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Clonus
SpecialtyNeurology
Ankle clonus

Clonus is a set of involuntary and rhythmic muscular contractions and relaxations. Clonus is a sign of certain neurological conditions, particularly associated with upper motor neuron lesions involving descending motor pathways, and in many cases is accompanied by spasticity (another form of hyperexcitability).[1] Unlike small spontaneous twitches known as fasciculations (usually caused by lower motor neuron pathology), clonus causes large motions that are usually initiated by a reflex. Studies have shown clonus beat frequency to range from three to eight Hz on average, and may last a few seconds to several minutes depending on the patient's condition.[1]

Signs

[edit]

Clonus is most commonly found at the ankle, specifically with a dorsiflexion/plantarflexion movement (up and down).[2] Some case studies have also reported clonus in the finger, toe, and laterally in the ankle (as opposed to the typical up and down motion).[3][4]

Cause

[edit]

Clonus is typically seen in people with cerebral palsy, stroke, multiple sclerosis, spinal cord damage and hepatic encephalopathy.[2] It can occur in epilepsy as part of a generalized tonic–clonic seizure, and in pregnant women presenting with severe pre-eclampsia and eclampsia.[5] It can also be an adverse drug reaction, such as after ingestion of potent serotonergic drugs, where clonus strongly predicts imminent serotonin toxicity (serotonin syndrome).

Mechanism

[edit]

Hyperactive stretch reflexes

[edit]

The self re-excitation of hyperactive stretch reflexes theory involves a repetitive contract-relax cycle in the affected muscle, which creates oscillatory movements in the affected limb.[1] In order for self re-excitation to exist, both an increase in motor neuron excitability and nerve signal delay are required.[1] Increased motor neuron excitability is likely accomplished by alterations to the net inhibition of neurons occurring as a result of injury to the central nervous system (CNS) (stroke/ spinal cord injury).[1] This lack of inhibition biases neurons to a net excitatory state, therefore increasing total signal conduction.[1] Signaling delay is present due to an increased nerve conduction time.[1] Long delays are primarily due to long reflex pathways, which are common in distal joints and muscles.[1] This may therefore explain why clonus is typically found in distal structures like the ankle. Frequency of clonus beats have been found to be directly proportional to the length of the reflex pathway it is found in.[1]

Central oscillator

[edit]

Clonus, with respect to the presence of a central oscillator, functions on the theory that when the central oscillator is turned on by a peripheral event, it will continue to rhythmically excite motor neurons, therefore creating clonus.[1]

Although the two proposed mechanisms are very different in [theory] and are still debated, some studies now propose the potential of both mechanisms co-existing to create clonus.[1] It is thought that the stretch reflex pathway may be stimulated first, and through its events, cause a decreased synaptic current threshold.[1] This decreased synaptic current threshold would enhance motor neuron excitability as nerve impulses would be more readily conducted, and thus turn on this central oscillator.[1] This theory is still being investigated.[1]

Clonus and spasticity

[edit]

Clonus tends to co-exist with spasticity in many cases of stroke and spinal cord injury likely due to their common physiological origins.[1] Some consider clonus as simply an extended outcome of spasticity.[1] Although closely linked, clonus is not seen in all patients with spasticity.[1] Clonus tends to not be present with spasticity in patients with significantly increased muscle tone, as the muscles are constantly active and therefore not engaging in the characteristic on/off cycle of clonus.[1]

Clonus results due to an increased motor neuron excitation (decreased action potential threshold) and is common in muscles with long conduction delays, such as the long reflex tracts found in distal muscle groups.[1] Clonus is commonly seen in the ankle but may exist in other distal structures as well.[2]

Diagnosis

[edit]

Clonus at the ankle is tested by rapidly flexing the foot into dorsiflexion (upward), inducing a stretch to the gastrocnemius muscle.[1] Subsequent beating of the foot will result, however only a sustained clonus (5 beats or more) is considered abnormal.[citation needed] Clonus can also be tested in the knees by rapidly pushing the patella (knee cap), towards the toes.

