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Biomedical subjects

N S Chu

Publications and source records attributed to N S Chu.

At least 127 records · Page 7Linked to original sources
PubMed1981

Caffeine- and aminophylline-induced seizures.

The epileptogenicity of caffeine and aminophylline was studied in rats. Intraperitoneal administration of caffeine produced an immediate excitation and seizures followed by an encephalopathy. A progression from encephalopathy to seizures was observed following aminophylline administration. During the development of behavioral seizures, the EEGs showed a progression from fast activity isolated or bursts of spikes and/or sharp waves to full-blown epileptiform discharges. A wide spectrum of cardiac arrhythmias was observed during and following the seizures. Epileptiform activities ranging from isolated or bursts of spikes and/or sharp waves to continuous epileptiform discharges were observed following local application of the drugs to the cerebral cortex.

Aminophylline↗
PubMed1980

Tuberculous meningitis. Computerized tomographic manifestations.

In a verified case of tuberculous meningitis, computerized tomographic scans showed a striking postcontrast enhancement of the cisterns around the base of the brain and the brainstem as well as the cortical meninges. Hydrocephalus and an infarct presumably from panarteritis were also demonstrated.

Adult↗
PubMed1980

Periodic lateralized epileptiform discharges with preexisting focal brain lesions. Role of alcohol withdrawal and anoxic encephalopathy.

Periodic lateralized epileptiform discharges (PLEDs) occurred in three patients during alcohol withdrawal, in two patients with episodes of anoxic ischemia, and in one patient under both conditions. In contrast to previous observations that PLEDs are often associated with acute gross destructive lesions, autopsy results and neurological studies reported here indicated that alcohol withdrawal and/or anoxic ischemia may activate preexisting focal hemispheric lesions to produce PLEDs.

Aged↗
PubMed1980

Auditory brainstem response study of alcoholic patients.

Auditory brainstem responses were obtained from 52 alcoholic patients with or without neurological complications of alcoholism. Almost half of the patients had abnormal auditory brainstem responses manifested by a prolonged central conduction time (Wave I to V interval) without significant alterations in morphology. The incidence of abnormal auditory responses was related to the type and the number of neurological complications. Patients with Wernicke-Korsakoff syndrome, dementia or cerebellar degeneration had high incidence of brainstem abnormalities. All patients with 3 or more neurological complications had abnormal auditory brainstem responses.

Alcohol Withdrawal Delirium↗
PubMed1979

Acute subdural hematoma and the periodic lateralized epileptiform discharges.

Focal motor seizures associated with periodic lateralized epileptiform discharges (PLEDs) were observed in two patients with acute subudral hematoma. Following the surgery, one patient continued to exhibit PLEDs but clinical seizures were absent PLEDs recurred in the second patient due to inadequate anticonvulsant medication. Autopsy study in one patient suggests that underlying cerebral contusion was not responsible for the occurrence of PLEDs.

Adult↗
PubMed1979

Carbamazepine: prevention of alcohol withdrawal seizures.

Effects of carbamazepine on alcohol withdrawal seizures and symptoms were studied in rats. Carbamazepine was administered during alcohol feeding and continued during alcohol withdrawal. When carbamazepine serum levels were above 3 micrograms per milliliter, alcohol withdrawal seizures were not observed. Carbamazepine also alleviated alcohol withdrawal symptoms, especially heightened spontaneous activity, startle to noise, stereotyped chewing movements, and intermittent body stiffening.

Alcoholism↗
PubMed1978

Acute effects of alcohol on auditory brainstem potentials in humans.

Auditory brainstem potentials were recorded from human subjects before and after an intoxicating dose of alcohol. Following alcohol ingestion there were significant, progressive increases in the latencies of brainstem potential peaks III through VII. No changes in peak amplitudes were found. The results indicate that alcohol has a depressive effect on neural transmission within the primary auditory brainstem pathway.

Adult↗
PubMed1978

Auditory brain stem potentials in chronic alcohol intoxication and alcohol withdrawal.

Auditory brain stem evoked responses were in unrestrained rats during periods of acute and chronic alcohol intoxication, alcohol withdrawal, and recovery. Acute alcohol administration altered the auditory brain stem potentials by a prolongation of both peak latency and central conduction time, beginning with early peaks. Similar but lesser effects affecting only the latter peaks were observed during chronic alcohol intoxication. By contrast, alcohol withdrawal resulted in a decrease in the peak latencies of auditory brain stem potentials and a facilitation of central conduction time. Recovery of the auditory brain stem potentials to the normal form required at least three to four weeks. The present study provides the first quantitative data, to our knowledge, on manifestations of alcohol tolerance and withdrawal.

Acoustic Stimulation↗
PubMed1978

Auditory brain stem potentials with alcohol.

Auditory brain stem potentials were recorded from unrestrained rats and from cats paralyzed with Flaxedil, before and after ingestion of intoxicating dosages of alcohol. The acute effect of alcohol was a cumulative increase in the central conduction times of successive brain stem potential peaks. Statistically significant latency changes were found for peaks attributed to neural structures as far peripherally as the medulla. This depressive influence of alcohol on sensory transmission was independent of variations in stimulus intensity and body temperature.

Acoustic Stimulation↗
PubMed1978

Enhancement of alcohol withdrawal seizures with 6-hydroxydopamine.

The relationship between central catecholamine neurons and alcohol withdrawal seizures was studied in rats pretreated with 6-hydroxydopamine to selectively destroy the central catecholamine nerve terminals. The alteration of alcohol withdrawal seizures was manifested by (1) a higher percentage of the rats developing the seizures, (2) an earlier onset of seizures, and (3) a greater severity of seizure activity. Seizure status was exhibited in 25% of the 6-hydroxydopamine-treated rats.

Acoustic Stimulation↗
PubMed1976

Alcoholic cerebellar disease and seizures.

Forty-eight chronic alcoholic patients with a clinical picture consistent with midline cerebellar disease were evaluated regarding alcohol related seizures. These seizures were noted in about 15% of this patient group. This seizure incidence approximates that in the severely alcoholic hospitalized population. Thus, the midline cerebellar degeneration does not appear to influence the seizure diathesis in the chronic alcoholic.

Adult↗
PubMed1975

Focal seizures and aminophylline.

Intravenous aminophylline therapy for acute exacerbation of chronic obstructive pulmonary disease may trigger prolonged and difficult to control focal motor seizures with generalization. This can occur in previously neurologically asymptomatic patients and be associated with a poor outcome. Most patients exhibited periodic lateralized epileptiform discharges or had autopsy-proved focal central nervous system lesions, or both. If focal and generalized seizures develop during aminophylline therapy, drug toxicity should be suspect as announcing a focal central lesion. Careful individual monitoring of aminophylline dose and administration rate is essential.

Aged↗