Osama Elazouni etl al. 421 Study of The Occurrence of Abnormal Involuntary Movements after Cerebral Stroke Osama M.M.A. Elazouni 1 , Amal SE Elmotayam 1 , Karam Selim 1 , Said A. Elmonem 2 Departments of Neurology 1 , Radiology 2 , Zagazig University ABSTRACT Introduction: Abnormal involuntary movements (AIM) following cerebral stroke were reported after lesions in certain areas of the brain, but most of these studies were case reports or series of patients with a given type of abnormal movement or anatomical lesion. Aim of The Work: The aim is to study pattern of occurrence of AIM that may occur after cerebral stroke and their relationship to the cause of stroke, clinical and personal data of patients as well as sites of lesions based on imaging studies. Patients and Methods: Thirty four patients with AIM after cerebral strokes were included in this study. These patients were selected suffering first ever clinical stroke, with negative history of previous attacks. These patients were subjected to medical history taking, and thorough neurological examination. The type of AIM was evaluated by more than one of the authors separately with consultation of every case. Clinical follow up of these AIM was done using abnormal involuntary movements scale (AIMS) for detection of improvement or deterioration of these abnormal movements. Also clinical follow up of the motor power, sensory deficits, cerebellar manifestations etc was done. Follow up was done every two weeks in the first month and every month afterward and patients were followed up for at least a year after onset of AIM. Patients that died or did not comply with the study were excluded, also patients with previous history of AIM before onset of stroke were excluded as well. All patients were subjected to CT brain in the acute stage of stroke and those that had normal CT in the acute stage were resubjected to CT or MRI brain. Another 3 cases of central thalamic ischemic lesions, authors came across while doing this research, were included and studied as previously. Results: Thirteen (38.2%) of patients suffered chorea, while only 4 (11.7%) suffered parkinsonism and patients with tremor and dystonia were 9 (26.4%), and 8 (23.5%) respectively. Group of patients with chorea were found significantly (P<0.05) the elder among the other groups. The shortest mean interval time between onset of stroke and development of AIM was that for chorea with statistical significant difference (P<0.05). Most of the patients with AIM were grade 4 and 5 on MRC scale, and of moderate to severe affection of proprioceptive sensation and ataxia. Although lesions of the thalamus and/or basal ganglia were found common in these patients, good percent of patients were found suffering lesions in other areas of the brain. Central thalamic lesion was accompanied with contralateral hypothesis, chorea, and ataxia. Summary and Conclusion: Correlation between site of lesion and type of AIM could be difficult to establish. Although thalamic and basal ganglion lesions are common underlying cause for AIM, these AIM could occur in a good percentage after lesions in other areas of the brain and that could be due to concurrent ataxia and proprioceptive sensory impairment beside reasonable motor strength. Finally, pathogenesis of AIM needs more speculation and more scrutinized analysis of imaging studies with paying more attention to functional brain imaging studies. (Egypt J. Neurol. Psychiat. Neurosurg., 2007, 44(2): 421-435) INTRODUCTION Abnormal involuntary movements (AIM) caused by cerebral strokes were reported 1-6 . These reported involuntary movements are in the form of chorea 7-11 , tremor 12-15 , dystonia 16-20 , parkinsonism 21-25 , and myoclonus 26 , as well as hemiballismus 27 , and all have been associated with both cerebral infarctions and haemorrhages. AIM may be part of acute clinical manifestation of stroke 9,14,15,27,28 or delayed in onset with progressive course 12,13,19 . Previous studies attributed AIM (dystonia, myoclonus, tremor) to
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Osama Elazouni etl al.
