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PubMed2000

Anatomical and psychological mechanism of reduplicative misidentification syndromes.

Reduplicative misidentifications syndromes (RMS) are rare memory disorders characterized by the subjective conviction that a place, person or event is duplicated. Even if RMS often follow a right frontal lesion, several studies have stressed the importance of bilateral hemispheric pathology. Moreover, from a psychological perspective, there is uncertainty if this symptom should be considered just as a kind of confabulation or if it should be associated with personal psychosocial and behavioral aspects. We report a patient who developed normal pressure hydrocephalus and RMS one year after a post-traumatic right frontal lesion. At the first neuropsychological evaluation, we found mild impairment of all functions, associated with the presence of reduplicative paramnesia. After the ventricle-peritoneal shunt intervention, we observed a progressive improvement of all functions but the frontal ones. The memory deficit became less specific and the RMS disappeared. We therefore postulate that a focal right frontal lesion is not sufficient to cause RMS per se. Our clinical report suggests that paramnesic events held on reasonable ground, not being just a kind of confabulation.

Aged↗

PubMed2006

Reduced Self-Referential Source Memory Performance is Associated with Interpersonal Dysfunction in Borderline Personality Disorder.

Source memory is impaired in schizophrenia, and this deficit is related to symptoms of interpersonal antagonism such as suspiciousness and hostility. The present study evaluated source memory in borderline personality disorder (BPD) and its relation to interpersonal antagonism. Forty-one noninpatient adults with BPD according to the DSM-IV and 26 healthy control subjects performed a verbal source memory test requiring completion of sentences with and without emotional content ("Hot" vs. "Cold" sentences). Subjects also completed self-report measures of suspiciousness and interpersonal antagonism (Buss-Durkee Hostility Inventory) and depression (Beck Depression Inventory). The BPD group showed no significant difference from the control group in self-referential source memory, recognition memory, response bias, and performance enhancement for items with emotion content. However, in the BPD group, poorer self-referential source memory was significantly related to Hostility measures including suspiciousness, but not with Depression scores. In contrast, generic item recognition memory was unrelated to Hostility. Heterogeneity in source memory function may be specifically related to some of the hallmark interpersonal disturbances of BPD, independent of the effects of general negative affect or general memory impairment.

Adult↗

PubMed1991

Amnesia in relation to fugue states--distinguishing a neurological from a psychogenic basis.

A case of transient amnesia is described in which a patient reported memory loss for five days, during which he had wandered extensively. Analysis showed that he did not have selective amnesia for the public events which had occurred during the five days for which he professed memory loss. This finding was incompatible with our case having a neurologically based global memory disorder during the fugue state. These findings offer support for a distinction between personal and public episodic memory.

Adult↗

PubMed1978

[Clinical side and adverse effects of antidepressant drugs (author's transl)].

Cases of extrapyramidal-motoric and psychologic side effects are reported when treatment with antidepressant drugs was performed. They have not been mentioned in the literature before. Hypokinetic disorders of speech and motion, tonic-atonic disturbances, dyskinesia and myoclonic muscle contractions are listed. Besides the latter movement disorders, "dreamy state", episodic amnesia ("ictal" amnesia) and amnestic "black out" as transient memory disorders have been observed.

Adult↗

PubMed1985

Thiamine deficiency depletes cortical norepinephrine and impairs learning processes in the rat.

