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At least 1,369 records · Page 76Linked to original sources
PubMed1985

[Transient global amnesia].

The clinical picture of transient global amnesia (TGA) is discussed on the basis of the clinical findings in 19 patients. The central symptom is an acute memory loss, leading to disorientation, helplessness and pseudo-confusion. The symptoms last for several hours and then fade away. Pathogenetically a functional impairment of the limbic system is proposed. Most cases of TGA are due to ischaemic disease; rare causes are epileptic seizures, tumours, encephalitis and toxic or metabolic conditions. In order to clarify the aetiology and initiate appropriate therapy meticulous neurological investigation is necessary. The spontaneous prognosis of ischaemic forms is favourable, whilst in other cases it depends on the primary condition.

Adult↗
PubMed1979

[Amnestic episode (transient global amnesia) (author's transl)].

The appearance of the amnestic episode is discussed by presentation of 4 own cases and by means of literature. The amnestic episode is a mental disorder, which exclusively affects short-term memory with a sudden onset and a duration of some hours, seldom up to several days, and often it is connected with a retrograde amnesia. The latter disappears in all cases, but there remains a permanent lack of memory for the time of the episode. Recidivism is rare. Internal, neurological and neurophysiological findings during and after the amnestic episode regularly are normal, at least certainly without characteristic findings. The main age of manifestation lies between the 40th and 70th year of life, there is no priority between women and men. Probably a disturbance of blood flow in the supplying area of the basilaric arteria is responsible, though the proof is still missing.

Aged↗
PubMedDate not supplied

Animal models of infantile amnesia, benign senescent forgetfulness, and senile dementia.

The Jacksonian principle of hierarchical development and dissolution of function was applied to infantile amnesia and memory loss in senescence. When the Jacksonian model is generalized to include life-span changes in memory it predicts a last-in, first-out appearance and disappearance of memory processes. Those memory capacities that are the last to appear in ontogeny should be the first to be compromised in aging. To evaluate this proposition in a specific context, the rodent literature on long-term memory in infant, adult, and aged animals was surveyed. Three types of memorial processes that emerged sequentially in development were identified and then examined in adult and aged rats. Although strong support of the Jacksonian principle did not emerge from this analysis, the data were sufficiently positive to suggest that the theory was still viable and even vigorous enough to guide future research on both the normal and pathological processes of development and aging.

Aging↗
PubMed1981

[The value of the EEG in patients with transient global amnesia (author's transl)].

The EEG findings from 30 patients with transient global amnesia (TGA) of vascular origin are described. A pathological result was seen in 18 cases, from which 17 had predominantly focal changes. 12 EEG's were normal. With increasing time interval between the TGA and the EEG investigation a normal record was slightly commoner. 20 patients had CT results, of which 8 cases were pathological. In 12 cases the EEG and CT results were correspondingly pathological or normal. The EEG shows functional disturbances even after the neurological deficits have resolved, which are related to transient metabolic or diminished blood-flow disturbances, but do not result in structural lesions to bae seen in the CT.

Adult↗
PubMedDate not supplied

[Use of lysine-vasopressine in the treatment of post-traumatic amnesia (author's transl)].

Following experimental works on the role of vasopressine (ADH) on learning and memory process, we have treated seven subjects suffering from post-traumatic amnesia with Lysine-Vasopressine (LVP), as a nasal spray for 15 days (14 UI per day). All subjects (males, aged 20 to 63) presented a deficit for 3 years, did not follow any treatment and did not hope for any improvement. Five subjects presented a real improvement, either immediately during the treatment, or in a way more progressive some weeks after the end of the treatment. The improvement as today was evidenced by psychological tests (attention and short term visual retention tests) and by electrophysiological methods (measure of amplitude of the VCN). The improvement was mainly on general activity, motivation and capacity for social adaptation. It was associated for four subjects with a marked increases in the level of Neurophysine I. The mode of action of LVP is discussed in light of recent neurochemical and neurophysiological works.

Adult↗
PubMed1995

Transient global amnesia and cortical blindness after vertebral angiography: further evidence for the role of arterial spasm.

We describe a series of six patients who experienced severe retrograde amnesia (five cases) or cortical blindness (one case) during selective vertebral angiography. All angiograms were obtained with the same nonionic contrast medium. Analysis of the contrast batch demonstrated no abnormalities, but investigation of the angiographic suite revealed a faulty contrast warming cabinet resulting in injection of contrast material above body temperature. The warming cabinet was withdrawn, and the complication has not recurred. We believe that these symptoms reflect ischemia caused by vertebral arterial spasm.

Adult↗
PubMedDate not supplied

Effect of dotarizine on electroconvulsive shock or pentylenetetrazol-induced amnesia and on seizure reactivity in rats.

