Destructive lesions of the basal forebrain are often associated with memory impairment and this structure is thought to contribute to memory function by providing a cholinergic input to critical structures associated with memory such as the hippocampus and amygdala. In previously reported cases of amnesia associated with damage in the basal forebrain, multiple neuroanatomical regions were damaged, and the critical lesion responsible for amnesia has not been identified clearly. We report a patient who developed primarily anterograde amnesia after clipping of an unruptured anterior communicating artery aneurysm. Postoperative magnetic resonance imaging showed a discrete lesion, centring in the right diagonal band of Broca and including the anterior hypothalamus, septal nucleus, lamina terminalis, and paraterminal gyrus, and an indiscrete patchy lesion in the corresponding area on the opposite side. The nucleus basalis of Meynert was minimally aVected and the diencephalon was not damaged. Single photon emission computed tomography showed marked hypoperfusion in the midline frontobasal region corresponding to the MRI lesion and hypoperfusion in the hippocampus bilaterally. It is concluded that disconnection of the pathway between the diagonal band of Broca and the hippocampus contributed to memory impairment. (J Neurol Neurosurg Psychiatry 1998;65:126-130) Keywords: diagonal band of Broca; amnesia; time taggingThe amnesic syndrome has been found in patients with relatively discrete lesions in several cerebral sites including (a) the medial temporal lobes including the hippocampus, (b) median thalamic nuclei, (c) anterior thalamic nuclei, (d) basal forebrain, (e) fornix, (f) mammillary bodies, and (g) retrosplenial cortex. 1-3The basal forebrain has been considered to contribute to memory function by way of the pathways between nuclei of the diagonal band or the septal nucleus and the hippocampal region, thus providing a cholinergic input to the hippocampus. [1][2][3][4] In most previously reported cases of amnesia 4-14 associated with basal forebrain lesions, multiple neuroanatomically identified areas were damaged, and it has been diYcult to identify the minimal lesion necessary to produce an amnesic syndrome except for patients in whom basal forebrain lesions were relatively well circumscribed. 5We describe a patient who developed anterograde amnesia as the result of a discrete lesion in the basal forebrain after clipping of an unruptured anterior communicating artery aneurysm. Case reportA 61 year old right handed high school teacher, who had taught science for more than 35 years and had had good memory function, experienced a sudden onset of weakness in the right upper and lower limbs in July 1993, but recovered the next day. He was admitted to a hospital elsewhere and underwent MRI, which showed a small haemorrhage in the left external capsule. He underwent cerebral angiography, which showed an aneurysm 5 mm in diameter in the anterior communicating artery. He underwent surgical clipping of the aneur...

Background/Aims: Existing cognitive measures for moderate-to-severe dementia have shown floor effects and an inability to assess the remaining cognitive function, especially for profound dementia. Methods: We constructed the Cognitive Test for Severe Dementia (CTSD), which consists of 13 items covering 7 cognitive domains, and examined its reliability and validity. Results: Cronbach's α in severe dementia participants was 0.896. Interrater and test-retest reliability were 0.961 and 0.969, respectively. The CTSD showed a significant correlation with 3 other measures of cognitive function (Mini-Mental State Examination, Severe Cognitive Impairment Rating Scale, and Hasegawa Dementia Scale-Revised: r values = 0.870-0.922, p values <0.001). While the other measures showed floor effects, the CTSD did not. Conclusion: The CTSD was able to sensitively capture the remaining cognitive function in severe dementia patients when compared with other cognitive tests.

In order to investigate the underlying mechanism of ideomotor apraxia, we studied 9 patients who could not mime using tools despite the ability to manipulate actual tools normally. In all the mime tasks, visually presented tools or model gestures by examiners were fundamentally ineffectual in improving the patients’ performances. Even the remarkable improvement demonstrated when using actual tools disappeared immediately after the subjects took their hands off them. In a further experiment, 4 of the 9 patients were required to pretend to use tools while holding a stick, resulting in significant improvements or normal miming. These findings suggest that the somatosensory feedback continuously supplied from a handheld tool is a crucial component in enabling patients with ideomotor apraxia to actually use tools.

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