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)

The GABAergic drug baclofen and the cholinergic drug physostigmine were administered to patients with upbeat and downbeat nystagmus. Baclofen (orally, 5 mg three times daily) reduced nystagmus slow phase velocity and distressing oscillopsia by 25-75% in four out of five patients (two upbeat nystagmus; two downbeat nystagmus). Physostigmine (1 mg single intravenous injection) increased nystagmus in five additional patients with downbeat (1) or positional downbeat nystagmus (4) for a duration of 15-20 minutes. The different interactions of baclofen and physostigmine on neurotransmission subserving vertical vestibulo-ocular reflex could account for these effects. The response to baclofen appears to be a GABA-B-ergic effect with augmentation of the physiological inhibitory influence of the vestibulo-cerebellum on the vestibular nuclei. Similarly baclofen has an inhibitory effect on the velocity storage mechanism. Cholinergic action may cause the increment of nystagmus by physostigmine.
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PMID:The effects of baclofen and cholinergic drugs on upbeat and downbeat nystagmus. 165 96

Toluene, an aromatic solvent, prolongs the duration of nystagmus induced by a rotatory acceleration or by an optokinetic stimulation in the pigmented rat. Baclofen, an agonist of GABAB receptors, and 4,5,6,7-tetrahydroisoxazolo[5,4-c]-pyridin-3-ol (THIP), an agonist of GABAA receptors are able to block this toluene effect on the vestibular system. On the contrary diazepam, which by itself causes an evident reduction of the duration of acceleratory nystagmus, is not able to block the toluene effect. The results indicate that the toluene effect is related to GABA transmission and that the solvent interacts by a rather receptor specific mechanism of action.
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PMID:The effect of toluene on the vestibulo- and opto-oculomotor system in rats, pretreated with GABAergic drugs. 216 15

Baclofen affects in experiments the reactivity of the vestibuloocular reflex by influencing the time constant of the vestibular nystagmus. The authors compare in three healthy volunteers the reactivity of the vestibular apparatus after administration of Baclofen and a new muscle-relaxant drug tizanidine. The authors evaluate basic parameters of the vestibular and optokinetic nystagmus (gain and time constant), discuss the problem of GABAergic (Baclofen) and monoaminergic (tizanide) receptors kin the area of the vestibular apparatus. As regards the effect on the reactivity of the vestibular system, tizanidine does not affect immediately the response of the vestibuloocular reflex but interferes with processes ensured by the central neuronal integrator.
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PMID:[The effect of muscle relaxants on the function of the vestibulo-ocular reflex arc]. 234 48

Familial spastic paraplegia (FSP) was recorded in three families. The pattern of familial transmission and the onset in the second and third decade of life strongly suggested autosomal dominant inheritance. FSP in this series showed the consistent, classical, clinical features with some inconstant findings (nystagmus, dysarthria, posterior column involvement). Baclofen for the treatment of spasticity is beneficial in this condition and genetic counselling should be considered.
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PMID:Familial spastic paraplegia. 273 87

1. Baclofen had a characteristic effect on vestibular and optokinetic nystagmus in rhesus monkeys. Each aspect of nystagmus that is dependent on the velocity-storage mechanism in the vestibulo-ocular reflex (v.o.r.) was altered by the drug: (a) Baclofen reduced the dominant time constant of the v.o.r. in a dose-dependent manner up to 5 mg/kg, the highest dosage used. The alteration in v.o.r. time constant began within 15 min of injection, was maximal between 1 and 4 h, and lasted for 14-18 h. This effect mirrors changes in plasma levels of baclofen after oral doses in humans (Faigle, Keberle & Agen, 1980). (b) Slow-phase velocities of steady-state nystagmus induced by rotation about axes tilted from the vertical (off-vertical axis rotation, o.v.a.r.) were reduced after baclofen and could not be maintained at previous levels. (c) There was a dose-dependent decline in the steady-state gain of optokinetic nystagmus (o.k.n.), and at the highest dosages little o.k.n. was induced. In parallel, the peak velocity and falling time constant of optokinetic after-nystagmus (o.k.a.n.) were reduced. Since baclofen is a GABA agonist, systems utilizing GABA and acting on GABAB receptors appear to produce inhibitory control of velocity storage. 2. The step gain of the v.o.r., measured at the beginning and end of constant-velocity rotation in darkness, was unaffected by baclofen, as were saccades, quick phases of nystagmus, and the ability to hold positions of fixation or to generate linear slow phases of nystagmus. This indicates that it is possible to use baclofen to manipulate the dominant time constant of the v.o.r. and of o.k.a.n. in relative isolation from effects on other oculomotor components. 3. Baclofen caused a dose-dependent reduction in the initial jump in eye velocity at the onset of o.k.n., suggesting that the initial jump is also under inhibitory control of GABAB receptors. However, there were still occasional slow phases with velocities up to 30-40 deg/s after baclofen, and animals were capable of visually suppressing the v.o.r. This indicates that pathways responsible for causing rapid changes in slowphase velocity were capable of functioning, at least intermittently, in the presence of the drug.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Baclofen and velocity storage: a model of the effects of the drug on the vestibulo-ocular reflex in the rhesus monkey. 344 8