421
Study of The Occurrence of Abnormal Involuntary
Movements after Cerebral Stroke
Osama M.M.A. Elazouni1, Amal SE Elmotayam
1, Karam Selim
1, Said A. Elmonem
2
Departments of Neurology1, Radiology2, Zagazig University
ABSTRACT
Introduction: Abnormal involuntary movements (AIM) following cerebral stroke were reported after lesions in
certain areas of the brain, but most of these studies were case reports or series of patients with a given type of
abnormal movement or anatomical lesion. Aim of The Work: The aim is to study pattern of occurrence of AIM that
may occur after cerebral stroke and their relationship to the cause of stroke, clinical and personal data of patients as
well as sites of lesions based on imaging studies. Patients and Methods: Thirty four patients with AIM after cerebral
strokes were included in this study. These patients were selected suffering first ever clinical stroke, with negative
history of previous attacks. These patients were subjected to medical history taking, and thorough neurological
examination. The type of AIM was evaluated by more than one of the authors separately with consultation of every
case. Clinical follow up of these AIM was done using abnormal involuntary movements scale (AIMS) for detection of
improvement or deterioration of these abnormal movements. Also clinical follow up of the motor power, sensory
deficits, cerebellar manifestations etc was done. Follow up was done every two weeks in the first month and every
month afterward and patients were followed up for at least a year after onset of AIM. Patients that died or did not
comply with the study were excluded, also patients with previous history of AIM before onset of stroke were excluded
as well. All patients were subjected to CT brain in the acute stage of stroke and those that had normal CT in the acute
stage were resubjected to CT or MRI brain. Another 3 cases of central thalamic ischemic lesions, authors came
across while doing this research, were included and studied as previously. Results: Thirteen (38.2%) of patients
suffered chorea, while only 4 (11.7%) suffered parkinsonism and patients with tremor and dystonia were 9 (26.4%),
and 8 (23.5%) respectively. Group of patients with chorea were found significantly (P<0.05) the elder among the
other groups. The shortest mean interval time between onset of stroke and development of AIM was that for chorea
with statistical significant difference (P<0.05). Most of the patients with AIM were grade 4 and 5 on MRC scale, and
of moderate to severe affection of proprioceptive sensation and ataxia. Although lesions of the thalamus and/or basal
ganglia were found common in these patients, good percent of patients were found suffering lesions in other areas of
the brain. Central thalamic lesion was accompanied with contralateral hypothesis, chorea, and ataxia. Summary and
Conclusion: Correlation between site of lesion and type of AIM could be difficult to establish. Although thalamic and
basal ganglion lesions are common underlying cause for AIM, these AIM could occur in a good percentage after
lesions in other areas of the brain and that could be due to concurrent ataxia and proprioceptive sensory impairment
beside reasonable motor strength. Finally, pathogenesis of AIM needs more speculation and more scrutinized
analysis of imaging studies with paying more attention to functional brain imaging studies. (Egypt J. Neurol. Psychiat. Neurosurg., 2007, 44(2): 421-435)
INTRODUCTION
Abnormal involuntary movements (AIM)
caused by cerebral strokes were reported1-6.
These reported involuntary movements are in the
form of chorea7-11, tremor
12-15, dystonia
16-20,
parkinsonism21-25, and myoclonus
26, as well as
hemiballismus27, and all have been associated
with both cerebral infarctions and haemorrhages.
AIM may be part of acute clinical manifestation
of stroke9,14,15,27,28
or delayed in onset with
progressive course12,13,19. Previous studies
attributed AIM (dystonia, myoclonus, tremor) to
Egypt J. Neurol. Psychiat. Neurosurg. Vol. 44 (2) – July 2007
422
lesions of various structures including the striato-
pallidal complex, the mesencephalon, and the
thalamus10,29,30. In the thalamus, lesions associated
with movement disorders have been described in
the ventrolateral, ventral posterolateral, and
paramedian territories10,29,31,32
. Some other studies
of the thalamic lesions that are responsible for
dystonia have attributed lesion to the subnuclei of
the thalamus33. The basal ganglia (caudate,
putamen, globus pallidus, subthalamic nucleus,
and substantia nigra) are a complex
interconnected link of several nuclear groups
within the brain and brainstem. They are involved
in parallel modular loops that leave and return to
the cortex much modulated and processed. They
receive afferents from many motor and limbic
areas to process motor information, and they
modulate the excitement level of the thalamus
motor nuclei that project to motor cortices. Basal
ganglia circuitry have two major pathways: the
direct and the indirect. The indirect pathway
includes a connection via the glutamatergic
subthalamic nucleus. Both pathways are in
balance and affect level of excitation of the motor
thalamus and its effect on the output of the
cerebral cortex. Diminished inhibitory output via
the direct pathway of the basal ganglia allows for
facilitation of the thalamic neurons. Increased
inhibition via the indirect pathways leads to
suppression of thalamic neurons. Altered output
or imbalance of these inhibitory pathways in the
diseased brain can account for the hyperkinesias
or hypokinesia as in Parkinson's disease34. Details
of the movement disorders were often lacking as
most of these studies were case reports or series of
patients with a given type of anatomical lesion.
