Anatomically, each thalamus lies rostral to the brainstem, lateral to the third ventricle, and medial to the internal capsule. As most blood to the thalamus arrives from the tip of the basilar artery and the proximal portions of the posterior cerebral arteries (PCAs), thalamic lesions may be associated with simultaneous lesions in the midbrain or in the distal territory of the PCA. Microangiopathy is the cause of most lateral thalamic infarcts although embolic sources are occasionally found. Large thalamic hemorrhages involve more nuclei and tracts, with or without ventricular extension, resulting in overlapping clinical syndromes. Common features seen in patients with thalamic hemorrhages include rapid onset of symptoms, inconstant impairment of consciousness even in large size hematomas, and a relatively good prognosis as compared with that for hemorrhages in the pons and basal ganglia. Venous thrombosis of the deep cerebral venous system usually leads to bilateral thalamic edema.

Memory systems are usually divided in five main categories: semantic, episodic, primary, procedural, and perceptual representation systems. Both semantic and episodic memories are forms of long-term memory with an unlimited capacity. The arterial blood supply of anatomical structures involved in memory comes from different sources. Memory impairment after stroke results from the cumulative effects of stroke and preclinical Alzheimer's disease or to unrecognized preexisting dementia. Mild memory complaints are frequent in stroke survivors. Confusion and memory loss can also result from infarction of the inferior genu of the internal capsule. This syndrome features fluctuating alertness, inattention, memory loss, apathy, abulia, psychomotor retardation, and severe memory loss. Concerning the influence of treatment modalities on memory defects, there are no differences between early and late aneurysmal surgery. Objective memory impairment is more frequent after surgical than after endovascular treatment of the ruptured aneurysm.