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Basal Forebrain Amnesia: Does the Nucleus Accumbens Contribute to Human Memory?

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Basal Forebrain Amnesia: Does the Nucleus Accumbens Contribute to Human Memory? J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.67.2.163 on 1 August 1999. Downloaded from J Neurol Neurosurg Psychiatry 1999;67:163–168 163 Basal forebrain amnesia: does the nucleus accumbens contribute to human memory? Georg Goldenberg, Uwe Schuri, Olaf Grömminger, Ursula Arnold Abstract and anterior portions of the thalamus can Objective—To analyse amnesia caused by cause amnesia.2–7 The evidence for a selective basal forebrain lesions. role of the basal forebrain in human memory is Methods—A single case study of a patient weaker and more indirect. It has originally with amnesia after bleeding into the ante- been derived from degeneration of cholinergic rior portion of the left basal ganglia. cells within the basal forebrain in Alzheimer’s Neuropsychological examination included disease.89 As amnesia is a core symptom of tests of attention, executive function, Alzheimer’s disease it has been concluded that working memory, recall, and recognition basal forebrain lesions can cause amnesia. This of verbal and non-verbal material, and conclusion is not compelling as neuronal recall from remote semantic and autobio- degeneration in Alzheimer’s disease aVects graphical memory. The patient’s MRI and medial temporal structures as well.10 11 More those of other published cases of basal direct evidence for basal forebrain amnesia is forebrain amnesia were reviewed to provided by patients with amnesia after cir- specify which structures within the basal cumscribed damage to only the basal forebrain are crucial for amnesia. forebrain.12–22 In most of them, the lesion was Results—Attention and executive function caused by haemorrhage from anterior commu- were largely intact. There was antero- nicating artery aneurysms and subsequent inf- grade amnesia for verbal material which arction of perforating arterial branches or aVected free recall and recognition. With Heubner’s recurrent artery.12–14 16 17 19–22 How- both modes of testing the patient pro- ever, subarachnoidal or intraventricular haem- duced many false positive responses and orrhage may cause hydrocephalus and di use intrusions when lists of unrelated words V had been memorised. However, he con- brain damage. This raises the possibility that at fabulated neither on story recall nor in least some of the symptoms of these patients are due to diVuse brain damage rather than to day to day memory, nor in recall from 23 remote memory. The lesion aVected the basal forebrain lesion. mainly the nucleus accumbens, but en- The anatomicoclinical relation of basal fore- croached on the inferior limb of the brain amnesia is further complicated by the capsula interna and the most ventral por- proximity of the basal forebrain to the frontal tion of the nucleus caudatus and globus lobe. Lesions from anterior artery aneurysms pallidus, and there was evidence of some often aVect the orbital and medial frontal http://jnnp.bmj.com/ atrophy of the head of the caudate nu- lobe.12 17 24 25 Disinhibition or unconcern re- cleus. The lesion spared the nucleus basa- lated to frontal lobe pathology may distort or lis Meynert, the diagnonal band, and the conceal the amnesic syndrome.16 Particularly, septum, which are the sites of cholinergic confabulations which are a frequent feature of cell concentrations. basal forebrain amnesia have been related to Conclusions—It seems unlikely that false accompanying frontal lobe pathology rather positive responses were caused by insuY- than to the basal forebrain lesion itself.26 cient strategic control of memory re- on September 28, 2021 by guest. Protected copyright. Neuropsychological The uncertainty of the anatomicoclinical Department, trieval. This speaks against a major role of relation increases when localisation within the Bogenhausen Hospital, the capsular lesion which might discon- basal forebrain is considered. Inspired by the Munich, Germany nect the prefrontal cortex from the thala- parallel with Alzheimer’s disease, some authors G Goldenberg mus. It is proposed that the lesion of the have considered damage to cholinergic cells in U Schuri nucleus accumbens caused amnesia. O Grömminger the septum, the diagonal band, or the nucleus (J Neurol Neurosurg Psychiatry 1999;67:163–168) U Arnold basalis of Meynert as being the cause of 12 18 Keywords: amnesia; basal forebrain; nucleus accumbens amnesia. An alternative account holds that Correspondence to: lesions of fibre tracts rather than cells are cru- Dr G Goldenberg, 15 20 Neuropsychologische cial for amnesia. The basal forebrain is tra- Abteilung, Krankenhaus Research in human amnesia has identified versed by the inferior and anterior thalamic München Bogenhausen, peduncles which connect the dorsomedial Englschalkingerstrasse 77, D three core regions where localised brain 81925 München, Germany. damage can cause a lasting amnesic syndrome: nucleus of the thalamus with the amygdalae Telephone 0049 89 9270 the medial temporal