Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We performed a double-blind, randomized trial of intravenous scopolamine, benztropine, and glycopyrrolate in 7 patients with acquired nystagmus and oscillopsia. Five patients had pendular nystagmus and 2, downbeat nystagmus. We recorded eye movements with a magnetic search coil technique and tested visual acuity and motion perception before and after administration of each drug. Scopolamine reduced nystagmus in all patients. Benztropine was moderately effective and glycopyrrolate had a negligible impact. Visual acuity improved only with scopolamine; motion discrimination and oscillopsia improved significantly with scopolamine and benztropine. Pendular and downbeat nystagmus respond to intravenous antagonists of central muscarinic receptors.
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PMID:Muscarinic antagonists in the treatment of acquired pendular and downbeat nystagmus: a double-blind, randomized trial of three intravenous drugs. 812 84

In order to elucidate the effect of scopolamine on the vestibular system in humans, various experimentally-induced forms of nystagmus, i.e. caloric nystagmus, rotational nystagmus, optokinetic nystagmus, visual-vestibular interaction and optokinetic after nystagmus, were evaluated before and after the administration of two pieces of Scopoderm-TTS or placebo patches retro-auricularly. Scopolamine reduced the responses of both the caloric and optokinetic after nystagmus compared with the placebo. The possible action site of this drug is discussed.
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PMID:Effect of transdermally administered scopolamine on the vestibular system in humans. 847 May 31

The aim of the present study was to investigate the effects of scopolamine (1.5 mg, transdermal patch) and cyclizine (50 mg tablet), at the doses usually used for the relief of motion sickness, on postural sway, optokinetic nystagmus (OKN) and circularvection (CV) in humans, using a within-subjects, double-blind, placebo-controlled design. Scopolamine and cyclizine were found to have no significant suppressive effect on these aspects of visual-vestibular interaction. Postural sway and CV were not significantly affected by either drug treatment; OKN SPV was significantly increased (p < 0.05), although OKN amplitude and frequency were unaffected. These results suggest that scopolamine and cyclizine, at doses used for the relief of motion sickness, may have minimal suppressive effects on these aspects of visual-vestibular interaction.
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PMID:The effects of scopolamine and cyclizine on visual-vestibular interaction in humans. 1093 83

Patients with acquired forms of nystagmus may suffer from oscillopsia and blurred vision; abolishing or reducing nystagmus ameliorates these symptoms. Ideally, treatment of nystagmus should be directed against the pathophysiologic mechanism responsible. Identification of nystagmus pattern is important in directing therapy and occasionally requires electronic eye movement recording for precise characterization. Patients with acquired pendular nystagmus, particularly those with multiple sclerosis, often benefit from gabapentin, a drug with few side effects. Scopolamine, clonazepam, and valproate are also useful in some patients. A new drug, memantine, was effective in treating pendular nystagmus in one study, but it has not yet been approved for use in the United States. Periodic alternating nystagmus usually responds to baclofen. Central vestibular nystagmus, including downbeating and upbeating forms, can be treated with baclofen or clonazepam. In some patients, treatment of an underlying condition, such as periodic ataxia, Whipple's disease, and Chiari malformation, abolishes nystagmus and improves vision. If pharmacologic therapy fails, optical devices can be considered in selected patients. Injections of botulinum toxin and surgery to weaken extraocular muscles are prone to induce diplopia and may precipitate plastic-adaptive ocular motor changes that eventually negate the beneficial effect.
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PMID:Acquired Nystagmus. 1109 97

Motion sickness is a common and distressing but poorly understood syndrome associated with nausea/vomiting and autonomic nervous system accompaniments that develops in the air or space as well as on sea or land. A bidirectional aetiologic link prevails between migraine and motion-sickness. Motion sickness provokes jerk nystagmus induced by both optokinetic and vestibular stimulation. Fixation of gaze or closure of eyes generally prevents motion sickness while vestibular otolithic function is eliminated in microgravity of space, indicating a predominant pathogenetic role for visuo-sensory input. Scopolamine, dimenhydrinate, and promethazine reduce motion-related nystagmus. Contraction of extraocular muscles generates proprioceptive neural traffic and can provoke an ocular hypertensive response. It is proposed that repetitive contractions of the extraocular muscles during motion-related jerk nystagmus rapidly augment brain stem afferent input by increasing proprioceptive neural traffic through connections of the oculomotor nerves with the ophthalmic nerve in the lateral wall of the cavernous sinus as well as by raising the intraocular pressure thereby stimulating anterior segment ocular trigeminal nerve fibers. This verifiable hypothesis defines the pathophysiological basis of individual susceptibility to motion sickness, elucidates the preventive mechanism of gaze fixation or ocular closure, advances the aetiologic link between MS and migraine, rationalizes the mechanism of known preventive drugs, and explores new therapeutic possibilities.
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PMID:Motion sickness is linked to nystagmus-related trigeminal brain stem input: a new hypothesis. 1582 12