Movement Disorders

After Stroke

Suroto
Dep of Neurology, Fac of Medicine
Sebelas Maret University
Stroke related MD
Stroke related Hyperkinetic MD
Stroke related Hypokinetic MD
Stroke related Seizure-like MD
 Stroke Related MD
• Stroke is usually characterized by loss of movement.
• However, in a small percentage of (1%) cases, patients
can have various abnormal movements: 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)
• Hemorrhagic strokes appear to be more likely to lead
to MD than ischemic ones.
• 90% of the acute-onset MD resolved within 6 months.
 Stroke Related MD
• Abnormal movements following stroke occur in men and
women equally.
• Average age of onset 63.3 (range 17–90).
• The age of predilection for different movement disorders
varies; chorea affects older people while pts who
develop dystonia are younger.
• 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 tx, and can importantly
contribute to disability and long-term outcome.
Classification of Stroke related MD
• Hyperkinetic Movement Disorders:
Hemichorea with or without hemiballismus, dystonia,
tremors , segmental or focal myoclonus, athetosis,
pseudoathetosis and asterixis.

• Hypokinetic Movement Disorders:

Vascular Parkinsonism; have been described and occur at
presentation of the stroke, in the delayed setting or as a
progressive condition.

• Seizure-like Movement Disorders

Stroke related MD
Stroke related Hyperkinetic MD
Stroke related Hypokinetic MD
Stroke related Seizure-like MD
 The spectrum

Myoclonus Ballismus Chorea Athetosi Dystonia

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
Stroke related Chorea & Ballism
• Chorea: brief, arrhythmic, non-repetitive
movements that appear to move from one muscle
to the next and is typically worsened by volitional
movements.
• Hemiballism : vigorous, irregular, poorly
patterned, high-amplitude movements of the
limbs ( a severe type of chorea).
• In ballism:
- 4% had a lesion restricted to the STn
- 23% STn combined with other BG or midbrain structures
- 14% STn combined with cortical lesion
- 59% had no evident STn lesion.
Stroke related Hemiballism & Hemichorea

• Hemiballism&hemichorea is the most common

MD reported to occur after stroke (40%) .
• 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 & Hemichorea
• 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).
• Post-stroke hemichorea tend to have MRI
hyperintensities in the BG, particularly the putamen.
• 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
 DD: Hyperglycemic Chorea
• 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.
• Both the involuntary movements and MRI changes
are reversible with appropriate treatment of the
hyperglycemia (Asian descent).
 Treatment Ballism & Chorea
Ballism and chorea typically respond to the same
therapies.
• DRBs, particularly haloperidol (resolution of
symptoms in 3–15 days: 56%)
• Clonazepam and diazepam,
• Topiramate, tetrabenazine, valproic acid
• Local i.m. inj. of botulinum toxin in severe cases
• Atypical dopamine antagonist drug risperidone
since it tends to have fewer side effects.
• Ventrolateral thalamotomy
Stroke related Dystonia
• 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.
 Stroke related Dystonia
• 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.
• This disturbance, is thought to increase thalamocortical
drive, which in turn induces dystonia.

• 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.
 Management of Stroke related Dystonia
• Oral Drugs: Baclofen, Benzodiazepines, Tizanidines,
Anticholinergics,
• Chemodenervation: Botulinum toxin
• Surgical: DBS, Pallidotomy, Myectomi, Selective peripheral
denervation
• Other: Physical tx, Occcupational tx

• Once present after stroke, dystonia stabilizes over time, and

rarely resolves completely.
• Dystonia following stroke usually has a poor response to medical
tx, typically being refractory to oral medications.
• Local i.m. injections of botulinium toxin can lessen stroke-
induced dystonia and is probably the best medical approach.
 Surgical Intervention
of Stroke related Dystonia
• Surgical interventions (thalamotomy, pallidotomy, DBS)
yielded the best results, showing benefit in 96% of
treated patients; however, 39% had only transient
improvement.
• DBS of either the thalamus or the internal globus
pallidus appears to be more successful than lesioning
approaches in producing a longer lasting response.
• However, ?? which target is more effective.
 Stroke related Myoclonus