A case of periodic alternating nystagmus (PAN), probably of congenital type, was reported. A 25-year-old woman, who has been suffering from cerebral palsy, was referred to our clinic for the consultation of a peculiar nystagmus and intermittent oscillopsia. Electronystagmographic examination revealed that the horizontal nystagmus on straight ahead gaze in the light continuously changed its direction alternately about 110 sec in right direction and about 90 sec in left direction with about 5 sec of an interlude, during which no nystagmus was observed, between each span. Electronystagmographic recording also illustrated that the amplitude and slow phase eye velocity of PAN first increase and then decrease in each span. Since other various kind of examination including neuroradiological examination revealed no special abnormality except for the signs of cerebral palsy, congenital PAN was suspected in this case. Although previous report indicated that baclofen dose not control congenital PAN in contrast to that of acquired type, we tried baclofen in this case. Baclofen reduced the strength of the nystagmus remarkably and patient also recognized the considerable improvement of her oscillopsia. We are of the opinion that the baclofen may improve the strength of congenital PAN and oscillopsia as well as those of acquired type PAN.
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PMID:A case of periodic alternating nystagmus: with a special reference to the efficacy of baclofen treatment. 403 8

Two patients with longstanding acquired periodic alternating nystagmus (PAN) were treated with baclofen, 30 mg/day. Baclofen abolished the PAN and relieved oscillopsia in both patients but was ineffective in another patient with congenital PAN.
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PMID:Treatment of periodic alternating nystagmus. 721 48

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

The horizontal vestibulo-oculomotor reflex was studied in pigmented rats during the first 5 days after a unilateral chemical or surgical vestibular deafferentation. Spontaneous eye movements in darkness and slow phase velocity gain of compensatory eye movements during horizontal sinusoidal rotation were evaluated. The most evident vestibulo-oculomotor symptom immediately after a unilateral vestibular loss was a spontaneous nystagmus, which gradually abated during the following days. Further, an asymmetry between ipsi- and contra-lesional gains was evident during sinusoidal vestibular stimulation. Single systemic doses of the GABA(B) receptor antagonist [3-[1-(S)-[[3-(cyclohexylmethyl)-hydroxyphosphinoyl]-2-(S)-hydroxypropyl]amino]ethyl]-benzoic acid (CGP 56433A), the agonist baclofen, or the GABA(A) receptor agonist (4,5,6,7-tetrahydroisoxazolo-[5,4-c]-pyridin-3-ol (THIP) were given at different intervals after unilateral vestibular deafferentation. CGP 56433A highly aggravated the vestibulo-oculomotor symptoms, observed as an increase in spontaneous nystagmus and slow phase velocity gain asymmetry. This effect was most pronounced during the first 2 days after unilateral vestibular loss, when CGP 56433A even decompensated the vestibular system to the extent that all vestibular responses were abolished. Baclofen caused no effect during the first days after unilateral vestibular loss, but in parallel with the abatement of spontaneous nystagmus, the drug equilibrated or even reversed the remaining spontaneous nystagmus with corresponding effects on the slow-phase velocity gain asymmetry. The effects of baclofen were very similar after both chemical and surgical deafferentation. THIP caused a slight depression of all vestibular responses. All single dose effects of the drugs were transient. Altogether these results reveal that endogenous stimulation of GABA(B) receptors in GABA-ergic vestibulo-oculomotor circuits are important for reducing the vestibular asymmetry during the early period after unilateral vestibular deafferentation. A possible role for GABA(B) receptors in the reciprocal inhibitory commissural pathways in the vestibular nuclei is suggested.
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PMID:Early compensation of vestibulo-oculomotor symptoms after unilateral vestibular loss in rats is related to GABA(B) receptor function. 1203 49

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


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