Several lines of evidence indicate that thiamine deficiency causes the Wernicke-Korsakoff syndrome, a human memory disorder. The present study examined behavioral deficits in rats after recovery from a bout of thiamine deficiency. Following behavioral testing, the brains were dissected into regions and assayed biochemically for levels of dopamine, norepinephrine, serotonin and the primary metabolites of these monoamines. Based on previous findings in this laboratory, we predicted that thiamine deficiency not only produces behavioral deficits but loss in catecholamines as well. Impairments were observed for a spatial delayed alternation task that had been learned prior to experimental treatment. In addition, experimental animals were impaired in their ability to acquire two novel tasks, active and passive shock avoidance, after recovery from the acute effects of thiamine deficiency. Comparable deficits were not observed for a number of reflex responses that were measured to assess the general neurological state of the animals. Biochemical analyses revealed that the concentration of norepinephrine was reduced significantly in cortex-hippocampus and olfactory bulb but not in other regions, while dopamine and serotonin levels were not altered in any brain region examined. These data demonstrate that a bout of thiamine deficiency can produce persistent deficits in brain norepinephrine and concomitant decrements in behavioral measures of learning and memory. These results are consistent with our hypothesis and evidence that noradrenergic deficits contribute to the amnesic symptoms of Korsakoff's psychosis.

Alcohol Amnestic Disorder↗

PubMed1999

[Neuropsychological aspects of dementia diagnosis].

In the interdisciplinary diagnostics of dementia neuropsychology is applied in early detection, in differential diagnostics and in progressive course assessment. With standardized neuropsychological testing severity and nature of cognitive dysfunction is assessed. In particular memory disorders, aphasia, apraxia, agnosia and disorders of executive functions are assessed by these methods. In early stage of Alzheimer's Disease episodic and semantic memory as well as certain language functions are affected. Apractic and agnostic disorders often appear only in the later course of the disease. Depending on localization and nature of lesion cognitive dysfunction patterns tend to be more lateralized in vascular dementia (e.g. aphasic, apractic or visual-constructive disorders). In the various forms of fronto-temporal dementia executive functions and/or personality are mainly affected.

Aged↗

PubMedDate not supplied

Atypical cognitive disorders in a man with developmental surface dyslexia.

The neuropsychological profile of a man with a developmental surface dyslexia is presented here. This case study is of interest because J.C. exhibited a pattern of cognitive disorders rarely documented in previous data. Results showed that JC's difficulties in reading comprehension were closely related to complex memory disorders and were also associated with cognitive slowness. The present observations do not support the visual memory failure hypothesis. The data rather suggest that the core difficulty primarily lies with the nonautomatization of grapheme-phoneme correspondence rules, which in turn dramatically contributed to lexicon weaknesses. The hypothesis of a timing mechanism in reading disorders is discussed.

Adult↗

PubMed1997

Effects of scopolamine on delayed-matching-to-sample and paired associates tests of visual memory and learning in human subjects: comparison with diazepam and implications for dementia.

Two experiments examined dose-related effects of 200, 400 and 600 micrograms scopolamine (n = 24, s.c.) and 5 and 10 mg diazepam (n = 6, PO) on parallel tests of visual memory and learning taken from the CANTAB battery. Scopolamine significantly impaired accuracy of performance on a delayed matching to sample test of visual recognition memory in a dose- and delay-dependent manner, but had only marginal decremental effects on a test of visuospatial paired associates learning. Scopolamine significantly lengthened decision times in a visual search matching to sample task at the 400 and 600 micrograms doses, without significantly affecting accuracy. The drug also impaired performance on tests of spatial (on accuracy and response time measures) and pattern (on response time only) memory. Most of the deleterious effects on scopolamine were removed by covariance analyses with indices of subjective sedation, but the effects of delayed matching accuracy and latency remained. By contrast, diazepam significantly impaired paired associates learning but affected delayed matching to sample in a delay-independent manner. These results suggest that scopolamine can produce selective deficits in tests of short-term visual recognition memory which do not depend on overall impairments in arousal and which contrast with deficits in visual associative learning produced by diazepam. They have implications for the pharmacological modelling of dementia and memory disorders in man and for the neurochemical substrates of the short-term recognition memory and associative learning for visual stimuli.

Adult↗

PubMed2001

Dissociation of regional activation in mild AD during visual encoding: a functional MRI study.

