Spasticity
Spasticity is a motor disorder characterized by a velocity-dependent increase in muscle tone and tonic stretch reflexes, leading to hypertonia, stiffness, and involuntary muscle contractions that disrupt normal movement patterns.[1] It arises as a component of upper motor neuron syndrome, where damage to the brain or spinal cord pathways impairs the balance between excitatory and inhibitory signals to muscles, resulting in exaggerated reflexes and resistance to passive movement.[1] This condition is estimated to affect 50% to 80% of individuals with spinal cord injuries and is common in neurological disorders, often leading to complications such as pain, contractures, and reduced quality of life if unmanaged.[2] The primary causes of spasticity stem from lesions or injuries to the central nervous system, particularly the upper motor neurons that control voluntary movement.[1] Common etiologies include stroke, traumatic brain injury, spinal cord injury, multiple sclerosis, and cerebral palsy, with the latter accounting for spasticity in over 80% of cases among affected children.[3] Less frequent causes encompass infections, tumors, or degenerative diseases like amyotrophic lateral sclerosis, where the disruption occurs due to loss of descending inhibitory pathways from the brain, heightening spinal reflex excitability.[1] In spinal cord injuries, spasticity typically emerges weeks to months post-injury and can vary in severity based on the lesion's location and extent.[4] Symptoms of spasticity manifest as increased muscle stiffness, particularly in the limbs, with velocity-dependent resistance that worsens with rapid stretching.[1] Affected individuals often experience muscle spasms, clonus (rhythmic contractions), pain, abnormal postures such as flexed elbows or equinus foot, and difficulties with gait, speech, or fine motor tasks like grasping objects.[5] In severe cases, it can lead to secondary issues including joint deformities, pressure ulcers, sleep disturbances, and fatigue, while milder forms may paradoxically assist with posture or weight-bearing in ambulatory patients.[1] Symptoms are often asymmetrical and more pronounced in antigravity muscles, such as hip adductors or ankle plantar flexors.[1] Diagnosis involves a thorough clinical evaluation, including patient history to identify underlying neurological conditions and physical examination assessing muscle tone, reflexes, and range of motion using standardized scales like the Modified Ashworth Scale (graded 0-4 based on resistance to passive movement).[1] Imaging such as MRI or CT scans may confirm the causative lesion, while electromyography can quantify reflex hyperactivity.[5] Treatment is multidisciplinary and tailored to severity, starting with non-invasive approaches like physical therapy, stretching, and orthotics to maintain flexibility, followed by oral medications such as baclofen or tizanidine to reduce tone.[6] For refractory cases, options include botulinum toxin injections, intrathecal baclofen pumps, or surgical interventions like selective dorsal rhizotomy, aiming to alleviate symptoms and improve function without a cure for the underlying disorder.[5]Overview
Definition
Spasticity is defined as a velocity-dependent increase in muscle tone, clinically manifested as an increase in the resistance encountered during passive stretching of muscles, attributable to exaggerated stretch reflexes as a consequence of an upper motor neuron (UMN) lesion.[7] This motor disorder arises from disruption in the central nervous system's control over muscle activity, leading to abnormal sensorimotor control that affects movement and posture.[8] The hallmark features of spasticity include hypertonia, characterized by elevated muscle stiffness; hyperreflexia, an exaggerated response to tendon reflexes; and the clasp-knife phenomenon, where initial resistance to passive movement gives way to sudden relaxation, mimicking the opening of a pocket knife.[9] These components collectively contribute to the clinical presentation, with the velocity-dependent nature distinguishing spasticity as a dynamic hypertonia that intensifies with faster movements.[10] Spasticity must be differentiated from other forms of hypertonia, such as rigidity, which involves a constant, velocity-independent increase in muscle tone often seen in extrapyramidal disorders like Parkinson's disease, and dystonia, which features sustained or intermittent muscle contractions causing abnormal postures without the characteristic velocity dependence.[10][11] Unlike rigidity's uniform resistance throughout the range of motion, spasticity's resistance varies with speed and includes reflex components, while dystonia emphasizes patterned, twisting movements rather than pure stretch reflex exaggeration.[12] At its physiological core, spasticity stems from lesions affecting upper motor neurons, particularly disrupting descending inhibitory pathways within the corticospinal tract that normally modulate spinal reflex arcs, resulting in unopposed excitatory influences on alpha and gamma motor neurons.[13][14] This imbalance leads to hyperexcitability of the stretch reflex, amplifying responses to muscle stretch and contributing to the disorder's motor impairments.[15]Epidemiology