The aim of this work is to study pattern of
occurrence of AIM that may occur after cerebral
stroke and their relationship to the cause of stroke,
clinical and personal data of patients as well as
sites of lesions based on imaging studies.
PATIENTS AND METHODS
Thirty four patients, suffered involuntary
movements after cerebral stroke, were included in
this study which was carried out in the ICU and
neurology outpatient clinic, in Zagazig university
hospitals from the period from July 2003 to June
2006. All patients selected were suffering first
ever clinical stroke with negative history of
previous attacks. This patients were subjected to
thorough neurological examination in the acute
stage and the medical history was obtained. The
type of AIM was evaluated by more than one of
the authors separately with final consultation
about every case. Clinical follow up included
reporting onset or disappearance of AIM and
calculation of the time from onset of cerebral
stroke to beginning of AIM, also period from
onset to disappearance of these AIM,
improvement of motor power, sensory deficit, and
cerebellar manifestations. Patients that did not
comply with follow up, and those died before
follow up period, were excluded. Also patients
with history of previous AIM before onset of
stroke were excluded as well. Some of the patients
were followed up from the beginning especially
those who showed evidence of beginning
abnormal movements in early post-stroke period
or whom suffered lesions in areas suspected to
develop AIM (thalamus, basal ganglia,
mesencephalon). Other group of patients affected
later and they were studied retrospectively and
then followed up as well. These patients were
followed up every two weeks in the first month,
and every month afterward. The patients were
followed up for at least a year after onset of AIM.
Definitions of AIM used by the authors were the
followings: Dystonia, sustained contractions of
both agonist and antagonist muscles frequently
causing twisting and repetitive movements or
abnormal postures35; Myoclonus, brief sudden
shock like jerks that may be caused not only by
active muscle contractions (positive myoclonus)
but also by lapses of muscle contraction (negative
Right striatocapsular infarction * Right hemiparkinsonism more prominent in upper limb (rigidity, bradykinesia, and postural tremor). ** Right hemiparkinsonism more prominent on the lower limb in the form of rigidity, and bradykinesia. *** Right hemiparkinsonism in the form of rigidity, bradykinesia, and rest tremor. **** Left hemiparkinsonism, more prominent in the upper limb, in the form of rigidity and bradykinesia, hemidystonic
movements were reported as well.
Fig. (1): Axial brain CT showing right and left central thalamic lacunar infarctions.
Osama Elazouni etl al.
427
Fig. (2): Axial T1 and T2 weighted images reveal left anterior thalamic and capsular infarctions.
Fig. (3): Axial CT brain showing right frontoparietal haemorrhagic infarction with incomplete effacement of
the frontal horn of lateral ventricle of female patient presented with left hemichoreic movements.
Egypt J. Neurol. Psychiat. Neurosurg. Vol. 44 (2) – July 2007
428
DISCUSSION
Most of the AIM reported in this study were
cases of chorea followed in frequency by tremor
and dystonia, and the least reported pattern was
parkinsonism. The mean age of patients with
chorea was significantly (P<0.05) higher than
other patients, whereas, patients who suffered
dystonia were the youngest group. This finding
came to agree with a clinical evidence that brain
damage early in life most probably leads to
dystonia rather than other abnormal movement
disorders, an example is that young onset
Parkinson's disease tends to present with dystonia
rather than parkinsonism46, and this might be a
result of changes in neuronal development related
to age or brain plasticity as demonstrated in
experimental focal cortical lesions inducing
changes in the adjacent cortex and in the
contralateral hemisphere47.
