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Articles by H Walter
Total Records ( 4 ) for H Walter
  B Vyssoki , P Steindl Munda , P Ferenci , H Walter , P Hofer , V Bluml , F Friedrich , D Kogoj and O. M. Lesch

Aims: To assess the clinical and biological status of alcohol-dependent patients admitted to a psychiatric or a gastroenterological ward, assessing and comparing dimensions important for prescribing treatment for withdrawal and relapse prevention. Methods: Eighty patients, alcohol-dependent according to international classification of diseases tenth revision and diagnostic and statistical manual, text revised, version IV, admitted to the Vienna General Hospital between January 2005 and  November 2006, were examined, of whom 44 were admitted to the psychiatric ward and 36 to the gastroenterological ward. Dimensions of alcohol dependence were assessed using a computerized structured interview, the Lesch alcoholism typology (LAT). Biological markers and the model for end-stage liver disease (MELD) score defined the severity of alcohol-related physical disturbances. Results: As might be expected, gastroenterological patients had more advanced physical diseases than psychiatric patients, and affective disorders and suicidal tendencies were significantly commoner among the psychiatric patients. Thus, LAT Type II patients were overrepresented at the gastroenterological ward and LAT Type III patients at the psychiatric ward. Conclusion: The severity of somatic diseases and psychiatric disorders as well as the distribution of the four types according to Lesch differ between alcohol-dependent patients admitted to a psychiatric ward or a gastroenterological ward. Regarding the positive long-term outcome, different evidence-based medical treatment approaches for withdrawal and relapse prevention are needed for these patients.

  M Feyder , R. M Karlsson , P Mathur , M Lyman , R Bock , R Momenan , J Munasinghe , M. L Scattoni , J Ihne , M Camp , C Graybeal , D Strathdee , A Begg , V. A Alvarez , P Kirsch , M Rietschel , S Cichon , H Walter , A Meyer Lindenberg , S. G. N Grant and A. Holmes

Research is increasingly linking autism spectrum disorders and other neurodevelopmental disorders to synaptic abnormalities ("synaptopathies"). PSD-95 (postsynaptic density-95, DLG4) orchestrates protein-protein interactions at excitatory synapses and is a major functional bridge interconnecting a neurexinneuroligin-SHANK pathway implicated in autism spectrum disorders.


The authors characterized behavioral, dendritic, and molecular phenotypic abnormalities relevant to autism spectrum disorders in mice with PSD-95 deletion (Dlg4–/–). The data from mice led to the identification of single-nucleotide polymorphisms (SNPs) in human DLG4 and the examination of associations between these variants and neural signatures of Williams' syndrome in a normal population, using functional and structural neuroimaging.


Dlg4–/– showed increased repetitive behaviors, abnormal communication and social behaviors, impaired motor coordination, and increased stress reactivity and anxiety-related responses. Dlg4–/– had subtle dysmorphology of amygdala dendritic spines and altered forebrain expression of various synaptic genes, including Cyln2, which regulates cytoskeletal dynamics and is a candidate gene for Williams' syndrome. A signifi-cant association was observed between variations in two human DLG4 SNPs and reduced intraparietal sulcus volume and abnormal cortico-amygdala coupling, both of which characterize Williams' syndrome.


These findings demonstrate that DLG4 gene disruption in mice produces a complex range of behavioral and molecular abnormalities relevant to autism spectrum disorders and Williams' syndrome. The study provides an initial link between human DLG4 gene variation and key neural endophenotypes of Williams' syndrome and perhaps corticoamygdala regulation of emotional and social processes more generally.

  O. A Onur , H Walter , T. E Schlaepfer , A. K Rehme , C Schmidt , C Keysers , W Maier and R. Hurlemann

Multiple lines of evidence implicate the basolateral amygdala (BLA) and the noradrenergic (norepinephrine, NE) system in responding to stressful stimuli such as fear signals, suggesting hyperfunction of both in the development of stress-related pathologies including anxiety disorders. However, no causative link between elevated NE neurotransmission and BLA hyperresponsiveness to fear signals has been established to date in humans. To determine whether or not increased noradrenergic tone enhances BLA responses to fear signals, we used functional magnetic resonance imaging (fMRI) and a strategy of pharmacologically potentiating NE neurotransmission in healthy volunteers. 18 subjects were scanned two times on a facial emotion paradigm and given either a single-dose placebo or 4 mg of the selective NE reuptake inhibitor reboxetine 2 h prior to an fMRI session. We found that reboxetine induced an amygdala response bias towards fear signals that did not exist at placebo baseline. This pharmacological effect was probabilistically mapped to the BLA. Extrapolation of our data to conditions of traumatic stress suggests that disinhibited endogenous NE signaling could serve as a crucial etiological contributor to post-traumatic stress disorder (PTSD) by eliciting exaggerated BLA responses to fear signals.

  H Walter , A Ciaramidaro , M Adenzato , N Vasic , R. B Ardito , S Erk and B. G. Bara

In this fMRI study, we investigated theory of mind (ToM) in patients with paranoid schizophrenia. We hypothesized that the network supporting the representation of intentions is dysfunctional in patients with schizophrenia dependent on the type of intention involved. We used a paradigm including a control condition (physical causation) and three intention conditions (private intention, prospective social intention and communicative intentions) differing in the degree of social interaction. In all four experimental conditions patients performed worse than controls regarding accuracy and reaction time. They showed significantly less activation in three regions typically activated in ToM tasks, i.e. paracingulate cortex and bilateral temporo-parietal junctions. However, this dysfunction was dependent on the type of intention represented, i.e. was present only for social but not for non-social intentions. Moreover, part of the reduced activation was related to the fact that there was no signal drop in these regions for the physical causality condition as usually found in controls. This may be due to the tendency of schizophrenic patients to attribute intentionality to physical objects. Our findings have implications for the study and understanding of ToM in schizophrenia but also in other disorders like autism.

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