post-stroke involuntary movement

1. ””‫علم‬ ‫ل‬ ‫سبحانك‬ ‫قالوا‬‫علم‬ ‫ل‬ ‫سبحانك‬ ‫قالوا‬
‫علمتنا‬ ‫ما‬ ‫إل‬ ‫لنا‬‫علمتنا‬ ‫ما‬ ‫إل‬ ‫لنا‬
‫العليم‬ ‫أنت‬ ‫إنك‬‫العليم‬ ‫أنت‬ ‫إنك‬
‫الحكيم‬‫الحكيم‬““
‫العظيم‬ ‫ا‬ ‫صدق‬
‫ايه‬ ‫البقرة‬ ‫سورة‬32
‫ا‬ ‫بسم‬‫ا‬ ‫بسم‬
‫الرحيم‬ ‫الرحمن‬‫الرحيم‬ ‫الرحمن‬

2. Movement Disorders
After Stroke
Dr/ Ayman Al-malt
Assistant Lecturer Neurology
Faculty Of Medicine
Tanta University.
2/10/2015

3. Stroke is defined as a focal neurological
deficit lasting for more than 24 hours with no
cause other than that of vascular origin (1).
Ischemic stroke is responsible for about 80%
of all strokes, intracerebral hemorrhage for
15% and subarachnoid hemorrhage for 5%
(2).
 A transient ischemic attack (TIA) has the
same complex symptoms as stroke, but with
a resolution of these symptoms within 24
hours (2).
DEFINITION

4. Since introduction of thrombolytic therapy
in acute ischemic stroke; The American Heart
Association and American Stroke Association
(AHA/ASA) 2009 Guidelines shift from the
time-based definition of TIA to a tissue-based
definition in 2002(3)
with a new definition for
TIA as :
"a brief episode of neurological
dysfunction caused by focal brain or retinal
ischemia, with clinical symptoms typically
lasting less than one hour and without
evidence of acute infarction"(4)
INTRODUCTION

5. American Heart Association, Inc. Circulation. 2011;123:e18-e209
Stroke Statistics

6. American Heart Association, Inc. Circulation. 2011;123:e18-e209
Stroke Statistics

7. 1. Typical Stroke Symptoms (stroke)
2. Typical Stroke Symptoms ( not stroke..
….. Mimics)
3. Atypical Stroke Symptoms (stroke…….
Chameleons)
4. Atypical Stroke Symptoms ( not
stroke…….. Non stroke)
Acute Neurological Symptoms

8. 1- Classical Stroke Symptoms:
1- Sudden numbness or weakness of face, arm
or leg, especially on one side of the body
2- Sudden confusion, trouble understanding or
speaking
3- Sudden trouble seeing in one or both eyes
4- Sudden trouble walking, dizziness, loss of
balance or coordination
5- Sudden severe headache with no known
cause

9. I- Non-localising symptoms
• Neuropsychiatric symptoms
• Acute confusional state
• Altered level of consciousness
II- Abnormal movements or seizures
• Abnormal movements
• Limb-shaking transient ischemic attacks
•Alien hand syndrome
• Localized asterixis
• Isolated hemifacial spasms
•Disappearance of previous essential tremor
Seizures like
2- Non- Classical Stroke Symptoms

10. IV- Atypical symptoms
• Isolated dysarthria
• Isolated dysarthria-facial
paresis syndrome
• Isolated visual symptoms{
Anton’s syndrome (cortical
blindness with denial of deficit)
Balint’s syndrome, Isolated visual
field disturbances}
• Foreign accent syndrome
• Isolated dysphagia or
stridor
III- Peripheral nervous
system symptoms
• Acute vestibular
syndrome
• Other cranial nerve
palsies (especially 3 and 7)
• Acute monoparesis
Cortical hand syndrome
Cortical foot syndrome
• Isolated sensory
symptoms
2- Non- Classical Stroke Symptoms

11. V- Isolated headache
• Subarachnoid hemorrhage
• Cerebral venous sinus thrombosis
• Cervical artery dissections
• Cerebellar infarction
VI- Acute neurological syndrome with
negative brain imaging
• Negative non-contrast CT in SAH , CVST , arterial
dissection, and acute ischemic stroke
• Negative MRI in acute ischemic stroke
2- Non- Classical Stroke Symptoms

