Anna Werrett
Stroke-related movement disorders are uncommon but can be either hypo- or hyperkinetic. They can occur at any time after a stroke, from the acute phase to years later. The most common post-stroke movement disorder is dystonia, followed by hemiataxia. Ischemic stroke is more likely to cause movement disorders than haemorrhagic stroke. The posterolateral thalamus is the part of the brain most often implicated in post-stroke movement disorders.
Post-stroke movement disorders are usually self-limiting and resolve within a year of onset. However, drug treatment may be required for symptom control. Surgical intervention may be considered for patients with severe, persistent and disabling movement disorders.
| 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 | Short-term pharmacotherapy, stereotactic functional neurosurgery |
What You'll Learn
- Post-stroke movement disorders can be hyperkinetic or hypokinetic
- Post-stroke dyskinesias are involuntary hyperkinetic movements
- Post-stroke chorea usually presents as a hemichoreiform dyskinesia
- Post-stroke dystonia is often associated with hypertonia due to underlying spasticity
- Post-stroke tremor is a heterogeneous group of movement disorders
Post-stroke movement disorders can be hyperkinetic or hypokinetic
Hyperkinetic Movement Disorders
- Hemichorea: unilateral, rapid, and purposeless movements of flexion and extension, rotation, or crossing.
- Hemiballismus: severe, violent, and arrhythmic movements of a limb from a proximal joint with an element of rotation.
- Dystonia: a syndrome characterised by sustained muscle contractions causing abnormal postures and twisting movements.
- Tremor: rapid, rhythmic, and oscillatory movements, generally of the hands.
- Myoclonus: sudden, involuntary, and jerky movements of a single muscle or a group of muscles.
- Athetosis: slow, sinuous, and writhing movements, mainly of the hands and feet.
- Pseudoathetosis: abnormal writhing movements caused by a failure of joint position sense.
Hypokinetic Movement Disorders
- Asterixis: failure to sustain muscle contraction, with intermittent lapses in muscle tone.
- Parkinsonism: characterised by bradykinesia, increased muscle tone, and tremors.
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Post-stroke dyskinesias are involuntary hyperkinetic movements
Post-stroke dyskinesias are usually associated with lesions in the basal ganglia or thalamus but can occur with strokes at many different locations in the motor circuit. The basal ganglia represents an area in the brain most often interested in post-stroke movement disorders. The basal ganglia circuitry provides a tonic inhibitory output to the thalamus and thus the motor cortex. The output of the cortico-cerebellar loop (cerebellar circuitry) is tonically excitatory. Glutamate is the major excitatory neurotransmitter and gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in this motor network.
The pathogenesis of post-stroke dyskinesias is still incompletely understood but suggested mechanisms include post-synaptic denervation hypersensitivity, trans-synaptic neuronal degeneration, as well as aberrant axonal and dendritic plasticity after the cerebrovascular injury. Post-stroke dyskinesias are relatively rare even with marked lesions, but they can arise after any stroke subtype at any level within the motor circuitry and after any interval period.
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Post-stroke chorea usually presents as a hemichoreiform dyskinesia
Post-stroke chorea is treated with anti-dopaminergic drugs, which block the D1 and D2 receptors. These include typical neuroleptics such as haloperidol, pimozide, perphenazine, and fluphenazine, as well as atypical neuroleptics such as olanzapine, quetiapine, and sulpiride. Presynaptic dopamine-depleting agents and catecholamine-depleting drugs, as well as GABA receptor agonists such as clonazepam and valproic acid, can also be used.
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Post-stroke dystonia is often associated with hypertonia due to underlying spasticity
Spasticity is a stretch reflex disorder, manifested clinically as an increase in muscle tone that becomes more apparent with more rapid stretching movement. It is due to a pathological stretch reflex, i.e. a tonic stretch reflex present in a relaxed muscle. Spasticity is one of the positive phenomena of the upper motor neuron syndrome (UMNS), which is characterised by the inability to relax a muscle leading to a spontaneous, although stretch-sensitive, tonic contraction. Spastic dystonia is usually viewed as an efferent phenomenon, mediated by a tonic supraspinal drive to spinal motor neurons.
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Post-stroke tremor is a heterogeneous group of movement disorders
Post-stroke dyskinesias are a group of movement disorders that arise from cerebrovascular insults. They are a rare complication of a relatively common disease, with an estimated prevalence of 1% to 4% of all strokes. The pathogenesis of post-stroke dyskinesias is still not fully understood, but it is believed to be caused by post-synaptic denervation hypersensitivity, trans-synaptic neuronal degeneration, and aberrant axonal and dendritic plasticity (remodelling) after the cerebrovascular injury.
Post-stroke dyskinesias can be classified as hyperkinetic or hypokinetic, with hyperkinetic being the most frequent. Hyperkinetic disorders can be further classified into choreiform dyskinesias (ballism, chorea, and athetosis), dystonia, and non-choreo-dystonic dyskinesias (eg, tremor, asterixis, and myoclonus). The most common type of post-stroke dyskinesia is hemichorea-hemiballism, but other reported mixed movements include chorea-ballism-dystonia, chorea-athetosis-dystonia, and dystonia-athetosis with or without action tremor or myoclonic jerks.
The pathophysiology of post-stroke dyskinesias is thought to be caused by lesions in the basal ganglia circuitry, particularly the striatum and thalamus. These lesions are believed to cause underactivity of the indirect pathway (and/or overactivity of the direct pathway), leading to a decreased pallidal inhibitory output to the thalamus. This results in thalamic disinhibition, which releases the motor cortex and allows movements that are normally suppressed.
The treatment of post-stroke dyskinesias depends on the specific type of dyskinesia. For example, the treatment of post-stroke choreiform dyskinesias consists mainly of anti-dopaminergic therapy with typical or atypical antipsychotics (neuroleptics), while post-stroke dystonia is usually treated with botulinum toxin (BTX) injections. Post-stroke tremor is particularly refractory to pharmacotherapy, and post-stroke myoclonus and asterixis usually improve spontaneously and do not require pharmacotherapy.
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Frequently asked questions
Yes, strokes can cause involuntary movements. These are known as post-stroke movement disorders, and they can occur after any type of stroke, at any level of the motor circuit, and at any time after the stroke.
Post-stroke movement disorders can be hyperkinetic or hypokinetic. Hyperkinetic movement disorders include choreiform dyskinesias (ballism, chorea, and athetosis), dystonia, and non-choreo-dystonic dyskinesias (e.g. tremor, asterixis, and myoclonus). Hypokinetic movement disorders include parkinsonism.
Symptoms of post-stroke movement disorders vary depending on the type of movement disorder. Choreiform dyskinesias usually present as hemichorea, hemiballism, and/or hemiathetosis on the side of the body opposite to the vascular insult. Dystonia usually affects the opposite limb and is often associated with hypertonia due to underlying spasticity. Post-stroke tremor is heterogeneous and characterised by various tremor phenomenologies. Post-stroke myoclonus and asterixis are usually focal or segmental.
Treatment of post-stroke movement disorders involves addressing the underlying cause and controlling vascular risk factors to reduce the incidence of vascular dyskinesias. Symptomatic pharmacotherapy may be required for severe cases. Surgical treatment may be considered for severe and persistent cases.
Post-stroke movement disorders are usually self-limiting and tend to resolve within 6 to 12 months. The overall long-term prognosis for patients with post-stroke movement disorders is similar to that of other stroke patients.