OBJECTIVE: The authors studied mild patients with AD with a visual learning paradigm to determine whether activations of medial temporal regions on fMRI differ in AD compared to nondemented individuals. BACKGROUND: Changes in activation patterns of medial temporal lobe regions may serve as a biologic marker of altered brain function early in the course of AD. METHODS: The authors studied eight healthy young subjects, eight late middle-age nondemented volunteers, and seven patients with mild AD. All subjects underwent fMRI scanning in which they viewed a set of geometric designs for 45 seconds. Changes in blood flow were analyzed by comparing the prestimulus fMRI signal with that present during the stimulus presentation. RESULTS: Patients with AD, who had very poor recall of the geometric designs subsequently, showed increased blood flow (activation) during stimulus presentation only in a visual association area. Both the young and older nondemented subjects, all of whom had good recall of the designs, showed activations during stimulus presentation of the right entorhinal cortex, right supramarginal gyrus, right prefrontal regions, and left anterior-inferior temporal lobe. The younger and older nondemented subjects did not differ in fMRI activation patterns. CONCLUSIONS: Failure of activation in AD of either temporal lobe or prefrontal regions is consistent with established clinical-pathologic correlations in AD. fMRI may be useful in confirming a memory disorder diagnosis and also may be useful in detecting individuals with incipient dysfunction in learning as a result of disorders such as AD.

Adult↗

PubMed1991

Piracetam. An overview of its pharmacological properties and a review of its therapeutic use in senile cognitive disorders.

Piracetam is the first of the so-called 'nootropic' drugs, a unique class of drugs which affect mental function. In animal models and in healthy volunteers, the drug improves the efficiency of the higher telencephalic functions of the brain involved in cognitive processes such as learning and memory. The pharmacology of piracetam is unusual because it protects against various physical and chemical insults applied to the brain. It facilitates learning and memory in healthy animals and in animals whose brain function has been compromised, and it enhances interhemispheric transfer of information via callosal transmission. At the same time, even in relatively high dosages it is devoid of any sedative, analeptic or autonomic activities. How piracetam exerts its effects on memory disorders is still under investigation, although among other proposed mechanisms of action it is thought to facilitate central nervous system efficiency of cholinergic neurotransmission. Results from trials involving elderly patients with senile cognitive disorders have been equivocal, as have the results obtained when piracetam has been combined with acetylcholine precursors. Piracetam seems to be almost completely devoid of adverse effects, and is extremely well tolerated. In conclusion, opinion is divided as to the benefits of piracetam in the treatment of senile cognitive decline. Although double-blind studies in the elderly have produced mixed results, some such trials (particularly those involving larger numbers of patients) have reported favourable findings, thus offering some reason for cautious optimism in a notoriously difficult area of therapeutics. However, further investigations of piracetam alone and in combination therapy are required before any absolute conclusions can be drawn.

Aged↗

PubMed1997

Discrimination and response bias in memory: effects of depression severity and psychomotor retardation.

Although memory disorders have been well documented in depression, there is controversy concerning depressives' performance on recognition memory tasks; e.g. whether they have impaired discrimination and conservative or liberal response bias according to signal detection theory. In addition, symptomatic correlates of discrimination and response bias indices have been lacking. A word recognition memory task analyzed according to the two high threshold theory was administered to 26 depressives and 26 controls. Depressives obtained a lower index of discrimination (Pr) than controls. The index of response bias (Br) was not different between groups. In the depressed group, overall severity of depression was related to discrimination, whereas psychomotor retardation level was related to response bias. Cognitive performance of depressives could be advantageously analyzed in terms of these two dimensions of symptomatology.

Adult↗

PubMed1999

Explicit memory in anxiety disorders.

Two experiments were conducted to study selective memory bias favoring anxiety-relevant materials in patients with anxiety disorders. In the 1st experiment, 32 patients with generalized anxiety disorder (GAD), 30 with social phobia (speaking anxiety), and 31 control participants incidentally learned GAD-relevant words, speech anxiety-relevant words, strongly pleasant words, and words with a neutral valence. Participants did not show any explicit memory bias for threatening materials. Thirty patients suffering from panic disorder (PD) with agoraphobia and 30 controls took part in the 2nd experiment. The design was similar to the 1st experiment. This time a highly specific selective memory bias for threatening words was found. Words describing symptoms of anxiety were better recalled by PD patients. Results are consistent with previous findings but are inexplicable by existing theories.