12. Stroke is usually characterized by loss of movement.
 However, in a small percentage of (1%) cases,
patients can have various abnormal movements:
(hyperkinetic, hypokinetic, or seizure-like) at stroke
onset (acute) or delayed.
 In most cases, the lesions were due to small vessel
CVD in the MCA or PCA territories. (blood supply of
the BG)
Movement Disorders after Stroke (chameleon)

15. Hemorrhagic strokes appear to be more likely to
lead to MD than ischemic ones.
90% of the acute-onset MD resolved within 6
months.
Despite the low frequency and tendency to
resolve, the recognition of a MD in the setting of
stroke can be important in localizing the lesions and
in suggesting an underlying etiology.
They may need to be a target for therapy, and can
importantly contribute to disability and long-term
outcome.
Movement Disorders after Stroke

16. CLASSIFICATION
I- Hyperkinetic movement Disorders:
hemichorea with or without hemiballismus, Dystonia,,
tremors , segmental or focal myoclonus ,athetosis,
pseudoathetosis and Asterixis
Transient dyskinesias or 'limb shaking' spells have been
described as a symptom of TIAs.
II- Hypokinetic movement Disorders
Vascular Parkinsonism.
have been described and occur at presentation of the
stroke,in the delayed setting or as a progressive condition.
III-seizure-like movement Disorders

18. The spectrum
Ballismu
s
DystoniaChorea Athetosi
s
Movements become - Less violent / explosive / jerky
- Smoother and more flowing
- More sustained
They differ from tics in that they cannot be
suppressed by voluntary control
Myoclonus

19. Abnormal movements following stroke occur in men
and women equally.
 Average age of onset (57.5) 63.3 (range 17–90).[20]
The age of predilection for different movement
disorders varies; chorea affects older people while
patients who develop dystonia are younger.
Nonketotic hyperglycemia and autoimmune diseases
Demography and Risk Factors

21. I- Hyperkinetic Movement
Disorders

22. Hemiballism is characterized by vigorous, irregular,
poorly patterned, high-amplitude movements of the
limbs on one side of the body ( a severe type of chorea).
Chorea consists of brief, arrhythmic, non-repetitive
movements that appear to move from one muscle to the
next and is typically worsened by volitional movements.
Hemiballism / hemichorea is the most common MD
reported to occur after stroke (40%) .
 ballism can involve one limb (monoballism) or all
limbs (biballism or paraballism).
1- Hemiballism

23. The majority of patients with hemiballism have both
choreic and ballistic movement and with time, the
ballistic movements become less severe and resemble
chorea.11
 May be associated with dyskinesias like orobuccal,
oromandibular, lingual and dystonia.
 72% of cases of hemiballism are caused by stroke,
with an average age of 66 years (older than other MD).
Hemichorea, had a prevalence of > 0.5% of stroke.
Although rare, hemichorea has been described as a
manifestation of a TIAs.
Hemiballism

24. 80% of hemiballism are acute onset after stroke,
while 20% is delayed by days, weeks, or months with
the longest reported delay being 5 months.
When chorea is observed in the setting of CVD, we
should consider the possibility of underlying vasculitis
(e.g., SLE) APLs or vasculopathy (e.g.,
paraproteinemia).
In ballism 4% had a lesion restricted to the STn, 59%
had no evident STn lesion, and the remainder had
lesions of the STn combined with other BG or midbrain
structures (23%) or cortical lesions (14%).
Hemiballism

25.  Post-stroke hemichorea tend to have MRI
hyperintensities in the BG, particularly the putamen.10
Hemiballism rarely may be a grave disorder with
progression to death within weeks, or benign course
and spontaneous recovery( 24%).4
85% of patients with cortical lesions and 54% of
those with BG lesions recovered completely, but none
of the patients with isolated lesions in the STn
recovered.
Hemiballism

