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REVIEW ARTICLE
Year : 2021  |  Volume : 69  |  Issue : 2  |  Page : 272-283

Post-stroke Movement Disorders: Clinical Spectrum, Pathogenesis, and Management


Department of Neurology, Govind Ballabh Pant Postgraduate Institute of Medical Education and Research, New Delhi, India

Date of Submission03-Aug-2018
Date of Decision30-Nov-2019
Date of Acceptance20-Jan-2020
Date of Web Publication24-Apr-2021

Correspondence Address:
Dr. Sanjay Pandey
Department of Neurology, Academic Block, Room No 503, Govind Ballabh Pant Postgraduate Institute of Medical Education and Research, New Delhi - 110 002
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.314574

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 » Abstract 


Involuntary movements develop after 1–4% of strokes and they have been reported in patients with ischemic and hemorrhagic strokes affecting the basal ganglia, thalamus, and/or their connections. Hemichorea-hemiballism is the most common movement disorder following a stroke in adults while dystonia is most common in children. Tremor, myoclonus, asterixis, stereotypies, and vascular parkinsonism are other movement disorders seen following stroke. Some of them occur immediately after acute stroke, some can develop later, and others may have delayed onset progressive course. Proposed pathophysiological mechanisms include neuronal plasticity, functional diaschisis, and age-related differences in brain metabolism. There are no guidelines regarding the management of post-stroke movement disorders, mainly because of their heterogeneity.


Keywords: Dystonia, stroke, tremor
Key Message: Post-stroke movement disorders are one of the commonest causes of secondary movement disorders. They can manifest in hypokinetic or hyperkinetic movement disorders. They are often associated with lesions in the basal ganglia, however, there is emerging evidence that in this setting most movement disorders result from a network dysfunction rather than from a single lesion.


How to cite this article:
Tater P, Pandey S. Post-stroke Movement Disorders: Clinical Spectrum, Pathogenesis, and Management. Neurol India 2021;69:272-83

How to cite this URL:
Tater P, Pandey S. Post-stroke Movement Disorders: Clinical Spectrum, Pathogenesis, and Management. Neurol India [serial online] 2021 [cited 2021 May 11];69:272-83. Available from: https://www.neurologyindia.com/text.asp?2021/69/2/272/314574




Movement disorders secondary to strokes are diverse and their natural history, prognosis, and treatment differ from their idiopathic counterpart. The frequency of post-stroke movement disorders has been estimated to range between 1–4% of all strokes [Table 1].[1],[2],[3] They either manifest acutely with stroke[1],[2] or as a delayed sequela of stroke.[4],[5] As with all secondary movement disorders, post-stroke movement disorders can also be divided into hyperkinetic disorders characterized by excessive, abnormal involuntary movements and hypokinetic disorders manifesting as paucity or slowness (bradykinesia) of movement. Movement disorders reported after cerebrovascular events include chorea-ballism-athetosis, dystonia, tremor, myoclonus, asterixis, stereotypies, akathisia, tics, vascular parkinsonism, progressive supranuclear palsy, isolated freezing of gait, and cortico-basal syndrome.[6],[7] Despite the greater number of patients experiencing the resolution of symptoms, the disability associated with it in the form of social, financial, and occupational burden plus the therapy available to treat them appropriately, makes their early recognition and management imperative. Most of the data regarding post-stroke movement disorder stem from individual case series and stroke registries alone. Thus, the objective of this review is to understand the different types of movement disorders reported in the literature and describe their pathogenesis and outcome.
Table 1: Published literature on poststroke movement disorder

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Search strategy

We searched the PubMed on 30th June 2018 and found 47 articles on “Post-stroke tremor;” 61 articles on “Post-stroke dystonia,” 7 articles on “Post-stroke hemichorea,” 97 articles on “Post-stroke hemiballism,” 6 articles on “Post-stroke hemichorea hemiballism,” 10 articles on “Post-stroke tics,” 9 articles on “Post-stroke vascular parkinsonism,” 1581 articles on “Vascular parkinsonism,” 5 articles on “Post-stroke restless leg syndrome,” 6 articles on “Post-stroke stereotypy,” 94 articles on “Post-stroke asterixis,” 17 articles on “Post-stroke myoclonus,” 8 articles on “Post-stroke akathisia.” We included data from English literature only and the final reference list was based on the relevance to the topic of review.

