INTRODUCTION

Movement disorders are rare, but may present as a consequence of stroke [1,2]. Involuntary movements related to any type of stroke comprise one important part of secondary movement disorders. Post-stroke movement disorders 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 [1,3]. Thus, movement disorder after stroke is a heterogeneous condition. Abnormal involuntary movements (AIM) following stroke can be classified as hyperkinetic or hypokinetic [4]. Various presentations including tremor, chorea-ballism, dystonia, athetosis, myoclonus, ataxia, and parkinsonism have been associated with vascular brain lesions [1,2,5,6]. The time course for the development of AIM attributed to stroke is not easily predicted, as the course differs according to the type of AIM; they can manifest with a variety of presentations or even in the same movements [4]. Similar to the typical stroke symptoms, the duration of AIM also varies from paroxysmal and/or transient to persistent and progressive [1]. The manifestation of stroke varies even in the same vascular territory [7]. Accordingly, mixed movements are one of the characteristics of secondary AIM associated with a stroke lesion with an extensive involvement. Although the frequency of AIM following stroke is low, it is important to know the possible clinical conditions, its course and symptoms and the proper management strategies, as these aspects could considerably affect a stroke patient’s quality of life as much as the paretic stroke symptoms. This article describes the etiology, treatment options and prognosis of post-stroke movement disorders.

ETIOLOGY OF POST-STROKE MOVEMENT DISORDERS

Stroke lesion location

Post-stroke movement disorders can develop in any stroke subtype and at any brain level of the motor circuit. In the extrapyramidal system, however, the basal ganglia and thalamus are the primary lesion sites associated with post-stroke movement disorders [1,4]. A comparison between stroke patients and case-controls (without movement disorders) revealed that stroke patients with movement disorders feature significantly greater involvement of deep brain lesions affecting the basal ganglia, thalamus, internal capsule, diencephalon, and mesencephalon than stroke patients without movement disorders. Strokes in deep brain lesions are also associated with a higher probability of AIM (odds ratio 3.38, 95% confidence interval 1.64 to 6.99) [1]. For cortical lesions, the areas most commonly associated with post-stroke movement disorders include those involved in the cortical motor system, including the primary motor, supplementary motor and premotor cortical areas. The parietal cortex is also involved in processing somatosensory information related to movement. However, “pure” or “isolated” stroke-related cortical movement disorders are rare, as most “cortical” strokes also affect subcortical structures. Therefore, consideration is needed for the possibility that many “structural” cortical strokes actually have functional defects arising from lesions affecting subcortical structures. Several case reports have described cortical stroke-related movement disorders, including parietal lobe stroke with choreo-ballism [8], focal dystonia [9,10], arm levitation due to distortion of the body schema and athetosis [11]. Frontal lobe stroke is associated with asterixis (negative myoclonus) [7], secondary painless leg moving toe syndrome [12], and resting and action tremor (with strokes affecting the anterior cerebral artery territory) [7,13]. Structural cystic lesions with mass effects of the middle fossa involving the fronto-temporo-parietal area can mimic Holme’s tremor [14]. Alleviation of a previous tremor is also possible after frontal cortical stroke [15]. Some cortical stroke-related movement disorders feature a laterality component: bilateral cortical ptosis can occur with a large right-side, hemispheric lesion [16,17]. Secondary restless legs syndrome (RLS) after stroke has been reported with temporo-occipital cortical lesions, as well as with stroke affecting the basal ganglia, thalamus, internal capsule and pons [18].

