full work associated with tarsometatarsal joint pain. These horses can generally be successfully managed by intra- articular medication.

However, despite careful selection, we still have a 22% failure rate. Generally, these horses have persistent lameness or early recurrence of lameness and lameness is resolved by infiltration of local anaesthetic solution around the origin of the suspensory ligament, or by perineural analgesia of the tibial nerve. Some of these failures may be due to adhesion formation (see above).

In a small number of horses we have identified postoperative complications. Three of 283 horses have developed proximal injuries of the accessory ligament of the deep digital flexor tendon. Four of 278 horses with good hindlimb conformation have developed progressive degenerative changes of the suspensory ligament body within three to nine months post-operatively. One horse developed a suspensory branch injury.

References

1. Dyson, S. and Romero, J. An investigation of injection techniques for local analgesia of the equine distal tarsus and proximal metatarsus. Equine Vet J 21993; 5: 30 - 35.

2. Contino, E., King, M., Valdés-Martínez, A., McIlwraith, C.W. In vivo diffusion characteristics following perineural injection of the deep branch of the lateral plantar nerve with mepivacaine or iohexol in horses. Equine Vet J 2014; doi: 10.1111/evj.12261

3. Dyson, S. Hindlimb lameness associated with proximal suspensory desmopathy and injury of the accessory ligament of the suspensory ligament: five horses. Equine Vet Educ 2014; 26: 538-542.

4. Dyson, S. Proximal injuries of the accessory ligament of the deep digital flexor tendon in forelimbs and hindlimbs: 12 horses (2006 – 2010) Equine Vet Educ 2012; 24: 134-142.

5. Dyson, S. Lameness associated with mineralisation of the central tarsal bone and a small Osseous cyst-like lesion in two sports horses. J Equine Vet Sci 2013, 33: 51-56.

66 6. Plowright E, Dyson S. Concurrent proximal suspensory desmopathy and injury of the accessory ligament of the deep digital flexor tendon in forelimbs or hindlimbs of 19 horses. Equine Vet Educ 2015; 27: 355 – 364.

7. Dyson, S., Murray, R., Pinilla, M. Proximal suspensory desmopathy in hindlimbs: a correlative clinical, ultrasonographic, gross post mortem and histological study. Equine Vet J 2017; 49: 65-72.

8. Launois M, Vandeweerd J, Perrin R, et al. Use of computed tomography to diagnose new bone formation associated with desmitis of the proximal aspect of the suspensory ligament in third metacarpal or third metatarsal bones of three horses. J Am Vet Med Assoc 2009; 234: 514-518.

9. Labens R, Schramme M, Robertson I, et al. Clinical, magnetic resonance and sonographic findings in horses with proximal plantar metatarsal pain. Vet Radiol Ultrasound 2010; 51: 11- 18.

10. Werpy N, Denoix J-M, McIlwraith C, et al. Comparison between standard ultrasonography, angle contrast ultrasonography and magnetic resonance imaging characteristics of the normal proximal suspensory ligament. Vet Radiol Ultrasound 2013; 54: 1-12.

11. Denoix J-M, Bertoni L. The angle contrast ultrasound technique in the flexed limb improved assessment of proximal suspensory ligament injuries in the equine pelvic limb. Equine Vet Educ 2015; 27: 209-217.

12. Dyson, S., Pinilla, M-J., Bolas, N., Murray, R. Proximal suspensory desmopathy in hindlimbs: magnetic resonance imaging, gross post mortem and histological study. Equine Vet J 2017; doi: 10.1111/evj.12756

13. Dyson, S., Blunden, A., Murray, R. Magnetic resonance imaging and gross post mortem and histological findings of the soft tissues of the plantar aspect of the tarsus and proximal metatarsal region in non-lame horses. Vet Radiol Ultrasound 2017; 58: 217-227.

14. Dyson, S., Murray, R.C. Management of hindlimb proximal suspensory desmopathy by neurectomy of the deep branch of the lateral plantar nerve and plantar fasciotomy: 155 horses (2003-2008). Equine Vet J 2012; 44: 361-367.

15. Dyson S, Weekes J, Murray R. Scintigraphic evaluation of the proximal metacarpal and metatarsal regions of horses with proximal suspensory desmitis. Vet Radiol Ultrasound 2007; 48: 78 – 85.

16. Routh, J., Strang, C., Gilligan, S., Dyson, S. An investigation of the association between hindlimb conformation and suspensory desmopathy in sports horses.

17. Murray, R., Dyson, S., Tranquille, C., Adams, V. Association of type of sport and performance level with anatomical site of orthopaedic injury diagnosis. Equine Vet J 2006; 38 (Suppl. 36): 411-416.

18. Holmström, M., Fredricson, I., Drevemo S. Biokinematic effects of collection on the trotting gaits in the elite dressage horse. Equine Vet J 1995; 27: 281-287.

19. Clayton, H. Comparison of the stride kinematics of the collected, working, medium and extended trot in horses. Equine Vet J 1994; 26: 230-234.

20. Weishaupt, M., Byström A., von Peinen, K., Wiestner, T., Meyer, H., Waldern, N., Johnston, C., van Weeren R., Roepstorff, L. () Kinetics and kinematics of the passage. Equine Vet J 2009; 41: 263-267.

21. Walker, V., Tranquille, C., Newton, J., Dyson, S., Brandham, J., Northrop, A., Murray R. Comparison of limb kinematics between collected and lengthened (medium/extended) trot in two groups of dressage horses on two different surfaces. Equine Vet J 2017; 49: 1-8.

22. Hobbs S, Northrop A, Mahaffey C, et al. Equine Surfaces White Paper. 2014. Available at: http://www.fei.org/fei/about-fei/publications/fei-books

23. Murray R, Walters J, Snart H, et al. Identification of risk factors for lameness in dressage horses. Vet J 2010; 184: 27-36.

