Samra et al.

The Egyptian Journal of Neurology,

Egypt J Neurol Psychiatry Neurosurg (2025) 61:11
[Link] Psychiatry and Neurosurgery

RESEARCH Open Access

Frequency, phenotypes, and neuroimaging

of early post stroke movement disorders:
a prospective study
Eslam Samra1, Tamer Roushdy2, Amr S. Zaki2, Alia H. Mansour2, Ahmed Elbassiouny2 and Ali Shalash2*   

Abstract
Background A prospective observational study recruited patients with acute stroke. Patients were assessed
for the presence of post-stroke movement disorders PSMDs during the first week of stroke. This study aimed to iden-
tify the frequency, clinical characteristics, and neuroimaging of early PSMDs (within the first week) and followed
for 1 year.
Results A total of 600 patients were recruited; 21 patients (3.5%) with PSMDs were detected. Thirteen (2.2%) patients
presented with intention tremor/ataxia and eight (1.3%) presented with other movement disorders (most commonly,
chorea and tremor). One patient presented with periodic left upper limb shaking with right subcortical water-
shed infarction, and one patient developed palatal myoclonus with right middle cerebral artery infarction. Patients
with PSMDs had significantly lower stroke severity (NIHSS) and were more likely to have lacunar strokes (p < 0.001
and < 0.006, respectively) than patients without PSMDs. Early PSMDs were more associated with posterior circulation
strokes (84.25%).
Conclusions Early PSMDs are commonly hyperkinetic, more associated with small vessel disease, and less severe
and posterior circulation strokes, implying their clinical importance for the proper management of stroke patients.
Keywords Stroke, Movement disorders, Chorea, Tremors, MRI

Background concerning stroke, variable phenotypes, and potential

According to the estimates, 1–4% of stroke patients will response to treatment [3, 4]. Although they are uncom-
experience post-stroke movement disorders (PSMDs), mon, PSMDs might help in localizing the stroke site,
with the basal ganglia, thalamus, and cerebellum being determining its etiology, and increasing patients’ disabil-
the most affected areas. Following either an ischemic or ity that requires specific treatment [5].
hemorrhagic stroke, both hyperkinetic and hypokinetic PSMDs occur after strokes that affect the basal gan-
PSMDs have been observed with different latencies [1, 2]. glia, thalamus, or the networks that connect them,
PSMDs were reported as the most common second- either immediately or after months to years [6]. While
ary movement disorders (22.3%), with variable onset some PSMDs, such as dystonia and tremor, can develop
months to years after a stroke, others, such as hemibal-
lism, occur early and can get better or even go away
*Correspondence:
within a few weeks. Moreover, PSMDs were reported
Ali Shalash
Ali_neuro@[Link] as presenting symptoms of stroke that mandate urgent
1
Department of Neurology, Faculty of Medicine Kafr El-Sheikh University, thrombolytic therapy or thrombectomy [7, 8].
Elgeish St., Kafr El‑Sheikh, Egypt
2 Therefore, clinicians should consider and recognize
Department of Neurology, Faculty of Medicine, Ain Shams University,
Cairo, Egypt early PSMDs to localize lesions, determine the underly-
ing etiology, and provide early and appropriate therapies.

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Samra et al. Egypt J Neurol Psychiatry Neurosurg (2025) 61:11 Page 2 of 10

