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

Institutionalized epileptic patients on long-term anticonvulsant diphenylhydantoin (DPH) therapy were examined clinically. DPH plasma levels were unexpectedly high in 54% despite rather poor seizure control. No patient was free from side effects, which included gingival hypertrophy (90% of patients), increased alkaline phosphatase activity (55%), suggestion of a sensory peripheral neuropathy (34%), central nervous system (CNS) intoxication (22%), coarsened facial features (19%), tendency to bleed excessively (15%), hirsutism (12%), and mild megalocytic anemia (5%). CNS intoxication correlated with high plasma DPH levels, reports of deteriorating behavioral and motor performance, and the findings of nystagmus on vertical gaze or truncal ataxia, though not all patients with high plasma levels were clinically intoxicated. Alarming were the often disfiguring changes of gums and facial structures and the tendency to develop signs of vitamin D deficiency secondary to therapy. Hirsutism was rare in black patients. Plasma DPH level determinations are recommended as part of the management of mentally retarded epileptic patients but do not replace clinical acumen and skill.
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PMID:Effects of diphenylhydantoin in 41 epileptics institutionalized since childhood. 19 Jul 7

1. In precollicular decerebrate cats the electrical activity of single pontine neurons was recorded before, during and after the episodes of postural atonia produced by i.v. injection of 0.03-0.1 mg/kg of eserine sulphate. These episodes were characterized by the regular occurrence of horizontal conjugate eye movements, which were mainly grouped in bursts of REM; moreover, a burst of REM in one direction was generally followed by a burst of REM in the opposite direction. 2. Among the recorded units, 32 showed an increase in their discharge rate during these cataplectic episodes. However, while these units fired at regular frequency when postural rigidity was present, they showed periodic changes in their discharge rate as soon as the bursts of REM appeared in the electrooculogram. In particular a nearly sinusoidal increase in the discharge rate was related to the appearance of an ocular burst in one direction, while a decrease in the unit discharge occurred during an ocular burst in the opposite direction. In some instances neighbouring pontine units located within each side of the brain stem showed reciprocal rate profiles during REM bursts oriented in a given direction, making it likely that the cyclic alternation of their activity depended upon their reciprocal interaction. 3. The alternative hypothesis, i.e., that these periodic changes in unit discharge depend upon the proprioceptive feedback due to the eye movements was excluded by the fact that these changes started before the occurrence of the bursts of REM and began to decline before the end of the burst. Moreover no variation in their firing rate was observed during the positional nystagmus induced by tilting the animal in the control period, i.e., when postural rigidity had reappeared following the end of the cataplectic episode. 4. Most of the neurons showing periodic changes in their discharge frequency during the bursts of REM were located in the pontine reticular formation. Scattered units were also found within the region of the locus coeruleus and the raphe system, close to the surrounding reticular structures. 5. In addition to these neurons, 60 pontine units were recorded, which did not show any changes in their discharge rate during transition from the control period to the cataplectic episode. However, phsiic increases or phasic decreases in their discharge rate appeared synchronously with the individual eye movements. Since in most instances these phasic changes in unit activity coincided with the appearance of the individual monophasic potentials recorded from the ascending MLB, which immediately preceded the rapid eye movements, these units could be attributed either to the premotor neurons responsible for these REM or to the closely related structures which generate their rhythmic discharge. In only a few instances did the discharge of these units not precede but follow the individual eye movements, indicating that they resulted from a proprioceptive feedback originating during the eye movements. 6...
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PMID:The oscillatory system responsible for the oculomotor activity during the bursts of REM. 19 Sep 62

Direct current electronystagmographic recordings of spontaneous nystagmus, in the light, in darkness, and with eye closure were carried out on 34 patients with peripheral lesions of the vestibular system with a view to determining their specificity. In 60% of patients the responses were characterised by an enhancement of the nystagmus both with eye closure and in darkness. The remainder exhibited no nystagmus under any recording condition.
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PMID:Electronystagmographic criteria in neuro-otological diagnosis. 1. Peripheral lesions. 20 49

Secondary nystagmus is frequently seen following cessation of prolonged unidirectional vestibular stimulation. It is explained on the basis of an adaptation during the application of the stimulus which leads to an apparent stimulus in the opposite direction when the stimulus is removed. The same phenomenon would be expected with vestibular disease when after a period of adaptation to the vestibular asymmetry, the affected ear recovers some or all of its function. The seondary nystagmus in this instance beats toward the affected ear and has been termed recovery nystagmus because it is generated by recovery of function. Two cases with recovery nystagmus following acute attacks of vertigo are presented.
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PMID:Recovery nystagmus. 20 16

