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.
Psychopharmacology (Berl) 1978 Sep 15
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

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.
Klin Monbl Augenheilkd 1978 Sep
PMID:[Oculomotor signs in cerebellar disease shown in ataxia telangiectasia (Louis Bar) (author's transl)]. 10 55

Ten monkeys were stimulated unilaterally and bilaterally through bipolar electrodes placed stereotactically on each side of the midline under light barbiturate anaesthesia. Bilateral simultaneous stimulation elicited straight downward binocular movements from a core of tissue about 40 mm3 on each side which included the fields of Forel, zona incerta, subthalamic nucleus, oral pole of the red nucleus, fasciculus retroflexus and 'area tegmentalis'. Unilateral stimulation of the same points yielded downward eye movements in only 25 per cent of the instances. Upward deviation of the globes could be elicited by bilateral stimulation of tissue located more caudal, ventral and medial than that from which downward movements were obtained. Bilateral electrolytic lesions within the region outlined above caused significant defects in downward gaze both in saccadic and slow pursuit binocular movements. Passive bending of the head backwards, however, resulted in downward deviation of the globes (oculocephalic reflex). Optokinetic nystagmus and after-nystagmus downward were abolished. Oblique (45 degrees) optokinetic stimulation elicited a perverted response in the horizontal plane. Vestibulo-ocular reflexes elicited by bilateral warm irrigation of both ear canals with the monkey in the erect position, or by turning the animal while lying on one side, caused a strong tonic deviation upward with absence of nystagmus downward. Some of these monkeys showed additional alterations in upward gaze but they were less severe in intensity and duration than those of downward gaze. All eye deviations in the horizontal plane were consistently normal. Recovery occurred in all types of vertical binocular movements except in the rapid motions (saccades and quick phases of nystagmus) below the horizontal meridian. A unilateral lesion had no effect. The minimal damage producing downward gaze defects was about 1.7 mm in diameter, cetred in the prerubral fields, rostral and medial to the red nuclei with minimal involvement of the oral pole of these structures. The nuclei of Cajal, Darkschewitsch and interstitialis of the posterior commissure, as well as the fasciculus retroflexus and the posterior commissure, were spared by this lesion. The so-called rostral interstitial nucleus of the medial longitudinal fasciculus and the nucleus campi Foreli appear to be destroyed. These structures are known to receive an input from the paramedian pontine reticular formation and project on to the oculomotor nerve nucleus. These results demonstrate that the prerubral fields contain structures which are critical for rapid eye movements downward, and therefore an isolated downward gaze palsy is a strong indicator of a bilateral lesion of this zone. The findings in the few reported cases with this sign and available pathological analysis suggest that our conclusions from the experimental monkey apply to man as well. The concept of bilateral innervation for vertical eye movements is amply confirmed for the downward vectors...
Brain 1979 Sep
PMID:Downward gaze in monkeys: stimulation and lesion studies. 11 43

In rabbits, participation of the extraocular muscles' sensitive innervation in extinguishing of the eyes nystagmus elicited by periodical rotations, was studied. Either limitation or complete abolishing of the above muscles motor activity were used, as well as the passive forced movements of the eyes. No considerable difference was revealed between the intact and the experimental animals. In both cases the course of nystagmus extinguishing was the same. On the other hand, repeated forced movements of the eye had no effect on the reflectory evoked nystagmus. The data obtained suggest that the proprioceptive afferents of the extraocular muscles take no part in the habituation of vestibular-oculomotor responses.
Fiziol Zh SSSR Im I M Sechenova 1977 Sep
PMID:[Assessment of the role of the sensory innervation of the intraocular muscles in habituation of vestibulo-oculomotor reactions]. 30 82

A rare case of the choroid plexus papilloma originating from the extraventricle was reported. A 48-hear-old woman began not to walk well about two years ago. Then, she was complained of vertigo, hearing disturbance of the right ear and nausea. These symptoms gradually increased. On admission she had papilledema, Brun's nystagmus, hearing disturbance of right ear and cerebellar ataxia. Cerebral angiogram and CT scan showed dilated ventricles and a large tumor in the posterior fossa. At operation, tumor was found in extramedullary space at the right cerebello-pontine angle and extended to the foramen magnum. This was removed totally. Histological examination revealed choroid plexus papilloma. Her postoperative course was satisfactory and shunting procedure was not necessary. According to the electron microscopic findings, the ultrastructure of tumor was similar to that of normal choroid plexus. We could not clear the morphological features which were considered essential for overproduction of CSF in the tumor.
No Shinkei Geka 1978 Sep
PMID:[A case of choroid plexus papilloma at the right cerebello-pontine angle (author's transl)]. 30 61

