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M P Remler

Publications and source records attributed to M P Remler.

35 records · Page 2Linked to original sources
PubMed1986

The late effects of radiation on the blood brain barrier.

Rats were irradiated with 60 to 20 Gy in a single dose focussed to a volume of 0.5 cc in the center of the left hemisphere. Breakdown of the BBB was detected by the presence of spikes on EEG after subcutaneous injection of Bicuculline methiodide, and the presence of staining following Evans Blue dye injection. Breakdown of the BBB (mean and standard deviation) occurred in 38/46 of the 60 Gy rats at 98 +/- 16 days, 7/11 of the 50 Gy rats at 128 +/- 25 days, 11/18 of the 40 Gy rats at 162 +/- 3 days, 5/11 of the 30 Gy rats at 178 +/- 5 days and, 7/12 of the 20 Gy rats at 217 +/- 7 days post irradiation. This study suggests that endothelial damage could be the principle mechanism mediating the late radiation syndrome.

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PubMed1984

The blood-brain barrier lesion and the systemic convulsant model of epilepsy.

Systemic kainic acid (KA) at 1 mg/kg crosses the normal blood-brain barrier (BBB) of rats to produce scattered sharp waves for approximately 10 min on the EEG, but is without observable effect, producing no EEG or behavioral changes, at 0.5 mg/kg. When the BBB is opened in most of one hemisphere by 6,000 rads, the rats are clinically normal and have a normal EEG. When the irradiated rats are challenged with 0.5 mg/kg KA, intense, highly lateralized epileptiform bursts result; these bursts last 1-10 s and recur for 90 mins. This phenomenon is repeatable for the 1 week that the BBB is open. The results are identical when the BBB is opened with a pin lesion. Because endogenous glutamate agonists are common, these data suggest a possible pathophysiologic mechanism for human epilepsy.

Animals↗
PubMed1983

A GABA-EEG test of the blood-brain barrier near epileptic foci.

The permeability of the blood-brain barrier (BBB) to gamma-aminobutyric acid (GABA) in the region of an epileptic focus may be assessed by infusing GABA and measuring a change in epileptic spike activity on the EEG. GABA does not cross the normal BBB but will suppress epileptic spike activity when it does cross where the BBB is damaged. 9 alumina-cobalt experimental epileptic foci were all initially suppressible, but 7 then became unsuppressible . When the foci were irradiated to lower the BBB, all 7 became temporarily suppressible. The experiments demonstrate that (1) epileptic foci can be equally active both with the BBB 'open' and 'closed'; (2) the intravenous GABA-EEG test can detect whether the BBB near the epileptic focus is open to GABA, and (3) anatomic tests of BBB integrity (in these experiments intravenous trypan blue) cannot determine if whether BBB near the focus is 'open' to GABA. Since the intravenous GABA-EEG test reveals the permeability of the BBB in the immediate environment of the epileptic focus, it may be very useful in the selection of a susceptible therapeutic group for inhibitory amino acid therapy.

Animals↗
PubMed1983

Theophylline-induced seizures: clinical and pathophysiologic aspects.

The clinical features and management of theophylline-induced seizures are not well appreciated in spite of their unique aspects. These seizures tend to occur in neurologically intact patients and leave no or only minor neurologic sequelae if controlled early. They begin with focal motor seizures with or without secondary generalization and are followed by stupor or coma. They are responsive only to adjustment of theophylline dosage. Should the motor phenomenon persist, it takes the form of epilepsia partialis continua. Extensive workup for a structural brain lesion may be unrewarding. The electroencephalogram typically shows periodic lateralized epileptiform discharges, which may provide a diagnostic clue.

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PubMed1982

EEG monitoring of focal lesions of the blood-brain barrier.

This paper presents a modified method for the EEG detection and monitoring of small focal blood-brain barrier (BBB) lesions. The method uses high dose IV penicillin (1.2 X 10(6) mu/kg) to produce a spike focus at BBB lesions, penicillin encephalopathy. The EEG is recorded and the epileptic spikes are counted by an automatic computer program. The computer produces an objective quantitative results. The method is verified empirically on traumatic and radiation BBB lesions.

Animals↗
PubMed1981

Radiation-controlled focal pharmacology in the therapy of experimental epilepsy.

