ReviewCureus2026
Central Auditory Pathway Dysfunction in Type 2 Diabetes Mellitus: A Narrative Review of Auditory Brainstem Response Alterations.
Review in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes mellitus (T2DM) is increasingly recognized as a disorder affecting both the peripheral and central nervous systems. Although diabetic neuropathy has traditionally been associated with peripheral nerve damage, accumulating evidence suggests that central auditory pathways are also vulnerable to chronic hyperglycaemia. This narrative review synthesizes current evidence regarding auditory brainstem response (ABR) abnormalities in adults with T2DM, with emphasis on their pathophysiological basis, characteristic electrophysiological alterations, clinical associations, and potential diagnostic significance. A structured search of PubMed/MEDLINE, Scopus, and Google Scholar identified 10 observational studies published between 2000 and 2024 that evaluated ABR parameters in adults with T2DM. Across the included studies, the most consistent findings were prolonged wave III and wave V absolute latencies together with extended interpeak intervals (I-III, III-V, and I-V), while wave I latency remained normal in most patients, indicating predominant central auditory pathway dysfunction. A smaller proportion of studies demonstrated additional peripheral auditory nerve involvement, suggesting mixed neuropathic changes. Higher glycated haemoglobin (HbA1c) levels and longer duration of diabetes were generally associated with greater ABR abnormalities, supporting the role of cumulative metabolic injury in central neural conduction delay. Despite methodological heterogeneity and predominantly cross-sectional study designs, the evidence consistently indicates that the auditory brainstem is an early target of diabetes-related neural injury. ABR represents a non-invasive and reproducible tool with potential utility for detecting subclinical central diabetic neuropathy before overt auditory impairment becomes clinically evident. Further multicentre longitudinal studies using standardized ABR protocols are required to validate its diagnostic and prognostic value in routine clinical practice.
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