Voluntary induction in healthy people

[edit]

Gregory Bateson described the induction of clonus in healthy people:[6]

Balance is a partly involuntary and unconscious business, dependent on "spinal reflexes." When provided with appropriate context, these reflexes go into oscillation that is called "clonus," a phenomenon that is familiar to everybody and which is easily produced. (While sitting, place the leg with thigh horizontal and foot supported on the floor. Move the foot inward toward you so that the heel is off the floor and the ball of the foot supports the weight of the leg. When the weights and angles are correctly adjusted, an oscillation will start in the muscle of the calf with a frequency of about six to eight per second and an amplitude of about half an inch at the knee. This oscillation is called clonus in neurophysiology and is a recurrent series of patellar reflexes, generated in a feedback circuit. The effect of each contraction is fed back as a modification of tension to the calf muscle. This change of tension triggers the next patellar reflex.)

— Gregory Bateson, A Sacred Unity, p. 85

In the text, Bateson goes on to describe induction of clonus as a key element of Balinese ritual.

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Clonus

View on Grokipedia
from Grokipedia
Clonus is a series of involuntary, rhythmic contractions and relaxations of a muscle, elicited by a sudden stretch, characterized by oscillations at a of approximately 5-8 Hz and typically signaling damage to upper motor neurons in the . The term "clonus" derives from the Greek word κλόνoς (klónos), meaning "turmoil" or "violent motion," and has been used in since the to describe this phenomenon. It is most commonly observed in the ankle, where brisk dorsiflexion of the foot produces repetitive plantar flexion beats, but can also occur at the , , or . In adults, sustained clonus exceeding 10 beats is considered pathological, distinguishing it from occasional normal responses in newborns. Clonus often coexists with hyperreflexia, spasticity, and muscle weakness, contributing to impaired gait, posture, and daily function in affected individuals. Clinically, it serves as a key indicator of upper motor neuron syndrome during neurological examinations, aiding in the differentiation of central versus peripheral nervous system pathology.

Introduction

Definition

Clonus is a series of involuntary, rhythmic muscle contractions and relaxations triggered by rapid passive stretch of the muscle, typically requiring at least three successive beats to be considered pathological. This oscillatory response arises from an exaggerated stretch reflex and is a hallmark of upper motor neuron (UMN) pathology. Key characteristics of clonus include its rapid cycling between and relaxation at a of 5-8 Hz, with the period averaging 160-200 milliseconds per cycle. It is most readily elicited at specific sites such as the ankle (via dorsiflexion), (through hyperextension), (by sharp downward depression of the patella with the knee extended), (by sudden depression of the ), though it can occur in other muscles like the or . Sustained clonus, defined as more than 10 beats, is particularly indicative of severe UMN involvement. As a clinical , clonus signifies disrupted from upper motor neurons, differentiating it from normal monosynaptic reflexes by its repetitive, self-sustaining nature. At the anatomical level, it involves the arc: muscle spindles sense the initial stretch, Ia afferent fibers relay the signal to the , and alpha motor neurons subsequently activate the extrafusal muscle fibers, perpetuating the cycle due to loss of supraspinal modulation. Clonus often co-occurs with , highlighting broader UMN dysfunction.

