Editors' Note: Progressive Auditory Verbal Agnosia Secondary to Alzheimer Disease

Abstract

In this issue of Neurology ®, Dr. Buciuc et al. describe the case of a patient with suspected Alzheimer disease and progressive auditory verbal agnosia. The clinical diagnosis is supported by nicely rendered [18F]-fluorodeoxyglucose PET imaging demonstrating hypometabolism in Heschl gyrus (primary auditory cortex), which corresponds with the patient's auditory verbal agnosia. The diagnosis of Alzheimer disease was reached on the basis of radiographic evidence of cortical atrophy with increased flortaucipir uptake in the bilateral temporal lobes (reflecting tau accumulation) and β-amyloid deposition on PET imaging, in the absence of other cognitive impairment. In response, Dr. Dasheiff commends the imaging findings and biologic explanation of this patient's condition; however, Dr. Dasheiff questions the diagnosis of Alzheimer disease given the lack of clinical pathology. The DSM-5 currently requires longitudinal follow-up and confirmation of progressive impairment in one or more cognitive domains to make the diagnosis of Alzheimer disease. The authors emphasize that their findings are consistent with Alzheimer pathology; however, they cannot confirm that an alternative tauopathy (or other clinical pathology) may account for this patient's neuroimaging and clinical manifestations. In this issue of Neurology ®, Dr. Buciuc et al. describe the case of a patient with suspected Alzheimer disease and progressive auditory verbal agnosia. The clinical diagnosis is supported by nicely rendered [18F]-fluorodeoxyglucose PET imaging demonstrating hypometabolism in Heschl gyrus (primary auditory cortex), which corresponds with the patient's auditory verbal agnosia. The diagnosis of Alzheimer disease was reached on the basis of radiographic evidence of cortical atrophy with increased flortaucipir uptake in the bilateral temporal lobes (reflecting tau accumulation) and β-amyloid deposition on PET imaging, in the absence of other cognitive impairment. In response, Dr. Dasheiff commends the imaging findings and biologic explanation of this patient's condition; however, Dr. Dasheiff questions the diagnosis of Alzheimer disease given the lack of clinical pathology. The DSM-5 currently requires longitudinal follow-up and confirmation of progressive impairment in one or more cognitive domains to make the diagnosis of Alzheimer disease. The authors emphasize that their findings are consistent with Alzheimer pathology; however, they cannot confirm that an alternative tauopathy (or other clinical pathology) may account for this patient's neuroimaging and clinical manifestations.