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At least 991 records · Page 55Linked to original sources
PubMed1997

Recent and remote memory dissociation: medication effects and hippocampal function in schizophrenia.

Neuropsychological measures of recent and remote memory as well as general attention were administered to two groups of DSM-III-R schizophrenic patients in a within-subject repeated measures design across a 3-week interval. One group of patients (n = 12) was maintained on haloperidol for both test sessions, whereas a second group (n = 9) was tested first on haloperidol and again 3-weeks drug free. Patients received no adjunctive anticholinergic medication during the study. No differences were observed between the patient groups in level of psychotic symptomatology or general attention across the two test sessions. Patients withdrawn from haloperidol showed significant decreases in recent verbal memory function, while at the same time demonstrating significant increases in remote verbal memory. We speculate that the observed pattern of results is consistent with medial temporal lobe dysfunction particularly prominent in the left hemisphere as patients become drug free, and provides support for the existence of state-dependent cognitive changes in schizophrenia.

Adult↗
PubMed1998

Magnetic resonance imaging correlates of depression in early- and late-onset Alzheimer's disease.

BACKGROUND: Depressive symptoms are frequent complications of Alzheimer's disease (AD). We hypothesized that AD patients with depression would be more likely than nondepressed AD patients to show deep white-matter, subcortical gray-matter, and periventricular hyperintensities on magnetic resonance imaging (MRI). METHODS: In a retrospective study of 31 AD patients, depression was characterized by clinical diagnosis (DSM-III-R major depression, depressive symptoms, or no depression), a clinician-rated depression scale, and informant ratings of premorbid (before memory disorder) as well as current depression using the NEO Personality Inventory (NEO-PI), and related to qualitative and quantitative ratings of MRI hyperintensities. RESULTS: In contrast to reports in nondemented elderly patients, there was no relationship between clinical diagnosis of major depressive episode and hyperintensities; however, clinician-rated depressive symptoms were higher in subjects with large anterior hyperintensities. In the early-onset AD group only, MRI abnormalities were related to greater premorbid depression, and less increase in depression after the onset of dementia, as rated by informants on the NEO-PI. CONCLUSIONS: Results highlight the need to consider early- and late-onset AD separately when assessing relationships between personality and MRI abnormalities, and to consider premorbid personality style when drawing conclusions about the etiology of depressive features seen in AD.

Age of Onset↗
PubMed2000

Cannabinoid receptor activation in CA1 pyramidal cells in adult rat hippocampus.

Intracellular assessments of the physiological actions of cannabinoid receptor agonists and antagonists on adult hippocampal CA1 pyramidal cells in the in vitro slice preparation were performed using current clamp and conventional sharp-electrode intracellular recording procedures. Several manipulations were performed to delineate putative currents and conductance mechanisms affected by the cannabinoid receptor agonist WIN 55,212-2 (WIN-2). This compound produced a tonic hyperpolarization of the pyramidal cell membrane that was bicuculline sensitive, reversed by changing the chloride gradient, and abolished by the addition of TTX to the bathing medium. Instantaneous membrane input resistance, computed from hyperpolarizing current pulses (peak R(in)) was also reduced significantly in the presence of WIN-2 and was accompanied by enhancement of a superimposed slow depolarization that reduced steady-state R(in) (SSR(in)); both effects were resistant to barium. Intracellular perfusion of cesium acetate (CsAc) and the sodium/potassium channel blocker, QX314, each blocked the effect of WIN-2 on R(in) and SSR(in). WIN-2 also reduced input resistance calculated from depolarizing current injections (R(d)). This effect was also blocked by atropine, as well as media containing TTX or low Ca(2+). Each of the above effects of WIN-2 was blocked by the cannabinoid receptor antagonist SR141716A, showing a dependence on CB1 cannabinoid receptors. Several known pre- and postsynaptic processes in adult pyramidal cells are discussed which could be responsible for these cannabinoid-produced changes in membrane resistances.