Historical Context

The term "clonus" originates from the word klonos, denoting turmoil or violent, confused motion, reflecting the rhythmic, involuntary muscular oscillations it describes. In the mid-19th century, as emerged as a distinct discipline, French clinicians first systematically recognized clonus as a pathological . Jean-Martin , a pioneering neurologist at the Salpêtrière Hospital, described it around 1862 as "provoked trepidation" or "provoked spinal ," emphasizing its elicitation by sudden muscle stretch and its association with lesions in the . Charcot's observations built on earlier anecdotal reports from the by French physicians, who noted the phenomenon in patients with hemiplegia and other , distinguishing it from or peripheral nerve issues. By the 1870s, the sign gained wider recognition through German contributions that formalized its examination. In 1875, Wilhelm Heinrich Erb and Carl Friedrich Otto Westphal independently published on deep tendon reflexes, with Erb specifically detailing ankle clonus as a series of rapid, alternating contractions and relaxations elicited by dorsiflexion. Erb coined the term "clonus" (from the Greek root) to describe this "reflex clonus" or "Fussphaenomen" (foot phenomenon, as termed by Westphal), viewing it as evidence of exaggerated spinal reflex activity rather than a mere local muscular response. These descriptions built directly on Charcot's work, incorporating clonus into routine neurological assessments for involvement. In the late , clonus became firmly embedded in neurological practice alongside Charcot's seminal characterizations of , as both were hallmarks of pyramidal tract dysfunction in conditions like and . Charcot's clinical-pathological correlations, detailed in his lectures from the and , highlighted clonus as a reliable indicator of central lesions, influencing of reflex testing protocols. Throughout the early , research shifted toward dissecting the spinal arcs underlying clonus, with foundational studies exploring its integration with . A major milestone came in the with electrophysiological investigations using (EMG), which confirmed clonus's oscillatory nature as a self-sustaining loop of hyperactivity driven by spinal mechanisms. Pioneering EMG recordings, such as those examining the timing and amplitude of muscle bursts during sustained stretch, demonstrated frequencies of 5-7 Hz and reinforced its dependence on disinhibition. These findings solidified the reflex-based model without significant alterations since, as clonus's clinical and mechanistic understanding has remained stable into the , with post-2000 research focusing primarily on therapeutic modulation rather than redefining its core features.

Clinical Features

Signs and Symptoms

Clonus is elicited through a sudden and sustained stretch of the affected muscle, most commonly by brisk dorsiflexion of the ankle while applying pressure to maintain the position, leading to an initial followed by a series of rhythmic, involuntary oscillations typically involving five or more beats. The oscillations occur at a of approximately 5-8 Hz, with the first beat being the longest in duration and , progressively decreasing until a consistent is established by the fourth or fifth beat. The ankle represents the most frequent site for clonus, particularly involving the Achilles tendon reflex, though it can also manifest at the (via ), , and less commonly the (masseter reflex). In these locations, the response is characterized by alternating contractions and relaxations, such as repeated plantarflexion and dorsiflexion at the ankle, which may persist as long as the stretch is maintained. Sustained clonus, defined as more than 10 beats, signifies a more severe manifestation and is graded highly on clinical scales, often as 4+ or 5. The amplitude of the oscillations generally diminishes over time, reflecting the progressive adaptation of the arc. In syndromes, clonus frequently occurs alongside associated symptoms such as , , and the presence of the Babinski sign. This hyperactivity is closely linked to , enhancing the overall clinical picture of neuromuscular dysfunction.

Types and Locations

Clonus is classified primarily by its duration and persistence, distinguishing between sustained and unsustained forms based on the number of rhythmic contractions elicited during clinical testing. Sustained clonus, considered pathological, involves more than 10 beats of oscillation and persists as long as the stretching force is maintained, often graded as 5 on the scale. In contrast, unsustained clonus features fewer than 10 beats—typically 5 to 9—and subsides spontaneously, graded as 4+, representing a borderline or less severe manifestation. Clonus is generally inducible through rapid muscle stretch or percussion. Anatomically, clonus predominantly affects the lower limbs, with ankle clonus being the most common site, elicited by dorsiflexion of the foot and involving the (S1-S2 nerve roots). Patellar clonus, tested by downward pressure on the (L4 nerve root), occurs less frequently in the . In the upper limbs, or finger clonus (C5-C6 nerve roots) can be observed through flexion maneuvers, exhibiting higher-frequency oscillations compared to lower limb sites. Axial clonus is rare but may involve the or masseter muscles via percussion of the . Variations in clonus presentation include asymmetry, often seen in unilateral lesions such as those from , where it affects one side more prominently. Bilateral clonus is more typical in diffuse conditions like , reflecting symmetric involvement of central pathways. Intensity is graded on a 0-5 scale, where 0 indicates no response, 1-3 reflect increasing reflex hyperactivity without clonus, 4 denotes unsustained clonus, and 5 signifies sustained clonus, aiding in severity assessment. The location of clonus provides clinical insight into the underlying site, as it correlates with specific spinal or supraspinal levels; for instance, ankle clonus frequently indicates involvement of lower segments in injuries affecting the thoracolumbar region.

