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Background <p>Posterior cortical atrophy (PCA) is a rare neurodegenerative syndrome most commonly associated with atypical Alzheimer’s disease. It is characterized by progressive visuospatial and visuoperceptual deficits with relative sparing of memory and language in early stages. Diagnosis is frequently delayed or missed due to clinical heterogeneity, subtle early symptoms, and limited sensitivity of routine cognitive screening tools. Psychiatric symptoms may further obscure the underlying neurological disorder. This case highlights the diagnostic challenges posed by PCA presenting in the context of prominent psychiatric symptoms, combined with a rapid clinical decline.</p> Case presentation <p>A 68-year-old white Danish male presented with suicidal ideation and was initially admitted to a psychiatric ward. He had a remote history of a suicide attempt and a family history of suicide but no known neurodegenerative disease. Within a short period, severe cognitive and functional impairment became evident, dominated by visuospatial deficits, apraxia, simultanagnosia, optic ataxia, and features of Gerstmann and Balint syndromes, with relative preservation of memory and language. Neuroimaging revealed marked posterior cortical atrophy and parieto-occipitotemporal hypometabolism with sparing of the posterior cingulate cortex. Cerebrospinal fluid analysis showed mildly reduced amyloid-β1–42 and markedly elevated neurofilament light chain levels. Electroencephalography demonstrated focal posterior slowing without epileptiform activity. Extensive evaluation excluded autoimmune, epileptic, metabolic, and prion-related causes. Based on the clinical syndrome, characteristic neuroimaging findings, and supportive CSF biomarkers, a diagnosis of posterior cortical atrophy likely related to underlying Alzheimer’s disease pathology was made. Disease-specific treatment was discussed but not initiated due to patient preference.</p> Conclusions <p>This case illustrates how posterior cortical atrophy may be overlooked, particularly when psychiatric symptoms dominate the initial presentation. It underscores the importance of considering neurodegenerative disorders in older patients with atypical psychiatric presentations or unexplained functional decline. Early recognition of PCA is crucial for accurate diagnosis, appropriate counseling, and tailored supportive care.</p>

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Posterior cortical atrophy with initial psychiatric presentation: a case report

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月23日

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  • Vivian Swane,
  • Bo Biering-Sørensen

摘要

Background

Posterior cortical atrophy (PCA) is a rare neurodegenerative syndrome most commonly associated with atypical Alzheimer’s disease. It is characterized by progressive visuospatial and visuoperceptual deficits with relative sparing of memory and language in early stages. Diagnosis is frequently delayed or missed due to clinical heterogeneity, subtle early symptoms, and limited sensitivity of routine cognitive screening tools. Psychiatric symptoms may further obscure the underlying neurological disorder. This case highlights the diagnostic challenges posed by PCA presenting in the context of prominent psychiatric symptoms, combined with a rapid clinical decline.

Case presentation

A 68-year-old white Danish male presented with suicidal ideation and was initially admitted to a psychiatric ward. He had a remote history of a suicide attempt and a family history of suicide but no known neurodegenerative disease. Within a short period, severe cognitive and functional impairment became evident, dominated by visuospatial deficits, apraxia, simultanagnosia, optic ataxia, and features of Gerstmann and Balint syndromes, with relative preservation of memory and language. Neuroimaging revealed marked posterior cortical atrophy and parieto-occipitotemporal hypometabolism with sparing of the posterior cingulate cortex. Cerebrospinal fluid analysis showed mildly reduced amyloid-β1–42 and markedly elevated neurofilament light chain levels. Electroencephalography demonstrated focal posterior slowing without epileptiform activity. Extensive evaluation excluded autoimmune, epileptic, metabolic, and prion-related causes. Based on the clinical syndrome, characteristic neuroimaging findings, and supportive CSF biomarkers, a diagnosis of posterior cortical atrophy likely related to underlying Alzheimer’s disease pathology was made. Disease-specific treatment was discussed but not initiated due to patient preference.

Conclusions

This case illustrates how posterior cortical atrophy may be overlooked, particularly when psychiatric symptoms dominate the initial presentation. It underscores the importance of considering neurodegenerative disorders in older patients with atypical psychiatric presentations or unexplained functional decline. Early recognition of PCA is crucial for accurate diagnosis, appropriate counseling, and tailored supportive care.