Assessment of Traumatic Nerve Injuries

American Association of Neuromuscular & Electrodiagnostic Medicine AANEM

ASSESSMENT OF TRAUMATIC NERVE INJURIES

Lawrence R. Robinson, MD Jeffrey G. Jarvik, MD, MPH David G. Kline, MD

2005 AANEM COURSE G AANEM 52nd Annual Scientific Meeting Monterey, California

Assessment of Traumatic Nerve Injuries

Lawrence R. Robinson, MD Jeffrey G. Jarvik, MD, MPH David G. Kline, MD

2005 COURSE G AANEM 52nd Annual Scientific Meeting Monterey, California AANEM

PRINTED BY JOHNSON PRINTING COMPANY, INC. ii Assessment of Traumatic Nerve Injuries

Faculty

Lawrence R. Robinson, MD David G. Kline, MD Professor Boyd Professor and Head Department of Rehabilitation Medicine Department of Neurosurgery University of Washington Louisiana State University Medical Center Seattle, Washington New Orleans, Louisiana Dr. Robinson attended Baylor College of Medicine and completed his res- Dr. Kline is currently a Boyd Professor and Head of the Department of idency training in rehabilitation medicine at the Rehabilitation Institute of Neurosurgery at Louisiana State University (LSU) Medical Center in New Chicago. He now serves as professor and chair of the Department of Orleans. He earned his medical degree from the University of Rehabilitation Medicine at the University of Washington and is the Pennsylvania, then performed his internship at the University of Michigan. Director of the Harborview Medical Center Electrodiagnostic Laboratory. He performed residencies at the University of Michigan and Walter Reed He is also currently Vice Dean for Clinical Affairs at the University of General Hospital and Institute of Research. Dr. Kline has served on sever- Washington. His current clinical interests include the statistical interpreta- al editorial boards including Neurosurgery, Microsurgery, and the Journal tion of electrophysiologic data, laryngeal electromyography, and the study of Reconstructive Microsurgery, among others. He is also active in many of traumatic neuropathies. He recently received the Distinguished medical societies. Dr. Kline was recently named a Boyd Professor at LSU, Academician Award from the Association of Academic Physiatrists and this which is only given to faculty members who have attained national or year is receiving the AANEM Distinguished Researcher Award. international distinction for outstanding teaching, research, or other cre- ative achievement. Jeffrey G. Jarvik, MD, MPH Professor Department of Radiology and Neurology

Adjunct Professor Faculty had nothing to disclose. Department of Health Services University of Washington Seattle, Washington As Director of Neuroradiology at the University of Washington, Dr. Jarvik’s clinical work encompasses the entire range of neuroradiology. His clinical and research focus has been on spinal and peripheral nerve imaging. His academic focus has been on health services as it relates to diagnostic imaging, e.g., how diagnostic imaging influences therapeutic decision making and patient outcomes. Dr. Jarvik is a member of the American Society of Neuroradiology, the American College of Radiology, and the Radiological Society of North America, among others.

Please be aware that some of the medical devices or pharmaceuticals discussed in this handout may not be cleared by the FDA or cleared by the FDA for the specific use described by the authors and are “off-label” (i.e., a use not described on the product’s label). “Off-label” devices or pharmaceuticals may be used if, in the judgement of the treating physician, such use is medically indicated to treat a patient’s condition. Information regarding the FDA clearance status of a particular device or pharmaceutical may be obtained by reading the product’s package labeling, by contacting a sales representative or legal counsel of the manufacturer of the device or pharmaceutical, or by contacting the FDA at 1-800-638-2041.

Course Chair: Alan R. Berger, MD

The ideas and opinions expressed in this publication are solely those of the specific authors and do not necessarily represent those of the AANEM. iii Assessment of Traumatic Nerve Injuries

Contents

Faculty ii

Objectives iii

Course Committee iv

Traumatic Nerve Injury to Peripheral Nerves 1 Lawrence R. Robinson, MD

Peripheral Nerve Magnetic Resonance Imaging: The Median Nerve in Carpal Tunnel Syndrome 11 Jeffrey G. Jarvik, MD, MPH Surgical Management of Nerve Injuries 19 David G. Kline, MD

CME Self-Assessment Test 29

Evaluation 31

Member Benefit Recommendations 33

Future Meeting Recommendations 35

O BJECTIVES—This course will provide an overview of the evaluation and management of traumatic nerve injuries. After attending this course, the participant will (1) understand the importance and time frame for the electrodiagnosis of nerve trauma, (2) learn the “state- of-the-art” concepts and future potential of neuroimaging of peripheral nerve injuries, and (3) learn the most important principles of the clinical and surgical management of peripheral nerve injuries. P REREQUISITE—This course is designed as an educational opportunity for residents, fellows, and practicing clinical EDX physicians at an early point in their career, or for more senior EDX practitioners who are seeking a pragmatic review of basic clinical and EDX principles. It is open only to persons with an MD, DO, DVM, DDS, or foreign equivalent degree. A CCREDITATION S TATEMENT—The AANEM is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education (CME) for physicians. CME CREDIT—The AANEM designates attendance at this course for a maximum of 3.25 hours in category 1 credit towards the AMA Physician’s Recognition Award. This educational event is approved as an Accredited Group Learning Activity under Section 1 of the Framework of Continuing Professional Development (CPD) options for the Maintenance of Certification Program of the Royal College of Physicians and Surgeons of Canada. Each physician should claim only those hours of credit he/she actually spent in the activity. The American Medical Association has determined that non-US licensed physicians who participate in this CME activity are eligible for AMA PMR category 1 credit. CME for this course is available 9/05 - 9/08. iv

2004-2005 AANEM COURSE COMMITTEE

Kathleen D. Kennelly, MD, PhD Jacksonville, Florida

Thomas Hyatt Brannagan, III, MD Dale J. Lange, MD Jeremy M. Shefner, MD, PhD New York, New York New York, New York Syracuse, New York

Timothy J. Doherty, MD, PhD, FRCPC Subhadra Nori, MD T. Darrell Thomas, MD London, Ontario, Canada Bronx, New York Knoxville, Tennessee

Kimberly S. Kenton, MD Bryan Tsao, MD Maywood, Illinois Shaker Heights, Ohio

2004-2005 AANEM PRESIDENT

Gary Goldberg, MD Pittsburgh, Pennsylvania Traumatic Injury to Peripheral Nerves

Lawrence R. Robinson, MD Professor and Chair Department of Rehabilitation Medicine University of Washington Seattle, Washington

EPIDEMIOLOGY OF PERIPHERAL NERVE TRAUMA 60% have a traumatic brain injury.30 Conversely, of those with traumatic brain injury admitted to rehabilitation units, Traumatic injury to peripheral nerves results in considerable 10-34% have associated peripheral nerve injuries.7,14,39 It is disability everywhere in the world. In peacetime, peripheral often easy to miss peripheral nerve injuries in the setting of nerve injuries commonly result from trauma due to motor CNS trauma. Since the neurologic history and examination vehicle accidents, and less commonly from penetrating trau- is limited, early hints to a superimposed peripheral nerve ma, falls, and industrial accidents. Out of all patients admit- lesion might be only flaccidity, areflexia, and reduced move- ted to Level I trauma centers, it is estimated that roughly 2- ment of a limb. 3% have peripheral nerve injuries.30,36 If plexus and root injuries are also included, the incidence is about 5%.30 Peripheral nerve injuries are of significant import as they impede recovery of function and return to work, and carry In the upper limb, the most commonly reported nerve risk of secondary disabilities from falls, fractures, or other sec- injured is the radial nerve, followed by the ulnar and median ondary injuries. An understanding of the classification, nerves.30,36 Lower limb peripheral nerve injuries are less com- pathophysiology, and electrodiagnosis of these lesions is crit- mon, with the sciatic nerve most frequently injured, followed ical to the appropriate diagnosis, localization, and manage- by the peroneal and rarely tibial or femoral nerves. Fractures ment of peripheral nerve trauma. of nearby bones are commonly associated, such as humeral fractures with radial neuropathy. CLASSIFICATION OF NERVE INJURIES In wartime, peripheral nerve trauma is much more common and most of physician’s knowledge about peripheral nerve There are two predominant schemes that have been proposed injury, repair, and recovery comes from experience derived in for classification of peripheral nerve traumatic injuries; that World Wars I and II, and subsequent wars.20,35,40 of Seddon35 and that of Sunderland40 (Table 1). The former is more commonly used in the literature. Seddon has used the Peripheral nerve injuries may be seen as an isolated nervous terms “neurapraxia,” “axonotmesis,” and “neurotmesis” to system injury, but may also accompany central nervous sys- describe peripheral nerve injuries.35 Neurapraxia is a compar- tem (CNS) trauma, not only compounding the disability, but atively mild injury with motor and sensory loss but no evi- making recognition of the peripheral nerve lesion problemat- dence of Wallerian degeneration. The nerve distally conducts ic. Of patients with peripheral nerve injuries, approximately normally. Focal demyelination and/or ischemia are thought 2 Traumatic Injury to Peripheral Nerves AANEM Course to be the etiologies of the conduction block. Recovery may intact stroma and corresponds to Seddon’s classification of occur within hours, days, weeks, or up to a few months. neurapraxia. Prognosis is good. Second degree injury involves Axonotmesis is commonly seen in crush injuries. The axons transection of the axon but with intact stroma. Recovery can and their myelin sheaths are broken, yet the surrounding occur by axonal regrowth along endoneurial tubes. Third stroma (i.e., the endoneurium, perineurium, and epineuri- degree injury represents transection of the axon and um) remains partially or fully intact. Wallerian degeneration endoneurial tubes, but the surrounding perineurium is occurs, but subsequent axonal regrowth may proceed along intact. Recovery depends upon how well the axons can cross the intact endoneurial tubes. Recovery ultimately depends the site of the lesion and find endoneurial tubes. Fourth upon the degree of internal disorganization in the nerve as degree injury involves loss of continuity of axons, endoneur- well as the distance to the end organ. ial tubes, and perineurium. Individual nerve fascicles are transected and the continuity of the nerve trunk is main- Sunderland’s classification further divides peripheral nerve tained only by the surrounding epineurium. Traction injuries injuries category. Neurotmesis describes a nerve that has been commonly produce these types of lesions. Prognosis is usual- either completely severed or is so markedly disorganized by ly poor absent surgical intervention because of the marked scar tissue that axonal regrowth is impossible. Examples are internal disorganization of guiding connective tissue ele- sharp injury, some traction injuries, or injection of noxious ments and associated scarring. Fifth degree injury describes drugs. Prognosis for spontaneous recovery is extremely poor transection of the entire nerve trunk and is similar to without surgical intervention. Seddon’s neurotmesis.

