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IntroductionComorbidity is increasingly regarded as important for both diagnosis and treatment of psychiatric disorders.ObjectivesElectrophysiological neuroimaging such as low-resolution brain electromagnetic tomography (LORETA) may be utilized to obtain insight into the pathogenesis of mental diseases.AimsThe aim of the present study was to compare EEG tomographic data obtained in generalized anxiety disorder (GAD) with and without nonorganic insomnia.MethodsIn the first study, LORETA was performed in 44 untreated patients (25 females) with the primary diagnosis of nonorganic insomnia (F51.0) associated with GAD (F41.1) and 44 age- and sex-matched normal controls. In the second study, 18 patients (9 females) with the primary diagnosis of GAD without mandatory insomnia were compared with 18 controls.ResultsWhile patients with F51.0 and concomitant F41.1 showed an increase in LORETA power in the delta, theta, alpha-1 and alpha-2 frequencies, GAD patients without mandatory insomnia demonstrated a decrease in LORETA power - specifically in delta (more left than right hemisphere, involving occipital cortex, insula, cingulate and frontal cortex) and beta (occipital cortex), mirroring neuroimaging findings on the neural circuitry of anxiety.ConclusionsDifferent EEG LORETA findings were obtained in GAD patients, depending on the comorbidity: While in daytime recordings patients with nonorganic insomnia demonstrated increased slow activities reflecting daytime tiredness and sleepiness, GAD patients without insomnia exhibited a decrease in slow activity and thus hypervigilance. According to the key-lock principle different pharmacological strategies have to be applied, which will be demonstrated on the basis our own data sets.

ObjectivesExperience-dependent cortical plasticity observed during post-training sleep has been hypothesized to be part of the global process of memory consolidation. Combining the temporal resolution of microstructure detectors and the spatial resolution of low-resolution brain electromagnetic tomography (LORETA) makes it possible to investigate when and where the experience-dependent reactivation occurs under normal (undisturbed) sleeping conditions.MethodsAfter an adaptation night, in the 2nd and 3rd night 48 young healthy volunteers were randomly assigned either to a control condition or to an experimental condition (declarative memory task: paired-associate word list or procedural memory task: mirror tracing). Sleep stages and sleep microstructures (slow waves, spindles and theta bursts) were detected automatically by means of the Somnolyzer 24x7. Changes in LORETA sources (experimental minus control night) were correlated with changes in memory performance (morning minus evening recall).ResultsOvernight improvements in the mirror tracing task were correlated with increased slow-wave sources in the right posterior parietal cortex (r = .70,p < 0.01) during NREM sleep and with desynchronized (r = −.76,p < 0.01) and synchronized (r = .62,p < 0.01) rolandic mu rhythm sources during periods with theta bursts in REM sleep. Overnight improvements in the declarative memory task were significantly correlated with increased spindle sources (r = .52, p < .01) in frontal, temporal and cingulate brain regions.ConclusionsThe present study supports the hypotheses of (1) a use-dependent reset of synaptic plasticity during slow-wave sleep (restorative function), (2) an experience-dependent reactivation during spindle episodes (stabilizing function) and (3) an off-line neuronal reprocessing during REM sleep (improvement without further training for novel tasks).

IntroductionSomatoform pain disorder (SPD) is frequently associated with sleep disorders, specifically restless legs syndrome and insomnia, which in turn lowers the pain threshold and worsens pain.ObjectivesThe aim of the present study was to investigate differences in wake-EEG by low-resolution electromagnetic tomography (LORETA) and objective and subjective sleep and awakening quality in SPD patients as compared with controls and study acute and chronic effects of trazodone CR on these variables and pain measures.MethodsFifteen patients with SPD (F45.4) and co-morbid insomnia (F51.0) were compared with 15 controls and participated in a single-blind, placebo-controlled, cross-over study on the acute effect of 100 mg trazodone CR, followed by a six-week open titration period. Statistics involved clinical, EEG-LORETA, PSG and psychometry.ResultsLORETA showed reduced power, mainly in the beta band in almost all pain matrix areas (SI, SII, ACC, SMA, PFC, PPC, insula, amygdala, hippocampus). PSG demonstrated a lack of deep sleep and increased arousals and stage shifts, with opposite changes induced by trazodone after acute and chronic therapy. Improvement of sleep was associated with improvement of pain, evaluated by visual-analog scales.ConclusionOur LORETA findings demonstrate a dysfunctional pain modulation in SPD. Trazodone induced changes in subjective and objective sleep and awakening quality that were opposite to the differences between SPD patients and controls (key-lock principle) and associated with pain improvement.

