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)

See-saw nystagmus is a pendular nystagmus with two distinct components: a conjugate torsional component and a disjonctive vertical component. The acquired form of nystagmus is usually seen with parasellar mass and less frequently in head injury or brainstem infarction. Almost all patients with parasellar mass or head injury have associated bitemporal hemianopia. We report the case of a 27-year-old man who developed intermittent daily oscillopsia five years after a severe head injury. On neurological examination, the patient showed a congenital left eye divergence with left eye convergence paresis, an anosmia, a right optic atrophy and a bitemporal hemianopia. Visual acuity was 7/10 and 3/10 for the right and left eyes. The rest of the neurological examination was unremarkable. Electroencephalogram during oscillopsia was normal. MRI revealed bilateral orbito-frontal low signal intensity on T1 weighted images. The brainstem, the diencephalon and the ventricular system appeared to be intact. Eye movement recordings exhibited intermittent see-saw nystagmus. Clonazepam treatment resolved the see-saw nystagmus. Slowly withdrawal of clonazepam was done without return of the see-saw nystagmus.
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PMID:[Intermittent sea-saw nystagmus successfully treated with clonazepam]. 767 33

This report documents a case of voluntary inhibition of acquired pendular nystagmus after head trauma. A 30-year-old male developed oscillopsia and decreased visual acuity, as well as findings of acquired pendular nystagmus with voluntary inhibition after head trauma. The EOG finding was horizontal 18-20 Hz bilateral symmetrical pendular nystagmus in all directions of gaze at near and distant fixation. Nystagmus did not change with 14 Prism Diopter base-out prisms on both eyes, but it was possible to abolish it intentionally. Baclofen and Clonazepam had no effect in improving the patient's symptoms and EOG finding.
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PMID:Acquired pendular nystagmus with voluntary inhibition. 1145 3

Acquired and congenital nystagmus often causes decreased visual acuity as a direct result of the inability to maintain stable foveal vision. In addition, acquired nystagmus causes a disabling subjective sensation of movement of the visual world called oscillopsia. The eye movements themselves do not require treatment if the patient is asymptomatic. However, therapy is necessary if visual disability is present. Treatments based in pharmacologic mechanisms are preferred. There are few controlled treatment trials and therapeutic efficacy generally is sought in a trial and error approach, depending on the type of nystagmus present. Treatment with 3,4-diaminopyridine and 4-aminopyridine recently have been shown to be effective for downbeat nystagmus. Gabapentin, baclofen, and clonazepam also are useful in some patients with downbeat nystagmus. Baclofen is the therapy of choice for periodic alternating nystagmus. Gabapentin often is effective for acquired pendular nystagmus. Clonazepam and valproate also may be effective for acquired pendular nystagmus. Memantine now is available in the United States and is promising in the treatment of pendular nystagmus. Optical devices that negate the negative effects of nystagmus continue to undergo development research. These and other medical, surgical, and optical devices are potentially useful alone or in combination with other therapies.
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PMID:Current Treatment of Nystagmus. 1561 Jul 9