26. An important condition to distinguish from stroke-
induced chorea is hyperglycemic chorea, which often
presents acutely as hemichorea and may have basal
ganglia hyperintensities on MRI.
It occurs in the setting of non-ketotic hyperglycemia
(usually RBS greater than 400 mg/dl) and has been
attributed to hyperosmolarity.14,15
 Both the involuntary movements and MRI changes
are reversible with appropriate treatment of the
hyperglycemia (Asian descent).
Hemichorea

28. Ballism and chorea typically respond to the same therapies.
1- DRBs, particularly haloperidol {resolution of
symptoms in 3–15 days (56%)}
2- clonazepam and diazepam,
3- topiramate, tetrabenazine, valproic acid, and, in
severe and persistent cases,
4- local intramuscular injections of botulinum toxin or
ventrolateral thalamotomy.
Despite absence of published support, we generally
treat disabling ballism or chorea with the atypical
dopamine antagonist drug risperidone since it tends to
have fewer side effects.
Treatment Hemiballism & chorea

29. Dystonia consists of involuntary sustained muscle
contractions causing twisting and repetitive
movements or abnormal postures.
Poststroke dystonia is the 2nd most common MD
20%.
Stroke is the most common cause of hemidystonia
50%. ( may be focal).
Most patients who have onset of hemidystonia after
stroke are young (below age 25), suggesting increased
susceptibility in the younger brain.
2- Dystonia

30. Irregular
The motor circuits of the basal ganglia in dystonia. Thin
arrows show a decrease in output and thick arrows show
an increase in output.
Irregular lines indicate irregular S-P-T outputs.

31. Post-stroke dystonia has been attributed to lesions of
the putamen (the most common site of isolated lesions
causing dystonia), caudate, pallidum, thalamus, and the
midbrain.22–24
Dystonia induced by an interruption of the cortico-
striato-pallido-thalamo-cortical loop by (PET) studies.
This disturbance, proposed to be caused by specific
lesions of the sensorimotor part of the striatiopallidal
complex and/or the putamen, is thought to increase
thalamocortical drive, which in turn induces
dystonia.25
Dystonia

32. In contrast to hemiballism, which typically begins at
the time of stroke, dystonia is delayed by an average of
9.5 months, with a range between 3 months and 3-5
years.
Dystonia often follows hemiplegia, appearing once
muscle strength begins to recover.
Dystonia

34. Once present after stroke, dystonia stabilizes over
time, and rarely resolves completely.21
Dystonia following stroke usually has a poor
response to medical therapy, typically being refractory
to oral medications. Anticholinergic drugs,
benzodiazepines, baclofen.
Local intramuscular injections of botulinium toxin
can lessen stroke-induced dystonia and is probably
the best medical approach.
Dystonia

35.  Surgical interventions (thalamotomy, pallidotomy,
deep brain stimulation (DBS)) yielded the best results,
showing benefit in 96% of treated patients; however,
39% had only transient improvement.
The recent literature suggests that DBS of either the
thalamus or the internal globus pallidus appears to be
more successful than lesioning approaches in
producing a longer lasting response since its
parameters can be altered for maximum benefit.
However, ?? which target is more effective.
Dystonia

36. 3- Myoclonus &Asterixis
Myoclonus involves brief, shock like involuntary of
muscles or muscle groups.
Post-stroke myoclonus (focal or segmental
) is not too helpful in localizing the vascular lesion
(frontoparietal lobes, BG, midbrain, pons, and
cerebellum).
Post-stroke myoclonus can affect the arms, legs,
face, or voice; however, facial myoclonus is
infrequent after stroke.29

37. Asterixis, is negative myoclonus, is characterized
by arrhythmic interruptions of sustained voluntary
muscle contraction causing brief lapses of posture.
Astrexis been described in association with stroke
in mesodiencephalen, resulting in impaired
processing of proprioceptive input, and in cortical
strokes that involve the primary motor cortex, with
subsequent impairment of centrally generated motor
command signals that control the postural tone of the
distal upper limbs.
 Asterixis, may result from ACA infarction (DD
metabolic derangement). 31
ASTERIXIS