Pathophysiology of movement disorders

Post-stroke movement disorders can manifest with lesions affecting any segment of the motor circuitry; be it cortical which includes the primary motor, supplementary motor, and premotor cortical areas; or subcortical affecting the basal ganglia, thalamus, internal capsule, diencephalon, and mesencephalon; or cerebellar circuitry.[8] The basal ganglia are the central subcortical component of the motor circuitry, which relays information from the cortex to the thalamus and back. The cerebellar circuitry involves two pathways: cortico-cerebello-cortical or dentate-rubro-thalamic pathway and GMT (Guillain Mollaret triangle) or dentate-rubro-olivary pathway [Figure 1].[9] It has been observed that strokes affecting the subcortical structures are more prone to develop abnormal movements than cortical strokes.[10]
Figure 1: The above figure illustrates the basal ganglia and cerebellar circuitries involved in the generation of movement disorders. The cortex as an excitatory influence over the striatum from where arise two pathways direct and indirect basal ganglia pathways. In the direct pathway, the striatum sends inhibitory signals to the globus pallidus interna (Gpi) which is further unable to inhibit the VpL nucleus of the thalamus. Thus, via the direct pathway, the thalamus has an excitatory influence over the cortex. In the indirect pathway, the striatum sends inhibitory signals to the globus pallidus externa (GPe) which is further unable to inhibit the subthalamic nucleus (STN). Thus, the STN now excites the GPi which has an inhibitory influence over the thalamic VpL nucleus. Thus, via the indirect pathway, the thalamus becomes inhibitory to the cortex. In the cerebellar circuitry, the cortex sends excitatory signals to the pontine nuclei which further on the cross the midline and have an inhibitory influence over the Purkinje cells of the cerebellum. Thus, the Purkinje cells are now unable to inhibit the dentate nucleus and continue further as the crossed dentatorubrothalamic pathway, which is excitatory to the cortex. Moreover, the STN has an excitatory influence over the pontine nuclei and thereby facilitates the excitatory cerebellar influence over the cortex. The Guillain-Mollaret triangle (GMT) is formed by the dentate nucleus of one side; red nucleus (RN) and inferior olivary nucleus (ION) of the opposite side. The red nucleus keeps the ION under check via inhibitory signals thus, it cannot go on to excite the Purkinje cells

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Damage to the direct basal ganglia pathway gives rise to hypokinetic movement whereas the involvement of the indirect pathway gives rise to hyperkinetic movement disorder.[8] Some movements develop acutely with stroke whereas others are delayed and some progressive.[1],[2],[4],[5] Any acute lesion leads to a sudden functional interruption in these motor circuitries giving rise to the abnormal movement which subsides once there is a return to normal function. Most often the abnormal movement begins to develop after improvement in motor weakness and thus are delayed in presentation.[5],[11],[12],[13],[14] This aspect brings to light the concept of neuronal plasticity wherein there is the formation of a parallel network that overcomes the motor loss, and formation of the pathological circuit gives rise to the abnormal movements.[15],[16] The type of movement disorder seen in adults and children following stroke is also different. The proposed reasoning for this could be related to differences in brain metabolism at different ages and their susceptibility to damage caused by stroke.[5] There are patients with thalamic stroke having sensory deficits leading to abnormal proprioceptive signals to muscle joints leading to impaired synergistic muscle contractions and abnormal movements.[5]

Mostly the abnormal movements were developed contralateral to the site of stroke but there have been cases wherein the abnormal movement has been ipsilateral to the site of the lesion. The proposed mechanism for this is a compensatory increase in the functioning of structures contralateral to stroke site and thus giving rise to ipsilateral abnormal movements.[17]

It has been observed that there is no definite relation between the type of abnormal movement and the site of stroke, that is the same type of movement can be seen with lesions at different places.[18] A probable explanation is that poor resolution of the imaging cannot pick up these lesions and moreover, functional diaschisis might have played a role.

The incidence of movement disorders is three times higher with subcortical strokes than cortical strokes, basal ganglia (44%) and thalamus (33%) being involved in most cases.[1],[10] Post-stroke movement disorders are rarely seen with lesions affecting the cerebellum in isolation.[19] In a study by Netravathi et al. on 103 patients of secondary movement disorders, it was found that the most common cause was vascular of which arterial stroke comprised 65% of the cases.[20]

Clinical studies: Demographics and types of movement disorders

Since stroke affects the elderly age group more often, there also seems to be a higher prevalence of post-stroke movement disorders in the same age group. In a study comprising of 56 patients by Alacron et al., the mean age of presentation was 63.3 years (range: 17–90 years). Similarly, it was 70 years (range: 32–90 years) in Lausanne stroke registry study.[1],[2] In a case series of thalamic strokes by Kim et al., 35 patients with post-stroke movement disorders, age ranged from 28–74 years with the mean age being 53.5 years.[5] In the systematic review by Suri et al. among 284 patients with post-stroke movement, disorders were found to be 63 years.[21] They also reported a slightly higher prevalence of the movements in males. Stroke-induced movement disorders are also seen in children.[22]