Sunderland40 uses a more subdivided scheme to describe Some authors have described another “degree” of injury, peripheral nerve injuries, with five groups instead of three. First known as sixth degree injury.25 This is a mixed lesion with degree injury represents conduction block with completely both axon loss and conduction block each occurring in some

Table 1 Classification Systems for Nerve Injury

Seddon Sunderland Classification Classification Pathology Prognosis Neurapraxia First degree Myelin injury or ischemia Excellent recovery in weeks to months Axonotmesis Axons disrupted Good to poor, depending upon integrity of Variable stromal disruption supporting structures and distance to muscle Second degree Axons disrupted Good, depending upon distance to muscle Endoneurial tubes intact Perineurium intact Epineurium intact Third degree Axons disrupted Poor Endoneurial tubes disrupted Axonal misdirection Perineurium intact Surgery may be required Epineurium intact Fourth degree Axons disrupted Poor Endoneurial tubes disrupted Axonal misdirection Perineurium disrupted Surgery usually required Epineurium intact Neurotmesis Fifth degree Axon disrupted No spontaneous recovery Endoneurial tubes disrupted Surgery required Perineurium disrupted Prognosis after surgery guarded Epineurium disrupted

Adapted from Dillingham.8 AANEM Course Assessment of Traumatic Nerve Injuries 3 fibers. This type of lesion is probably quite common and described elsewhere10,27 and will be only briefly reviewed. requires skillful electrodiagnostic data collection and analysis There are changes in both the axon and the nerve cell body. to separate from pure axon loss lesions. In the axon, a number of changes occur in the first 2 days including leakage of axoplasm from the severed nerve, swelling of the distal nerve segment, and subsequently disap- EFFECTS OF NEURAPRAXIA ON NERVE AND MUSCLE pearance of neurofibrils in the distal segment. By day three, there is fragmentation of both axon and myelin with the As noted above, neurapraxic injuries to peripheral nerves may beginning of digestion of myelin components. By day eight, be due to ischemia or focal demyelination. When ischemia the axon has been digested and Schwann cells are attempting for a brief period (i.e., up to 6 hours) is the underlying cause, to bridge the gap between the two nerve segments. Nerve there are usually no structural changes in the nerve, though fibers may also degenerate for a variable distance proximally; there may be edema in other nearby tissues.18 depending upon the severity of the lesion, this retrograde degeneration may extend for several centimeters. On the other hand, in neurapraxic lesions due to focal demyelination, there are anatomic changes predominantly If the lesion is sufficiently proximal, there are also a number affecting the myelin sheath, but sparing the axon. Tourniquet of changes at the nerve cell body level occurring after nerve paralysis has been used to produce an animal model of a neu- trauma. Initially, within the first 48 hours, the Nissel bodies rapraxic lesion, though it is recognized that acute crush (the cell’s rough endoplasmic reticulum) break apart into fine injuries may be different in mechanism than prolonged particles. By 2 to 3 weeks after injury, the cell’s nucleus application of a tourniquet.31 In this model, anatomic becomes displaced eccentrically and the nucleolus is also changes along the nerve are most marked at the edge of the eccentrically placed within the nucleus. These changes may tourniquet where a significant pressure gradient exists reverse as recovery occurs. between the tourniquet and nontourniquet areas. The pressure gradient essentially “squeezes” out the myelin with resulting invagination of one paranodal region into the next. ELECTRODIAGNOSIS: TIMING OF CHANGES AND As a result, there is an area of focal demyelination at the edge DETERMINING DEGREE OF INJURY of the tourniquet.31 Larger fibers are more affected than smaller fibers. The Compound Motor Action Potential

In this area of focal demyelination, impulse conduction from Neurapraxia one node of Ranvier to the next is slowed as current leakage occurs and the time for impulses to reach threshold at succes- In purely neurapraxic lesions, the compound muscle action sive nodes of Ranvier is prolonged. Slowing of conduction potential (CMAP) will change immediately after injury, velocity along this nerve segment ensues. More severe assuming one can stimulate both above and below the site of demyelination results in complete conduction block. This the lesion (Figure 1a-c). When recording from distal muscles has been reported to occur when internodal conduction and stimulating distal to the site of the lesion, the CMAP times exceed 500-600 ms.33 Since there are very few sodium should always be normal since no axonal loss and no channels in internodal segments of myelinated nerves, con- Wallerian degeneration has occurred. Moving stimulation duction in demyelinated nerves cannot simply proceed slow- proximal to the lesion will produce a smaller or absent ly as it would for normally unmyelinated nerves. Thus, suffi- CMAP, as conduction in some or all fibers is blocked. It cient demyelination results in block of conduction rather should be remembered that amplitudes normally fall with than simply more severe slowing. increasing distance between stimulation and recording; hence there is some debate about how much of a drop in amplitude There are relatively few changes in muscle as a result of neu- is sufficient to demonstrate conduction block. Amplitude rapraxic lesions. Disuse atrophy can occur when neurapraxia drops exceeding 20% over a 25 cm distance or less are clear- is more than transient. There remains debate as to whether ly abnormal; smaller changes over smaller distances are likely muscle fibrillates after a purely neurapraxic lesion. also suggestive of an abnormality. In addition to conduction block, partial lesions also often demonstrate concomitant slowing across the lesion. This slowing may be due to either EFFECTS OF AXONOTMESIS ON NERVE AND MUSCLE loss of faster conducting fibers or demyelination of surviving fibers. All these changes in the CMAP will generally persist Soon after an axonal lesion, the process of Wallerian degen- until recovery takes place, typically by no more than a few eration begins to occur in nerve fibers. This process is well months postinjury. Most importantly, the distal CMAP will 4 Traumatic Injury to Peripheral Nerves AANEM Course

A B

Figure 1 Representation of changes in the compound muscle action potential (CMAP) after neurapraxia (A), axonotmesis (B), neurotmesis (B), and mixed lesions (C).

never drop in amplitude in purely neurapraxic injuries, since looks the same as conduction block and can be confused with no axon loss or Wallerian degeneration occurs and the distal neurapraxia. Hence neurapraxia and axontomesis cannot be nerve segment remains normally excitable. distinguished until sufficient time for Wallerian degeneration in all motor fibers has occurred, typically about 9 days Axonotmesis and Neurotmesis postinjury.6

Electrodiagnostically, complete axonotmesis (equivalent to As Wallerian degeneration occurs, the amplitude of the Sunderland grades 2, 3, and 4) and complete neurotmesis CMAP elicited with distal stimulation will fall. This starts at look the same, since the difference between these types of about day three and is complete by about day nine.6 lesions is in the integrity of the supporting structures, which Neuromuscular junction transmission fails before nerve have no electrophysiologic function. Thus these lesions can excitability.15,16 Thus in complete axonotmesis at day nine, be grouped together as axonotmesis for the purpose of this one has a very different picture than neurapraxia. There are discussion. absent responses both above and below the lesion. Partial axon loss lesions will produce small amplitude motor Immediately after axonotmesis and for a “few days” there- responses, with the amplitude of the CMAP roughly propor- after, the CMAP and motor conduction studies look the tional to the number of surviving axons. Side-to-side CMAP same as those seen in a neurapraxic lesion. Nerve segments amplitudes can be compared to estimate the degree of axon distal to the lesion remain excitable and demonstrate normal loss, though inherent side-to-side variability of up to 30-50% conduction while proximal stimulation results in an absent or limits the accuracy of the estimate. Using the CMAP ampli- small response from distal muscles. Early on, this picture tude to estimate the degree of surviving axons is also most AANEM Course Assessment of Traumatic Nerve Injuries 5 reliable only early after injury, before axonal sprouting has ing nerve action potentials, there is normally a greater drop occurred. Use of this technique later after injury will tend to in amplitude over increasing distance between stimulating underestimate the degree of axon loss. and recording electrodes, due to temporal dispersion and phase cancellation.22 Amplitude drops of 50-70% over a 25 Mixed Lesions cm distance are not unexpected and it is less clear just what change in amplitude is abnormal. A large focal change over a Lesions which have a mixture of axon loss and conduction small distance is probably significant. Slowing may also block provide a unique challenge. These can usually be sort- accompany partial conduction blocks, as for the CMAP. ed out by carefully examining amplitudes of the CMAP Responses elicited with stimulation and recording distal to elicited from stimulation both above and below the lesion the lesion are normal in pure neurapraxic injuries. and by comparing the amplitude with distal stimulation to that obtained from the other side. The percentage of axon Axonotmesis and Neurotmesis loss is best estimated by comparing the CMAP amplitude from distal stimulation with that obtained contralaterally. Of Immediately after axonotmesis, the SNAP looks the same as the remaining axons, the percentage with conduction block seen in a neurapraxic lesion. Nerve segments distal to the are best estimated by comparing amplitudes or areas obtained lesion remain excitable and demonstrate normal conduction with stimulation distal and proximal to the lesion. Thus if a while proximal stimulation results in an absent or small 1 mV response is obtained with proximal stimulation, a 2 response. Hence neurapraxia and axontomesis can not be dis- mV response is obtained distally, and a 10 mV response is tinguished until sufficient time for Wallerian degeneration in obtained with distal stimulation contralaterally, the clinician all sensory fibers has occurred, typically about 11 days post can deduce that probably about 80% of the axons are lost, injury.6 It takes slightly longer for sensory nerve studies to and of the remaining 20%, half are blocked (neurapraxic) at demonstrate loss of amplitude than for motor studies (i.e., 11 the lesion site. As previously mentioned, this analysis is most days versus 9 days), due to the earlier failure of neuromuscu- useful only in the acute phase, before reinnervation by axon- lar junction transmission compared to nerve conduction. al sprouting occurs. Needle Electromyography F Waves Neurapraxia F waves may change immediately after the onset of a neurapraxic lesion. In a complete block, responses will be absent. The needle electromyography (EMG) examination in purely However, in partial lesions, changes can be more subtle since neurapraxic lesions will show neurogenic changes in recruit- F waves are dependent upon only 3-5% of the axon popula- ment with debatable abnormalities in spontaneous activity. tion to elicit a response.12 Thus partial lesions may have nor- As mentioned earlier, there is debate as to whether fibrillation mal miminal F-wave latencies, and mean latencies, with potentials are recorded after a purely neurapraxic lesion. One reduced or possibly normal penetrance. While F waves are study of peripheral nerve lesions in baboons has failed to conceptually appealing for detecting proximal lesions (e.g., demonstrate fibrillations in purely neurapraxic lesions.17 On brachial plexopathies) it is in few instances that they truly the other hand, study of purely neurapraxic lesions in rats5 provide useful additional or unique information. They are has suggested fibrillations occur in blocked, but not dener- sometimes useful in very early proximal lesions when conven- vated, muscle fibers. There are limited reports of fibrillations tional studies are normal since stimulation does not occur in humans with apparently predominantly neurapraxic nerve proximal to the lesion, but they are not good at distinguish- lesions,43,48 but it is difficult to know whether or not any ing axon loss lesions from conduction block. axon loss had occurred in these patients, since nerve conduction studies (NCSs) are not sensitive for detecting minimal Compound or Sensory Nerve Action Potentials axon loss. Needle EMG is more sensitive for detecting motor axon loss than NCSs, and hence it is easy to imagine situa- Neurapraxia tions in which NCSs are within normal limits, but needle EMG detects minimal or mild axon loss. The sensory nerve action potential (SNAP) and compound nerve action potential (CNAP) will show changes similar to Independent of whether or not the needle EMG demon- the CMAP after focal nerve injury. In the setting of neu- strates fibrillation potentials in neurapraxia, the most appar- rapraxia, there is a focal conduction block at the site of the ent change on needle EMG will be changes in recruitment. lesion, with preserved distal amplitude. However, the criteria These occur immediately after injury. In complete lesions for establishing conduction block in sensory nerve fibers are (i.e., complete conduction block) there will be no motor unit substantially different than that for the CMAP. When record- action potentials (MUAPs). In incomplete neurapraxic 6 Traumatic Injury to Peripheral Nerves AANEM Course lesions, there will be reduced numbers of MUAPs firing more fibrillation numbers does not predict recovery, but rather rapidly than normal (i.e., reduced or discrete recruitment). muscle fibrosis. Recruitment changes alone are not specific for neurapraxia or axon loss. Fibrillations may also occur after direct muscle injury, as well as nerve injury. Partanen and Danner32 have demonstrated Since no axon loss occurs in neurapraxic injuries, there will that patients after muscle biopsy have persistent fibrillation be no axonal sprouting and no changes in MUAP morphol- potentials starting after 6-7 days and extending for up to 11 ogy (e.g., duration, amplitude, or phasicity) anytime after months. In patients who have undergone multiple trauma, injury. coexisting direct muscle injury is common and can be potentially misleading when trying to localize a lesion. Axonotmesis and Neurotmesis When there are surviving axons after an incomplete axonal A number of days after an axon loss lesion, needle EMG will injury, remaining MUAPs are initially normal in morpholo- demonstrate fibrillation potentials and positive sharp waves. gy, but demonstrate reduced or discrete recruitment. Axonal The time between injury and onset of fibrillation potentials sprouting will be manifested by changes in morphology of will be dependent in part upon the length of distal nerve existing motor units. Amplitude will increase, duration will stump. When the lesion is distal and the distal stump is short, become prolonged, and the percentage of polyphasic MUAPs it takes only 10-14 days for fibrillations to develop. With a will increase as motor unit territory increases.9,11 This process proximal lesion and a longer distal stump (e.g., ulnar-inner- occurs soon after injury. Microscopic studies demonstrate vated hand muscles in a brachial plexopathy), 21-30 days are outgrowth of these nerve sprouts starting at 4 days after par- required for full development of fibrillation potentials and tial denervation.21,27 Electrophysiologic studies utilizing sin- positive sharp waves.42 Thus, the electrodiagnostic (EDX) gle-fiber EMG demonstrates increase in fiber density starting physician needs to be acutely aware of the time since injury, at 3 weeks postinjury.26 so that severity is not underestimated when a study is performed early after injury, and also so that development of In complete lesions, the only possible mechanism of recovery increased fibrillation potentials over time is not misinterpret- is axonal regrowth. The earliest needle EMG finding in this ed as a worsening of the injury. case is the presence of small, polyphasic, often unstable MUAPs previously referred to as “nascent potentials.” Fibrillation and positive sharp wave density are usually grad- ed on a 1-4 scale. This is an ordinal scale, meaning that as Observation of these potentials is dependent upon establish- numbers increase findings are worse. However, it is not an ing axon regrowth as well as new neuromuscular junctions interval or ratio scale, i.e., 4+ is not twice as bad as 2+ or 4 and this observation represents the earliest evidence of rein- times as bad as 1+. Moreover, 4+ fibrillation potentials does nervation, usually preceding the onset of clinically evident not reflect complete axon loss, and in fact may represent only voluntary movement.9 These potentials represent the earliest a minority of axons lost.3,9 Evaluation of recruitment and definitive evidence of axonal reinnervation in complete particularly of distally elicited CMAP amplitude are neces- lesions. When performing the examination looking for new sary before a determination can be made whether or not MUAPs, the clinician must be sure to accept only “crisp,” complete axon loss has occurred. nearby MUAPs with a short rise-time, since distant potentials recorded from other muscles can be deceptive and could erro- Fibrillation potential size will decrease over time since injury. neously suggest intact innervation. Kraft24 has demonstrated that fibrillations initially are several hundred microvolts in the first few months after injury. Mixed Lesions However, when lesions are more than 1 year old, they are unlikely to be over 100 µV in size. Fibrillations will also When there is a lesion with both axon loss and conduction decrease in number as reinnervation occurs, however this block, needle EMG examination can be misleading if inter- finding is not usually clinically useful for two reasons. First, preted in isolation. If, for example, a lesion results in destruc- since a qualitative or ordinal scale of fibrillation density is tion of 50% of the original axons and conduction block of typically used and an accurate quantitative measurement of the other 50%, then needle EMG will demonstrate abundant fibrillation density is not available, comparison of fibrillation (4+) fibrillation potentials and no voluntary MUAPs. The numbers from one examination to the other is not reliable.9 EDX physician should not then conclude that there is a com- Second, even in complete lesions, fibrillation density will plete axonal lesion, but should instead carefully evaluate the eventually reduce since the muscle becomes fibrotic and the motor NCSs to determine how much of the lesion is neu- number of viable muscle fibers falls; in this case, reduction in rapraxic and how much is axonotmetic. The important point AANEM Course Assessment of Traumatic Nerve Injuries 7 here is to not take the presence of abundant fibrillations and equina, spinal cord) tend to have normal SNAP amplitudes, absent voluntary MUAPs as evidence of complete denerva- even in the setting of reduced or absent sensation.1,41 This is tion. a particularly bad prognostic sign when seen in the setting of possible root avulsion. On the other hand, lesions occurring distal to the dorsal root ganglion have small or absent SNAPs LOCALIZATION OF TRAUMATIC NERVE INJURIES (when these are recorded in the appropriate distribution). Thus, SNAPs may be useful to differentiate root versus The localization of peripheral nerve injuries is sometimes plexus or other pre- versus postganglionic locations. A limi- straightforward but is potentially complicated by a variety of tation, particularly in partial lesions, is the wide variability in possible pifalls. Localization is usually performed by two SNAP amplitudes seen in normal individuals. Mixed pre- methods: (1) detecting focal slowing or conduction block on and postganglionic lesions are also potentially difficult to NCSs, or (2) assessing the pattern of denervation on needle interpret. EMG. The other major EDX method of determining the site of Localizing peripheral nerve lesions by NCSs usually requires nerve injury is by needle EMG. Conceptually, if the branch- that there be a focal slowing or conduction block as the EDX ing order to various muscles under study is known, the clini- physician stimulates above and below the lesion. To see such cian can determine that the nerve injury is between the a change there must either be focal demyelination or branches to the most distal normal muscle and the most ischemia, or the lesion should be so acute that degeneration proximal abnormal muscle. There are, however, a number of of the distal stump has not yet occurred. Thus lesions with potential problems with this approach. First, the branching partial or complete neurapraxia (due to either demyelination and innervation for muscles is not necessarily consistent from or ischemia) can be well localized with motor NCSs, as can one person to another. Sunderland40 has demonstrated a very acute axonal injuries. great deal of variability in branching order to muscles in the limbs, variability in the number of branches going to each In pure axonotmetic or neurotmetic lesions, it is more diffi- muscle, and variability in which nerve or nerves supply each cult if not impossible to localize the lesion using NCSs. In muscle. Thus, the typical branching scheme may not apply to such a case, there will be mild and diffuse slowing in the the patient being studied and consequently the lesion site can entire nerve due to loss of the fastest fibers, or there will be be misconstrued. no response at all. Conduction across the lesion site will be no slower than across other segments. In addition, provided Second, the problem of muscle trauma and associated needle enough time for Wallerian degeneration has elapsed (i.e., at EMG findings can be misleading. As mentioned earlier, least 9 days for motor fibers or 11 days for sensory fibers), direct muscle trauma can result in positive sharp waves and there will be no change in amplitude as one traverses the site fibrillations for months or longer after injury.32 Practically of the lesion. Thus, pure axon loss lesions are not well local- speaking, this can result in erroneously proximal lesion sites, ized along a nerve by NCSs. or error in diagnosing more than one lesion. For example, in the setting of humeral fracture with radial neuropathy, the There are some cases in which indirect inferences can be triceps not infrequently demonstrates fibrillation potentials, made about the location of purely axonal lesions. For due to direct muscle trauma. However, a clinician could be instance, if the ulnar motor response is very small or absent misled to localize the lesion to the axilla or higher rather than and the median motor response is normal, this implies an spiral groove, if the triceps findings are not recognized to ulnar neuropathy rather than a lower brachial plexus lesion. come from direct muscle rather than nerve injury. However, in such an instance, the site of pathology along the ulnar nerve may not be well defined. Third, the problem of partial lesions can make for misdiag- nosis to more distal sites. In partial ulnar nerve lesions at the Another indirect inference that can be made based upon sen- elbow, for example, the forearm ulnar-innervated muscles are sory NCSs is placement of the lesion at a pre- versus postgan- often spared.4 This is thought at least partially to be due to glionic location. Lesions that are proximal to the dorsal root sparing of the fascicles in the nerve that are preparing to ganglion, i.e. at the preganglionic level (proximal root, cauda branch to the flexor digitorum profundus and the flexor carpi 8 Traumatic Injury to Peripheral Nerves AANEM Course ulnaris, i.e., they are in a relatively protected position. This sprouts) near denervated muscle fibers.21 Partial recovery in finding could lead a clinician to inadvertently localize the twitch tension has been reported as early as 7-10 days post lesion distally to the distal forearm or wrist. Similarly, a lesion injury,2 though electrophysiologic correlates (e.g., polyphasic involving the median nerve in the arm (above the elbow) has long duration motor units) usually take longer. Sometimes, been reported to cause findings only in the anterior when axonal regeneration occurs, those muscle fibers reinner- interosseous distribution.46 Intraneural topography needs to vated by distal sprouting become dually innervated, i.e., by be considered when making a diagnosis based on branch- both the sprout and the newly regenerated fiber.19,21 It is not ing.45 well understood how multiple synapses are reduced.

