Functional MRI revealed that AVHs were associated with activation in the right STG and posterior insula, the right middle temporal gyrus, and hippocampus/parahippocampal gyrus. (2006) using PET reported a positive correlation between hallucinations and activation of anterior cortex and a negative correlation with hippocampus-parahippocampus. (2006) suggest that the abnormal laterality of the supplementary motor area activity accounts for the failure to attribute speech generated by one’s own brain to one’s self and that the activation of Wernicke’s area accounts for the perceptual nature (hearing) of the patient’s experience. Activation was also observed in the left superior frontal area, right superior temporal pole and right orbitofrontal region (Parellada et al., 2008). Using PET during auditory verbal hallucinations (AVH), patients demonstrated a significant activation of the supplementary motor area, anterior cingulum, medial superior frontal area and cerebellum.
These temporal regions are important for visual object recognition, and these rCBF changes are associated with inappropriate visual processing and are responsible for nonpsychotic visual hallucinations in PD (Oishi et al., 2005). Nonpsychotic visual hallucinations in Parkinson’s disease (PD) were associated with hypoperfusion in the right fusiform gyrus and hyperperfusion in the right superior and middle temporal gyri. (1993) reported that hallucinatory state was associated with greater blood flow in language-related areas, significantly so in a region corresponding to Broca’s area and anterior cingulate and left temporal cortices. (2000) found increased rCBF in the left temporal region in hallucinating patients. This explains the occurrence of hallucinations following specific sensory modality deprivation. If by any chance there is stoppage or impairment of sensory input (e.g., in case of excessive affects during “functional psychosis,” prolonged periods of sensory deprivations), then earlier perception or memory traces emerge into the conscious, and the individual experiences hallucinations. But the censorship mechanism can operate only when there is constant flow of sensory inputs. The perceptual release theory (West, 1975) postulated the presence of a censorship mechanism in the brain which actively excluded from the consciousness the majority of sensory information that is received continually by the brain. The neurophysiologic dissociation theory (Marrazzi, 1970) proposes that hallucinations result from a dissociation between primary sensory cortex and cortical association areas which exert a regulatory influence on the former. He proposed the theory of abnormal brain excitation as a mechanism of production of hallucinations. (1950) demonstrated that electrical stimulation of certain cortical or subcortical structures induced different types of hallucinations. This model is known as disinhibition model. Hughlings Jackson (1932) suggested that hallucinations occur when the usual inhibitory influences of the uppermost level are impeded, thus leading to release of middle-level activity, which takes the form of hallucinations.
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