Stroke subtypes

A large epidemiologic study previously examined post-stroke movement disorders but was limited by a small number of patients. However, in that study, basal ganglia and thalamus involvement in stroke was frequent [2]. Overwhelmingly, the typical stroke symptoms that occur in the acute phase play a role in overlooking combined movement disorders. In one registry study that enrolled 1,500 consecutive stroke patients, 59 (3.9%) developed post-stroke movement disorders, with chorea as the most common movement disorder subtype [1]. Ischemic stroke can be etiologically classified as a small vessel disease, large vessel disease or cardioembolic stroke [19]. Among the ischemic stroke subtypes, multifocal small vessel stroke is the most commonly associated with movement disorders following stroke, and it is the leading cause of post-stroke AIM. However, cardioembolic stroke and large- and medium-sized atherosclerotic stroke are also included in the etiology of movement disorders [2,20]. Hemorrhagic stroke has a high probability of developing post-stroke movement disorders when compared to ischemic stroke. Generally speaking, there is no specific preference to the vascular region or subtype in post-stroke movement disorders, with only a trend for some of the clinical factors described [21]. Chronic small vessel disease or Binswanger’s disease can develop into secondary parkinsonism (vascular parkinsonism). Vascular parkinsonism is phenomenologically characterized by bilateral slowness and rigidity, which is predominant in the lower extremities, causing gait problems and lower-body parkinsonism [22]. Subcortical small vessel pathology, rather than the typical Lewy body pathology, was reported in the pathologic study of vascular parkinsonism [23].

MOVEMENT DISORDERS IN SPECIFIC STROKE SYNDROMES

CADASIL

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a progressive vascular disease characterized by migraine headache, stroke syndromes, and dementia [24]. CADASIL patients have a variety of movement disorders, including dystonia as an atypical late presentation secondary to chronic ischemic insults. Abnormal findings in dopamine transporter single-photon emission computed tomography imaging without response to dopaminergic treatment has implicated vascular parkinsonism in the CADASIL family [25,26]. Mutations in the NOTCH 3 gene have been reported in potential cases of progressive supranuclear palsy, along with cases of multiple system atrophy with scattered white matter signals [27,28].

MELAS

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a distinct clinical syndrome involving skeletal muscles and the brain [29]. As the name suggests, the most common movement disorder in MELAS is myoclonus. Parkinsonism and gait freezing are other symptoms associated with MELAS [30-32]. Nakagaki et al. [33] reported a case of chorea-ballism in MELAS that might accelerate hyperglycemic movement disorders. Although brain lesions in MELAS are not confined to a specific vascular territory [34], the brain pathology might contribute to most of the related secondary movements.

Moyamoya disease

Moyamoya disease is defined by progressive occlusion of the internal carotid artery and arteries in the circle of Willis [35]. Movement disorders in moyamoya disease are rare and have been reported mainly in pediatric patients [36-38]. Regardless of age, the most common AIM in moyamoya disease is chorea [39]. The reported occurrence in one study was 31 of 42 (67.4%) patients, which was followed by dystonia in 8 of 42 (17.4%) patients, with a mean age of onset of 21.4 years [40]. In another study, 5 of 513 pediatric patients with moyamoya disease had AIM, 4 had chorea, and one had dystonia. The symptoms improved in all cases after bypass surgery, suggesting that cerebral ischemia even in the absence of stroke lesions might be a pathogenic mechanism in moyamoya disease [37]. Another retrospective review study of 316 surgically treated children with moyamoya disease reported that 10 (3.2%) children had chorea that resolved following the revascularization surgery. The same authors postulated that dysfunction of the basal ganglia via the hypertrophic collateral vessels was causative for chorea [36].

