Effect of chronic hypoxia on adrenoceptor responses of ovine foetal umbilical vessels

OBJECTIVE: To evaluate the relevance of hypometabolism in the hippocampal head to the pathophysiology of memory impairment. BACKGROUND: Neurofunctional imaging studies with an image reslicing technique provided by using software suggest that dysfunction of the amygdalohippocampal system causes memory impairment. However, metabolic and morphologic profiles of the whole hippocampal formation have not been evaluated in detail. METHODS: By tilting the gantry of a high-resolution PET scanner in a plane parallel to the hippocampal longitudinal axis determined beforehand by MRI, we performed quantitative measurement of glucose metabolism in the subdivisions of the hippocampal formation (head, body, tail) in 10 patients of normal intelligence with pure amnesia, in eight patients with AD, and in eight normal subjects. RESULTS: Although the volumes of the amygdala and hippocampal formation in pure amnesics were not different significantly from those of normal subjects, glucose metabolism in the head of the hippocampus was significantly lower in pure amnesics. In patients with AD, marked hypometabolism was found extending to the amygdala, the hippocampal head, and the parietotemporal cortex, along with amygdalohippocampal atrophy. CONCLUSION: Hippocampal head dysfunction plays an important role in memory impairment in amnesic patients. Further metabolic impairment over the amygdalohippocampal system and the surrounding association cortex reflects the pathophysiology of AD.     

Amnestic mild cognitive impairment: Difference of memory profile in subjects who converted or did not convert to Alzheimer's disease.

Episodic long-term, short-term, and implicit memory were investigated in 79 elderly subjects who fulfilled criteria for the amnestic form of mild cognitive impairment (a-MCI; i.e., by having an idiopathic amnestic disorder with absence of impairment in cognitive areas other than memory and without confounding medical or psychiatric conditions) and who developed Alzheimer's disease (AD) after 2 years as well as in 111 subjects affected by a-MCI who did not develop dementia. Results document a memory profile in a-MCI subjects characterized by preserved short-term and implicit memory and extensive impairment of episodic long-term memory. In virtually all episodic memory indexes examined (learning, forgetting, recognition abilities), a-MCI subjects who converted to AD were more severely impaired than were subjects who did not become demented. This memory profile, which closely resembles that exhibited by amnestic patients with bilateral mesial-temporal lobe lesions, confirms a precocious phase in preclinical AD characterized by selective involvement of mesial-temporal areas and worsening of the memory impairment as atrophic changes progress in hippocampal structures. In this context of pervasive episodic memory impairment, tests assessing the free recall of verbal material following a delay interval demonstrated the greater sensitivity to memory deficits of a-MCI subjects who developed AD. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Memory impairment in monkeys following lesions limited to the hippocampus.

Investigated the degree of memory impairment produced by a lesion limited to the hippocampus in 13 cynomolgus monkeys (Macaca fascicularis) with circumscribed hippocampal lesions who were tested on the delayed-nonmatching-to-sample task, a test of recognition memory that is sensitive to amnesia in humans. Ss were given no preoperative training and were given no postoperative experience prior to training on the task. A marked deficit was observed. The results, taken together with those from previous studies, also provide information about the role of factors that could potentially influence the level of memory impairment following hippocampal lesions. The level of impairment does not appear to be due to any of the following factors: time of testing after surgery, prior postoperative testing, surgical techniques, species differences, or behavioral training methods. However, preoperative training experience does appear to reduce the severity of the impairment, and this factor may account for the observation that the memory impairment associated with hippocampal lesions is sometimes mild. A recent case of human amnesia is discussed in which a bilateral lesion limited to a portion of the hippocampus produced a well-documented memory deficit. (27 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Impaired recognition memory in patients with lesions limited to the hippocampal formation.

A recent literature survey of results from a widely used recognition memory test raised questions about the extent to which recognition memory impairment ordinarily occurs in human amnesia and, in particular, whether recognition memory is impaired at all after damage limited to the hippocampal region (J. P. Aggleton & C. Shaw, 1996). Experiment 1 examined the performance of 6 amnesic patients on 11 to 25 different recognition memory tests. Three patients had bilateral lesions limited primarily to the hippocampus (G.D.) or the hippocampal formation (W.H. and L.M.), as determined by postmortem, neurohistological analysis (N. Rempel-Clower, S. M. Zola, L. R. Squire, & D. G. Amaral, 1996). All 6 patients exhibited unequivocally impaired recognition memory. In Experiment 2, the 3 patients still available for study were each markedly impaired on a test of object recognition similar to the kind used to test recognition memory in nonhuman primates. Recognition memory impairment is a robust feature of human amnesia, even when damage is limited primarily to the hippocampus. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Influence of opioid peptides on learning and memory processes in the chick.