Previous retrospective studies reported the prevalence Within the current study, an operational definition for
of PSMDs through patient registries and described their PSMDs was movement disorders that can occur immedi-
phenotypes and associated imaging [1, 9]. Moreover, lim- ately at the onset of the acute stroke and even be part of
ited data about the frequency and clinical characteristics the acute stroke presentation [1] and manifests because
of early PSMDs are available, which were obtained from of a vascular lesion encountered along any motor-provid-
previous studies and case series with few prospective ing area within the brain or because of a vascular lesion
studies, implying the need for further studies [6, 9–11]. along a motor circuitry [13]. Different types of trem-
Therefore, this prospective study aimed to investigate ors including Holmes and palatal tremors were defined
the frequency, clinical phenotypes, and neuroimaging according to experts’ consensus. For example, Holmes
of early PSMDs in patients with acute stroke (within the tremor is characterized by proximal and distal rest, pos-
first week). tural, and intention tremor of low frequency (< 5 Hz)
[14]. Other hyperkinetic MDs were defined according to
their diagnostic criteria and defined clinical characteris-
Methods tics. Hemichorea was identified as involuntary, irregular,
In this prospective observational study, all patients with non-stereotyped, and non-patterned involuntary move-
acute stroke were recruited for a 1-year duration. Acute ment involving one side of the body [15].
stroke was defined as the rapid development of signs of Patients with PSMDs were assessed using the Montreal
focal or global disturbance of cerebral function, lasting Cognitive Assessment (MoCA) for cognitive function
over 24 h or leading to death [12]. [4, 16, 17] and the Beck Depression Inventory (BDI) for
Patients who had an acute ischemic or hemorrhagic depression [4, 16, 17].
stroke, of either sex and who were ≥ 18 years were Furthermore, tremors were evaluated with the Fahn–
included after reviewing the case histories. Patients with Tolosa–Marín tremor rating scale [18], chorea was eval-
PSMDs during the first week of stroke were examined uated by the Abnormal Involuntary Movement Scale
and videotaped by a trained neurologist, and then vid- (AIMS) [19], ataxia was assessed by the Scale for the
eos were revised by two movement disorders experts to Assessment and Rating of Ataxia (SARA) [20], and dys-
confirm phenomenology, which included the description tonia was evaluated using the Fahn–Marsden–Dystonia
and classification of the PSMDs. We selected the first Rating Scale [21]. Patients with early PSMDs were fol-
week in an attempt to demonstrate that PSMDs might be lowed for 1 year to detect their prognosis.
the onset of stroke symptoms rather than their afteref- Statistical analysis was performed by SPSS for Windows
fects. Exclusion criteria included a history of any abnor- (Statistical Package for the Social Sciences) (standard
mal movements before the patient’s stroke, participation version 26). The one-sample Kolmogorov‒Smirnov test
in other pharmacological or rehabilitation intervention was used to initially check for data normality. Quantita-
studies that can confound the results of this study, and tive and percentage descriptions were used for qualita-
Patients with other possible causes of MDs, such as sys- tive information. The chi-square test was used for testing
temic disease or drugs that might underlie recent move- associations between categorical variables; Fisher’s exact
ment disorders. test and the Monte Carlo test were used for testing cell
All patients were subjected to complete clinical assess- counts below 5. For properly distributed data, the mean
ment by a trained neurologist, scoring with the National and standard deviation (SD) were used, and for nonnor-
Institutes of Health Stroke Scale (NIHSS), and full stroke mally distributed data, the median (Min–Max) was used.
protocol investigations including laboratory workup, Independent t tests (parametric) and Mann‒Whitney U
electrocardiogram, echocardiography, carotid duplex, tests were used to compare the two sets of data (nonpara-
and non-contrast brain computed tomography (CT) or metric). P < 0.05 was considered statistically significant.
magnetic resonance imaging (MRI) (stroke protocol; T1 The sample size was calculated using the Epi-info soft-
weighted image (WI), T2WI, FLAIR, WI, T2*, diffusion- ware statistical package. The criteria used for the calcula-
weighted image). Patients with acute stroke were fol- tion are as follows: 95% confidence limit, 80% power of
lowed for 1 week to evaluate PSMDs occurrence. the study, a precision of 2%, and an expected post-stroke
The rationale for using specific neuroimaging protocols movement disorders percentage of 3.7%. A sample size
was to help detect lesion location and correlate with the based on the previously mentioned criteria was to be a
clinical phenomenology of PSMDs. For example, lesions total of 343 stroke cases. To compensate for a possible
to the nigrostriatal tract can cause hemi parkinsonism dropout, 20% were added to the total sample size to reach
contralateral to the lesion, and lesions involving the sub- 412 patients.
thalamic nucleus can cause contralateral hemichorea– To minimize selection bias, all patients presenting with
hemiballism [51]. acute stroke to our facility over 1 year were consecutively
Samra et al. Egypt J Neurol Psychiatry Neurosurg (2025) 61:11 Page 3 of 10

