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J Neurol Neurosurg Psychiatry 1999;67:163-168 doi:10.1136/jnnp.67.2.163
  • Paper

Basal forebrain amnesia: does the nucleus accumbens contribute to human memory?

  1. Georg Goldenberg,
  2. Uwe Schuri,
  3. Olaf Grömminger,
  4. Ursula Arnold
  1. Neuropsychological Department, Bogenhausen Hospital, Munich, Germany
  1. Dr G Goldenberg, Neuropsychologische Abteilung, Krankenhaus München Bogenhausen, Englschalkingerstrasse 77, D 81925 München, Germany. Telephone 0049 89 9270 2106; fax 0049 89 9270 2089; emailGeorg.Goldenberg{at}lrz.tum.de
  • Received 20 October 1998
  • Revised 12 January 1999
  • Accepted 19 January 1999

Abstract

OBJECTIVE To analyse amnesia caused by basal forebrain lesions.

METHODS A single case study of a patient with amnesia after bleeding into the anterior portion of the left basal ganglia. Neuropsychological examination included tests of attention, executive function, working memory, recall, and recognition of verbal and non-verbal material, and recall from remote semantic and autobiographical memory. The patient’s MRI and those of other published cases of basal forebrain amnesia were reviewed to specify which structures within the basal forebrain are crucial for amnesia.

RESULTS Attention and executive function were largely intact. There was anterograde amnesia for verbal material which affected free recall and recognition. With both modes of testing the patient produced many false positive responses and intrusions when lists of unrelated words had been memorised. However, he confabulated neither on story recall nor in day to day memory, nor in recall from remote memory. The lesion affected mainly the nucleus accumbens, but encroached on the inferior limb of the capsula interna and the most ventral portion of the nucleus caudatus and globus pallidus, and there was evidence of some atrophy of the head of the caudate nucleus. The lesion spared the nucleus basalis Meynert, the diagnonal band, and the septum, which are the sites of cholinergic cell concentrations.

CONCLUSIONS It seems unlikely that false positive responses were caused by insufficient strategic control of memory retrieval. This speaks against a major role of the capsular lesion which might disconnect the prefrontal cortex from the thalamus. It is proposed that the lesion of the nucleus accumbens caused amnesia.

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