Search

Palatal myoclonus is usually due to a brainstem or cerebellar lesion disrupting the dentato-rubro-olivary pathway. Rarely it may be caused by a cortical lesion. The precipitating factor in 70% of all cases is an infarct. We describe an unusual case of a patient with palatal myoclonus who had an old ipsilateral cerebellar infarct and a new contralateral subcortical (corona radiata) infarct. We postulate that the new infarct caused disinhibition of the old cerebellar infarct, resulting in palatal myoclonus. Magnetic resonance imaging (MRI) of the brain did not show any hypertrophy of the inferior olivary nucleus. Her myoclonus proved refractory to clonazepam, valproate and phenytoin.

Sciatic neuropathy is an uncommonly diagnosed focal mononeuropathy. We reviewed the aetiology and electrodiagnostic features of 29 patients studied at the Neurodiagnostic Laboratory, Tan Tock Seng Hospital from January 1989 to April 1995. External nerve compression was the most common cause (38%) followed by trauma (21%). Other rare causes in this series included intragluteal injections, hip surgery and diabetic mononeuropathy while 24% had uncertain aetiology. Electrodiagnostic studies showed preferential involvement of the peroneal division in 51%. Axonal loss was found in 97%. We conclude that sciatic neuropathy often mimics distal peroneal nerve dysfunction and neurophysiological studies are essential for diagnosis. Furthermore, these studies are necessary for assessing prognosis in relation to axonal loss.

Fibromuscular dysplasia (FMD) of the internal carotid arteries and its relationship with focal cerebral ischaemia is unproven. This vasculopathy is often detected incidentally during a cerebral angiogram for non-ischaemic cerebral events. FMD affects the proximal one-third of the internal carotid artery in almost all cases and is bilateral in 60% to 85%, with middle-aged women affected in 85% of the cases. Ischaemic stroke has been postulated to result from severe stenosis or thrombotic occlusion at the FMD site. Cerebral embolism from FMD has rarely been reported. We report 3 young patients with acute ischaemic stroke who had FMD on cerebral angiography. They presented with a focal hemispheric stroke where the probable pathophysiology is embolism to the distal internal carotid artery from thrombus formed at the proximal FMD site. The patients were all males, with unilateral proximal internal carotid artery FMD lesions and occlusion of the internal carotid artery distally on the same side. All were extensively investigated and no other causes for stroke were found.

Acute mutism with paralysis of the bulbar and facial muscles following discrete bilateral internal capsular infarction is a rare stroke syndrome. We describe a 62 year-old male who suddenly became unable to speak or swallow. The paucity of facial expression and inability to voluntarily move the facial, lingual and pharyngeal muscles were persistent and contrasted with a relatively mild limb paresis which recovered. High resolution CT scan revealed infarcts in the posterior limbs of both internal capsules. It is important to recognise this stroke syndrome because of the permanence of dysarthria and dysphagia associated with it.

We describe a 30 year-old female who presented with severe orthostatic hypotension despite appropriate compensatory tachycardia on standing, following a viral infection. Clinical assessment and laboratory evaluation failed to detect other causes of her illness besides sympathotonic orthostatic hypotension. She responded to fludrocortisone and recovered completely after 3 months. We postulate that her acute reversible illness was due to a post-viral immunological response selectively affecting the alpha adrenergic receptors subserving the post-ganglionic sympathetic vasomotor fibres.

We describe a 40 year-old male with a ball-cage mitral valve prosthesis who suddenly developed bilateral ptosis, bilateral dilated and unreactive pupils, right third nerve palsy, bilateral failure of vertical gaze, somnolence and mild ataxia without major motor deficits. Computed Tomography (CT) revealed bilateral thalamic infarcts in the distribution of the rostral basilar artery. Infarction in this case occurred despite adequate anticoagulation. The recognition of the entity of rostral basilar artery occlusion is important as interruption of anticoagulation may be avoided.