Underlying Causes

Clonus primarily arises from lesions in the (UMN) pathways, particularly the or , which interrupt descending inhibitory signals to spinal motor neurons, leading to reflex hyperactivity. These disruptions result in a loss of supraspinal control, allowing exaggerated stretch reflexes to manifest as rhythmic oscillations. Acute causes of clonus include cerebrovascular accidents such as , traumatic brain injury (TBI), and spinal cord injury (SCI), where sudden damage to UMN pathways triggers the sign within hours to days post-insult. For instance, up to 46% of survivors develop , which may manifest with clonus, by 12 months, reflecting the vulnerability of descending motor tracts to ischemic or traumatic events. Chronic conditions associated with clonus encompass , , and , all involving progressive or persistent UMN degeneration. In MS and CP, clonus often occurs as part of , which affects approximately 80% of cases due to demyelination or perinatal injury affecting inhibitory pathways. In , clonus can present as part of UMN signs, such as . Other etiologies include toxic exposures, such as , which blocks glycine-mediated inhibition in the , mimicking UMN disinhibition and producing clonic convulsions. Metabolic disturbances like , often from drug interactions (e.g., SSRIs or ), can induce ankle clonus through excessive serotonergic activity enhancing reflex excitability, as can from liver dysfunction. Rare genetic disorders, such as (HSP), feature clonus as a hallmark of progressive lower limb due to affecting in corticospinal neurons. Risk factors for clonus primarily involve those predisposing to UMN lesions, including age over 50 years, which heightens risk via vascular , and underlying vascular disease accelerating pathway damage. Clonus is a common clinical indicator of inhibitory failure in UMN disorders.

Associated Neurological Conditions

Clonus is frequently observed in (MS), particularly in advanced cases where involvement leads to and . Ankle clonus is a common manifestation, often presenting with a relapsing-remitting pattern that aligns with disease flares, affecting approximately 10-17% of patients in early to progressive stages based on assessments. In , clonus is prominent in the subtype, characterized by bilateral lower limb involvement due to perinatal affecting motor pathways. This form of clonus tends to be persistent and lifelong, contributing to disturbances and muscle stiffness as part of the syndrome. Following an ischemic stroke, clonus typically manifests unilaterally on the affected side, emerging as an early sign of disruption within weeks of the event. It may resolve spontaneously in a of cases, with spasticity-related features including clonus improving in up to 20-30% of patients within the first few months through and rehabilitation. Spinal cord injury often results in sustained clonus below the level of the lesion, driven by disinhibited spinal reflexes in incomplete or complete injuries. This rhythmic activity is commonly exacerbated by specific positioning, such as hip extension or ankle dorsiflexion, which can trigger or prolong episodes in the lower extremities.

Pathophysiology

Stretch Reflex Hyperactivity

Clonus can arise from hyperactivity of the due to lesions, which reduce descending inhibition on spinal reflex arcs, leading to exaggerated responses to muscle stretch. In this model, rapid stretch evokes a myotatic reflex, and the resulting shortens the muscle, unloading muscle spindles and allowing relaxation, which then restretches the muscle, perpetuating oscillations through self-reexcitation without requiring an independent central generator. This reflex-based mechanism explains the dependence of clonus frequency on mechanical properties like limb and , as observed in biomechanical studies. Sustained clonus thus reflects spinal hyperexcitability, where the reflex loop gain exceeds unity, enabling rhythmic activity at 5-8 Hz.

