Beyond amnesia: neuropsychological deficits in acute unilateral posterior cerebral artery infarction involving the hippocampus.

BACKGROUND

Acute unilateral posterior cerebral artery (PCA) infarction involving the hippocampus can cause clinically relevant cognitive impairment, yet the acute neuropsychological syndrome remains insufficiently defined.

METHODS

This retrospective observational study included 78 patients with unilateral PCA stroke involving the hippocampus who underwent assessment at a median of 5 days (IQR, 3-7 days) after symptom onset. Thirty-two patients had right-hemispheric and 46 had left-hemispheric infarctions. Cognitive symptoms at onset, structured behavioral observations, standardized clinical tasks, and formal norm-referenced neuropsychological testing were used to characterize impairment across cognitive domains. Group differences were examined, and multivariable logistic regression analyses were performed to identify predictors of cognitive dysfunction.

RESULTS

Neuropsychological deficits involved memory, language, attention, executive functions, and visuoconstructive performance, indicating a broad range of cognitive symptoms rather than an isolated amnestic disturbance. Left-hemispheric infarctions were more often associated with amnestic symptoms at onset, and aphasic symptoms occurred exclusively in this group. Compared with right-sided lesions, left-hemispheric infarctions showed higher rates of subjective memory complaints and objective impairment in episodic memory, language production, and comprehension. Formal testing further demonstrated more frequent deficits in naming, categorical word fluency, verbal recall, verbal recognition, and visual recall. In multivariate analyses, lesion side emerged as the main predictor of neuropsychological impairment, whereas additional thalamic ischemia did not significantly improve prediction.

DISCUSSION: Acute unilateral PCA infarction involving the hippocampus is associated with multidomain and possibly network-mediated early cognitive dysfunction with more extensive impairment after left-hemispheric lesions independent of thalamic involvement.