38. Post-stroke myoclonus often does not require ttt.
When intolerable: the two most commonly used ttt
include clonazepam and sodium valproate (both
GABAergic drugs). piracetam and levitiracetam may
be used .
clonazepam and levitiracetam, sometimes used in
combination, are the most effective medications for
myoclonus.
The appropriate ttt for asterixis remains unknown.
Myoclonus &Asterixis

39. 4- Holmes’ Tremor
HT (also called rubral, midbrain, or cerebellar outflow
tremor) is a resting tremor of a limb with marked
accentuation on action, intention and goal-oriented
movement.
 It is typically irregular, of low frequency (4.5 Hz) UL.
HT occurs with stroke in the brainstem, the
cerebellum and thalamus have also been reported.
These localizations suggest involvement of both the
nigrostriatal and dentato-rubro-thalamic pathways
(supported by MRI).

40. The onset of post-stroke HT is typically delayed by
weeks to months.
 propranolol, clonazepam, levodopa, other
dopaminergic agents, valproate, topiramates and
levetiracetam.
However, response to drugs is usually poor in these
patients.
So many patients with HT require surgical
intervention, such as ventrointermedius thalamotomy
and thalamic DBS.
28% of patients had complete resolution (64% partial).
Holmes’ Tremor

41. PT consists of brief, rhythmic involuntary movements
of the soft palate. (Essential # secondary)
Renamed as PT because of rhythmic nature.
Stroke is one of the most common causes of SPT
( trauma, neoplasm, brainstem angioma, MS, syringobulbia , encephalitis,
degenerating conditions). (Occurs 2-49 months)
SPT patients have other signs of cerebellar and
brainstem dysfunction.
 SPT persists and varies in rate during sleep as an
audible clicking sound + APN(vertical) = OPM.
5- Palatal Tremor

42. Imaging studies show lesions in the triangle of
Guillain–Mollaret (red nucleus, inferior olive, dentate
nucleus).
Post-stroke PT tends not to resolve spontaneously,
particularly when associated with other cerebellar
dysfunction.
This may be tolerable and not require specific ttt.
When intolerable or functionally impairing, local
intramuscular botulinum toxin injections.
Palatal Tremor
Pendular Nystagmus and Palatomyoclonus - YouTube.flv

43. Conversely, disappearance of abnormal movements
might be the presenting feature of a stroke.
 In a few reports, improvement of patients’ essential
tremors has been described after strokes that affect
the cerebellum, frontal lobe, thalamus, and basis
pontis.
 These authors speculated that interruption of
transcortical motor and cerebellar-thalamic-cortical
loops by a stroke could result in disappearance of the
tremors.
6- Disappearance Of Previous ET

44. Isolated hemifacial spasms might be the only
presenting signs of an ipsilateral lacunar pontine
stroke.45
The hemifacial spasms are thought to result from
irritation of the intra-pontine roots of the facial nerve
or its nucleus by ischaemic oedema, leading to
hyperexcitability of the facial motor neurons and
interneurons that mediate the blink reflex.
When intolerable or functionally impairing, local
intramuscular botulinum toxin injections.
7- Isolated Hemifacial Spasms

45. One of the most interesting rare presentations of
stroke is the so-called AHS, in which one hand seems to
have a mind of its own and acts independently of the
patient’s voluntary control.
 This syndrome can be seen in patients with strokes
involving the corpus callosum, frontal lobe, or
posterolateral parietal lobe.
AHS is thought to result from disconnection of the
area of the primary motor cortex that controls the hand
from the premotor cortex, while retaining its ability to
execute hand movements.
Physicians misdiagnosed as a psychiatric disorder.
8-Alien Hand Syndrome

46. Tics consist of rapid nonrhythmic sterotyped
involuntary twitches (motor tics) or sounds (phonic
tics).
There are a few case reports of tics developing
after stroke localized to the basal ganglia and one
case following hemorrhage of a left frontal
arteriovenous malformation.48
If disabling, tics can be treated with alpha-receptor
agonists (clonidine, guanfacine) or dopamine
receptor antagonists such as risperidone or
fluphenazine.
9- Tics