Axonal regeneration contributes to recovery in both partial MECHANISMS OF RECOVERY and complete axonotmesis and, with surgical approximation, neurotmesis. In complete axon loss lesions, this is the only There are several possible mechanisms of recovery after trau- mechanism for muscle recovery. It is noted that in the 24-36 matic nerve injury; knowledge of these mechanisms, along hours after injury, the proximal nerve stump has started to with the type of nerve injury, allows estimation of the prob- sprout regenerating axons and these have started to penetrate able course of recovery. the area of injury. The recovery that results from this process depends upon the degree of injury, presence of scar forma- For motor fibers, resolution of conduction block (in neu- tion, approximation of the two nerve ends, and age of the rapraxic lesions), muscle fiber hypertrophy (in partial patient. lesions), distal axonal sprouting of spared axons, and axonal regeneration from the site of injury, may contribute to recov- In relatively more minor axonotmetic lesions, in which the ery of strength. endoneurial tubes are preserved (i.e., Sunderland 2nd degree injuries), the axons can traverse the segment of injury in 8-15 Resolution of conduction block, whether based upon days and then regenerate along the distal nerve segment at a ischemia or demyelination, is probably the first mechanism rate of 1-5 mm/day,40 slightly faster for crush injuries than to promote recovery of strength after nerve injury. for sharp laceration, slightly faster for proximal than distal Improvement after a solely ischemic lesion is relatively quick. injuries, and slightly faster for younger individuals. Demyelinating injuries take longer as remyelination over an injured segment may take up to several months,13 depending In more severe axonotmetic lesions in which there is distor- upon the severity of demyelination and the length of the tion of endoneurial tubes with or without perineurial disrup- demyelinated segment. tion (Sunderland 3rd and 4th degrees), prognosis for spontaneous regrowth is worse. Extensive scarring reduces the speed In normal adults performing strengthening exercises, there at which regenerating axons can traverse the lesion and more are generally two mechanisms of increasing force production: importantly reduces the likelihood that they will ever reach initial neural mechanisms followed by later muscle fiber their end organs. When regrowth occurs, it may also be mis- hypertrophy. The initial neural mechanisms are thought to directed to the wrong end organ. In some of these cases, par- involve improved synchronization of motor unit firing,28,29 ticularly when a large neuroma is present, surgical interven- and they result in increased efficiency (defined as muscle tion is required. force per unit of electrical activity) in the absence of muscle fiber changes. After several weeks, there is muscle fiber hyper- In complete neurotmesis (Sunderland 5th degree), axonal trophy, which results in further increases in strength. In regrowth will usually not occur unless the nerve ends are patients with partial nerve lesions, it is unclear how much freed from scar and surgically re-approximated. After surgical neural changes alone (i.e., increased efficiency of firing) can intervention, using either direct approximation or cable contribute to increased strength since there is loss of nerve grafting, nerve growth will often occur along the endoneurial fibers. However, it is likely that working the existing muscle tubes of the distal segments. Use of cable grafts (e.g., sural fibers to fatigue in the setting of partial nerve injuries does nerve graft) does not provide axons directly since these die produce enlargement of muscle fibers and consequent after harvesting; the graft simply provides a pathway for increases in force production. axonal regrowth to occur.34,47

Partial axonotmesis of motor nerves also produces distal In complete lesions, recovery of motor function will also sprouting of motor fibers from intact axons. It has been depend upon integrity of the muscle when the axon reaches observed that within 4 days after nerve injury, sprouts are it. Muscles remain viable for reinnervation for 18-24 months starting to form from intact axons, typically from distal nodes post injury. However, past this time, due to fibrosis and atro- of Ranvier (nodal sprouts) or from nerve terminals (terminal phy, motor axon regrowth makes little difference since muscle AANEM Course Assessment of Traumatic Nerve Injuries 9 fibers (the end organ), are no longer viable. For example, in complete lower trunk brachial plexus lesions, recovery of hand function is usually not expected no matter how good the surgical grafting might be; it simply takes too long for axons to reach the muscle.

Recovery of sensory function is dependent upon different mechanisms than motor recovery. There may be redistribu- tion of sensory distribution after an axonal injury, such that intact fibers provide cutaneous sensation to a larger area than previously.38,44 The mechanisms of axonal regeneration are similar to those mentioned above for motor axons. An Figure 3 Conceptual representation of mechanisms for important difference, however, is that one does not have end improvement in sensation after a mixed lesion to a peripheral organs that may degenerate after 18-24 months as muscle nerve. The processes represented are not necessarily temporally does; hence sensory recovery may continue for a longer peri- distinct, but may merge. Recovery may continue for longer than od of time than motor recovery does. 18 months since it is not dependent upon muscle viability.

