Biomedical subjects
Publications and source records attributed to K Sonka.
Ageing is associated with deterioration of the quality of nocturnal sleep, more frequent siestas in the afternoon, a forward shift of sleep in the 24-hour cycle. In old age sleep disorders are more frequent such as sleep apnoea, the restless feet syndrome, periodic movements of the lower extremities and others. The authors present an account of changes of sleep and vigilance and the most frequent sleep disorders in old age.
The purpose of the presented work was to investigate the relationship between the length of I-III and I-V intervals during BERA examinations on the intensity of the stimulus in healthy subjects. Furthermore to assess the normal range of the maximum length of I-III and I-V intervals. Twenty-seven subjects aged 15-57 years, incl. 10 men, were examined. The stimuli were 100 us clicks, the repeating rate was 30/s, the stimulation intensity 0-85 dB nHL. The examination was made after administration of diazepam or rohypnol. TDH 49 earphones were used. Into the external auditory meatus on the examined side an electrode of the authors' own design in the shape of an open tube was introduced. The length of I-III and I-V intervals depended on the intensity of stimulation. The differences of mean values of the length intervals at stimulation intensities of 65 dB nHL and 45 dB nHL were statistically significant: p less than 0.02 for interval I-III and p less than 0.0001 for interval I-V. We take as the upper borderline of the normal length of intervals I-III approximately 2.8 ms and of intervals I-V 4.7 ms, if the latency of wave I is smaller than 2.5 ms. When the latency of wave I is greater, even longer I-III and I-V intervals may be still normal.
A simple blind study with small doses of naloxone (0.8-1.6 mg i.v.) was carried out in 11 patients with hypersomnia with sleep apnoea (HSA). The effect was studied by diurnal polysomnography. It was found that the administration of naloxone was followed by significant prolongation of wakefulness and by significant shortening of the total duration of the second stage of NREM sleep. The duration of the apnoeic episodes was also significantly shortened after naloxone, although their number did not alter. Increased activity of the endorphinergic system (which naloxone inhibits by receptor competition) evidently plays a role in the pathophysiology of HSA.
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.
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.
The authors examined HLA antigens in 124 narcoleptics. In addition to narcolepsy, 122 patients suffered also from cataplexy. The two patients without cataplexy suffered also from sleep paralysis and hypnagogic hallucinations. These two symptoms were also present in many of the other patients. HLA group DR2 was found in 120 patients including all six symptomatic cases. In four patients HLA DR2 was not present. Two of these were fully pronounced narcolepsy-cataplexy cases whereas the two other did not suffer from cataplexy. Since several other cases with negative DR2 have already been published it is necessary to admit the existence of DR2-negative narcolepsy, albeit very rare. Among 5 patients with isolated sleep paralysis HLA DR2 was present in one familial and 1 sporadic case. The authors further discuss some aspects of the classification of narcolepsies in the light of recent HLA studies as well as their delimitation from idiopathic hypersomnia.
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This article describes a quantitative assessment of pathological diurnal sleepiness in three groups of patients with excessive daytime sleepiness: narcoleptic patients, idiopathic hypersomniac patients, hypersomniac patients with sleep apnea syndrome. We analyzed polygraphic diurnal recordings of 45 min duration obtained under standardized conditions. We called the percentage of total sleep time during the 45-min recording the polygraphic index of sleepiness. The polygraphic score of sleepiness is determined by the latencies and total durations of the individual sleep stages. Because deeper sleep stages correspond to more pronounced sleepiness than do superficial sleep stages, we introduced coefficients for each sleep stage. We present a formula for calculating a score in a single figure that gives a good indication of the patient's sleepiness and makes inter- and intraindividual comparison possible. Separate REM and NREM sleep scores are also given.
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