recruited, resulting in 600 participants being included in Most patients with PSMDs had infarctions along the
the study. distribution of posterior circulation (vertebrobasilar
To address potential attrition bias, several proac- system) (16 patients, 84.25%), while 3 patients (15.75%)
tive measures were implemented throughout the study had infarctions related to the anterior circulation. Most
to minimize the loss of participants during the follow- patients with PSMDs had lacunar infarctions/small ves-
up period and mitigate its impact on the findings. All sel disease, except one patient who presented with pala-
patients diagnosed with PSMDs during the first week tal myoclonus had a territorial middle cerebral artery
were closely monitored for 1 year, with scheduled fol- infarction.
low-up visits to track their prognosis. Detailed contact The most common site of infarction was along the
information was collected during recruitment, enabling right cerebellum (4 patients, 20%) with right ataxia, fol-
effective communication with participants throughout lowed by right pontine infarction (2 patients, 10%) with
the study. Regular reminders were provided to partici- left ataxia. Chorea was related to caudate and putami-
pants through phone calls and text messages, ensuring nal lesions (Table 2). Out of 60 patients with basal gan-
they remained engaged with the study and attended their glia strokes (39 infarctions and 21 hemorrhages), only
scheduled assessments. 3 patients with infarction developed PSMDs (5%). Four
patients (4.4%) with brainstem strokes developed PSMDs
Results (3 patients with intention tremor/ataxia and 1 patient
Frequency and characteristics of early PSMDs with Holmes tremor) out of 91 cases.
Of 600 patients with acute stroke (510 patients with In the PSMDs group, there were five patients with
ischemic stroke (85%) and 90 patients with hemorrhagic mild depression (23.8%), three with moderate depression
stroke (intracerebral hemorrhage) (15%)), 21 patients (14.3%), seven with severe depression (33.3%), three with
(3.5%) with PSMDs were detected. Thirteen (2.2%) very severe depression (14.3%), and one patient without
patients presented with intention tremor/ataxia (Sup- depression (4.8%). Moreover, 18 patients with PSMDs
plementary Table 1) and 8 (1.3%) presented with other showed cognitive impairment (85.7%, MOCA < 26)
PSMDs (Table 1). (Table 1, Supplementary Table 1).
Of patients with other PSMDs, 3 patients had trem-
ors (2 patients had unilateral tremors and one patient Short‑ and long‑term prognosis of PSMDs
had bilateral tremors, while one of them was associated Four patients (19%) in the PSMDs group had missed fol-
with dystonia), 3 patients had hemichorea (left), and one low-ups, and five patients (23.8%) died during the year.
patient had palatal myoclonus. Intention tremor/ataxia, Within the first week, 8 patients with intention tremor/
hemichorea, and limb shaking occurred with stroke onset ataxia (61.5%) showed partial improvement. Out of the
(first day), while the mean latency of other tremors was 3 patients who had tremors; 2 (66.7%) did not improve,
6 days. The mean latency of chorea was 4 days (range: and 1 (33.3%) died. Two patients with hemichorea
1–7 days), while palatal myoclonus occurred on the sec- improved on risperidone 2 mg/day, while a patient was
ond day of stroke onset. Table 1 shows the clinical char- lost to follow-up. The patient with periodic limb shak-
acteristics of stroke patients with PSMDs. ing improved with maintaining average normal blood
Imaging clinical correlation analysis is challenging due pressure, while the patient with the palatal myoclonus
to clinical and neuroimaging heterogeneity. PSMDs were showed resolution.
traditionally thought to be caused by lesions in specific Six patients with intention tremor/ataxia showed par-
anatomical brain structures, more recent evidence has tial improvement after a year of follow-up; four of them
shown that this is often not true [52]. Similar clinical responded well to low doses of propranolol 40mg/day,
phenotypes are seen with lesions in heterogeneous ana- two of them improved without therapy, three patients
tomical locations, and clinical heterogeneity is seen with did not improve, three patients died, and one patient
lesions affecting the same anatomical structures [4]. For lost follow-up. Out of the 3 patients who had tremors;
example, only a minority of patients with hemichorea– one patient improved without treatment, one patient
hemiballism have lesions in the subthalamic nucleus, and died, and one patient lost follow-up. One patient with
lesions in the globus pallidus have led to multiple abnor- hemichorea improved on risperidone 2 mg/day, one
mal movements [52]. It has been estimated that lesion patient was lost to follow-up and one patient died. The
locations considered atypical can occur in approximately patient with palatal myoclonus experienced focal and
half of PSMD cases [4], but these estimates are based on generalized fits that were managed with levetiracetam
limited data, which can include diagnostic and reporting 2gm daily, while the patient with periodic limb shaking
biases. lost follow-up (Table 1, Supplementary Table 1).
Table 1 Demographics and characteristics of patients with post-stroke hyperkinetic movement disorders
n Age Sex Risk factors Stroke Stroke type NIHSS Movement Latency Follow-up after MOCA BDI FTM AIMS Infarction site
presentation disorder 1 year (severity)
presentation

