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Published on: March 26, 2019
Cortical auditory disorder caused by bilateral strategic cerebral bleedings. Analysis of two cases
Imre Szirmai1, Marianna Farsang, Maria Csüri
1Department of Neurology, Faculty of Medicine, Semmelweis University, Balassa u.6., Budapest H-1083, Hungary. szirmai@neur.sote.hu
Insights
Hypertensive bleedings causing bilateral temporal lobe damage led to evolving auditory dysfunction, from pure word deafness to generalized auditory agnosia in two patients. Brainstem auditory evoked potentials remained normal, indicating intact lower auditory pathways.
Area of Science:
- Neurology
- Neuroscience
- Otolaryngology
Background:
- Cortical auditory dysfunction can arise from lesions affecting auditory processing centers in the brain.
- Hypertensive hemorrhages are a significant cause of cerebrovascular damage, potentially impacting various brain regions.
Observation:
- Two patients experienced sequential hypertensive bleedings affecting bilateral temporal lobes, destroying cortical auditory centers and surrounding white matter.
- Clinical presentation evolved over time, progressing from pure word deafness to cortical deafness and generalized auditory agnosia.
Findings:
- Destruction of bilateral temporal white matter isolated the cortical hearing centers.
- Brainstem auditory evoked potentials (BAEPs) showed normal patterns, suggesting the auditory pathways below the cortex were preserved.
Implications:
- The transformation of clinical symptoms suggests a dynamic tissue response to subcortical bleeding within the auditory cortex.
- Understanding these evolving patterns is crucial for diagnosing and managing complex auditory processing disorders following cerebrovascular events.
Abstract:
The authors present the anatomical and clinical features of cortical auditory dysfunction in two patients, in whom hypertensive bleedings destroyed the cortical auditory centres in both hemispheres. The second haemorrhage occurred four years after the first bleeding in both cases. The bleedings isolated the cortical hearing centres due to the destruction of the right and left temporal white matter. During the clinical course the symptomatology has changed in both patients: pure word deafness has transformed to cortical deafness and generalised auditory agnosia. Normal pattern of brain stem auditory evoked potentials suggested intact auditory pathways. Authors conclude that transformation of clinical forms of cortical auditory disorder can be explained by the tissue reaction to the subcortical bleeding in the cortical auditory centres.