Adult↗

PubMed1999

[Behavioral pharmacological characterization of mice lacking the nociceptin receptor].

Nociceptin and nociceptin receptor, which show structural similarities to opioid peptides and opioid receptors, respectively, have been recently found to constitute a novel neuromodulatory system. In the central nervous system, however, the physiological role of modulation via the nociceptin receptor is still unclear. Here, we report the behavioral pharmacological characterization of mice lacking the nociceptin receptor. Nociceptin produced hyperalgesia and hypolocomotion, whereas the nociceptin receptor-knockout mice showed no significant abnormalities in nociceptive thresholds (tail-flick, hot-plate, electric, and acetic acid-induced writhing tests) and locomotion. In the learning and memory tests, nociceptin induced impairment of learning and memory in wild-type mice. Nociceptin receptor-knockout mice possessed greater learning ability and had better memory than wild-type mice. These results suggest that the nociceptin system plays a role in regulation of nociception or locomotion and seems to play negative roles in learning and memory. Next, we compared nociceptive responses induced by various opioids between the nociceptin receptor-knockout and wild-type mice. As previously reported, morphine (mu-opioid receptor agonist), U-50,488 H (kappa 1-opioid receptor agonist), and naloxone benzoylhydrazone (NalBzoH; kappa 3-opioid receptor agonist) induced antinociceptive effects in wild-type mice. Surprisingly, knockout mice lacked the antinociceptive effect induced by NalBzoH, but not by morphine and U-50,488H. Further, NalBzoH completely inhibited nociceptin-induced hyperalgesia and hypolocomotion in wild-type mice. Experiments on the cultured cells transfected with the nociceptin receptor cDNA showed that NalBzoH competed in [3H]-nociceptin binding and attenuated the nociceptin-induced inhibition of cyclic AMP accumulation induced by forskolin. These results clearly suggest that NalBzoH acts as a potent antagonist for the nociceptin receptor. Our studies suggest that the nociceptive system and/or learning and memory processes could be modulated by ligands to the nociceptin receptor, and further that the antagonists are worth testing for the alleviation of pain and memory disorders.

Animals↗

PubMed2004

Enhanced excitability compensates for high-pressure-induced depression of cortical inputs to the hippocampus.

High pressure (>1.0 MPa) induces the high-pressure neurological syndrome (HPNS) characterized by increased excitability of the CNS and cognitive impairments involving memory disorders. The perforant-path transfer of cortical information to the hippocampal formation is important for memory acquisition. High pressure may alter information transfer in this connection. We used rat corticohippocampal slices for studying the effect of pressure on the transfer function between synaptic inputs from the medial perforant path (MPP) and spike generation by granule cells (GC) of the dentate gyrus. High pressure (10.1 MPa) reduced single MPP field excitatory postsynaptic potential (fEPSP) amplitude and slope by nearly 50%. Field antidromic action potentials (AAPs) elicited by stimulation of GC axons, and population spike (PS) generation by the pressure-depressed MPP fEPSP were not significantly altered at hyperbaric conditions. Nevertheless the relationship PS/fEPSP increased at high pressure, indicating dendritic hyperexcitability in the GC. PSs elicited by paired-pulse MPP fEPSPs at 10- to 200-ms interstimulus intervals and PS generated by trains of five fEPSPs at 25 Hz were also not affected in spite of severe pressure-induced synaptic depression. Similarly, trains of AAPs at 25-50 Hz were not significantly changed. Trains of fEPSPs at higher frequency (50 Hz), however, induced additional spikes at high pressure, indicating pressure disruption of the regular low-pass filter properties of the DG. Such effect was closely mimicked by partial blockade of GABAA inhibition. High pressure depresses synaptic activity while increases excitability in the neuronal dendrites but not in the axons. This mechanism, allowing neuronal communication at low input signals, may partially cope with pressure effects at the low frequency range (<25 Hz) but losses reliability at higher frequencies (>50 Hz).

