You are on page 1of 10

Post-stroke Movement Disorders: The Clinical, Neuroanatomic,

and Demographic Portrait of 284 Published Cases

Ritika Suri, MD,* Federico Rodriguez-Porcel, MD,† Kelly Donohue, MD,*


Erin Jesse, BA,‡ Lilia Lovera, MD,† Alok Kumar Dwivedi, PhD,§ and
Alberto J. Espay, MD, MSc*

Purpose: Abnormal movements are a relatively uncommon complication of strokes.


Besides the known correlation between stroke location and certain movement dis-
orders, there remain uncertainties about the collective effects of age and stroke
mechanism on phenomenology, onset latency, and outcome of abnormal movements.
Materials and Methods: We systematically reviewed all published cases and case
series with adequate clinical-imaging correlations. A total of 284 cases were ana-
lyzed to evaluate the distribution of different movement disorders and their association
with important cofactors. Results: Posterolateral thalamus was the most common
region affected (22.5%) and dystonia the most commonly reported movement dis-
order (23.2%). The most common disorders were parkinsonism (17.4%) and chorea
(17.4%) after ischemic strokes and dystonia (45.5%) and tremor (19.7%) after hem-
orrhagic strokes. Strokes in the caudate and putamen were complicated by dystonia
in one third of the cases; strokes in the globus pallidus were followed by par-
kinsonism in nearly 40%. Chorea was the earliest poststroke movement disorder,
appearing within hours, whereas dystonia and tremor manifested several months
after stroke. Hemorrhagic strokes were responsible for most delayed-onset move-
ment disorders (>6 months) and were particularly overrepresented among younger
individuals affected by dystonia. Conclusions: This evidence-mapping portrait of
poststroke movement disorders will require validation or correction based on
a prospective epidemiologic study. We hypothesize that selective network

From the *James J. and Joan A. Gardner Center for Parkinson Disease and Movement Disorders, Department of Neurology and Rehabil-
itation Medicine, University of Cincinnati, Cincinnati, Ohio; †Department of Neurology, Medical University of South Carolina, Charleston,
South Carolina; ‡Department of Chemistry, Ohio State University, Columbus, Ohio; and §Department of Biomedical Sciences, Division of
Biostatistics and Epidemiology, Texas Tech University Health Sciences Center El Paso, El Paso, Texas.
Received March 2, 2018; revision received April 7, 2018; accepted April 23, 2018.
Financial disclosure: Dr. Dwivedi is supported by the NIH (1R01HL125016-01) as a Co-Investigator and (R21 AI118228) as a Collaborator.
He has also been serving as a statistician in 4 CPRIT grants (PP110156, PP140211, PP150031, and PP130083), Coldwell (Co-Investigator), MSA
Coalition (Collaborator), and as a principal investigator in a TTUHSC ELP mini seed grant. Dr. Dwivedi is a director of Biostatistics and
Epidemiology Consulting Laboratory at the TTUHSC ELP. Dr. Espay has received grant support from the NIH, Great Lakes Neurotechnologies,
and the Michael J. Fox Foundation; personal compensation as a consultant/scientific advisory board member for Abbvie, TEVA, Impax, Acadia,
Acorda, Cynapsus/Sunovion, Lundbeck, and US WorldMeds; publishing royalties from Lippincott Williams & Wilkins, Cambridge Univer-
sity Press, and Springer; and honoraria from Abbvie, UCB, US WorldMeds, Lundbeck, Acadia, the American Academy of Neurology, and the
Movement Disorders Society.
Conflict of interest: Drs. Suri, Rodriguez-Porcel, Donohue, and Lovera, and Ms. Jesse declare that they have no conflict of interest to disclose.Author
contributions: Case Series Project: Conception: R.S., F.R.P., L.L., and A.J.E.; Organization: R.S. and A.J.E.; Execution: R.S., F.R.P, E.J., and K.D.
Statistical Analysis: A.D. Manuscript: Writing of the First Draft: R.S. and F.R.P.; Review and Critique: E.J., K.D., L.L., A.D., and A.J.E.
Address correspondence to Alberto Espay, MD, MSc., Department of Neurology and Rehabilitation Medicine, University of Cincinnati Academic
Health Center, 260 Stetson St., Suite 2300 (PO Box 670525), Cincinnati, OH 45267-0525. E-mail: espayaj@ucmail.uc.edu.
1052-3057/$ - see front matter
© 2018 National Stroke Association. Published by Elsevier Inc. All rights reserved.
https://doi.org/10.1016/j.jstrokecerebrovasdis.2018.04.028

2388 Journal of Stroke and Cerebrovascular Diseases, Vol. 27, No. 9 (September), 2018: pp 2388–2397
POST-STROKE MOVEMENT DISORDERS 2389
vulnerability and resilience may explain the differences observed in movement
phenomenology and outcomes after stroke. Key Words: Movement disorders—
stroke—ischemic stroke—hemorrhage—dystonia.
© 2018 National Stroke Association. Published by Elsevier Inc. All rights reserved.