The prevalence of post-stroke movement disorder stems from two large series; by Ghika et al. in 1997 and Alarcon et al. in 2004; which amounts to 1–4%. In the Lausanne registry, 29 patients were identified with post-stroke movement disorders out of the 2500 patients studied, whereas Alarcon et al. reported them in 56 out of the 1500 patients they evaluated. These two studies stated a higher prevalence of post-stroke movement disorders in patients with hemorrhagic stroke.[1],[2] But the systematic review by Suri et al. stated that two-thirds of the cases of post-stroke movement disorders reported in the literature were secondary to ischemic stroke rather than hemorrhagic stroke.[21] A similar observation was reported by Gupta et al. in their review on post-thalamic stroke movement disorders.[23]

The various movement disorders described by Alarcon et al. following stroke included chorea (n = 20), dystonia (n = 16), tremor (n = 14), and vascular parkinsonism (n = 6) whereas movement disorders observed in Lausanne registry included hemichorea–hemiballism (n = 11), hemidystonia (n = 5), stereotypies (n = 2), jerky dystonic unsteady hand (n = 3), asterixis (n = 2), initial limb-shaking (n = 2), bilateral tremor (n = 1), bilateral jaw myoclonus (n = 1), hemi-akathisia (n = 1), and dysarthria-dyskinetic hand (n = 1). Thus, the most common movement disorder observed by them was hemichorea followed by dystonia.[1],[2] In a systematic review on post-thalamic stroke movement disorders, authors reported 102 cases of dystonia, 72 cases of hemiataxia, 70 cases of chorea, 69 cases of tremor, 55 cases of vascular parkinsonism, 37 cases of asterixis, 35 cases of athetosis, 15 cases of myoclonus, and 14 cases of ballism with dystonia as the most common movement disorder and hemiataxia as the most common acute movement disorder following thalamic stroke. They found chorea to be the third most common movement disorder following a stroke. Other rare movement disorders seen secondary to thalamic stroke include pseudochoreoathetosis, myorhythmia, jerky unsteady dystonic hand, clonic perseveration, stereotypy, bilateral eyelid tremor, cerebellar syndrome, hemiakathisia, jerky dystonia of shoulder, orofacial dyskinesia, restless leg syndrome, and paroxysmal kinesigenic dystonic choreoathetosis.[23] In the systematic review by Suri et al., they found that dystonia (n = 66) was the most common movement disorder following a stroke, followed by chorea (n = 46) and myoclonus (n = 43). They also found that dystonia was commoner in the younger age group (>50 years), whereas chorea was more prominent in the elderly age group. The other movement disorders stated by them include tremor (n = 39), parkinsonism (n = 42), restless legs syndrome (n = 20), alien hand syndrome (n = 9), periodic limb movements (n = 9), stereotypy (n = 8), akathisia (n = 1), and tics (n = 1).[21]

Hemichorea-hemiballism

Hemichorea is unilateral, rapid involuntary motions of flexion and extension, rotation or crossing, which may involve all body parts but predominantly distal parts.[3],[24] Hemiballismus is a severe, violent, arrhythmic, and large amplitude excursion of a limb from a proximal joint with an element of rotation.[3],[24] Hemichorea-hemiballism is the commonest post-stroke movement disorder. In a study of 2500 patients by Ghika Schimd et al., 29 patients had post-stroke abnormal movements of which 11 (38%) patients had hemichorea-hemiballism.[1] In a study of 56 patients by Alarcon et al., chorea was the most common movement disorder present in 20 (36%) patients.[2] Hemiballism has traditionally been described in lesions of the contralateral STN but can also be associated with lesions in other parts of the brain. The lesions in the thalamus or lentiform nucleus are more frequently associated with hemiballism than lesions in the subthalamus.[1],[2],[22],[25],[26] Alarcon et al., reported that in eight patients with hemiballismus of which one had subthalamic lesions, one had a pallidal lesion, and six had thalamic lesions.[2] The syndrome of hemiballismus associated with acute limb pain has been described due to an anterior parietal artery stroke.[27] In another study of 25 patients with hemiballism by Vidakovic et al., it was reported that only one patient had an isolated contralateral subthalamic nucleus lesion, five had subthalamus with other central nervous system parts (pons, midbrain, basal ganglia) involvement, five with basal ganglia involvement, one had thalamic involvement, and three had cortical involvement.[28] Hemichorea is commonly seen with lesions involving the lentiform nucleus or thalamus but has also been reported with lesions involving the subthalamus, striatum, posterior limb of the internal capsule, corona radiata, frontal lobe, parietal lobe, temporal cortex, external capsule, and pons.[3]