ELECTRODIAGNOSTIC EVALUATION OF PROGNOSIS rience a relatively rapid partial, but incomplete, recovery followed a slower further recovery. Sensory recovery may pro- Determining the pathophysiology of a peripheral nerve trau- ceed for a longer time than motor (Figure 3). matic injury can help with estimating prognosis. Those injuries that are completely or largely neurapraxic have a Partial axon loss lesions usually represent axonotmesis, good prognosis for recovery within a few months (usually up though a partial neurotmesis (e.g., a laceration through part to 3 months postinjury). Resolution of ischemia and remyeli- of the nerve) cannot always be excluded in such cases. In nation should be complete by this time. axonotmesis, recovery will depend upon axonal sprouting and regeneration. Thus there will be some early recovery fol- Mixed injuries typically have two or more phases of recovery lowed possibly by a later recovery if or when regenerating (Figure 2). The neurapraxic component resolves quickly as axons reach their end organs. The amplitude of the CMAP above and muscle fiber hypertrophy can provide additional provides some guide to prognosis. In facial nerve lesions, it recovery, but the axonal component is slower, since it has been demonstrated that patients with CMAP amplitudes depends upon distal axonal sprouting and on axonal regener- 30% or more of the other side have an excellent outcome, ation from the site of the lesion. Thus patients usually expe- those with 10-30% have good, but not always complete, recovery, and those with less than 10% have a poor outcome.37

Complete axonotmesis and neurotmesis have the worst prognosis. Recovery depends solely upon axonal regeneration which may or may not occur, depending upon the degree of injury to the nerve. In many cases of complete axon loss, it is not possible to know the degree of nerve injury except by surgical exploration with or without intraoperative recording, or looking for evidence of early reinnervation after the lesion.

SUMMARY

Figure 2 Conceptual representation of mechanisms for As a consequence, it is often recommended that an EDX increases in strength after a mixed lesion to a peripheral nerve. The processes represented are not temporally distinct, but may physician should wait 2-4 months before looking for evi- merge. Maximal recovery is usually achieved by 18-24 months. dence of reinnervation in previously completely denervated muscles near the site of the lesion.23,47 Those lesions that have 10 Traumatic Injury to Peripheral Nerves AANEM Course some spontaneous recovery are usually treated conservatively 18. Gilliatt RW. Acute compression block. In: Sumner AJ, editor. The since operative repair is unlikely to improve upon natural physiology of peripheral nerve disease. Philadelphia: WB Saunders; recovery. Those with no evidence of axonal regrowth usually 1980. p 287-315. 19. Guth L. Neuromuscular function after regeneration of interrupted have operative exploration with possible grafting. nerve fibers into partially denervated muscle. Exp Neurol 1962;6:129-141. 20. Haymaker W, Woodhall B. Peripheral nerve injuries. Philadelphia: REFERENCES WB Saunders; 1953. 21. Hoffman H. Local reinnervation in partially denervated muscle: a 1. Brandstater ME, Fullerton M. Sensory nerve conduction studies in histophysiological study. Aust J Exp Biol Med Sci 1950;28:383. cervical root lesions. Can J Neurol Sci 1983;10:152. 22. Kimura J, Machida M, Ishida T, Yamada T, Rodnitzky RL, Kudo Y, 2. Brown MC, Holland RL, Hopkins WG. Motor nerve sprouting. Suzuki S. Relation between size of compound sensory or muscle Ann Rev Neurosci 1981;4:17-42. action potential, and length of nerve segment. Neurology 3. Buchthal F. Fibrillations: clinical electrophysiology. In: Culp WJ, 1986;36:647-652. Ochoa J, editors. Abnormal nerves and muscle generators. New York: 23. Kline DG. Surgical repair of peripheral nerve injury. Muscle Nerve Oxford University Press; 1982. p 632-662. 1990;13:843-852. 4. Campbell WW, Pridgeon RM, Riaz G, Astruc J, Leahy M, Crostic 24. Kraft GH. Fibrillation amplitude and muscle atrophy following EG. Sparing of the flexor carpi ulnaris in ulnar neuropathy at the peripheral nerve injury. Muscle Nerve 1990;13:814-821. elbow. Muscle Nerve 1989;12:965-967. 25. Mackinnon SE, Dellon AL. Surgery of the peripheral nerve. New 5. Cangiano A, Lutzemberger L, Nicotra L. Non-equivalence of impulse York: Thieme Medical Publishers; 1988. blockade and denervation in the production of membrance changes 26. Massey JM, Sanders DB. Single-fiber EMG demonstrates reinnerva- in rat skeletal muscle. J Physiol 1977;273:691-706. tion dynamics after nerve injury. Neurology 1991;41:1150-1151. 6. Chaudhry V, Cornblath DR. Wallerian degeneration in human 27. Miller RG. AAEE minimonograph #28: Injury to peripheral motor nerves: serial electrophysiological studies. Muscle Nerve nerves. Muscle Nerve 1987;10:698-710. 1992;15:687-693. 28. Milner-Brown HS, Stein RB, Lee RG. Synchronization of human 7. Cosgrove JL, Vargo M, Reidy ME. A prospective study of peripheral motor units: possible role of exercise and supraspinal reflexes. nerve lesions occuring in traumatic brain-injured patients. Am J Phys Electroencephalogr Clin Neurophysiol 1975;38:245-254. Med Rehabil 1989;68:15-17. 29. Moritani T, deVries HK. Neural factors versus hypertrophy in the 8. Dillingham TR. Approach to trauma of peripheral nerves. In: 1998 time course of muscle strength gain. Am J Phys Med 1979;58:115- AAEM Course C: Electrodiagnosis in traumatic conditions. 130. Rochester, MN: American Association of Electrodiagnostic 30. Noble J, Munro CA, Prasad VS, Midha R. Analysis of upper and Medicine. p 7-12. lower extremity peripheral nerve injuries in a population of patients 9. Dorfman LJ. Quantitative clinical electrophysiology in the evaluation with multiple injuries. J Trauma 1998;45:116-122. of nerve injury and regeneration. Muscle Nerve 1990;13:822-828. 31. Ochoa J, Fowler TJ, Gilliatt RW. Anatomical changes in peripheral 10. Dumitru D. Electrodiagnostic medicine. Philadelphia: Hanley & nerves compressed by a pneumatic tourniquet. J Anat 1972;113:433- Belfus; 1995. p 341-384. 455. 11. Erminio F, Buchthal F, Rosenfalck P. Motor unit territory and mus- 32. Partanen JV, Danner R. Fibrillation potentials after muscle injury in cle fiber concentration in paresis due to peripheral nerve injury and humans. Muscle Nerve 1982;5:S70-S73. anterior horn cell involvement. Neurology 1959;9:657-671. 33. Rasminsky M, Sears TA. Internodal conduction in undissected 12. Fisher MA. AAEM minimonograph #13: H reflexes and F waves: demyelinated nerve fibres. J Physiol 1972;227:323-350. physiology and clinical indications. Muscle Nerve 1992;15:1223- 34. Seddon HJ. Nerve grafting. J Bone Joint Surg Br 1963;45:447-461. 1233. 35. Seddon HJ. Surgical disorders of the peripheral nerves, 2nd edition. 13. Fowler TJ, Danta G, Gilliatt RW. Recovery of nerve conduction after New York: Churchill-Livingstone; 1975. p 21-23. a pneumatic tourniquet: observations on the hind-limb of the 36. Selecki BR, Ring IT, Simpson DA, Vanderfield GK, Sewell MF. baboon. J Neurol Neurosurg Psychiatry 1972;35:638-647. Trauma to the central and peripheral nervous systems: part II, a sta- 14. Garland DE, Bailey S. Undetected injuries in head-injured adults. tistical profile of surgical treatment in New South Wales, 1977. Aust Clin Orthop Relat Res 1981;155:162-165. N Z J Surg 1982;52:111-116. 15. Gilliatt R, Hjorth RJ. Nerve conduction during Wallerian degenera- 37. Sillman JS, Niparko JK, Lee SS, Kileny PR. Prognostic value of tion in the baboon. J Neurol Neurosurg Psychiatry 1972;35:335- evoked and standard electromyography in acute facial paralysis. 341. Otolaryngol Head Neck Surg 1992;107:377-381. 16. Gilliatt R, Taylor JC. Electrical changes following section of the facial 38. Speidel CC. Studies of living nerves: growth adjustments of cuta- nerve. Proc R Soc Med 1959;52:1080-1083. neous terminal arborization. J Comp Neurol 1942;76:57-73. 17. Gilliatt R, Westgaard RH, Williams IR. Extrajunctional acetylcholine 39. Stone L, Keenan MA. Peripheral nerve injuries in the adult with trau- sensitivity of inactive muscle fibres in the baboon during prolonged matic brain injury. Clin Orthop Relat Res 1988;233:136-144. nerve pressure block. J Physiol 1978;280:499-514. AANEM Course Assessment of Traumatic Nerve Injuries 11

40. Sunderland S. Nerves and nerve injuries, 2nd edition. New York: 45. Wertsch JJ, Oswald TA, Roberts MM. Role of intraneural topogra- Churchill-Livingstone; 1978. p 133-138. phy in diagnosis and localization in electrodiagnostic medicine. Phys 41. Tackmann W, Radu EW. Observations of the application of electro- Med Rehabil Clin N Am 1994;5:465-475. physiological methods in the diagnosis of cervical root compressions. 46. Wertsch JJ, Sanger JR, Matloub HS. Pseudo-anterior interosseous Eur Neurol 1983;22:397-404. nerve syndrome. Muscle Nerve 1985;8:68-70. 42. Thesleff S. Trophic functions of the neuron. II. Denervation and reg- 47. Wood MB. Surgical approach to peripheral nervous system trauma. ulation of muscle. Physiological effects of denervation of muscle. Ann In: 1998 AAEM Course C: Electrodiagnosis in traumatic conditions. N Y Acad Sci 1974;228:89-103. American Association of Electrodiagnostic Medicine: Rochester, 43. Trojaborg W. Early electrophysiological changes in conduction block. MN; p 27-36. Muscle Nerve 1978;1:400-403. 48. Yuska MA, Wilbourn AJ. Incidence of fibrillation potentials in “pure” 44. Weddell G, Glees P. The early stages in the degeneration of cutaneous conduction block mononeuropathies. Muscle Nerve 1998;21:1572. nerve fibers. J Anat 1941;76:65-93. 12 AANEM Course 13

Peripheral Nerve Magnetic Resonance Imaging: the Median Nerve in Carpal Tunnel Syndrome

Jeffrey G. Jarvik MD, MPH Professor Departments of Radiology, Neurosurgery, and Health Services University of Washington Seattle, Washington