Several experiments were conducted to examine the effects of intracranial injection of opioid peptides and antagonists on learning and memory in the chick. Pretraining injection of [leu–5]enkephalin and the selective delta receptor agonist [D-Pen–2,L-Pen–5]enkephalin (DPLPE) into the intermediate medial hyperstriatum ventrale (IMHV) produced impairment. ICI 174,864, a delta-selective antagonist, reversed the impairment produced by either [leu–5]enkephalin or DPLPE, results indicating that delta receptors may play a role in learning in the chick and suggesting that the impairment produced by [leu–5]enkephalin is mediated through delta opioid receptors. β-endorphin produced a naloxone-reversible impairment in performance, which suggests that this impairment is mediated by opioid receptors. Bilateral injection of β-endorphin into the IMHV produced impairment, as did unilateral injection into the right, but not left, IMHV. Only bilateral injections into IMHV of [leu–5]enkephalin were effective. These results suggest that the effects of β-endorphin are centrally mediated whereas the effects of [leu–5]enkephalin may be localized to other brain regions or are peripherally mediated. These initial results suggest that opioids are associated with learning and memory in the chick. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Neuropsychological differences among empirically derived clinical subtypes of schizophrenia.

Neuropsychological profile differences between empirically derived clinical subtypes of schizophrenia were examined. Two hundred five patients and 209 demographically matched controls were administered a neuropsychological battery examining 8 domains. Subtypes included negative, disorganized, paranoid, Schneiderian, and mild. All subtypes displayed a neuropsychological profile of generalized impairment with greater deficits in learning, memory, and attention. Results were suggestive of diffuse cognitive dysfunction in schizophrenia with more severe deficits in learning and memory relative to executive skills. This pattern of greater learning and memory impairment was pronounced for disorganized patients. In contrast, paranoid patients outperformed disorganized and negative patients in several domains. These findings reflect bilateral frontal–temporal dysfunction, particularly in disorganized and negative patients. Subtype differences highlight the importance of conceptualizing schizophrenia as a multifocal disorder. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Medial temporal lesions in monkeys impair memory on a variety of tasks sensitive to human amnesia.

Relative to 3 unoperated controls, 4 cynomolgus monkeys with conjoint bilateral lesions of the hippocampus and amygdala were impaired on 4 tests of memory—delayed retention of object discriminations, concurrent discrimination, delayed response, and delayed nonmatching to sample. In 3 of the tasks, relatively long-delay intervals between training and test trials were used, and in 2 tasks, distraction was introduced during the delay intervals. The severity of the impairment increased with the length of the delay, and distraction markedly increased the memory impairment. For 1 task given on 2 occasions (delayed nonmatching to sample), the severity of the impairment was unchanged over 1.5 yrs. It is concluded that monkeys with medial temporal lesions constitute an animal model of human amnesia and that the 4 tasks used in the present study appear to constitute a sensitive and appropriate battery that could be used in other studies of the neuroanatomy of memory functions in the monkey. (47 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A permanent pure amnestic syndrome of insidious onset related to Alzheimer's disease

A 55-year-old patient experienced a pure amnestic syndrome of insidious onset that worsened progressively. Subsequently, her memory disorder stabilized and remained her only cognitive impairment for several years. She ultimately developed more widespread cognitive decline and terminal dementia. Postmortem examination 18 years after the onset revealed numerous senile plaques and neurofibrillary tangles consistent with Alzheimer's disease. A permanent pure amnestic syndrome of insidious onset may represent a further type of focal cerebral degeneration.     

Neurocognitive deficit in schizophrenia: a quantitative review of the evidence

The neurocognitive literature on test performance in schizophrenia is reviewed quantitatively. The authors report 22 mean effect sizes from 204 studies to index schizophrenia versus control differences in global and selective verbal memory, nonverbal memory, bilateral and unilateral motor performance, visual and auditory attention, general intelligence, spatial ability, executive function, language, and interhemispheric tactile-transfer test performance. Moderate to large raw effect sizes (d > .60) were obtained for all 22 neurocognitive test variables, and none of the associated confidence intervals included zero. The results indicate that schizophrenia is characterized by a broadly based cognitive impairment, with varying degrees of deficit in all ability domains measured by standard clinical tests.     

The effects of NMDA lesions centered on the postrhinal cortex on spatial memory tasks in the rat.