Introduction demographics (e.g., age and gender), type and location


of stroke, reported movement disorder, latency to
Poststroke movement disorders (PSMDs) represent up
onset and, if available, outcome (e.g., improvement or
to 22% of all secondary movement disorders. However,
persistence).
PSMDs are only observed in 1%-4% of all strokes.1,2 Despite
the fact that the basal ganglia, thalamus, and cerebel-
lum are commonly affected, the vast majority of strokes Statistical Analysis
in these regions do not complicate their course with a A total of 74 articles yielding 284 patients were found
movement disorder.1,3 This remains an intriguing phe- suitable for the analysis.4-75 Because the majority of the
nomenon, considering the role of these structures in the articles were case reports, each subject from each study
pathophysiology of idiopathic and degenerative move- was considered to be a unit of analysis, and thus no weight
ment disorders. Furthermore, while selected movement was assigned to any studies. Type of stroke (ischemic
disorders may emerge after lesions in distinct parts of versus hemorrhagic), average age, gender distribution, type
the brain, the topographical specificity for many move- and location of movement disorders, latency period
ments may be poor, and there remains uncertainty about between stroke and movement disorder, and outcomes
the effects of age and stroke type on phenomenology, onset were extracted from each report. All data were de-
latency, and outcome of abnormal movements. The reasons scribed using frequencies and proportions. All data were
for these discrepancies remain unclear. compared according to type of stroke, gender, and age
In this study, we sought to elucidate the role of type groups using Fisher’s exact tests. Comparison of latency
of stroke (ischemic versus hemorrhagic), location, and age period according to different factors was assessed using
on the phenomenology, latency to onset, and outcome chi-square test. All the statistical analyses were carried
of PSMDs based on a review of published cases. out using STATA 13 (StataCorp, College Station, TX).

Methods Results
We conducted a systematic review of the literature to General Features of PSMD
identify cases of PSMDs reported between 1986 and 2016. Of a total of 323 qualifying cases, 39 were excluded
We performed a PubMed search with the following terms: due to insufficient data. In total, 284 cases fulfilled our
(stroke or infarct or hemorrhage or ischemia) AND (move- research criteria and were used for analyses. Reported
ment disorders or hyperkinetic or dystonia or myoclonus PSMDs were more common in men (58%), with a mean
or chorea or Parkinson’s or parkinsonism or tremor or age at presentation of 62 years (range 18-93). Ischemic
restless legs syndrome or periodic limb movements or strokes preceded more than three quarters of PSMDs. Pos-
stereotypy or akathisia or alien hand syndrome or tics). terolateral thalamus (23%) was the region most frequently
Search results, titles, and abstracts were reviewed to include affected, followed by the putamen (19%) and caudate (14%).
case reports and case series pertinent to our research ob- Dystonia was the most common PSMD (23%), followed
jectives. Among the identified articles, we included in the by chorea (16%) and myoclonus (15%) (Table 1).
review those that contained (1) well-documented pa-
tients with movement disorders developing after a stroke;
Basic Demographics and PSMD
(2) characterization of the stroke type (e.g., ischemic, hem-
orrhagic) and location; (3) report of the latency between In patients between 50 and 70 years (51.4%), the pos-
the stroke and onset of the movement disorder; and terolateral thalamus was the most common location (29%),
(4) patients who did not present alternative causes for while myoclonus and dystonia were the most common
the emergence of the movement disorder (e.g., metabol- PSMD (27% and 24%, respectively). In those younger than
ic abnormalities, medications). Additional articles were age 50, the putamen and caudate (28% and 19%, respec-
identified by screening secondary research articles (reviews, tively) were the most common locations, and dystonia
commentaries, and letters) yielded by the initial PubMed the most common PSMD (40%). In those older than 70
search. We excluded articles with incomplete character- years, the putamen was most frequently affected (25%)
ization of the movement disorder or the imaging data and chorea the most common PSMD (24%) (Supplementary
regarding localization. Subjects from criteria-meeting ar- Table S1). Women showed greater putaminal involvement
ticles were included in a database, which included than men (26% versus 14.0%) but similar frequency of
2390 R. SURI ET AL.
Table 1. General characteristics of poststroke movement disorders

Men Age Ischemic


affected, years cases Hemorrhagic
Movement disorder N (%) N (%) (range) N (%) cases N (%) Most common location N (%)