Hemichorea-hemiballism is usually seen contralateral to the lesion site but there have been few case reports where it was found to be present on the ipsilateral side of the lesion.[29],[30],[31] One patient had developed ipsilateral hemiballism postoperatively due to infarct in the right anterior cerebral artery territory.[31] In a clinicoradiological study of vascular hemichorea by Galiano et al., all lesions were contralateral to the side of the body affected except in one case with a left thalamic hematoma and ipsilateral hemichorea.[32]

Hemiballism is usually seen to occur immediately with the onset of stroke; however, there have been cases which reported a delay of up to 5 months[8] while hemichorea seems to occur within a few days after stroke.[8]

Although small vessel disease is implicated as the common cause of these movement disorders, vascular malformations such as cavernous malformation, moyamoya disease and carotid stenosis are also observed.[1],[2],[32],[33] In a study of 42 patients with moyamoya disease with a mean age of onset of 21.4 years, chorea was present in 24 patients and dystonia in 8 patients.[34] After bypass surgery, symptoms improved in all patients suggesting that the pathogenic process is cerebral ischemia in moyamoya disease, which is reversible.[35] Infrequently, ballism and chorea can occur bilaterally or may involve only one limb (monochorea).[36] Distal choreiform movements are seen in many patients with ballism, and, when recovery takes place, hemiballism often transforms into hemichorea and hemidystonia.[37],[38]

Contrary to popular belief that hemiballism has a grave prognosis and progresses to death within weeks; more recent studies have shown evidence of a more benign course and spontaneous recovery.[28] In a study by Ristic et al., of 27 vascular hemiballism patients, the survival rate free from recurrent stroke was found to be 80% after 2 years.[39] Though most cases resolve spontaneously, the serious and adverse nature of the movement capable of inflicting injury makes the pharmacological treatment necessary. Pharmacological therapy can be offered in the form of antidopaminergic therapy with typical and atypical neuroleptics and catecholamine-depleting agents. Typical neuroleptic agents such as haloperidol, pimozide, perphenazine, and fluphenazine work by blocking dopamine receptors (D1 and D2).[10],[39],[40] The atypical neuroleptic drugs olanzapine, quetiapine, and sulpiride work by blocking the D3 and D4 dopamine receptors, and have fewer tendencies to cause drug-induced parkinsonism and tardive dyskinesia.[10],[39] In refractory cases, clozapine has been used but it causes agranulocytosis.[41] Tetrabenazine depletes presynaptic dopamine by inhibiting brain synaptic vesicular monoamine transporter type 2 (VMAT2) and blocks postsynaptic dopamine receptors. Reserpine also acts presynaptically but causes side effects including profound depression, suicidal tendencies, hypotension, and parkinsonism.[42] Other GABAergic drugs such as clonazepam and sodium valproate have also been used.[42] Levetiracetam and topiramate have also been proven to be effective in a few studies.[42],[43],[44],[45],[46] In cases of intolerability to medical therapy or its ineffectiveness, surgical intervention can be effective such as stereotactic ventral intermediate thalamotomy and chronic thalamic stimulation.[47] There have been three cases of acute hemiballism-hemichorea which were treated with intravenous thrombolysis following which the movements subsided despite which all developed restricted diffusion on imaging in the putamen, striatum, and globus pallidus, respectively.[48],[49],[50]

Dystonia

As per the 2013 consensus criteria, dystonia is defined as a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both. Dystonic movements are typically patterned and twisting, and may be tremulous. Dystonia is often initiated or worsened by voluntary action associated with overflow muscle activation.[51]

