[Dramatic changes in the age structure for medical specialists in the field of mental health]. / Dramatische Veränderungen der Altersstruktur bei Fachärzten im Bereich psychischer Gesundheit.

BACKGROUND: Over the past 20 years the importance of treatment of people with mental and neurological disorders has greatly increased. Parallel to this development it has become more difficult to attract young physicians to this field. The aim of this study was to examine the development of the number of physicians specialized in the care of patients suffering from neurological, mental and psychosomatic disorders with special consideration of the age structure. MATERIAL AND METHODS: The analyses were based on the number of professionally active physicians and specialized physicians published by the German Medical Association for the years 2000-2020. Separate age groups were looked at for psychiatry and psychotherapy (PPT), psychosomatic medicine and psychotherapy (PMPT), Nervenheilkunde (formerly psychiatry and neurology together, NHK) and neurology. RESULTS: In comparison to the year 2000 the number of specialized physicians working in PPT (4736 vs. 12,053), neurology (2226 vs. 8355) and PMPT (3543 vs. 4130) increased in 2020, while the number of specialists actively working in NHK decreased (5184 vs. 2301). Parallel to this the proportion of women increased. Dramatic changes occurred concerning the age structure. Currently, 77.7% of specialists working in NHK and 59.7% working in PMPT are over 60 years old. In 2020 there were 2988 specialists aged over 60 years in the discipline of PPT compared to only 1070 under 40 years, which is dramatically different from 20 years earlier when only 181 were over 60 years but 1491 were under 40 years old. CONCLUSION: The overaging of professional specialists and the shortage of junior physicians jeopardize modern and adequate provision of care for mentally ill patients. Possible solutions include a marked increase in medical school capacities as well as strategies to convince young physicians to work in the disciplines of PPT and PMPT.

[Internet-based cognitive behavioral therapy of insomnia and nightmare disorder]. / Internetbasierte kognitive Verhaltenstherapie der Insomnie und Albtraumstörung.

Cognitive behavioral therapeutic interventions are considered to be one of the most effective forms of treatment of various mental disorders. Besides being very frequent, sleep disorders, such as insomnia and nightmare disorder are often not treated effectively and guideline-conform, mainly due to the lack of qualified psychotherapists. Implementation of modern technical options, such as web-based psychotherapy can help to overcome this problem. This article presents the current situation in the treatment of insomnia and nightmare disorders as particularly well-suited fields of application. For insomnia there are several English language and also recently German language options, which for example were also evaluated for the application to work-related stress and sleep disorders. In this respect, procedures with and without contact to a therapist or multicomponent procedures and single interventions can be differentiated. For nightmare disorders imagery rehearsal therapy provides a structure, which can also easily be transferred to an internet-based therapy program. The currently beginning use of internet-based treatment of sleep disorders does not yet utilize all theoretically available technical possibilities. The potential of internet-based therapy is extremely versatile and it remains for medical sleep experts to consider which method can be used for which indications.

Narcolepsy - clinical spectrum, aetiopathophysiology, diagnosis and treatment.

Narcolepsy is a rare brain disorder that reflects a selective loss or dysfunction of orexin (also known as hypocretin) neurons of the lateral hypothalamus. Narcolepsy type 1 (NT1) is characterized by excessive daytime sleepiness and cataplexy, accompanied by sleep-wake symptoms, such as hallucinations, sleep paralysis and disturbed sleep. Diagnosis is based on these clinical features and supported by biomarkers: evidence of rapid eye movement sleep periods soon after sleep onset; cerebrospinal fluid orexin deficiency; and positivity for HLA-DQB1*06:02. Symptomatic treatment with stimulant and anticataplectic drugs is usually efficacious. This Review focuses on our current understanding of how genetic, environmental and immune-related factors contribute to a prominent (but not isolated) orexin signalling deficiency in patients with NT1. Data supporting the view of NT1 as a hypothalamic disorder affecting not only sleep-wake but also motor, psychiatric, emotional, cognitive, metabolic and autonomic functions are presented, along with uncertainties concerning the 'narcoleptic borderland', including narcolepsy type 2 (NT2). The limitations of current diagnostic criteria for narcolepsy are discussed, and a possible new classification system incorporating the borderland conditions is presented. Finally, advances and obstacles in the symptomatic and causal treatment of narcolepsy are reviewed.

Functional microstates within human REM sleep: first evidence from fMRI of a thalamocortical network specific for phasic REM periods.

High thalamocortical neuronal activity characterizes both, wakefulness and rapid eye movement (REM) sleep, but apparently this network fulfills other roles than processing external information during REM sleep. To investigate thalamic and cortical reactivity during human REM sleep, we used functional magnetic resonance imaging with simultaneous polysomnographic recordings while applying acoustic stimulation. Our observations indicate two distinct functional substates within general REM sleep. Acoustic stimulation elicited a residual activation of the auditory cortex during tonic REM sleep background without rapid eye movements. By contrast, periods containing bursts of phasic activity such as rapid eye movements appear characterized by a lack of reactivity to sensory stimuli. We report a thalamocortical network including limbic and parahippocampal areas specifically active during phasic REM periods. Thus, REM sleep has to be subdivided into tonic REM sleep with residual alertness, and phasic REM sleep with the brain acting as a functionally isolated and closed intrinsic loop.