All 284 164 (57.7) 61.8 (18-93) 218 (76.7) 66 (23.2) Posterolateral thalamus: 64 (22.5)
Dystonia 66 (23.2) 39 (40.9) 61.7 (37-76) 19 (28.7) 20 (30.3) Posterolateral thalamus: 22 (66.6)
Chorea 46 (16.1) 25 (54.3) 61.72 (42-85) 19 (41.3) 6 (13.0) Caudate: 5 (50)
Myoclonus 43 (15.1) 25 (58.1) 66.6 (47-83) 20 (46.5) 5 (11.6) Frontal lobe: 9 (75)
Parkinsonism 42 (14.7) 26 (61.9) 60.7 (18-80) 25 (59.5) 1 (2.4) Putamen: 9 (64.2)
Tremor 39 (13.7) 24 (61.5) 53.3 (18-76) 16 (41) 8 (20.5) Midbrain: 6 (54.5)
Restless legs syndrome 20 (7.04) 7 (35.0) 65.2 (46-83) 7 (35) 0 (0) Pons: 2 (28.5); putamen: 1 (14.2)
Alien hand syndrome 9 (3.1) 4 (44.4) 62.9 (25-83) 4 (44.4) 0 (0) Parietal lobe: 2 (40)
Periodic limb 9 (3.1) 4 (44.4) 60.5 (53-75) 4 (44.4) 0 (0) Pons: 3 (50)
movements
Stereotypy 8 (2.8) 6 (75) 63.8 (40-93) 6 (75) 0 (0) Putamen: 3 (37.5)
Akathisia 1 (.35) 1 (100) 60 (N/A) 1 (100) 0 (0) Posterior thalamus: 1 (100)
Tics 1 (.35) 1 (100) 71 (N/A) 1 (100) 0 (0) Caudate: 1 (100)

Abbreviation: N/A, not applicable.

stroke involvement in other localizations. While dystonia affecting the globus pallidus exhibited parkinsonism in
and myoclonus were of relatively similar frequency in men nearly 40%. Thalamic strokes yielded distinct pheno-
and women (~23% and ~15%, respectively), parkinsonism types depending on the region affected (Fig 1).
was among the top 3 disorders in men (16%) and chorea
among the top 3 in women (18%) (Supplementary Table S2). Latency to PSMD after Stroke
Most PSMDs (46%) manifested within the first 7 days
Type of Stroke and PSMD
after a stroke. Chorea was the earliest PSMD, appearing
Ischemia was the most common mechanism of stroke within 24 hours, whereas dystonia and tremor had a
in those older than 70, whereas hemorrhage was more poststroke latency measured in several months (Fig 2).
common between the ages of 50 and 70. The distribu- Ischemia remained the most common mechanism of stroke
tion of ischemic and hemorrhagic strokes was similar for movement disorders manifesting in less than a month.
between men and women. Ischemic strokes complicat- Hemorrhagic strokes were responsible for most cases of
ed with PSMD were more frequently located in the delayed onset of movement disorders (>6 months) (Fig 3).
putamen (22%), followed by frontal lobe (16%), mid- The latency period varied depending on stroke loca-
brain (16%), and caudate (15%), whereas hemorrhagic tion. For patients who manifested PSMDs within the first
strokes frequently affected the posterolateral thalamus week, the posterolateral thalamus was the most common
(42%), midbrain (15%), and pons (9%). Parkinsonism, location. The putamen was the most common location
chorea, and dystonia (17% each) were the most com- involved in patients presenting with symptoms within
monly observed movement disorders in patients with a day, and the caudate was most commonly involved in
ischemic strokes, whereas dystonia (46%), tremor (20%), patients presenting with symptoms within 6 months.
and myoclonus (15%) were commonly experienced by
patients with hemorrhagic stroke. Compared with hem- Outcome of PSMD
orrhagic strokes, parkinsonism and restless legs syndrome
Outcome data were reported in 64% of cases re-
were significantly the more frequent type of PSMD after
viewed. Over 70% of these patients exhibited spontaneous
ischemic strokes (6% versus 17% and 0% versus 9%, re-
improvement or resolution. Of those with persistent symp-
spectively); compared with ischemic strokes, dystonia (46%)
toms, only half experienced benefit from symptomatic
and tremor (20%) were significantly more frequent after
treatment. The most common movement disorder to
hemorrhagic strokes, complicating almost two thirds of
improve or resolve spontaneously was myoclonus (84%),
such cases (P < .001) (Table 2 and Supplementary Table S3).
tremor was the most to persist (38%), and parkinson-
ism was the most common to improve with treatment
Stroke Location and Type of PSMD
(36%) (Fig 4). The frontal lobe was the most common lo-
PSMDs varied depending on the location of the stroke. cation involved in cases that spontaneously improved or
While caudate and putaminal strokes were complicated resolved, the putamen in cases that persisted despite treat-
by dystonia in one third of the cases, those selectively ment, and the midbrain in cases that responded to
POST-STROKE MOVEMENT DISORDERS 2391
Table 2. Type of stroke and movement disorders

