1/22. Basal forebrain amnesia: does the nucleus accumbens contribute to human memory?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.- - - - - - - - - - ranking = 1keywords = nucleus (Clic here for more details about this article) |
2/22. Loss of psychic self-activation after paramedian bithalamic infarction.BACKGROUND AND PURPOSE: Loss of psychic self-activation has been described after bilateral lesions to the globus pallidus, striatum, and white matter of the frontal lobes, but it is a very rare sign of bithalamic lesions. The exact functional-anatomic mechanism underlying loss of psychic self-activation following bithalamic lesions remains to be elucidated. CASE DESCRIPTION: We present clinical, neuropsychological, structural, and functional neuroimaging data of an 18-month follow-up period of a man with prominent loss of psychic self-activation after coronary arteriography. Except for memory decline, accompanying symptoms remained restricted to the acute phase. The neurobehavioral syndrome consisted mainly of apathy, indifference, poor motivation, and flattened affect, and this remained unchanged during the entire follow-up period. MRI showed a bithalamic infarction involving the nucleus medialis thalami bilaterally. Single-photon emission CT revealed a severe relative hypoperfusion of both thalami, a relative hypoperfusion of both nuclei caudati, and a relative hypoperfusion mesiofrontally. CONCLUSIONS: Single-photon emission CT data support the hypothesis that the neurobehavioral manifestations after bithalamic paramedian infarction are caused by disruption of the striatal-ventral pallidal-thalamic-frontomesial limbic loop. Probably, bilateral disruption at different levels of the striatal-ventral pallidal-thalamic-frontomesial loop may lead to a similar clinical picture consisting of loss of psychic self-activation.- - - - - - - - - - ranking = 0.11111111111111keywords = nucleus (Clic here for more details about this article) |
3/22. Transient crossed aphasia and persistent amnesia after right thalamic haemorrhage.A 45-year-old right-handed woman suffered transient aphasia and persistent amnesia after a right thalamic haemorrhage. This patient appeared to have crossed aphasia, although it disappeared within 8 weeks. It is noteworthy that the patient had a unilateral right thalamic lesion but exhibited both verbal and non-verbal memory impairment. Computed tomography and magnetic resonance imaging revealed cerebral haemorrhage in the right thalamus involving the ventral anterior nucleus, medioventral nucleus, mamillothalamic tract, internal medullary lamina, and mediodorsal nucleus. An amytal test was performed and suggested that the right hemisphere was dominant for language functions and the left hemisphere was dominant for visuospatial functions. Single photon emission CT revealed a low perfusion area only in the right thalamus. These findings suggest that the right hemisphere might be dominant for both verbal and non-verbal memory function in this patient, although visuospatial function was lateralized in the left hemisphere.- - - - - - - - - - ranking = 0.33333333333333keywords = nucleus (Clic here for more details about this article) |
4/22. Memory disorder in Korsakoff's psychosis: a neuropathological and neuropsychological investigation of two cases.Neuropathological findings in the brains of two alcoholic patients with Korsakoff's psychosis are reported. Their memory defects had been studied in detail quantitatively over a period of nine years in one case and three years in the other, relevant details of which are presented. Both patients had had a relatively pure long-term memory impairment in the absence of other cognitive deficits and in the absence of a short-term memory impairment. Their retrograde amnesia for public events and famous faces had been measured and found to have extended backwards over at least twenty-five years. There was severe impairment in anterograde recognition memory for both verbal and non-verbal material. On a newly prepared memory quotient battery both patients had scored well below the bottom of the normal scale (less than 60, where 100 is the mean with a standard deviation of /- 15). Both patients had also shown the characteristic differential improvement in retention when tested by cued recall and also the characteristic 'prior learning effect', i.e. normal retention of one list of words when tested by cued recall but impaired retention of a second list sharing the same cues as the first list. There had been a slight but significant deterioration in intelligence in one of the patients in the two years prior to his death, although his IQ still fell within the normal range. The other patient remained undeteriorated until his death, and his IQ also was close to an estimated measure of his premorbid IQ. In the brains of both patients there was marked gliosis, shrinkage and discolouration bilaterally in the medial nuclei of the mammillary bodies. In addition there was a thin band of gliosis bilaterally between the wall of the third ventricle and the medial dorsal nucleus, the rostral limit lying anterior to the medial dorsal nucleus. In the patient with