After hemiballism-hemichorea, dystonia is the second most common movement disorder after stroke, representing about 20% of cases.[1] In a study at a Toronto hospital, of the 100 children with basal ganglia stroke, only 21% developed dystonia, seen more likely to occur in younger children and girls, onset was frequently 6–12 months after stroke.[44],[52] It can be slow, rapid, or jerk-like in nature.[30],[53] Dystonia can either be segmental, focal, or involve the ipsilateral side of the face, arm, and leg (hemidystonia).[2],[54],[55] It is frequently unilateral (contralateral to the brain lesion site) but can be bilateral or generalized. Infrequently, ipsilateral dystonia has also been seen.[54] Focal hand dystonia (involving upper limbs) is the most common form of post-stroke dystonia presentation; other sites involved include the foot, facial, or lingual muscles.[2],[5] Dystonia can be associated with other movement disorders such as tremor, myoclonus, or athetosis.[20],[54] Dystonia worsens on voluntary action and has the property of overflow muscle activation.[28] Vascular dystonia is the most common cause of secondary movement disorders nearly accounting to 50% of the cases.[4] In a study by Ghika et al., 87% of the 32 patients of parietal stroke had dystonia and this was attributed to faulty sensory processing and distortion of body position perceptions.[1] Post-stroke spasticity occurs typically within the first few days or weeks after stroke. It occurs due to muscle weakness and loss of inhibitory impulses differentiating it from dystonia, which occurs due to, increased muscle activity caused by reduced inhibition at many levels of the motor system.[3] Lesions are seen most frequently in the lentiform nucleus, particularly the putamen other sites being caudate, pallidum, thalamus (posterolateral, paramedian, and centromedian nuclei are typically involved), and the midbrain.[56],[57],[58],[59] Dystonia also occurs after vascular lesions in the brainstem-diencephalic junction; manifesting as blepharospasm, oromandibular dystonia, or other combinations of cranial dystonia.[60] In Alarcon study, dystonia of the hand was reported secondary to a pontine hemorrhage and foot dystonia in two patients with a severe proprioceptive deficit.[2] Contrary to popular belief, Russmann et al., reported that dystonia is a rare sequela of lenticular infarction.[11] CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) is an arteriopathy in which dystonia is seen secondary to chronic ischemic insults.[61]

Dystonia is associated with a significant disability if left untreated. In the Alarcon study, in five patients (31.2%) the dystonia disappeared completely and in ten patients there was a partial improvement (62.5%) with treatment.[2] Botulinum toxin has become the mainstay of therapy in the management of dystonia.[3],[48] Medical treatment includes benzodiazepines, baclofen, anticholinergic drugs, and dopamine-depleting/blocking agents.[4] Commonly used benzodiazepines include clonazepam and diazepam but higher dosages of these may cause drowsiness. Dystonic posturing results due to muscular contractions, thus botulinum toxin and anticholinergic drugs, which block the release of acetylcholine resulting in a decrease in muscle contractions, are useful. Trihexyphenidyl is used in younger patients with dystonia as compared to the elderly due to the side effects causing confusion and drowsiness.[3],[4] Tetrabenazine has also been used in cases of dystonia. Benzhexol and tetrabenazine combination has been found useful in younger patients.[62] Gabapentin at lower dosages also improved the severity of dystonia on animals in a study conducted by Richter et al.[63] In addition, Chuang et al. showed that 22 out of 23 patients in literature and 5 out of the six cases in the series of 33 hemidystonia patients had benefit with surgical interventions (thalamotomy, pallidotomy, and deep brain stimulation (DBS).[4] DBS of either the thalamus or the GPi (globus pallidus interna) appears to be more successful than lesioning approach in producing a long-lasting response as evidenced by recent literature. However, which target is more effective, still needs to be supported by studies further.[4]

Tremor

Tremor is a rhythmic, oscillatory movement produced by alternating or synchronous contractions of antagonist muscles that can occur at rest or during an action.[6] It is usually a delayed presentation following a stroke but can also occur acutely.[1] Action tremors can either be postural or kinetic; seen when holding the limb against gravity or seen when moving the limb.[9],[10] Post-stroke tremor occurs on action mainly, though can be a combination of rest, postural, and kinetic tremor.[5],[25],[64],[65] It can be focal, multifocal, segmental, or generalized though most often multifocal or segmental and unilateral.[2],[3],[19],[25],[60],[64],[65] Post-stroke tremor is often seen with other abnormal movement disorders.[5],[19],[64],[66]

Lesions in the posterior thalamus or lesions affecting either of the pathways (dentatorubrothalamic, cerebellothalamic, or nigrostriatal) can give rise to post-stroke tremors.[3],[19],[61],[67],[68],[69] Lesions involving the cerebellothalamic loops would give rise to kinetic or postural tremors whereas those affecting the nigrostriatal pathways would give rise to rest tremors. Acute onset of a Parkinsonian tremor and head tremor has been seen with a stroke of the medial tract of the substantia nigra and paramedian pontomesencephalic infarct.[10],[32] Brain stem syndromes like Claude's and Benedikt causes contralateral tremors. Dopaminergic dysfunction may also be leading to vascular orthostatic tremor.[70] Task-specific writing tremor has been described following a small frontal cortical infarct.[71] A resting tremor that becomes more severe on maintaining posture and most severe during movement is called rubral, midbrain, or Holmes' tremor, although a lesion of the red nucleus has not always been identified.[72],[73] It is irregular in nature, involving the proximal and distal part, with a frequency of 4.5 Hz.[74] Strokes involving the posterior circulation can involve the thalamus, producing slow (1–3 Hz) rest and postural tremors, referred to as myorhythmia.[63] The presence of myorhythmia, which can be mistaken for Parkinson's disease tremor, is distinguished on the basis of its slower frequency which indicates a vascular lesion in the thalamus, rostral brainstem (particularly the substantia nigra), inferior olivary nucleus, or the cerebellum.[75] Palatal myoclonus is another slow, 1–3 Hz, rhythmical movement, often associated with hypertrophy of the inferior olivary nucleus, seen with lesions involving the Guillain-Mollaret triangle linking the dentate nucleus, red nucleus, and inferior olivary nucleus. It affects primarily the levator veli palatini muscle, which has been described in pontine or bulbar strokes but was also reported in one patient with lateral thalamic infarction.[76]

