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FRIMEDBIO-Fri prosj.st. med.,helse,biol

Auditory Verbal Hallucinations (AVH) in Schizophrenia

Awarded: NOK 5.6 mill.

Project Number:

221550

Application Type:

Project Period:

2013 - 2018

Location:

Schziophrenia is a severe mental disorder that handicaps the patients suffering from the disorder, and where it also is a large economic burden of the disorder. Auditory hallucinations are a characteristic symptom of the disorder, which is characterized by "hearing voices that do not exist". Auditory hallucinations are therefore a subjective conviction of perceiving a verbal message that does not have an external source explanation. A main question in the present project has therefore been how we could empirically understand what is happening in the brain during auditory halluicnations, and in particular what is the underlying neurochemistry of auditory hallucinations, which has not previously been investigated. A second question was if there were differences in the composition of nerve fiber structure between hallucinating and non-hallucinating patients, and controls. A third question was how large-scale activation networks in the brain interact in hallucinating and non-hallucinating patients, as well in schizophrenia patients in general. The project has utilized different MR-techniques to answer these questions, some of them being state-of-art techniques internationally. Results have essentially confirmed the hypoteses and questions, with elevated concentrations of the transmitters glutamate and glutamine in selected regions in the brain in hallux\cinating patients, and that they have altered composition of white matter nerve fiber structure between language areas in the brain, and finally that activation netork dynamics is different for schizophrenia, and hallucinating patients, and controls.

Auditory verbal hallucinations (AVH) is the most characteristic symptom in schizophrenia and psychosis, and iin a sense it "defines" the disorder from a clinical and phenomenological point of view. For this reason we have taken the approach that in order to understand the heterogenity of schizophrenia it may be more fruitful to focus on a single symptom than on the disorder as such. From our own (and others) previous research we know that: a) AVHs are speech percetual mis-representations originating in t he left posterior temporal lobe, b) neurons in the left temporal lobe show hyper-excitation to elicit AVHs, but are at the same time hypo-excited to an external speech sound, b) AVHs are not cognitively inhibited once they occur, due to frontal lobe defic it in excecutive control, c) AVH attract available attention resources inwards, leaving the patient unable to attend to outwards events during AVH episodes. Thus, AVHs engage large cortical networks in complex activation patterns. What we do not know: a) how are temporal lobe hyper- and hypo-excitation during AVH mediated at the transmitter and receptor level, what is the role of glutamate (excitatory) and GABA (inhibitory) to produce the "paradoxial" activation pattern seen, b) is the deficit in frontal lobe executive inhibition caused by a deficit in prefrontal cortex (anterior cingulate) deficit or in a deficit in fronto-temporal connectivity, or both, c) does the attention abnormality originating from the parietalk lobe, actually indicate a more globa l cortical network connectivity deficit in AVHs, affecting large-scale networks. We intend to address these three "unknowns" with an extended MR procol with fMRI, MRspectroscopy, diffusion tensor imaging (DTI), strcutural MR, and network connectivity anal ysis in hallucinating patients (N = 60) and heakthy controls over a period of 3 years. The access to and expertize in the Bergen fMRI Group will be available for the empirical studies.

Funding scheme:

FRIMEDBIO-Fri prosj.st. med.,helse,biol

Funding Sources