Action Potentials↗

PubMed1994

Ameliorative effects of chronic treatment using DX-9386, a traditional Chinese prescription, on learning performance and lipid peroxide content in senescence accelerated mouse.

DX-9386 is a traditional Chinese prescription consisting of ginseng, polygala, acorus and hoelen. The effect of chronic oral treatment with this preparation on learning behaviors and lipid peroxide concentration was studied in senescence accelerated mouse (SAM). SAM P8, a senescence prone of SAM, and SAM R1, a senescence resistant substrain of SAM, were started on a diet containing 1% of DX-9386 from the age of 2 months. All the experiments were performed at the age of 10 months. The prescription ameliorated the memory disorders of SAM P8, as evaluated in a step down test as well as a spatial memory test. The preparation, however, did not affect the learning behaviors in SAM R1. DX-9386 reduced the elevated levels of lipid peroxide in the serum and liver of SAM P8, while it did not alter that in SAM R1. These results suggested that DX-9386 slowed the aging process of SAM P8 in terms of learning behaviors and lipid peroxidation.

Administration, Oral↗

PubMed1986

Encoding, memory, and thought disorder in schizophrenia and mania.

Schizophrenic (n = 24) and manic (n = 20) inpatients were compared with a normal comparison sample (n = 10) on memory and encoding performance for both self- and other-generated speech. It was found that the level of encoding, as indexed by the level of organization present in the recalled speech, predicted memory performance for both schizophrenic and normal samples. Schizophrenics were less effective at encoding than normals, although the relationship between level of encoding and memory performance was similar for both samples. For the manic patients, however, clinically rated thought disorder predicted memory performance better than encoding performance. It appeared that thought disorder specifically disrupted recall performance, with less of an effect on encoding. These relationships, as well as the lack of a significant relationship between thought disorder and task performance in the schizophrenics, are discussed in terms of their implications for later research in the area of information processing in psychotic patients.

Adult↗

PubMed1999

The role of nociceptin in cognition.

The physiological role of the modulation via the nociceptin receptor is still unclear. Here we report the role of the nociceptin system in learning and memory. Nociceptin-knockout mice possess greater learning ability in the water maze task, show an enhanced latent learning in the water finding task, have better memory in the passive avoidance task, and further, show larger long-term potentiation in the hippocampal CA1 region than wild-type mice. Nociceptin itself induces an impairment of the passive avoidance task in wild-type mice. This impairment is reversed by naloxone benzoylhydrazone (NalBzoH), but not by other opioids in wild-type mice. Further, experiments on cultured cells transfected with nociceptin receptor cDNA show that NalBzoH competes [3H]-nociceptin binding and attenuates the nociceptin-induced inhibition of cAMP accumulation induced by forskolin. These results demonstrate that the nociceptin system seems to play a negative role in learning and memory and that NalBzoH acts as a potent antagonist for the nociceptin receptor. In addition, the antagonists for the nociceptin receptor may be worth testing for alleviating memory disorders.

Animals↗

PubMed1995

Do cognitive changes of Parkinson's disease result from dopamine depletion?

Cognitive changes have long been observed in patients with Parkinson's disease: visuo-spatial deficits, memory disorders, dysexecutive syndrome. Given the modulatory role of the basal ganglia and related structures, these deficits might result from more fundamental disorders concerning the allocation of attentional resources, the temporal organization of behavior, the maintenance of representations in working memory or the self-elaboration of internal strategy, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of parallel, segregated loops that interconnect well defined subregions of the basal ganglia to discrete areas of the prefrontal cortex via the thalamus may give some support to this hypothesis.

Cerebral Cortex↗