24. Murray R, Walters J, Snart H, et al. How do features of dressage arenas influence training surface properties which are potentially associated with lameness? Vet J 2010; 186: 172-179.

25. Dyson, S. Proximal suspensory desmitis in the hindlimb: 42 cases. Br Vet J 1994; 150: 279- 291.

26. Norvall, A., Allen, K., Johns, S., Giguère, S., Selberg, K. Diagnosis, treatment and outcome of hindlimb proximal suspensory desmopathy in sport horses: 75 cases (2008-2014). Proceedings of the 61st Annual Convention of the American Association of Equine Practitioners, Las Vegas, 2015; 358.

27. Crowe O, Dyson S, Wright I, et al. Treatment of chronic or recurrent proximal suspensory desmitis using radial pressure wave therapy. Equine Vet J 2004; 36: 313-316.

28. Lischer C, Ringer S, Schnewlin M, et al. Treatment of chronic proximal suspensory desmitis in horses using focused electrohydraulic shock wave therapy. Schweizer Arch. Tierheilk 2007; 148:561-568.

29. Kelly G. Results of neurectomy of the deep branch of the lateral plantar nerve for treatment of proximal suspensory desmitis, in Proceedings, 16th Annual Convention of the European College of Veterinary Surgeons, Dublin, 2007; 130.

30. Barstow, A., Dyson, S. Clinical features and diagnosis of sacroiliac joint region pain in 296 horses: 2004 – 2014. Equine Vet Educ 2015; 27: 637-647.

68 MY HORSE WON’T BEND CERVICAL STIFFNESS AND DYSFUNCTION Carla W Pasteur MS DVM 4500 NW 95th Avenue Rd Ocala, FL 34482 [email protected] Introduction Our knowledge of the equine axial skeleton and related soft tissue has increased dramatically in the last few years. Imaging equipment has improved to allow clear imaging of the cervical vertebrae. Research is elucidating normal cervical movement, correct biomechanics, muscle recruitment and development of pathology. Conditions that have gone untreated and even unrecognized on the past can now be treated. In this paper, we will review normal biomechanics, axial skeletal physiology, the effects of pain, and rehabilitation therapies for the neck.

Cervical Movement Normal movement of the head and neck is important for locomotion, balance, and adjusting the load on individual limbs.1 Changing the head position changes input to vision, vestibular, and proprioceptive systems. It also has a mechanical effect on weight distribution. The head is a large cantilevered weight at a distance from the center of mass (COM) and creates a powerful moment arm. Raising or lowering the head changes the COM and the amount of weight carried by each limb. It also changes the tension on the supraspinous ligament and affects flexion and extension of the thoracolumbar vertebrae. Flexion and extension of the spine is an integral part of locomotion and helps to move the ribcage for respiration2, 3.

Changes in the position and movement of the head and neck are used to affect the center of mass and the load on individual limbs in sound horses4 and in lame horses.5-7 Normally, horses have a greater range of motion (ROM) of the head and neck at the walk, both sagittally and transversely, than at the trot. At the walk, the muzzle should move craniocaudal and laterally left and right, in a figure 8 pattern. The body COM moves in a craniocaudal direction at the walk and in a dorsoventral direction at the trot and mirrors the movement of the head and neck. The neck is stabilized in the direction of travel at the trot allow for greater movement efficiency. A high head position at the trot reduces the dorsoventral motion of the thoracolumbar spine and reduces gait efficiency. In the ridden horse both lifting the neck and holding the neck in a low flexed position shifted the COM towards the hindquarters.3 Waldern et al. showed that induced variations in head and neck positions changed vertical ground reaction forces, stride length and timing when compared to an unrestrained head and neck in sound horses.4 Buchner et al. induced lameness in 11 horses and found that the vertical acceleration of the head and neck as well as the displacement amplitude of the tuber sacrale were the best indicators of lameness compensation.6

69 In the study by Clayton et al., skin markers were used to measure sagittal vertebral angulations (flexion/extension) in the live horse.8 The C1 segment and the C6 segment had the largest changes in angulation. C1 changes the angle of the head relative to the neck whereas C6 raises and lowers the head. In a neutral position the lower cervical vertebrae are in extension due to the ventrally convex lower cervical curve. Therefore, the lower cervical joints are able to have a larger change in angulation as the neck goes into flexion.

Range of motion in other planes was addressed in another study by Clayton et al, in which skin markers were placed on the head, transverse processes of the cervical vertebrae, and at several other specific sites caudal to the neck.9 The measurements were taken at three positions, chin to girth, chin to hip, and chin to tarsus. As in their previous study on sagittal motion,8 the horses were enticed into the different positions with food. A ten-camera motion analysis system was used to collect data. The angular difference for at all three positions was greatest at C1 and at C6 while the difference at C2 through C5 was fairly uniform. Some left-right asymmetries were found with more lateral bend to the left. In the horse lateral bend is coupled with axial rotation. Only the component of lateral bend was considered in this study. Using a baited technique to induce lateral bend may encourage increased axial rotation and affect lateral bend.

For survival, the neuromuscular system can accomplish a given task in several different ways. If one structure, muscle, joint or neuromuscular unit is compromised, there is another way or several other ways to complete the task. This compensatory movement can be used as an indication of a lack of normal neuro-musculoskeletal function. Horses that have full range and normal neuro-musculoskeletal function are able to bring the head laterally to the axillary area without rotation at C1-C2. Horses that have difficulty with lateral bend at C3-C7 often compensate by prematurely rotating at C1-C2. Rotation was not measured in these studies. In all three of these studies,8-10 C6 was found to have a larger ROM than C2-C5. The greater range of motion at C6 may be a factor in the high incidence of osteoarthritis in lower cervical region in horses.11

Muscle Recruitment Muscles have dual functions that seem contradictory, to create movement and to create stability. The neck must have a large ROM to aid in locomotion, to allow for grazing and to focus vision. However, the vertebrae must be stabilized within the physiologic ROM. The head must be kept stable during trot and gallop. To fulfill these contradictory roles muscles are arranged in several layers with different primary functions. Closest to the vertebrae are small muscles that cross only just one joint or joints with the same function. These are activated with low load and are predominately type I fibers. Type I muscle fibers are slow twitch and do not fatigue easily. Muscles that are used to keep the body upright against gravity, the postural muscles, are usually type I. Even within the muscles closest to the spine there are layers. The smallest muscles close to the vertebrae have a high concentration of proprioceptors for accurate positioning. The next layer consists of slightly larger local muscles that dynamically stabilize the spine. The superficial muscles cross several joints and are either a mix of fiber types or mostly type II. These are the muscles that provide ROM.

