Amnesia (PCA Infarct)
OBJECTIVES
To review the anatomic circuits and connecting pathways involved in amnesia.
To identify disorders associated with acute-onset memory loss.
To evaluate the leading causes of amnestic syndromes.
VIGNETTE
A 50-year-old right-handed man had sudden difficulties in comprehending written words and remembering the names of family members and associates. He also had right-sided headaches and right-sided visual field impairment. Past medical history was remarkable for hypertension and thrombocytopenia of unknown cause.

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Our patient had acute onset of memory loss, anomia, alexia, and a right superior homonymous quadrantanopia consistent with an infarct in the territory of the left posterior cerebral artery (PCA). T2-weighted magnetic resonance imaging (MRI) of the brain showed hyperintensities involving the inferomedial left PCA. Follow-up brain MRI showed hyperintensities on T2-weighted and fluid-attenuated inversion recovery (FLAIR) images involving the left hippocampus, amygdala, and left occipital lobe (Fig. 30.1). On diffusion-weighted images these areas showed restricted diffusion. Magnetic resonance angiography (MRA) showed focal stenosis of the left PCA at the P1-P2 junction.
Our patient was initially thought to have herpes simplex encephalitis. Herpes simplex encephalitis, the most common cause of sporadic viral encephalitis, often presents with a subacute and progressive course characterized by headache, fever, altered sensorium, seizures, and occasionally focal neurologic deficits. Our patient had no recorded fever. Moreover, the course of his illness was acute and nonprogressive. Indeed, he awoke with his deficits. Although herpes viruses have a predilection for the limbic system, involving one or both mesial temporal lobes, involvement of the diencephalon and occipital cortex is rare.

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