Acknowledgements noninvasively visualize anatomic detail may lead to a better understanding and diagnosis of nerve injury in general. This work was supported by the National Institute of Arthritis and Musculoskeletal Skin Disease (NIAMS) (P60 AR48093) and the Why bother to image the carpal tunnel if nerve conduction University of Washington’s Multidisciplinary Clinical Research studies are already widely available? While electrodiagnostic Center. (EDX) studies are useful and widely employed for patients with suspected carpal tunnel syndrome (CTS), there is room for improvement. In patients with suspected CTS, there is INTRODUCTION varying evidence as to how well they correlate with symptom severity and response to treatment. For example, Prignac and The first reports of using magnetic resonance imaging (MRI) to colleagues found no relationship between EDX severity and image the median nerve in the carpal tunnel appeared in the well-accepted measures of clinical disease, the Katz-Stirrat mid-1980s.40,50 Much progress has been made in the interven- Hand Pain Diagram and the Carpal Tunnel Syndrome ing two decades and currently, even on a standard 1.5 Tesla MR Assessment Questionnaire (CTSAQ).45 In contrast, system, radiologists can now routinely obtain high-resolution Dennerlein and colleagues found that distal motor and sen- images of peripheral nerves.1,7,10,14,15,19,20,26,28,36,37,51 The dis- sory latencies did correspond to preoperative symptom sever- semination of MRI systems using even higher field strength ity.16 There is also conflicting evidence regarding EDX stud- (>3 Tesla) promises further improvement in imaging.6,18,41 ies ability to predict outcome. Several investigators have These advances and refinements in MRI have allowed inves- found a correlation between various EDX parameters and tigators to visualize several types of peripheral nerve patholo- outcomes after surgery.16,24,4,8 For example, Bland found that gies. It is now possible to see morphological and signal patients with middle grade EDX abnormalities did the best changes in nerve entrapment disorders, cervical radiculopa- after surgery, compared to those with either very severe or thy, traumatically injured and surgically repaired peripheral very mild findings. Dennerlein and colleagues showed that nerves, and peripheral nerve tumors. The ability of MRI to distal motor latency correlated with outcome.16 Others have 14 Peripheral Nerve Magnetic Resonance Imaging AANEM Course not found such a relationship.54,3,35,21 In the only large In postoperative patients, the author repeats the T1-weighted randomized controlled trial of surgery versus conservative axial images with fat saturation after giving contrast to detect therapy for CTS, Gerritsen and colleagues found that EDX scar formation. was not a significant predictor of which patients would improve without surgery.22 Thus, there may be a useful role Chappell and colleagues pointed out a potential pitfall in for MRI in further clarifying which patients would benefit interpreting MRIs of peripheral nerves: the magic angle from surgery for CTS. effect.11 When highly ordered structures, such as nerves and tendons, are aligned at particular angles to the main magnetic field, the signal within these structures increases on T2- MAGNETIC RESONANCE TECHNIQUE weighted images with moderate or short echo times (TE). This “magic angle” is achieved when the following formula is High-resolution MRI of peripheral nerves requires the use of satisfied: 3cos2q-1=θ. Thus, when the nerve is at 55 degrees surface coils to increase signal-to-noise ratio. While this to the main magnetic field, the signal will be hyperintense on author uses a custom-designed phased-array wrist coil, com- T2-weighted images. The authors point out that this condi- mercially available coils provide excellent images as well. tion is routinely satisfied when imaging the brachial plexus, Higher field strength systems (> 1.5 Tesla) also provide better but may also be present on studies of the carpal tunnel. signal-to-noise ratio, although their use in the peripheral Careful attention must be given when positioning patients nervous system has been limited to date. for these studies, and interpretation of signal intensity must take into account the magic angle phenomenon. This author’s group uses axial T1- and T2-weighted fast short tau inversion recovery (STIR) images in an attempt to image in a plane perpendicular to the long axis of the nerve. The ANATOMY T1-weighted images are best for demonstrating normal anatomy. Fat is bright, muscle and nerves are intermediate Peripheral nerves have three distinct layers: endoneurium, signal, and tendons are dark. The natural contrast provided perineurium, and epineurium. Endoneurium consists of con- by the fat that surrounds nerves, vessels, and muscle allows nective tissue and extracellular fluid that surrounds the axons ready identification of these structures. The fast STIR images and their Schwann cells. Perineurium is a sheath that bundles suppress fat signal, allowing greater conspicuity of structures fibers together to form a fascicle. The epineurium surrounds that have long T2 relaxation. This includes pathological the multiple fascicles to form the nerve.23 peripheral nerves, acutely denervated muscle, inflammatory tissue surrounding nerves and tendons, and mass lesions such Magnetic resonance imaging can reliably identify the median as ganglions. Some groups use T2-weighted sequences with a nerve within the carpal tunnel and characterize its shape and frequency-selective fat saturation pulse, but because of the signal intensity.30 Frequently, MRI can also identify individ- difficulty in obtaining uniform fat saturation due to magnet- ual fascicles within the epineurium. Cross-sectional (or axial) ic field inhomogeneity, the author prefers to use the STIR images best demonstrate these features. sequence. Saturation pulses are also applied superior and inferior to the imaging plane to minimize vascular flow arti- In addition to the median nerve itself, MRI can delineate the fact. anatomy of adjacent structures within and around the carpal tunnel. The median nerve is usually superficial or volar to the This author’s current imaging protocol is as follows: flexor digitorum superficialis tendons (usually the latter) (Figure 1) but may also be interposed between the flexor dig- (1) coronal T1-weighted spin echo: (TR=600, TE=min- itorum superficialis tendons (Figure 2a) and/or between the imum, 18 cm field of view (FOV), 256x192 matrix, flexor pollicis longus and flexor digitorum superficialis ten- 4 mm slice thickness); dons (Figure 2b).55

(2) axial T1-weighted spin echo: (TR=450, TE=mini- Guyon’s canal, located at the ulnar side of the carpal tunnel, mum, 10 cm FOV, 256x256 matrix, 4 mm slice contains the ulnar nerve, artery and vein. Ulnar entrapment thickness, 1 mm skip, 5.5 minutes); at the wrist may occur at Guyon’s canal, especially in patients with hook of hamate fractures. (3) axial fast STIR: (TR=3650, TE=54, TI=160, echo train length = 6, 10 cm FOV, 256x224 matrix, 4 The MRI findings in patients with CTS include flattening of mm slice thickness, 1 mm skip, 5.25 minutes). the median nerve within the carpal tunnel (Figure 3), high signal of the nerve on T2-weighted images (Figure 4), AANEM Course Assessment of Traumatic Nerve Injuries 15

Figure 1 Axial T1-weighted image at the level of the pisiform Figure 2a Axial T1-weighted image at the level of the hamate (P) demonstrates a normal position of the median nerve (MN- hook shows the median nerve (asterisk) interposed nerve arrow), volar to the flexor tendons. between flexor digitorum tendons.

enlargement of the nerve either proximal or distal to the point of maximal compression (Figure 5), bowing of the flex- or retinaculum, and thickening with increased signal of the flexor tendon sheaths (Figure 6), and deep palmar bursa (Figure 7).

Configurational changes in the nerve are probably the most reliable imaging finding. Britz and colleagues9 described a flattening ratio that is frequently used to measure nerve configuration changes. It is the ratio of the major to minor axes of the median nerve at the level of the hamate bone. The swelling ratio is also used, which is the ratio of the nerve cross-sectional area at the level of the pisiform compared with the cross-sectional area at the level of the distal radioulnar joint.32 Figure 2b Axial T1-weighted image at the level of the hamate The median nerve may occasionally divide proximal to the hook in a different patient demonstrate the median nerve carpal tunnel and result in a bifid median nerve.27,46 This rel- interposed between the flexor pollicis longus and flexor digitorum atively uncommon anatomic variant (approximately 3% of tendons. patients) is important to recognize when using size criteria to determine nerve abnormality. The bifid nerve may not measure as large as an undivided nerve, leading to decreased sensitivity of imaging. can cause variability in signal. For example, shading of images because of surface coils can make superficial structures appear more hyperintense than deep structures. Moreover, the nerve DIAGNOSTIC PERFORMANCE will normally appear hyperintense compared with the relatively black signal of the adjacent tendons.39 A useful internal Increased T2 signal appears to be a consistent finding, standard is the thenar muscles, which compared with the although as pointed out above, must be interpreted with cau- median nerve should be iso- to slightly hyperintense (Figure tion due to the magic angle effect as well as other factors that 8). The nerve signal frequently returns to near normal at the 16 Peripheral Nerve Magnetic Resonance Imaging AANEM Course

Figure 3 Axial T2-weighted short tau inversion recovery image Figure 4 Axial T2-weighted short tau inversion recovery image shows flattened and hyperintense median nerve (asterisk). shows a median nerve that is extremely hyperintense (asterisk).

Figure 5 Axial T2-weighted short tau inversion recovery image Figure 6 Axial T2-weighted short tau inversion recovery image. demonstrates an enlarged and hyperintense median nerve. The There is marked thickening and high signal of the flexor tendon fascicles are prominent as well. interspace and deep palmar bursa (asterisks). The median nerve is normal in signal.

site of maximal compression, perhaps due to a loss of fluid. Swelling of the median nerve proximal to the carpal tunnel Quantification of nerve signal is still not clinically practical seems to be a consistent finding among several studies as an and evaluation relies on the judgement of the observer. important discriminator between patients with CTS and those without. Monagle found that cross-sectional area of the In addition to spatial variation in nerve signal, there is also nerve was 50% larger in patients compared to asymptomatic temporal variation. Experimental evidence by a number of volunteers.41 Keberle found that a swelling ratio greater than authors have demonstrated T2 prolongation in injured or equal to 1.3 and a flattening ratio of greater than or equal nerves.2,13 with T2 signal peaking around day 14 after injury to 3.4 had a 100% sensitivity and negative predictive value, and normalizing by 2 months. Moreover, Cudlip and col- with a specificity of 68% and positive predictive value of leagues demonstrated a strong temporal correlation between 75%.32 In their series of 37 patients, Wu and colleagues T2 signal and functional assessment of an animal’s gait. found proximal nerve enlargement to have the strongest asso- AANEM Course Assessment of Traumatic Nerve Injuries 17

tenosynovitis/bursitis. Thenar muscle denervation is rare unless symptoms are severe. With acute denervation, there is high signal on STIR images in the thenar muscle that may persist for months. Chronic denervation results in fatty infiltration of the muscle as well as atrophy.1

Studies that have examined the diagnostic accuracy of MRI for patients with CTS have generally suffered from small sample sizes and various biases, such as spectrum bias, that tend to inflate estimates of accuracy.9,17,20,25,33,34,42,43,44,47,48, 49,51,53,55 The author’s experience, the most reliable imaging findings were high T2-signal, configurational changes, and an overall global rating of nerve abnormality.30 It has also been found that the length of signal abnormality on T2- Figure 7 Axial T2-weighted short tau inversion recovery image. weighted images correlates with the degree of median nerve 30 There is high signal in the deep palmar bursa (arrows). There is conduction slowing. also high signal in the median nerve. Several authors have failed to find a strong correlation between imaging findings and EDX studies. Deryani and colleagues found no correlation between median nerve diameter or flexor retinaculum bowing and median sensory nerve action potential distal peak latency or amplitude.17 The author’s group also failed to find a strong correlation between imaging and EDX studies.30

POTENTIAL IMAGING INDICATIONS

Magnetic resonance imaging has the potential to offer new insight into the diagnosis and management of patients with hand and wrist neurological symptoms. Unlike EDX studies, MRI directly visualizes the median nerve and can detect abnormalities of both configuration (nerve compression) as well as signal (possibly indicating intraneural edema and demyelination).20,29-31 Either or both of these findings have Figure 8 Axial T2-weighted short tau inversion recovery image. the potential to be better predictors of patient outcomes than The median nerve (arrow) is isointense to muscle (asterisk). EDX studies.