Entire cohort Ischemic Hemorrhagic

Characteristics N (%) N (%) N (%) P value

Age (y) .002


<50 58 (20.4) 42 (19.3) 16 (24.2)
50-70 146 (51.4) 104 (47.7) 42 (63.6)
>70 80 (28.2) 72 (33) 8 (12.1)
Gender .478
Male 164 (57.7) 123 (56.4) 41 (62.1)
Female 120 (42.3) 95 (43.6) 25 (37.9)
Movement disorders
Dystonia 66 (23.2) 36 (16.5) 30 (45.5) <.001
Tremor 39 (13.7) 26 (11.9) 13 (19.7) <.001
Chorea 46 (16.2) 38 (17.4) 8 (12.1) .346
Myoclonus 43 (15.1) 33 (15.1) 10 (15.2) 1.000
Parkinsonism 42 (14.8) 38 (17.4) 4 (6.1) .028
Restless legs syndrome 20 (7) 20 (9.2) 0 (0) .005
Alien hand syndrome 9 (3.2) 8 (3.7) 1 (1.5) .690
Periodic limb movements 9 (3.2) 9 (4.1) 0 (0) .123
Stereotypy 8 (2.8) 8 (3.7) 0 (0) .205
Akathisia 1 (.4) 1 (.5) 0 (0) 1.000
Tics 1 (.4) 1 (.5) 0 (0) 1.000
Latency <.001
Simultaneously 18 (6.3) 18 (8.3) 0 (0)
Within 1 d 40 (14.1) 33 (15.1) 7 (10.6)
1 d to 1 wk 74 (26.1) 60 (27.5) 14 (21.2)
>1 wk to <1 mo 18 (6.3) 16 (7.3) 2 (3)
1 mo to <6 mo 33 (11.6) 26 (11.9) 7 (10.6)
6-12 mo 18 (6.3) 7 (3.2) 11 (16.7)
>1 yr 14 (4.9) 6 (2.8) 8 (12.1)
Unknown 69 (24.3) 52 (23.9) 17 (25.8)
Outcome .124
Spontaneously resolved or improved 85 (29.9) 71 (32.6) 14 (21.2)
Improved with treatment 48 (16.9) 39 (17.9) 9 (13.6)
Persisted 50 (17.6) 38 (17.4) 12 (18.2)
Unknown 101 (35.6) 70 (32.1) 31 (47)

Significant values (p<.05) are in bold.

treatment. There was no difference in outcome among was significantly higher in patients with hemorrhagic
the different age groups. There was no statistical difference strokes, whereas the frequency of parkinsonism and rest-
in the outcomes of PSMD manifesting from ischemic or less legs syndrome was significantly higher in patients
hemorrhagic strokes, although there was a trend for move- with ischemic strokes. Delayed onset of movement dis-
ment disorders resulting from ischemic strokes to improve orders was mostly observed in patients with hemorrhagic
on their own or resolve with treatment compared with strokes associated with dystonia and tremor, whereas earlier
movement disorders resulting from hemorrhagic strokes. onset of movement disorders was due to ischemic strokes
In summary, an interesting portrait emerged from the leading to chorea (over one third persisted), parkinson-
analysis of these 284 cases. The most common PSMD was ism (over half improved with treatment or resolved), and
dystonia (both in men and women), and most post- restless legs syndrome (over two third improved or
stroke dystonia occurred in patients younger than age resolved).
50 years and after hemorrhagic strokes. The second most
common PSMD was chorea, with slightly higher fre-
Discussion
quency among those older than 70 years with ischemic
strokes. Myoclonus was the third most common PSMD, With the inherent biases of published case reports and
was mostly observed in the 50-70 age bracket, and was case series, the collective data suggest a relatively small
equally distributed among patients with hemorrhagic and but significant burden of poststroke movement-related com-
ischemic strokes. The frequency of dystonia and tremor plications. As with other studies, the type of stroke and
2392 R. SURI ET AL.

Figure 1. Frequency of post-stroke movement disorders according to stroke localization.

location provided only a rough estimate of the associ- differences in gender, latency, and outcome according to
ated movement disorder. 1,2 Posterolateral thalamus, the type of stroke, localization, type of movement dis-
putamen, and caudate emerged as the most commonly order, and age, assisted by the high number of cases
reported regions affected by stroke and dystonia as the retrieved compared with the 3 studies mentioned above.
most common movement disorder. Ischemia remained the The relatively poor association between stroke local-
most common mechanism of stroke across all PSMDs. The ization and movement phenomenology (most associations
type of stroke was important in predicting the phenom- were under 30%) may be explained by the inability to
enology, with parkinsonism and restless legs syndrome discern the different motor networks involved in the patho-
being more prevalent after ischemic strokes while dys- physiology of movement disorders. These networks
tonia and tremor after hemorrhagic strokes (more than represent the interaction between multiple regions of the
two thirds of hemorrhagic cases exhibited dystonia). Finally, brain and can be analyzed at different levels, from neurons
age was also a variable affecting location and move- and synapses to anatomical regions and fiber tracts.77 There-
ment phenomenology, with putamen and caudate fore, the focal damage caused by a stroke may affect 1
appearing more frequently affected in those under 50. or multiple neural networks within a single structure. Thus,
Three studies have examined the clinical characteris- patients with stroke involving a given region (e.g., the
tics of PSMDs and have reported chorea, including thalamus) may suffer damage in 1 or more varying neu-
hemiballism (the most severe form), as the most common ronal networks, resulting in a spectrum of motor deficits.
PSMD, followed by dystonia.1,2,76 Our literature reap- In addition, the disruption of the network architecture
praisal showed that chorea, parkinsonism, dystonia, and may trigger different adaptive responses to ensure the
myoclonus were most commonly disorders among maintenance of motor function, which stand to alter the
patients with ischemic strokes. Dystonia was dispropor- movement disorder phenomenology.78,79 In particular, mal-
tionately more prevalent (accounting for two thirds of adaptive mechanisms like diaschisis, dedifferentiation, and
the cohort) in hemorrhaging cases. Ischemia was the most abnormal axonal regeneration may lead to an aberrant
common stroke mechanism, with thalamus and basal network function potentially manifesting as PSMD.77
ganglia the most common stroke localizations. Prior studies We found that patients with PSMD after hemorrhagic
underscore the inconsistencies between stroke localiza- strokes were younger compared with those presenting
tion and phenomenology. Mehanna and Jankovic’s study after ischemic stroke. In addition, younger age and hem-
sought to correlate movement phenomenology with other orrhagic type of stroke were independently associated with
stroke features. Similar to our study, they uncovered a a later onset of PSMD, beyond at least 1 month. We spec-
higher incidence of dystonia in younger patients and chorea ulate that the differences between these groups may be
in older patients. Our review is the first to assess due to the higher degree of resilience and neuroplasticity
POST-STROKE MOVEMENT DISORDERS 2393