Radiation-controlled focal pharmacology is a method using intermediate-dose radiation of a portion of the brain to break down the blood-brain barrier (BBB) followed by the administration of a drug which does not cross the normal BBB but which has a desired pharmacologic effect when it does cross the BBB. Therefore, the drug affects only the radiated portion of the brain. Cats with alumina-cobalt chronic epileptic foci were given intravenous gamma-aminobutyric acid (GABA) with no suppression of their EEG-recorded, computer-analyzed epileptic spike frequency. When the focus received 6,000 rad of Bragg peak proton radiation, there was no significant change in spike frequency. Then, however, when GABA was again given, there was dramatic suppression of spike frequency, reaching a peak of 87% suppression at 9 days postradiation. The efficacy of GABA used in radiation-controlled focal pharmacology in the 7- to 9-day postradiation period was demonstrated with a confidence of p less than 0.01.

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PubMed1981

Primary position upbeat nystagmus. Another central vestibular nystagmus?

Recent studies of the vestibulo-ocular reflex have revealed a distinct pathway from the anterior semicircular canal to the contralateral oculomotor nucleus via the superior vestibular nucleus. Axons of this pathway ascend in the brachium conjunctivum, while axons of the other semicircular canal pathways ascend in the medial longitudinal fasciculus (MLF). We report two cases of primary position upbeat nystagmus where lesions of the brachium conjunctivum were suggested by computed tomography (CT) scans. One of these lesions was confirmed at autopsy. We concluded that primary position upbeat nystagmus, like downbeat nystagmus, is a type of central vestibular nystagmus resulting from an imbalance of vertical vestibulo-ocular reflex activity.

Adenocarcinoma↗
PubMed1973

A semiquantitative theory of synaptic vesicle movements.

Under the assumption that vesicles are the anatomic correlate of quantal release, the forces governing the movement of synaptic vesicles inside neurons are analyzed. Semiquantitative calculations are presented to show that a diffuse layer field penetrates a few Debye lengths into the axoplasm. This field binds tightly a monolayer of water to the membrane forming the potential barrier for miniature end-plate potential (mepp) release. The action potential destroys the monolayer and pulls the vesicle to the membrane. The vesicles are brought to the synaptic zone and held there by a Na(+) leak in the synaptic membrane. A stochastic theory of synaptic vesicle release is presented to explain experimental results. The rate of vesicle release is fractionated into a rate of membrane contacts by a vesicle and a rate of vesicle discharge per contact.

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PubMedDate not supplied

Bicuculline methiodide in the blood-brain barrier-epileptogen model of epilepsy.

Focal epilepsy can be produced by a blood-brain barrier (BBB)-excluded systemic convulsant (penicillin, folic acid, etc.) in the presence of a focal BBB lesion. Bicuculline methiodide, a gamma-aminobutyric acid blocking epileptogen, crosses the normal BBB of rats poorly and produces no consistent abnormality behaviorally or on EEG at 36 mg/kg. When the BBB is opened in 0.25 ml of cortex by 6,000 rad of alpha particles, by a pin trauma lesion, or by a heat lesion, the rats are normal clinically and on EEG. When these lesioned rats are challenged with bicuculline methiodide, 36 mg/kg, an intense, highly localized epileptiform discharge results that begins approximately 20 min after injection and lasts 30-90 min. The plausibility and experimental utility of the BBB-epileptogen model of epilepsy are enhanced by these observations.

Animals↗
PubMedDate not supplied

Systemic focal epileptogenesis.

Rats that receive radiation to 0.25 cc of one cerebral hemisphere are clinically and electroencephalographically normal until there is a breakdown of the blood-brain barrier (BBB) at 3 to 6 months postradiation. This BBB lesion can be detected by transient focal seizure activity produced by the BBB-excluded systemic convulsant bicuculline methiodide. In two rats the seizure activity induced by this one injection was self-sustaining. In seven of 15 other rats tested, the subsequent administration of repeated 2 mg/kg injections created a chronic focus that continued to spike with great frequency for 3 weeks or more without further administration of any convulsant. In three of eight other rats, implanted minipumps delivering 180 micrograms/h of bicuculline methiodide produced self-sustaining epileptic activity.

Animals↗
PubMedDate not supplied

Pharmacological response of systemically derived focal epileptic lesions.

Focal epileptic lesions were made in rats by systemic focal epileptogenesis. In this method, a focal lesion of the blood-brain barrier (BBB) is produced by focal alpha irradiation followed by repeated systemic injection of a convulsant drug that cannot cross the normal BBB, resulting in a chronic epileptic focus. Changes in the spike frequency of these foci in response to various drugs was recorded. The controls, saline and chlorpromazine, produced no change. Phenytoin, phenobarbital, chlordiazepoxide, and valproic acid produced the expected decrease in spike frequency. Pentobarbital and diazepam produced a paradoxical increase in spike frequency.

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