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Biomedical subjects

H Scherk

Publications and source records attributed to H Scherk.

7 recordsLinked to original sources
PubMed2006

[Drug addiction in young prison inmates with and without attention deficit hyperactivity disorder (ADHD)].

Prospective studies of children with ADHD have shown a high level of substance use disorder comorbidity, particularly when associated with social maladaptation and antisocial behavior. Conversely, studies of drug abusing participants and delinquents revealed a high prevalence of ADHD comorbidity. In this study 129 young male prison inmates were systematically examined for ADHD and substance use disorders. 64,3 % showed harmful alcohol consumption. 67,4 % fulfilled DSM-IV criteria for any drug abuse or dependence. 28,8 % of these participants were diagnosed with ADHD, combined type, other 52,1 % showed ADHD residual type. Opioid dependence was more common in delinquents without ADHD. Addicted delinquents with ADHD showed worse social environment and a higher degree of psychopathology, including externalizing and internalizing behavior, compared to addicted delinquents without ADHD. Neuroticism and conscientiousness ratings of the addicted ADHD group, but not of those without ADHD, differed from non-addicted delinquents. The results underline the need of adequate therapeutic programs for addicted young prison inmates considering ADHD comorbidity, which is associated with additional psychopathology and social problems.

Adult↗
PubMed2005

[Magnetic resonance spectroscopy in schizophrenia. Possibilities and limitations].

Magnetic resonance spectroscopy is a noninvasive investigative technique for in vivo detection of biochemical changes in neuropsychiatric disorders for which especially proton (1H-MRS) and phosphorus (31P-MRS) magnetic resonance spectroscopy have been used. In this review we explain the principles of MRS and summarize the studies in schizophrenia. A systematic literature review was carried out for 1H-MRS studies investigating schizophrenic patients compared to controls. The inconsistent results in the cited studies may be due to different study population, specific neuroimaging technique, and selected brain regions. Frequent findings are decreased PME and increased PDE concentrations (31P-MRS) linked to altered metabolism of membrane phospholipids and decreased N-acetylaspartate (NAA) or NAA/choline ratio (1H-MRS) linked to neuronal damage in frontal (DLPFC) or temporal regions in patients with schizophrenia. These results contribute to the disturbed frontotemporal-thalamic network assumed in schizophrenia and are supported by additional functional neuroimaging, MRI morphometry, and neuropsychological evaluation. The combination of the described investigative techniques with MRS in follow-up studies may provide more specific clues for understanding the pathogenesis and disease course in schizophrenia.

Brain↗
PubMed2004

[Changes in brain structure in bipolar affective disorders].

The neurobiological basis of bipolar affective disorders is unknown. However, neuroanatomic circuits of mood regulation have been hypothesized. Neuroimaging revealed volumetric changes of specific brain structures in these circuits. The most prominent abnormality is enlargement of the amygdala. In addition there might be structural changes in the frontal lobe, cerebellum, and pituitary. The findings in bipolar disorder differ from those in unipolar depression and schizophrenia. For further identification of the neurobiological basis of bipolar disorders, structural neuroimaging combined with functional neuroimaging such as magnetic resonance spectroscopy, neuroendocrinological studies, and genetical analyses are required to subgroup patients with bipolar disorder by diagnostic, prognostic, and therapeutic criteria.

Affect↗
PubMed2004

[Changes in brain structure caused by neuroleptic medication].

A couple of studies showed that neuroleptic treatment affects brain morphology. This paper reviews findings of volumetric longitudinal studies on treated schizophrenics, longitudinal studies considering the effect of different neuroleptic treatments on brain morphology, and studies on neuroleptic-naive patients with schizophrenia. The latter studies show enlargement of ventricles, diminished volume of the thalamus and reduced gray matter in different cortical regions. Findings on the nucleus caudatus, hippocampus, and amygdala are inconsistent. The volumes of the putamen and globus pallidus are unchanged. Medication with typical antipsychotics leads to increased volume of the nucleus caudatus while atypical antipsychotics do not change the volume of the nucleus caudatus.

Antipsychotic Agents↗
PubMed2003

[The importance of interneurons in schizophrenic and affective disorders].

In brains of patients with schizophrenic and affective disorders pathomorphological changes have been shown focussing in frontal and temporal cortex. The volume reduction in prefrontal cortex of schizophrenic patients is hypothesized to be based on a reduction of neuropil. A decrease of synaptic proteins and a decrease of dendritic spines of pyramidal cells can additionally be the origin of disconnections of neurons. Affection of the glutamatergic, GABA-ergic and dopaminergic system and reduction of interneurons could be the correlate of a deficient neuronal network which might be combined with exogen factors generate psychotic symptoms. Reelin and associated proteins are candidate molecules. Their dysregulation might explain essential features of the dysfunctional network of schizophrenia.

Brain↗
PubMed2000

Association between a functional polymorphism in the monoamine oxidase A gene promoter and major depressive disorder.

Various polymorphisms of the X-chromosomal monoamine oxidase A (MAO-A) gene were investigated for association with affective disorders. However, none of the studied variants could consistently be associated with either major depressive or bipolar affective disorder. Recently, a positive association between panic disorder and a novel functional repeat polymorphism in the MAO-A gene promoter, with the longer alleles being more active, was reported. Since monoaminergic neurotransmission is supposed to play an important role in affective disorders, we investigated a potential association of this polymorphism with major depressive illness in a sample of 146 unrelated patients of German descent and a control group of 101 individuals with a negative life history for affective disorders. Similarly to the recent findings in panic disorder, we observed a significantly increased frequency of genotypes containing only long alleles in female patients with recurrent major depression in comparison with age- and sex-matched controls. Thus, our data suggest that an excess of high-activity MAO-A gene promoter alleles resulting in an elevated MAO-A activity is a risk factor for major depressive disorder in females. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:801-803, 2000.

Adult↗