Rapid eye movement-related brain activation in human sleep: a functional magnetic resonance imaging study.

In animal models, ponto-geniculo-occipital waves appear as an early sign of rapid eye movement sleep and may be functionally significant for brain plasticity processes. In this pilot study, we use a combined polysomnographic and functional magnetic resonance imaging approach, and show distinct magnetic resonance imaging signal increases in the posterior thalamus and occipital cortex in close temporal relationship to rapid eye movements during human rapid eye movement sleep. These findings are consistent with cell recordings in animal experiments and demonstrate that functional magnetic resonance imaging can be utilized to detect ponto-geniculo-occipital-like activity in humans. Studying intact neuronal networks underlying sleep regulation is no longer confined to animal models, but has been shown to be feasible in humans by a combined functional magnetic resonance imaging and electroencephalograph approach.

Functional MRI during sleep: BOLD signal decreases and their electrophysiological correlates.

Prominent local decreases in blood oxygenation level (BOLD) can be observed by functional magnetic resonance imaging (fMRI) upon acoustic stimulation during sleep. The goal of this study was to further characterize this BOLD signal decrease with respect to corresponding neurophysiological phenomena using a simultaneous electroencephalography (EEG)/fMRI approach in sleeping human subjects. Healthy volunteers were subjected to acoustic stimulation during non-rapid eye movement (NREM) sleep. On the basis of statistical parametric maps, the correlations between the fMRI response (both amplitude and extent of the BOLD response) and the concomittant changes in the EEG (delta power and K-complexes) were calculated. Amplitude and extent of the stimulus-induced negative BOLD effect correlated positively with measures of EEG synchronization, namely an increase in the number of K-complexes and EEG delta power. Stimulus-induced BOLD decreases were most prominent during light (stage 2) NREM sleep and disappeared during slow wave sleep, indicating an influence of the baseline degree of hyperpolarization. Our observations provide first evidence that 'negative' BOLD signal changes during human sleep are associated with electrophysiological indicators of altered neuronal activity. Increased number of K-complexes and delta power reflecting hyperpolarization suggests true cortical deactivation upon stimulus presentation. This sleep stage-dependent deactivation might serve to protect the brain from arousing stimuli, particularly during the light phases of sleep shortly after sleep onset.

Epidemiology, implications and mechanisms underlying drug-induced weight gain in psychiatric patients.

Body weight gain frequently occurs during drug treatment of psychiatric disorders and is often accompanied by increased appetite or food craving. While occurrence and time course of this side effect are difficult to predict, it ultimately results in obesity and the morbidity associated therewith in a substantial part of patients, often causing them to discontinue treatment even if it is effective. This paper reviews the available epidemiological data on the frequency and extent of weight gain associated with antidepressant, mood-stabilizing, and antipsychotic treatment. Possible underlying pathomechanisms are discussed with special attention to central nervous control of appetite including the role of leptin and the tumor necrosis factor system. Metabolic alterations induced by drug treatment such as type 2 diabetes mellitus and the metabolic syndrome are also considered. Weight gain appears to be most prominent in patients treated with some of the second generation antipsychotic drugs and with some mood stabilizers. Marked weight gain also frequently occurs during treatment with most tricyclic antidepressants, while conventional antipsychotics typically induce only slight to moderate weight gain. Serotonin reuptake inhibitors may induce weight loss during the first few weeks, but some of them induce weight gain during long-term treatment. Several antidepressant and antipsychotic drugs are identified which reliably do not cause weight gain or even reduce weight. Based on these insights, countermeasures to manage drug-induced weight gain are suggested.

Altered processing of acoustic stimuli during sleep: reduced auditory activation and visual deactivation detected by a combined fMRI/EEG study.

Although there is evidence that acoustic stimuli are processed differently during sleep and wakefulness, little is known about the underlying neuronal mechanisms. In the present study, the processing of an acoustic stimulus was investigated during different non rapid eye movement (NREM) sleep stages using a combined EEG/fMRI approach in healthy human volunteers: A text stimulus was presented to sleep-deprived subjects prior to and after the onset of sleep, and single-slice silent fMRI were acquired. We found significantly different blood oxygenation level-dependent (BOLD) contrast responses during sleep compared to wakefulness. During NREM sleep stages 1 and 2 and during slow wave sleep (SWS) we observed reduced activation in the auditory cortex and a pronounced negative signal in the visual cortex and precuneus. Acoustic stimulation during sleep was accompanied by an increase in EEG frequency components in the low delta frequency range. Provided that neurovascular coupling is not altered during sleep, the negative transmodal BOLD response which is most pronounced during NREM sleep stages 1 and 2 reflects a deactivation predominantly in the visual cortex suggesting that this decrease in neuronal activity protects the brain from the arousing effects of external stimulation during sleep not only in the primary targeted sensory cortex but also in other brain regions.