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 anticonvulsant potency and neurological toxicity of two new catalytic inhibitors of GABA-transaminase have been assessed in acute experiments in baboons with a natural syndrome of photic epilepsy. gamma-Acetylenic GABA, 160--200 mg/kg, or gamma-vinyl GABA, 450--950 mg/kg, intravenously, gave complete protection against generalised myoclonus or seizure responses induced by photic stimulation (in baboons without or with priming with subconvulsant doses of allylglycine). The protection became maximal 1--3 h after injection, and continued for 7--24 h. Signs characteristic of the acute toxicity of anticonvulsant drugs (nystagmus and ataxia) were not seen. The potential use of these compounds in human epilepsy deserves investigation.
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PMID:Blockade of epileptic responses in the photosensitive baboon, Papio papio, by two irreversible inhibitors of GABA-transaminase, gamma-acetylenic GABA (4-amino-hex-5-ynoic acid) and gamma-vinyl GABA (4-amino-hex-5-enoic acid). 10 Aug 12

Optokinetic nystagmus (OKN) continues after the cessation of visual stimulation in complete darkness as primary optokinetic after-nystagmus (OKAN I). After variable periods of time, it is followed by secondary OKAN (OKAN II). Short periods of visual fixation during OKAN I in monkey and in man inhibit OKAN I, but enhance OKAN II. The enhanced OKAN II starts earlier, lasts longer, and often reaches higher slow-phase velocities than in control experiments. Therefore, OKAN II depends not on the ocurrence or strength of OKAN I, but mainly on parameters of the preceding optokinetic stimulus. Results suggest that OKAN I duration is partially determined by the development of OKAN II.
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PMID:Dynamic changes of optokinetic after-nystagmus (OKAN) caused by brief visual fixation periods in monkey and in man. 10 Nov 85

1. In the alert monkey, 74 neurons in the vestibular nuclei were investigated during sinusoidal rotation about a vertical axis at frequencies between 0.003 and 0.5 Hz. Phase and gain were determined by a fast Fourier analysis program. 2. Phase advance, relative to turntable velocity, was small between 0.05 and 0.5 Hz. At lower frequencies phase advance increased to 45 degrees at 0.007--0.02 Hz, and 90 degrees at 0.003--0.005 Hz. In agreement with the phase characteristics, a gain decrease of -3 dB was determined between 0.007 and 0.02 Hz. Assuming a linear system, time constants of 9.5, 11.9, and 24.5 s were calculated for three different monkeys. 3. Simultaneously recorded nystagmus exhibited similar time constants as the central vestibular neurons for each monkey. 4. Frequency responses of 11 neurons were recorded from the same monkeys while they were under general anesthesia and the time constants were reduced to 4--7 s. This is the range of time constants seen in the peripheral nerve. 5. The longer time constants in the alert state are due to an integration process, which provides a low-frequency compensation, and is thought to be achieved through a feedback loop involving the reticular formation. 6. In the alert and anesthetized state, monkeys were also exposed to velocity trapezoids. Time constants of decay of neuronal activity were in good agreement with the data obtained during sinusoidal stimulation. 7. A transfer function of the primary vestibular afferents is expanded to include the described low-frequency compensation found in central vestibular neurons in the alert animals.
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PMID:Transfer characteristics of neurons in vestibular nuclei of the alert monkey. 10 15

Vestibular and optokinetic nystagmus (OKN) of monkeys were induced by platform and visual surround rotation. Vision prolonged per-rotatory nystagmus and cancelled or reduced post-rotatory nystagmus recorded in darkness. Presumably, activity stored during OKN summed with activity arising in the semicircular canals. The limit of summation was about 120 degrees/s, the level of saturation of optokinetic after-nystagmus (OKAN). OKN and vestibular nystagmus, induced in the same or in opposite directions diminished or enhanced post-rotatory nystagmus up to 120 degrees/s. We postulate that a common storage mechanism is used for producing vestibular nystagmus, OKN, and OKAN. Evidence for this is the similar time course of vestibular nystagmus and OKAN and their summation. In addition, stored activity is lost in a similar way by viewing a stationary surround during either OKAN or vestibular nystagmus (fixation suppression). These responses were modelled using direct pathways and a non-ideal integrator coupled to the visual and peripheral vestibular systems. The direct pathways are responsible for rapid changes in eye velocity while the integrator stores activity and mediates slower changes. The integrator stabilizes eye velocity during whole field rotation and extends the time over which the vestibulo-ocular reflex can compensate for head movement.
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PMID:Velocity storage in the vestibulo-ocular reflex arc (VOR). 10 22