The muscles must be recruited i.e. activated in a precise order to allow smooth movement while stabilizing and protecting the vertebrae. The small local muscles should be recruited before or at the same time as the superficial muscles. Based on horses’ fiber type, the deep cervical muscles, longus colli, longus capitis, rectus capitis anterior, and rectus capitis lateralis are postural muscles designed to support the spine and protect it from overuse injury. With neck pain in humans, the activation of this muscle group is impaired.12 Higher electromyography (EMG) activity in the superficial cervical flexors (range of motion muscles), sternocleidomastoid (SCM), and anterior scalene muscles (SC) is seen in patients with neck pain and this may be a compensation for deep cervical flexor muscle (DCF) impairment. In other words, these subjects are using large superficial muscles to stabilize the vertebrae. These muscles should be used for ROM not vertebral stabilization. Lindstrom R et al. measured EMG activity in the SCM and SC in women with chronic neck pain and healthy controls.13 Higher EMG amplitude was found in the neck pain group in ramped flexion and extension in the antagonist muscle. The neck pain group also showed reduced directional specificity of EMG during circular contractions. The EMG amplitude was higher in the SC during flexion and was proportional to intensity of pain. They concluded neck pain impairs neuromuscular control and motor performance.

There is an optimal recruitment pattern however, the cervical region has a high muscular redundancy so that different recruitment patterns are possible to accomplish a specific task. Cervical pain changes the recruitment pattern. Gizzi L et al. injected hypertonic saline into the right splenius capitis muscle of human volunteers and found that while the kinematics of the task did not change, different muscles were active.14 It is interesting to note that different subject adopted different alternative patterns. This study demonstrated that the alteration of afferent input via a painful stimulus altered motor control.

Coordinated muscle activation with appropriate strength is an important mechanism to keep the head upright and protect the cervical structures. As discussed, neck pain changes recruitment patterns and decreases neuromuscular efficiency.15 These effects are seen in head movements, during upper limb movement12 and sudden unexpected whole-body perturbations.16 Boudreau et al. investigated the activation of the splenius capitis (SC) and the sternocleidomastoid (SCM) muscles during sudden unanticipated whole-body perturbations in humans with neck chronic neck pain and healthy controls.16 The neck pain group showed delayed onset and reduced EMG amplitude in the SCM and SC muscles in all perturbations. This altered neural control in response to sudden perturbations may leave the neck vulnerable to injury due to the delayed muscular response.

Delayed muscular response is seen with unilateral arm movements as well. Falla et al. compared cervical flexor (deep cervical flexors, SCM and SC) activity during rapid unilateral arm movements.17 In controls the DCF, SC and SCM were active 50ms after onset of deltoid activity, consistent with feed-forward control. The onset was delayed in the neck pain group and suggested a loss of feed-forward control. Neck pain can alter the activity patterns in muscles that are not in the neck. Testa M et al. measured the force generated between the first molars in a

71 jaw-clenching task and EMG activity in the masseter and anterior temporalis muscles.18 They found that neck pain altered the neuromuscular control of the masseter muscle in the absence of orofacial or temporomandibular disorders.

In addition to altered pattern recruitment, higher EMG activity, and delayed onset of action, early muscle fatigue is also seen with chronic neck pain.19 Two possible contributing factors are: 1) neck pain patients show an inability to relax the muscles after completion of a task, and 2) the muscle fiber type changes over time. Postural muscles typically have a predominance of type I slow twitch fibers. In chronic neck pain the fiber type changes to type IIB fast twitch fibers which fatigue more quickly than Type I fibers.20

Equine cervical pain Cervical pain and stiffness is commonly found in sport horses and is a cause of decreased performance and changes in gait.2 Presenting signs may include: resistance to turning, lameness not localized to the distal limb, poor performance, abnormal gait, loss of power, incoordination, and ataxia.2 Changes in range of cervical motion may be due to joint pathology, tendon/ligament strain, myofascial injury, hyper- or hypotonicity of the myofascia, or neuromuscular dysfunction.3, 21 All of these systems are inter-related and several or all may be involved concurrently. (Table 1) It has been shown that humans with neck pain have altered recruitment patterns, impaired function of cervical stabilizer muscles, poor motor control, and decreased proprioception.12-16, 21,22 These changes could leave the neck open to further injury and continued pain. Eliminating pain does not always lead to resolution of the neuromuscular changes and to be effective the treatment must do more than just eliminate pain.21

The lack of muscle development, muscle atrophy, and abnormal muscle tension that is seen with cervical stiffness often goes unrecognized. Resistance to lateral bend is seen as a training issue rather than a medical issue. If the horse is painful or lacks the appropriate neuromuscular control, it is not possible to improve lateral bend with standard training alone. Because the early signs often go unrecognized, horses that are presented for cervical pain often have advanced or severe pathology. A better understanding of normal function, biomechanics and pathogenesis will aid in early recognition and treatment. Horses presenting with advanced disease can be difficult to treat and often can only be managed. Earlier recognition may lead to improved outcomes and may involve observation of muscle mass, recruitment patterns and movement assessment.