Spasticity is a common neurological complication affecting millions globally, with estimates indicating it impacts over 12 million people worldwide.[3] This burden is particularly pronounced in low- and middle-income countries, where higher rates of traumatic injuries and infections contribute to elevated incidence compared to high-income settings.[16] Among specific conditions, spasticity manifests in up to 30-80% of stroke survivors, with community-based studies reporting incidence rates between 19% and 43% within the first year post-stroke.[17] In cerebral palsy, a leading pediatric cause, spasticity affects approximately 80% of individuals, representing the predominant subtype.[3] Similarly, in multiple sclerosis, prevalence reaches 80-86% among patients, often contributing to mobility impairments.[18] Demographic patterns reveal variations by age and gender. Pediatric prevalence is tied closely to cerebral palsy, which occurs in 1.5 to 2.5 per 1,000 live births globally, with spastic forms comprising the majority of cases.[19] In this population, males face a slightly higher risk, accounting for up to 60% of cerebral palsy diagnoses.[20] For traumatic etiologies, such as spinal cord injuries, onset often peaks in younger adults, though overall spasticity risk increases with age due to higher stroke incidence in older populations.[19] Recent trends indicate a rising global burden, driven by aging populations and improved survival rates from acute neurological events like stroke and trauma, with data highlighting increased prevalence in elderly cohorts.[21] This shift underscores the growing public health impact, particularly as geriatric-related neurological disorders become more common.[22]Causes and Risk Factors
Etiology
Spasticity primarily arises from damage to upper motor neurons (UMNs) in the brain or spinal cord, which disrupts the balance of inhibitory and excitatory signals to alpha motor neurons in the spinal cord, leading to hyperexcitability of the stretch reflex arc.[8] This UMN lesion results in the upper motor neuron syndrome, characterized by loss of descending inhibition from higher centers, allowing unchecked facilitatory influences on spinal reflexes.[23] Among acquired causes, stroke is the most common etiology, affecting approximately 19% to 43% of survivors depending on the timing of assessment post-event.[24] Traumatic brain injury (TBI) frequently induces spasticity through diffuse axonal damage or focal lesions interrupting corticospinal pathways.[25] Similarly, spinal cord injury (SCI) leads to spasticity below the level of the lesion due to interruption of descending inhibitory tracts, with prevalence varying by injury completeness and height.[26] Congenital and developmental causes include cerebral palsy, often resulting from perinatal hypoxic-ischemic encephalopathy or prematurity-related brain injury, which damages developing motor pathways and manifests as spastic diplegia, hemiplegia, or quadriplegia.[3] In such cases, the insult occurs during fetal or early postnatal brain development, leading to lifelong UMN dysfunction.[27] Other etiologies encompass central nervous system infections such as meningitis or encephalitis, which can cause inflammatory damage to UMN pathways, and brain or spinal tumors that compress or infiltrate motor tracts.[28] Degenerative conditions like amyotrophic lateral sclerosis (ALS) may present with spasticity in early stages due to selective UMN involvement before lower motor neuron predominance emerges.[29] Risk factors for developing spasticity include the severity and extent of the UMN lesion, with more complete or extensive damage increasing likelihood; lesion location, particularly involvement of the pyramidal tract or brainstem structures; and timing of onset, as spasticity typically emerges within 3 days to 6 weeks post-insult due to evolving neural plasticity.[30] Younger age and hemorrhagic stroke subtypes also heighten risk compared to ischemic events.[24]Associated Conditions
Spasticity frequently co-occurs with multiple sclerosis (MS), a demyelinating disease of the central nervous system that disrupts upper motor neuron pathways, leading to shared manifestations of muscle stiffness and impaired mobility. In MS, spasticity affects up to 84% of patients at some point, with severity varying from mild to severe and often contributing to gait disturbances through common inflammatory and neurodegenerative processes.[31] Hereditary spastic paraplegia (HSP), a group of over 90 genetic disorders primarily affecting the corticospinal tracts, is characterized by progressive lower limb spasticity as its hallmark feature, reflecting degeneration in long descending motor pathways. HSP typically presents with bilateral leg weakness and stiffness, progressing slowly over decades and sharing neural vulnerability with other spastic conditions due to axonal damage.