We have earlier reported two cases, one having a thumb and the other having tongue tremors, both of which developed following an acute stroke in the left frontoparietal cortex.[77],[78] We proposed that they were caused by a loss of cortical inhibition.

In dystonic tremor patients, the tremor is seen to occur in the same body part as the dystonia or with dystonia in a different part of the body. It is a postural/kinetic tremor and focal usually.[74] Patients with post-stroke dystonia have additional abnormal movements associated with dystonia in the form of tremor (dystonic tremor), myoclonus (dystonic myoclonus), or athetosis which occurs secondary to lesions affecting the thalamus or cerebellum.[3] Thalamic lesions, particularly in the thalamo-geniculate artery territory affecting the ventral intermediate nucleus and ventral caudal nucleus of the thalamus, produce these movements.[79],[80]

Post-stroke tremor is particularly refractory to pharmacotherapy. In the Alarcon study, in four patients (28.5%) the tremor disappeared completely and in nine patients (64.2%) partially.[2] Rubral and palatal tremor may respond to clonazepam and sodium valproate.[10] Balci et al. reported two patients with myoclonic tremor due to parietal cortical lesions with tremulous finger movements induced by action and posture and were treated well with both clonazepam and sodium valproate.[81] Topiramate has also been found to have a place in the treatment of tremors.[46],[82],[83],[84] Tremors can also be decreased by adding weights to the affected limbs or the use of larger utensils.[6] Propranolol and or primidone hardly show any benefit in the treatment of post-stroke cerebellar-outflow tremors.[3],[85] As the dopaminergic system is involved in most cases of Holmes' tremor, treatment with levodopa should be attempted.[74] In severe cases, DBS can be a useful treatment modality. Targets include the thalamic nuclei; ventralis intermedius, ventralis oralis posterior, or both, or the lenticular fasciculus.[3],[86],[87],[88],[89]

Myoclonus

Myoclonus refers to sudden involuntary, brief, jerk-like irregular contractions of certain muscle groups. It is seen usually with lesions in the thalamus, midbrain, and pons. It can be focal or segmental.[2],[3],[90] Myoclonus with focal neurological signs and superimposed asterixis with dystonic posturing may be observed in thalamic lesions.[91] Intention tremor with myoclonus was reported secondary to thalamic angioma in a case report by Avanzini et al.[92] Ghika et al. reported one case of focal action myoclonus of the jaw and tongue.[1] One case of generalized post-stroke myoclonus has been reported by Inoa et al. following STN infarct.[93] One neonate developed myoclonus following cerebellar stroke within 24 h of birth secondary to top of basilar artery syndrome.[94] Clonazepam and sodium valproate are useful in most cases but levetiracetam, piracetam, primidone, tetrabenazine, acetazolamide, and botulinum toxin injections can also be used.[48],[95],[96],[97]

Asterixis

Asterixis is one type of negative myoclonus occurring due to sudden cessation of electrical activity causing a sustained contraction in the extensor muscles, probably due to intermittent inhibition of the spinal neuronal system that regulates the voluntary tonic extension posture of the limb. Young and Shahani suggested that sustained muscle contraction is related to the neural subsystem involving the medial frontal cortex, parietal lobe, and the ventrolateral thalamus which are the supratentorial influence over the brainstem-spinal cord connections such as vestibulospinal, reticulospinal, or rubrospinal tracts.[98] Thus, lesions involving these supratentorial pathways results in loss of sustained muscle contraction and posture and thus giving rise to asterixis.