Action Potentials↗
PubMed2000

Regional changes in the hippocampal density of AMPA and NMDA receptors across the lifespan of the rat.

The current study dissected the fascia dentata (FD) and hilar region from the CA and subicular cell fields of the rat and conducted in vitro determinations of the number of binding sites for N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) glutamate receptors across the lifespan. We determined the density of binding of [3H]-glutamate or [3H]-AMPA to NMDA or AMPA receptor sites, respectively. The changes reported might be due to either a change in receptor number or an alteration in the binding characteristics of the receptor site with aging. We found an age-related decline in the number of NMDA receptors in the CA1, CA3 and subicular cell regions of the hippocampus, but not in the FD/hilar region, and an age-related decline in the number of AMPA receptors in the FD/hilar region, but not in the CA fields. The decline in the number of NMDA or AMPA receptors that occurs with aging was not a continuous or homogeneous process. These changes in receptor number might underlie selected age-associated changes in sensitivity to drugs that influence hippocampal function as well as to changes in NMDA-dependent long-term potentiation. A thorough understanding of the mechanisms underlying changes in glutamate receptor function in discrete brain regions, using combined neurochemical and electrophysiological methods, may ultimately provide insight into the fundamental substrates of age-associated memory disorders related to hippocampal dysfunction.

Aging↗
PubMed2001

Progressive brain dysfunction following intracerebroventricular infusion of beta(1-42)-amyloid peptide.

The behavioral, neurochemical and histological changes of rats subjected to 3 days treatment with intracerebroventricular infusion of beta-amyloid peptides(Abeta)(1-42) were investigated 20 days and 80 days after the surgery. Abeta(1-42) produced a dose-dependent and a time-dependent impairment in the spontaneous alternation performance in the Y-maze (spatial working memory), place navigation task in a water maze (spatial reference memory) and passive avoidance retention (non-spatial long-term memory) at doses of 10 and 20 microg/rat. The learning impairments were more severe at 80 days than 20 days after infusion of Abeta(1-42). At 25 days after the infusion, a significant decrease in hemicholinium-3 (HC-3) binding was observed only in the hippocampus, although choline acetyltransferase (ChAT) activity was unchanged in the brain regions tested as compared with the vehicle (Abeta(40-1)) treatment. In contrast, the reduction in ChAT activity 85 days after Abeta(1-42) infusion was significant in hippocampus and striatum. HC-3 binding was also significantly decreased in the posterior cortex, hippocampus and striatum. In the histological analysis, brain atrophy was observed inasmuch as ventricular enlargement and neuronal damage in the CA1 area of the hippocampus were seen 85 days after Abeta(1-42) infusion. These results suggest that the rats subjected to intracerebroventricular infusion of Abeta(1-42) suffered from progressive brain dysfunction, and could be useful as an animal model for evaluating the developmental processes at the early and/or middle stage of Alzheimer's-type dementia.

Alzheimer Disease↗
PubMed2003

Neonatal cerebral hypoxia-ischemia causes lateralized memory impairments in the adult rat.

Neonatal hypoxia-ischemia (HI) has been extensively studied in a rat model characterized by unilateral brain damage (Rice-Vannucci Model). However, as well as in humans, each rat brain hemisphere is distinctly involved in cognitive functions, as for example retrieval of emotionally based memory, and neurochemical asymmetries have been described. In this paper we investigated whether hypoxia-ischemia could cause distinct cognitive deficits depending on which hemisphere is damaged. Seven-day-old male Wistar rats were submitted to permanent occlusion of left or right common carotid artery and were exposed to a mixture of 8% oxygen-92% nitrogen for 2.5 h. On adulthood, these rats were trained in step-down inhibitory avoidance and in two tasks in the Morris water maze. Both experimental groups (right and left lesioned) showed a deficit of retrieval in the inhibitory avoidance task compared to controls, although rats with right hemisphere lesion showed a significantly greater deficit than the left damaged group (P<0.05). In the Morris maze, both damaged groups presented cognitive deficits in the reference memory task (P<0.05), however only the right damaged group had an impairment in the working memory task. Brain coronal areas, at levels +1.20 and -3.30 mm from bregma of both HI groups were smaller than those of control, with no differences between the right and left damaged groups (P<0.05). These results show that cerebral hypoxia-ischemia in neonatal rats causes asymmetric behavioral outcomes depending on which of the hemispheres is lesioned and support the hypothesis of lateralization of cognitive functions in the rodent brain.

