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Review Article *Corresponding author Ramiro Palazón, Department of Psychiatry, National Hospital of Paraplegics, Calle Plomo 3, Madrid, Spain, after Email: Submitted: 03 October 2017 Injury Part 1 - Clinical Features Accepted: 03 November 2017 Published: 07 November 2017 Ramiro Palazón-García* Copyright Department of Psychiatry, National Hospital of Paraplegics, Spain © 2017 Palazón-García

OPEN ACCESS Abstract Spasticity is a common complication after (SCI) within the upper motor Keywords neuron syndrome. The prevalence of spasticity is about 65% of people with SCI. • Spasticity • Spinal cord injury This article (part 1) addresses the characteristics of spasticity in SCI patient, its • pathophysiology, differences between spasticity of cerebral or spinal origin, exacerbating factors for spasticity, advantages and disadvantages caused by spasticity, and assessment of spasticity and its consequences. The treatment will be described in part 2.

INTRODUCTION according with American Spinal Injury Association Impairment Scale as grade A though patients with grade C injuries had the Spasticity is a common complication after spinal cord injury highest prevalence of ongoing spasticity treatment and functional (SCI) as a sign of damage of upper motor neurons. Spasticity limitation [11,12]. may develop months or years after the acute injury and lead to increased loss of function and hospitalization [1,2]. PATHOPHYSIOLOGY OF SPASTICITY The characteristics of the spasticity after SCI will be Spasticity is generally due to a lowered threshold of phasic manifestationsdescribed in two and parts: repercussions the first one and (part the 1) way presents of assessing general them; and becomeor tonic hyperactive stretch reflexes; [1]. when inhibitory signals are lost due inspecific the second characteristics one (part 2) of the the treatment spinal spasticity will be described. with its clinical to spinal cord damage the segmental reflexes are released and The classical motor unit path is formed by lower motoneurons by Lance in 1980: “Spasticity is a motor disorder characterized The most commonly cited definition of spasticity was created of 2 types: alpha that projects to extrafusal skeletal fibers, and gamma motor neuron that projects to intrafusal by a velocity dependent increase in tonic stretch reflexes (muscle spindlesmuscle fibers when within there is the any muscle stimulus spindle (not only[11,13]. stretching) The stretch and tone) with exaggerated tendon jerks, resulting from hyper travelsreflex is via a monosynaptica Ia afferent to reflex the spinal that originates cord where in itthe synapses muscle limitationsexcitability of because the stretch the observed reflex, as featuresone component of spasticity of the doupper not with correspondent alpha motor neuron (directly or via another motoneuron syndrome” [3]. Nevertheless, this definition has has been produced. If the stimulus goes on too long, Golgi tendon contractionsexclusively result of agonists from and hyper antagonists excitability [4]. of For the this stretch reason, reflex the interneuron) and finally contracts muscle fibers where stimulus nor are they all velocity dependent like , spasms or co developing management algorithms to guide and standardize the spasticityorgans can after be elicited, SCI [11,13]. and via Ib interneuron’s can relax previous assessment,Ability Network treatment, (an international and evaluation panel of of outcomes clinical experts of persons for contraction. The hyper excitability of stretch reflex can explain The mechanisms underlying spasticity and its consequences with spinal cord damage and disabling spasticity) recommends motor control, resulting from an lesion, can be classified in 2 groups: presentingadoption of as theintermittent definition or by sustained Pandyan: involuntary “disordered activation sensory- of muscles” [5,6]. - Alterations in spinal mechanisms [11,13,14]. Enhancement SCI.in the This excitability enhancement of motoneurons is attributed andto depolarizing interneuron’s current are most that The prevalence of spasticity is about 65% of people with SCI doeslikely not involved inactivate in the with pathophysiology prolonged membrane of spasticity depolarization following (persistent inward currents) whose activation is regulated through the monoaminergic drive from the brainstem, mediated chronic[1]; during SCI inpatient patients rehabilitation (more than 1 incidence year post is injury) only 25- spasticity 37% in traumatic SCI and 15- 36% of non traumatic SCI [7-10], and in been associated with cervical levels and severity of the injury on the other through neurotransmissions like serotonin or nor is present in 65- 93% [1,2,11,12]. Problematic spasticity has epinephrine. Other mechanisms are fusimotor hyper excitability, axonal sprouting, reduction in presynaptic inhibition and Cite this article: Palazón-García R (2017) Spasticity after Spinal Cord Injury Part 1 - Clinical Features. J Neurol Disord Stroke 5(3): 1130. 1/6 Palazón-García (2017) Email:

Central Bringing Excellence in Open Access CLINICAL FEATURES OF SPASTICITY AFTER potentials has been demonstrated as a very important mechanism SPINAL CORD INJURY developingreduction inspasticity Ia- reciprocal in animal inhibition. models but Induction not in humans of plateau [15]. These mechanisms have a neurophysiologic correlation: the H Time - course of developing spastic impairments following injury amplitude of the compound muscle ) ratio shows When a spinal cord injury comes abruptly (as occurs in max (maximum amplitude of an H reflex)/ M max (maximum traumatic or vascular injuries) there is an initial phase called by an electrical stimulus delivered to a , being greater thanthe percentage normal in upper of motor motor neurons neuron that lesions can be(greater reflex still activated when spasticity occurs) and lower than normal in spinal shock. Spinal shock is defined as temporary loss of spinal reflex activity occurring below a SCI and implies flaccid and loss of deep tendon reflexes below the level of the cord injury lesions or spinal shock [16], though this increase in the ratio may [21]. In first 3- 4 weeks following acute spinal transaction, the take up to 2 to 6 months from the time the injury occurs, while intrinsic properties underlying motor neuron excitability start to Clinicalrecovery features of F- waves of spasticity and flexor depend reflex on excitability the greater appears or lesser at loss the return [22,23]. If spasticity appears we can say spinal shock is ofend the of ability spinal to shock voluntarily and may modulate increase the as levelspasticity of activity develops of a given [17]. over but there is no relationship between first signs of spasticity As spasticity is part of the upper motor neuron syndrome, it motor pool and the capacity of the interneuron’s that project and time since injury beyond the spinal shock period [11]. to these motor pools to recruit the appropriate combination of syndrome. The anatomical segment above the conus medullar is motor pools [18]. cannot occur when the SCI feature is like a lower motor neuron

functionnamed the of epiconus, sacral segments. consisting According of spinal withcord thesegments International L4-S1; properties,- Plastic decrease alterations in the in number affected of sarcomeres, muscles [11]. accumulation Spasticity lesions in this zone affect lower lumbar roots with sparing of reflex ofcauses connective fibrosis, tissue,atrophy and of muscle alteration fibers, of decrease contractile in propertiesthe elastic [24], neurological levels of injury above T10 always present as an upperstandards motor for neuron neurological syndrome, classification and for that of reason spinal people cord injury with , and then the capacity for development of active tensiontoward is tonic less musclethan that characteristics. normally possible Muscle at longer shortening lengths causes L3these do injurynot develop levels spasticity are most [25,26]. likely to Those develop patients spasticity with injury when CLASSIFICATION OF SPASTICITY levelstheir spinal between shock T11 is and over, L2 while usually people present with with injury an upperlevels motorbelow neuron syndrome. [11,19]: In general, spasticity can be classified according to 2 criteria Differences between spasticity of cerebral and spinal origin differentiating between intrinsic if stimulus emerges within - Place where located stimulus for spasticity is allows When spasticity is of spinal origin it has several specific orCentral . Nervous System, and extrinsic if afferent input proceeds characteristics among which the following stand out [1,27- 30]: from other structures such skin, subcutaneous tissues, muscles patients with spasticity of spinal than cerebral origin. - Acute flaccid phase previous to spastic period is longer in movement tonic or static component is described, and if there is any -movement Components phasic of the or stretchdynamic reflex. component If there is isdescribed. no resulting The spinal is generalized and diffuse while focal spasticity is more - Most frequent presentation of spasticity when origin is concept of tonic spasticity is the one that best agrees with the prevalent when origin is cerebral.

