Study of The Occurrence of Abnormal Involuntary Movements ... · Study of The Occurrence of Abnormal Involuntary Movements after Cerebral ... involuntary movements after cerebral

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

myoclonus)36; Chorea, involuntary continuous

abrupt rapid brief unsustained irregular

movements that flow randomly from one body

part to another. Patients frequently incorporate

movements into semipurposeful activities36;

Tremor, rhythmic oscillatory involuntary

movements of a body part37; and Parkinsonism,


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the presence of bradykinesia and at least one of

the following: muscle rigidity, rest tremor, or

postural instability38. Ballismus (or hemiballismus

if unilateral) is a condition in which large scale,

violent, flail-like or ballistic movements occur39.

Dystonia, chorea and tremor, were defined focal if

affect single part of the body; segmental in case

two or more adjacent parts affected; multifocal,

more than one part of the body; and unilateral in

ipsilateral affection of arm and leg, as well as

generalized form. Sense of position and

movement were graded based on Nathan et al.40

and Davidoff41 findings into minimal (loss of the

sense of position in small finger or toes),

moderate (loss of sense of position and movement

in small finger or toes), severe (loss of sense of

position or movement in thumb or big toe). Motor

strength was assessed and followed up and graded

as I to V using the Medical Research Council

scale (MRC)42. Ataxia if present was graded as

mild (slight dysmetria on approaching the target,

or ataxia observed on reinforcement, resistance

applied by examiner on the volar surface of the

patient's forearm on doing finger to nose test),

Severe (severe oscillation of the arm from start of

movement with decomposition of movement and

severe overshooting, sometimes complete inability

to execute the act on finger to nose test).

Moderate is the grade between mild and severe43.

In follow up severity of AIM was assessed using

abnormal involuntary movement scale (AIMS)44,

this scale allows rating facial and oral movements,

extremity movements, trunk movements, and

global judgements of the severity of AIM, as well

as dental status. This scale allows global

judgements of the severity of abnormal

movements, incapacitation and also patient's

awareness of the abnormal movements. Score 1:

for none, 2: for minimal or extreme normal, and 3,

4, 5 for mild, moderate, and severe respectively.

Imaging studies:

All the patients were subjected to CT brain

in the acute stage of stroke, but patients who

showed AIM and their previous CT scans were

negative (CT brain scanning within first 72

hours), these patients were re-subjected to CT or

MRI brain imaging studies.

Finally, results were collected and data base

processing was done using statistical package of

social sciences (SPSS) version 0.845. Chi-Squared

Test was used for qualitative variables and

ANOVA test to compare group means of

quantitative variables and the results were

considered significant if P-value <0.05, while P-

value >0.05 indicates non significant and P‹0.001

highly significant values.

RESULTS

Thirty four patients suffered AIM after

cerebral strokes were included in this study. The

relationships were done between AIM to personal

data of patients (age and gender), clinical

findings, pattern of cerebral stroke, time interval

between onset of stroke and appearance and

disappearance of AIM, and analysis of these

abnormal movements, as well as description of

AIM reported in extra three cases of rare central

thalamic infarction we came across while doing

this study. The results of this study were as

follow:

Relationship between AIM and clinical

parameters of the patients in the form of muscle

strength, manifestation of proprioceptive

sensation, and ataxia were studies (Tables 2, 3 and

4).

Cases of chorea, tremor, and dystonia, as

well as parkinsonism were analysed separately in

relation to anatomical lesions evidenced by

imaging studies and the results were as shown in

tables (5), (6), (7) and (8). Although lesion of the

thalamus or basal ganglia are common among

these patients, good percentage of patients were

found suffering lesions in other areas of the brain

(Tables 5, 6, 7 and 8).

Central thalamic lesion: Three patients of

age 43, 57, and 65 year old were included in the

study and had unilateral central thalamic infarcts

(one right lesion and two on the left side). One of

these patients was known hypertensive with

medical treatment Bisoprolol fumarate 5mg once


424

daily, but his blood pressure on admission was

210/120. The other two cases showed high blood

pressure on admission (210/120 & 180/110) but

their relatives denied any history. Blood sugar

estimation was abnormal in random samples for

all patients. Lipid profiles for all the three patients

was abnormal (abnormally high LDL, low HD).

All these patients were admitted with low

conscious level, contralateral hemiparesis, and

hypoesthesia. On follow up these patients

regained full consciousness within few days but

cognition was impaired. Within 2 weeks, motor

power improved to grade 4 but two patients had

developed contralateral chorea and hemiataxia.

Table 1. AIM versus demographic data, and type of stroke, as well as time interval between onset of stroke

and AIM appearance and improvement.