The interval between onset of stroke and
development of chorea was the shortest among all
other AIM and the difference was statistically
significant (P<0.05). On the other hand, the time
interval for parkinsonism to develop was the
longest with mean time ± SD. 125.00±73.82 days
as shown in the table (1). The reason for the delay
in occurrence of AIM, remains speculative. This
delay may reflect the time required for the
unbalanced successful recovery of the motor
function and subsequent development of
pathological neuronal circuitry, or it may indicate
the time required for the possible changes in
neuronal synaptic activities13,48,49
. Another
explanation for the delay in appearance of
parkinsonism is due to deafferentation (indicated
by secondary or transsynaptic degeneration) or
certain functional changes in neuronal activities
and their connecting structures15.
Most of the patients suffering chorea, tremor,
and dystonia, have improved partially, but few of
them either showed complete resolution of these
abnormal movement or have not improved at all.
The partial or complete recovery might be a result
of a plastic reorganization or reinnervation with
partial or complete regaining of their functions15,47.
In this study, reported clinical manifestations
of patients with AIM showed that most of the
patients had reasonable muscle strength, grade 4,
on MRC scale, and moderate to severe affection
of proprioceptive sensation and ataxia as shown
in tables (2), (3) and (4). Despite these values
could not reach statistical significant level, we
may consider these values near significance or
border line and that might be due to paucity of the
cases. These findings made us hypothesize that
reasonable motor power accompanied with
manifest affection of the proprioceptive sensation
and moderate to severe ataxia are important to
develop AIM. In support to this hypothesis,
results of the previously published studies of
Chollet et al.50, and Lee and van Donkelaar51, that
showed the functional recovery of motor
dysfunction is related to a plastic reorganization
of the motor cortex or activation of the uncrossed
pyramidal pathways from the opposite
hemisphere. In the presence of persistent failure of
original proprioceptive and cerebellar inputs, the
newly organized proprioceptive-cerebellar-motor
integrative system should be unstable or even
misdirected. In addition, it has shown that
development of dystonia is related to
proprioceptive sensory dysfunction52,53,54
, and also
in Tinazzi et al.55 study they reported enhanced
cortical somatosensory evoked potentials in
patients with dystonia. Morover, in experimental
study with monkeys subjected to cerebellar injury,
Mackel56 found that compensation of cerebellar
deficits was considerably impaired if the sensory
cortex was concomitantly removed. From all these
previous data, one can suggest that decreased
proprioceptive sensory input may result in
excessive cortical activation and impair cerebellar
function in coordination of the movements and all
that could play a role in the pathogenesis of AIM.
and pontine lesions as shown in the table (7). This
finding shows that brain lesions behind the later
development of dystonia in this study, were not
confined to basal ganglia as the previously
established, indisputable evidence of the link
between basal ganglia and dystonia29,62,63. Our
results showed that lentiform nucleus lesion was
reported in 2 (25%) cases of dystonia. This
contrast with either Alarcón et al.64, that found
lentiform nucleus lesions the most frequent in
dystonia and we also contrast with Russman et
al.65, that reported no case of dystonia in their
patients with lentiform nucleus lesions. This
discrepancy might be due to paucity of the cases
or that the studies done were based on different
selection criteria either of the type of movement
disorder or the anatomical sites of the lesions.
Recently, Le Ber et al.66 have suggested that
dystonia at least in their patients, arises from
Egypt J. Neurol. Psychiat. Neurosurg. Vol. 44 (2) – July 2007
430
dysfunction of the cerebellum. This suggestion
based on their patients' brain MRI that revealed
prominent atrophy of the cerebellum without
obvious abnormalities of the basal ganglia. This
suggestion challenged traditional views of the
anatomy of dystonia which focus predominantly
on the basal ganglia. The link between the basal
ganglia and dystonia is supported by CT and MRI
studies that have repeatedly linked dystonia with
focal lesions of the basal ganglia29. PET and other
functional imaging techniques have also revealed
abnormal function of basal ganglia even when
focal lesions are not apparent62,63. Although Le
Ber and colleagues have acknowledged in the end
of their study that the cerebellar atrophy may be
unrelated to dystonia and that additional basal
ganglia defects may have escaped detection, some
other evidence for primary role of the cerebellum
in the genesis of dystonia have emerged. An
autopsy study established a link between cervical
dystonia and tumours of the cerebellum and in
some cases it improved or disappeared after
tumour removal67. Neuroimaging studies have
shown the most frequent abnormalities among
patients with cervical dystonia are in the
cerebellum or its afferents68. Thalamic lesions can
cause limb dystonia and the responsible lesions
occur most frequently in subnuclei linked to the
cerebellum, not the basal ganglia, and an effective
surgical target for deep brain stimulation in
dystonia also involves the thalamic regions
connected with the cerebellum3,10.