Muscles should be of sufficient mass for the tasks required of them. The neck should have a rounded appearance from dorsal to ventral. Atrophy or lack of development can be seen throughout the cervical region and may indicate poor biomechanics, stiffness and pain. In the upper cervical region, the capitis muscles may feel tense on palpation or be atrophied. A decrease in muscle mass of the paracervical muscles will allow the facets and transverse processes to be more evident. The caudal portion of the splenius muscle is often atrophied

72 leaving the caudal cervical region concave even to the point that the funicular part of the nuchal ligament is prominent. Concurrent with atrophy, the demarcation between muscles and the connective tissue within muscles can be prominent, these can be referred to as muscle tension lines.

Compensatory movement in the cervical region is easily seen in lateral bend. The horse should be able to bring the head laterocaudal to the level of the elbow at a neutral height without rotation. Horses that prematurely rotate at C1-C2 are likely to have a cervical issue. Structural changes in the caudal cervical facets are fairly common and increase with age.23 Because the facets are one of the borders of the intervertebral foramen (IVF) changes can cause nerve dysfunction. Effusion of the articular joint process may distend the joint capsule into the spinal canal and contribute to cord compression.24 Humans with changes in the IVF often have pain, weakness, numbness or abnormal sensation in their hands and arms. In horses, we can see front limb lameness due to cervical issues. Compensatory movement can also include holding the neck in extension or flexion rather than in a neutral position. Changes in neuromuscular control, recruitment pattern, and muscle mass are seen in humans with cervical pain and these changes do not return to normal after resolution of pain.25 Studies in this area of equine medicine are lacking, but it is possible that cervical pain has similar effects in both humans and equines. Certainly, it is common to find horses with changes in cervical muscle mass and poor lateral bend without clinical signs of pain. Chronic degenerative osseous changes of the cervical facets are seen in horses, especially in middle age to older horses.26-28 This indicates a chronic instability which may be due to a lack of appropriate support from soft tissue structures. Degenerative osteoarthritis leads to soft tissue pain and further neuromuscular changes perpetuating the cycle of pain and instability.21 The inflammation in the facet joints is treated with intra-articular anti-inflammatory medication, however, treatment should address pain, neuromuscular, and myofascial deficits.

Rehabilitation Rehabilitation should include pain management, removing restrictions, retraining muscle recruitment and range of motion in that order.27 Pain management may include facet joint injection, systemic anti-inflammatories and local pain relief. Ancillary treatment for pain should include myofascial techniques, acupuncture and stimulation of Ia afferent fibers to help block pain via the Gate Theory. Tui-na is a good myofascial technique that is simple and can be taught to owners for daily use. Stimulating the Ia afferent fibers can be easily done with a hand-held massager used over the entire cervical, poll and shoulder region.

Retraining muscle recruitment is done in humans but has not been studied in horses. Humans are put in good position and asked to move while consciously focusing on the correct muscle recruitment. As soon as they shift from proper biomechanics to a compensatory pattern the

73 movement is stopped and started again from the initial position. The disadvantage with horses is that we cannot ask them to think about using proper biomechanics. We can put them in a good position, ask for movement and praise the correct recruitment pattern. It is important to stop the movement immediately when compensatory patterns are observed. This may mean that only a few degrees of motion are trained initially. For example, if we are presented with a horse that has difficulty in lateral bend to the right and compensates with rotation and movement of the body, we may start with imaging and facet injections +/-systemic non-steroidal anti-inflammatory drugs (NSAIDs). Treatment to relieve restrictions may include spinal manipulation and myofascial therapy. Forty-eight to seventy-two hours post-injection we may begin retraining muscle recruitment. Starting with the head and neck in line with the thoracolumbar spine and at a relaxed level (neither extended or flexed), ask the horse for right lateral bend. Discourage rotation by using both hands on the halter, one near the muzzle and one near the poll. As soon as you feel the first indication of rotation stop the movement and reward the horse. The first attempts may only achieve a few degrees of bend. The goal is using the correct muscle recruitment not the range of motion. With repetitions the ROM will improve. Ideally each session would be only a few repetitions but with many sessions per day. Range of motion should be increased only as it can be done with proper biomechanics. ROM is the last priority.

Summary Cervical pain in humans has been shown to have wide ranging effects. These secondary effects do not necessarily recover after pain is resolved and need further treatment. Changes in muscle recruitment pattern, neuromuscular control and muscle fiber type secondary to pain leave the neck susceptible to injury. Treating these secondary issues is necessary to prevent recurrence of neck pain. Recognizing cervical pain in horses can be difficult. Horses can often maintain a high level of performance using compensatory movement patterns so that cervical pain may go unrecognized. Signs of compensatory movement include, pre-mature rotation with lateral bend, resisting lateral bend in neutral position, individual muscle atrophy or lack of development, and inappropriate muscle tension. Rehabilitation of cervical stiffness should include pain management, clearing restrictions and retraining proper muscle recruitment and ROM to prevent recurrence.

74 References 1. Dunbar D, Macpherson JM, Simmons RW, Zarcades A. Stabilization and mobility of the head, neck and trunk in horses during overground locomotion: comparisons with humans and other primates. 2008 The Journal of Experimental Biology 211, 3889-3907

2. 1. Dyson S Lesions of the equine neck resulting in lameness or poor performance in Divers T ed. Vet Clin North Am Equine Pract 2011 Dec;27(3):417-37

3. 3. Zsoldos RR, Licka TF The equine neck and its function during movement and locomotion 2015 Zoology 118:364-376

4. Waldern NM, Wiestner T, von Peinen K, Gomez Alvarez CG, Roepstroff L, Johnston C. Meyer H, Weishaupt MA Influence of different head-neck positions on vertical ground reaction forces, linear and time parameters in the unridden horse walking and trotting on a treadmill 2009 Eq Vet J 41:268-273

5. Buchner HH, Obermuller S, Scheidl M Body centre of mass movement in the lame horse Equine Vet J Suppl 2001 Apr;(33):122-7