[32] In cerebral palsy (CP), a non-progressive disorder arising from early brain injury, spasticity coexists with dystonia in approximately 50% of cases, where both stem from disrupted basal ganglia and pyramidal tract function, leading to mixed hypertonia and abnormal postures. Contractures, resulting from prolonged spasticity, further overlap in CP by causing joint limitations through sustained muscle shortening along shared upper motor neuron lesions. Additionally, about 45% of individuals with CP experience intellectual disabilities, exacerbating functional challenges via combined motor and cognitive impairments from perinatal brain damage.[33] Spinal cord injury (SCI) often involves spasticity in 65-93% of cases, frequently accompanied by pain syndromes such as neuropathic pain below the injury level, both arising from disrupted spinal reflex arcs and supraspinal inhibition. This overlap affects up to 81% of SCI survivors with chronic pain, where spasticity amplifies discomfort through hyperexcitable motor neurons.[34][35] Following stroke, spasticity commonly accompanies hemiplegia, unilateral paralysis resulting from upper motor neuron damage in the affected hemisphere, leading to asymmetrical tone increases and motor deficits via shared ischemic pathways. In traumatic brain injury (TBI), spasticity occurs in up to 38% of severe cases within the first year, often compounded by cognitive deficits like attention and memory impairments that hinder rehabilitation and mobility through widespread cortical and subcortical disruptions.[36][37]Pathophysiology
Neural Mechanisms
Spasticity arises primarily from upper motor neuron (UMN) lesions that disrupt descending pathways, leading to a loss of supraspinal inhibition on spinal motor circuits.[15] Reduced activity in the dorsal reticulospinal tract, which normally provides inhibitory control, results in unopposed facilitation from the medial reticulospinal and vestibulospinal tracts.[15] This imbalance causes hyperexcitability of alpha motor neurons in the spinal cord, amplifying responses to sensory inputs and contributing to the core features of spasticity.[38] At the spinal level, spasticity involves heightened excitability within the stretch reflex arc, where Ia afferents from muscle spindles synapse directly onto alpha motor neurons via monosynaptic connections.[38] Post-lesion adaptations reduce presynaptic inhibition of these Ia afferents and impair disynaptic reciprocal inhibition between antagonist muscles, further enhancing reflex gain.[15] Following UMN lesions, neural plasticity manifests as structural and functional reorganization in the spinal cord, including axonal sprouting from primary afferents and interneurons that form novel excitatory synapses.[38] This sprouting, along with the unmasking of previously silent synapses due to reduced inhibition, alters the balance of spinal circuits toward greater excitability over time.[15] Such changes contribute to the progressive development of spasticity, as compensatory adaptations reinforce pathological reflex pathways.[39] Biochemically, spasticity is associated with an imbalance in neurotransmitters, characterized by decreased inhibitory GABAergic signaling and increased excitatory glutamatergic activity.[39] Reduced GABA levels or receptor function, often due to downregulation of the potassium-chloride cotransporter KCC2, diminish postsynaptic and presynaptic inhibition, allowing unchecked motor neuron firing.[39] Concurrently, elevated glutamate release exacerbates excitotoxicity and amplifies excitatory drive on spinal neurons, perpetuating the hyperexcitable environment.[39] The velocity-dependent nature of spasticity stems from the stretch reflex's sensitivity to the speed of muscle lengthening, where reflex gain increases proportionally with stretch velocity due to dynamic responses of Ia afferents.[38] This property reflects the enhanced threshold and amplitude of the reflex arc, distinguishing spastic hypertonia from other forms of rigidity.[15]Relationship to Clonus
Clonus represents a specific hyperreflexic manifestation of spasticity, characterized by sustained, rhythmic muscle contractions occurring at a frequency of 5-8 Hz, typically elicited by rapid passive stretch of the affected muscle and serving as an indicator of severe spasticity.[40][41] This oscillatory response arises from exaggerated spinal reflex loops, where the loss of supraspinal inhibitory control—often due to upper motor neuron lesions—results in unchecked feedback between muscle stretch receptors and alpha motor neurons, perpetuating the rhythmic contractions.[42][40] Common types include ankle clonus, which is frequently observed in the lower limbs due to its accessibility for testing, and wrist clonus, involving the upper limbs; these are assessed by dorsiflexing the foot or flexing the wrist, respectively.[42] A duration of more than 10 beats is considered sustained clonus, signifying significant upper motor neuron involvement and a higher degree of spasticity.[42] Clinically, clonus acts as a reliable marker of spasticity severity, particularly in conditions involving pyramidal tract lesions such as spinal cord injury (SCI), where it correlates with the extent of neural hyperexcitability and impacts functional outcomes.[42][43] Its presence helps differentiate the intensity of upper motor neuron dysfunction from milder hyperreflexia, guiding prognostic assessments in spastic disorders.[42]Clinical Presentation
Signs and Symptoms