Central Oscillator Theory

The Central Oscillator Theory posits that clonus results from the activity of a spinal (CPG), composed of interconnected spinal that form a half-center oscillator capable of producing rhythmic, alternating bursts of activation without ongoing peripheral input. This emerged in the , with work by researchers like Walsh describing clonus as driven by an autonomous spinal oscillator rather than purely mechanisms. Unlike simple loops, the theory emphasizes intrinsic spinal network properties that sustain oscillations once initiated, though debate persists with evidence supporting reflex self-reexcitation as sufficient in some cases. In this model, the half-center oscillator consists of mutually antagonistic pools of corresponding to flexor and extensor muscle groups; excitatory drive to one pool inhibits the opposing pool via , leading to rhythmic alternation. Rebound excitation occurs in the disinhibited pool following removal of inhibition, allowing it to fire and reciprocally suppress the previously active pool, thereby perpetuating the cycle at frequencies typically 5–8 Hz in clonus. This mechanism draws from broader CPG principles observed in locomotion but adapts to explain the self-sustaining nature of clonus after an initial trigger, such as stretch. Supporting evidence from animal models includes decerebrate cat preparations, where rhythmic, clonus-like activity persists in hindlimb muscles following transection, demonstrating generation within isolated spinal circuits. In humans, (EMG) recordings during clonus reveal synchronized, rhythmic bursts across motor units at consistent frequencies (e.g., 4–7 Hz) that continue despite perturbations to peripheral feedback, confirming a spinal origin independent of supraspinal drive in chronic . Recent (fMRI) studies from the have provided insights into supraspinal modulation of these spinal oscillators, showing altered cortico-spinal functional connectivity in spastic conditions that correlates with oscillatory motor output and responds to interventions targeting spinal circuits. For instance, epidural reducing has been associated with normalized integration between premotor cortical areas and spinal networks, suggesting descending influences fine-tune the intrinsic spinal rhythmicity.

Relation to Spasticity

Clonus and both arise from disinhibition of (UMN) pathways, leading to exaggerated stretch reflexes as part of the UMN syndrome. This shared results from lesions in descending inhibitory tracts, such as the corticospinal and reticulospinal pathways, which normally modulate spinal reflex arcs. Clonus represents a rhythmic, oscillatory manifestation of this , functioning as a specific subset of the broader spastic observed in UMN disorders. While is characterized by a velocity-dependent increase in tonic stretch reflexes and muscle resistance to passive movement, clonus specifically requires phasic or sustained stretch to elicit its repetitive contractions and relaxations. This distinction highlights spasticity's emphasis on sustained , whereas clonus involves dynamic, alternating muscle activity, often tested through rapid joint dorsiflexion. Clinically, clonus frequently coexists with in conditions like , , and , where it may emerge as an early or concurrent sign of reflex hyperactivity. Both are assessed using scales such as the Modified Ashworth Scale, which incorporates clonus in higher grades of muscle tone resistance (e.g., intermittent or sustained clonus indicating grades 3 or 4). The presence of clonus often signifies a more profound degree of UMN compared to tonic alone, as its sustained oscillations reflect heightened spinal excitability and reduced supraspinal control. This pathological insight underscores clonus as an indicator of advanced reflex dysregulation within the UMN syndrome.

Clinical Assessment

Clinical assessment of clonus is performed during a routine to evaluate integrity, typically at the , , or . The patient is positioned with the slightly flexed for ankle testing to promote relaxation. The examiner supports the , such as the foot, and applies a quick, brisk stretch by dorsiflexing the ankle sharply while maintaining slight pressure and eversion; rhythmic oscillations, or beats, of alternating contraction and relaxation are then observed and palpated against the examiner's hand. The number of beats is counted, with a positive response indicated by three or more repetitive movements at a of approximately 5-8 Hz. Clonus is typically assessed as part of the deep tendon grading scale, where a 4+ response indicates the presence of clonus (three or more beats), and sustained clonus exceeding 10 beats may be graded as 5+. This grading helps quantify severity and is integrated into broader deep tendon assessment, where clonus corresponds to a 4+ hyperreflexic response. Precautions include avoiding the maneuver in acute injuries, such as recent spinal cord trauma, to prevent potential exacerbation of damage or pain. The assessment should always be combined with evaluation of other reflexes, like the Achilles deep tendon reflex, to provide context, as isolated clonus may not fully characterize the underlying pathology. Clonus demonstrates high sensitivity for identifying upper motor neuron lesions, often appearing alongside hyperreflexia and spasticity, but exhibits low specificity when assessed in isolation due to potential occurrence in non-pathological states or varied etiologies. It is commonly associated with neurological conditions such as stroke and multiple sclerosis.