Dotarizine (DOT), a compound performing both as calcium antagonist and as 5-HT2 receptor antagonist, was evaluated for its ability to protect against electroconvulsive shock (ECS)- and pentylenetetrazol (PTZ)-induced performance deficit in a passive avoidance "step-down" task in rats. Its effect on electric and PTZ seizure models was also studied. DOT administered orally at a dose of 50 mg/kg for 5 days before learning had no significant effect on retention tests given 3 h, 24 h and 7 days after the training session. It should be noted, however, that DOT completely prevented ECS- and PTZ-induced amnesia in passive avoidance situation. DOT had a pronounced protective effect against electric seizures but did not affect PTZ seizures. The present results provide additional evidence for the role of serotonergic neurotransmitter system and calcium homeostasis for memory and seizure reactivity and may be important in the development of effective treatment strategies for memory dysfunction.

Administration, Oral↗
PubMedDate not supplied

[Charcot and cerebral localizations. From aphasia to amnesia].

During the course of his convincing research into localizing cerebral motor areas, Charcot used the clinico-pathological method and his faith in localization for the study of aphasia. Thus, in 1883, he gave a course on the subject which is one of the most complex among the study of cerebral diseases. In this series of lessons, he was able to organize data from clinical studies, anatomy and psychology. In fact, for Charcot in 1883, aphasia was simple a particular kind of amnesia which could be taken as more or less severe partial loss of word memory. Memory itself would not exist, but would be divided into a number of autonomous partial memories. Charcot did not discover until some years later, basically from observing patients with hysteria, that memory is not only a stock of sensations but that it can also be used to save personal, autobiographical information. This led him to consider memory impairment not only as an organic disease but also as a psychological disease.

Amnesia↗
PubMed1994

ECT-induced anterograde amnesia: can the deficits be minimized?

To date, no pharmacological agent has been confirmed to lessen electroconvulsive therapy (ECT)-induced memory deficits. BR-16A is an herbal preparation, containing various organic extracts, used in India for the enhancement of cognition (among other applications). In the present study, adult male Sprague-Dawley rats received six once-daily electroconvulsive shocks (ECSs). Half the animals were treated with BR-16A (200 mg/kg/day) for 1 week before ECS, during the ECS course, and during the post-ECS learning assessment phase; the remaining animals received vehicle alone. In experiment 1, rats (n = 16/treatment group) were preassessed for learning on days 3 and 5 of exposure to the Hebb-Williams complex maze and were reassessed after comparable exposure to the maze starting from the second day post-ECS. In experiment 2, rats (n = 9/treatment group) were preassessed for number of trials to satisfactory learning and number of wrong arm entries in a T-maze and were reassessed on the second day post-ECS. The learning preassessments were conducted just prior to the commencement of the BR-16A/vehicle treatments. In both experiments, rats receiving BR-16A performed significantly better than controls. It is concluded that BR-16A protects against ECS-induced anterograde amnesia. BR-16A may therefore have scope in minimizing ECT-induced learning deficits.

Amnesia, Retrograde↗
PubMed1994

Infantile amnesia: through a glass darkly.

Memory for former preschool classmates was examined in 9- and 10-year-old children using measures of both explicit and implicit memory. Yes-no recognition of faces was at low levels but was significantly above chance. Skin conductance data showed similarly low but above-chance differentiation between classmates and controls. A median split of children based on their recognition memory scores showed that children with little evidence of explicit memory for classmates were as likely to show differential skin conductance responding to faces of former classmates as were children with higher recognition scores. Infantile amnesia, like the clinical syndrome for which it is named, may not always involve complete loss of encoded information.

Amnesia↗
PubMed1993

Effect of piracetam on electroshock induced amnesia and decrease in brain acetylcholine in rats.

Piracetam, a prototype of a new class of psychotropic agents, the nootropic agents, which improve learning ability and memory retention, was found to induce a dose-related prevention of disruption of acquisition of a passive avoidance response produced by electroshock application. The amnesia attenuating effect of piracetam was accompanied by prevention of the decrease in acetylcholine concentrations of rat brain induced by electroshock. The study indicates that the cognition enhancing effect of piracetam may be due to a facilitatory effect on cholinergic transmission.

Acetylcholine↗
PubMed1993

[Aggressive episodes without amnesia. Differential diagnostic problems based on a case report].

A 21-year-old patient suffered from recurrent attacks characterized by aggression and a varying disturbance of consciousness. He had no amnesia for these episodes. Loss of activity and social withdrawal had heralded the manifestation of the disease. He had delusions at times. The problems of differential diagnosis: schizophrenic disorder, frontal lobe epilepsy, or psychogenic seizures are discussed.

Adult↗
PubMed1993

Adafenoxate abolishes the amnesia induced by neonatal 6-hydroxydopamine treatment in rats.