6. Buchner HH, Savelberg HH, Schamhardt HC, Barneveld A Head and trunk movement adaptations in horses with experimentally induced fore- or hind limb lameness 1996 Eq Vet J Jan 28;1:71-76

7. Vorstenbosch MA, Buchner HH, Savelberg HH, Schamhardt HC, Barneveld A Modeling study of compensatory head movements in lame horses Am J Vet Res 1997 Jul;58(7):713-8

8. Clayton HG, Kaiser LJ, Lavagnino M, Stubbs NC Dynamic mobilizations in cervical flexion: effects on intervertebral angles Eq Vet J (2010) 42 (Suppl.38) 688-694

9. Clayton HG, Kaiser LJ, Lavagnino M, and Stubbs NC Evaluation of intersegmental vertebral motion during performance of dynamic mobilization exercises in cervical lateral bending in horses 2012 AJVR, Aug;73(8):1153-9

10. Clayton HG, Townsend HGG Kinematics of the cervical spine of the adult horse 1989 Equine Vet J 21;3:189-192

11. Levine JM, Adam E, MacKay RJ, Walker MA Frederick JD, Cohan ND (2007) Confirmed and presumptive cervical vertebral compressive myelopathy in older horses: a retrospective study (1992-2004) J Vet Intern Med 21, 812-819

12. Falla D, Bilenkij G and Jull G Patients with chronic neck pain demonstrate altered patterns of muscle activation during performance of a functional upper limb task Spine 2004 Jul 1;29(13):143-40

13. Lindstrom R, Shomacher J, Farina D, Rechter L and Falla D Association between neck muscle co-activation, pain and strength in women with neck pain Man Ther 2011 Feb;16(1):80-6 14. Gizzi L, Muceli S, Petke F, Falla D Experimental pain impairs synergistic modular control of neck muscles PLos One 2015 Sep 18;10(9)

15. Falla D, Jull G, Edwards S, Koh K and Rainoldi A Neuromuscular efficiency of the sternocleidomastoid and anterior scalene muscles in patients with chronic neck pain Disabil Rehabil 2004 Jun 17;26(12):712-7

16. Boudreau SA, Falla D Chronic neck pain alters muscle activation patterns to sudden movements Exp Brain Res 2014 Jun;232(6):2011-20

17. Falla D, Lindstrom R, Rechter L, Boudreau S, Petzke F Effectiveness of an 8 weeks exercise programme on pain and specificity of neck muscle activity in patients with chronic neck pain: a randomized controlled study Eur J Pain 2013 Nov;17(10):1517-28

18. Testa M, Geri T, Gizzi L, Petzke F, Falla D Alteration in masticatory muscle activation in people with persistent neck pain despite the absence of orofacial or temporomandibular disorders J Oral Facial Pain Headache 2015 Fall;29(4)340-8

19. Gogia PP and Sabbahi MA Electromyographic analysis of neck muscle fatigue in patients with osteoarthritis of the cervical spine Spine 1994 Mar 1;19(5)502-6

76 20. Falla D, Rainoldi A, Merletti R and Jull G Myoelectric manifestations of sternocleidomastoid and anterior scalene muscle fatigue in chronic neck pain Clin Neurophysiol 2003 Mar;114(3):488-95

21. Falla D Unraveling the complexity of muscle impairment in chronic neck pain Manual Therapy 9 (2004) 125-33

22. Falla D, Jull G and Hodges PW Feed-forward activity of cervical flexor muscles during voluntary arm movements is delayed in chronic neck pain Exp Brain Res 2004 Jul;157(1):43-8

23. Down SS, Henson FM Radiographic retrospective study of the caudal cervical articular process joints in the horse. Equine Vet J. 2009 Jul;41(6):518-24.

24. Claridge HA, Piercy RJ, Parry A, Weller R. The 3D anatomy of the cervical articular process joints in the horse and their topographical relationship to the spinal cord. Equine Vet J. 2010 Nov;42(8):726-31.

25. Sterling M, Jull G, Vicenzino B. Kenardy J, Darnell R Development of motor dysfunction following whiplash injury 2003 Pain 103:65-73

26. Dyson S The cervical spine and soft tissues of the neck In Dyson S, Ross M, ed Diagnosis and Management of Lameness in the Horse 2nd Ed St Luis Mo:Elsevier 2011 660-616

27. Comerford M Retraining strategies for uncontrolled movement in Kinetic Control: The Management of Uncontrolled Movement 1st Ed Chatswood, Austrailia Elsevier 2012 pg 63-82 27. Carr E, Maher O Neurologic causes of gait abnormalities in the athletic horse In Hinchcliff K, Kaneps A, Geor R eds. Equine Sports Medicine and Surgery 2nd Ed Saunders Elsevier 2014 503-526

28. Rombach N, Stubbs NC, Clayton HM Prevalence of osseous pathology in the articular process articulations in the equine cervical and cranial thoracic vertebrae 2014 British Equine Veterinary Medical Assn Congress Eq Vet J 46;S47

77 Table 1 Normal cervical function and changes seen with dysfunction

Normal Dysfunction Motion at walk Figure 8 Stiff +/- extended Lateral bend No rotation until past axilla Premature rotation Muscle mass Full Small. May see prominent vertebrae and nuchal ligament Muscle tone Good tone without tension Tension lines Muscle fiber type* Type I non-fatiguing Type II fatiguable Muscle recruitment Low load postural muscles Global mobility muscles used for stabilization for stabilization Muscle timing Quick onset Delayed onset *from human research

Abbreviations COM center of mass DCF deep cervical flexors EMG electromyography NSAID non-steroidal anti-inflammatory drug ROM range of motion SCM sternocleidomastoid muscle SC anterior scalene muscles

78 UNDERSTANDING BACK PAIN, THORACOLUMBAR FASCIA AND THE MIDDLE COMPARTMENT Carla W Pasteur MS DVM Rising Sun Equine Clinic LLC 4500 NW 95th Avenue Rd Ocala, FL 34482 [email protected]

Introduction Back pain in horses can be a frustrating problem for all involved, horses, owners and veterinarians. Finding the source or the damaged structure responsible can be difficult if not impossible. Even when a structural problem is found treatment may not resolve the pain long term. Habitual gaits patterns and poor recruitment of abdominal muscles may perpetuate vertebral instability and continued pain.

