JRSM >
Volume 94, Number 6 >
Pp. 301-302
Department of Neurosurgery, Newcastle General Hospital, Newcastle,
UK
1
Department of Neuroradiology, Newcastle General Hospital, Newcastle, UK
Correspondence to: Professor A D Mendelow, Department of Neurosurgery, Newcastle General Hospital, Newcastle upon Tyne NE4 6BE, UK
Cortical tremor is easily mistaken for parkinsonism. Ablation of the underlying lesion can be curative.
CASE HISTORY
A woman aged 50 sought advice because of continous shaking of her left hand, which interfered with her daily life. She was right-handed. The tremor had begun gradually about six weeks earlier, worsening to the point where she could not get food to her mouth with a fork in the left hand. Alcohol made it worse. There was no precipitating cause that she could recall; she had not been exposed to antiemetics, neuroleptics or antidepressants. On examination the tremor was present at rest and was aggravated by posture and action. There was no stimulus sensitivity. She had difficulty in performing rapidly alternating tasks and fine finger movements with the left hand. Neurological findings were otherwise normal. Early parkinsonism and epilepsia partialis continua were prominent in the differential diagnosis. Magnetic resonance imaging revealed an arteriovenous malformation, approximately 3 cm in maximum diameter, at the medial aspect of the right cerebral hemisphere just superior to the rostrum of the corpus callosum, affecting the cingulate gyrus (Figure 1). Digital subtraction arteriography indicated that its blood supply was from the right anterior cerebral artery (pericallosal and callosomarginal branches). Venous drainage was to the superior sagittal sinus (Figure 2).
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The nidus of the malformation was catheterized (1.2F microcatheter) and the lesion was partly embolized with glue mixture. Some of the arterial supply to the malformation was from small perforating vessels which could not be catheterized. The tremor improved somewhat. The malformation was then excised completely via a right parasagittal frontal craniotomy, with preservation of the pericallosal and callosomarginal arteries. Complete excision was confirmed by intraoperative angiography. The patient's symptoms resolved completely and she was discharged without further disability. On review at one year she had a very mild tremor in the left hand which did not interfere with her social or domestic activities.
COMMENT
Various tumours and vascular lesions, including arteriovenous malformations, have been reported as causing kinetic tremors1,2,3,4,5,6—hence the calls for brain scanning in patients with parkinsonsism7. Evidente et al.5 described improvement, though not abolition, of tremor after removal of a convexity meningioma. Others, by contrast, have described development of tremor after meningioma surgery3,8. The mechanism in our patient may have been rapid growth or enlargement of the malformation, with disruption of the pathways in the right motor cortex. With tumours, some workers suggest that the basal ganglia can be involved via oedema or vascular insufficiency; others hypothesize dysfunction of the premotor cortex or deafferentation of the primary motor cortex5. Wang et al.3 suggest that the sensory cortex is normally under inhibitory influences from the ipsilateral frontal motor cortex; thus damage from trauma or ischaemia might cause loss of such inhibition. In our patient we think the presentation and outcome suggestive of an ischaemic mechanism. The arteriovenous malformation was in the cingulate gyrus and we hypothesize that a vascular ‘steal’ phenomenon, more pronounced on activity, was responsible for the tremor and its variability.
Acknowledgments
We thank Dr David Burn, consultant neurologist, for his comments.
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