So, we can distinguish 3 main types of spasticity [4,13,19,20]: classic definition of spasticity. - As for spastic , patients with SCI develop a more a. Intrinsic tonic spasticity. Hypertonia is an involuntary intense spasticity than those with a stroke or a injury, especiallyand clasp- in knife lower phenomenon limbs, while is cerebral more prevalent spasticity when predominates origin is dependent. spinal. The muscles most commonly affected in SCI are extensor increase in resistance of muscle to passive stretch velocity- in flexor muscles. involuntary rhythmic that can result in distal prevalent when origin is spinal, and patellar clonus is rare if jointb. oscillation, Intrinsic andphasic it can spasticity. be result Clonus of the sudden is defined application as an origin- Asof spasticity for intrinsic is not phasic cerebral. spasticity ankle clonus is more of sustained stretch to a muscle too. Tendon hyper-reflexia is spasms in lower limbs are the most prevalent spastic feature applied tap of deep tendons. - Extrinsic spasticity is more frequent in SCI patients; extensor identified as an exaggerated muscle response to an externally (especially last 20 degrees), and most important receptors are hip mecanoceptors;among people with within SCI. cerebralMost important origin spasticity stimulus mostis hip importantextension c. Extrinsic spasticity. Spasms are involuntary and abrupt patientmuscle simultaneously. contractions. Although one type of , flexor or extensor usually predominates, they can coexist in the same receptors are mecanoceptors. - Influence of posture. SCI patients show shortening of J Neurol Disord Stroke 5(3): 1130 (2017) 2/6 Palazón-García (2017) Email:

Central Bringing Excellence in Open Access muscles due to prolonged postures not considered as spasticity, Differential diagnosis the most frequent affected muscles are hamstrings that are

We must distinguish spasticity from other tone disorders; the The first point is to make a correct diagnosis of spasticity. shortened by keeping the sitting in the wheelchair. However, stroke patients can maintain a posture due to spasticity when resistance to passive movement found in extrapiramidal rigidity, they develop spastic dystonia, whose principal example is elbow paratoniaMeasurement or simulation of tone are not velocity- dependent [1,20]. flexion posture. Triggering- Spinal spasticity factors is more exacerbated by visceral diseases. The most important factors are posture and bowel and Usually the severity of spasticity is identified with the intensity wayof the to tone,measure commonly the tone measured despite having with the demonstrated Modified Ashworth in some can produce that a patient with a SCI and normal or decreased Scale (MAS, Table 1) [41]. MAS is considered as the most adequate tonebladder can issuespresent [31]. with The intense presence or frequent of these spasms. exacerbating factors studies problems of reliability [1,11]; being a likert- type scale Supine position is associated with a more intense hypertonia may have problems of validity but its reliabilility and inter- rater and greater ease of causing spasms than sitting, the most scale is based upon the pendulum test; it consists of performing and test- retest agreement have been reported [42,43]. Tardieu frequent situation related by patients with SCI to suffer spasms is stretching of a muscle between 2 points at 2 speeds. It adheres during transfers (above all transfers to bed) [32,33]. There is an activation of involuntary contractions in high soleus and tibialis more closely to Lance’s definition of spasticity and some studies anterior during transfers from wheelchair to bed [34]. other measures to change following treatment with botulinum have identified the Tardieu Scale to be more sensitive than Bowel issues are related with spasticity, both the constipation maintained and the moments of evacuation and faecal impact; the toxin [44]. Inter-rater and test-retest agreement for its scores is former are related with hypertonia and the others with dynamic poor,substantial these tofacts almost suggest perfect its utility but inter-rater as a complementary reliability oftool some for symptoms [35,36]. measures for the hip adductor and knee extensor muscles are as the main scale for tone assessment [45]. detrusor hyperactivity, urinary tract infection or obstructions informing treatment decisions in patients with SCI, keeping MAS Most frequent bladder issues related with spasticity are Assessment of dynamic phenomena Although there is no correlation between the frequency and [35,37]. intensity of the phasic symptoms and the evolution of spasticity, conditions (pressure sores, ingrown nails), menstrual cycle, mentalOther stress, factors and like tight pregnancy, clothing alsocold, increase. circadian Acute, rhythm, serious skin intensity of spasms can be measured, but only frequency measure infections (sepsis) and syringomyelia may cause both increased they are collected in the physical examination [43]. Frequency and spasticity and a sudden absence of spasticity [2]. Clinical influence of spasticity on the SCI patient is validated through Penn Spasm Frequency Score (Table 2) [46]. There is a specific scale for phasic components assessment in SCI: Spasticity interferes in the patient causing functional Spinal Cord Assessment Tool for Spastic Reflexes (SCATS, Table disadvantages but can also provide some advantages. Spasticity 3) [47], that has a great inter-rater agreement and even shows can limit the ability for positioning, transfers, mobility, basic scores for lower limb joints [48]. a significant correlation between SCATS clonus scores and MAS activities of daily living and can interfere with sleep, occupation Functional assessment and social participation. Disabling spasticity can also lead to Goniometric measurements are performed to evaluate results and all of these effects can increase the number of primary care of or loss of motion. Neurophysiologic assessment is visitsfatigue, and pain, hospitalizations increased risk [6, of 11]. pressure For those ulcers reasons and infections, there can with activities of daily living can be measured with general scales not correlated with spasticity [27]. The interference of spasticity However, sometimes spasticity may increase stability in sitting andbe a standing, negative self-facilitate image the and performance a decreased of quality some activities of life [38]. of like Functional Independence Measure [49] or specific scales for SCI like Spinal Cord Independence Measure version III [50]. of spastic muscles (thereby helping prevent osteopenia), and increasedaily living venous and transfers, return diminishing increase muscle the probability bulk and strength of deep Ability for walking can be also measured with general scales such Table 1: vein thrombosis [11], and muscle contraction by spasticity can 0. No increase in tone. accelerate fracture healing [39]. . 1. Slight increase in tone with a catch, or minimal resistance at the end ASSESSMENT OF SPASTICITY AND ITS CONSEQUENCES 1+. Slight increase in tone with a catch, followed with minimal resistance of the range of movement (ROM) The International Spinal Cord Society (ISCOS) provides recommendations on how to assess various groups of symptoms, movedthroughout the remainder (less than half) of the ROM. 2. Marked increase in tone through most of the ROM, but limb is easily ítem and is only mentioned in the dataset corresponding to collected as basic dataset, but spasticity does not have a specific l disorders [40]. 3.4. ConsiderableLimb rigid or contractedincrease in tone; passive movement difficult musculoskeleta J Neurol Disord Stroke 5(3): 1130 (2017) 3/6 Palazón-García (2017) Email:

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Table 2: 0. No spasms. Penn Spasm Frequency Score. 10- Meters Walk Test [51] or 6 Minutes Walk Test [52] or specific scalesAssessment like Walking of the Index impact in Spinal on Cordthe quality Injury [53]. of life 1. Mild spasms brought on by stimulus Interferences of spasticity with leisure, sleep, physical activity 2. Infrequent spasms (occurring < 1 time/ hour) and quality of life can be measured with a general health scale 3. Spasms occurring > 1 time/ hour 4. Spasms occurring > 10 times/ hour impact of spasticity on SCI patient’s quality of life are preferred. Table 3: like Short Form Health Survey- 36 [54], but specific scales for Spinal Cord Assessment Tool for Spastic Reflexes. 0. No reaction Spinal Cord Injury Spasticity Evaluation Tool (SCISET, Table 4) is Clonus of ankle plantar flexors with rapid passive dorsiflexion of foot a scale to know how the patient estimates spasticity to influence ofon spasticity 35 components on SCI patient of his lifequality [55]. of Patientlife but effects Reported of patient Impact life of 1. Mild: clonus < 3 seconds 3. Severe: clonus > 10 seconds onSpasticity spasticity Measure [56]. (PRISM, Table 5) evaluates not only influence 2. Moderate: clonus lasts between 3 and 10 seconds Subjective assessment Flexor spasms in response to pinprick on foot plantar surface with leg 0. No reaction Usually patients can describe their spasticity with a number and hip in full extensión

1. Mild: extension of great toe or <10 degrees of hip/ knee flexion rating scale [6,11], but they can use SCISET or PRISM scales as 2. Moderate: 10 to 30 degrees of hip/ knee flexion self- administered inventories or even they can describe their 3. Severe: > 30 degrees of hip/ knee flexion spasticity through specific signs such the duration and intensity Extensor spasms of quadriceps muscle after extensión of leg from a of involuntary agonist- antagonist muscle coactivity during 0. No reaction position of hip/ knee flexion everydayChanges tasks after [34]. therapy

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Cite this article Palazón-García R (2017) Spasticity after Spinal Cord Injury Part 1 - Clinical Features. J Neurol Disord Stroke 5(3): 1130.

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