Figure 2. Latency for most common poststroke movement disorders.

in younger subjects and their decline with age.80,81 While are more likely to have more severe outcomes, includ-
diminished neuroplasticity results in limb paresis in some ing death or paresis (precluding later documentation of
cases, the ability of the neural networks to reorganize them- abnormal movements). Similar reasoning may apply to
selves may lead to aberrant network regeneration, ischemic strokes, where younger patients may be left with
manifesting as abnormal movements.82,83 In addition, the a lower prevalence of residual deficits compared with older
ability of the neural networks to reorganize themselves patients.
depends on the severity of the initial insult.84 We suggest There are several limitations to this literature reap-
that PSMDs are more likely to emerge after hemorrhag- praisal. First, it was based on reported cases that included
ic strokes in younger patients due to their higher degree a marked selection bias: while most PSMDs remain a small
of resilience (and at a longer latency due to stroke se- fraction of all strokes, it is likely that only a fraction of
verity), whereas older patients with hemorrhagic strokes this fraction has ever been reported, with more common
2394 R. SURI ET AL.

Figure 3. Latency according to type of stroke. * indicates significant difference (P < .05).

cases of poststroke chorea or dystonia becoming unlikely phenotype (e.g., potential for Lewy bodies and nigra de-
to be reported in the modern era. As a result, our find- generation in individuals with presumed poststroke
ings are not suitable to estimate prevalence assumptions parkinsonism). Despite these limitations, this is the first
after stroke types and localization in the general popu- comprehensive systematic review study to evaluate the
lation (e.g., it is uncertain whether the higher percentages distribution of PSMDs and their outcomes based on all
of movement disorders occurring in the first week after of the published cases (which may not be accrued from
strokes in patients older than 70 compared with those a single medical center) for which sufficient clinico-
younger than 50 are due to the shorter survival of the imaging data are available.
former group). Relatedly, a number of cases may have
been unique rather than representative of phenomena seen
Conclusion
during routine clinical practice. Moreover, most of these
case reports were not accompanied by video material and PSMDs remain an uncommon but important source of
the determination of the movement phenomenology may disability in neurology, with differences in phenomenol-
have been made by clinicians without specialized train- ogy and outcome that may result from selective network
ing in movement disorders, potentially leading to a vulnerability and resilience. A prospective epidemio-
percentage of mischaracterized phenotypes. Also, the ag- logic study would be desirable to determine which
gregated level of data from different studies did not allow elements of this evidence-mapping portrait may be ac-
the use of multivariable analysis. Due to mixed study curate and which may be embellished or misleading,
designs with small number of cases, the analysis could further refining the variables that may affect the frequen-
not account for weighting structure of each study. Finally, cy, type, and outcome of these secondary PSMDs.
we did not include abnormalities not considered “classic”
movement disorders, such as spasticity and apraxia, even
Appendix: Supplementary Material
though these may complicate strokes far more common-
ly and we lacked neuropathologic data to exclude Supplementary data to this article can be found online
comorbidities that may at least partially account for a given at doi:10.1016/j.jstrokecerebrovasdis.2018.04.028.
POST-STROKE MOVEMENT DISORDERS 2395

Figure 4. Outcome of poststroke movement disorders and locations involved for each.