1 65 F HTN, AF Lt hemiparesis CE 3 Palatal myo- 2nd day Patient devel- 22 10 Mild – – Rt middle cerebral
clonus oped further territorial (frontal
attacks of focal and parietal)
and general-
ized seizures,
that were
controlled
by Levetiracetam
Samra et al. Egypt J Neurol Psychiatry Neurosurg

2000 mg/day
2* 63 M HTN, 80% Lt Lt hemiparesis SVD – Episodes of Lt First day NA – – – Lt periventricular
carotid stenosis upper limb
by CT angiog- transient shaking:
raphy with distal course
tremors, followed
(2025) 61:11

by Lt hemiparesis
on the next day
3* 65 F HTN Lt hemiparesis Haemorrhage – Lt hemichorea Seventh day Died 14 32 Severe – 27 Rt microbleeds
after 10 months in basal ganglia
from stroke onset
4* 66 F HTN Lt hemiparesis SVD – Lt hemichorea First day NA – – - – Rt caudate
5 77 F HTN, IHD Lt hemiparesis SVD 11 Lt hemichorea Second day Improved on ris- 10 33 Severe – 19 Rt basal ganglia
peridone 2 mg/
day with no side
effect
6 64 F DM, HTN Lt hemiparesis SVD 3 Postural tremors Fifth day Improved with- 18 14 Mild 11% mild – Rt periventricular
in both upper out therapy
limbs
7 73 M DM, HTN, Previ- Lt hemiparesis SVD 6 Rt upper Fifth day Not improved 19 17 Moderate 51% marked – Rt pontine
ous Stroke limb postural
and kinetic
tremors (Holmes
tremor) and dys-
tonic posture
8 70 M HTN, Previous Rt hemiparesis SVD 6 Rt upper Sixth day Died 5 22 Moderate 53% marked – Lt thalamic
Stroke limb postural after 2 months
and kinetic from stroke onset
tremors
CE cardioembolic stroke, M male, F female, IHD ischemic heart disease, HTN hypertension, DM: diabetes, NIHSS national institutes of health stroke scale, LAA large artery atherosclerosis, MOCA Montreal cognitive
assessment, BDI Beck depression inventory, FTM Fahn–Tolosa–Marin tremor rating scale, AIMS acute involuntary movement scale, SVD small vessel disease, Rt right, Lt left, NA not applicable, dropped from follow-up
Page 4 of 10
Samra et al. Egypt J Neurol Psychiatry Neurosurg (2025) 61:11 Page 5 of 10

