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At least 253 records · Page 14Linked to original sources
PubMed1993

[Visual perseveration and palinopsia: a visual memory disorder?].

Visual perseveration and palinopsia are defined as the persistence or the reappearance of the visual image. These infrequent symptoms are thought to be linked to the right hemisphere posterior areas. We report a case of this syndrome in which the initial fixation was foveal. The palinoptic image was sometimes moving. This suggests that palinopsia is due to a dysfunction of the visual memory, rather than of the visual system: this dysfunction may be related to hyperactivity of the visual buffer.

Brain Neoplasms↗
PubMed1993

[Pharmacologic correction of learning and memory disorders induced by exposure to high-frequency electromagnetic radiation].

Acute exposure of rats to microwaves (12.6 chr, 2375 MHz, power density 1 mW/cm2) induced the retrograde amnesia. It was show the role of opioidergic, benzodiazepine, GABAergic and cholinergic components in the amnesic effects of microwaves. Piracetam (100 mg/kg, i. p.) and oxiracetam (10 mg/kg, i. p.) prevented the negative effects of microwaves on memory processes.

Animals↗
PubMed1990

[Subacute familial thalamic atrophy. Memory disorders and complete insomnia].

Thalamic atrophy is rarely primitive. Selective atrophy of the dorso-medial and anterior thalamic nuclei has been reported in a few families. The clinical course is subacute. Symptoms and signs include sleep disorders and intellectual deficit. We report a new family with this uncommon disease and discuss its etiology.

Atrophy↗
PubMed1996

[Memory disorders due to extreme impacts and their pharmacological correction].

The review encompasses the author's and literary data concerning effects of various extreme impacts, i.e. SHF electromagnetic radiation, motion sickness, hypoxia, etc. on the cognitive and memorizing processes in humans and animals. Potentials for pharmacological correction, with nootropic drugs in the first place, of anamnestic disorders consequent to various extreme impacts are considered. Possible mechanisms of the protective action of pharmacological substances are analyzed.

Amnesia↗
PubMed2005

Effects of internal clock and memory disorders on duration reproductions and duration productions in patients with Parkinson's disease.

Patients with Parkinson's disease (PD) exhibit deficits in perceptual and motor timing as well as impairments in memory and attentional processes that are related to dysfunction of dopaminergic systems in the basal ganglia. The aim of the present study was to assess the relationships existing between impaired duration judgments and defective memory and attention in PD patients. We compared time performance of medicated PD patients and control subjects on a duration reproduction task that is highly memory-dependent, and on a duration production task that could reveal effects of changes in the speed of internal time-keeping mechanisms. Each task was performed in a control counting condition and in a condition requiring divided attention between the temporal task and a concurrent reading task. Moreover, PD patients and control subjects were assessed on memory and attention using a battery of neuropsychological tests. The results revealed that in the concurrent reading condition of the reproduction task, duration judgments tended to be more variable in PD patients than in control subjects. Moreover, variability of duration reproductions was correlated with both measures of memory and of disease severity. In the concurrent reading condition of the production task, duration judgments were significantly shorter in PD patients than in control subjects, and accuracy of duration productions was correlated with scores on sub-tests of short-term memory. The findings suggest that the administration of dopamine did not entirely remove the memory deficits in PD patients. Moreover, DA treatment would have abnormally accelerated the rate of the internal clock leading to shorter duration productions in PD patients. The whole results indicate that dopamine administration in patients might have overshadowed the slowing rate of the internal clock usually reported in non medicated PD patients, without entirely restoring all of the memory functions.

Aged↗
PubMed1988

Vasopressin and vasopressin analogues for treatment of memory disorders in clinical practice.

1. Beyond its antidiuretic and vasopressor effects, vasopressin has central nervous system effects, first described in rats by David de Wied in 1965. 2. Its first clinical use in humans, in 1978, confirmed its stimulant action in normal individuals, especially in middle-aged male subjects. 3. Its utility in mnemic problems is also worht considering when the pathology is relatively recent (less than 2 years prior) and unaccompanied by major neurological lesions. Behavioral modifications, such as improvement of "sociability", "mood" improvement, independent of its effects on memory have been described, and would justify complementary clinical investigation. 4. New synthetic vasopressin derivatives which would eliminate metabolic effects while maintaining behavioral effects intact, and the definition of clinical, neuroendocrine, and neurophysiological prognostic criteria, will be the two most important paths for investigation over the next years.

Cognition↗
PubMed1992

[Isolated memory disorders disclosing antiphospholipid antibody syndrome].

Most of the neurological complications of the antiphospholipid syndrome are consequences of arterial or venous cerebral thromboses. We report the case of a 46-year-old woman presenting with the main signs of antiphospholipid syndrome: Raynaud's phenomenon, livedo, leg ulcers, repeated miscarriages, presence of a circulating anticoagulant and of antiphospholipid antibodies, who developed an isolated amnestic syndrome with a peculiar pattern; 1) almost complete sparing of the ability to learn new skills and of short-term recall; 2) deterioration, followed by disappearance of recent memories after a sufficient delay; 3) progressive alteration of increasingly old memories including knowledge memory suggested a gradual alteration of mnestic traces. The lack of neuroradiological signs of multiple infarcts suggests a direct intervention of antibodies in this patient's memorisation mechanisms.

Antibodies, Antiphospholipid↗
PubMed2003

[Experience in the application of pramistar, a new nootropic preparation, in the treatment of memory disorders in patients with cerebrovascular pathology].

Morbidity rise of cerebrovascular pathology is followed by remarkable cognitive decline. Chronic cerebral blood insufficiency and stroke consequences compose a group of the diseases which lead to different types of memory deterioration, consecutive memory decline and as a result to professional and social dysadaptation. The morphological basis of the problem consists in progressive structural cerebral deficit with forming a new adaptive system. The activity of this system is often not effective due to a lack of mediator supply. We have investigated the effects of monotherapy by a new nootropic drug--pramiracetam (Pramistar) on neuropsychological symptoms of memory deterioration in patients with chronic cerebrovascular insufficiency and stroke consequences in basilar and carotid vascular basin. The data obtained suggest statistically significant heterogeneous influence of the medicine on intensity of the evaluated symptoms.

Adult↗
PubMed1989

[Pharmacological analysis of memory disorders of different origins].

The influence of nootropic drugs of different chemical structure and mechanism of action (piracetam 200-800 mg/kg, meclofenoxate 50-100 mg/kg, nicergoline 1-4 mg/kg) on amnestic disturbances induced with electroconvulsive shock (ECS), scopolamine (2.5 mg/kg) and phenazepam (2.0 mg/kg) was studied in mice using passive avoidance test. All the investigated drugs possess distinct protective properties concerning different models of amnesia. In ECS-induced amnesia meclofenoxate was most effective, in scopolamine-induced amnesia--meclofenoxate and nicergoline, in phenazepam-induced amnesia all drugs were equally potent in profundity. It is supposed that neurophysiological mechanism of action of nootropic drugs is connected with directed activation of weakened memory trace of different etiology and its transmission into form receivable for transcription.

Amnesia↗