• 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.
 Stroke related Asterixis
• Asterixis, is negative myoclonus, is characterized by
arrhythmic interruptions of sustained voluntary
muscle contraction causing brief lapses of posture.
• Asterixis been described in association with
- stroke in mesodiencephalon, 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 asterixis: metabolic derangement).
 Myoclonus & Asterixis Tx
• Post-stroke myoclonus often does not require Tx.
• When intolerable: the two most commonly used Tx
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 Tx for asterixis remains unknown.
 Holmes’ Tremor
• HT is a 3–4 Hz flexor extension oscillation, present at rest
and exacerbated with posture and additionally intensified
with action.
• The most common etiology is vascular.
• The onset of post-stroke is typically delayed by wks-mo’s.
• The most common site are mesencephalon and thalamus.
• The most common associated symptoms are hemiparesis
and ataxia.
• The most effective treatment is functional surgery
• Levodopa may be effective.
 Palatal Tremor
• PT consists of brief, rhythmic involuntary
movements of the soft palate. (Essential #
secondary)
• Stroke is one of the most common causes of SPT
(trauma, neoplasm, brainstem angioma, MS,
syringobulbia , encephalitis, degenerating
conditions).
• SPT patients have other signs of cerebellar and
brainstem dysfunction (eg nystagmus).
• SPT persists and varies in rate during sleep as an
audible clicking sound.
 Palatal Tremor
• 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 Tx.
• When intolerable or functionally impairing, local i.m.
botulinum toxin inj.
 Disappearance Of Previous ET

• 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.
 Isolated Hemifacial Spasms
• Isolated hemifacial spasms might be the only presenting
signs of an ipsilateral lacunar pontine stroke.
• The hemifacial spasms are thought to result from
irritation of the intra-pontine roots of the facial nerve or
its nucleus by ischaemic edema, leading to
hyperexcitability of the facial motor neurons and
interneurons that mediate the blink reflex.
• When intolerable or functionally impairing, local i.m.
botulinum toxin inj.
 Alien Hand Syndrome
• 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.
• AHS can be seen in pts with stroke 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.
 Tics
• Tics consist of rapid nonrhythmic sterotyped
involuntary twitches (motor tics) or sounds (phonic
tics), and can be temporarily uppressed by an effort
of will.
• 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.
• If disabling, tics can be treated with alpha-receptor
agonists (clonidine, guanfacine) or dopamine receptor
antagonists such as risperidone or fluphenazine.
Stroke related MD
Stroke related Hyperkinetic MD
Stroke related Hypokinetic MD
Stroke related Seizure-like MD
 Vascular Parkinsonism
• Stroke in critical locations, such as the midbrain
and BG, can cause the acute onset of
parkinsonism.
• VaP is clinically manifested primarily by bilateral,
symmetric bradykinesia and rigidity (idiopathic
PD typically begins on one side and tends to be
asymmetric)
• Predominant involvment of the legs = („lower-
body parkinsonism“)
– gait and balance disorder (frontal type gait,
apraxia of gate, shuffling, short steps)
– tremor is usually absent
 Vascular Parkinsonism
• Resting tremor may be present in VaP, 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.
• Two forms of leukoencephalopathy, Binswanger’s
disease and CADASIL (cerebral autosomal dominant
arteriopathy with subcortical infarcts and
leukoencephalopathy), and Moyamoya disease can
present with VaP.
 Vascular Parkinsonism

• VaP 20% of patient with bilateral or

hemiparkinsonism made a spontaneous recovery.
• misdiagnosis of VaP as PD is common with rates of
misdiagnosis of 15–30%.
• Levodopa and other dopaminergic drugs may improve
VaP, but the effects are usually modest and short-
lived
Stroke related MD
Stroke related Hyperkinetic MD
Stroke related Hypokinetic MD
Stroke related Seizure-like MD
 Seizures
• 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 Arterial) , watershed infarctions and AVM.
• Nearly 40% Cerebral Vein and Dural Sinus
Thrombosis had seizures at presentation.
 Seizures
• 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 hrs, such a distinction is
often difficult
• Ongoing headaches or symptoms and signs of
elevated ICP, such as papil-edema, in these pts
could provide clues to the correct Dx.
• The use of advanced brain imaging techniques,
such as perfusion and vascular imaging, is often
needed to discriminate
 Summary
• 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 wks but treatment may be
required for symptom control except delayed
dystonia.