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...

Left hemispatial neglect, confined to right-hand and verbal responses, was exhibited by a 56-yr-old right-handed male patient with callosal lesions due to cerebral infarction. Various disconnection signs were also present. His CT and MRI scans disclosed major lesions situated in the posterior half of the genu and the whole trunk of the corpus callosum, as well as in the left medial frontal and temporo-occipital lobes. Left hemispatial neglect was invariably demonstrated in right-hand performance such as copying drawings, line bisection, matching identical figures and copying multiple digit numbers, and in verbal performance such as confrontation naming and reading aloud multiple digit numbers. In contrast, little or no right hemispatial neglect was demonstrated in tasks performed with the left hand. These findings support the hypothesis that the left hemisphere is only concerned with attending to the contralateral hemispace and that the right hemisphere is specialized for attending to both sides of space although the preponderant tendency is for attending to the contralateral hemispace. The neglect symptoms observed in our patient may be a disconnection sign which was attributable to a combination of lesions in the corpus callosum and in the left medial frontal lobe.

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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.