Table 2 MRI characteristics of stroke patients with movement associated with lacunar and posterior circulation strokes.
disorders In addition, this study described comprehensively the
Stroke patients with Site of infarction n (%) phenotypic, prognosis, and localization of early PSMDs.
Movement disorders Our results are consistent with data from the Lausanne
n = 21 (3.5%) stroke registry, which reported an uncommon prevalence
Ataxia (n = 13, 61.9%) of PSMDs (1.16%, 29/2500) in acute stroke [1]. Another
Rt ataxia (n = 9) Rt cerebellar 4 (19) study showed a higher prevalence, but it included
Lt periventricular and internal 1 (4.8) patients with PSMDs for up to 1 year [2]. However, the
capsule frequency of reported PSMDs with short latency is com-
Cerebellar and brainstem 1 (4.8) parable to the current study.
Lt parathalamic infarction 1 (4.8) In the current study, an operational definition was
Rt pontine infarction 1 (4.8) given to diagnose PSMDs based on the clinical appear-
Lt thalamic hematoma 1 (4.8) ance of any form of involuntary movement in a patient
Lt ataxia (n = 4) Rt pontine infarction 2 (9.5) diagnosed with vascular stroke within 1 week to reflect
Rt parathalamic infarction 1 (4.8) the acute and associated link between the two disorders.
Lt cerebellar infarction 1 (4.8) However, currently, there are no criteria for the diagno-
Tremors (n = 3, 14.3%) sis of PSMDs [22]. Clinically, the majority of practitioners
Rt upper limb tremor (n = 2) Rt pontine 2 (9.5) consider the onset of a movement disorder within a day
Lt thalamic infarction of the stroke as either extremely or very useful for mak-
Tremor in both limbs (n = 1) Rt parietal infarction 1 (4.8) ing the diagnosis of PSMDs. However, this view may limit
Others (n = 5, 23.8%) the diagnosis of PSMDs, which can emerge several days
Lt hemi chorea (n = 3) Rt putaminal microbleeding 1 (4.8) to even months after a stroke (e.g., dystonia). The value of
Rt caudate infarction 1 (4.8) stability over time in the diagnosis of PSMDs is also dif-
Rt putaminal infarction 1 (4.8) ficult to interpret, as it depends on the phenomenology
Lt upper limb shaking (n = 1) Rt periventricular infarction 1 (4.8) and differential diagnoses [2].
Palatal myoclonus (n = 1) Rt parietal infarction 1 (4.8) The time course for the development of movement
Rt right, Lt left
disorders varies considerably from the day of the onset
of stroke to several years later and it also depends on
the type of movement disorder. Chorea appears earlier
Comparing stroke patients with and without PSMDs (mean 4.3 day post-stroke), while parkinsonism much
In our study, we divided the groups of stroke patients into later (mean 117.5 day post-stroke) which explains limited
a group that had movement disorders and a group that patients with vascular parkinsonism in this study [2].
did not have movement disorders. The patients with and The main focus of the studies and reports on PSMDs
without PSMDs showed similar mean age, sex, and vas- has been the correlation between the localization of the
cular risk factors. Patients with PSMDs had significantly stroke and phenomenology. Despite the lack of large
lower stroke severity (NIHSS) and were more likely to studies, one clear conclusion is that there is a poor cor-
have lacunar strokes (p < 0.001 and < 0.006, respectively) relation between stroke localization and phenomenol-
than patients without PSMDs (Table 3). ogy. Although stroke in certain regions, particularly
The effect size of the age was negatively low (Cohen’s subcortical nuclei, appears to be more often associated
d =− 0.10). The odds ratios of small vessel disease and with PSMDs, the association between stroke localiza-
hypertension were 2.96 and 1.51, respectively (Table 3). tion and phenomenology is often less than 30%. [1, 2,
In addition, both groups showed no significant differ- 4]. Recent research has shown that lesions in heteroge-
ences in cardiac and laboratory investigations except neous locations causing MDs may express as a manifes-
higher serum triglycerides among patients with MDs tation of a network disorder by impairing certain brain
(p = 0.003) (Supplementary Table 2). circuits rather than any single anatomical region [53,
54]. However, despite the growing acceptance of the
role of brain circuits over individual anatomical struc-
Discussion tures, the value and therapeutic implications of the
The current prospective study detected that early circuit-based approach in clinical practice remain to
PSMDs, within the first week, accounted for 3.5% of be validated. The use of advanced MRI sequences (dif-
stroke patients, including 2.2% with intention tremor/ fusion tensor imaging and functional MRI) in patients
ataxia and 1.3% with other PSMDs (most commonly, with PSMD is needed to further clarify the structural
tremors and hemichorea). Early PSMDs were mostly damage to white matter tracts and identify functional
Samra et al. Egypt J Neurol Psychiatry Neurosurg (2025) 61:11 Page 6 of 10

Table 3 Demographics and characteristics of stroke patients with and without movement disorders
Patients’ characteristics Total (n = 600) Stroke patients with Stroke patients without P value Effect size
movement disorders movement disorders
(n = 21, 3.5%) (n = 579, 96.5%)

