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 EEG response and drug kinetics after intravenous infusion of diazepam at 1-0 mg/min until nystagmus, dysarthria, and moderate sedation developed, has been investigated in five normal subjects and 17 patients with chronic liver disease. Diazepam induced adequate premedication with a similar clinical response in all subjects with no adverse reactions. Maximal response was during or within five minutes of infusion. The dose of diazepam required in liver chronic disease was 17-9 +/- 1-4 mg (M +/- SEM) compared with 27 +/- 5-4 mg in controls (p less than 0-01). Dose correlated significantly with serum albumin (p less than 0-05). Baseline mean dominant frequency (MDF) and slow wave index (SWI) significantly correlated with albumin (p less than 0-01). After diazepam, the MDF decreased and SWI increased. The change was greatest at the time of maximal clinical response. It was greater in liverdisease and was greatest in patients with previous hepaticencephalopathy. In spite of reduced dose requirements in liver disease, there was no significant difference in plasma concentration at the end of drug infusion...
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PMID:Intravenous administration of diazepam in patients with chronic liver disease. 101 18

1. Electrophysiological methods were used to investigate the pretectal and telencephalic control of units within the nucleus of the basal optic root (nBOR) of the accessory optic system of pigeons. 2. Electrical stimulation of the pretectal lentiform nucleus mainly produced excitatory effects on nBOR units with temporal-to-nasal directional preference (among 109 cells, 51% were excited, 23% were inhibited and 23% were not affected) and inhibitory effects on units with nasal-to-temporal preferences (among 88 cells, 43% were inhibited, 38% were not affected, and 19% were excited). 3. Electrical stimulation of the visual Wulst (considered to be the equivalent of the visual cortex) produced mainly inhibitory effects on units with downward preferences (among 123 units, 47% were inhibited, 24% were excited and 29% were not affected), and mixed effects on units with upward preferences (among 70 cells, 30% were excited, 36% were inhibited and 34% were not affected). 4. Excitatory effects of LM stimulation had first-spike latencies ranging from 2-20 ms (mean +/- SEM, 5.5 +/- 0.7 ms), whereas latencies of W stimulation ranged from 6 to 30 ms (13.0 +/- 0.9 ms). 5. These results provide additional information about the neural substrates of the optokinetic nystagmus.
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PMID:Extraretinal modulation of accessory optic units in the pigeon. 182 82

Dynamic changes of deficits in canal and otolith vestibulo-ocular reflexes (VORs) to high acceleration, eccentric yaw rotations were investigated in five subjects aged 25-65 years before and at frequent intervals 3-451 days following unilateral vestibular deafferentation (UVD) due to labyrinthectomy or vestibular neurectomy. Eye and head movements were recorded using magnetic search coils during transients of directionally random, whole-body rotation in darkness at peak acceleration 2,800 degrees/s2. Canal VORs were characterized during rotation about a mid-otolith axis, viewing a target 500 cm distant until rotation onset in darkness. Otolith VOR responses were characterized by the increase in VOR gain during identical rotation about an axis 13 cm posterior to the otoliths, initially viewing a target 15 cm distant. Pre-UVD canal gain was directionally symmetrical, averaging 0.87 +/- 0.02 (+/-SEM). Contralesional canal gain declined from pre-UVD by an average of 22% in the first 3-5 days post-UVD, before recovering to an asymptote of close 90% of pre-UVD level at 1-3 months. This recovery corresponded to resolution of spontaneous nystagmus. Ipsilesional gain declined to 59%, and showed no consistent recovery afterwards. Pre-UVD otolith gain was directionally symmetrical, averaging 0.56 +/- 0.02. Immediately after UVD, the contralesional otolith gain declined to 0.30 +/- 0.02, and did not recover. Ipsilesional otolith gain declined profoundly to 0.08 +/- 0.03 (P < 0.01), and never recovered. In contrast to the modest and directionally symmetrical effect of UVD on the human otolith VOR during pure translational acceleration, otolith gain during eccentric yaw rotation exhibited a profound and lasting deficit that might be diagnostically useful in lateralizing otolith pathology. Most recovery of the human canal gain to high acceleration transients following UVD is for contralesional head rotation, occurring within 3 months as spontaneous nystagmus resolves.
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PMID:Temporal dynamics of semicircular canal and otolith function following acute unilateral vestibular deafferentation in humans. 1709 Dec 90

On the basis of reports by patients with downbeat nystagmus (DBN) that their symptoms were worse during the morning but better during the daytime, we investigated whether the intensity of DBN changes during the daytime. DBN was measured at 9 am, 11 am, and 1 pm. The mean peak slow phase velocity (MPSPV) of DBN was determined in different eye positions, with and without fixation, as well as in three different body positions: sitting upright, lying supine with the nose up, and lying prone with the nose down. Twelve patients with DBN either due to cerebellar degeneration or of idiopathic etiology were examined. The major findings of this study were as follows. First, the intensity of DBN significantly decreased during the daytime. When measured in the sitting upright position and primary eye position, MPSPV decreased from 4.32 deg/sec (+/-SEM 1.02) at 9 am to 2.12 deg/sec (+/- 0.5) at 11 am (P < 0.01) and stayed constant around 1.93 deg/sec (+/- 0.57) at 1 pm (P < 0.01 from 9 am to 1 pm) and 2.08 deg/sec (+/- 0.75) at 3 pm (P < 0.01 from 9 am to 3 pm). Second, this change did not depend on fixation during the measurements. Third, this effect was not influenced by the eye position during the measurements (upward, downward, or straight ahead). Our data show that the intensity of DBN decreases during the daytime. This decrease correlates with the symptoms of the patients. This change during daytime did not depend on visual fixation. Another possible mechanism is the modulation of DBN by head position relative to gravity, that is, by otolith input. This should be evaluated in further studies.
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PMID:The intensity of downbeat nystagmus during daytime. 1964 14