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Stroke impairs episodic memory, while retaining immediate and remote memory. Cerebral hemorrhage/infarction in the Papez and Yakovlev circuits (episodic memory) manifests as memory loss. Extensive medial temporal lobe damage impairs retrieval of old memories. Hippocampal damage causes anterograde amnesia. Damage to the hippocampus and parahippocampal gyri causes severe retrograde amnesia. Retrosplenial lesions may cause memory loss if the fibrous communication between the hippocampus and anterior thalamic nucleus is impaired. Basal forebrain amnesia impairs recall but the aspect providing retrieval clues remains relatively intact. Corpus striatum and basal forebrain damage results in serious memory loss. Other cognitive functions require evaluation using intelligence (WAIS-IV) and executive function tests, along with memory loss assessments. The WMS-R can evaluate memory after stroke. The RBMT elucidates the nature of memory loss, especially in the elderly. Cognitive rehabilitation with repetitive training and internal-memory strategies aims to activate the memory processes. External strategies and environmental adjustments provide effective clues and replicate the environment. Rehabilitation protocols should directly solve problems encountered in daily life. This chapter provides an overview of the anatomical basis of memory, pathophysiology of underlying memory loss, and assessment for stroke.
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