Age (years) Mean ± SD 65.57 ± 9.90 64.61 ± 10.14 65.61 ± 9.89 0.652 Cohen’s d = − 0.10
95% CI 64.78–66.36 59.99–69.23 64.80–66.42
Sex
Male n (%) 340 (56.7%) 12 (57.1%) 328 (56.6%) 0.964 OR = 1.00
95% CI 20.2–70.4 34.3–78.2 50.2–60.4
Female n (%) 260 (43.3%) 9 (42.9%) 251 (43.4%) OR = 0.98
95% CI 40.3–50.6 21.4–65.7 30.3–40.8
Medical history
None n (%) 42 (7.0%) 0 (0%) 42 (7.3%) 0.178 –
95% CI 50.3–90.4 0 50.4–90.6
Hypertension, n (%) 444 (74.0%) 17 (81.0%) 427 (73.7%) 0.460 OR = 1.51
95% CI 70.3–80.2 50.5–90.7 60.2–70.4
DM n (%) 294 (49.0%) 7 (33.3%) 287 (49.6%) 0.144 OR = 0.51
95% CI 40.2–50.3 10.2–50.2 45.1–53.2
IHD n (%) 53 (8.8%) 1 (4.8%) 52 (9.0%) 0.503 OR = 0.51
95% CI 1.1–11.3 10.1–23.8 1.2–11.4
Smokers n (%) 63 (10.5%) 1 (4.8%) 62 (10.7%) 0.383 OR = 0.42
95% CI 8.1–13.2 10.1–23.8 8.3–13.5
Recurrent stroke n (%) 14 (2.3%) 0 (0%) 14 (2.4%) 0.493 –
95% CI 10.2–13.3 0 10.2–14.3
AF n (%) 33 (5.5%) 1 (4.8%) 32 (5.5%) 0.809 OR = 0.85
95% CI 30.2–70.3 10.1–23.8 38.1–77.1
Presentation
LSW n (%) 436 (72.7%) 15 (71.4%) 421 (72.7%) 0.897 OR = 0.98
95% CI 60.9–76.2 47.8–88.7 68.8–76.3
RSW n (%) 248 (41.3%) 6 (28.6%) 242 (41.8%) 0.227 OR = 0.56
95% CI 37.3–45.3 11.2–52.8 37.7–45.9
Dysarthria n (%) 25 (4.2%) 0 (0%) 25 (4.3%) 0.331 –
95% CI 20.7–60.9 0 20.8–60.3
NIHSS Median (IQR) 7 (4–10) 4.5 (3–6) 7 (5–10) 0.001 Cohen’s d = 0.50
Stroke type by TOAST classification
Large artery atherosclerosis n (%) 186 (32.1%) 6 (28.6%) 180 (36.7%) 0.731 OR = 0.85
95% CI 27.3–34.8 11.2–52.2 27.3–35.2
Small vessel disease n (%) 168 (29.0%) 12 (57.1%) 156 (31.8%) 0.006 OR = 2.96
(lacunar) 95% CI 24.4–31.7 34.1–78.2 23.3–30.7
Cardioembolic n (%) 77 (13.3%) 1 (4.8%) 76 (15.5%) 0.253 OR = 0.28
95% CI 10.2–15.7 10.1–23.8 10.4–16.2
Unclassified n (%) 79 (13.6%) 0 (0%) 79 (16.1%) 0.069 –
95% CI 10.5–16.2 0 10.9–16.7
DM Diabetes Mellitus, IHD Ischemic Heart Disease, AF Atrial Fibrillation, LSW Left-sided Weakness, RSW Right-sided Weakness; NIHSS National Institutes of Health
Stroke Scale, TOAST Trial of Org 10172 in Acute Stroke Treatment, CI confidence interval; OR Odds ratio

abnormalities caused by the lesion. Most of the neu- versus rare lesion locations, acute versus delayed phe-
roimaging data for PSMDs come from case reports nomena, and single versus multiple lesions [53].
or case series, and there are only a limited number of The types of PSMDs in our study are consistent with
case–control or prospective studies systematically previous reports. Chorea and tremors are common and
investigating PSMDs. This can lead to bias regarding usually have short latency. Parkinsonism could not be
common versus uncommon stroke locations, classic detected, which could be explained by its usual long
Samra et al. Egypt J Neurol Psychiatry Neurosurg (2025) 61:11 Page 7 of 10