The effect of neonatal 6-hydroxydopamine (6-OHDA) treatment on learning and memory and on the levels of biogenic monoamines in some brain structures, as well as the influence of the nootropic drug adafenoxate on 6-OHDA effect was studied in shuttle box and step down trained rats. In mature rats injected with 6-OHDA postnatal, learning and retention were impaired and the noradrenaline (NA) level in the frontal cortex and hippocampus was decreased. Adafenoxate abolished the amnestic effect of 6-OHDA and restored the NA level to normal in the above-mentioned brain structures. This finding suggests the important role of the noradrenergic neurotransmitter system in 6-OHDA-induced amnesia and the favorable effect of adafenoxate on learning and memory impaired by 6-OHDA.

Amnesia↗
PubMed1995

Adapting symptom validity testing to evaluate suspicious complaints of amnesia in medicolegal evaluations.

Symptom validity testing was adapted to assess suspicious complaints of amnesia. In the adaptation, two-alternative, forced-choice memory questions were generated for subject matter claimed to be forgotten. The number of questions correctly answered was then compared to the expected number of questions to be correctly answered if no knowledge actually existed. Three case studies are presented, two of competency-to-stand-trial evaluees and one of an insurance medical examinee. In each case, the use of this procedure generated the conclusion that the knowledge claimed to be forgotten was actually remembered; however, not all individuals were classified as malingerers.

Accidents, Traffic↗
PubMed1995

Sex offenders who claim amnesia for their alleged offense.

Information relating to demography, history, and psychiatric functioning was collected for 20 consecutive individuals presenting to the Sexual Behaviours Clinic of the Royal Ottawa Hospital who claimed amnesia for their alleged sexual offenses. In addition, comparison groups of admitter and nonadmitter sex offenders were established to isolate relevant psychopathological constructs within the primary study group. Amnestic offenders displayed higher degrees of violence and fulfilled diagnostic criteria for potentially more harmful paraphilia.

Adult↗
PubMed1996

[Transient global amnesia. Case-control study of 24 cases].

Transient global amnesia (AGT) is a well-defined syndrome of unknown aetiology. It is generally believed to be of vascular origin. Other theories suggest epilepsy or migraine as the cause. We studied the clinical features and associated risk factors in 24 patients with AGT, comparing them with two control groups with 24 people in each group, paired for age and sex. The first control group contained healthy individuals (CN) and the second patients with transient ischaemic attacks (AIT). Of the patients with AGT, 70% were women and 30% men. Their average age was 60 (range 14-76). The attacks were abrupt in onset in 100%. In 8% there was a recognisable trigger factor (driving, physical exercise, etc). The average duration was 7 hours. On study of the cardiovascular risk factors, it was found that 36% were hypertensive, 24% had cardiopathy, 12% had diabetes mellitus, 8% were smokers, 4% had polycythaemia, 16% had hyperlipidaemia, 4% were alcoholics. There was a history of migraine in 29%. No patient had a past history of epilepsy. Further investigation showed ECG changes in 12%. In 24% there were non-specific changes in the EEG. On cerebral CT scan there were lesions compatible with ischaemia in 12.5% of the patients. Levels of arterial hypertension were significantly higher in the AGT group as compared to the normal control group (Odds ratio 7.86; CI. 1.29-11.38). A past history of migraine was seen to be a risk factor associated with AGT as compared with both groups of controls (AGT/CN Odds ratio 9.47; CI 1.01-444.92; AGT/AIT Odds ratio > 1.72).

Adolescent↗
PubMedDate not supplied

[The molecular basis of dopamine synapse activity in the mechanisms of learning and amnesia].

Neurochemical events underlying the activity of the dopamine synapse during the retrieval of memory and its impairment ("psychogenic" amnesia) are considered in the paper. Physico-chemical parameters of operation of D2 receptor and catechole content were investigated in various brain areas (striatum, neostriatum, hypothalamus, amygdala, frontal cortex, hippocampus, nuclei accumbens, A9, and A10) in intact, learned, and amnestic rats. The impairment in the memory trace retrieval was found to be associated with a significant decrease in activation of synaptic dopamine receptors and a modification of the dopamine transformation pathway.

Amnesia↗
PubMed1996

Peripherally administered GM-CSF interferes with scopolamine-induced amnesia in mice: involvement of interleukin-1.

We studied the effects of granulocyte-macrophage colony stimulating factor (GM-CSF) on the classical behavioral test of scopolamine-induced amnesia for a passive avoidance response in the mouse. Pre-training intraperitoneal administration of this cytokine (1.25, 2.5, 5.0 or 10 micrograms/mouse) partially, although significantly, reduced the amnesic action of the muscarinic receptor antagonist. The peripheral administration of a specific interleukin-1 receptor antagonist (IL-1 ra, 50 micrograms/mouse i.p.) blocked the effect of GM-CSF. Our results suggest that GM-CSF is able to exert neuromodulatory actions and that it is involved (probably via IL-1) in the interactions between the immune system and the central nervous system.

Amnesia↗