Movement and Stability The greatest range of motion (ROM) in flexion/extension of the thoracolumbar (TL) spine is at the lumbosacral junction, followed by T18-L1 and T1-T2. The divergent angle of the dorsal spinous processes at L6-S1 allows for greater ROM in extension compared to other joints in the thoracolumbar spine. Axial rotation and lateral bend were greatest in the caudal thoracic region, T14-T16.1 Lateral bend and axial rotation are coupled movements in the equine spine.2

There are 254 joints from T1 to L6 in the horse. Each one needs to be able to move through a normal range of motion and at the same time remain stable. Movement must be contained within the physiologic ROM and controlled at every position throughout the range. The ability to stiffen the spine during limb movements is essential for efficient locomotion. Stabilization of the TL spine is important for locomotion and efficient energy transfer from the limbs. Stabilization is necessary to keep each joint within its physiologic range of motion (ROM). When joint ROM exceeds its physiologic limits, clinical instability may result. Clinical instability is damage or disruption of structures that limit joint movement. Functional instability is an inability to hold a joint in the desired position i.e. resist movement.3 Functional instability may be seen when the primary stabilizing structure is not available due to pain or dysfunction. In this case a secondary strategy will be used to stabilize the joints. Often the secondary strategy is slower and less efficient and the functional instability remains.

79 Appropriate spinal stability depends on three systems neural, active and passive. Neural control provides proper timing and recruitment of muscles as well as integrating sensory and proprioceptive feed-back. The active system includes muscles which need the ability to respond to neural control and strength to initiate and control movement. The passive system includes ligaments, fascia, joint capsules and osseous conformation.4 Functional instability can lead to microdamage. This microdamage is sub-clinical but as it is repeated over time microdamage can accumulate until the structure fails. Horses with back pain often present with chronic changes. One model to explain this is the functional instability model. Pain is initiated due to stress or fatigue which leads to a change in muscle recruitment. Typically, the local stabilizer, in this case the multifidus, has delayed or sub-optimal recruitment. The horse compensates by using a global stabilizer, the longissimus, to stabilize the spine. Horses and especially those with athletic ability are able to compensate for the functional instability using this secondary strategy with little to no loss of performance. Microdamage due to the instability eventually accumulates until it overwhelms the horse’s ability to compensate and the horse is presented for back pain.

The greatest ROM of the TL spine is in flexion and extension. Flexion of the thoracolumbar column is induced by contraction of abdominal muscles, lowering of the neck, retraction of the forelimb and protraction of the hindlimb.5 During flexion the longissimus dorsi (LD) must be eccentrically active to resist flexion and stabilize the spine. For example, in gallop the hind limbs are propelled forward by release of stored energy in the elastic elements and muscular action. This explosive protraction induces rapid flexion of the thoracolumbar spine. Flexion must be controlled to prevent movement outside of the physiologic range, damage to vertebrae and surrounding structures. The LD is part of the active system that controls flexion. The main action of the LD is to stabilize the vertebral column against dynamic forces.5 Loss of control of back flexion can be seen in humans with chronic non-specific low back pain.6 Interestingly, in humans this hyperflexion of the thoracolumbar spine can be compensation for to a lack of hip flexion. In a forward bending task, excessive flexion occurs in the thoracolumbar spine because the hip joints do not flex enough.7 Extension of the TL spine is due to contraction of the epaxial muscles, elevating the head, protraction of the forelimbs, retraction of the hindlimbs, weight of the abdominal viscera.5 The abdominal muscles and fascia control thoracolumbar extension.

Epaxial Muscles Muscles can be divided into three groups; local stabilizers, global stabilizers and global mobilizers.7 In the equine back the multifidus could be considered a local stabilizer, the longissimus a global stabilizer. Although these muscles are used for movement as well, their primary role seems to be stabilization.

The multifidus muscle typically has 5 muscle bundles per segment. These bundles originate on

80 the lamina and dorsal spinous processes. The fibers run from cranial to caudal and insert on the mammillary processes and sacrum. The multifidus has a high concentration of proprioceptors and connective tissue and aids in controlling flexion and axial rotation. The size of the multifidus increases where the vertebrae have increased ROM. The multifidus has more bulk at the lumbosacral junction. The pennation angle is greater in this region as well. A large physiologic cross section and a greater pennation angle imply that the muscle can generate high isometric force and is used to stabilize joints.8,9 In humans, the multifidus is recruited in preparation for movement. Stabilization of the spine occurs prior to movement. This would protect the spine and aid in efficient transfer of energy from the limbs. In rats the multifidus is tonically active during all movements that need trunk stabilization.10 The same was found in cats and horses trotting on a treadmill.11,12

In people with low back pain the recruitment of the multifidus was delayed. Delayed recruitment of the multifidus and alterations in recruitment of other trunk muscles indicate changes in neuromuscular control that may leave the spine open to injury. EMG studies “indicate that the neural system in back pain patients may have more difficulty in maintaining a coordinated and controlled exertion during axial rotation”. 13 As stated above the atrophy of the multifidus is seen with back pain. This atrophy does not spontaneously resolve with resolution of pain perhaps because of the changes in neural control.14 It is thought that this may be why back pain tends to recur. If the multifidus does not recover sufficient mass to stabilize the spine, functional instability and pain may follow. Specific exercise programs increased the size of the multifidus in low back pain patients and healthy controls and decreased pain.15,16

