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G Vanhooren

Publications and source records attributed to G Vanhooren.

5 recordsLinked to original sources

Benign paroxysmal positional vertigo of the horizontal canal.

OBJECTIVES: To review the clinical features, electronystagmography findings, the possible mechanism, and a possible therapeutic approach to benign paroxysmal positional vertigo (BPPV). METHODS: Sixty-three cases of BPPV of the horizontal canal type have been reviewed. It is characterised by horizontal nystagmus and an intense vertigo, provoked by rotation of the head in a supine patient. The horizontal nystagmus beats towards the ground on both sides, becomes more pronounced when lying on the pathological side, and then the nystagmus often changes direction. RESULTS: Forty-eight patients underwent electronystagmography. On the pathological side, the first phase nystagmus had a mean latency of three seconds and a mean duration of 31.6 seconds. Nystagmus inversion occurred in 36 patients after a nystagmus free interval. The mean second phase nystagmus duration lasted 33.4 seconds. On the healthy side, the nystagmus had a mean latency of 3.4 seconds and a mean duration of 39.5 seconds. Fatigue was seen in six patients. Simultaneous involvement of the posterior canal was present in 16 patients. A liberatory manoeuvre was successful in six patients. CONCLUSIONS: The liberatory manoeuvre should be tried in patients with horizontal canal vertigo. It should not be performed in patients with severe cervical arthrosis, vertebrobasilar insufficiency, or when the patient has neck pain during the manoeuvre.

Adult

Apraxia of eyelid opening secondary to right frontal infarction.

Apraxia of eyelid opening is the incapacity of voluntarily eyelid opening in the absence of motor dysfunction or blepharospasm. It has mostly been described in extrapyramidal diseases and only very rarely in cortical lesions. We report a right-handed patient with a right frontal infarction exhibiting eyelid opening apraxia.

Aged

Polyneuropathy in lithium intoxication.

Two patients developed acute sensorimotor polyneuropathy after intoxication with lithium carbonate. Nerve conduction studies, electromyography, and sural nerve biopsy proved it to be an axonal neuropathy. Recovery of muscle strength, reflexes, and sensory function started weeks after discontinuation of lithium therapy. One patient fully recovered within a year. In the literature we found nine other cases of lithium polyneuropathy.

Adult