no intellectual deterioration these were the only pathological changes that were seen. In neither patient was there evident local loss of nerve cells, gliosis or any other qualitative evidence of abnormality in the hippocampi, the white matter of the temporal lobes or the greater part of the medial dorsal nuclei, although it is difficult to be certain whether there was any overlap between the band of gliosis and the most medial region of the medial dorsal nueleus and other adjacent thalamic nuclei. In the other patient there was also a small zone of softening in the cerebellum and an increase in astrocytes in other regions of the cerebral hemispheres, including the basal ganglia, amygdala, and brain-stem, but without noticeable loss of cells. The question of the minimal lesion for the alcoholic Korsakoff amnesic state, and some aspects of the related anatomy, is discussed in the context of other reports in the literature which are, however, difficult to assess in the absence of details of the specificity, severity and character of the memory disorders.- - - - - - - - - - ranking = 0.22222222222222keywords = nucleus (Clic here for more details about this article) |
5/22. Dorsal thalamic lesion in a noted case of human memory dysfunction.The extensively studied patient N.A. has had a severe verbal memory deficit since 1960, when he sustained a stab wound to the brain with a miniature fencing foil. His amnesia occurs in the absence of any other known cognitive defect. Recent CT scans have localized a lesion in the left dorsal thalamus of this patient in a position corresponding to the dorsomedial nucleus; there is no radiographic evidence of other damage in the diencephalon or cerebral cortex. The dorsomedial thalamus may be critical in the neuropathology of diencephalic amnesia and, in humans, may be required for normal memory functions.- - - - - - - - - - ranking = 0.11111111111111keywords = nucleus (Clic here for more details about this article) |
6/22. A case of frontal network amnesia.A 63 year old man developed an amnesic syndrome coupled with an array of "frontal lobe" signs after bilateral small subcortical infarcts. His amnesia was characterised by severe difficulty in voluntary recall of recently memorised verbal and non-verbal materials, while his recognition for the same materials was less affected. The symptoms remained unimproved at a follow up evaluation eight months after onset. magnetic resonance imaging showed two small circumscribed lesions, one in the dorsomedial nucleus of the left thalamus and the other in a region of the right globus pallidus and anterior limb of the right internal capsule. The mammillothalamic tracts and anterior nuclei of the thalami were clearly spared bilaterally. The left dorsomedial nucleus lesion disrupted the thalamofrontal circuit, while the anterior limb lesion of the right internal capsule disconnected the same circuit by damaging part of the anterior thalamic radiation. Thus the amnesia in this patient may have been caused by disruption of the bilateral thalamofrontal circuits. This type of amnesic pathology should be separated from more conventional types of amnesia that are produced by disruption of the so called Papez circuit or the Delay-Brion memory system.- - - - - - - - - - ranking = 0.22222222222222keywords = nucleus (Clic here for more details about this article) |
7/22. amnesia following a discrete basal forebrain lesion.Destructive lesions of the basal forebrain are associated with memory impairment in both humans and experimental animals. The basal forebrain is thought to contribute to memory function by providing cholinergic innervation to critical memory structures such as the hippocampus and amygdala. In previously reported clinical cases of basal forebrain amnesia, multiple neuroanatomical regions have been damaged, preventing identification of the minimal critical lesion necessary to produce an amnestic syndrome. We describe a patient who developed persistent, global anterograde and retrograde amnesia following resection of a low-grade glioma. Post-surgical magnetic resonance imaging studies revealed a small discrete lesion, centred in the right diagonal band of broca, that included the preoptic area, the anterior hypothalamus, the lamina terminalis and the paraterminal gyrus. The septal nuclei and the cell bodies of the nucleus basalis of Meynert appeared to have been spared, as were other structures in the medial temporal lobe and diencephalon. Our case provides critical support for the independent contribution of the basal forebrain, in particular the diagonal band nuclei, in memory function. We propose that our patient's amnesia resulted from disconnection of pathways between the diagonal band nuclei and the hippocampal region, depriving the hippocampus of cholinergic innervation.- - - - - - - - - - ranking = 0.11111111111111keywords = nucleus (Clic here for more details about this article) |