It occurs mainly during the acute phase of the stroke with lesions involving the thalamus, basal ganglia, frontoparietal cortex, cerebellum, midbrain, and pons.[1],[3],[58],[99],[100] It is usually unilateral but bilateral cases have been reported and mainly affect the upper limbs.[1],[62],[99] Paliwal et al. reported a case of lower limb asterixis following stroke.[101] The incidence was found to be 0.08% in the Lausanne stroke registry and 1.9% in the Kim et al. series. In a case series of 12 patients of asterixis secondary to a focal lesion, 75% were due to stroke, with lesions involving contralateral thalamus in the majority, rest involving other structures (lenticular nucleus, frontal lobe, internal capsule, precentral regions and cerebellum).[102] In another series of 30 patients of post-stroke asterixis, the majority of the patients had lesions involving the thalamus followed by the frontal lobe. Bilateral lesions were seen in four of them.[99] In a series of movement disorders following anterior cerebral artery territory infarction, four out of the nine patients developed asterixis of which all had infarcts involving the prefrontal cortex and one of which had bilateral asterixis. In a series of 45 patients with asterixis, 95.5% of them had a stroke in the thalamus.[103] Post-stroke asterixis is usually self-limiting and does not require any treatment.[99]

Vascular parkinsonism

Vascular parkinsonism (VP) was first described by Critchley in 1929 and comprises of 2.5–5% of all cases of parkinsonism in the clinical cohort and population-based studies.[104] In the Equador stroke, the registry found parkinsonism in 10% of their patients.[1] It is called by various names such as arteriosclerotic parkinsonism, vascular pseudoparkinsonism, and lower body parkinsonism.[104] There are two forms of vascular parkinsonism, one being the acute form seen immediately with basal ganglia and thalamic infarction and other being the chronic diffuse white matter degeneration changes in the lentiform nucleus and the striatum.[10]

In a study of 10 patients with VP by Fitzgerald et al., 90% presented with gait abnormality, and only 22% responded to levodopa.[105] In another study by Zijlmans et al. of 17 patients with pathologically proven VP; 15 presented with bradykinesia, 13 with rigidity, 11 with gait abnormality, 8 with tremors, 5 with cognitive decline, and with 70% of the patients responding to levodopa. Bilateral features were seen in all but two patients, with acute onset presentation in 4 patients having basal ganglia and thalamic involvement.[106] Similarly, Winikates et al. studied 69 patients of VP and 277 patients with Parkinson's disease (PD) and observed that patients with VP were older, had more gait problems, postural instability, predominant lower-body involvement, pseudobulbar affect, corticospinal signs, urinary incontinence, dementia, and less response to levodopa.[107] The olfactory function seems to be normal in patients with VP.[108] In a study of 20 patients with parkinsonism, age at onset in PD patients was lower than patients with VP (Mean ± standard deviation: 55 ± 12 versus 62 ± 13 years).[109] In another study by Rampello et al. on 45 patients with VP, only 29% of patients were responsive to levodopa treatment.[110] Binswanger's disease, CADASIL, Fabry's disease, central nervous system vasculitis, and moyamoya disease can also present with VP.[110],[111],[112],[113],[114],[115],[116] Vascular parkinsonism has also been described in a series following dural arterio-venous fistulas.[117],[118],[119],[120],[121],[122],[123] Vascular progressive supranuclear palsy (PSP) has also been described following lesions of the basal ganglia, thalamus and rostral brainstem, where 33 of the 128 patients of PSP were vascular.[120]

On brain imaging in VP patients commonly noted lesions are lacunar infarcts, white matter changes involving subcortical white matter, basal ganglia, thalamus, frontal lobes and upper brainstem, and rarely, territorial infarcts.[32],[33] As observed that coincidental vascular lesions in idiopathic PD are common, only the presence of these lesions on brain imaging is not conclusive or diagnostic of VP.[124] In VP patients, the dopamine transporter (DAT) scan usually shows normal dopamine content of the striatum when compared with idiopathic PD.[125] Though the DAT scan deficit can also be seen in VP, it tends to be more asymmetric when compared with PD.[126] In the VADO study of 158 patients with parkinsonism, the DAT scan was normal in 48 (30.4%) and abnormal in 110 (69.6%) patients and those with normal DAT binding had higher vascular load on brain imaging.[127] Transcranial sonography of brain parenchyma has been used as a tool to differentiate VP from idiopathic PD, where the substantia nigra is seen to be hyperechogenic.[128]

Various therapies have been tried for vascular parkinsonism in literature in the form of vitamin D supplementation, transcranial magnetic stimulation, lumbar puncture and levodopa.[105],[129],[130],[131],[132],[133],[134] The first three options have not been promising and data on them is very limited. In a meta-analysis, it was found that 30% of patients of vascular parkinsonism responded to levodopa. As patients with vascular parkinsonism can present with lesions anywhere in the external capsule, corona radiata, thalamus, pons, basal ganglia, and substantia nigra, it was seen that those with lesions in the substantia nigra were 15 times more likely to respond to levodopa as compared to the rest. Patients of vascular parkinsonism with dopamine transporter deficiency on SPECT studies also would respond better to levodopa.[135]