Rats with bilateral N-methyl-D-aspartate lesions centered on the postrhinal cortex (POR) and sham lesions were tested in a series of spatial memory tasks. The POR-lesioned rats were significantly impaired compared with sham rats in the reference memory version of both the water maze and radial arm maze tasks and in the standard radial arm maze working memory task. The POR-lesioned rats displayed a delay-independent impairment in the working memory versions of the water maze and in a delayed nonmatching-to-place (DNMP) version of the radial arm maze task. The POR-lesioned rats were also impaired in a DNMP procedure conducted in the T-maze. These findings indicate that the POR has a delay-independent role in the processing of spatial information. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Melatonin as an antiaging drug: between facts and fantasy

Structural neuroimaging has been used to correlate lesional patterns with the cognitive profile of patients with multiple sclerosis (MS), especially for "frontal" dysfunction. However, a clear-cut anatomical explanation has yet to be found for the long-term memory deficit which is a hallmark of MS cognitive impairment. We have used PET to measure regional cerebral glucose metabolism (rCMRglc) in a group of 15 MS patients with involvement of verbal and/or spatial long-term memory. These patients were compared with 10 normal controls and 13 MS patients unimpaired on all neuropsychological tests. Relative to the controls, MS patients with memory deficits showed a significant bilateral reduction of rCMRglc in the hippocampus, cingulate gyrus, thalamus, associative occipital cortex, and cerebellum. Direct comparisons between patients with memory deficits and the group of unimpaired MS patients showed a metabolic reduction in the left thalamus and in both hippocampi. Seven of the memory-impaired patients also had neuropsychological signs of frontal dysfunction. These patients were compared with patients who had isolated memory deficit. Here we observed a further metabolic reduction in a number of brain regions including bilateral prefrontal cortex, inferior parietal cortex, and basal ganglia. Our findings indicate that hypometabolism of thalamic and deep cortical gray structures of the temporal lobe is associated with episodic memory dysfunction in MS. On the other hand, pathological performance on tests designed to assess frontal functions was associated with widespread reduction of glucose metabolism.     

Effects of chronic infusion of nerve growth factor (NGF) in rats with nucleus basalis magnocellularis lesion

We attempted to evaluate the effects of bilateral injection of ibotenic acid (IA) into the nucleus basalis magnocellularis (nbm) of rats as well as the potential recovery mediated by the infusion of nerve growth factor (NGF). The lesion caused an impairment of learning and memory processes. Also, a severe depletion of choline acetyl transferase activity was detected in cortical areas. After the NGF administration, a significant reversion of these functional changes was observed. Thus, IA-lesioned rats might serve as a model for the evaluation of neurotrophic factors actions on basal forebrain damaged neurons.     

Attributions (beliefs) and job satisfaction associated with back pain in an industrial setting

Transient cerebral ischemia can produce irreversible neuronal damage and permanent learning and memory impairments in humans. This study examined whether ischemia-induced brain damage in rats results in impairments on the delayed nonmatching-to-sample (DNMS) task, a nonspatial recognition task analogous to tests on which amnesic patients display impairments. Male Wistar rats received either sham surgery or 20-min forebrain ischemia induced by bilateral carotid occlusion and hypotension. Four weeks after surgery, ischemic rats were significantly impaired in both learning and performing the DNMS task at retention intervals up to 5 min. Extensive presurgical training did not reduce this impairment. Observable cell loss in ischemic rats was limited to CA1 pyramidal neurons and a subset of cells in the dentate gyrus. The results indicate that ischemic damage to the hippocampus in rats results in recognition memory deficits similar to those produced by ischemic damage in humans.     

Lesions of rat perirhinal cortex exacerbate the memory deficit observed following damage to the fimbria-fornix.

Rats that had received bilateral lesions of the perirhinal cortex, fimbria-fornix, combined lesions of both these structures, or sham operations were tested on an object-guided delayed non-match-to-sample task. Perirhinal lesioned and fimbria-fornix lesioned rats were moderately impaired when delay intervals of 30 s or more were introduced between the sample and test phases of the experiment. Animals with combined lesions displayed a considerably greater impairment than animals with lesions of either structure alone. The combined lesioned animals were severely impaired in the initial acquisition of the task and displayed a profound memory deficit at delay intervals of greater than 4 s. These results emphasize the importance of the perirhinal cortex to memory function and suggest that the perirhinal cortex and the hippocampal formation may function interactively in the execution of memory processes. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Bilateral paramedian thalamic infarction: Neuropsychological and perfusional followup study.