IntroductionIn contrast to the abundance of visual qualitative EEG reports in patho-endocrinology, there is a paucity of quantitative EEG findings.ObjectivesElectrophysiology may be utilized for differential diagnosis of hypersomnolence.AimsTo investigate long-term daytime sleepiness in a young female neurologist with the tentative diagnosis of narcolepsy in addition to moderate depression/anxiety and congenital thyroid hypoplasia treated with thyroxin.MethodsThree-night polysomnography, multiple sleep latency test (MSLT), visual EEG/ERP-mapping, LORETA, psychometrics and blood analyses were performed.ResultsPolysomnography revealed normal sleep efficiency and sleep architecture, but a high arousal index of up to 63/h TST. The MSLT showed a shortened mean sleep latency of 3.7 min. without REM-sleep onsets, objectifying the high Epworth Sleepiness score of 18. Visual EEG evaluation exhibited a fast alpha rhythm with intermittent theta and delta intrusions and paroxysmal activities. EEG-mapping showed an accelerated dominant frequency and ubiquitous increase in absolute (especially delta and beta) power, ERP revealed shortened N1 latency and very high amplitudes in all components (P300 > 5 SD). LORETA demonstrated significant regional increases in delta, alpha-2 and beta-1 power in the anterior cingulate, orbital, ventromedial, dorsolateral prefrontal cortex and temporal cortex, predominantly right hemispherically. Psychometry showed increased anxiety (SAS) and depression (SDS) and reduced quality of life. Finally, hormonal analysis pointed to thyrotoxicosis factitia (ICD-10 E05.4).ConclusionDiagnostic investigations clearly elucidated the pathogenesis of the presenting diagnosis of organic hypersomnia triggered by increased sleep-microarousals due to thyrotoxicosis factitia. Discontinuation of hormone substitution led to a normalization process that will be discussed.

IntroductionEarlier studies reported that subjective sleep quality correlates with objective polysomnographically measured sleep initiation and continuity, but less with sleep architecture.AimsThis study aimed to investigate relations between subjective and objective sleep in normals (N), insomnia comorbid with generalized anxiety disorder (G) and apnea (A).MethodsOne hundred and seventy-seven normals (50.9±19.6a), 100 insomniac G patients (37.9±10.6a) and 51 A patients (51.3±9.7a) completed the self-rating scale for sleep and awakening quality (Saletu et al. 1997) regarding two polysomnographic nights analyzed by the Somnolyzer (Anderer et al. 2005). Correlations were calculated based on changes between the first (adaptation) and second polysomnographic night to diminish inter-individual variances of sleep perception.ResultsIn N, subjective sleep quality (S-QUA) demonstrated correlations (p < 0.01) with sleep efficiency (EFF), wake after sleep onset (WASO), S2, S1%, REM, S1, frequency of awakenings (FW), latency to continuous sleep (L-CONT), sleep latency (S-LAT) and slow-wave sleep, while awakening quality (A-QUA) showed weak (p < 0.05) correlations with EFF and WASO. Somatic complaints (S-COM) correlated (p < 0.05) with WASO and REM. In G, correlations (p < 0.01) were obtained between S-QUA and EFF, WASO, S2, L-CONT and S-LAT (p < 0.05), while A-QUA correlated with S2, WASO and EFF. In A, S-QUA correlated (p < 0.01) with EFF, S2, S1%, S2%, L-CONT, WASO and less (p < 0.05) with S-LAT and S1. A-QUA correlated with S2, S2% (p < 0.01), L-CONT and EFF (p < 0.05). S-COM correlated with S-CONT (p < 0.01) and S-LAT (p < 0.05).ConclusionEFF, WASO, S2 and less S-LAT determine good S-QUA in all groups.