Sleepwalking episodes are preceded by arousal-related activation in the cingulate motor area: EEG current density imaging.

OBJECTIVE: To investigate local arousal fluctuations in adults who received ICSD-2 diagnosis of somnambulism. METHODS: EEG neuroimaging (eLORETA) was utilized to compare current density distribution for 4s epochs immediately preceding sleepwalking episode (from -4.0 s to 0 s) to the distribution during earlier 4s epochs (from -8.0 s to -4.0 s) in 20 EEG segments from 15 patients. RESULTS: Comparisons between eLORETA images revealed significant (t>4.52; p<0.05) brain activations before onset of sleepwalking, with greater current density within beta 3 frequency range (24-30 Hz) in Brodmann areas 33 and 24. CONCLUSIONS: Sleepwalking motor events are associated with arousal-related activation of cingulate motor area. SIGNIFICANCE: These results support the notion of blurred boundaries between wakefulness and NREM sleep in sleepwalking.

Fully parametric sleep staging compatible with the classical criteria.

We present an open system for sleep staging, based explicitly on the criteria used in visual EEG analysis. Slow waves, theta and alpha waves, sleep spindles and K-complexes are parameterized in terms of time duration, amplitude, and frequency of each waveform by means of the matching pursuit algorithm. It allows the detection of these structures using mostly the criteria from visual EEG analysis. For example, within this framework for the first time we compute directly the relative duration of slow waves, which is a basic parameter in recognition of deep sleep stages. Performance of the system is evaluated on 20 polysomnographic recordings, scored by experienced encephalographers. Seven recordings were scored by more than one expert. Proposed system gives concordance with visual staging close to the inter-expert concordance. The algorithm is implemented in a user-friendly software system for display and analysis of polysomnographic recordings, freely available with complete source code from http://signalml.org/svarog.html .

[Vagus nerve stimulation in severe, treatment-resistent depression]. / Stymulacja nerwu blednego w ciezkiej, opornej na leczenie depresji.

Since a few years, attempts are taken at the application of vagus nerve stimulation in the treatment of severe depression. It appears that the vagus nerve exerts a direct influence on areas of the brain associated with the regulation of mood and increases the level of biogenic amines. What is more, studies have confirmed an increased activity of fronto-orbital and prefrontal cortex, hypothalamus, cingulum and an increased concentration of serotonin and noradrenalin in the CNS and in the cerebro-spinal fluid. Preliminary clinical trials have confirmed the efficacy, good tolerance and safety of this treatment modality, although some objections have been raised whether these promising results were not partly due to the placebo effect. Therefore new, multicenter clinical studies have been designed, enabling an unbiased evaluation of usefulness of this method in the treatment of depression.

Sleepwalking and night terrors: psychopathological and psychophysiological correlates.

Sleepwalking and night terrors are considered to be manifestations of the same nosologic continuum. It has been proposed that a sudden arousal from non-rapid eye movement (NREM) sleep is the cause of these disorders. Benign forms of NREM arousal parasomnias occur frequently in childhood and attenuate in teen years; however, they can persist into or begin in adulthood. The available literature documents high levels of psychopathology in adult patients. Sleepwalking and night terrors are most likely to manifest during the first episode of slow wave sleep, but may also appear any time during NREM sleep. The hypersynchronous delta activity, previously considered to be a hallmark of somnambulism, has proven to be unspecific. Post-arousal EEG activity reveals altered consciousness during sleepwalking and sleep terror episodes. Pathophysiology of NREM arousal parasomnias consists of predisposing factors, which may be a genetically determined tendency for deep sleep, facilitating factors which deepen sleep and increase slow wave sleep, and triggering factors which increase sleep fragmentation, such as stress, environmental or endogenous stimuli, and stimulants. Recently published data on low delta power in the first sleep cycle and slow decline of delta power in successive sleep cycles suggest a chronic inability to sustain slow wave sleep.