Diagnostic Tests

Electrophysiological studies play a crucial role in confirming clonus and quantifying its characteristics beyond clinical observation. (EMG) records the electrical activity of muscles during clonus, allowing measurement of contraction frequency, typically ranging from 5 to 8 Hz, and amplitude to assess severity and rhythmicity. Automated algorithms applied to EMG data can detect and analyze clonic bursts in extended recordings, aiding in objective evaluation of involuntary muscle activity. The , elicited by submaximal stimulation of the , evaluates spinal reflex excitability, which is often heightened in conditions producing clonus due to involvement, while the F-wave assesses motor axon conduction to the , helping identify proximal nerve or spinal root pathology contributing to . Imaging modalities are essential for identifying structural lesions underlying clonus. (MRI) of the brain and spinal cord detects demyelinating plaques in , tumors, or traumatic injuries that disrupt pathways, thereby confirming etiological factors. Computed tomography (CT) scans are particularly useful in acute settings, such as suspected , to rapidly visualize ischemic or hemorrhagic events in the that may precipitate clonus. These imaging techniques provide anatomical context to correlate with clinical findings of clonus. Somatosensory evoked potentials (SSEPs) assess the integrity of sensory pathways from periphery to cortex, which can be impaired in neurological disorders causing clonus, such as or injury. By stimulating peripheral and recording cortical responses, SSEPs help evaluate conduction delays or blocks in dorsal column pathways, offering insights into mixed sensorimotor involvement in syndromes. Although less specific for motor phenomena like clonus compared to direct tests, SSEPs are valuable in preoperative or intraoperative monitoring to predict neurological outcomes. Emerging wearable sensors, including accelerometers and surface EMG devices, enable quantitative, real-time assessment of clonus in settings during the . These portable systems measure and muscle patterns to quantify clonic frequency, amplitude, and duration noninvasively, facilitating longitudinal monitoring in patients with or . For instance, integrated accelerometer-EMG probes detect involuntary movements with high sensitivity, supporting objective tracking of treatment responses without requiring clinical visits.

Induction in Healthy Individuals

Voluntary Methods

Physiological clonus in healthy adults is uncommon and typically transient, occurring under specific conditions such as following prolonged exercise, where passive stretch can elicit brief rhythmic oscillations. It is generally not inducible by voluntary self-initiated movements due to intact cortical inhibition of the . When present, it is most readily observed at the ankle following brisk passive dorsiflexion after exhaustive activity, producing unsustained responses of fewer than 5 beats that fatigue rapidly due to normal refractory periods in the reflex arc. Sustained clonus exceeding 10 beats is pathological and not observed in healthy individuals. Such responses share the 5-8 Hz frequency with pathological clonus but lack persistence, occurring sporadically without large-scale documentation of prevalence.

Physiological Mechanisms

In healthy individuals, physiological clonus arises from temporary overload of the intact stretch reflex arc due to enhanced excitability following conditions like prolonged exercise, leading to brief rhythmic oscillations upon passive muscle stretch without underlying neurological damage. This involves excitatory Ia afferent fibers from muscle spindles activating α-motoneurons, with the gamma loop enhancing spindle sensitivity during contraction, potentially contributing to the oscillatory response at 5–7 Hz lasting fewer than 5 beats. Unlike pathological clonus, this self-limiting phenomenon is constrained by preserved supraspinal descending control that maintains inhibitory feedback via , preventing sustained activity. Electromyographic (EMG) studies show similar burst patterns in physiological and pathological clonus, with synchronized soleus at 5–7 Hz, but healthy episodes are shorter in duration and lower in amplitude, inducible only under conditions. This suggests a shared spinal oscillator mechanism, limited in normals by intact regulatory pathways.