The LD muscle is primarily a global stabilizer. The LD muscle has different architecture in different regions of the spine indicating that its function varies. In the cranial thoracic region, the muscle fibers are longer and have a smaller pennation angle. This muscle architecture indicates more of a mobilizing role. Stabilization in this area is aided by the ribs and sternum. The spinalis muscle is also present in this region. The fibers of the spinalis course from craniodorsal to caudoventral while the fibers of the LD are oriented in the opposite direction, caudodorsal to cranioventral. The different orientation of the muscle fibers of the spinalis and the LD could contribute to stabilization of the cranial thoracic vertebrae when the muscles are active simultaneously. In the lumbar region, the fibers of the LD are shorter and have a larger pennation angle indicating its role as a stabilizer. EMG recordings show that the LD is active at times when the propulsion from the hind limbs would cause flexion of the spine. At the walk, the longissimus shows weak activity during mid-stance, at trot it is most active during late stance and early swing and at canter during swing phase of the leading hind limb.17,18

The Middle Compartment A common strategy to hold a joint in a specific position and keep it stable to resist other forces, is co-contraction. Co-contraction means simultaneous, isometric contraction of both flexors and extensors. For example, imagine someone handing you a heavy object. In anticipation of the weight you would isometrically contract your biceps and triceps to stabilize your elbow. This co- contraction is used to prevent elbow extension. In the caudal thoracic and cranial lumbar region

81 co-contraction of the abdominal and epaxial muscles helps to stabilize the spine. One difference between the arrangement of flexor and extensors in this region compared to the limbs is that the flexors (abdominal muscles) are far removed from the vertebrae. The rectus abdominis muscle helps to limit vertebral extension by supporting the weight of the viscera and encouraging ventroflexion. It does little to stabilize individual vertebrae.

The cranial thoracic region has the sternal ribs and sternum for added stabilization and the sacral region has the bony ring of the pelvis. But the caudal thoracic and lumbar spine lacks additional osseous stabilization and perhaps due to the lack of osseous stabilization, it is the area with the greatest ROM. Increased intra-abdominal pressure may aid in stabilizing the caudal thoracic and lumbar spine. In humans, the transversus abdominis (TA) is vital for maintaining proper tension on the lumbar vertebrae and sacroiliac joint. The TA attaches to the thoracolumbar fascia which is a dense aponeurosis with limited elasticity. Tension on the thoracolumbar fascia may help limit or control vertebral flexion while contraction of the TA and abdominal muscles limits or controls extension. There must be a certain amount of pressure in the abdominal cavity to keep tension on the myofascia. The transversus abdominis works with the epaxial musculature, diaphragm and pelvic floor muscles to modulate intra-abdominal pressure. However, most of these same muscles are needed for respiration and to maintain continence. Fine, coordinated control of this myofascial system is needed to maintain continence and breathing while at the same time supporting the vertebrae. Tensing the thoracolumbar fascia supports the lumbar spine (in pigs and humans) Studies in pigs showed that electrostimulation of diaphragm increases intra-abdominal pressure and stabilizes the lumbar vertebrae. Cutting the thoracolumbar fascia reduces lumbar stability and injury to porcine thoracolumbar fascia produces changes also seen in humans with chronic low back pain.19-21 These findings using a porcine model indicate that intra-abdominal pressure may be part of the thoracolumbar stabilization system in quadrupeds as well as in bipeds.

Some of the muscles used for respiration are also used to stabilize the spine by regulating intra- abdominal pressure i.e. the diaphragm, TA, abdominal muscles and pelvic floor muscles. In humans and in horses breathing is linked to the stride cycle. The tensioning system is "weakest" at the end of inspiration in humans and when running neither people nor horses have heel strike at that point. It is "strongest" at the end of expiration and there is always heel strike at that point. Marathon runners are able to keep this relationship but high-altitude climbers are not. During arm movement with normal O2 the diaphragm and transverse abdominal are tonically active to stabilize the spine, on top of this tonic activity, there are bursts of higher activity during respiration. When hypercapnia is induced the tonic activity disappears and the phasic activity continues; the CNS prioritizes breathing over spinal stability. People with COPD don't use the diaphragm for postural control; it is prioritized to breathing. They also don't use the transverse abdominal for breathing instead use superficial ab muscles. they don't use the fascial tensioning system for postural control they stiffen and brace. People with COPD have significantly more back pain than people without.22

82 Standardbred horses at high speed on a treadmill (11m/s) had synchronized respiration and stride cycle with one inspiration/expiration per stride. Approximately 57% of the stride duration was available for inspiration and only 43% for expiration. Hypercapnia, acidosis and muscular fatigue may occur quickly at high speed because of this decrease in expiration duration which is mechanically linked to the stride cycle both at the trot and gallop.23 Cotrel et al found that Standardbred trotters exercise on a track at velocities of 8.3 to 21.4 m/s found that some horses had a 3:2 ratio of strides:respirations. Better performers had higher ratios.24 Preventing hypercapnia may allow the muscles of respiration to continue to be used for both respiration and spine stability and thereby indirectly help prevent back pain.

Back Pain Horses with back pain have decreased F/E and axial rotation and a decrease in stride length.25 Much of the flexion and extension of the spine is due to protraction and retraction of the limbs. A decrease in stride length will help to decrease F/E of the back. Persistent muscular activity is used decrease ROM and to stabilize the lumbar spine in humans with back pain.26 The kinematics of horses with back pain was studied at walk and trot. Because the center of rotation for the hind limb at gallop is the lumbosacral junction it is possible that the decrease in stride length may be even greater at gallop. In another study, Wennerstrand et al looked at kinematic changes with unilateral induced back pain.27 After lactic acid injection into the left longissimus dorsi muscle the caudal thoracic region was more extended at walk and trot and was held in left lateral bend. After a week, this lateral bend was reversed to right lateral bend at the walk. Induced back pain in trotters led to stiffness of the TL spine, reduced performance and changes in stride characteristics.