References tractography study. J Stroke Cerebrovasc Dis 2013;


22:e240-e244.
1. Ghika-Schmid F, Ghika J, Regli F, et al. Hyperkinetic 10. Kloesel B, Czarnecki K, Muir JJ, et al. Sequelae of a
movement disorders during and after acute stroke: the left-sided parietal stroke: posterior alien hand syndrome.
Lausanne Stroke Registry. J Neurol Sci 1997;146:109-116. Neurocase 2010;16:488-493.
2. Alarcon F, Zijlmans JC, Duenas G, et al. Post-stroke 11. Kim YD, Lee ES, Lee KS, et al. Callosal alien hand sign
movement disorders: report of 56 patients. J Neurol following a right parietal lobe infarction. J Clin Neurosci
Neurosurg Psychiatry 2004;75:1568-1574. 2010;17:796-797.
3. Russmann H, Vingerhoets F, Ghika J, et al. Acute 12. Groom KN, Ng WK, Kevorkian CG, et al. Ego-
infarction limited to the lenticular nucleus: clinical, syntonic alien hand syndrome after right posterior cerebral
etiologic, and topographic features. Arch Neurol artery stroke. Arch Phys Med Rehabil 1999;80:162-
2003;60:351-355. 165.
4. Sabrie M, Berhoune N, Nighoghossian N. Alien hand 13. Schirinzi T, Chiaravalloti A, Davoli A, et al. Transient
syndrome and paroxystic dystonia after right posterior parkinsonism after unilateral midbrain stroke: a
cerebral artery territory infarction. Neurol Sci compensatory intervention from the healthy side? Neurol
2015;36:1709-1710. Sci 2014;35:2013-2015.
5. Serrano-Vicente J, Duran-Barquero C, Garcia-Bernardo L, 14. Milanov I, Bogdanova D, Georgiev D. Contralateral
et al. Bilateral alien hand syndrome in cerebrovascular hemi-parkinsonism and atypical tremor after stroke (a
disease: CT, MR, CT angiography, and 99mTc-HMPAO- case report). Parkinsonism Relat Disord 1998;4:143-
SPECT findings. Clin Nucl Med 2015;40:e211-e214. 145.
6. Nowak DA, Bösl K, Lüdemann-Podubecka J, et al. 15. Defer GL, Remy P, Malapert D, et al. Rest tremor and
Recovery and outcome of frontal alien hand syndrome extrapyramidal symptoms after midbrain haemorrhage:
after anterior cerebral artery stroke. J Neurol Sci clinical and 18F-dopa PET evaluation. J Neurol Neurosurg
2014;338:203-206. Psychiatry 1994;57:987-989.
7. Shereef H, Cavanna AE. The “brother’s arm:” alien hand 16. Hirota N, Sakajiri K, Nitta E, et al. Hemiparkinsonism
syndrome after right posterior parietal lesion. J due to a solitary infarction of the right external segment
Neuropsychiatry Clin Neurosci 2013;25:E02. of the globus pallidus: a case report. Rinsho Shinkeigaku
8. Huang Y, Jia J. Corpus callosum hematoma secondary 2011;51:215-218.
to cerebral venous malformation presenting as alien hand 17. Pedroso JL, Godeiro-Junior C, Felício AC, et al. Multi-
syndrome. Neurocase 2013;19:377-381. lacunar strokes mimicking atypical parkinsonism with
9. Jang SH, Lee J, Yeo SS, et al. Callosal disconnection an unusual neuroimaging presentation: état criblé. Arq
syndrome after corpus callosum infarct: a diffusion tensor Neuropsiquiatr 2008;66:906-907.
2396 R. SURI ET AL.
18. Orta Daniel SJ, Ulises RO. Stroke of the substance nigra 41. Kim JS. Delayed onset mixed involuntary movements
and parkinsonism as first manifestation of systemic lupus after thalamic stroke: clinical, radiological and
erythematosus. Parkinsonism Relat Disord 2008;14:367-369. pathophysiological findings. Brain 2001;124(Pt 2):299-309.
19. Gonzalez-Alegre P. Monomelic parkinsonian tremor 42. Gille M, Van den Bergh P, Ghariani S, et al. Delayed-onset
caused by contralateral substantia nigra stroke. hemidystonia and chorea following contralateral infarction
Parkinsonism Relat Disord 2007;13:182-184. of the posterolateral thalamus. A case report. Acta Neurol
20. Ohta K, Obara K. Hemiparkinsonism with a discrete Belg 1996;96:307-311.
lacunar infarction in the contralateral substantia nigra. 43. Choi HY, Jung YJ, Shin HW. Multifocal dystonia as a
Mov Disord 2006;21:124-125. manifestation of acute midbrain infarction. J Neurol Sci
21. De la Fuente Fernandez R, López J, Rey del Corral P, 2015;356:217-218.
et al. Peduncular hallucinosis and right hemiparkinsonism 44. Franzini A, Messina G, Marras C, et al. Poststroke fixed
caused by left mesencephalic infarction. J Neurol dystonia of the foot relieved by chronic stimulation of