Can high-resolution MRI of the median nerve identify patients for whom early surgery might be more efficacious ciation with recurrent CTS after surgery.52 Prominence of the than conservative therapy? There are currently no definitive fascicles frequently accompanies nerve swelling; this finding studies that can answer this question. Cudlip and colleagues, is best demonstrated on T2-weighted images. in their series of 30 patients, showed that low T2 signal in the median nerve was associated with worse outcome,12 although A less common finding is bowing of the flexor retinaculum. they only had one patient with a poor outcome following This is presumably caused by increased pressure within the surgery. The author’s group is conducting a trial that will carpal tunnel. Britz and colleagues described drawing a line hopefully shed some light on this issue.38 As part of a treat- from the tip of the hamate hook to the trapezial tubercle, and ment trial comparing surgery with nonsurgical therapy, considered that abnormal bowing was present if the flexor patients are being recruited with mild to moderate CTS from retinaculum extended more than 2 mm anterior to this line.9 both primary care as well as subspecialty offices (orthopedic Other less commonly cited findings include high signal and surgery, neurosurgery, physical medicine and rehabilitation, thickening of the flexor tendon sheath interspaces as well as and neurology). Subjects undergo high resolution MRI of the the palmar bursa which may reflect an inflammatory carpal tunnel prior to randomization, and are followed for a 18 Peripheral Nerve Magnetic Resonance Imaging AANEM Course year. Both subjects and physicians are blinded to the results REFERENCES of the MRI. This will allow the group to determine how well MRI predicts change in symptoms and functional status, and 1. Aagaard B, Maravilla KR, Kliot M. MR neurography. MR imaging more importantly, if it can preoperatively help to determine of peripheral nerves. Magn Reson Imaging Clin N Am 1998;6:179- the benefit of surgery. 194. 2. Aagaard BD, Lazar DA, Lankerovich L, Andrus K, Hayes CE, Maravilla K, Kliot M. High-resolution magnetic resonance imaging Magnetic resonance imaging may prove useful as a postoper- is a noninvasive method of observing injury and recovery in the ative evaluative tool. Wu and colleagues found that contin- peripheral nervous system. Neurosurgery 2003;53:199-203. ued proximal enlargement of the median nerve and evidence 3. al-Qattan MM, Bowen V, Manktelow RT. Factors associated with of tenosynovitis were associated with recurrent CTS.52 While poor outcome following primary carpal tunnel release in non-diabet- ic patients. J Hand Surg Br 1994;19:622-625. preliminary in nature, this potential use as a problem-solving 4. Atroshi I, Johnsson R, Ornstein E. Patient satisfaction and return to tool shows promise. work after endoscopic carpal tunnel surgery. J Hand Surg Am 1998;23:58-65. What does the future hold? As high field-strength MRI sys- 5. Bendszus M, Stoll G. Caught in the act: in vivo mapping of tems proliferate, MRI will better delineate anatomic defini- macrophage infiltration in nerve injury by magnetic resonance imag- tion of the median nerve and its surrounding structures.18,41 ing. J Neurosci 2003;23:10892-10896. 6. Bilgen M, Heddings A, Al-Hafez B, Hasan W, McIff T, Toby B, Farooki and colleagues, using a clinical 8 Tesla magnet, were Nudo R, Brooks WM. Microneurography of human median nerve. able to resolve tertiary tendon fiber bundles, achieving a res- J Magn Reson Imaging 2005;21:826-830. olution of approximately 200 microns. Bilgen and colleagues, 7. Blake LC, Robertson WD, Hayes CE. Sacral plexus: optimal imag- on a 9.4 Tesla system, identified structures at the subfascicu- ing planes for MR assessment. Radiology 1996;199:767-772. lar level and were able to quantify diffusion characteristics 8. Bland J. Do nerve conduction studies predict the outcome of carpal tunnel decompression? Muscle Nerve 2001;24:935-940. along the nerve. The role of diffusion and perfusion charac- 9. Britz GW, Haynor DR, Kuntz C, Goodkin R, Gitter A, Kliot M. teristics of peripheral nerves, as well as functional activation Carpal tunnel syndrome: correlation of magnetic resonance imaging, studies of the spinal cord and brain will also surely be inves- clinical, electrodiagnostic, and intraoperative findings. Neurosurgery tigated. 1995;37:1097-1103. 10. Britz GW, Haynor DR, Kuntz C, Goodkin R, Gitter A, Maravilla K, Molecular imaging is a new field that uses a variety of tech- Kliot M. Ulnar nerve entrapment at the elbow: correlation of magnetic resonance imaging, clinical, electrodiagnostic, and intraopera- nologies, such as micro-positive emission tomography, opti- tive findings. Neurosurgery 1996;38:458-465. cal imaging, microcomputed tomography, and MRI to mon- 11. Chappell KE, Robson MD, Stonebridge-Foster A, Glover A, Allsop itor fundamental cellular events in living subjects. Using JM, Williams AD, Herlihy AH, Moss J, Gishen P, Bydder GM. molecular agents, it promises unparalleled specificity. Magic angle effects in MR neurography. AJNR Am J Neuroradiol Bendszus and Stoll imaged macrophages in vivo using super- 2004;25:431-440. 5 12. Cudlip SA, Howe FA, Clifton A, Schwartz MS, Bell BA. Magnetic paramagnetic iron oxide (SPIO) particles. Macrophages resonance neurography studies of the median nerve before and after concentrate SPIO, and thus processes that result in carpal tunnel decompression. J Neurosurg 2002;96:1046-1051. macrophage migration and activation will demonstrate signal 13. Cudlip SA, Howe FA, Griffiths JR, Bell BA. Magnetic resonance neu- alteration. Using a nerve crush injury in a rat model, the rography of peripheral nerve following experimental crush injury, and authors were able to observe accumulation of local iron and correlation with functional deficit. J Neurosurg 2002;96:755-759. hence signal loss, at the site of crushed nerves. This signal 14. Dailey A, Tsuruda JS, Goodkin R, Haynor DR, Filler AG, Hayes CE, Maravilla KR, Kliot M. Magnetic resonance neurography for cervical change peaked at day 4 and then normalized by 14 days after radiculopathy: a preliminary report. Neurosurgery 1996;38:488-492. injury. As the field of molecular imaging matures, other trac- 15. Dailey AT, Tsuruda JS, Filler AG, Maravilla KR, Goodkin R, Kliot ers will undoubtedly be developed that will be able to identi- M. Magnetic resonance neurography of peripheral nerve degenera- fy specific characteristics of nerve injury and healing. tion and regeneration. Lancet 1997;350:1221-1222. 16. Dennerlein JT, Soumekh FS, Fossel AH, Amick BC 3rd, Keller RB, Katz JN. Longer distal motor latency predicts better outcomes of carpal tunnel release. J Occup Environ Med 2002;44:176-183. SUMMARY 17. Deryani E, Aki S, Muslumanoglu L, Rozanes I. MR imaging and electrophysiological evaluation in carpal tunnel syndrome. Yonsei While EDX studies will probably remain the primary diag- Med J 2003;44:27-32. nostic test for patients with suspected CTS, MRI holds great 18. Farooki S, Ashman CJ, Yu JS, Abduljalil A, Chakeres D. In vivo high- promise and may well play an expanded role as the technol- resolution MR imaging of the carpal tunnel at 8.0 tesla. Skeletal Radiol 2002;31:445-450. ogy matures. AANEM Course Assessment of Traumatic Nerve Injuries 19

19. Filler AG, Howe FA, Hayes CE, Kliot M, Winn HR, Bell BA, 38. Martin BI, Levenson LM, Hollingworth W, Kliot M, Heagerty PJ, Griffiths JR, Tsuruda JS. Magnetic resonance neurography. Lancet Turner JA, Jarvik JG. Randomized clinical trial of surgery versus con- 1993;341:659-661. servative therapy for carpal tunnel syndrome [ISRCTN84286481]. 20. Filler AG, Kliot M, Howe FA, Hayes CE, Saunders DE, Goodkin R, BMC Musculoskelet Disord 2005;6:2. Bell BA, Winn HR, Griffiths JR, Tsuruda JS. Application of magnet- 39. Mesgarzadeh M, Schneck CD, Bonakdarpour A. Carpal tunnel: MR ic resonance neurography in the evaluation of patients with peripher- imaging. Part I. Normal anatomy. Radiology 1989;171:743-748. al nerve pathology. J Neurosurg 1996;85:299-309. 40. Middleton WD, Kneeland JB, Kellman GM, Cates JD, Sanger JR, 21. Gerritsen A, Korthals-de Bos I, PM L, de Vet H, Scholten R, Bouter Jesmanowicz A, Froncisz W, Hyde JS. MR imaging of the carpal tun- L. Splinting for carpal tunnel syndrome: prognostic indicators of suc- nel: normal anatomy and preliminary findings in the carpal tunnel cess. J Neurol Neurosurg Psychiatry 2003;74:1342-1344. syndrome. AJR Am J Roentgenol 1987;148:307-316. 22. Gerritsen AA, Scholten RJ, Assendelft WJ, Kuiper H, de Vet HC, 41. Monagle K, Dai G, Chu A, Burnham RS, Snyder RE. Quantitative Bouter LM. Splinting or surgery for carpal tunnel syndrome? Design MR imaging of carpal tunnel syndrome. AJR Am J Roentgenol of a randomized controlled trial [ISRCTN18853827]. BMC Neurol 1999;172:1581-1586. 2001;1:8. 42. Murphy RX Jr, Chernofsky MA, Osborne MA, Wolson AH. 23. Grant GA, Goodkin R, Kliot M. Evaluation and surgical manage- Magnetic resonance imaging in the evaluation of persistent carpal ment of peripheral nerve problems. Neurosurgery 1999;44:825-839. tunnel syndrome. J Hand Surg Am 1993;18:113-120. 24. Higgs PE, Edwards DF, Martin DS, Weeks PM. Relation of preoper- 43. Oneson SR, Scales LM, Erickson SJ, Timins ME. MR imaging of the ative nerve-conduction values to outcome in workers with surgically painful wrist. Radiographics 1996;16:997-1008. treated carpal tunnel syndrome. J Hand Surg Am 1997;22:216-221. 44. Pierre-Jerome C, Bekkelund SI, Husby G, Mellgren SI, Osteaux M, 25. Horch RE, Allmann KH, Laubenberger J, Langer M, Stark GB. Nordstrom R. MRI of anatomical variants of the wrist in women. Median nerve compression can be detected by magnetic resonance Surg Radiol Anat 1996;18:37-41. imaging of the carpal tunnel. Neurosurgery 1997;41:76-82. 45. Priganc VW, Henry SM. The relationship among five common 26. Howe FA, Filler AG, Bill BA, Griffiths JR. Magnetic resonance neu- carpal tunnel syndrome tests and the severity of carpal tunnel syn- rography. J Magn Reson Imag 1992;28:328-338. drome. J Hand Ther 2003;16:225-236. 27. Iannicelli E, Chianta GA, Salvini V, Almberger M, Monacelli G, 46. Propeck T, Quinn TJ, Jacobson JA, Paulino AF, Habra G, Darian VB. Passariello R. Evaluation of bifid median nerve with sonography and Sonography and MR imaging of bifid median nerve with anatomic MR imaging. J Ultrasound Med 2000;19:481-485. and histologic correlation. AJR Am J Roentgenol 2000;175:1721- 28. Jarvik J, Yuen E, Haynor DR, Bradley C, Fulton-Kehoe D, Smith- 1725. Weller T, Franzblau A, Kliot M, Franklin G. Magnetic resonance 47. Radack DM, Schweitzer ME, Taras J. Carpal tunnel syndrome: are neurography (MRN) in carpal tunnel syndrome (CTS). American the MR findings a result of population selection bias? AJR Am J Society of Neuroradiology (ASNR), 1999; San Diego. Roentgenol 1997;169:1649-1653. 29. Jarvik JG, Kliot M, Maravilla KR. MR nerve imaging of the wrist and 48. Soccetti A, Raffaelli P, Giovagnoni A, Ercolani P, Mercante O, hand. Hand Clin 2000;16:13-24, vii. Pelliccioni G. MR imaging in the diagnosis of carpal tunnel syn- 30. Jarvik JG, Yuen E, Haynor DR, Bradley CM, Fulton-Kehoe D, drome. Ital J Orthop Traumatol 1992;18:123-127. Smith-Weller T, Wu R, Kliot M, Kraft G, Wang L, Erlich V, Heagerty 49. Timins ME, O’Connell SE, Erickson SJ, Oneson SR. MR imaging PJ, Franklin GM. MR nerve imaging in a prospective cohort of of the wrist: normal findings that may simulate disease. patients with suspected carpal tunnel syndrome. Neurology Radiographics 1996;16:987-995. 2002;58:1597-1602. 50. Weiss KL, Beltran J, Shamam OM, Stilla RF, Levey M. High-field 31. Jarvik JG, Yuen E, Kliot M. Diagnosis of carpal tunnel syndrome: MR surface-coil imaging of the hand and wrist. Part I. Normal anato- electrodiagnostic and MR imaging evaluation. Neuroimaging Clin N my. Radiology 1986;160:143-146. Am 2004;14:93-102. 51. West GA, Haynor DR, Goodkin R, Tsuruda JS, Bronstein AD, Kraft 32. Keberle M, Jenett M, Kenn W, Reiners K, Peter M, Haerten R, Hahn G, Winter T, Kliot M. Magnetic resonance imaging signal changes in D. Technical advances in ultrasound and MR imaging of carpal tun- denervated muscles after peripheral nerve injury. Neurosurgery nel syndrome. Eur Radiol 2000;10:1043-1050. 1994;35:1077-1085. 33. Kleindienst A, Hamm B, Hildebrandt G, Klug N. Diagnosis and 52. Wu HT, Schweitzer ME, Culp RW. Potential MR signs of recurrent staging of carpal tunnel syndrome: comparison of magnetic reso- carpal tunnel syndrome: initial experience. J Comput Assist Tomogr nance imaging and intra-operative findings. Acta Neurochir 2004;28:860-864. 1996;138:228-233. 53. Yoshioka S, Okuda Y, Tamai K, Hirasawa Y, Koda Y. Changes in 34. Kleindienst A, Hamm B, Lanksch WR. Carpal tunnel syndrome: carpal tunnel shape during wrist joint motion. MRI evaluation of staging of median nerve compression by MR imaging. J Magn Reson normal volunteers. J Hand Surg Br 1993;18:620-623. Imaging 1998;8:1119-1125. 54. Yu GZ, Firrell JC, Tsai TM. Pre-operative factors and treatment out- 35. Kouyoumdjian JA, Morita MP, Molina AF, Zanetta DM, Sato AK, come following carpal tunnel release. J Hand Surg Br 1992;17:646- Rocha CE, Fasanella CC. Long-term outcomes of symptomatic elec- 650. trodiagnosed carpal tunnel syndrome. Arq Neuropsiquiatr 55. Zeiss J, Skie M, Ebraheim N, Jackson WT. Anatomic relations 2003;61:194-198. between the median nerve and flexor tendons in the carpal tunnel: 36. Kuntz C 4th, Blake L, Britz G, Filler A, Hayes CE, Goodkin R, MR evaluation in normal volunteers. AJR Am J Roentgenol Tsuruda J, Maravilla K, Kliot M. Magnetic resonance neurography of 1989;153:533-536. peripheral nerve lesions in the lower extremity. Neurosurgery 1996;39:750-756. 37. Maravilla KR, Bowen BC. Imaging of the peripheral nervous system: evaluation of peripheral neuropathy and plexopathy. AJNR Am J Neuroradiol 1998;19:1011-1023. 20 AANEM Course 21

