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Abstract
Auditory hallucination is false perception of sounds (usually voices but also other noises such as music) which is not under voluntary control and occurs in wakeful state. It’s the most common hallucination in psychiatric disorders, mean while, it’s the most common symptom of schizophrenia being reported by about 65% of schizophrenic patients. Auditory hallucinations can occur in any age with diversity of etiology and occur with no sex difference. Auditory hallucinations may occur in wide range of circumstances that can be classified into psychiatric conditions like schizophrenia and mood disorders, neurological or structural brain lesions like temporal lobe tumors, hearing impairment and systemic conditions. Cognitive approaches for auditory hallucinations focus respectively over that it may be either: 1) inner speech with erroneous interpretation that it’s of non self origin, 2) dysfunction of speech perception, 3) defect in reality monitoring or 4) auditory verbal imagery.
Auditory hallucinations may differ considerably in their phenomenology. They may be ill formed like tinnitus which is more common in neurological causes and hearing impairment or well formed like auditory verbal hallucination which is more common in psychiatric disorders. AVH are even variable in areas of form, content and frequency which differ from one disorder to another and even from one patient to another with the same disorder.
Understanding the biological bases of auditory hallucinations requires knowledge about the anatomy and physiology of the CANS and its complexity till reading auditory cortex with subsequent complex auditory processing. Cortical auditory areas include primary auditory cortex in the superior and transverse temporal gyri, which is surrounded by 2ry auditory cortex responsible for more complex processing. Yet, auditory cortex has wide spread connections and functional integration with other related cortical areas related to speech, memory and attention. Auditory integrative functions and complex auditory processing include speech comprehension, perception of auditory spatial location, modulation by attention and functional integration with other cortical areas for other sensory modalities and other related functions. Central auditory processing can be simply seen as implying change from sounds to speech and space leading to auditory scene segregation. This process can be simplified as two streams known as: anterior “what pathway” for intelligible speech with more anterior temporal and frontal lobe involvement, posterior or “where” pathway with posterior auditory and inferior parietal cortical responses for spatial localization.
These widespread cortical areas involvement in auditory processing and auditory integrative functions makes us not astonished with functional imaging results for auditory hallucination which may show discrete cortical and subcortical areas of activation during auditory hallucinations.
Application of unified pathophysiological model for auditory hallucination in neurological and psychiatric conditions is based on dysfunction in thalamocortical circuits and their regulation. Auditory perception is subserved by thalamocortical circuits between specific thalamic nuclei and auditory cortex. These thalamocortical circuits have basal intrinsic activity. These circuits are controlled by excitatory effect from glutamatergic corticothalamic projection, arousal mechanisms and attention from prefrontal cortex and limbic system together with A.ch from nucleus basalis during arousal. Meanwhile, inhibitory effect comes from reticular thalamic nucleus GABAergic neurons to thalamic nuclei. Regulatory input comes also from cholinergic, adrenergic and serotonergic brain stem systems.
In schizophrenia, there’s biological susceptibility apparent as hyperactive base line of thalamocortical circuits due to decreased inhibitory GABAergic transmission from reticular thalamic nucleus to the thalamus. This occurs together with increased dopamine that adds more to disinhibition of thalamocortical circuits. With increased attention, cortical glutamatergic and cholinergic output facilitate more thalamocortical circuits leading to auditory hallucination.
In hearing impairment there’s increased back ground activity in thalamic nuclei due to sensory deprivation together with increased cortical cholinergic arousal mechanisms that again may lead to hallucination. In brain diseases abnormal cerebral excitation may predispose to auditory hallucination. In peduncular hallucinosis, mid brain lesions disrupt brain stem regulatory serotonergic and cholinergic systems controlling thalamic nuclei and reticular thalamic nucleus. While in neurodegenerative diseases like Parkinson disease and Lewy body disease, there is disruption of brain stem and cortical regulatory systems over thalamic nuclei.