Parkinsonism: The authors have got 4
patients suffering contralateral parkinsonism after
lesions in basal ganglia and cortical lesion
(frontoparietal infarction). Parkinsonian
manifestations were not isolated in all the cases
but combined with hemidystonia and postural
tremor in two of them. Previous studies have
suggested two forms of vascular parkinsonism:
one form with acute onset associated with basal
ganglionic infarction and the other form is
insidious and progressive possibly associated with
diffuse subcortical white matter ischaemia22,69.
This approach neither explain our patient with
frontoparital infarction nor that of Kims' patients58
that had anterior cerebral artery territory
infarction lesion underlying later development of
parkinsonism. Despite, previous authors have
attributed vascular parkinsonism to the lesions of
the basal ganglia in the striatum or lentiform
nucleus whether unilateral24,25 or bilateral22,70.
Other authors have showed that vascular
parkinsonian symptoms could be due to vascular
lesions disrupting the interconnecting fibre tracts
between the basal ganglia, the thalamus, and the
motor cortex that leads to disruption not only of
sensorimotor integration22,23,24
, but also of
descending reticular pathways to the major centres
of the brain stem23. The parkinsonian symptoms
could be due to vascular lesions disrupting the
interconnecting fibre tracts between the basal
ganglia, the thalamus, and the motor cortex that
leads to disruption not only of sensorimotor
intergeration, but also of descending reticular
pathways to the major centres of the brain
stem22,23,24
. None of our patients showed evidence
of improvement even those with lesion in basal
ganglia in contrast to Tolosa and Santamarǐa
study71.
Central thalamic lesion: Central thalamic
infarction is rare among other infarcts of the
thalamus31,72. Low conscious level could be due to
affection of adjacent structures as dorsomedian
nucleus (DM), and intralaminar nuclei (IL) that
may together play an important role in
maintaining wakefulness73. Sensory deficit is
related to affection of ventroposterolateral (VPL)
nucleus31,72 but this nucleus is mainly affected in
the posterior lateral thalamic lesion74 but that
could be due to affection of the adjacent part of
this nucleus. Ventrolateral (VL) nucleus affection
in these cases was the underlying cause of
hemiataxia reported75. From all these previous
data, one can report that central thalamic lesion is
associated with combination of neuropsychiatric
manifestations due to affection of adjacent nuclei
in anteromedian and posterolateral areas of the
thalamus. Study of a large number of these
patients would help to clarify neuropsychiatric
manifestations linked to this lesion more
accurately.
Osama Elazouni etl al.
431
In summary, the authors reported that
correlation between site of lesion and type of AIM
could be difficult to establish. Although lesions
that involved the thalamus and basal ganglia most
commonly cause movement disorders on the
contralateral side, involvement of basal ganglia or
thalamic lesion was not the case in all the patients
of AIM, as lesions in some other regions of the
brain were found linked to AIM. Accepted models
of basal ganglia circuitry do not fit well with
clinical observations. Most of the patients with
AIM had suffered a manifest proprioceptive
sensory impairment, and ataxia in contrast to
motor strength which was affected to a lesser
degree. Therefore, authors conclude that although
thalamic and neighbouring basal ganglion lesions
are the common lesions underlying later
development of contralateral AIM after cerebral
stroke, these AIM could occur in a good
percentage after lesions in other areas of the brain
and that could be due to concurrent ataxia and
proprioceptive sensory impairment beside
reasonable motor strength, or the CT or MRI
might be neither show the full extent of pathology
nor the functional effects of such lesions,
furthermore concurrent or previous ischemic
lesions might be not detected by current imaging
techniques. Finally, pathogenesis of AIM needs
more speculation and more scrutinized analysis of
imaging studies with paying more attention to
functional brain imaging studies.
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