8/22. Diencephalic amnesia.The anatomical basis and cognitive profile of diencephalic amnesia remain unclear. We report a two-part study. First, we studied 4 patients with bilateral medial thalamic infarctions using magnetic resonance imaging and comprehensive neuropsychological testing. All patients were followed for more than 1 year. Using a stereotactic method, we plotted the lesions in an atlas delineating the probable structure involved. Secondly, in 2 monkeys, using autoradiography, we traced the pathway from the amygdala to the dorsomedial nucleus, paying particular attention to the intrathalamic course of the amygdalothalamic projections. Our findings were (1) patients develop amnesia when infarctions are located anteriorly; (2) in patients with amnesia, the lesions can be small and strategically located, probably interfering with both hippocampal-related neural structures such as the mamillothalamic tract, and amygdala-related neural structures such as the ventroamygdalofugal pathway; and (3) a specific component of the latter is situated lateral but immediately adjacent to the mamillothalamic tract in the monkey, enabling both structures to be damaged bilaterally by small mirror image lesions. The amnesia is characterized by deficits in anterograde verbal and visual learning and in retrograde amnesia, but motor learning is preserved. We raise the possibility that bilateral diencephalic lesions may interfere particularly with temporal aspects of memory.- - - - - - - - - - ranking = 0.11111111111111keywords = nucleus (Clic here for more details about this article) |
9/22. Description of brain injury in the amnesic patient N.A. based on magnetic resonance imaging.N.A. has been amnesic since 1960 when at the age of 22 years he sustained a penetrating brain injury with a miniature fencing foil. The amnesia primarily affects verbal material and occurs in the absence of other detectable cognitive deficits. Previous CT scans demonstrated a lucency in the region of the left mediodorsal thalamic nucleus, but no additional damage was revealed. Beginning in 1986 when he was 48 years old, N.A. was evaluated with a series of magnetic resonance imaging (MR) studies. Three major areas of damage were identified. In the left thalamus there is a prominent 3- to 4-mm-wide linear lesion that approximates the position and orientation of the internal medullary lamina. The defect extends for approximately 20 mm anteroposteriorly and likely involves the rostral group of intralaminar nuclei (central medial, paracentral, central lateral, rhomboid, and reuniens nuclei), the caudal group of intralaminar nuclei (centrum medianum and parafascicular nuclei), the ventral aspect of the mediodorsal nucleus, and the ventral lateral and ventral anterior nuclei. It also likely interrupts the trajectories of the mammillothalamic tract and postcommissural fornix. The posterior hypothalamus is markedly disrupted and the mammillary nuclei appear to be missing bilaterally. Finally, the right anterior temporal lobe is damaged for a distance of about 3.5 cm from the pole to midway through the amygdaloid complex. This damage probably occurred during exploratory neurosurgery done at the time of N.A.'s injury. The hippocampal formation appears intact on both sides. A comparison of these findings with those from other patients with diencephalic amnesia suggests that amnesia can result when several diencephalic structures are damaged conjointly, including the internal medullary lamina, the intralaminar nuclei, the mediodorsal nucleus, and the mammillothalamic tract. Whether amnesia as severe as N.A.'s would result from selective damage to any one of these structures remains to be determined.- - - - - - - - - - ranking = 0.33333333333333keywords = nucleus (Clic here for more details about this article) |
10/22. Location of lesions in Korsakoff's syndrome: neuropsychological and neuropathological data on two patients.Psychometric and neuropathological findings on two Korsakoff amnesics are described. Both patients showed anterograde and retrograde amnesia, poor performance on the Peterson short-term memory task, on the wisconsin card sort test and on certain visuo-spatial tasks. Patient J.W. performed consistently worse on tests of anterograde, but not retrograde amnesia, whereas patient B.C. showed more perseverative difficulties and, unlike J.W., his measured intelligence seemed to have declined from its premorbid level. Both patients showed marked neuronal loss from the medial mammillary bodies and a narrow band of gliosis in the medial thalamus, adjacent to the wall of the third ventricle, a region known as the paratenial nucleus. Only B.C. showed visible signs of cortical atrophy. Morphometric measures did, however, reveal reduced nucleolar volumes in layers III and V of the frontal cortex, with B.C. also showing more marked neuronal loss from these layers. B.C. also showed neuronal loss from the CA1 region of the hippocampus and reduced nucleolar volumes in the septum. Significantly, both patients had normal neuronal numbers and nucleolar volumes in the nucleus basalis of Meynert. J.W. only showed greater dysfunction than B.C. in one region: the locus caeruleus. This finding was related to his more severe amnesia.- - - - - - - - - - ranking = 0.22222222222222keywords = nucleus (Clic here for more details about this article) |
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