Management

Treatment Options

Treatment of clonus primarily focuses on reducing the underlying and muscle oscillations associated with , often through a combination of pharmacological, physical, and surgical approaches. Pharmacological Interventions
, a GABA-B receptor , is commonly used to manage clonus by inhibiting excitatory neurotransmitter release in the , thereby relieving flexor spasms and clonus in conditions such as and . Oral is initiated at low doses (e.g., 5 mg three times daily) and titrated up to 80 mg daily, while intrathecal delivery via pump is reserved for severe cases unresponsive to oral therapy, providing targeted spinal inhibition with doses typically ranging from 300-800 μg daily for spinal-origin . , a centrally acting alpha-2 , reduces and clonus frequency by decreasing facilitation and excitatory release; it is dosed starting at 2 mg every 6-8 hours, up to a maximum of 36 mg daily, and has shown efficacy comparable to in placebo-controlled trials for spastic conditions. For focal clonus, type A injections target affected muscles, with a 2017 systematic review of 14 studies (181 patients) demonstrating improvement in clonus severity across various assessment scales, including clonus scores and duration, though results varied due to inconsistent measurement tools. Physical Interventions
Stretching exercises, often incorporating range-of-motion techniques and proprioceptive neuromuscular facilitation, help optimize muscle length, reduce , and diminish clonus by addressing the length-tension relationship in spastic muscles, particularly in where contractures affect up to 66% of patients within the first year. Bracing or splinting maintains joint positions and applies consistent stretch to hyperreflexic muscles, thereby minimizing clonus triggers and supporting functional positioning as part of focal therapy for . (FES) delivers targeted electrical impulses to activate muscles, reducing lower extremity as evidenced by of 10 studies showing significant decreases in Modified Ashworth Scale scores (e.g., 70-98% reduction in some cohorts), which may indirectly attenuate clonic oscillations through enhanced . Focal vibration therapy applies localized mechanical vibration to affected muscles and has been shown to reduce , particularly in post-stroke rehabilitation, with a 2024 review of randomized controlled trials indicating improvements in motor function and . Surgical Interventions
For clonus, selective dorsal rhizotomy involves sectioning abnormal rootlets in the spine to interrupt hyperactive reflex arcs, effectively reducing and improving mobility in , as demonstrated in studies combining it with pump removal for sustained benefits. Intrathecal pumps provide for severe, generalized clonus unresponsive to oral agents, offering precise dosing (e.g., 90-703 μg daily for cerebral origins) and superior tone reduction compared to , particularly in pediatric populations. Emerging options include cannabinoids, with 2020s trials such as a randomized controlled study of in pediatric showing tolerability but no significant spasticity reduction overall, though further research explores potential anti-spastic effects in severe cases. , targeting the or , is under investigation in 2020s clinical trials for dyskinetic , aiming to modulate including clonus, with preliminary safety data but limited efficacy evidence specific to clonic symptoms. Recent 2024-2025 studies have demonstrated that high-frequency epidural electrical stimulation and stimulation can reduce clonus and in individuals with and .

Prognosis and Outcomes

The prognosis for clonus is highly variable and largely determined by the underlying neurological condition causing the . In acute cases, such as those following or traumatic injury, clonus often improves or resolves as the primary heals, particularly with early intervention and rehabilitation; for instance, symptoms may diminish within weeks to months in reversible etiologies like vascular events or infections. In contrast, clonus tends to persist chronically in progressive disorders such as or , where ongoing demyelination or permanent damage sustains the reflex hyperactivity. Several factors influence the persistence of clonus, including the acuity and reversibility of the . Acute, treatable causes, such as post-stroke or transient ischemia, generally offer a more favorable outlook due to potential neural recovery, whereas irreversible damage from complete spinal transection or advanced neurodegenerative processes leads to prolonged or permanent clonus. Early therapeutic management further enhances prognosis by mitigating secondary complications, though complete elimination is rare in non-reversible cases. Untreated clonus can result in adverse outcomes, including the development of muscle contractures from sustained , which restrict joint range and contribute to . This progression significantly impairs mobility, balance, and overall , increasing fall risk and limiting daily activities. In long-term scenarios, such as , regular monitoring is essential to detect disease progression that may exacerbate clonus; while no curative options exist, effective symptom control can substantially improve functional independence and reduce disability.

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  58. https://clinicaltrials.gov/study/NCT06122675
  59. https://www.science.org/doi/10.1126/scitranslmed.adp9607
  60. https://pubmed.ncbi.nlm.nih.gov/41019413/
  61. https://www.healthline.com/health/neurological-health/clonus
  62. https://www.webmd.com/a-to-z-guides/what-is-clonus-reflex
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