MANAGEMENT OF POST-STROKE MOVEMENT DISORDERS

Pharmacological treatment

Decisions regarding the management of post-stroke movement disorders should be individualized and based on each clinician’s experience. This reflects the scarcity of case-controlled, randomized clinical trials resulting from the difficulty in collecting appropriate sample sizes. Medical treatment of post-stroke movement disorders is similar to that for primary movement disorders, as they share common underlying pathomechanisms (Table 1). Many cases of post-stroke movement disorders are transient and self-remitting, so no treatment or intervention is needed [41]. Chorea is the most common post-stroke movement disorder [22]. Persistent choreaballism in acute stroke patients needs to be treated, as this might cause significant patient discomfort [3]. Anti-dopaminergic drugs that block the D1 and D2 receptors are the first choice in choreic movements. D3 and D4 receptor antagonists can be used and have the merit of a low risk of extrapyramidal side effects, such as parkinsonism and akinesia. Other atypical neuroleptics should be applied only in refractory cases [5]. Presynaptic dopamine-depleting agents and catecholamine-depleting drugs, as well as GABA receptor agonists, can also be used in selected cases [42]. Consideration for the side effects of each drug is important when choosing a drug for the devastating post-stroke chorea [22]. For post-stroke dystonia, the symptoms rarely improve completely with treatment [43]. Focal injections of botulinum toxin is the usual treatment option, and intrathecal baclofen can be tried for partial symptom relief [5]. Other medical treatments include anticholinergics, baclofen, and benzodiazepam, which is similar to the treatment of primary dystonia. In addition, anti-dopaminergic agents can be tried. Tremor activation in post-stroke tremor disorder is both resting and postural/kinetic [7,13,41]. Although the response to pharmacological treatment of vascular tremors is limited, the treatment options should be decided based on the type of tremor. Of the specific forms of tremor, symptomatic rubral (midbrain) and palatal tremor are usually caused by stroke lesions in the dentate-rubro-thalamic circuits. Limited but potential benefits were reported for propranolol, clonazepam, dopaminergic agents and anti-epileptic drugs, including valproic acid and levetiracetam [22,44]. However, for most refractory cases, surgical intervention and focal botulinum toxin injections are required [45-47]. Post-stroke secondary myoclonus is mostly transient and does not require management. GABAergic drugs (valoproic acid and clonazepam) enhance inhibitory neurotransmission, and levetiracetam and piracetam can be used for symptomatic treatment [48,49]. Some clinicians recommend a combination of these drugs to lessen adverse events. Vascular parkinsonism is characterized by symmetric akinesia and gait impairment [50,51]. The effect of representative treatment with levodopa for vascular parkinsonism may be poor and short-lasting [1,3]. Post-stroke RLS is not uncommon in the acute stroke phase (17 out of 137 cases) and has been associated with dysfunction of the subcortical dopaminergic system of the basal ganglia and thalamus [18,52]. Secondary RLS associated with acute stroke is mostly transient and improves without medication. When treatment is required, dopaminergic agents might help to relieve symptoms [18]. Treatment of post-stroke tics is the same as with primary tics: clonidine, neuroleptics, dopaminedepleting agents can be applied [53].

Surgical treatment

In drug-resistant and devastating post-stroke movement disorders, surgical intervention can be considered. For secondary movement disorders caused by vascular hypoperfusion of the carotid or vertebrobasilar artery, revascularization surgery may result in near complete symptom improvement [54-58]. Chronic motor cortex stimulation was originally used for post-stroke pain control, but effective control of involuntary movements (choreo-athetosis, action and resting tremor) can also be obtained [59]. Several mechanisms of action, including hyperdirect motor cortex-subthalamic nucleus input, cortical inhibition, and plastic changes, have been proposed for motor cortex stimulation in various movement disorders [60]. Movement disorders attributed to moyamoya syndrome can be improved through bypass surgery [38]. Deep brain stimulation (DBS) targeting the globus pallidus and thalamic nucleus (nucleus ventralis oralis posterior, nucleus ventralis intermedius) are other useful options for treating drug-refractory chorea and/or dystonia [5,43,61,62]. Pallidotomy, thalamotomy and DBS of the thalamus in patients with severe tremor, including a high amplitude and low frequency, are several treatment options worth trying for symptomatic control [5,45].

Physical therapy and rehabilitation

Proper rehabilitation is needed for most stroke patients [63]. Physical and occupational therapy have become important assistive therapeutic options for secondary movement disorders. Physical therapy is helpful for both hypokinetic and hyperkinetic movement disorders, such as vascular parkinsonism and dystonia, which are associated with postural deformity and balance problems [64,65]. Physical therapy and brace devices [3,5], as well as proprioceptive rehabilitation [66], may be applied for movement disorders after stroke.

PROGNOSIS OF POST-STROKE MOVEMENT DISORDERS

Onset latency

Many of the post-stroke movement disorders develop during the acute phase, especially within several days of the stroke onset. The timing can cause clinicians to overlook and under-diagnose the presence of post-stroke movement disorders because of the overwhelming motor and sensory deficits [1]. The clinical course of post-stroke movement disorders is variable, but some tendencies are apparent according to which type of AIM is presented [3]. The period for developing a movement disorder after stroke is between the stroke onset to years after the onset [1,2]. The latency interval of post-stroke movement disorders is shortest for chorea (4.3 days) and longest for parkinsonism (117.5 days) [1]. Transient hemichorea-ballism can develop even before stroke in the form of transient ischemic attacks and can serve as a warning sign [67-69]. Post-stroke RLS can appear within a week after the onset of stroke (mean 1.8 days) [18].