Spasticity primarily presents as an abnormal increase in muscle tone, characterized by stiffness that intensifies with rapid movements or attempts to stretch the affected muscles.[1] This velocity-dependent resistance to passive elongation is most evident in antigravity muscles, such as the elbow flexors, hip adductors, and ankle plantar flexors, leading to a sensation of tightness during daily activities.[44] Involuntary muscle spasms, which are sudden, forceful contractions often triggered by touch or position changes, frequently occur and can involve flexor or extensor patterns depending on the affected limbs.[6] These motor impairments result in significant functional limitations, including gait disturbances like scissoring, where the legs cross involuntarily due to adductor muscle tightness, complicating walking and balance.[45] Patients often experience reduced range of motion in joints, as sustained hypertonia limits passive and active movements, alongside fatigue that arises during prolonged physical efforts or even routine tasks like dressing and transferring.[1] Clonus, a rhythmic series of involuntary contractions and relaxations, may accompany these signs, particularly in the ankles or wrists upon sudden stretch.[44] Associated sensory symptoms include pain or discomfort, stemming from the persistent muscle contractions that strain soft tissues and joints over time.[6] The progression of these manifestations varies: acute onset is typical after traumatic events such as stroke or spinal cord injury, where symptoms emerge rapidly post-event, whereas in degenerative diseases like multiple sclerosis, spasticity develops gradually and may fluctuate with disease exacerbations.[1]Characteristics
Spasticity is fundamentally characterized by velocity-dependent hypertonia, where muscle resistance to passive stretch increases with the speed of movement, distinguishing it from the low or absent tone seen in flaccid paralysis.[1] This hallmark feature arises from exaggerated tonic stretch reflexes, as originally defined by Lance as a motor disorder involving a velocity-dependent increase in these reflexes with heightened tendon jerks.[46] The resistance is not uniform but escalates nonlinearly with faster stretching velocities, often manifesting as a "catch" during rapid passive maneuvers.[1] Distribution patterns of spasticity vary based on the underlying neurological insult, ranging from focal involvement to more widespread generalization. Focal spasticity typically affects a single limb or muscle group, such as the upper extremity following a unilateral stroke, allowing for targeted interventions.[36] In contrast, generalized spasticity involves multiple body regions bilaterally, as commonly observed in cerebral palsy where it contributes to hemiplegia, diplegia, or quadriplegia patterns.[47] Temporal features of spasticity include both phasic and tonic components, leading to intermittent flexor or extensor spasms superimposed on a baseline of sustained hypertonia.[38] These manifestations can fluctuate, with spasms occurring episodically—ranging from rare to frequent (>10 per hour)—while constant tone persists variably.[1] Spasticity intensity is often modulated by posture, increasing in positions that stretch affected muscles, and by arousal states, such as emotional stress or noxious stimuli, which can exacerbate reflex excitability.[48][1] Electrophysiological studies reveal distinct traits in spasticity, including enhanced amplitudes of the H-reflex and F-wave on electromyography (EMG), reflecting hyperexcitability of spinal motor neurons.[49][50] The H-reflex, elicited by submaximal stimulation of Ia afferents, shows increased magnitude in spastic muscles, indicating amplified stretch reflex gain, while F-wave persistence and amplitude are elevated due to recurrent discharges in alpha motor neurons.[51][52] These EMG findings provide objective quantification beyond clinical observation, correlating with the severity of velocity-dependent resistance.[50]Diagnosis
Clinical Assessment
The clinical assessment of spasticity begins with a thorough history taking to determine the onset, progression, and potential underlying causes. Clinicians inquire about the sudden or gradual emergence of symptoms, such as following a neurological event like stroke, spinal cord injury, or traumatic brain injury, and evaluate how the condition has evolved over time, including any fluctuations influenced by factors like fatigue, infections, or medication changes.[1] Associated neurological events are explored, including details on prior diagnoses such as multiple sclerosis or cerebral palsy, alongside impacts on daily activities, sleep, and quality of life.[53] This step helps identify triggers like urinary tract infections, deep vein thrombosis, or positioning issues that may exacerbate symptoms.[54] During the physical examination, observation of posture and spontaneous movements reveals characteristic patterns, such as flexed postures in the upper limbs (e.g., shoulder adduction and elbow flexion) or equinus foot positioning in the lower limbs, indicative of sustained muscle activity.