latency after stroke. Dystonia was reported in one patient precentral gyrus infarctions without brainstem lesions,
only, which could be explained by its common occur- which were attributed to associated epileptogenic activ-
rence in younger patients and its long latency [1, 23]. ity [28, 29]. Moreover, palatal tremor was reported as a
Hemichorea is characterized by a range of involuntary presenting symptom of Epilepsia partialis continua sec-
movements involving one side of the body, is the most ondary to cortical lesions, particularly the operculum
frequent post-stroke hyperkinetic movement disorder, [30, 31]. On the other hand, few cases were reported
and always emerges as an acute manifestation. Previous secondary to cortical infarction without evidence of
reports suggest that the most common subtype of stroke epileptogenic etiology, suggesting another mechanism,
leading to hemichorea is cerebral small vessel disease such as diaschisis or disruption of corticobulbar fibers
with small deep infarcts in the contralateral subthalamic secondary to ischemia [32, 33]. Interestingly, one of our
nucleus or adjacent structures [7]. patients with early PSMDs presented with a transient
All patients with hemichorea had contralateral palatal–lingual tremor that occurred on the second day
ischemic and hemorrhagic strokes of the basal ganglia, of right frontoparietal infarction and developed seizures
similar to previous reports [24]. Consistently, lentiform on follow-up with an abnormal electroencephalogram,
was the most frequently reported site for hemichorea, implying the underlying epileptogenic etiology and the
followed by other sites, such as the thalamus, subtha- importance of close follow-up of those patients.
lamic nucleus, and cortical regions [4, 24]. Hemichorea Limb shaking is one of the reported PSMDs with tran-
appears to occur within a few days after stroke, whereas sient ischemic attacks and acute strokes. It has been
hemiballismus is typically seen to start promptly with described as brief trembling, jerky involuntary movement
the onset of stroke [24]. Similar to our reported patients, of any limb and is related to the impaired hemodynamic
hemichorea might be the presenting or the only symp- state of the brain [4, 22]. MRI brain might be normal or
tom of acute stroke that mandates urgent intervention by associated with watershed ischemia [1]. Its identifica-
thrombolysis or thrombectomy if patients present in the tion is of clinical significance, as it is usually associated
appropriate window [7, 8]. with significant carotid stenosis and heralding disabling
Holmes tremor is an irregular resting, kinetic, or pos- stroke, which could be prevented by medications and
tural tremor with a frequency below 4.5 Hz. It is caused carotid stenting [4, 22]. Moreover, differentiating it from
by a combined disruption of dopaminergic nigrostriatal, seizures is essential to avoid misdiagnosis [22, 34]. In our
and cerebello-rubro-thalamic tracts. Apart from inten- cohort, we identified one case that presented with left
tion tremors, patients with post-stroke postural and limb shaking and left hemiparesis, with significant (80%)
Holmes tremors were detected. [25] Similarly, previous carotid stenosis confirmed by CT angiography. This is
reports described postural tremors as the most common consistent with previously published cases individually
type, usually associated with thalamic and brainstem or within cohorts, confirming the clinical implications
strokes, disrupting cerebello-thalamo-striatal circuits of proper neurovascular assessment and management [1,
[4]. The low number of detected patients with post- 34].
stroke tremors is attributed to their long latency from Previous cohorts of PSMDs did not include patients
stroke onset; however, the early occurrence of tremors with intentional tremors associated with ataxia. This may
with acute stroke has been reported [1, 4]. Stroke was be related to the lack of clear definitions and diagnostic
the most commonly reported cause of Holmes tremor criteria for PSMDs [13]. We included those patients who
[13, 16, 17]. Interestingly, we detected the occurrence represented 2.2% of PSMDs, according to the MDS Con-
of Holmes tremor in the first week of stroke after pon- sensus Statement on the classification of tremors, which
tine infarction, although it is usually reported as delayed included cerebellar tremors (tremors with prominent
onset. Holmes tremor might improve by levodopa while additional signs) similar to Holmes and palatal tremors
responding significantly to ventral intermediate nucleus [14]. This frequency is consistent with the low frequency
thalamotomy or thalamic DBS [4, 17]. of cerebellar ischemic strokes, which account for 2–3%
Stroke is the most common cause of symptomatic of all ischemic strokes [35]. Expectedly, intention tremor
palatal tremor (myoclonus), which is usually associated was associated with posterior circulation strokes, which
with cerebellar and brainstem infarctions and occurs 1 were reported to cause limb ataxia in 76.1% of patients
week to 49 months after lesion onset [26, 27]. Less com- [36].
monly, symptomatic palatal tremor has been reported in The current literature on treatment for PSMD is largely
association with cortical ischemia, which was explained based on anecdotal evidence without controlled clinical
by associated epileptic activity, disruption of cortico- trials to support current treatment practices. The lack of
olivary fibers, or diaschisis. Few cases of palatal tremor treatment evidence-based guidelines drives practitioners
were reported secondary to left frontoparietal and left to translate treatment options from other conditions with
Samra et al. Egypt J Neurol Psychiatry Neurosurg (2025) 61:11 Page 8 of 10