Basic research in autism is reviewed. There is mounting indication, but as yet inconclusive evidence, of unique physiologic disturbances etiologically related to autism. Additionally there is indication that some of the physiologic disturbances found in autistic children are also present in children with other developmental disorders. Children called autistic probably represent a complex of clinically similar manifestations in a variety of different subgroups of children, each subgroup representing a basically different physiologic disturbance. However, the possibility remains that there is only one basic disturbance that in varying degrees affects many body systems and thus manifests in a variety of overlapping syndromes. Objective markers are needed so as to allow the demarcation of subgroups of autistic children for further study. Possible markers may be decreased duration of postrotatory nystagmus, auditory evoked response deviations, lymphocytic hyporesponsivity, increased blood platelet serotonin efflux, and/or the presence of urinary DMT or bufotenin.
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PMID:Overview of selected basic research in autism. 22 98

Senegalese baboons (Papio papio), with a natural syndrome of photosensitive epilepsy, consistently show generalized myoclonic jerks if stimulated stroboscopically at hourly intervals, two to eight hours after the intravenous administration of allylglycine, 200 mg/kg. This provides a model for testing the acute antiepileptic effects of established or new drugs. The relationship between concentration of drug, antiepileptic action, and acute neurological toxic effects can be studied. Pnehobarbital (15 mg/kg) and diazepam (0;5 to 1.5 mg/kg) were highly effective in the absence of signs of toxic reaction (plasma levels: phenobarbital sodium, 0.7 to 1.7 mg/100 ml; diazepam, greater than 0.5 mug/ml). After administration of carbamazepine (30 to 40 mg/kg) and diphenylhydantoin sodium (40 to 50 mg/kg), antiepileptic action was seen, but was accompanied by severe toxic signs (nystagmus and ataxia). Sulthiame (20 to 125 mg/kg) and ethosuximide (50 to 100 mg/kg) had little antiepileptic activity and no acute toxic effects. This primate model may aid the identification of new drugs that are active against grand mal seizures and status epilepticus.
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PMID:A primate model for testing anticonvulsant drugs. 23 98

The case histories of four patients who developed choreoathetoid movements during intoxication with phenytoin are presented. Drug intoxication was confirmed in each case by measuring the serum phenytoin concentration. Drug interactions were, in part, responsible for the occurrence of intoxication in three of them. Phenytoin intoxication is not always easy to recognize, particularly when nystagmus is minimal or absent, as in these four patients. The estimation of the serum phenytoin concentration is invaluable in this situation.
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PMID:Involuntary movements caused by phenytoin intoxication in epileptic patients. 23 1

The visual afferent pathways affect the oculogyric centres in two ways: (1) By maintaining the oculomotor tonus; (2) By inducing optically elicited movements. In organic amblyopia the diminution of central visual acuity is not sufficient to impair the oculomotor reflexes which usually remain unchanged until the vision becomes very poor. Howver, abnormal movements are typically observed in the inhibition of strabismic amblyopia. Sensorimotor difficulties are observed in both version and vergence movements. Abnormal version patterns have two main effects: suppression of optokinetic nystagmus and kinetic anarchy of pursuit and saccadic movements. Vergences are found to be much more brittle and vulnerable to amblyopia than versions, and amblyopia is often accompanied by anomalies of fusional, accommodative, and fast vergence movements.
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PMID:Abnormal ocular movements in amblyopia. 29 22

Eye-tracking and optokinetic nystagmus (OKN) abmormalities in patients with focal lesions of the nervous system are reviewed. Patients with peripheral labyrinthine lesions can have deficits in smooth pursuit and OKN, but they are rapidly compensated after an acute lesion. By contrast, patients with large, cerebellopontine angle tumors have progressive impairment of pursuit and OKN as the tumor enlarges. Abnormalities of saccadic eye movements suggest intrinsic central nervous system (CNS) dysfunction. Saccade accuracy is severely impaired with cerebellar lesions, while brain stem disease frequently results in a slowing of saccade maximum velocity. Smooth pursuit and OKN abnormalities are common with all types of CNS lesions. The pattern of eye-tracking and OKN abnormality can be useful in anatomically localizing nervous system lesions.
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PMID:Eye-tracking and optokinetic nystagmus. Results of quantitative testing in patients with well-defined nervous system lesions. 29 96

Visual suppression of caloric nystagmus was studied in normal adults and in 98 clinical cases in order to justify the application of the procedure as a clinical test. The maximum slow phase velocity during ten seconds in darkness and the slow phase velocity during ten seconds in light were taken from the recordings and measured. The mean values of these slow phase velocities were calculated and the mean slow phase velocity in darkness was assigned a value of 100%. The value which the slow phase velocity in light subtracts from the slow phase velocity in darkness, represents the visual suppression. It was determined that visual suppression of the slow phase velocity of caloric nystagmus was 48 +/- 10% in 22 normal adults. This was caused by the visual fixation mechanisms. Cases in which lesions were diagnosed in the cerebellum, such as spinocerebellar degeneration and cerebelitis, showed reduced or abolished visual suppression. The lesion side can be determined by this test. Compensation following unilateral sudden loss of inner ear function can be measured by the visual suppression test.
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PMID:Visual suppression test. 29 97


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