lobe, the thalamus, and and with the prefrontal cortex. Amnesia may be 2106; fax 0049 89 9270 1 caused by interruption of an amygdala- 2089; email the basal forebrain. However, the weight of the [email protected] evidence for a selective correlation between thalamic-prefrontal loop rather than by basal circumscribed lesions and amnesia is diVerent forebrain damage itself.11527 Received 20 October 1998 for these three locations. There are many case In this paper we describe a patient with and in revised form 12 January 1999 reports showing that circumscribed lesions of amnesia from a circumscribed basal forebrain Accepted 19 January 1999 the medial temporal lobes and of the medial lesion which did not extend into the frontal J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.67.2.163 on 1 August 1999. Downloaded from 164 Goldenberg, Schuri, Grömminger, et al A which had been talked about only a few minutes ago. In addition he noted an impover- ishment of his autobiographical memories and a loss of professional knowledge. He could not remember geographical facts, names of other companies, mathematical formulae, or phone numbers which he had known by heart before. He said that he had lost his previous knowledge of foreign languages. He had to translate labo- riously even English which had been the every- day language in his job. Visiting a place where he had spent several holidays, his wife and he noted that he had diYculties in finding familiar routes. As well as his memory problems the patient complained of a loss of libido and of a flattening of emotional reactions. He said: “There is nothing which makes me really happy or really sad. It’s all far away”. Neurological examination showed only a slight reduction of fine motor skill of the right B hand, which disappeared completely during the subsequent weeks. NEURORADIOLOGICAL EXAMINATION Brain MRI (figure) showed a sharply demar- cated, slit-like, lesion which ran from the bottom of the left frontal horn in a slightly Cd curved way laterally. The caudal limit of the lesion was at the level of the anterior commis- sure. The lesion destroyed a large portion of CI the nucleus accumbens and encroached on the GP inferior limb of the capsula interna and the most ventral portions of the anterior nucleus caudatus and globus pallidus. There was no Acb general enlargement of ventricles, but the wall of the left frontal horn was slightly widened and DB flattened, indicating some atrophy of the head of the caudate nucleus. Tc-99-HMPAO SPECT showed hypoper- (A)T1weighted MRI of the lesion. (B) Anatomical scheme of the centre of the lesion, corresponding to the leftmost image of the bottom row of the MRI. The right side of the fusion of left basal ganglia (92% of homologu- figures corresponds to the left side of the brain. GP=globus pallidus; Cd=caudate nucleus; ous right brain region), left frontal cortex Acb=nucleus accumbens; CI=capsula interna; DB=diagonal band. (91%) and left basal and medial temporal cor- http://jnnp.bmj.com/ lobes and which largely spared structures rich tex (91% and 90%). on cholinergic cells. NEUROPSYCHOLOGICAL EXAMINATION Attention Case report The patient scored well within the normal The patient was a 55 year old right handed range on a battery of computerised tests prob- engineer who held a managing position in an ing reaction time, speed of visual scanning, 28 international computer company. He had arte- divided attention, and shifting of attention. on September 28, 2021 by guest. Protected copyright. rial hypertension. In July 1996 he became His attention/concentration index value on the somnolent and confused. On emergency ad- WMS- R29 was 111. mission, CT showed bleeding into the anterior portion of the left basal ganglia with invasion Language into the left frontal horn of the lateral ventricle. In German, his native language, speech was No source of bleeding could be identified on well articulated, fluent, and syntactically cor- angiography. During the subsequent weeks the rect. Only when talking about diYcult and medical records noted mild right sided weak- complex matters did his expression become ness, word finding diYculties, and paraphasia. imprecise and circumstantial with occasional His ability to store new information was confusions of low frequency words. He per- severely defective and he was disoriented to fectly named 20 highly familiar items from the time. Snodgrass-Vanderwart pictures30 31 but made He was admitted as an outpatient to our two errors for 20 unfamiliar items (“perhaps a department in October 1996. The hemiparesis goose?” for ostrich, and skittle for spinning had resolved and conversation was inobstru- top). Knowledge of second languages was not sive. He was fully oriented, but complained of assessed. memory problems: He rated himself as very poor at remembering names, places, and the Intelligence content of conversations. His spouse con- On a multiple choice lexical decision test with firmed that he often enquired about details words of decreasing frequency,32 reflecting pre- J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.67.2.163 on 1 August 1999.
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