PubMed Health⌕ Search

Biomedical subjects

P Neu

Publications and source records attributed to P Neu.

11 recordsLinked to original sources
PubMed2006

Association between cerebral glutamate and human behaviour: the sensation seeking personality trait.

INTRODUCTION: Brain imaging studies have linked the anterior cingulate cortex (ACC) to motivation, drive, and personality traits like novelty and sensation seeking. Animal studies have shown glutamatergic neurotransmission to be important in ACC function as well as motivated behaviour. However, the role of glutamate in related personality traits like sensation seeking has not been investigated in humans. METHODS: The associations between sensation seeking personality scores and absolute glutamate concentrations in the ACC and the hippocampal region measured by 3-Tesla proton magnetic resonance spectroscopy (1H-MRS) were investigated. RESULTS: ACC glutamate concentration was negatively correlated with the sensation seeking sum score and the experience seeking subscore. A weak negative correlation was also observed between the hippocampal glutamate and the sensation seeking sum score. The reexamination of the glutamate concentration after 4 weeks revealed a similar relationship with sensation seeking. DISCUSSION: Although preliminary, the results are in line with the key role of the ACC for motivation and executive control and with the impact of glutamate on novelty related behaviour observed in animal experiments. The role of the hippocampus for novelty processing is discussed. Glutamate measurement with 1H-MRS may facilitate the understanding of biological underpinnings of personality traits and psychiatric diseases associated with dysfunctions in motivation and drive.

Adult↗
PubMed2006

Cerebrovascular reactivity in depressed patients without vascular risk factors.

INTRODUCTION: Cerebrovascular reactivity (CVR) seems to be gaining importance as a prognostic factor for stroke risk. CVR reflects the compensatory dilatory capacity of cerebral arterioles to a dilatory stimulus; this mechanism plays an important role in maintaining a constant cerebral blood flow. Evaluating factors that influence CVR will help prevention or early detection of cerebrovascular disease (CVD). In this study we aimed to measure the CVR in vascular-risk free depressed individuals so as to evaluate the effect depression has on CVR and hence its role as a stroke risk factor. METHODS: Using acetazolamid (ACZ) stimulation, CVR was assessed with a transcranial Doppler ultrasound in 25 non-smoking depressed patients (average age: 48.48 +/- 14.40) and in 25 healthy non-smoking controls (average age: 46.76 +/- 13.69) by calculating the difference between the maximal mean blood flow velocity at baseline and the maximal mean blood flow velocity after ACZ stimulation. RESULTS: Basal Cerebral Blood flow in Patients was 50.6 cm/s (SD: 11.6) versus controls 52.80 cm/s (SD: 12.70) whereas after stimulation maximal blood flow velocity was 72.64 cm/s (SD: 15.75) in patients versus 80.20 cm/s (SD: 18.43) in controls. In an analysis of covariance we found that cerebrovascular reactivity was significantly reduced in the vascular-risk free depressed sample. Age had a significant influence whereas gender did not. DISCUSSION: Major Depression appears to decrease cerebrovascular reactivity supporting the idea of increased risk for stroke in depressed patients. The mechanisms leading to this phenomenon and its subtle subgroup differences should be further investigated.

Acetazolamide↗
PubMed2006

Cerebrovascular reactivity over time course in healthy subjects.

INTRODUCTION: Cerebrovascular reactivity (CVR) reflects the compensatory dilatory capacity of cerebral arterioles to a dilatory stimulus and is an important mechanism for maintaining constant cerebral blood flow. Many pathological conditions are associated with an impaired CVR thus contributing to a higher risk of cerebrovascular disease. Since an impaired CVR might contribute to a cerebrovascular disease if it lasts for a longer period of time, it is of importance to know what the time-course of CVR might be under healthy conditions. METHODS: We investigated CVR in 33 healthy subjects on baseline and on follow-up after 1 to 3 years. CVR was determined by calculating the difference between maximal blood flow velocity after stimulation with acetazolamide and during rest. Blood flow velocities were measured by transcranial Doppler ultrasound. RESULTS: CVR did not differ significantly in a group of healthy persons when reevaluated after 1 to 3 years. Possible influencing factors like age, gender, interval between testing, and smoking did not show a significant influence. DISCUSSION: This is the first study to investigate within-subject-differences in healthy subjects. CVR seems to remain constant under healthy conditions. Even this short period of life-span is of importance because an altered CVR can improve under treatment within weeks. Nevertheless further studies should follow-up longer periods of time.

Adult↗
PubMed2005

What accounts for vertigo one year after neuritis vestibularis - anxiety or a dysfunctional vestibular organ?