Atrophy of the multifidus muscle ipsilateral to osseous pathology is seen in humans, pigs and horses.28 There is a significant association between the grade of osseous pathology and the degree of multifidus asymmetry. It is unknown which is the primary lesion. The multifidus is a stabilizer of the spine; dysfunction in this muscle would lead to a functional instability and to osseous change. The study by Stubbs et al was done Thoroughbred racehorses that train and compete at a gallop. The lumbosacral junction is the center of rotation of the hind limb at gallop and ROM in flexion/extension of the lumbosacral joint is linearly correlated with speed. These two factors combined may predispose these subjects to pathology of the TL region and perhaps even more so in higher quality race horses.

Osseous pathology is common in Thoroughbred race horses even without a history of back pain.29 Osseous changes are not limited to horses that gallop. A study by Coutsy et al of French Trotters found radiographic lesions in 62% of horses without back pain and in 98% of horses with back pain.30 This type of bony change indicates a chronic instability and lack of stabilization from the active and passive components, the muscles and the fascia, tendons and ligaments. Pain can cause a change in the timing of muscle action, a change in the muscles used for stabilization, and a change in the muscle fiber type.31-33 With chronic pain onset of action of stabilizer muscles

83 is delayed, secondary muscles are used for stabilization and with chronic pain type I postural muscle fibers are replaced with type II fibers which fatigue more quickly. All of these changes decrease stability of the vertebrae leaving the spine open to injury and chronic bony pathology. While the paralumbar muscles should be used to actively stabilize the vertebrae in patients with back pain, muscle atrophy is commonly seen. Spine and peripheral joint disease with pain can cause reflex inhibition of motor neurons, resulting in weakness and atrophy of associated muscles.34

Atrophy of the multifidus is seen in with osseous abnormalities and clinically back pain and atrophy of the LD are seen together.28 In young Thoroughbreds in racing training changes in LD and middle gluteal mass and tone can be observed and may correlate with growth patterns and stage of training. A decrease of tone in the longissimus lumborum and an apparent hypertrophy of the middle gluteal dorsal at the level of the lumbosacral junction and sacroiliac joint is often seen with a croup high stage of growth. This same pattern of muscle change is seen in some horses when they begin increasing gallop speed during training. Research needs to be done in this area to determine the exact changes associated with these observations and the effect on spinal stabilization and biomechanics.

Neck and back pain leads to changes in muscle recruitment, both in timing of muscle action and the muscles recruited for the task. There is some evidence to indicate these changes occur quickly after onset of pain.35 Resolution of pain does not always lead to resolution of the neuromuscular changes.35,36 The finding that the neuromuscular changes remain after resolution of pain is one reason that neck and back pain tends to recur. Treatment of pain is needed so that it does not interfere with neuromuscular retraining. Complete treatment of back pain should address the neuromuscular changes as well as the pain itself.

Summary The function of the TL spine is vital to the athletic performance of the horse. The vertebrae need to be mobile and at the same time resist movement. Stability of the spine is needed for efficient energy transfer from the limbs and to protect the vertebrae and spinal cord from injury. At trot and canter flexion and extension of the equine spine is largely due to movement of the limbs and the weight of the viscera. The epaxial muscles are used to stabilize the spine and limit/control flexion. Extension of the spine is controlled by the abdominal muscles. Increasing intra- abdominal pressure helps to stabilize the spine in both flexion and extension.

Abbreviations F/E flexion/extension LD longissimus dorsi

84 ROM range of motion TA transversus abdominis TL thoracolumbar

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88 BISPHOSPHONATES IN EQUINE PRACTICE Robert P. Boswell, DVM

Bisphosphonates have been widely used in human medicine to treat conditions of abnormal bone remodeling for 40 years. Its use in patients with tumor metastasis to bone has been associated with significant pain relief. Two bisphosphonates, Clodronate and Tiludronate (Osphos® and Tildren®), are currently approved for use in horses older than 4 years of age. These two drugs entered the market in 2014, and have a narrow FDA approval for use to treat navicular syndrome in horses older than 4 years of age. They are both reported to work by osteoclast inhibition in cases of excess bone resorption, thereby returning a “balance” between osteoclast mediated bone resorption and osteoblast mediated new bone production. Although there are several published reports of the benefits of Tildren®, I have not seen those same benefits in my practice. My experience with the use of Osphos® however has been positive. The ease of administration and the overall difference in cost also favor the use of Osphos®. As would be expected their extra-label use has been broad. In many cases reported benefits would seem to be unrelated to their anti-resorptive properties. The literature is full of published works regarding the use, benefits, and complications associated with the use of bisphosphonates in human medicine. Of the reports of adverse events, most are associated with the use of the nitrogenous family of bisphosphonates, and atypical femoral fracture and osteonecrosis of the jaw are the most serious. Several prominent equine veterinarians have recently expressed serious concerns regarding the use of bisphosphonates in equine practice. It is their opinion that inappropriate case selection and overzealous use could interfere with normal bone remodeling and predispose normal bone to fracture. Have veterinarians in practice using bisphosphonates experienced this complication or other adverse events? If so, what are they, what were the outcomes, and how have veterinarians adjusted their case selection? A recent paper reports no measurable change in bone remodeling with either Tildren® or Osphos® in horses when administered at the recommended dose for each drug. Nevertheless, the use of bisphosphonates is now widespread and the benefits are real. If not from decreasing osteoclastic activity, how are these benefits explained? What is really going on? The anti- inflammatory and analgesic properties of bisphosphonates are well known and perhaps are responsible for part, or in some cases all, of the reported benefits. Therefore, from a practical standpoint when do I consider or recommend the use of bisphosphonates in my practice? Once selected, what is the best dose and frequency? When should I expect to see benefit? How concerned should I be with respect to any adverse events, and what would that/they most likely be?

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