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EV0865

Rapid progression to mutism: a case of frontotemporal dementia with subcortical frontal hyperintensity

RAPID PROGRESS TO MUTISM: A CASE REPORT OF FRONTOTEMPORAL DEMENTIA WITH SUBCORTICAL FRONTAL HYPERINTENSITY

In a case showing left frontal-predominant cortical atrophy and left prefrontal subcortical white matter hyperintensities, speech output declined to near-mutism within 15 months.

The patient was a 57-year-old man with no known personal or family history of neurodegenerative or psychiatric disorders. The clinical course began with a gradual reduction in spontaneous speech; verbal output became limited to brief responses, and the patient rarely initiated speech, while comprehension and object naming remained preserved. After eight months, the condition progressed to near-mutism, verbal repetition became impaired, and executive dysfunction and job loss occurred. Seven months later, behavioral symptoms emerged, including apathy, reduced initiative, aimless wandering, and altered eating behavior with an increased preference for sweets. Neurological examination revealed glabellar, grasp, snout, and palmomental release reflexes, indicating frontal lobe dysfunction. Cognitive assessment yielded an ADAS-Cog score of 56 out of 120, demonstrating marked difficulties in verbal recall and word finding, along with severe deficits in memory and language. Biomarker testing showed a low plasma p-tau217 level of 2.4 pg/mL, ruling out Alzheimer’s disease; an oligomerized amyloid-beta value of 0.54 supported this exclusion, and the APOE ε3/ε3 genotype was not associated with an increased risk of Alzheimer’s disease. Imaging revealed knife-blade cortical atrophy, most pronounced in the left frontal, left orbitofrontal, and left insular regions, along with marked asymmetric white matter hyperintensities (WMHs) in the left prefrontal subcortical white matter. The authors suggest that disruption of frontal-subcortical networks may affect language networks, driving the rapid decline in speech initiation and verbal output, and note that this pattern has been associated with hereditary frontotemporal dementia and progranulin mutations.

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