Biomedical subjects

A Oksenberg

Publications and source records attributed to A Oksenberg.

28 records · Page 2Linked to original sources

PubMed1995

Effects of hemi-thalamic damage on K-complexes evoked by monaural stimuli during midafternoon sleep.

Polygraphic recording of midafternoon sleep were made in two patients with unilateral hemorrhagic infarction in the thalamus. One patient had massive signs of reduced attention in the contralesional space following right lateral thalamic lesion. The other patient had infarction centered in the left posterior ventrolateral thalamus with no signs of hemineglect. In both cases, waking and sleep records showed symmetric background EEG at C3 and C4. In contrast, monaural sounds (clicks) elicited bilaterally symmetrical K-complexes only in the second patient. In the other patient with right thalamic lesion, both left- and right-ear clicks failed to elicit K-complexes in the right cerebral hemisphere, whereas normal K-complexes continued to appear at C3 as well as at Fz. In neither patient did the frequency of evoked K-complexes depend on the side of the stimulated ear. Unlike K-complexes, sleep spindles were bilaterally absent in patient 1. The right hemisphere does not seem to have a special role in control of circuits generating K-complexes.

Acoustic Stimulation↗

PubMed1995

Is obstructive sleep apnea a common cause of essential hypertension?

Obstructive sleep apnea (OSA) occurs in about 10% of the middle-aged population but in about 30% of the hypertensive population of the same age. About 20% of the middle-aged population has hypertension but about 50% of patients with OSA have hypertension. Despite this close relationship between these two entities, previous attempts to determine whether the respiratory abnormalities in OSA were responsible for the hypertension were inconclusive, particularly because of the confounding effect of obesity which is common to both conditions. Data from recent observational and intervention studies, however, have succeeded in avoiding many of the pitfalls of earlier studies and it is now becoming evident that OSA may be a major cause of hypertension--responsible for about 30% of all cases. Successful treatment of OSA by any means has been shown in most studies to cause significant reductions in blood pressure throughout the 24 h period, while at the same time alleviating the vast array of symptoms and clinical abnormalities associated with this common and serious condition. Despite the encouraging results of these recent data, more studies are urgently required which should include larger numbers of patients and controls in order to clarify further the relationship between OSA and hypertension.

Airway Obstruction↗

PubMed1993

Spontaneous nystagmus across the sleep-wake cycle in vegetative state patients.

The presence of spontaneous CNS nystagmus during wakefulness was documented for the first time in 6 vegetative-state (VS) patients. Nystagmus of smaller amplitude as compared to the awake state was consistently detected in each patient during stage 1 of sleep. There was complete absence of nystagmus during stage 2 and slow wave sleep (SWS) in all the patients. Clear nystagmus episodes were observed during rapid eye movement (REM) sleep in all patients. Some nystagmus episodes followed rapid eye movements (REMs), some were unrelated to REMs while others were superimposed on REMs. It is suggested that spontaneous neural activation during REM sleep may allow the episodic emergence of nystagmus during this sleep stage.

Adult↗

PubMed1992

Temporally related changes of sleep complaints in traumatic brain injured patients.

Sleep complaints were obtained from 22 hospitalised patients with traumatic brain injury of recent onset (median 3.5 months after injury) and were compared with those of 77 discharged patients who had sustained brain injury about two to three years (median 29.5 months) previously. A high incidence of sleep complaints was noted in both groups (72.7% and 51.9% respectively). Disorders in initiating and maintaining sleep (DIMS) were the most common complaints among hospitalised patients (81.2%), whereas disorders of excessive somnolence (DOES) were common in discharged patients (72.5%). This difference in the nature of the complaints was apparently due to differences between the two groups in the time elapsed since injury, duration of coma, and immediate environmental conditions. In discharged patients with sleep complaints, neurobehavioural impairments and a poorer occupational outcome were more common than in those discharged patients without sleep complaints. It is suggested that early evaluation and treatment of sleep disturbances must be considered an integral part of the rehabilitation process.

Adult↗

PubMed1991

Polysomnography in locked-in syndrome.

Sleep patterns were evaluated in a case of 'locked-in' syndrome. This patient had an ischemic infarction involving the ventral portion of the upper half of the pons bilaterally, with a posteromedial extension into the tegmentum. Reticular structures, notably the median raphe nuclei, supposed to play a major regulatory role in sleep, were most probably involved. Unexpectedly, repeated polysomnographic studies revealed sleep patterns with only minor abnormalities.

Electroencephalography↗

PubMed1982

Dissociation between sleep-related and TRH-induced prolactin secretion in seminiferous tubule failure.