One year after neuritis vestibularis, 29% from a sample of 75 patients still complained of vertigo. The objective of this investigation was to study why patients suffer from persisting vertigo. The alternative hypotheses were that the vertigo experienced could be explained either by a persisting vestibular dysfunction or by psychopathological changes. To elucidate this question, patients were examined with dynamic posturography, the symptom check list (SCL 90 R), the state-trait anxiety inventory (STAI), the agoraphobic cognitions questionnaire (ALQ) and the body sensations questionnaire (BSQ). After one year, only two patients had overall pathological results in the posturography. Following the assumption that sub-clinical dysfunction of the organs of balance can also lead to an altered body perception in combination with anxiety, the pathological results of posturographic sub-tests were related to experiences of vertigo. Here also there were no significant associations. However, vertigo correlated highly significantly with body-related anxiety and anxiety-related apprehension. In conclusion, chronic vertigo after an acute vestibular disorder could be regarded as a somatopsychic process. Persisting experience of vertigo is not explained by sub-clinical organic changes. Anxiety seems to be the crucial factor in persisting vertigo.

Anxiety↗
PubMed2005

Electroconvulsive monotherapy in the treatment of acute confusion psychosis. A case report.

This report focuses on the successful treatment of a most acute case of confusion psychosis according to the concept of Karl Leonhard. The 18-year-old patient was hospitalized three times before the current episode and his case has been characterized as pharmacologically treatment-resistant psychosis since he failed to respond to any psychopharmacological therapy including sufficient clozapine medication. In the patient's history, typical and atypical antipsychotic as well as mood-stabilizing and sedating pharmacological treatments have been conducted. However, only adverse effects could be observed. When receiving electroconvulsive monotherapy (ECT), the patient showed a marked reduction of symptoms while experiencing no adverse effects. The implications of this finding are discussed with regard to Leonhard's diagnostic system.

Acute Disease↗
PubMed2003

[First onset of panic disorder and agoraphobia induced by a series of inappropriate shocks of an implanted cardioverter/defibrillator].

We report on a 61-year-old patient with an implanted defibrillator due to malignant arrhythmia after myocardial infarction. After several years of appropriate function, the patient suffered a cluster of 16 shocks due to a defect in the defibrillator. Soon the patient developed a panic disorder with agoraphobia which was successfully treated with cognitive-behavioral therapy. Possible cognitive-behavioral mechanisms of panic disorder and special issues of behavioral therapy of patients with serious organic diseases are discussed.

Agoraphobia↗
PubMed2001

Time-related cognitive deficiency in four different types of depression.

Mild cognitive impairment often occurs in depressive illness. But it is unknown whether the occurrence or severity of cognitive deficits has diagnostic specificity. It is of interest to investigate whether there are time-related differences in cognitive functions characteristic of different kinds of depressive diagnoses, and therefore whether such differences might help to distinguish between types of depressive disorder. Eighty inpatients with a DSM-IV depressive episode (unipolar, bipolar, dysthymic and schizoaffective disorder, depressive type) were assessed with a series of neuropsychological tests at the beginning and at the end of their hospital stays. A group of 62 matched healthy controls were assessed with the same series of tests at comparable intervals. The diagnostic sub-groups could not be distinguished by cognitive parameters in the time-course. At the time of admission the inpatient group had a worse performance than the control group. After a significant decrease of their mean depression score, the patients still continued to show an outcome worse than the controls. We conclude that the variation of cognitive dysfunction with time in depression seems to be a phenomenon which does not depend on the kind of depressive sub-diagnosis. The results indicate that cognitive deficits might persist longer than the period of illness, but this seems to be true for all depressive sub-diagnoses.

Adult↗
PubMed2000

Comorbidity of mild cognitive disorder and depression--a neuropsychological analysis.

Mild cognitive impairment is found in many cases of depression, and it is mostly assumed to improve during the time course of depression remission. Recent data question the reversibility of low cognitive test performance in depression. The aim of this study is to determine the degree of reversibility and the proportion of patients who will not demonstrate reversibility of cognitive dysfunction. Consecutive inpatients suffering from depression (N=102) were investigated and N=82 matched control subjects. N=57 of the patients were diagnosed as major depression according to DSM-IV. A total of N=67 could be retested after remission of depression (N=32 of the patients with major depression) and a matched control group (N=62). Neuropsychological tests were applied in a test session which avoids the effects of fatigue in the patients by the short duration of strenuous tests. For most neuropsychological tests an impaired performance in the depressed patients was found. About one third of the depression subjects performed at an impaired level in tests of averbal memory and verbal fluency (below 5th percentile). In the follow-up investigation, a slight improvement in performance could be assessed for both the depression and the control group, which was, however, attributed to a general test training effect. No normalization of cognitive test performance was found in spite of complete recovery of the affective symptoms. No correlation between the duration of the disease before the index episode or number of episodes and cognitive deficits could be found. The data of the neuropsychological deficits of depressed patients, which are stable in the time course of the affective disorder, may indicate that these patients may suffer from comorbidity of both depression and mild cognitive disorder. The findings are discussed as 1) indicating only a minor impact of the depressed mood on the cognitive performance and 2) they are consistent with a role of brain lesions which have been reported in several studies in a subgroup of depression.

Cognition Disorders↗