Chorea Tremor Dystonia Parkinsonism

Number and percent of patients

Mean age of patients

Gender of patients Male

Female

Patients of ischemic stroke

Patients of hemorrhagic stroke

Hemorrhagic infarct or combined

Mean time to develop AIM (days)

Improvement of AIM Partial

(No and % of patients) Total

None

13 (38.2%)

67.69±5.99*

5 (38.46%)

8 (61.54%)

4 (30.8%)

8 (61.5%)

1 (7.7%)

7.61±4.44*

9 (69.23%)

1 (7.69%)

3 (23.08%)

9 (26.4%)

53.77±6.01

7 (77.78%)

2 (22.22%)

3 (33.3%)

5 (55.6%)

1(11.1%)

23.22±9.43

6 (66.66%)

2 (22.22%)

1 (11.12%)

8 (23.5%)

46.5±10.9

6 (75.00%)

2 (25.00%)

3 (37.5%)

5 (62.5%)

0

29.25±13.44

6 (75.00%)

2 (25.00%)

None

4 (11.7%)

56.75±4.03

1 (25.00%)

3 (75.00%)

4 (100%)

None

0

125.00±73.82

None

None

4 (100.00%)†

* statistically significant difference (P<0.05), ANOVA.

† statistically significant difference (P<0.05), Chi-Squared Test.

Table 2. Relationship between AIM and muscle strength (MRC scale).

Muscle strength Grade 0 Grade 1 Grade 2 Grade 3 Grade 4 Grade 5

No. & % of patients

Chorea:

Tremor:

Dystonia:

Parkinsonism:

0

0

0

0

0

0

0

0

1 (7.7%)

0

0

0

0

2 (22.2%)

0

0

9 (69.2%)

7 (77.8%)

8 (100.00%)

2 (50.00%)

3 (23.1%)

0

0

2 (50.00%)

Chi-Squared Test, x2 = 14.72, P = 0.09 (non significant).

Table 3. Relationship between AIM and severity of sensory affection.

Sensory Affection Normal Mild Moderate Severe

No. & % of patients

Chorea:

Tremor:

Dystonia:

Parkinsonism:

0

0

0

1 (25%)

1 (7.7%)

0

1(12.5%)

1 (25%)

7 (53.8%)

3 (33.33%)

3 (37.5%)

2 (50%)

5 (38.5%)

6 (66.7%)

4 (50%)

0



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Table 4. Relationship between AIM and Ataxia.

Severity of Ataxia Normal Mild Moderate Severe

No. & % of patients

Chorea:

Tremor:

Dystonia:

Parkinsonism:

0

0

0

1 (25%)

1 (7.7%)

0

0

1 (25%)

8 (61.5%)

4 (44.44%)

3 (37.5%)

2 (50%)

4 (30.8%)

5 (55.6%)

5 (62.5%)

0


Table 5. Cases of chorea reported after cerebral stroke in relation to CT/MRI findings.

Age of

patients

Sex of

patients Handedness

Clinical

manifestations CT/MRI findings

68 year

75 year

69 year

72 year

69 year

76 year

70 year

55 year

67 year

71 year

65 year

64 year

59 year

Male

Male

Female

Female

Male

Male

Male

Female

Female

Female

Female

Female

Female

Right

Right

Right

Right

Right

Right

Right

Right

Right

Right

Right

Right

Right

Left hemichorea*

Right hemichorea

Left hemichorea

Left hemichorea

Generalized chorea

Right hemichorea

Right hemichorea*

Left hemichorea

Left hemichorea*

Left hemichorea

left hemeichorea

Left hemichorea

Left hemichorea

Bilateral cerebellar with right thalamic hge

Bilateral temporal infarction

Bilateral corona radiata infarction

Right lenticulocapsulostriatal infarction

Bilateral thalamic hge

Left thalamic with bilateral cerebellar hge

Left putaminocapsulothalamic hge

Right thalamocapsulolenticular hge

Right pallidal capsular infarction

Left thalamic hge

Right frontoparital haemorrhagic infarction

Bilateral parietal hge

Bilateal cerebellar hge

* Hemichorea with hemiballismus abnormal movements.

Table 6. Cases of tremor reported after cerebral stroke in relation to CT/MRI findings.

Age of

patients Gender Handedness Clinical manifestations CT/MRI findinges

55 year

57 year

63 year

50 year

44 year

51 year

61 year

49 year

54 year

Female

Male

Male

Male

Male

Female

Male

Male

Male

Right

Right

Right

Right

Right

Right

Right

Right

Right

Right hemichorea.

Right upper limb tremor, and

right chorea.

Bilateral upper limb tremor,

right foot dystonia.

Right upper limb tremor,

myoclonic jerk.

Tremor in left upper limb, and

ataxia.

Right upper limb tremor.

Right hemiataxia, head tremor,

right upper limb tremor.

Left upper limb tremor.

Cranial tremor, left foot tremor,

and dystonia.

Left frontotemproparietal hge

Left temproparietooccipital infarction

Left thalamic infarction.

Bilateral pontine infarctions.

Subarachnoid hge.

Subarachnoid hge.

Bilateral cerebellar haematoma & right

medullary infarction.

Right frontotemporal hge.

Right lenticulocapsular hge.