Long term prognosis

Most of the post-stroke movement disorders typically have a short duration and improve over time. Among the post-stroke movement disorder subtypes, chorea, myoclonus, and especially asterixis, do not last long and are self-limiting. Vascular parkinsonism tends to persist and progressively deteriorates [1]. Dystonia also has a poor prognosis with significantly worsened activities of daily living and quality of life. Tremor, especially symptomatic cerebellar-outflow tremor with low frequency, persists and worsens, and it is specifically refractory to medical treatment [5].

CONCLUSIONS

Post-stroke movement disorders are rare, but they account for an important part of secondary AIM. Various manifestations of hyperkinetic and hypokinetic movements, as well as overwhelming stroke symptoms, make timely diagnosis of combined movement disorders challenging. Any stroke lesion occurring in the motor system from the cortex to brainstem, any etiologic subtype of stroke, regardless of the lesion size, and a variety of systemic syndromes that can cause stroke may cause involuntary movement. Therefore, clinicians should consider the possibilities associated with AIM when treating acute stroke patients in clinical practice. Concerning the clinical course, most post-stroke movement symptoms are transient and self-limiting. However, proper diagnosis with a treatment strategy is critical because sometimes these might persist and become life-threatening with significant detriment to the victim’s quality of life. Timely treatment could hasten the recovery and prevent a worsening of symptoms. Although there are no established treatment guidelines based on randomized case-controlled studies, which reflects the low prevalence of these disorders, most of the pharmacological treatment options for secondary movements are not dissimilar to those for primary movement disorders based on similar underlying pathomechanisms. The treatment strategies include controlling dopaminergic excitability and modulating GABAergic transmission. Catecholamine-depletion and anti-cholinergic drugs are other options used to control AIM. Recently, symptomatic control with botulinum toxin injections, which blocks peripheral release of acetylcholine at the muscle level or intrathecal baclofen infusion, has been introduced as a therapeutic option for drug-resistant post-stroke dystonia. Repeated transcranial magnetic stimulation is another useful treatment option in limited cases of drug-resistant secondary dystonia and tremor. In cases of irresistible post-stroke movement disorder, surgical intervention might be considered. Exercise and physical therapy should always be considered to achieve better outcomes.

Notes

Conflicts of Interest

The author has no financial conflicts of interest.