Prolactin (PRL) secretion has been measured during sleep and following TRH administration in 8 patients aged 24-39 yr with seminiferous tubule failure and 36 controls. Basal LH levels were 25.7 +/- 14.7 mIU/ml in the patients compared to 11.5 +/- 4.2 mIU/ml in the controls (p less than 0.01) Corresponding FSH levels were 26.2 +/- 10.7 mIU/ml and 5.9 +/- 2.1 mIU/ml (p less than 0.001) Mean estradiol 17B and testosterone levels were similar in the 2 groups. The mean PRL secretion during sleep was 16.5 +/- 11.7 ng/ml in the patients and not different in 11 of the controls (12.4 +/- 3.2 ng/ml). One patient had a mean nocturnal PRL concentration of 44.1 ng/ml. In both groups, the mean sleep related PRL concentration was greater than that during waking hours. The average number of peaks in the 2 groups was similar. In the same patients, the peak PRL response to TRH (200 ug IV) was 81.9 +/- 18.8 ng/ml as compared to 32.1 +/- 10.7 ng/ml in the controls (p less than 0.001). It is concluded that PRL concentrations following pharmacological stimulation are increased in seminiferous tubule failure, whereas levels are normal in relation to the physiological stimulus of sleep.

Adult↗

PubMed1979

"It's time, you must wake up now".

Seven subjects who claimed to be able to awake accurately from sleep at a predetermined time were required to awake in the sleep laboratory at 03:30 and 05:30 on two separate nights. Eight of the 12 spontaneous awakenings were within +/- 20 min. from the target time, and 8 awakenings were from REM sleep. The two best performing subjects were tested for additional 7 nights in the laboratory but accuracy deteriorated considerably with only 2 awakenings within +/- 20 min. from target time. Approximately 50% of all awakenings, however, were from REM sleep. It is concluded that some individuals are able to awake at predetermined times and that this ability might be dependent on motivational level and the sleep stage.

Adult↗

PubMedDate not supplied

A functional role for REM sleep in brain maturation.

The biological function of REM sleep is defined in terms of the functions of neural processes that selectively operate during the REM sleep state. The high amounts of REM sleep expressed by the young during a period of central nervous system plasticity suggest that one function of REM sleep is in development. The phenomenon of activity-dependent development has been clearly shown to be one mechanism by which early sensory experience can affect the course of neural development. Activity-dependent development may be a ubiquitous process in brain maturation by which activity in one brain region can influence the developmental course of other regions. We hypothesize an ontogenetic function of REM sleep; namely, the widespread control of neuronal activity exerted by specific REM sleep processes help to direct brain maturation through activity-dependent developmental mechanisms. Preliminary tests of the hypothesis have been conducted in the developing feline visual system, which has long been known to incorporate information derived from visual experience in establishing neuronal connectivity. We find that suppression of REM sleep processes by an instrumental REM deprivation procedure results in a significant enhancement of the effects of altered visual experience by monocular occlusion. Bilateral brainstem lesions that selectively block the occurrence of ponto-geniculo-occipital (PGO) waves are sufficient to produce similar results. These data indicate that the propagation of phasic influences during REM sleep interacts with other processes subserving neural development. This source of influence appears not to derive from the environment but rather stems from an intrinsic source of genetic origin. Examination of the neural activity associated with PGO waves in the lateral geniculate nucleus reveals a distribution of facilitatory influence markedly different from that induced by visual experience. We conclude that REM sleep directs the course of brain maturation in early life through the control of neural activity.

Animals↗

PubMedDate not supplied

Is vasoactive intestinal polypeptide (VIP) a sleep factor?

Vasoactive intestinal peptide (VIP) was tested in order to determine its hypnogenic properties in cats. VIP was administered intraventricularly in doses of 10 and 100 ng and compared to Ringer controls. In addition the dose of 100 ng was tested in cats pretreated with 150 mg/kg of chloramphenicol (CAP). The results showed that the 100 ng dose of VIP had small but significant REM enhancing properties, but that it did not protect the animals from the specific REM inhibiting properties of CAP. The results suggest that VIP may participate in the regulation of REM sleep.

Animals↗

PubMedDate not supplied

Obstructive sleep apnea and hypertension: from correlative to causative relationship.

Sleep-disordered breathing, manifested by repetitive episodes of partial or complete cessation of breathing during sleep associated with brief arousal and autonomic activation, is estimated to affect as many as 4% of adult men and 2% of adult women. Studies conducted during the 1980s revealed a strong association between sleep-disordered breathing and hypertension. The results of these early studies, which relied on relatively small samples of patients, have been confirmed in recent years by large-scale epidemiologic studies that are controlled for all possible confounding factors. This paper reviews the evidence suggesting a causative relationship between hypertension and disordered breathing in sleep. The authors discuss the possible underlying mechanisms of the two entities and address the clinical implications of this relationship. They conclude by recommending a proactive approach to the diagnosis of breathing disorders in sleep, in order to prevent the cardiovascular sequelae of this syndrome.

Confounding Factors, Epidemiologic↗