different pathophysiologies that share the same phenom- versus atypical lesion locations, acute versus delayed phe-
enology with the PSMDs [22]. nomena, and single versus multiple lesions [13]. It has
Management of some of the PSMDs was achieved with been observed that there is no definite relation between
atypical antipsychotics, beta-blockers, or antiepilep- the type of involuntary movement and the site of infarc-
tics; meanwhile, some patients improved spontaneously. tion, which has been attributed to poor resolution of
Unfortunately, there are no guidelines for the manage- the imaging and poor localization of lesions. Moreover,
ment of PSMDs available at the moment due to the lim- functional diaschisis might have played a role as well as
ited number of patients in different studies. the involvement of lesions within a functional motor
After a year of follow-up, six patients with intention circuitry rather than a specific anatomical lesion which
tremor/ataxia showed improvement, and four of them requires further studies assessing neuroimaging through
showed partial response to low doses of propranolol in tractography and functional studies [44].
line with Duhigg and colleagues’ findings regarding the Depression and cognitive impairment are commonly
effects of propranolol in patients with ataxia, which is associated with stroke, increasing the patients’ disability
intriguing considering the possible shared cerebellar ori- and impairing their quality of life [23, 45, 46]. The preva-
gins of these diseases. A few clinical papers reported that lence rates of post-stroke depression are estimated to
propranolol temporarily alleviated ataxia [37]. range between 30 and 40% in the initial few months [47].
The current study confirmed that lacunar strokes/ In addition, post-stroke cognitive impairment is most
small vessel disease is the common underlying stroke common in the first year after stroke, occurring in up to
type of PSMDs (57.1%), followed by large artery athero- 60% (cumulative incidence) of stroke survivors, with the
sclerosis, which involves posterior circulation and basal highest rate seen shortly after stroke [46, 48]. Remark-
ganglia, thalamus, and cerebellar connections, inconsist- ably, the current study showed their high association in
ency with previous cohorts. Small vessel disease repre- patients with PSMDs, which has an important implica-
sented approximately two-thirds of strokes with early and tion for patient management. This association could be
delayed PSMDs according to hospital stroke registries [1, attributed to lesions in strategic areas, including the basal
9]. Small vessel disease leads to hypoperfusion and con- ganglia, thalamus, and cerebellum, and disruption of
sequent disruption of basal ganglia–thalamic–cerebellar their connections, resulting in different PSMDs, in addi-
circuits, which could be linked to various forms of hyper- tion to depression and cognitive impairment [26, 39, 49,
kinetic PSMDs [38, 39]. The low incidence of PSMDs 50].
among patients with basal ganglia stroke might be related The current study has some strengths as well as limi-
to stroke severity, individual susceptibility, and variable tations. Limitations include the drop-out of patients
brain plasticity [38]. with PSMDs for longer follow-ups, lack of anatomi-
In this study, stroke severity was significantly lower in cal and clinical correlation, heterogeneity in the choice
patients with PSMDs. Similarly, patients with ataxia had of neuroimaging modality (CT vs. MRI), and report-
lower stroke severity [40]. This could be explained by the ing bias regarding classic and atypical lesion locations.
common association of PSMDs with lacunar strokes and Strengths include the prospective design of the study and
small vessel disease. Moreover, major strokes are usu- the recruitment of a large number of patients with acute
ally associated with disturbed consciousness and severe stroke among a different population. Reaching an agree-
weakness. In addition, the NIHSS does not include scor- ment on the definition of PSMDs and creating consensus
ing for all manifestations of posterior circulation strokes, standards.
including movement disorders.[41] In addition, this study A systematic review of the available data, the creation
revealed that patients with PSMDs had higher serum tri- of a PSMDs rating scale to track response, prospective
glycerides, which could be attributed to the commonly large-scale data that features comprehensive details on
associated small vessel disease [42]. Triglycerides, rather treatments and treatment response, and multi-centric
than other lipid fractions, have been correlated with studies to evaluate treatment response are all appropriate
small vessel disease in older persons [43]. Interestingly, implications for the future research outlook.
other factors, including age, sex, risk factors, and stroke
recurrence, were not different among patients with
PSMDs in this study. Conclusion
Most of the neuroimaging data for PSMDs come from Early PSMDs are commonly hyperkinetic, especially
case reports or case series, and there are only a limited tremors and chorea, more associated with small ves-
number of case–control or prospective studies systemati- sel disease, less severe, and poster circulation strokes.
cally investigating PSMDs. This can lead to bias regard- Although early PSMDs are uncommon, their early
ing common versus uncommon stroke locations, classic identification might have an essential role in the
Samra et al. Egypt J Neurol Psychiatry Neurosurg (2025) 61:11 Page 9 of 10

localization of stroke lesions, diagnosis of hyperacute Received: 16 August 2024 Accepted: 25 January 2025
stroke, and proper management of patients to decrease
their disability.
Abbreviations
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