REFERENCES

• 1. Alarcón F, Zijlmans JC, Dueñas G, Cevallos N. Post-stroke movement disorders: report of 56 patients. J Neurol Neurosurg Psychiatry 2004;75:1568–1574.ArticlePubMedPMC
• 2. Ghika-Schmid F, Ghika J, Regli F, Bogousslavsky J. Hyperkinetic movement disorders during and after acute stroke: the Lausanne Stroke Registry. J Neurol Sci 1997;146:109–116.ArticlePubMed
• 3. Mehanna R, Jankovic J. Movement disorders in cerebrovascular disease. Lancet Neurol 2013;12:597–608.ArticlePubMed
• 4. Béjot Y, Giroud M, Moreau T, Benatru I. Clinical spectrum of movement disorders after stroke in childhood and adulthood. Eur Neurol 2012;68:59–64.ArticlePubMed
• 5. Handley A, Medcalf P, Hellier K, Dutta D. Movement disorders after stroke. Age Ageing 2009;38:260–266.ArticlePubMedPDF
• 6. Lee MS, Lyoo CH, Chung TS. Parkinsonism and dementia associated with giant Virchow-Robin spaces. J Mov Disord 2015;8:106–107.ArticlePubMedPMC
• 7. Kim JS. Involuntary movements after anterior cerebral artery territory infarction. Stroke 2001;32:258–261.ArticlePubMed
• 8. Mizushima N, Park-Matsumoto YC, Amakawa T, Hayashi H. A case of hemichorea-hemiballism associated with parietal lobe infarction. Eur Neurol 1997;37:65–66.ArticlePubMed
• 9. Ghika J, Ghika-Schmid F, Bogousslasvky J. Parietal motor syndrome: a clinical description in 32 patients in the acute phase of pure parietal strokes studied prospectively. Clin Neurol Neurosurg 1998;100:271–282.ArticlePubMed
• 10. Burguera JA, Bataller L, Valero C. Action hand dystonia after cortical parietal infarction. Mov Disord 2001;16:1183–1185.ArticlePubMed
• 11. Gondim FA, Oliveira GR, Cruz-Flores S. Position-dependent levitation of the dominant arm after left parietal stroke: an unreported feature of posterior alien limb syndrome? Mov Disord 2005;20:632–633.ArticlePubMed
• 12. Oh SM, Yoon WT, Kim JY, Shin HY, Lee WY. Painless legs and moving toes as an initial presentation of ischemic stroke. J Mov Disord 2009;2:40–42.ArticlePubMedPMCPDF
• 13. Kim JS, Lee MC. Writing tremor after discrete cortical infarction. Stroke 1994;25:2280–2282.ArticlePubMed
• 14. Menon B, Sasikala P, Agrawal A. Giant middle fossa epidermoid presenting as holmes’ tremor syndrome. J Mov Disord 2014;7:22–24.ArticlePubMedPMCPDF
• 15. Kim JS, Park JW, Kim WJ, Kim HT, Kim YI, Lee KS. Disappearance of essential tremor after frontal cortical infarct. Mov Disord 2006;21:1284–1285.ArticlePubMed
• 16. Averbuch-Heller L, Leigh RJ, Mermelstein V, Zagalsky L, Streifler JY. Ptosis in patients with hemispheric strokes. Neurology 2002;58:620–624.ArticlePubMed
• 17. Blacker DJ, Wijdicks EF. Delayed complete bilateral ptosis associated with massive infarction of the right hemisphere. Mayo Clin Proc 2003;78:836–839.ArticlePubMed
• 18. Lee SJ, Kim JS, Song IU, An JY, Kim YI, Lee KS. Poststroke restless legs syndrome and lesion location: anatomical considerations. Mov Disord 2009;24:77–84.ArticlePubMed
• 19. Adams HP Jr, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, et al. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke 1993;24:35–41.ArticlePubMed
• 20. Kim JS. Delayed onset mixed involuntary movements after thalamic stroke: clinical, radiological and pathophysiological findings. Brain 2001;124(Pt 2):299–309.ArticlePubMedPDF
• 21. Edlow JA, Selim MH. Atypical presentations of acute cerebrovascular syndromes. Lancet Neurol 2011;10:550–560.ArticlePubMed
• 22. Bansil S, Prakash N, Kaye J, Wrigley S, Manata C, Stevens-Haas C, et al. Movement disorders after stroke in adults: a review. Tremor Other Hyperkinet Mov (N Y) 2012;Mar. 20. [Epub]. http://dx.doi.org/10.7916/D86W98TB. Article
• 23. Mark MH, Sage JI, Walters AS, Duvoisin RC, Miller DC. Binswanger’s disease presenting as levodopa-responsive parkinsonism: clinicopathologic study of three cases. Mov Disord 1995;10:450–454.ArticlePubMed
• 24. Dichgans M, Mayer M, Uttner I, Brüning R, Müller-Höcker J, Rungger G, et al. The phenotypic spectrum of CADASIL: clinical findings in 102 cases. Ann Neurol 1998;44:731–739.ArticlePubMed