Animals↗
PubMed1997

WAY 100635, a 5-HT1A receptor antagonist, prevents the impairment of spatial learning caused by intrahippocampal administration of scopolamine or 7-chloro-kynurenic acid.

The effect of WAY 100635, a 5-HT1A receptor antagonist, on the impairment of spatial learning caused by intrahippocampal administration of scopolamine, a cholinergic muscarinic receptor antagonist, or 7-chloro-kynurenic acid, an antagonist at the glycine site associated with the NMDA receptor complex, was studied in a two-platform spatial discrimination task. Scopolamine (4 microg/microl) or 7-chloro-kynurenic acid (3 microg/microl), administered bilaterally into the CA1 region of the dorsal hippocampus 10 min before each training session, impaired choice accuracy with no effect on choice latency and errors of omission. Administered subcutaneously at 1 (but not at 0.3) mg/kg 30 min before each training session, WAY 100635 did not modify the acquisition of spatial learning, but prevented the impairment of choice accuracy caused by intrahippocampal scopolamine or 7-chloro-kynurenic acid. These findings suggest that blockade of 5-HT1A receptors can compensate the loss of cholinergic or NMDA-mediated excitatory input to pyramidal cells in the hippocampus. The mechanisms involved and the importance of these findings for the symptomatic treatment of memory disorders in man are discussed.

Animals↗
PubMedDate not supplied

Déjà vu in France during the 19th century: a conceptual history.

The feeling of déjà vu features as prominently in the creative as in the clinical literature. However, its meaning and mechanisms remain unclear, and it is posited here that this has partially resulted from the way in which this symptom was originally conceptualized. During the late 19th century, medical opinion seemed agreed that déjà vu was a disorder of memory (a paramnesia). However, its study was obfuscated by an overemphasis on its secondary features (e.g., "feeling of conviction," "fleetingness") and by "parapsychological" interpretations. Around the turn of the century, the problem was compounded by the development of narrow models of memory (inspired by association psychology) that left no room for the descriptive complexities of déjà vu. Consequently, it soon became (and has remained) a "symptom without a psychological function." French psychological writers played a crucial role in the conceptualization of déjà vu and this report presents a detailed history of their contribution.

Deja Vu↗
PubMed1993

Focal retrograde amnesia in neurological disease: a critical review.

The condition of focal retrograde amnesia represents a new and challenging concept to our understanding of human memory disorders. Cases of both permanent and transient focal retrograde amnesia, dating from early clinical descriptions to more recent experimental reports, are critically reviewed. It is concluded that the condition of focal retrograde amnesia does represent a distinct and reliable neurological entity. Four sets of issues are discussed--methodological issues, conceptual issues, anatomical issues and therapeutic issues. Current evidence indicates an important role for temporal lobe structures in mediating focal retrograde amnesia. Both storage and retrieval deficits may contribute to the presence of focal retrograde amnesia, though available evidence points to a greater role for engram destruction/fragmentation rather than disruption of access mechanisms. In general, pharmacological and other therapies have had minimal effects in alleviating focal retrograde amnesia.

Amnesia↗
PubMed1975

The relation of visuospatial dysfunction to digit span performance in patients with cerebral lesions.