Neurosurg Psychiatry 1994;57:870. the posterior limb of the internal capsule. J Neurosurg
22. Kuo SH, Kenney C, Jankovic J. Bilateral pedunculopontine 2009;111:1216-1219.
nuclei strokes presenting as freezing of gait. Mov Disord 45. Burguera JA, Bataller L, Valero C. Action hand dystonia
2008;23:616-619. after cortical parietal infarction. Mov Disord 2001;16:1183-
23. Sibon I, Guyot M, Allard M, et al. Parkinsonism following 1185.
anterior choroidal artery stroke. Eur J Neurol 2004;11:283- 46. Kajimoto Y, Miwa H, Ueno M, et al. Sensorimotor
284. hemiparesis with secondary cervical dystonia following
24. Morgan JC, Sethi KD. Midbrain infarct with parkinsonism. lateral caudal medullary infarction without signs and
Neurology 2003;60:E10. symptoms of Wallenberg syndrome. J Neurol Sci
25. Fénelon G, Houéto JL. Unilateral parkinsonism following 2004;219:167-168.
a large infarct in the territory of the lenticulostriate arteries. 47. Tan EK, Chan LL, Auchus AP. Hemidystonia precipitated
Mov Disord 1997;12:1086-1090. by acute pontine infarct. J Neurol Sci 2005;234:109-111.
26. Kulisevsky J, Berthier ML, Avila A, et al. Unilateral 48. Marom T, Flaksman H, Ben-David N, et al. Isolated
parkinsonism and stereotyped movements following a myoclonus of the vocal folds. J Voice 2013;27:95-97.
right lenticular infarction. Mov Disord 1996;11:752-754. 49. Fabiani G, Teive HA, Sá D, et al. Palatal myoclonus: report
27. Friedman A, Kang UJ, Tatemichi TK, et al. A case of of two cases. Arq Neuropsiquiatr 2000;58(3B):901-904.
parkinsonism following striatal lacunar infarction. J Neurol 50. Inoa V, McCullough LD. Generalized myoclonus: a rare
Neurosurg Psychiatry 1986;49:1087-1088. manifestation of stroke. Neurohospitalist 2015;5:28-31.
28. Domingos J, Moreira B, Magalhaes M. Hemiparkinsonism 51. Alves PN, de Carvalho M, Peralta R, et al. Axial
secondary to a contralateral globus pallidus hemorrhagic myoclonus after ischemic stroke. Neurology 2015;85:654.
lesion [abstract]. Mov Disord 2012;27(Suppl 1):1141. 52. Jagota P, Bhidayasiri R. Lingual myoclonus secondary
29. Kim JS. Involuntary movements after anterior cerebral to bilateral cortical strokes in a probable case of
artery territory infarction. Stroke 2001;32:258-261. antiphospholipid syndrome. Mov Disord 2010;25:2000-
30. Navalpotro-Gomez I, Rodríguez-Campello A, 2002.
Vivanco-Hidalgo RM, et al. Progressive gait disorder and 53. Gomis M, Puente V, Pont-Sunyer C, et al. Adult onset
epilepsy secondary to venous stroke due to dural simple phonic tic. Mov Disord 2008;23:765-766.
arteriovenous fistula type III. Neurologia 2015;30:450-451. 54. Kim JS. Asterixis after unilateral stroke: lesion location
31. Li JY, Lai PH, Chen CY, et al. Postanoxic parkinsonism: of 30 patients. Neurology 2001;56:533-536.
clinical, radiologic, and pathologic correlation. Neurology 55. Lee SJ, Kim JS, Song IU, et al. Post stroke restless legs
2000;55:591-593. syndrome and lesion location: anatomical considerations.
32. Pedroso JL, Vale TC, Knobel M, et al. Clonic perseveration Mov Disord 2009;24:77-84.
after acute ischemic stroke: an insight into the 56. Han SH, Park KY, Youn YC, et al. Restless legs syndrome
pathophysiological mechanisms. J Stroke Cerebrovasc Dis and akathisia as manifestations of acute pontine infarction.
2016;25:e109-e110. J Clin Neurosci 2014;21:354-355.
33. Nguyen FN, Pauly RR, Okun MS, et al. Punding as a 57. Unrath A, Kassubek J. Symptomatic restless leg syndrome
complication of brain stem stroke? Report of a case. Stroke after lacunar stroke: a lesion study. Mov Disord
2007;38:1390-1392. 2006;21:2027-2028.
34. Yasuda Y, Akiguchi I, Ino M, et al. Paramedian thalamic 58. Sechi G, Agnetti V, Galistu P, et al. Restless legs syndrome
and midbrain infarcts associated with palilalia. Rinsho and periodic limb movements after ischemic stroke in
Shinkeigaku 1989;29:186-190. the right lenticulo striate region. Parkinsonism Relat
35. Pandey S, Sarma N. Stereotypy after acute thalamic Disord 2008;14:157-160. [Epub 2007 Apr 17].
infarct. JAMA Neurol 2015;72:1068. 59. Woo HG, Lee D, Hwang KJ, et al. Post stroke restless
36. Lee D, Lee D, Ahn TB. Stereotypy after cerebellar leg syndrome and periodic limb movements in sleep. Acta