• 25. Miranda M, Dichgans M, Slachevsky A, Urbina F, Mena I, Venegas P, et al. CADASIL presenting with a movement disorder: a clinical study of a Chilean kindred. Mov Disord 2006;21:1008–1012.ArticlePubMed
• 26. Ragno M, Berbellini A, Cacchiò G, Manca A, Di Marzio F, Pianese L, et al. Parkinsonism is a late, not rare, feature of CADASIL: a study on Italian patients carrying the R1006C mutation. Stroke 2013;44:1147–1149.ArticlePubMed
• 27. Erro R, Lees AJ, Moccia M, Picillo M, Penco S, Mosca L, et al. Progressive parkinsonism, balance difficulties, and supranuclear gaze palsy. JAMA Neurol 2014;71:104–107.ArticlePubMed
• 28. Rice CM, McGuone D, Kurian KM, Love S, Renowden SA, Giffin NJ. Autopsy-confirmed, co-existent CADASIL and multiple system atrophy. Parkinsonism Relat Disord 2011;17:390–392.ArticlePubMed
• 29. Hammans SR, Sweeney MG, Hanna MG, Brockington M, Morgan-Hughes JA, Harding AE. The mitochondrial DNA transfer RNALeu(UUR) A-->G(3243) mutation. A clinical and genetic study. Brain 1995;118(Pt 3):721–734.ArticlePubMedPDF
• 30. De Coo IF, Renier WO, Ruitenbeek W, Ter Laak HJ, Bakker M, Schägger H, et al. A 4-base pair deletion in the mitochondrial cytochrome b gene associated with parkinsonism/MELAS overlap syndrome. Ann Neurol 1999;45:130–133.ArticlePubMed
• 31. Schapira AH. Mitochondrial DNA in Parkinson’s disease. Adv Neurol 1999;80:233–237.PubMed
• 32. Singmaneesakulchai S, Limotai N, Jagota P, Bhidayasiri R. Expanding spectrum of abnormal movements in MELAS syndrome (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes). Mov Disord 2012;27:1495–1497.ArticlePubMed
• 33. Nakagaki H, Furuya J, Santa Y, Nagano S, Araki E, Yamada T. [A case of MELAS presenting juvenile-onset hyperglycemic chorea-ballism]. Rinsho Shinkeigaku 2005;45:502–505.PubMed
• 34. Finsterer J. [MELAS syndrome as a differential diagnosis of ischemic stroke]. Fortschr Neurol Psychiatr 2009;77:25–31.ArticlePubMedPDF
• 35. Suzuki J, Kodama N. Moyamoya disease--a review. Stroke 1983;14:104–109.ArticlePubMed
• 36. Ahn ES, Scott RM, Robertson RL Jr, Smith ER. Chorea in the clinical presentation of moyamoya disease: results of surgical revascularization and a proposed clinicopathological correlation. J Neurosurg Pediatr 2013;11:313–319.ArticlePubMed
• 37. Lee JY, Kim SK, Wang KC, Chae JH, Cheon JE, Choi JW, et al. Involuntary movement in pediatric moyamoya disease patients: consideration of pathogenetic mechanism using neuroimaging studies. Childs Nerv Syst 2014;30:885–890.ArticlePubMed
• 38. Pandey P, Bell-Stephens T, Steinberg GK. Patients with moyamoya disease presenting with movement disorder. J Neurosurg Pediatr 2010;6:559–566.ArticlePubMed
• 39. Jung HY, Lee JE, Kang I, Kim YB, Park HE, Kim JS. Acute chorea onset after hot food consumption in a patient with moyamoya disease. J Mov Disord 2016;9:50–52.ArticlePubMedPMCPDF
• 40. Baik JS, Lee MS. Movement disorders associated with moyamoya disease: a report of 4 new cases and a review of literatures. Mov Disord 2010;25:1482–1486.ArticlePubMed
• 41. Siniscalchi A, Gallelli L, Labate A, Malferrari G, Palleria C, Sarro GD. Post-stroke movement disorders: clinical manifestations and pharmacological management. Curr Neuropharmacol 2012;10:254–262.ArticlePubMedPMC
• 42. Siniscalchi A, Gallelli L, De Sarro G. Use of antiepileptic drugs for hyperkinetic movement disorders. Curr Neuropharmacol 2010;8:359–366.ArticlePubMedPMC
• 43. Chuang C, Fahn S, Frucht SJ. The natural history and treatment of acquired hemidystonia: report of 33 cases and review of the literature. J Neurol Neurosurg Psychiatry 2002;72:59–67.ArticlePubMedPMC
• 44. Striano P, Elefante A, Coppola A, Tortora F, Zara F, Minetti C, et al. Dramatic response to levetiracetam in post-ischaemic Holmes’ tremor. J Neurol Neurosurg Psychiatry 2007;78:438–439.ArticlePubMedPMC
• 45. Lyons KE, Pahwa R. Deep brain stimulation and tremor. Neurotherapeutics 2008;5:331–338.ArticlePubMedPMC
• 46. Dijk JM, Tijssen MA. Management of patients with myoclonus: available therapies and the need for an evidence-based approach. Lancet Neurol 2010;9:1028–1036.ArticlePubMed
