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July2007 Vol.44 Issue:      2 Table of Contents
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Study of The Occurrence of Abnormal Involuntary Movements after Cerebral Stroke

Osama M.M.A. Elazouni1, Amal SE Elmotayam1, Karam Selim1, Said A. Elmonem2

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, tremor12-15, dystonia16-20, parkinsonism21-25, and myoclonus26, 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 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, 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 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

Chi-Squared Test, x2 = 13.21, P = 0.15 (non significant).

 

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

Chi-Squared Test, x2 = 15.03, P = 0.09 (non significant).

 

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.

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.

 

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.


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 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 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.   

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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الملخــص العربـــى

 

دراسة حدوث الحركات اللاإرادية المرضية بعد الإصابة بالسكتة الدماغية

 

مقدمة عن البحث :

قامت بعض الدراسات السابقة من قبل باستعراض ودراسة حدوث الحركات اللاإرادية المرضية بعد الإصابة بالسكتة الدماغية ولكن معظم هذه الدراسات كانت فقط دراسات عن حدوث نوع معين من هذه الحركات أو دراسة الحركات اللاإرادية الناجمة عن إصابة في منطقة معينة بالمخ أو فقط تقارير عن حالات نادرة. 

 

الهدف من البحث :

إن الهدف من أجراء هذا البحث هو دراسة الحركات اللاإرادية المرضية في المرضى بعد الإصابة بالسكتات الدماغية من حيث نوعية هذه الحركات أيا كان مكان الإصابة بالمخ وعلاقة حدوث هذه الحركات اللاإرادية بنوع السكتة الدماغية من حيث نزيف أو جلطات الدماغ وأيضا دراسة علاقة هذه الحركات بالحالة الإكلينيكية للمرضى والتاريخ الشخصي للمرضى مثل السن والجنس ومكان الإصابة بالمخ معتمدا على الدراسات الإشعاعية.

 

طرق البحث :

تضمن هذا البحث عدد 43 مريضا يعانون من حدوث الحركات اللاإرادية المرضية بعد الإصابة بالسكتة الدماغية وقد تم اختيار هؤلاء المرضى على أساس الإصابة للمرة الأولى وذلك بناء على دلائل إكلينيكية و إشعاعية للمرضى وهؤلاء المرضى إما قد تم ضمهم إلى الدراسة في الفترة الأولى وهؤلاء هم الذين قد ظهرت فيهم الحركات اللاإرادية مبكرا وقد تم متابعتهم منذ البداية أو هؤلاء الذين ظهرت فيهم الحركات اللاإرادية بعد ذالك وقد تم فحصهم و تدوين تاريخ حدوث السكتة الدماغية وتاريخ حدوث هذه الحركات ونوع السكتات الدماغية وغير ذالك من التاريخ الطبي ومتابعتهم مثل الآخرين من المرضى وقد تم استبعاد المرضى الذين قد أصيبوا بحركات لاإرادية قبل هذه الدراسة والذين لم يخضعوا بالكامل لمدة المتابعة الكاملة أو الذين قد توفوا قبل هذه المدة وقد تم إخضاع هؤلاء المرضى للاتي:

·     فحص اكلينيكى شامل للجهاز العصبي متضمنا الحصول على التاريخ الطبي من المرضى أو من مرافقيهم عند تدهور مستوى الوعي للمرضى. وقد تم تحديد وتشخيص نوع هذه الحركات اللاإرادية عن طريق اثنين من الباحثين في هذه الدراسة كلآ على حده ثم الاستشارة للخروج للتشخيص النهائي ومتابعة هذه الحركات باستخدام مقياس الحركات اللاإرادية المرضية وأيضا متابعة الحالة الإكلينيكية للمرضى من حيث القوة الحركية والإصابة الحسية وأيضا الاختلاج العصبي وقد تمت هذه المتابعة كل أسبوعين في الشهر الأول ثم بعد ذلك فترة كل شهر لمدة عام على الأقل بعد ظهور هذه الحركات.

·     دراسات إشعاعية (أشعة مقطعية أو رنين مغناطيسي على المخ) في الفترة الأولى بعد الإصابة بالسكتة الدماغية وقد أعيد عمل هذه الدراسات لبعض المرضى وذلك لعدم وضوح الإصابة.

أيضا اشتملت الدراسة على ثلاث حالات نادرة من جلطات منطقة مهاد المخ المركزية, وقد أجريت عليهم نفس الدراسات السابقة.

 

نتائج البحث :

اظهر البحث النتائج آلاتية:

·           اكبر نسبه من المرضى 38.2% مصابين بالحركة اللاإرادية الراقصة واقل نسبة من المرضى كانت تعانى من الشلل الرعاش 11.7%

·           متوسط أعمار مرضى الحركة اللاإرادية الراقصة هو الأعلى بالنسبة لباقي المجموعات و بفارق ذا دلالة إحصائية.

·     اقل متوسط مدة لحدوث الحركات الللاارادية هي تلك الخاصة لحدوث الحركات اللاإرادية الراقصة وهي تقل بفارق ذا دلالة إحصائية عن بقية المجوعات

·           بفارق ذا دلالة إحصائية لم يتم شفاء أيا من مرضى الشلل الرعاش

·     معظم المرضى المصابين بالحركات اللاإرادية المرضية كانوا على درجة 4 على مقياس القوة الحركية وكانت درجة تأثرهم الحسية والاختلاج العصبي متوسطة و شديدة

·     لم تكن جميع الإصابات الدماغية للمرضى في منطقة المهاد المخى أو النواة القاعدية بل وجدت نسبة من الإصابات خارج هذه المناطق مثل الإصابات القشرية الأمامية, الجدارية, الصدغية, الخلفية وأيضا نزيف تحت العنكبوتية, إصابات المخيخ, إصابات جزع المخ و غير ذالك

·           المرضى المصابين بجلطات بالمنطقة المركزية للمهاد المخى قد أصيبوا بالحركة اللاإرادية الراقصة وأيضا الاختلاج العصبي.

 

ملخص البحث :

أن إيجاد علاقة بين مكان الإصابة في المخ ونوع الحركات اللاإرادية المرضية يمكن إن يكون في بعض الأحيان صعب وغير واضح وعلى الرغم من إن الإصابة بمنطقة المهاد المخى أو النواة القاعدية هي السبب الشائع للحركات اللاإرادية إلا إن نسبة من هؤلاء المرضى كانوا قد أصيبوا في أماكن أخرى من المخ ويمكن تفسير ذالك بحدوث اختلاج عصبي وإصابة حسية عميقة بدرجة متوسطة أو شديدة مع إصابة بسيطة في الجهاز الحركي وهذا يمكن إن يكون السبب وراء حدوث هذه الحركات في إصابات المخ خارج ألاماكن السابقة. وأخيرا يمكن القول إن دراسة كيفية حدوث الحركات اللاإرادية يحتاج إلى الكثير إلى الدراسة العميقة و التحليل الدقيق للدراسات الإشعاعية مع النظر بعين الاعتبار إلى الدراسات الإشعاعية الوظيفية.



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