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Biomedical subjects

M Posmurová

Publications and source records attributed to M Posmurová.

11 recordsLinked to original sources

"Epileptosis"--a syndrome or useless speculation?

102 patients were divided into 3 groups: epileptics, psychotics and epileptics with psychotic symptoms. All had long been monitored for a number of clinical and laboratory parameters. Though different in many respects, all share states of sudden dysphoria, cacophoria, panic anxiety, horror, and EEG (stereo-EEG, too) signs of epileptic or other gross anomalies, often correlated to those affective disorders. Attacks of dysphoria, epilepsy, and psychosis come spontaneously and in response to biological (hypoglycemia, sleep deprivation, alcohol, menses) or psychosocial stimulation (agitation, quarrels, fear of redundancy, psychic trauma). These states (attacks, dysphoria, "neurotic" or even psychotic episodes) often provoke one another. -Calling this syndrome epileptosis, we believe its mechanism is due to lesions of the limbic and brainstem modulation systems. At the start of the process there is an epileptic focus in the amygdalo-hippocampal complex (AHC) which in itself can trigger simple or complex partial paroxysm but also-by means of electric stimulation of the AHC-states of dysphoria, anxiety, and psychotic hallucinations. Besides, a form of pathological learning develops in premorbid "hypersensitive" personality which can be put down to associative learning and to Overton's phenomenon of "state-dependent retention of learned responses". This may give rise to mutual stimulation where epileptic focal activity in AHC can provoke dysphoria while an external psychosocial situation can trigger epileptic activity there, too (AHC). Since there need not always be mydriasis (though other vegetative signs such as tachycardia, tachypnoea, nausea, blush and others are frequent) or unconsciousness, and some psychomotor manifestations may be out of the ordinary, and scalp EEG may be normal, such patients are often regarded as "hysterics" or malingerers.

Adult↗

[Naltrexone in narcolepsy. Initial experience].

The administration of 550 mg naltrexon in the course of 13 days did not four patients with narcolepsy-cataplexy to improvement of symptoms of the disease and did not improve their appetite or increase their body weight. No side-effects of naltrexon were observed.

Adult↗

The effect of naloxone on the symptoms of narcolepsy.

The effect of Naloxone (0.4 mg i.v.) was studied in 10 patients suffering from narcolepsy. The diurnal polysomnographic recordings showed that Naloxone leads to an increase in the latency of REM sleep (P less than 0.05), to a shortening of its total duration and to a decrease in the average amount of phasic manifestations in 1 min. of REM sleep (P less than 0.05). The Polygraphic sleepiness score for REM sleep decreased significantly (P less than 0.01). Naloxone led also to the disappearance of stages 3 and 4 NREM sleep, and to an increase in the total duration of stage 1 NREM sleep. Naloxone caused no change in the total performance in Bourdon's test; though it did enhance attention. There were no changes in the subjective perception of the state of arousal or of the psychomotor tempo. It was found no post-Naloxone alterations of blood pressure, body temperature, pulse or pupillary diameter. The above findings support the hypothesis that an hyperactive endorphinergic system participates in the pathophysiology of narcolepsy.

Adult↗

Pharmacogenetic study with diazepam in twins.

In a study with healthy volunteers (6 monozygotic and 4 dizygotic twin pairs) we followed up diazepam serum levels and psychotropic effects of diazepam after single-dose administration. We found that pharmacokinetic properties of diazepam as well as its influence on memory and performance are probably not under genetic control. On the other hand, genetic factors seem to contribute to effects of diazepam on affectivity.

Adult↗

Genetic aspects in chronic schizophrenia. Morbidity risks and contributory factors.

112 schizophrenics, over 55 years old, and their relatives were studied. Aims of the study were (1) to evaluate the assumption that using an appropriate selection of probands and methods of the morbid risk estimation, one may expect to obtain a higher (and probably more realistic) value of risk to children; and (2) to assess the possible influence of patients' and relatives' characteristics on the magnitude of the morbid risk. The main results were (1) the values of risks (0.04 +/- 0.02 for spouses; 0.08 +/- 0.02 for siblings; 0.17 +/- 0.04 for offspring); (2) the risk to siblings and to children increased with the numbers of other relatives affected; (3) no clinical symptoms in probands (evaluated throughout the lifetime course of the disease) were associated with an increased/decreased value of risk to any class of relatives.

Adult↗