DSF and DSB performance was compared in hospitalized controls and right and left brain lesion groups dichotomized for the presence or absence of visuospatial deficits. Digit Span performance was also correlated with WAIS Similarities and Block Design and Raven Coloured Progressive Matrices. No differences between groups were observed on DSF. On DSB patients with brain lesions had lower scores than controls and brain-lesioned patients with visuospatial deficits had lower scores than those without. DSB correlated significantly with WAIS Block Design and Raven Coloured Progressive Matrices supporting the hypothesis that visuospatial ability is needed to mediate proper DSB performance. The correlation of DSB with WAIS Similarities, however, lends support to the idea that low DSB may merely reflect severity of cognitive deficit.

Aphasia↗
PubMed1977

Memory function after closed head injury: a review of the quantitative research.

Studies which provide quantitative analyses of memory function following closed head injury were reviewed. Specific issues covered include criteria for assessing post-traumatic amnesia (PTA), PTA duration, relation of PTA duration to later memory impairment, memory functions within PTA, and comparisons between PTA and other amnesic conditions. Issues associated with the assessment of retrograde amnesia were also reviewed. With regard to memory function after PTA has terminated, we described and discussed normative data, the time course of recovery, and issues related to the nature of the later memory impairment. Directions for future work which seem particularly useful from a practical and theoretical viewpoint were also considered.

Amnesia↗
PubMed1980

Amnesia is not caused by cognitive slowness.

It has been suggested that the memory disorder in human organic amnesia might be caused by the slow processing of information. Such slowness might be differentially greater for semantic tasks, and/or for tasks requiring the extraction of multiple features of stimuli, or it might simply be a non-specific slowing. These possibilities were tested in a group of alcoholic amnesics and matched normal controls by presenting subjects with a series of words and requiring them to identify one specified word or one of two specified words, or membership of a specified category or one of two specified categories. Although amnesics' reaction times were slightly slower than controls' the effect was insignificant, and there was no hint of differential slowing in the semantic or multiple processing tasks. It was concluded from these results and a consideration of the reaction time literature that cognitive slowness is unrelated to the main cause of amnesia.

Alcohol Amnestic Disorder↗
PubMed1982

Retrograde amnesia for forty years.

We describe a patient who, in the absence of anterograde amnesia, experienced sudden onset of profound retrograde amnesia for the last forty years of his life. The amnesia encompassed all knowledge, including motor skills, acquired during these forty years. There has been no recovery in over eighteen months. His symptoms seem most consistent with a vascular etiology. Current understanding of memory disorders fails to explain these symptoms. It may be that his case represents a previously undescribed disorder.

Activities of Daily Living↗
PubMed1986

Short term retention with lateralized temporal lobe epilepsy.

This investigation focused upon whether individuals with lateralized temporal-lobe epilepsy have impairments in short term memory and, if so, whether these impairments are of a material-specific nature. The Peterson short term memory distractor paradigm which consists of single, brief presentations of stimuli with varying decay intervals and appropriate interpolated distractors was employed. A significant deficit in both left and right temporal lobe seizure groups was documented in comparison to controls for verbal but not for non-verbal materials. The results suggest that one aspect of the memory problem observed in temporal lobe seizure patients relates to relatively early components of information processing where encoding is primarily based upon physical rather than semantic characteristics of the stimulus and material-specificity is less evident.

Adolescent↗
PubMed1987

Memory impairment associated with progression of Huntington's disease.

Huntington's Disease (HD) has been described as one example of a "subcortical" dementia, characterized by slowed cognitive processing and impairment of memory. We examined the relationship between slowed cognitive processing and memory impairment as a function of disease progression in patients with HD. Results from three experiments suggest that in the early stages of HD there is slowed cognition with intact memory acquisition and retrieval processes. In later stages, cognition is further slowed and specific impairments of memory become evident. Thus, memory impairment in HD would appear to change qualitatively with progression of the disease.

Adult↗