infarction. J Neurol Sci 2014;344:227-228. Neurol Scand 2016;135:204-210.
37. Nishimura K, Uehara T, Toyoda K. Early-onset dystonia 60. Lee JS, Lee PH, Huh K. Periodic limb movements in sleep
after supplementary motor area infarction. J Stroke after a small deep subcortical infarct. Mov Disord
Cerebrovasc Dis 2014;23:1267-1268. 2005;20:260-261.
38. Waln O, Ledoux MS. Delayed-onset oromandibular 61. Kim JS, Lee SB, Park SK, et al. Periodic limb movement
dystonia after a cerebellar hemorrhagic stroke. during sleep developed after pontine lesion. Mov Disord
Parkinsonism Relat Disord 2010;16:623-625. 2003;18:1403-1405.
39. O’rourke K, O’riordan S, Gallagher J, et al. Paroxysmal 62. Jones HR Jr, Baker RA, Kott HS. Hypertensive putaminal
torticollis and blepharospasm following bilateral cerebellar hemorrhage presenting with hemichorea. Stroke
infarction. J Neurol 2006;253:1644-1645. 1985;16:130-131.
40. Zadro I, Brinar VV, Barun B, et al. Cervical dystonia due 63. Chung SJ, Im JH, Lee MC, et al. Hemichorea after stroke:
to cerebellar stroke. Mov Disord 2008;23:919-920. clinical-radiological correlation. J Neurol 2004;251:725-729.
POST-STROKE MOVEMENT DISORDERS 2397
64. Saris S. Chorea caused by caudate infarction. Arch Neurol 75. Rieder CR, Rebouças RG, Ferreira MP. Tremor
1983;40:590-591. in association with bilateral hypertrophic olivary
65. Miwa H, Hatori K, Kondo T, et al. Thalamic tremor: case degeneration and palatal tremor: chronological
reports and implications of the tremor-generating considerations. Case report. Arq Neuropsiquiatr 2003;
mechanism. Neurology 1996;46:75-79. 61(2B):473-477.
66. Kim JS, Lee MC. Writing tremor after discrete cortical 76. Mehanna R, Jankovic J. Movement disorders in
infarction. Stroke 1994;25:2280-2282. cerebrovascular disease. Lancet Neurol 2013;12:597-608.
67. Kim JS. Delayed onset hand tremor caused by cerebral 77. Fornito A, Zalesky A, Breakspear M. The connectomics
infarction. Stroke 1992;23:292-294. of brain disorders. Nat Rev Neurosci 2015;16:159-172.
68. Miyagi Y, Shima F, Ishido K, et al. Posteroventral 78. Holtbernd F, Eidelberg D. Functional brain networks in
pallidotomy for midbrain tremor after a pontine movement disorders: recent advances. Curr Opin Neurol
hemorrhage. Case report. J Neurosurg 1999;91:885-888. 2012;25:392-401.
69. Shepherd GM, Tauböll E, Bakke SJ, et al. Midbrain tremor 79. Scott BL, Jankovic J. Delayed-onset progressive movement
and hypertrophic olivary degeneration after pontine disorders after static brain lesions. Neurology 1996;46:68-
hemorrhage. Mov Disord 1997;12:432-437. 74.
70. Dethy S, Luxen A, Bidaut LM, et al. Hemibody tremor 80. Rice JE 3rd, Vannucci RC, Brierley JB. The influence of
related to stroke. Stroke 1993;24:2094-2096. immaturity on hypoxic-ischemic brain damage in the rat.
71. Cosentino C, Velez M, Nuñez Y, et al. Bilateral Ann Neurol 1981;9:131-141.
hypertrophic olivary degeneration and Holmes tremor 81. Hosp JA, Luft AR. Cortical plasticity during motor
without palatal tremor: an unusual association. Tremor learning and recovery after ischemic stroke. Neural Plast
Other Hyperkinet Mov (N Y) 2016;6:40. 2011;2011:871296.
72. Paviolo JP, Raina GB, Conti E, et al. Writing tremor 82. Ohye C, Shibazaki T, Hirai T, et al. Plastic change of
secondary to ischemic stroke: a report on a case with a thalamic organization in patients with tremor after stroke.
remarkable response to topiramate. Clin Neuropharmacol Appl Neurophysiol 1985;48:288-292.
2015;38:57-59. 83. Ohara S, Lenz FA. Reorganization of somatic sensory
73. Martins WA, Marrone LC, Fussiger H, et al. Holmes’ function in the human thalamus after stroke. Ann Neurol
tremor as a delayed complication of thalamic stroke. J 2001;50:800-803.
Clin Neurosci 2016;26:158-159. 84. Andersen KK, Olsen TS, Dehlendorff C Kammersgaard
74. Raina GB, Cersosimo MG, Folgar SS, et al. Holmes tremor: LP. Hemorrhagic and ischemic strokes compared: stroke
clinical description, lesion localization, and treatment in severity, mortality, and risk factors. Stroke 2009;40:2068-
a series of 29 cases. Neurology 2016;86:931-938. 2072.

You might also like