Involuntary Movements: A Stroke's Unseen Impact

can a stroke cause involuntary movements

Involuntary movements can occur after a stroke, and these are known as post-stroke movement disorders. They are relatively uncommon, but they can be a significant complication of this common disease. Post-stroke movement disorders can be either hypo- or hyperkinetic and can develop in any stroke subtype and at any brain level of the motor circuit. The basal ganglia and thalamus are the primary lesion sites associated with post-stroke movement disorders. The most common post-stroke movement disorder is chorea, which usually presents as a hemichoreiform dyskinesia on the side of the body opposite the vascular insult. Dystonia is another common post-stroke movement disorder, which often affects the contralateral limb and is associated with hypertonia due to underlying spasticity. Post-stroke movement disorders are usually self-limiting and resolve within 6 to 12 months of onset, but a short-term treatment may be required for symptom control.

Characteristics Values
Prevalence 1% to 4% of all strokes
Sex Both sexes are affected equally
Onset Early/acute or delayed/chronic
Course Transient, recurrent, persistent, or progressive
Treatment Pharmacotherapy, chemodenervation, stereotactic functional neurosurgery

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Post-stroke movement disorders: clinical manifestations and pharmacological management

Post-stroke movement disorders: clinical manifestations

Involuntary abnormal movements have been reported after ischaemic and haemorrhagic stroke. Post-stroke movement disorders can appear as acute or delayed. The frequency of post-stroke abnormal movements is unclear, with studies showing that 3.7% and 1% of stroke patients developed movement disorders. The time course for the development of movement disorders varies from the day of stroke onset to several years later. The basal ganglia is the area in the brain most often affected by post-stroke movement disorders.

Post-stroke movement disorders can be hyperkinetic or hypokinetic. Hyperkinetic movement disorders include:

  • Chorea, which consists of irregular, purposeless, abrupt, rapid, brief, jerky, un-sustained movements that may involve all parts of the body.
  • Ballism, a severe form of chorea, is characterised by wide-amplitude, flinging movements, usually involving the proximal limbs.
  • Dystonia, a neurological disorder dominated by sustained muscle contractions, which frequently causes twisting, repetitive, and patterned movements or abnormal postures.
  • Tremor, which occurs most commonly with a multifocal or segmental distribution and is related to action.
  • Myoclonus, defined as sudden jerks typically lasting 10 to 50 milliseconds, with movements rarely lasting more than 100 milliseconds.
  • Parkinsonism, which has been associated with unilateral or bilateral basal ganglia infarcts in the striatum or lentiform nucleus.

Hypokinetic movement disorders include:

Vascular parkinsonism, characterised by symmetric akinesia and gait impairment.

Pharmacological management

The knowledge of pharmacological treatment for post-stroke movement disorders is still inadequate. Dopaminergic and GABAergic systems may be involved in post-stroke movement disorders. Drugs that can modulate dopaminergic or GABAergic tone are usually used in management, including:

  • Typical neuroleptics (e.g. haloperidol, pimozide, perphenazine, fluphenazine)
  • Atypical neuroleptics (e.g. olanzapine, quetiapine, sulpiride, clozapine)
  • Tetrabenazine and reserpine, which deplete presynaptic dopamine and block post-synaptic dopamine receptors
  • Clonazepam, a long-acting central-type GABA-A receptor agonist
  • Sodium valproate, an indirect agonist of GABA receptors
  • Levetiracetam, which has several action mechanisms, including the inhibition of calcium release from intraneuronal stores and the modulation of GABA- and glycin-gated currents
  • Topiramate, which has shown several action mechanisms, including the inhibition of calcium release from intraneuronal stores and the modulation of GABA- and glycin-gated currents
  • Botulinum toxin, which blocks the release of acetylcholine
  • Benzodiazepines, baclofen, and anticholinergic drugs
  • Dopamine-depleting/blocking agents

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Post-thalamic stroke movement disorders: a systematic review

Yes, a stroke can cause involuntary movements.

Involuntary abnormal movements have been reported after ischaemic and haemorrhagic stroke. Post-stroke movement disorders can appear as acute or delayed sequel. The most common post-stroke abnormal movement disorder reported is dystonia followed by hemiataxia. There was a higher association between ischaemic stroke and movement disorder. Acute onset movement disorders were more common than delayed. The posterolateral thalamus was most commonly involved in post-thalamic stroke movement disorders.

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Post-stroke dyskinesias

Chemodenervation with botulinum toxin (BTX) injections is the cornerstone of the symptomatic treatment of focal or segmental post-stroke dystonia. Vascular dystonia usually has a poor response to oral pharmacotherapy, including dopamine blocking and depleting agents, anticholinergic drugs, baclofen, and benzodiazepines. Oral medications, however, are widely used in generalized dystonia, dystonia mixed with other movement disorders, or as an adjuvant therapy in focal or segmental dystonia when there is an unsatisfactory response to BTX.

Post-stroke tremor is particularly refractory to pharmacotherapy. Trials of medications with GABA-agonistic activity (eg, clonazepam, valproate, topiramate, or primidone), alone or in combination, may be effective in individual cases. Because of the dopaminergic (nigrostriatal) system involvement in Holmes tremor, treatment with levodopa or dopamine agonists seems to be useful. Propranolol, one of the first-line treatments in essential tremor, is usually of limited benefit in vascular tremor. Dystonic and parkinsonian tremors are treated as vascular dystonia and parkinsonism, respectively.

