Benign Paroxysmal Positioning Vertigo and Sleep:
A Polysomnographic Study of Three Patients
Per Monstad

In three elderly patients with a clinical diagnosis of Benign Paroxysmal Positioning Vertigo (BPPV), two with posterior canal BPPV and one with horizontal canal BPPV, polysomnography was performed with a position detector attached to the forehead. A total of 14 head movements were recorded during sleep. None of these were followed by nystagmus, while head movements during awake induced the expected nystagmus. However, a low sleep efficiency was seen in all cases, and 13 of the head movements were followed by at least one epoch of awake. BPPV might be a cause of sleep problems, but the polysomnographic findings are unspecific, as the oculovestibular reflexes are abolished during sleep.

A Qualitative and Quantitative Assessment
of the Sleep-Wakefulness Cycle Architecture
in the Post-Paradoxical Sleep Deprivation Period
Lia M. Maisuradze, Nani D. Lortkipanidze,
Marine D. Eliozishvili, Niko T. Oniani, Tengiz N. Oniani

The aim of this study was to assess post-deprivation sleep-wakefulness cycle (SWC) architecture following two versions of paradoxical sleep deprivation (PSD): rapid eye movements (REM) and ponto-geniculo-occipital (PGO) spikes. Mature cats were chronically implanted with electrodes for SWC registration during baseline, deprivation and recovery days. Differences between the two versions are expressed in the quantity and quality of sleep phases. Thus, the paradoxical sleep (PS) rebound and enhancement of its intensity clearly testifies to the pressure from the unsatisfied PS need accumulated in the course of the REM-deprivation period. Although following PGO-deprivation an increase in the amount of PS is available, quantitatively it is markedly less than PS rebound after REM-deprivation, and PS quality does not differ from baseline; in contrast to REM-deprivation, there is a significant slow-wave sleep (SWS) rebound in quality and quantity that leads to the increase in the amount of PS. However, the absence of changes in the post-deprivation ratio of deep slow-wave sleep (DSWS) and PS in relation to total sleep time indicates that an increase of the total amount of PS is not only a consequence of enhanced PS need, but also an increased SWS that suppresses wakefulness. The enhanced intensity of brain mechanisms during SWS takes up the responsibility for PS triggering. It is suggested that this occurs because of the pressure from the system of SWS on that of wakefulness, which becomes weak and is unable to control and delay the triggering of PS; having been released from the control of wakefulness, PS follows DSWS in full-developed episodes.

Prediction of Performance during Sleep Deprivation
and Alcohol Intoxication using a Quantitative Model
of Work-Related Fatigue
Adam Fletcher, Nicole Lamond,
Cameron J. van den Heuvel and Drew Dawson

Shift work and particularly night work can cause fatigue with subsequent negative impacts on health, sleep, and alertness. To facilitate better management of work-related fatigue, we have developed, optimized and validated a computerized model that can predict changes in performance, vigilance, sleepiness, and tiredness. The present study is a laboratory-based validation that demonstrates the further utility of the model in predicting performance impairment resulting from sleep deprivation and alcohol intoxication. Twenty-two healthy volunteers (mean age=22.0 years) each completed three counter-balanced laboratory conditions: sleep deprivation, alcohol intoxication, and a placebo control condition. In each condition, subjects were woken at 0700 h and performance on a variety of tests was measured hourly from 0800 h. The tests at 0800 h were then used as a relative baseline to which all other performance data were expressed. The six measures of performance assessed were grammatical reasoning (response latency and accuracy), unpredictable tracking score, vigilance (response latency and accuracy), and simple sensory comparison score. Regression analyses indicated that the fatigue model predicted between 47 and 98% of the variance in actual performance measures. Thus, there were moderate to very strong significant relationships between work-related fatigue model predictions and neurobehavioral performance as measured under laboratory conditions.

Insomnia and Depression: Which Comes First?
David Morawetz

It has been well documented that depression can lead to insomnia. However, evidence from previous research and from clinical experience indicates that the reverse can also be the case: long-standing insomnia can often lead to depression. The aim of this study is to test the hypothesis that, for many people suffering from both depression and insomnia, treating the insomnia successfully without medication can lead the depression to lift as well. The sample consisted of 86 consecutive patients or clients who presented as suffering from chronic insomnia. Two thirds of these people were also suffering from depression at intake. During an initial hour-long interview, self-report estimates of key sleep parameters were recorded, and the Beck Depression Inventory was administered. Subjects were then introduced to the "Sleep Better Without Drugs" self-help program (a book and three audio cassettes), which they used at home to improve their sleep. At follow-up, six to eight weeks later, the sleep parameters were recorded again and the Beck Depression Inventory was re-administered. Results showed that 70% of the insomnia sufferers who were depressed before treatment and learned to sleep better were no longer depressed, or were significantly less depressed, once their sleep had improved. By contrast, among people who did not learn to sleep better, none experienced a significant reduction in depression. The conclusion is that, for many people who suffer from both depression and insomnia, treating the insomnia successfully without medication can eliminate or significantly reduce the depression.