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Table 7. Cases of dystonia reported after cerebral stroke in relation to CT/MRI findings.

Age of

patients Gender Handedness

Clinical

Manifestations CT/MRI findings

43 year

35 year

43 year

41 year

50 year

71 year

48 year

41 year

Male

Male

Female

Male

Male

Male

Male

Female

Right

Right

Right

Right

Right

Right

Right

Right

Generalized dystonia.

Left hemidystonia.

Left upper limb dystonia.

Oromandibular, and left cervical

dystonia.

Left upper limb dystonia.

Dystonia in left foot.

Right hemidystonia.

Left foot dystonia, and left hemitremor.

Bilateral cerebellar ischaemia.

Bilateral pontine infarctions.

Right temporal infarction.

Right frontoparietal hge.

Right temporal hge.

Right thalamic hge.

Left lenticulocapsulothalamic hge.

Right lenticulocapsular hge.

Table 8. Cases of parkinsonism reported after ischemic cerebral stroke in relation to CT/MRI findings.

Age of

patients Gender Handedness Clinical manifestations CT/MRI findings

57 years

60 years

59 years

51 years

Male

Female

Female

Female

Right

Right

Right

Right

Right hemiparkinsonism*

Right hemiparkinsonism**

Right hemiparkinsonism***

Left hemiparkinsonism****

Left frontoparital infarction

Left lenticulocapsular infarction

Left mesencephalic ischemic lesion

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.


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.


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.

Chorea: Most of the cases of chorea, had

underling thalamic lesion (6 patients, 46.1%),

followed in frequency by lesions in lentiform

nucleus and neighbouring structures (4 patients,

30.8%), whereas surface lesions (frontal, parietal, &

temporal), were reported in 3 patients (23.1%).

Only one patient had lesion in corona radiate and


429

another patient suffered cerebellar lesion alone as

shown in the table (5). Based on the previous data,

one can conclude that most of cases of chorea in

this study are due to deep lesions particularly in

thalamus and lentiform nucleus with contralateral

development of chorea. In spite of this previous

finding, more than quarter of patients had lesions in

other regions so we can suggest that although most

of the cases of chorea are due to lesions in thalamus

or lentiform nucleus, lesions in other regions as

cortical areas (temporal, frontal, parietal),

cerebellum, and corona radiate, could be

incriminated in the pathogenesis of chorea. Our

finding came to agree with that of Dewey and

Jankovic9, and Lee and Marsden10, that reported the

most frequent lesion in cases of chorea is thalamic

lesion, and Chang, et al.11, that found lentiform

nucleus lesions were common cause of chorea.

Through reduction of inhibitory output of the

globus pallidus on the thalamus10, lesions in the

thalamus and lentiform nuclei presumably leads to

excess excitatory output to the cortex with

subsequent contralateral hyperkinetic movements30.

Hemiballismus: Rather than subthalamus, we

found in this study that ballismus movement was

present in patients having lesion in thalamus,

putamin, globus pallidus and neighbouring

structures as shown in table (5). This finding could

be explained based on previous studies9,10,30

, that

attributed hemiballismus movement after

subthalamus lesion to reduction of the inhibitory

output of the globus pallidus on the thalamus by

diminishing the normal excitatory drive to the

internal segment of the globus pallidus, and this

disinhibition gives rise to excessive excitatory drive

to the cortex which is expressed as a contralateral

hyperkinetic movement. From this previous data,

one can report that subthalamus, globus pallidus,

and thalamus, all of them are involved in

pathogenesis of ballismus movement.

Tremor: Tremor reported in this study were

mainly intention type and most of them in the

upper limb, 5 (55.5%) patients out of 9 had both

resting and intention pattern, and all the patients

had postural element but to varying degrees.

Cortical lesions were reported in 3 patients

(33.3%), in agreement with Kim in 1992, 1994,

and 200112,57,58

, who reported upper limb tremor,

especially of the hand in patients with cortical

lesion. Kim in 1992, and 1994 has suggested that

cortical strokes may modulate the sensorimotor

circuitry and produce movement disorders. Other

patients with tremor had thalamic, pontine,

medullary, and cerebellar lesions as well as

subarachnoid haemorrhage. This finding match

with results reported by previous studies59,60,61

,

that posterior thalamic lesion including thalamic

infarction, haemorrhage, traumatic brain injury,

infection, or neoplasm, was reported as well as

dentatorubrothalamic tract involvement to cause

intention tremor. Subarachnoid haemorrhage itself

or its complications (hydrocephalic lesion), might

induce its tremogenic effect via global

compromise of brain functions or secondary

hydrocephalic changes with dilatation of

ventricles and subsequent compression of

structures adjacent to ventricular system as basal

ganglia, thalamus, etc.

Dystonia: As far as dystonia is concerned,

our patients who suffered dystonia have lesions in

different regions of the brain rather than basal

ganglia, as cortical lesions (frontal, parietal,

temporal), thalamus, lenticulocapsular, cerebellar,

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


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.


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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434

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