[Quality improvement of multiple choice examinations: in psychiatry, psychosomatic medicine, psychotherapy, and neurology]. / Qualitätsverbesserung von Multiple-Choice-Prüfungen: In Psychiatrie, Psychosomatik, Psychotherapie und Neurologie.

We describe a continuous improvement process in planning, performance, and evaluation of multiple choice examination questions in psychiatry, neurology, psychosomatic medicine, and psychotherapy. We analyzed 640 multiple choice questions of 1,419 students during a period of 4 years. Crucial changes concerned the abolishment of problematic question types, implementation of validated new question formats, extension of case-based questions, elongation of question stems, quantitative evaluation of item difficulty, discriminatory value, and the introduction of a peer review system. Consequences of these improvements were greater item difficulty (average 18%) and discriminatory value (average 67%) and reduced post hoc analysis times. Introduction of peer reviews resulted in longer preparation time, which was however appreciated by the peers due to a clear improvement in item quality.

BOLD fMRI deactivation of limbic and temporal brain structures and mood enhancing effect by transcutaneous vagus nerve stimulation.

UNLABELLED: Direct vagus nerve stimulation (VNS) has proved to be an effective treatment for seizure disorder and major depression. However, since this invasive technique implies surgery, with its side-effects and relatively high financial costs, a non-invasive method to stimulate vagal afferences would be a great step forward. We studied effects of non-invasive electrical stimulation of the nerves in the left outer auditory canal in healthy subjects (n = 22), aiming to activate vagal afferences transcutaneously (t-VNS). Short-term changes in brain activation and subjective well-being induced by t-VNS were investigated by functional magnetic resonance imaging (fMRI) and psychometric assessment using the Adjective Mood Scale (AMS), a self-rating scale for current subjective feeling. Stimulation of the ear lobe served as a sham control. fMRI showed that robust t-VNS induced BOLD-signal decreases in limbic brain areas, including the amygdala, hippocampus, parahippocampal gyrus and the middle and superior temporal gyrus. Increased activation was seen in the insula, precentral gyrus and the thalamus. Psychometric assessment revealed significant improvement of well-being after t-VNS. Ear lobe stimulation as a sham control intervention did not show similar effects in either fMRI or psychometric assessment. No significant effects on heart rate, blood pressure or peripheral microcirculation could be detected during the stimulation procedure. CONCLUSIONS: Our study shows the feasibility and beneficial effects of transcutaneous nerve stimulation in the left auditory canal of healthy subjects. Brain activation patterns clearly share features with changes observed during invasive vagus nerve stimulation.

Non-pharmacologic prevention of Alzheimer's disease: nutritional and life-style risk factors.

We conducted a review of cohort studies and interventional studies on nutritional and life-style risk factors and primary prevention of Alzheimer's Disease. Studies were assessed by the Oxford classification. Interventional studies exist for mental training and vitamin supplementation. For alcohol, fat and fish intake, mediterranean diet, homocysteine, overweight/caloric intake, physical and social activity, hypercholesterolemia, diabetes and smoking, currently there is only evidence from cohort studies. Cognitive stimulation by mental training increases mental functions and can be recommended on the basis of positive interventional studies. Vitamin supplementation cannot prevent AD on the basis of interventional studies. Hyperlipidemia, hyperhomocysteinemia, diabetes and typical life-style factors (alcohol, smoking, obesity etc.) modestly increased AD risk, fish, mediterranean diet and unsaturated fat or n-3 fatty acids and social activity are protective in observational cohorts, but interventional studies are lacking.

[Folate against hyperhomocysteinemia. A new approach for the prevention and therapy of alcoholism-associated disorders?]. / Folsäure gegen Hyperhomocysteinämie. Ein neuer Ansatz zur Prävention und Therapie Alkoholismus-bedingter Störungen?

There is growing evidence that chronic alcoholism is associated with a derangement in the sulfur amino acid metabolism. Excitatory aminoacids such as glutamate, aspartate, and homocysteine have been shown to be increased in patients with chronic alcoholism who underwent alcohol withdrawal. Furthermore, sustained hyperhomocysteinemia occurred in chronic alcoholics with active drinking pattern. Excitotoxicity can be induced by increased hormocysteine levels via rebound activation of NMDA receptor-mediated glutamatergic neurotransmission upon the removal of ethanol-evoked inhibition. Therefore, hyperhomocysteinemia may be responsible for the higher incidence of complications during alcohol withdrawal (e.g.stroke,convulsions). In addition, an association between brain atrophy and increased levels of homocysteine in chronic alcoholism was shown. This may have important implications for the pathogenesis of brain atrophy in alcoholics. Taking into account that high plasma homocysteine levels are helpful in the prediction of alcohol withdrawal seizures, early anti-convulsive therapy could prevent this severe complication. Supplementation of folate, a cofactor of the homocysteine metabolism, lowers raised homocysteine levels and therefore could be established as a new therapeutic strategy in alcohol withdrawal treatment. The results of various studies highlight the need for further research to prove whether alcoholics benefit from a reduced homocysteine level with respect to both, alcohol-related disorders and alcohol withdrawal symptoms.

A post mortem study on neurochemical markers of dopaminergic, GABA-ergic and glutamatergic neurons in basal ganglia-thalamocortical circuits in Parkinson syndrome.

Functional models of the circuitry of the basal ganglia have recently been proposed to account for the vast spectrum of motor disorders associated with the loss of anatomical or neurochemical integrity within the basal ganglia. On the basis of these hypothetical models, hypokinetic disorders such as Parkinson's disease, are thought to be associated with excessive tonic and phasic inhibition of the output from the basal ganglia to the thalamus. In the present study we have attempted to determine the validity of the proposed model by measuring neurochemical markers of inhibitory and excitatory neurotransmission in post mortem human brain tissue. We have determined the concentrations of the excitatory neurotransmitters aspartate/glutamate and of the inhibitory neurotransmitter GABA in 18 relevant regions of the thalamocortical circuits of the basal ganglia of patients who had manifested Parkinsonian symptoms, and compared them with controls of individuals who had died without any history of neurological or psychiatric disorders and had no neuropathological abnormalities. Additionally, the receptor subtype for the excitatory amino acid N-methyl-D-aspartate (NMDA) was studied in the same brain tissue in which neurotransmitter concentrations had been analysed as neurochemical markers of post-synaptic excitatory neurotransmission. In patients who had manifested Parkinsonian symptoms, glutamate and aspartate levels were found to be unchanged in all examined brain regions. In contrast, the binding of [3H]MK-801, which identifies the NMDA receptor, was reduced in the head (-42%) and body (-38%) of the caudate nucleus. In parkinsonian patients, GABA levels were diminished by 36% in the centromedial thalamus, compared to control values. These results do not confirm the changes in neurotransmitter concentrations predicted according to the model, although we cannot rule out that the predicted changes might have been observed if the Parkinsonian group had been further subdivided into groups diagnosed on the basis of the patients' clinical picture (akinetic-rigid, tremor-dominant, equivalent type) and compared with the control group.

The cortico-nigral projection: reduced glutamate content in the substantia nigra following frontal cortex ablation in the rat.

Unilateral ablation of the frontal cortex results in a significant reduction (19.5%) of glutamic acid in the ipsilateral compared with the contralateral substantia nigra. The GABA level in the substantia nigra and both the glutamate and GABA levels in the hippocampus remain unchanged. The results suggest that glutamate is a transmitter in the cortico-nigral fibre tract.