[1] Passive movement testing assesses resistance to joint motion, noting a velocity-dependent increase where faster stretching elicits greater opposition due to hypertonia, a key feature distinguishing spasticity from other tone abnormalities.[55] Reflex elicitation involves tapping tendons to evaluate stretch reflexes, which are typically hyperactive, often accompanied by clonus or an upgoing plantar response (Babinski sign).[53] Functional tests complement the exam by measuring range of motion through gentle manipulation of affected joints to quantify limitations and detect early contractures, ensuring movements are performed at varying speeds to highlight spastic resistance.[1] Gait analysis observes walking patterns for asymmetries, such as circumduction, toe-walking, or scissoring, which reflect spasticity's interference with normal locomotion and balance.[54] These bedside evaluations provide insights into functional impairments without relying on advanced tools. Differential diagnosis during assessment focuses on distinguishing spasticity, an upper motor neuron disorder, from lower motor neuron conditions like flaccid weakness. Spasticity presents with velocity-dependent hypertonia and hyperreflexia, whereas lower motor neuron lesions feature hypotonia, areflexia, and muscle atrophy without increased resistance to passive movement.[1] This differentiation guides appropriate management by confirming the upper motor neuron origin.[54]Grading Scales
Spasticity severity is quantified using validated clinical and neurophysiological scales to provide objective measures for diagnosis, treatment planning, and outcome evaluation. These tools assess muscle tone, velocity-dependent resistance, and reflex excitability, helping differentiate spasticity from other forms of hypertonia.[56] The Modified Ashworth Scale (MAS) is a widely used clinical tool for assessing muscle tone in spasticity, though recent guidelines critique its specificity for true spasticity and recommend the Tardieu Scale as preferred.[56][57] It evaluates the increase in muscle tone through passive range of motion across a joint. It employs a 6-point ordinal scale from 0 to 4, where 0 indicates no increase in tone and 4 denotes rigidity in flexion or extension; intermediate grades capture varying degrees of resistance, such as a "catch" followed by minimal resistance (grade 1) or considerable difficulty in passive movement (grade 3). Despite its simplicity and frequent use in clinical settings like stroke and cerebral palsy, the MAS has limitations due to its subjective nature and moderate inter-rater reliability, which can lead to inconsistencies in scoring.[58][59] The Tardieu Scale, including its modified version (MTS), offers a more dynamic assessment by measuring spasticity at specified movement velocities, capturing the velocity-dependent nature of the condition as defined by Lance. It evaluates two key angles: R1 (angle of arrest due to tonic stretch reflex at fast velocity, V3) and R2 (angle of catch due to spastic reaction at slower velocities, V1 or V2), along with a qualitative muscle reaction score from 0 (no reaction) to 4 (disordered movement).[60] This approach distinguishes true spasticity from contractures more effectively than static scales like the MAS, with evidence showing superior reliability in identifying velocity-specific responses in neurological conditions such as multiple sclerosis and spinal cord injury.[61][59] Other validated tools include the Tone Assessment Scale (TAS), which provides a comprehensive evaluation of tone in upper and lower limbs through passive movements, scoring resistance, clonus, and associated reactions on a 0-4 scale per segment; it demonstrates good reliability in conditions like cervical spondylotic myelopathy and is useful for tracking changes in spinal cord-related spasticity.[62] Additionally, H-reflex quantification via electromyography (EMG) serves as an objective neurophysiological measure, assessing the ratio of H-reflex amplitude to M-wave (H/M ratio) in muscles like the soleus to gauge spinal reflex excitability; elevated ratios correlate with spasticity severity in disorders such as stroke and cerebral palsy, offering quantitative insights beyond clinical observation.[63][64] Emerging frameworks, such as the Five-Step Assessment (FSA), integrate Tardieu measurements to differentiate spasticity from other impairments like weakness and contracture, showing moderate to excellent reliability in recent studies (as of 2024).[65] These grading scales establish a baseline for monitoring treatment efficacy, such as responses to botulinum toxin or physical therapy, and ensure standardization in clinical research trials evaluating interventions for spasticity in populations with upper motor neuron lesions.[56][65]| Grade | Description |
|---|---|
| 0 | No increase in muscle tone |
| 1 | Slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the range of motion when the affected part(s) is moved in flexion or extension |
| 1+ | Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the range of motion |
| 2 | More marked increase in muscle tone through most of the range of motion, but affected part(s) easily moved |
| 3 | Considerable increase in muscle tone, passive movement difficult |
| 4 | Affected part(s) rigid in flexion or extension |