Surgical Management of Nerve Injuries

David G. Kline, MD Boyd Professor and Head Department of Neurosurgery Louisiana State University Medical Center New Orleans, Louisiana

INTRODUCTION SHARP TRANSECTION OR LACERATION

Three large categories of peripheral neuropathies may be Sharp transection or laceration injuries usually involve a helped by operative intervention—nerve injuries, entrap- knife, glass, or a sharp metal edge. The forces necessary to ments, and tumors. There are a number of excellent books divide the nerve are minimal and thus, force to the stumps is available concerning surgical nerve lesions.2,7,8,22,27,31 There minimal. As a result, these are excellent cases for relatively are, of course, also occasions where the surgeon can help the acute nerve repair when performed within the first 72 hours electrodiagnostic physician in working up and managing a postinjury.16 This approach offers many advantages because medical neuropathy.6 This is usually accomplished by nerve the nerve can be repaired with the expectation of a reasonable and/or muscle biopsy, and under exceptional circumstances result at the same time as the repair of associated injuries to operative exploration for suspected (but not proven) neural adjacent structures such as vessels and tendons.2 Such early pathology. repair, when possible, has the best outcome—even for the brachial plexus (Table 1). If it is not repaired relatively acutely, the stumps retract and the need for grafts to bridge the gap NERVE INJURIES AND TRANSECTIONS increases. Positive outcomes with grafting are possible but not as good as with end-to-end repair. There are two categories of mechanical nerve injury. The smallest category is transection or partial laceration of the nerve or plexus element. However, physicians most often pre- BLUNT TRANSECTION sume the cause of nerve injury to be from transaction or partial laceration. However, although an important category to Blunt transection injuries are usually due to fan and propeller consider, these injuries represent approximately 30% of all blades, auto metal, or other blunt objects. The blunt injury is serious nerve injuries. There are two categories of lacerations best managed secondarily, after a delay of several weeks.27,31 and transactions—sharp, and dull or blunt, and thus contu- This is because the forces of transection are large and blunt, sive. This is far from a mechanistic stratification because and there is a degree of proximal and distal injury which is these two categories have a different management algorithm. unpredictable acutely. After several weeks, the extent of dam- 22 Surgical Management of Nerve Injuries AANEM Course

femoral nerve function. It is even less certain whether subpec- Table 1 Surgical outcome in 71 brachial plexus lacerations toral, axillary, popliteal, and subgluteal clots will resolve without acute surgical intervention. Elements in Sharp Blunt continuity Transection Transection Totals Another relatively acute indication for surgery is a pseudoaneurysm or atrioventricular fistula usually due to a penetrat- Plexus cases 20 28 2 71 ing wound and affecting axillary or popliteal artery.31 The Plexus elements 57 83 61 201 pseudoaneurysm or fistula needs resection and a neurolysis Neurolysis 24/26 0/0 0/0 4/26(92%) performed of the affected cord and nerve elements or tibial (+NAPs) nerve. Primary suture 0/0 25/31 0/0 25/31(81%) Sometimes when a nerve in an extremity is badly swollen by Secondary suture 9/7 12/8 3/5 18/26(70%) trauma, it needs exposure and neurolysis acutely, especially if Secondary graft 22/17 21/40 25/56 63/118(118%) it is near a potential area of tightness or entrapment. In many Total elements 48/57 54/83 28/61 130/201(65%) of these cases fasciotomies will be necessary, but under some circumstances neurolysis of the nerves is also be needed.22 A Results are given as number of elements recovering to grade 3 or better (LSUHSC good example of this is Volkman’s ischemic contracture. This system). Primary = repair within 72 hours of injury; secondary = delayed repair, usually is due to distal humeral fracture and often due to usually after several weeks. elbow dislocation and brachial artery compromise. Here, in addition to volar and dorsal forearm fasciotomies, it may be NAP = nerve action potential. advisable to expose the median, radial, and sometimes even the ulnar nerve. age can be both palpated and visualized, permitting resection LESIONS OR NEUROMAS IN CONTINUITY back to healthy tissue (coapting good to good rather than bad to bad). If blunt transection is encountered acutely, it is best Lesions or neuromas in continuity are the largest and most to tack the stumps down with nonresorbable sutures to adja- difficult category of injury to manage and therefore require cent fascial planes. This maintains length so that later end-to- special attention. The mechanisms of injury are usually blunt end repair rather than graft repair can be performed. and associated with contusion and stretch involving nerve or plexus elements. Classic, but by no means exclusive, injuries Despite a penetrating mechanism, nerves can be displaced, include fractures and gunshot wounds (GSWs) involving contused, stretched, or sometimes partially divided, leading limb, neck, shoulder, or pelvis. A large category which can be to neuromas or lesions in continuity. It is best to wait 2 to 3 associated with or without fracture(s) is stretch-contusion to months to evaluate whether surgery is necessary. After 2 to 3 the plexus with or without avulsion of nerve roots. As seen months, operative nerve action potential (NAP) recordings under the transection-laceration category, these mechanisms can be used to guide decisions about resection and repair, can occasionally lead to either partial or complete division of partial resection and split repair, or simple neurolysis where the element. More often than not, lesions in continuity result the nerve is cleared 360 degrees around, over a length, and from stretch/contusion either at a supraclavicular or infra- freed up from surrounding scar or other injury. clavicular level.

An important first step is a careful clinical examination with OTHER INDICATIONS FOR ACUTE OPERATION grading of all muscles and sensation, especially that of the hand or foot. An early needle electromyography (EMG) There are some other urgent indications for operating on study may be indicated if the clinician suspects prior injury, nerve(s) acutely. The most obvious is a blood clot, where entrapment, or disease. It may also be helpful to conduct acute compression of the nerve (unless ameliorated) can lead early nerve conduction studies centered on sites commonly to either long-standing or irreversible neuropathy.22 For involved by potential neurapraxic injuries.14 Usually with example, not all pelvic clots associated with anticoagulants more serious injuries, the initial needle EMG study is per- sufficiently resolve spontaneously to permit recovery of formed at approximately 3 weeks postinjury because the AANEM Course Assessment of Traumatic Nerve Injuries 23

Wallerian degenerative process takes time. For most suspect- axonotmesis or neurotmesis where there is gross continuity. ed lesions in continuity, an approximate 3 month period of To confirm regeneration or lack of regeneration, it is impor- repetitive clinical and needle EMG studies is needed before tant to wait several months before recording NAPs. Also, the resorting to surgery since some patients can have evidence of presence of a NAP beyond a lesion in continuity a year or early clinical or electrical recovery and thus not require an more postinjury may not have the predictive ability of one operation. When this does not occur, operative exploration, recorded in the early months. If a tourniquet is used, it needs external neurolysis of the involved elements, and operative to be removed or deflated for 30 minutes before recordings NAP recordings should be performed. Based on information are attempted. The technique will not work if local anesthet- from these studies, resection of the lesion in continuity may ic has bathed the nerve being tested. be indicated.

