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| Year : 1999 | Volume
: 47
| Issue : 1 | Page : 40-2 |
Movement disorders caused by brain tumours.
Bhatoe HS
Department of Neurosurgery, Command Hospital (Sc), Pune, Maharashtra, 411040, India.
Correspondence Address:
Department of Neurosurgery, Command Hospital (Sc), Pune, Maharashtra, 411040, India.
Movement disorders are uncommon presenting features of brain tumours. Early recognition of such lesions is important to arrest further deficit. We treated seven patients with movement disorders secondary to brain tumours over a period of seven years. Only two of these were intrinsic thalamic tumours (astrocytomas) while the rest were extrinsic tumours. The intrinsic tumours were accompanied by hemichorea. Among the extrinsic tumours, there was one pituitary macroadenoma with hemiballismus and four meningiomas with parkinsonism. Symptoms were unilateral in all patients except one with anterior third falcine meningioma who had bilateral rest tremors. There was relief in movement disorders observed after surgery. Imaging by computed tomography or magnetic resonance imaging is mandatory in the evaluation of movement disorders, especially if the presentation is atypical, unilateral and/or accompanied by long tract signs.
How to cite this article:
Bhatoe H S. Movement disorders caused by brain tumours. Neurol India 1999;47:40 |
Brain tumours rarely present with movement disorders (MDs). Such tumours may be intrinsic or extrinsic with reference to basal ganglia and thalamus. We treated seven patients with MDs secondary to brain tumours over a period of seven years (1990-1996). While only two of these were intrinsic thalamic astrocytomas, the rest were extrinsic tumours (pituitary macroadenoma and meningiomas). Relevant literature is briefly reviewed.
This report is based on analysis of seven patients with brain tumours, who had MDs either as their principal presenting feature or these were important part of clinical presentation. Diagnosis was made by computed tomography (CT). All the patients underwent surgery and excision of tumour. Tumour excision was partial in patients with thalamic tumours and subtotal in one patient with sphenoid ridge meningioma. MDs disappeared in all the patients after surgery. There was no preoperative mortality. No recurrence of MDs was observed during the follow up period of 6 months to 5 years. The clinical profile, diagnosis, surgical procedure and results in all seven patients is given in [Table 1.]
The basal ganglia play a major role in the control of posture and movement. Although the presence of a space occupying lesion (a tuberculoma) involving the substantia nigra (SN) was the first indication that the SN played a role in the pathogenesis of Parkinsonism,[1] reported cases of brain tumours manifesting as MDs are rare. How brain tumours manifest clinically as MDs only in some cases is a matter of conjecture, and clinicopathological correlation should be made with certain reservations. Intrinsic basal ganglia and thalamic lesions as well as extrinsic compressive lesions have been reported to be causing MDs. Direct mechanical pressure and/or torsion of basal ganglia by a hemispheric mass might in itself cause dysfunction of these nuclei. Others have proposed that MDs occurred in brain tumours due to midbrain compression from upward or downward herniation.[3],[4] It is reasonable to postulate that such herniation may be accompanied by an impairment of blood flow to the basal ganglia via the posterior cerebral arteries, leading to ischaemia of the subthalamic nuclei.[5] Coexisting lacunar infarct of the basal ganglia, especially in the presence of coexisting hypertension may be responsible in certain cases.[6] In intrinsic tumours, the basal ganglia and thalamus involved primarily by the tumour may lead to `internal' compression of neurons or pathways, or from altered metabolism by reduced vascular supply.[7] Tumours or peritumoural oedema may also induce symptoms by `external' compression of adjacent structures or their vascular supply leading to hemichorea.
The functional state of tumours causing MDs has only rarely been studied. In a case of left frontal meningioma with right sided hemi-parkinsonism, PET studies indicated impaired oxygen metabolism and tissue perfusion in the striato-pallidal region.[8] In one case of Parkinsonism, secondary to craniopharyngioma, biochemical findings on autopsy revealed considerably reduced striatal catecholamines and severely decreased dopamine binding sites in the caudate.[9]
It is thus clear that interaction of different mechanisms may or may not lead to MDs in patients with brain tumours. Since these tumours/lesions may also involve structures of basal ganglia or their connections which are known to reduce or abolish MDs when lesioned (ventrolateral thalamus, zona incerta, pulvinar thalami) tumours of basal ganglia or thalamus are rarely accompanied by MDs.[7]
MDs are p lesions.[10] Most of such extrinsic lesions are laterally placed. These lesions may be frontal,[11] temporal,[11] or parietal.[10],[13],[14] Almost all these extrinsic lesions have been meningiomas. Gliomas and metastatic tumours in the frontal lobes have also been associated with parkinsonian tremor.[10],[11],[15] Subdural haematoma has also been reported producing Parkinsonism.[2],[6]
Midline extrinsic lesions producing MDs are even more rare. Wakai et al[16] reported an anterior third ventricular meningioma producing parkinsonism. Although pituitary adenoma and craniopharyngioma too have been reported with Parkinsonian features,[9] hemiballismus accompanying pituitary adenoma has not been reported earlier. Rarely Parkinsonism may be seen due to posterior fossa lesions.[4],[9],[17]
In contrast to trinsic tumours which produce rest tremor intrinsic thalamic or basal ganglia tumours usually produce chorea. Krauss et al[7] reported dystonia and chorea in most of their patients of thalamic tumours with MDs. Hemiparkinsonism secondary to thalamic and basal ganglia astrocytoma, is rare[18] as is chorea due to an extrinsic compressive lesion.[19]
Patients with brain tumours who present with MDs may also have other associated neurological manifestations such as alteration in sensorium, involvement of corticospinal tracts, features of raised intracranial pressure, etc would seem appropriate to obtain CT or MRI in any patient with appropriate clinical profile, especially if the patient is young, has long tract signs and features of raised intracranial pressure. Excision of the offending mass should be considered without delay in these patients. Several authors have shown the reversibility of clinical findings after tumour excision. This was true in our patients as well. Further, functional studies are needed which will provide deeper insights into the pathophysiological processes underlying the generation of MDs in patients with brain tumours.
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