Conducted a 2-yr follow-up of a woman (aged 35 yrs) who had a bilateral paramedian thalamic infarction and suffered from a sudden impairment of consciousness followed by a global deficit of cognitive functions. Two years after clinical onset, verbal and visuospatial memory, verbal fluency, constructional praxia, and categorization were mainly affected. In the acute phase, a single-photon emission-computed tomography study showed a severe and diffuse cerebral blood flow (CBF) impairment, more marked on the right side. Radioisotope uptake in frontal and temporal cortices was still reduced 2 yrs later. The CBF depression in these regions suggests that the decline of cognitive functions could be due to an interruption of thalamocortical projections. A degenerative process rather than a "diaschisis" could be responsible for the long-lasting deficit of cognitive functions. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Predictors of perceived memory impairment: do they differ in Alzheimer's disease versus normal aging?

Predictors of perceived memory impairment were investigated in 40 elderly normal adults and 28 individuals with Alzheimer's disease. Measures of perceived memory impairment, global cognitive functioning, memory, use of memory strategies, memory strategy efficacy, and depressive symptomatology were obtained for all participants. The elderly normal and Alzheimer's disease groups did not differ in the extent to which they reported perceived memory impairment. For both participant groups, more frequent use of memory strategies and lower perceived memory strategy efficacy were significant predictors of perceived memory impairment. Depressive symptomatology was an additional, significant determinant of perceived memory impairment for the elderly normal group.     

Diminished ability to interpret and report internal states after bilateral medial temporal resection: Case H.M.

Conducted 2 experiments on a 54-yr-old man who became amnesic when he was 27 yrs old following a bilateral resection in the medial temporal lobe region for epilepsy. To document the clinical reports that he rarely commented on such internal states as pain, hunger, and thirst, his thermal pain perception was examined in relation to his other somatosensory capacities, and his reports of hunger and thirst were assessed before and after meals. To investigate the effect of limited memory ability on the reporting of internal states, S's performance was compared with that of 5 other Ss (aged 22–48 yrs) with global amnesia. 19 22–74 yr old normal controls were also assessed. Results show that S's information about his internal states was less available or less accessible than normal and that his impairment was not attributable to his memory deficit. Instead, it is believed that the bilateral resection of the amygdala accounted for S's poor understanding of his internal states. (41 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Memory impairment in multiple sclerosis: A quantitative review.

To assess the nature and magnitude of memory impairment in multiple sclerosis (MS), the authors analyzed quantitatively 36 studies comparing the memory performance of MS participants to healthy controls. The authors studied (a) the pattern of impairment across short-term memory (STM), working memory (WM), and long-term memory (LTM); (b) the moderating influence of retrieval support on LTM impairment; (c) the covariation of WM and LTM impairment; and (d) the moderating influence of clinical characteristics of the MS sample on memory impairment. The analyses revealed significant impairment across all memory domains and failed to support a retrieval-based account of LTM dysfunction in MS patients. In addition, robust associations were found between clinical features of MS and memory impairment. The findings suggest a more global pattern of memory deficits in MS than has been previously believed, with deficits clearly associated with neurological disability and disease course. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Memory loss resulting from fornix and septal damage: Impaired supra-span recall but preserved recognition over a 24-hour delay.

Despite increasing evidence that the fornix is important for memory, uncertainty remains about the exact nature of subsequent impairments arising from damage to this tract. This uncertainty is often created by pathology in additional brain structures. The present study involved a young man, DN, who had almost complete bilateral loss of the rostral columns of the fornix and much of the surrounding septum in the left hemisphere following the surgical removal of a cavernous angioma. Quantitative MRI analyses of structure size, normalized to intracranial volume, showed no difference in any of the additional brain regions measured, apart from those areas removed to expose the tumor. DN showed a marked, stable anterograde memory impairment that was still present 4 years postsurgery. In contrast, DN performed within normal levels on most tests of recognition memory. This sparing was most striking when given a 24-hr delay between study and test of the Warrington Recognition Memory Test. This recall/recognition dissociation provides further evidence for neuroanatomical divisions within recognition memory processes. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Evidence for involvement of orbitofrontal cortex in memory functions: An interference effect.

Although it is frequently stated that the frontal lobes play a significant role in memory function, research proof has been ambiguous at best. The present study investigated this problem by administering a variety of memory tests (e.g., Wechsler Memory Scale, WAIS) to 16 schizophrenic patients who had undergone prefrontal leukotomy approximately 25 yrs earlier. Ss were divided into 3 groups on the basis of recovery after surgery. Two comparison groups (5 psychiatric and 5 normal controls) were established to control for psychiatric symptomatology, years of institutionalization, age, and years of education. Results indicate that large bilateral orbitofrontal lesions may not result in amnesia; in fact, the nonoperated schizophrenic control group performed the most poorly. Proactive interference was demonstrated, however, resulting in significant impairment for all Ss with prefrontal lobe damage despite normal scores on commonly used memory tests. Ability to maintain consistent and directed attention and to overcome interference is proposed as a role of the frontal lobes in memory function. (55 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)