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  1. Che Awang CMA, Abdul Wahab NA, Mohammad Tahir SA, Maamor N, Zakaria MN, Wahab S
    Sci Rep, 2025 Mar 20;15(1):9662.
    PMID: 40113860 DOI: 10.1038/s41598-025-94412-4
    Auditory hallucination is a complex and not yet fully understood phenomenon, and further research is necessary to elucidate the underlying mechanisms. Previous research has shown the possible contribution of abnormal efferent auditory pathways to auditory hallucinations. Given the structural and functional top-down connection between the auditory cortex and the cochlea, this study investigated the efferent auditory system in schizophrenia patients experiencing verbal auditory hallucinations (VAHs). Alternate Auditory Attention (ALAUDIN©) tasks were integrated with Contralateral Suppression of Otoacoustic Emissions (CSOAE) tasks as an assessment method. A total of 57 healthy controls (HCs) and 10 schizophrenia patients-five with recent hallucinations (SRH group) and five with nonrecent hallucinations (SNRH group) participated. Contralateral suppressors, which included white noise (WN) alone and WN in combination with ALAUDIN© tasks, were integrated with an otoacoustic emission (OAE) system to measure the suppression of cochlear outer hair cells. While no significant differences in suppression were found between the left and right ears across all groups, the SRH group demonstrated significantly greater suppression than did the HC group for contralateral suppressor 4 (CS4). Notably, incorporating the ALAUDIN© tasks could be used to measure abnormalities in the efferent auditory pathway in patients with schizophrenia with VAHs. These results suggest that the ALAUDIN©-CSOAE test could be used to examine efferent auditory pathways and differentiate schizophrenia patients with recent VAHs from healthy individuals, but further research with larger sample sizes is warranted to validate these findings.
    Matched MeSH terms: Efferent Pathways/physiopathology
  2. Chua AS, Keeling PW
    World J Gastroenterol, 2006 May 07;12(17):2688-93.
    PMID: 16718754 DOI: 10.3748/wjg.v12.i17.2688
    Functional dyspepsia (FD) is a common disorder of yet uncertain etiology. Dyspeptic symptoms are usually meal related and suggest an association to gastrointestinal (GI) sensorimotor dysfunction. Cholecystokinin (CCK) is an established brain-gut peptide that plays an important regulatory role in gastrointestinal function. It inhibits gastric motility and emptying via a capsaicin sensitive vagal pathway. The effects on emptying are via its action on the proximal stomach and pylorus. CCK is also involved in the regulation of food intake. It is released in the gut in response to a meal and acts via vagal afferents to induce satiety. Furthermore CCK has also been shown to be involved in the pathogenesis of panic disorder, anxiety and pain. Other neurotransmitters such as serotonin and noradrenaline may be implicated with CCK in the coordination of GI activity. In addition, intravenous administration of CCK has been observed to reproduce the symptoms in FD and this effect can be blocked both by atropine and loxiglumide (CCK-A antagonist). It is possible that an altered response to CCK may be responsible for the commonly observed gastric sensorimotor dysfunction, which may then be associated with the genesis of dyspeptic symptoms.
    Matched MeSH terms: Efferent Pathways/physiopathology
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