BRACHIAL PLEXUS INJURIES OPERATIVE NERVE ACTION POTENTIAL RECORDINGS There are special circumstances where NAP recordings take To perform operative NAP recordings requires an EMG on a different dimension. One of these circumstances is the machine for both stimulation and recording, either bipolar or frequently seen stretch/contusive injury involving the preferably tripolar electrodes for stimulation, and bipolar brachial plexus.12,28 Cases involving the supraclavicular electrodes for recording.10 If possible this author prefers to plexus should be carefully worked up before surgery.1,23,30 check electrodes and equipment either by recording from an Workup should include not only the involved limb but also adjacent, less involved or intact nerve, or by both stimulating needle EMG studies of paraspinal muscles and more distal and recording above the lesion. An inter-electrode distance of sensory recordings, searching for sensory nerve action poten- at least 3 cm is needed. The recording electrodes are then tials (SNAPs) suggesting avulsion.25 A cervical computerized moved through the lesion in continuity to determine if a tomography (CT) myelogram is usually also a necessary pre- recorded response persists and whether the response is distal operative step.4,12 A CT scan is performed not only to look to the lesion or injury site. If found, a simple external neurol- for meningoceles—suggesting although not certifying—avul- ysis up and down the course at an epineurial level will suffice. sion(s) but to determine whether both the anterior and posterior nerve roots can be identified within the dye column at A recent analysis of NAP recordings is in press at the proceed- each C5 through T1 level. Usually, each potentially involved ings of the 13th World Congress of Neurological Surgery level is compared to the same level on the uninvolved side. held in Marrakesh, Morocco. Recovery to a Louisiana State Magnetic resonance imaging (MRI) using coils and the prop- University Health Science Center (LSUHSC) grade 3 or bet- er sequences is a wonderful advance for medicine and in the ter level occurred with neurolysis based on +NAPs in 1255 of hands of experienced neuroradiologists it can be an effective 1422 (94.7%) of injuries. A portion of the injury site some- tool for visualizing the nerve.8 The usual MRI performed times appeared worse than the rest. Facsicles or groups of fac- without such steps is currently useful for nerve tumors but sicles were individually tested and those with flat traces were not usually for nerve injury. At the present time, medicine resected and repaired. Those with positive traces were left continues to rely on the CT myelogram even though for alone. This is termed a split repair. Outcomes in the split either technique there is a false positive and false negative repair group of patients were uniformly good (94%). If there incidence. On the other hand, MRI of muscles provides the is no conduction across the lesion and the trace is flat just dis- earliest test for denervation.29 Due to increased water con- tal to the lesion, the lesion is resected and an epineurial end- tent, muscle distal to the nerve lesion may appear somewhat to-end repair is performed for shorter gaps. Graft repair is hypodense on T1 and more likely hyperdense on T2 within usually performed using the sural nerve for longer deficits. a few days of loss of axonal input. Analyzing 1975 repairs performed under these circumstances (including favorable and unfavorable elements or nerves such If possible, an operation is performed at 4-5 months postin- as the lower trunk, the medial cord, the ulnar nerve, and the jury for C5 and C6 (Erb’s), or C5, C6, and C7 (Erb’s plus) peroneal nerve or peroneal division of the sciatic nerve), stretches in adults. This timeframe is important because 40% recovery to a grade 3 or better LSUHSC level was 56%. or more of C5 and C6 and roughly 16% of C5, C6, and C7 lesions may be identified within this time frame. Early evi- Operative NAP recordings performed in the early weeks dence clinically or electrically of recovery will therefore postinjury may confirm neurapraxia or document a partial or negate the need for an operation.12 Flail arms involving the incomplete lesion. This will not be of use in differentiating C5 through T1 elements should be explored earlier if possi- between the complete traumatic neuropathy due to either ble since clinical and/or electrical-evidence of spontaneous 24 Surgical Management of Nerve Injuries AANEM Course recovery is less common (5%).11,21 There is a great interest or lateral cord is possible, this author will still transfer into worldwide in the use of nerve transfers or what is incorrectly the medial portion of the musculocutaneus nerve medial pec- termed neurotization (repair of nerve) for such lesions.2,9,22 toral branches on a C5 and C6, or C5, C6, and C7 stretch or This is accomplished by sectioning functional nerves such as take ulnar flexor fasicles to the motor branch of the muscu- accessory, phrenic, C3 or C4 spinal nerves, thoracodorsal locutaneous nerve. Even in the flail arm, if C6 or C7 have nerve, triceps branches, medial pectoral branches, intercostal useful outflow that will be taken to the lateral cord and some- nerves, or a portion of the ulnar nerve and transferring them times also the posterior cord while intercostal nerves are to nonfunctional elements such as suprascapular nerve, the taken to one-half of the more distal musculocutaneous nerve. divisions of the upper or middle trunk, or the axillary or Another example of direct repair coupled with nerve transfer musculocutaneous or proximal median nerves.3,19,24 Even the is that the C5, if useable for direct lead-out, may be extend- contralateral C7 spinal nerve or middle trunk has been ed by grafts to the posterior division of the upper trunk and extended by sural grafts to provide input to proximal median the distal accessory nerve transferred into the more proximal nerve. The preferential priorities for plexus repair for stretch- supraclavicular nerve. es are (1) elbow-flexion, (2) some shoulder abduction, (3) external rotation of shoulder, and (4) some wrist and finger Useful outcomes are still quite difficult to achieve in this cat- motion.16,21 egory of plexus injury.12,21 By comparison, outcomes with repair of plexus lacerations (Table 2) and even plexus gunshot This author continues to favor direct plexus repair for these wounds are far better (Table 3). Most operations for lacera- lesions whenever possible supplemented by nerve transfers.16 tions for plexus lacerations and GSWs are performed anteri- As a result, the involved portion of the plexus is exposed, orly, but if damage is close to the spine (especially on lower including a portion of the intraforaminal spinal nerves, and spinal nerves or roots) a posterior approach is indicated.5 Use operative NAP studies are performed. Thus, the spinal nerve of operative recordings is especially important with GSWs is stimulated and recordings are taken downstream on distal where some 40-50% of the lesions in continuity produced by trunks and divisions, depending on the distal extent of the this wounding mechanism have some potential for recovery injury on the cords of the plexus. If traces are flat, the lesion without direct repair. Provided these lesions can be identified may be postganglionic or pre- and postganglionic. Then, this by operative recording techniques. Thus, in a series of 118 author sections back to a more proximal level on the spinal cases involving brachial plexus elements with adequate fol- nerve and either finds healthy facsicular structure useful for low-up, 46% of lesions with a finding of complete preopera- lead-out of grafts or a scarred and sometimes avulsed ele- tive clinical and EMG loss in their distribution had NAPs ment, in which case direct repair at that level is not possible. transmitted across their lesions at 2-6 months post wound- Such an element or its distal outflows are then candidates for ing. These plexus elements had only a neurolysis with a 91% nerve transfer(s). If the lesion is preganglionic, a relatively recovery rate and did not require repair either by direct suture large amplitude and rapidly conducting NAP will be record- or by grafts.13 By comparison recovery rates to LSUHSC ed because of sensory fiber sparing. Direct repair in such a grade 3 or better in the suture repair group was 67% and distribution will not be useful, but nerve transfer to it may be with grafts it was 54%. These figures include repairs for ele- useful. The most favorable operative NAP finding would be ments known to have low recovery reates with repair such as a smaller amplitude and slower conducting (20-40 m/s) NAP C8, T1, lower trunk, and medial cord as well as those such as which provides strong evidence for regeneration even though C5, C6, C7, upper and middle trunks, and lateral and poste- more distal clinical loss is complete. This would be an ele- rior cords where repair is more likely to be successful. ment not to repair or transfer into more distally. Interestingly, despite clinical and EMG evidence of sparing of In patients with C5, C6, clinical, and needle EMG loss, it is function, there were nine plexus elements that did not con- extremely important to expose operatively C7 to the middle duct and thus required resection. These elements histologi- trunk and to perform operative recordings on that element. cally were neurotemetic. The preoperative evaluation as to This is because 1/7th of C5 andC6 patients also have serious severity of loss was probably complicated by anatomical involvement of C7. This needs assessment so that its poten- plexus variations especially at the cord level. tial repair is not neglected.12,16 Gunshot wounds as well as stretch injuries involving infra- In only 5% of flail arm cases will C5 be avulsed and in only clavicular plexus levels i.e., cords and cord-to-nerve levels, 5% of cases are all roots (C5 thru T1) avulsed. Therefore did not necessarily recover spontaneously and required oper- direct repair of one or more elements is usually possible.12 ation. They did relatively well even if repair by suture or graft Having said that, the results of nerve transfers are good so was necessary. The anatomy of these lesions can be complex they can almost always be added in. For example, if direct and the juxtaposition of the axillary artery and vein and their repair of lead out from C6 to anterior division of upper trunk branches make dissection difficult, but the outcomes warrant AANEM Course Assessment of Traumatic Nerve Injuries 25

Table 2 Overall postoperative grades on 366 patients with supraclavicular plexus stretch injuries patients

Postoperative grade Initial loss 0 1 1-2 2 2-3 3 3-4 4 4-5 Totals C5/C6 ( C ) 1 0 0 0 6 14 18 9 7 5 C5/C6/C7 ( C ) 1 0 0 2 14 23 20 9 6 75 C5 to T1 (C ) 21 8 15 29 62 40 20 13 0 208 C5 to C8 ( C ) 0 0 0 0 0 1 1 0 0 2 C6/C7/C8/T1 (C ) 0 0 0 1 0 2 1 0 0 4 C7 to T1 (C ) 0 0 0 0 1 1 0 0 0 2 C8 to T1 ( C ) 2 3 2 2 0 2 0 0 0 11 C8 to T1 (I) 0 0 0 0 0 0 2 2 3 7 C7/C8/T1 (I) 0 0 0 0 0 1 1 0 0 2

Total 25 11 17 34 83 84 63 33 16 366

C = complete or nearly complete loss; I = incomplete loss.

Table 3 Outcomes of Surgery for 118 gunshot wound injuries to plexus

No. of Neurolysis Type of Lesion Elements (+NAP) Suture Graft Lesions w/ 202 46/42 21/14 135/73 complete loss Lesions w/ 91 82/78 6/5 3/2 incomplete loss Totals 293 128/120 27/19 138/75 (94%) (70%) (54%)

Results are given as the total number of elements/ the number of elements recovering to grade 3 or higher.

NAP = nerve action potential. 26 Surgical Management of Nerve Injuries AANEM Course

Table 4 Outcomes of axillary nerve repair in 99 patients (Number of Nerves/Mean Postoperative LSUHSC Grade)

Partial Loss Complete Loss & Positive & Positive NAP/ Resection Resection Outcome NAP/Neurolysis* Neurolysis† & Suture† & Graft ‡ Solitary axillary palsy (56 cases) 4/4.3 6/3.8 3/3.8 43/3.8§ Axillary palsy w/ 1/4.5 3/4.3 0/0 7/3.2 2 suprascapular palsy (11 cases) Axillary palsy w/radial loss (14 cases) 3/4.3 2/4.5 0/0 9/3.0 Axillary palsy w/ 7/4.0 4/4.2 0/0 7/3.1 other plexus loss (18 cases)|| Totals** 15/4.1 ± 0.4 15/4.0 ± 1.0 3/3.8 ± 0.6 66/3.7 ± 1.1 * The mean preoperative grade was 2.2 (range 1-4) † Preoperative grade in each case was 0. ‡ Preoperative grade in most cases was 0, except in three in which it was 1 (trace only). § Includes two split repairs with a mean outcome grade of 4. || Two additional axillary nerves were exposed, but irreparable due not only to lengthy involvement, but also to distal avulsion. ** The mean values are expressed as means ± SDs.

LSUHSC = Louisiana State University Health Science Center; NAP = nerve action potential; SD = standard deviation.

this step. An interesting subset of such injuries are those of recovery. Parsonage-Turner syndrome can, of course, be the axillary nerve (Table 4). The incidence of associated responsible for loss in the plexus distribution.7,30 Like thoracic plexus injuries was relatively high, but despite this, the outlet syndrome, Parsonage-Turner syndrome is a diagnosis of patient outcome was relatively good in the author’s series as exclusion. Unless the patient has the classic neuropathies well as others.15,20 involving multiple somewhat desperate plexus elements, and a characteristic antecedent event such as immunization, pneu- monia, or excessive exercise or exertion, the clinician must POSSIBLE PITFALLS exclude such possibilities as cervical rib or elongation, “Parrott beaking” of the C7 transverse process, tumor, or Some cautions referable to both pre- and postoperative elec- direct trauma due to operative manipulation or malposition trical evaluation (especially regarding plexus lesions) are war- during anesthesia. Having said that, Parsonage-Turner syn- ranted. It is possible for the needle EMG to show a good deal drome remains an important differential diagnosis and the of denervational change in muscle(s) that have recovered patient’s recovery is not helped by operation.30 clinical contraction especially in the early months postinjury or repair, so examination and grading of muscle function Other Operative Electrophysiologic Tests remains a priority. Unfortunately, on the other hand, early weak contraction does not always mean eventual good con- The usefulness of skin level somatosensory studies in serious traction although it favors it. It is also possible, since needle plexus lesions at least in the first year or so postinjury is ques- EMG is a sampling procedure, to record nascents in one or tionable. The stimulus sites are usually well distal to the more areas of a muscle perhaps because a few fibers have injury site. For serious injuries such as GSWs, lacerations, found their way back to muscle and yet over time there may and stretches, the information gained can be minimal.26 not be enough regrowth for useful contraction of that mus- With the supraclavicular stretch injuries, the clinician should cle. However, if serial needle EMG shows an increasing num- perform distal sensory NAP studies to look for preganglionic ber of nascents (perhaps with decreasing numbers of fibrilla- injury of T1, C8, or C7. Reproducible studies for C6 pregan- tions) these repetitive observations strongly favor useful glionic injuries are possible but difficult using the lateral AANEM Course Assessment of Traumatic Nerve Injuries 27 cutaneous branch of musculocutaneous territory for stimula- fibers greater than 5 µm in diameter at the recording site. tion and recording. Reproducable studies are nonexistent for The relatively early presence of this many fibers beyond a C5 nerve roots and spinal nerve.14,23 lesion in continuity bodes well for future functional growth.

Direct stimulation of spinal nerve(s) on the operating table and recording a spinal evoked potential (EP) or evoked cor- SUMMARY tical response (ECR) does, if it is positive, document some integrity of the peripheral to central sensory pathway. It does It can be reassuring under some delayed circumstances to not, however, guarantee that the motor concomitant is intact, know that at least some fibers have reached muscle and made although it favors such.10,26 Experimental studies have indi- enough of a connection to record an evoked MUAP. Thus, cated that only a few hundred fibers need to be intact in the grading the amplitude or latency of such a response and using posterior root to record such a spinal EP or ECR after stim- that to decide for or against resection has been an unexpect- ulation of its more distal spinal nerve.32 ed consequence of such studies. This author will leaves the reader to their own assessment of when a nerve or element is Recently, in the case of the plexus from the spinal nerves, stimulated and whether recordings can be made from distal there is interest in motor evoked potentials (MEPs) where the muscle in the distribution of that nerve, no matter their cerebral motor cortex is stimulated and more distal record- amplitude or latency, and whether resection of the involved ings are made The implication is that if there is a positive nerve or element and the consequent repair necessitated is response then there is an intact motor root. Although likely, justified. that is not necessarily so since the descending pathways from the cortical stimulus site used may be other than motor, just The previous observations are based on adult nerve (and as they may be at a spinal cord level when used to evaluate especially plexus injuries) and may not be applicable to the corticospinal tract function. Of some promise, but awaiting unfortunate child with a birth injury to the plexus. further experience and confirmation, is the use of paraspinal motor unit action potential (MUAP) recordings after spinal nerve stimulation. If a response is positive after spinal nerve REFERENCES stimulation then the motor root is intact, although only 100 or less intact fibers may give such a response. The surgeon 1. Alnot JY. Traumatic brachial plexus palsy in the adult. Retro- and must take great care that the stimulus does not spread to adja- infraclavicular lesions. Clin Orthop Relat Res 1988;237:9-16. 2. Birch R, Bonney G, Wynn Parry C. Surgical disorders of the periph- cent intact spinal nerves since each segment of paraspinal eral nerve. Philadelphia: WB Saunders; 1998. muscle has input from multiple cervical spinal segments. 3. Brandt KE, Mackinnon SE. 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