• 47. Yamamoto T, Katayama Y, Kano T, Kobayashi K, Oshima H, Fukaya C. Deep brain stimulation for the treatment of parkinsonian, essential, and poststroke tremor: a suitable stimulation method and changes in effective stimulation intensity. J Neurosurg 2004;101:201–209.ArticlePubMed
• 48. Genton P, Gélisse P. Antimyoclonic effect of levetiracetam. Epileptic Disord 2000;2:209–212.ArticlePubMed
• 49. Van Zandijcke M. Treatment of myoclonus. Acta Neurol Belg 2003;103:66–70.PubMed
• 50. FitzGerald PM, Jankovic J. Lower body parkinsonism: evidence for vascular etiology. Mov Disord 1989;4:249–260.ArticlePubMed
• 51. Zijlmans J, Evans A, Fontes F, Katzenschlager R, Gacinovic S, Lees AJ, et al. [123I] FP-CIT spect study in vascular parkinsonism and Parkinson’s disease. Mov Disord 2007;22:1278–1285.ArticlePubMed
• 52. Wetter TC, Eisensehr I, Trenkwalder C. Functional neuroimaging studies in restless legs syndrome. Sleep Med 2004;5:401–406.ArticlePubMed
• 53. Yochelson MR, David RG. New-onset tic disorder following acute hemorrhage of an arteriovenous malformation. J Child Neurol 2000;15:769–771.ArticlePubMed
• 54. Galea I, Norwood F, Phillips MJ, Shearman C, McMonagle P, Gibb WR. Pearls & Oy-sters: resolution of hemichorea following endarterectomy for severe carotid stenosis. Neurology 2008;71:e80–e82.ArticlePubMed
• 55. Kim JS, Suh DC. Hemiballism-hemichorea and posterior communicating artery stenosis. Eur Neurol 2001;45:182–183.ArticlePubMed
• 56. Pareés I, Pujadas F, Hernández-Vara J, Lorenzo-Bosquet C, Cuberas G, Munuera J, et al. Reversible hemichorea associated with extracranial carotid artery stenosis. J Neurol Sci 2011;300:185–186.ArticlePubMed
• 57. Tatemichi TK, Young WL, Prohovnik I, Gitelman DR, Correll JW, Mohr JP. Perfusion insufficiency in limb-shaking transient ischemic attacks. Stroke 1990;21:341–347.ArticlePubMed
• 58. Kim DW, Ko Y, Jang SH, Yoon SJ, Oh GS, Lee SJ, et al. Acute hemichorea as an unusual presentation of internal carotid artery stenosis. J Mov Disord 2013;6:17–20.ArticlePubMedPMCPDF
• 59. Katayama Y, Oshima H, Fukaya C, Kawamata T, Yamamaoto T. Control of post-stroke movement disorders using chronic motor cortex stimulation. Acta Neurochir Suppl 2002;79:89–92.ArticlePubMed
• 60. Canavero S, Bonicalzi V. Extradural cortical stimulation for movement disorders. Acta Neurochir Suppl 2007;97(Pt 2):223–232.ArticlePubMed
• 61. Franzini A, Cordella R, Messina G, Marras CE, Romito LM, Carella F, et al. Deep brain stimulation for movement disorders. Considerations on 276 consecutive patients. J Neural Transm (Vienna) 2011;118:1497–1510.ArticlePubMed
• 62. Tseng KY, Tang CT, Chang CF, Chen KY. Treatment of delayed-onset post-stroke monochorea with stereotactic pallidotomy. J Clin Neurosci 2010;17:779–781.ArticlePubMed
• 63. Shinohara Y, Yanagihara T, Abe K, Yoshimine T, Fujinaka T, Chuma T, et al. VII. Rehabilitation. J Stroke Cerebrovasc Dis 2011;20(4 Suppl):S145–S180.ArticlePubMed
• 64. Ganesan V. Outcome and rehabilitation after childhood stroke. Handb Clin Neurol 2013;112:1079–1083.ArticlePubMed
• 65. Guerini F, Frisoni GB, Bellwald C, Rossi R, Bellelli G, Trabucchi M. Subcortical vascular lesions predict functional recovery after rehabilitation in patients with L-dopa refractory parkinsonism. J Am Geriatr Soc 2004;52:252–256.ArticlePubMed
• 66. Abbruzzese G, Trompetto C, Mori L, Pelosin E. Proprioceptive rehabilitation of upper limb dysfunction in movement disorders: a clinical perspective. Front Hum Neurosci 2014;8:961.ArticlePubMedPMC
• 67. Ali S, Khan MA, Khealani B. Limb-shaking transient ischemic attacks: case report and review of literature. BMC Neurol 2006;6:5.ArticlePubMedPMCPDF
• 68. Baquis GD, Pessin MS, Scott RM. Limb shaking--a carotid TIA. Stroke 1985;16:444–448.ArticlePubMed
• 69. Persoon S, Kappelle LJ, Klijn CJ. Limb-shaking transient ischaemic attacks in patients with internal carotid artery occlusion: a case-control study. Brain 2010;133(Pt 3):915–922.ArticlePubMedPDF