Stereotypies

Stereotypies are involuntary, coordinated, repetitive, patterned, and rhythmic seemingly purposeless movements.[9] Very few cases of stroke-induced stereotypies have been reported, some being part of the acute stroke presentation.[1],[136],[137] Parietal, lenticulostriatal, thalamic, midbrain, or left middle cerebral artery territory infarcts were seen in these patients.[138],[139] Most patients had unilateral lesions. Laplane et al. reported two cases of stereotypy with bilateral basal ganglia lesion.[140] Lee et al. reported a case of stereotypy, developed after a cerebellar infarction and suggested a functional mismatch between cerebellum and cortex combined with underlying diffuse cognitive dysfunction as a hypothetical mechanism of stereotypy related to cerebellar infarction.[141] Clonic perseveration may also occur due to stroke and may mimic stereotypy.[142] Tetrabenazine, while the most effective drug in the treatment of tardive stereotypies, has not been evaluated in patients with post-stroke stereotypies. Clonazepam can be used but stereotypy is usually refractory to benzodiazepines, amantadine, and anticholinergics.[6]

Restless leg syndrome and periodic limb movement disorder

Post-stroke restless leg syndrome (psRLS) and periodic limb movement disorder (psPLMD) are very rare with a prevalence of 12.4% and described to date in only 31 patients. They are more common in women.[143],[144] They occur with lesions in the pons (especially the tegmentum), corona radiata, basal ganglia, thalamus, cerebellum, cortex, and internal capsule. psRLS is predominantly bilateral in presentation whereas psPLMD can be ipsilateral, bilateral, or contralateral to the lesion.[145] psRLS can also involve the arm.[144] The presentation is acute following stroke ranging from 1–4 days for psRLS and 1–30 days for psPLMD.[145] The proposed mechanism is a disinhibition of supraspinal control over the reticulospinal and corticospinal tract in the brainstem, involvement of the sensory system in the form of medial lemniscus and the role of basal ganglia in bilateral symptom presentation.[146],[147] psRLS was found to be transient in some but mainly persisted in patients following stroke whereas psPLMD was transient and disappeared in a few days. The treatment includes levodopa, clonazepam, dopamine agonists, gabapentin, and pregabalin.[148]

Transient Limb shaking TIA (transient ischemic attacks)

Fischer et al. first described them as trembling, shaking, twisting, drawing up, or moving irregularly of any limb.[149] They are abnormal involuntary movements seen secondary to carotid artery stenosis.[150] One case has been described as secondary to internal carotid artery dissection and middle cerebral artery dissection as well.[151],[152] Carotid artery stenosis leads to ischemia of the contralateral cerebral hemisphere giving rise to this jerking of the limbs. These movements get precipitated by postural changes leading to lowering of blood pressure.[153] They are often mistaken for focal motor seizures but can be distinguished from them by lack of Jacksonian march and noninvolvement of the face. The electroencephalogram is normal during the event and there is no response to anticonvulsants.[154],[155] This is a heralding sign for disabling stroke and thus identifying its importance.[156],[157] Carotid artery stenting in these patients can lower the risk of future stroke.[158]

Post-stroketics

Jankovic et al. described the prevalence of post-stroke tics as 1.2% in a series of 155 patients with secondary tics and tourettism.[159] There have been cases of secondary tourettism described following subcortical stroke involving the basal ganglia, and superior cerebellar peduncle.[160] There have been cranial-lingual-cervical tics, coprolalia, suppressible arm shaking.[161],[162],[163] The tics have been seen to coexist with attention deficit hyperkinetic disorder, obsessive-compulsive disorder, dystonia, and hemiballism.[160]


 » Conclusion Top


Despite the data, which is available to us, not all is known about post-stroke movement disorders and how they differ from other secondary movement disorders. There is a need to further study these patients to look at various aspects in terms of the likelihood of hemorrhagic stroke versus ischemic stroke causing movement disorder, what are the chances of developing acute vs delayed movements, and reason for the similarity in movements despite lesions at different sites. Further studies are needed which can help to understand better the intricate networks involved in generating these abnormal movements and thereby help in guiding further management of the same. Generating interest in the identification of these abnormal movements following a stroke can help plan better management of these patients and beneficial outcomes.

Financial support and sponsorship

Nil.

Conflicts of interest

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