47. Limb-shaking transient ischemic attacks Involuntary
repetitive and stereotyped limb shaking might be the
manifestation of diminished perfusion of the fronto-
subcortical motor pathways.
Contra-lateral to a high-grade carotid occlusive
lesion.
 ?? epileptic in nature (brief and show postural
dependence; being precipitated by abrupt standing up
and relieved by lying down and no Jacksonian march).
10-Limb-shaking TIAs

48. LSTIAs preferentially affect the UL, spare facial
muscles and are almost always contralateral to a tight
carotid stenosis.
Early recognition of LSTIAs is crucial as these
patients are at high risk for stroke if steps to improve
cerebral perfusion (augmentation of blood pressure,
optimisation of intravascular volume, and carotid
revascularisation).
Limb-shaking TIAs

49. II- Hypokinetic Movement Disorders
II- Hypokinetic Movement
Disorder:

50. Vascular parkinsonism
Stroke in critical locations, such as the midbrain and
BG, can cause the acute onset of parkinsonism.
chronic small vessel CVD can develop a progressive
condition characterized by features resembling
Parkinson’s disease (PD). Termed ‘‘vascular
parkinsonism’’.
vPD is clinically manifested primarily by bilateral,
symmetric bradykinesia and rigidity (idiopathic PD
typically begins on one side and tends to be
asymmetric), usually in the presence of a gait disorder.

51. ‘‘lower half parkinsonism’’, in which there is rigidity
and bradykinesia of the legs with sparing of the upper
extremities, often accompanied by start hesitation (gait
ignition failure) and gait freezing.
Resting tremor may be present in vascular
parkinsonism, but it is usually mild.
On brain neuropathologic show evidence of
widespread, mostly subcortical small vessel CVD and
they do not have the characteristic Lewy body
(synucleinopathic) pathology of PD.
Vascular parkinsonism

52. Two forms of leukoencephalopathy, Binswanger’s
disease and CADASIL (cerebral autosomal dominant
arteriopathy with subcortical infarcts and
leukoencephalopathy), and Moyamoya disease can
present with vascular parkinsonism. 54,55
 vPD 20% of patient with bilateral or
hemiparkinsonism made a spontaneous recovery.[20]
misdiagnosis of vascular parkinsonism as PD is
common with rates of misdiagnosis of 15–30%.
Vascular parkinsonism

53. Pseudoparkinsonian signs (action tremor or
myoclonus, paratonic rigidity, apraxic slowness,
apraxic gait) that reflect multifocal or diffuse
hemispheric dysfunction that would be expected in
patients with cerebrovascular disease.
Levodopa and other dopaminergic drugs may
improve vascular parkinsonism, but the effects are
usually modest and short-lived
Vascular parkinsonism

55. III- Seizure-like
Movement Disorders

56. in the setting of acute stroke are not uncommon,
(1·5% to 5·7%)
 higher in younger patients, with haemorrhagic
strokes, infarcts involving the cerebral cortex (Venous
or Areterial) , watershed infarctions and AVM.
It is important for clinicians to differentiate postictal
Todd’s paralysis from deficits attributable to a stroke
with a seizure at onset.
In the initial minutes to hours, such a distinction is
often difficult on the basis of clinical examination
alone.
Seizures

57. The use of advanced brain imaging techniques, such
as perfusion and vascular imaging, is often needed to
discriminate paralysis attributable to seizures alone
from that caused by a stroke and these techniques
could facilitate treatment decisions.37,38
Nearly 40% Cerebral Vein and Dural Sinus
Thrombosis had seizures at presentation.39
 ongoing headaches or symptoms and signs of
elevated intracranial pressure, such as papilloedema,
in these patients could provide clues to the correct
diagnosis.
Seizures

58. Stroke chameleon must be in mind, Although rare.
Different varieties of abnormal movements can be
found after a stroke either acutely or as a delayed
sequel.
MD can be hyperkinetic ( hemichorea–hemiballismus)
hypokinetic (vascular parkinsonism) and seizure like.

Most are caused by stroke in the BG or thalamus but
can occur with different locations in the motor circuit.
Many are self limiting 2 w but treatment may be
required for symptom control except delayed dystonia.
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