Post-stroke myoclonus and asterixis usually improve spontaneously and do not require pharmacotherapy. When interfering with the patient’s functional abilities, like eating or writing, myoclonus is most frequently treated with GABAergic medications (eg, clonazepam and valproate), but levetiracetam or piracetam can be very useful. Monotherapy should be attempted first, although eventually several drug combinations might be required. Dystonic myoclonus is treated as vascular dystonia.

Finally, stereotactic functional neurosurgery, whether ablative or deep brain stimulation (DBS), should be considered for patients with severe and persistent dyskinesias (arbitrarily defined as duration longer than 1 year).

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Movement disorders following cerebrovascular lesions: aetiology, treatment options and prognosis

Movement disorders are a rare but possible consequence of stroke. They are defined as paroxysmal, recurrent, transient, permanent, and delayed movements in the acute phase or as a delayed syndrome occurring months or years after vascular events. These involuntary movements can be classified as hyperkinetic or hypokinetic and include various presentations such as tremor, chorea-ballism, dystonia, athetosis, myoclonus, ataxia, and parkinsonism. The time course for the development of these disorders is unpredictable, as the course differs according to the type of movement disorder. Similar to typical stroke symptoms, the duration of these disorders can vary from paroxysmal and/or transient to persistent and progressive.

Etiology

Post-stroke movement disorders can develop in any stroke subtype and at any brain level of the motor circuit. However, the basal ganglia and thalamus are the primary lesion sites associated with these disorders. Strokes in deep brain lesions are more likely to result in movement disorders. Ischemic stroke, the most common type of stroke, can be classified into small vessel disease, large vessel disease, or cardioembolic stroke. Hemorrhagic stroke has a higher probability of developing post-stroke movement disorders compared to ischemic stroke. Chronic small vessel disease can lead to secondary parkinsonism, which is characterized by bilateral slowness and rigidity, predominantly in the lower extremities.

Treatment Options

The management of post-stroke movement disorders should be individualized and based on each clinician's experience. Many cases are transient and self-remitting, requiring no treatment. Medical treatment for these disorders is similar to that for primary movement disorders as they share common underlying pathomechanisms. Chorea, the most common post-stroke movement disorder, is typically treated with anti-dopaminergic drugs that block D1 and D2 receptors. For dystonia, focal injections of botulinum toxin and intrathecal baclofen can be used for partial symptom relief. Tremor, which is often resistant to medical treatment, may require surgical intervention and focal botulinum toxin injections. Post-stroke myoclonus is usually transient and does not require management, but GABAergic drugs and levetiracetam can be used for symptomatic treatment. Vascular parkinsonism, characterized by symmetric akinesia and gait impairment, may be treated with levodopa, although the effect is often poor and short-lasting.

Prognosis

The clinical course of post-stroke movement disorders is variable. Many of these disorders develop during the acute phase, especially within several days of the stroke onset, which can lead to under-diagnosis. The period for developing a movement disorder after stroke can range from immediately before the stroke to years after the onset. The latency interval is shortest for chorea and longest for parkinsonism. Most post-stroke movement disorders have a short duration and improve over time. Chorea, myoclonus, and asterixis are typically self-limiting, while vascular parkinsonism tends to persist and progressively deteriorate. Dystonia and tremor have a poor prognosis, with significantly worsened activities of daily living and quality of life.

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Tremors following stroke

Tremors are a type of involuntary movement that can occur following a stroke. They are characterised by rhythmic shaking of the hands, arms, head, legs, or torso, and can cause challenges in performing daily tasks. Tremors can be categorised as rest or action tremors, depending on when they are activated. Rest tremors occur when a person is at rest, while action tremors occur when a muscle is moved voluntarily.

Post-stroke tremors can be caused by lesions in the basal ganglia or thalamus, which are areas of the brain that control movements. They can also be caused by damage to the cerebellum, which controls movement coordination, or by other medical conditions such as diabetes, liver or kidney failure, and thyroid disorders.

The treatment for post-stroke tremors depends on the type of tremor and its severity. Medications such as beta-blockers, anti-seizure drugs, tranquilizers, dopaminergic medications, and anticholinergic drugs may be used to slow down the tremors. In some cases, botulinum toxin injections or surgical procedures such as deep brain stimulation may be considered. Lifestyle changes, such as reducing caffeine intake, eliminating stress, and getting enough sleep, can also help manage tremors.

Frequently asked questions

The most common types of movement disorders that can occur after a stroke include both hypo and hyperkinetic syndromes. The most common post-stroke abnormal movement disorder is dystonia, followed by hemiataxia.

The symptoms of post-stroke movement disorders can vary depending on the type of disorder. Some common symptoms include involuntary hyperkinetic movements, such as chorea, dystonia, tremor, and myoclonus.

The treatment options for post-stroke movement disorders depend on the specific type of disorder and its severity. In some cases, the symptoms may resolve spontaneously within 6 to 12 months. For more severe or persistent cases, short-term pharmacotherapy or functional neurosurgical interventions, such as deep brain stimulation, may be considered.

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