Figure & Data

References

Citations

Citations to this article as recorded by  

• Post-stroke movement disorders disappearance: a report of disappearance of tardive dyskinesia after stroke and a literature review
  Min Seung Kim, InJa Shin, Don Gueu Park, Jung han Yoon
  Acta Neurologica Belgica.2023; 123(5): 2005.     CrossRef
• Monochorea after acute contralateral pontine infarction: A case report
  Yun Su Hwang, Byoung-Soo Shin, Han Uk Ryu, Hyun Goo Kang
  Medicine.2023; 102(3): e32660.     CrossRef
• Adult-onset sporadic chorea: real-world data from a single-centre retrospective study
  Roberta Bovenzi, Matteo Conti, Rocco Cerroni, Mariangela Pierantozzi, Alessandro Stefani, Antonio Pisani, Nicola Biagio Mercuri, Tommaso Schirinzi
  Neurological Sciences.2022; 43(1): 387.     CrossRef
• Parkinsonism and ataxia
  Giulia Franco, Giulia Lazzeri, Alessio Di Fonzo
  Journal of the Neurological Sciences.2022; 433: 120020.     CrossRef
• Movement Disorders Associated With Cerebral Artery Stenosis: A Nationwide Study
  Kye Won Park, Nari Choi, Eungseok Oh, Chul Hyoung Lyoo, Min Seok Baek, Han-Joon Kim, Dalla Yoo, Jee-Young Lee, Ji-Hyun Choi, Jae Hyeok Lee, Seong-Beom Koh, Young Hee Sung, Jin Whan Cho, Hui-Jun Yang, Jinse Park, Hae-Won Shin, Tae-Beom Ahn, Ho-Sung Ryu, So
  Frontiers in Neurology.2022;[Epub]     CrossRef
• Post-stroke Movement Disorders
  Priyanka Tater, Sanjay Pandey
  Neurology India.2021; 69(2): 272.     CrossRef
• Hemibalismo y hemicorea secundarios a un ataque cerebrovascular isquémico insular, una presentación inusual: reporte de caso
  Carlos Martínez-Rubio, Hellen Kreinter-Rosenbaum, Habib Moutran-Barroso
  Neurología Argentina.2020; 12(3): 207.     CrossRef
• Hemiballismus in subcortical lacunar infarcts
  ChinyeluUchenna Ufoaroh, OvercomerNnaemeka Agah, Nnamdi Morah, ErnestNdukaife Anyabolu
  Nigerian Journal of Medicine.2020; 29(3): 527.     CrossRef
• COVID-19 and stroke: Red flags for secondary movement disorders?
  Daniella Balduino Victorino, Marcia Guimarães-Marques, Mariana Nejm, Fulvio Alexandre Scorza, Carla Alessandra Scorza
  eNeurologicalSci.2020; 21: 100289.     CrossRef
• Post-stroke restless arm syndrome mimicking hemichorea–hemiballism
  Ha-yom Kim, Moon-Ho Park, Do-Young Kwon
  Acta Neurologica Belgica.2017; 117(3): 791.     CrossRef
• Vascular Pathology Causing Late Onset Generalized Chorea: A Clinico‐Pathological Case Report
  Paula Salgado, Ricardo Taipa, Joana Domingos, Daniel Dias, Manuel Melo Pires, Marina Magalhães
  Movement Disorders Clinical Practice.2017; 4(6): 819.     CrossRef

Comments on this article