Disturbances of the eye movements are described in 2 brothers with ataxia telangiectasia (Louis Bar): pathological smooth pursuit and command movements of the eyes (hypometry) with a preseved doll's phenomenon, increased reaction times of voluntary saccades, failure of gaze holding, gaze nystagmus, altered optokinetic nystagmus, and distinct convergence defect. These oculomotor defects are the result of cerebellar lesions. The E.N.G.-findings in pathologically changed pursuit movements are in accordance with those disturbances of eye movements shown by Westheimer and Blair in cerebellectomized monkeys.
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PMID:[Oculomotor signs in cerebellar disease shown in ataxia telangiectasia (Louis Bar) (author's transl)]. 10 55

On certain occasions it becomes important to evaluate vestibular function in a patient with otitis media. The potential application of the air caloric test in evaluating such patients was examined. Patients with unilateral otitis media before and after surgery were studied to answer certain clinical questions. More questions were raised than answers provided. The preliminary conclusions from this study are: 1. Patients with tympanostomy tubes or small perforation of one ear may show a caloric response in the perforated ear equal to that of the intact ear. 2. Patients with a large tympanic membrane perforation on one side may show hyperactive caloric responses on the perforated side. 3. Patients with a moist ear may show inverted horizontal nystagmus to warm air caloric testing. This applies to patients with a large perforation or mastoidectomy cavity. 4. Patients with a dry open mastoid or fenestration cavity are likely to show a hyperactive caloric response on the side of previous surgery, accompanied by vegetative symptoms. This size of the cavity appears to be less important than the presence of the cavity per se. 5. Patients may be safely tested in the early postoperative period.
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PMID:Air caloric testing in otitis media. (preliminary studies). 10 11

A young epileptic presented with spasticity as well as ataxia, diplopia and nystagmus; his serum phenytoin level was very high. All the abnormal signs disappeared after withdrawal of phenytoin. Spasticity, hyperreflexia, and clonus are features of phenytoin intoxication, present in this case, which are not commonly seen, and which have rarely been mentioned previously in the literature.
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PMID:Spasticity due to phenytoin toxicity. 10 44

Sigma-optokinetic nystagmus (sigma-OKN) can be elicited in awake Java monkeys (Macaca fascicularis) when stationary periodic visual patterns (grid of black white stripes, row of equally spaced dots) are illuminated stroboscopically. Three methods were found to be useful in inducing the sigma-OKN: postrotatory nystagmus, optokinetic afternystagmus (OKAN) following normal OKN and a gradual transition from phi-movement (phi-OKN) to sigma-OKN. The properties found for sigma-OKN in man are also present in monkeys with the one exception that monkeys have a long-lasting sigma-OKAN in darkness which is not present in man. The average angular speed Ve of sigma-OKN slow phases was related to the flash frequency fs and the spatial period Ps of the stripe pattern according to the following equation: Ve = k.Ps . fs [degrees . s-1] The constant k was 1 or close to 1.
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PMID:Three methods to elicit sigma-optokinetic nystagmus in Java monkeys. 11 Jun 12

A case of trisomy 6p21 leads to 6pter resulting from a maternal balanced t(2;6)(p25;p21) translocation is reported. The main clinical abnormalities were psychomotor retardation, hypotrophy, blepharophimosis, nystagmus, high nasal bridge, small mouth, sacral dimple, and systolic murmur. Other anomalies might have been due to partial 2p monosomy. Comparison with seven other cases of trisomy 6p allowed the delineation of a clinical entity. Direct proof of the localization of HLA genes was given by the presence of three haplotypes in the index patient.
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PMID:Partial trisomy 6p. 11 Jun 70

Squirrel monkeys of 2 subspecies, Bolivian and Colombian, were removed from their mothers on the day of birth and nursery reared for up to 2 years of age. Infants were tested weekly for 12 weeks, then monthly for 1 year, and at 2 years of age. Tests included morphology (body weight, crown-rump length, and head measurements), behavior (reflexes, activity, reaction to the surrogate), and physiology (heart rate, respiratory rate, temperature and optokinetic nystagmus). Data show some likenesses and some differences between the 2 subspecies.
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PMID:The growth and development of the squirrel monkey (Saimiri Sciureus). 11 54


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