The reported case of 2 brothers suffering from medullary sponge kindeys is unique in that uremia developed in spite of the absence of urinary tract obstruction, infection or hypertension. With the exception of congenital nystagmus and psoriasis, none of the extrarenal malformations often associated with medullary sponge kidneys was observed.
Schweiz Med Wochenschr 1979 Sep 22
PMID:[Familial medullary cystic kidney with progressive kidney failure]. 38 16

1. Velocity characteristics of optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN) induced by constant velocity full field rotation were studied in rhesus monkeys. A technique is described for estimating the dominant time constant of slow phase velocity curves and of monotonically changing data. Time constants obtained by this technique were used in formulating a model of the mechanism responsible for producing OKN and OKAN.2. Slow phase velocity of optokinetic nystagmus in response to steps in stimulus velocity was shown to be composed of two components, a rapid rise, followed by a slower rise to a steady-state value. Peak values of OKN slow phase velocity increased linearly with increases in stimulus velocity to 180 degrees /sec. Maximum slow phase eye velocities in the monkey are 2-3 times as great as in humans.3. At the onset of OKAN, slow phase velocity falls by about 10-20%, followed by a slower decline to zero. Peak OKAN slow phase velocities were linearly related to optokinetic stimulus velocities up to 90-120 degrees /sec. Above 120 degrees /sec OKAN slow phase velocity saturated although OKN slow phase velocity continued to increase.4. The charge and discharge characteristics of OKAN were studied. The OKAN mechanism charged in 5-10 sec and discharged over 20-60 sec in darkness. The time constants of decay in OKAN slow phase velocity decreased as stimulus velocities increased. They also decreased on repeated testing. In several monkeys there was a consistent difference in the rate of decay of OKAN slow phase velocity to the right and left.5. Extended visual fixation discharged the activity responsible for producing OKAN. Short fixation times caused only a partial discharge of the OKAN mechanism. Following brief periods of fixation, OKAN resumed but with depressed slow phase velocities.6. A model based on a state realisation of a peak detector was formulated which approximately reproduces the salient characteristics of OKN and OKAN. This model predicts the three dominant characteristics of OKAN: (1) charge over 5-7 sec, (2) slow discharge in darkness, and (3) rapid discharge with visual fixation. With the addition of direct fast forward pathways, it also correctly predicts the rapid and slow rise in OKN. We postulate that OKAN is produced by a central integrator which is also active during OKN. Presumably this integrator acts to maximize velocities during OKN and to smooth and stabilize ocular following during movement of the visual surround.
J Physiol 1977 Sep
PMID:Quantitative analysis of the velocity characteristics of optokinetic nystagmus and optokinetic after-nystagmus. 40 38

Two members of a family suffer from recurrent attacks of either vertigo or cerebellar incoordination. The occurrence of these two distinct types of attack in the same patient may reconcile the disparate features of previously reported cases of familial periodic ataxia. The finding of downbeating nystagmus suggests a medullary disturbance. As in a previously reported family, the attacks were relieved by acetazolamide.
Arch Neurol 1979 Sep
PMID:Familial periodic ataxia. 47 21

Vestibular nuclear neurons of the horizontal canal system (Vn) of albino rats (Wistar) failed to respond to optokinetic stimulation. Similarly, optokinetic nystagmus (OKN) could not be elicited in these animals. Brown (DA--HAN) rats, however, consistently showed optokinetic responses of Vn and OKN to identical stimuli.
Exp Brain Res 1979 Sep
PMID:Functional deficits in the optokinetic system of albino rats. 48 14

1. The firing rates of action potentials of abducens nerve single fibers were recorded in the cat's orbit during a variety of vestibular and optokinetic stimulations. 2. Comparison was made of the neural firing rates associated with agonist and antagonist responses during slow and fast components of vestibular and optokinetic nystagmus. It was found that the relationship between the motoneuron firing rates and the eye motion was independent of the reflex with which they were associated--vestibular or optokinetic, or the type of response--agonist or antagonist. No neurons were observed that responded only during the fast or only during the slow nystagmus phase. Motoneuron firing rates were proportional to both velocity and position of the eye in a ratio of 1 (spikes/s)/(deg/s) to 7.2 (spikes/s)/deg. The behavior of the motoneurons was compatible with the hypothesis that thier firing rates are sufficient to overcome both elastic and viscous forces by which the muscles and ligaments hold the eye in the orbit. 3. For low-frequency head rotations, eye displacement and neural responses showed a small phase angle difference. At higher frequencies, however, while the eyes maintained a fixed relationship to the head rotation, the neural responses showed an increasing phase lead. One component of this phase lead compensated for the phase lag introduced by the orbital mechanics. The other was modeled as a constant delay of approximately 70 ms, which may be accounted for by neuromuscular transmission and transduction.
J Neurophysiol 1979 Sep
PMID:Neural correlates of nystagmus in abducens nerve. 49 Jan 99


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