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PubMed1981

[Amnesia from bilateral ischemic lesions of the thalamus (author's transl)].

A 43-year-old woman developed during post-partum an axial amnesia of ischemic origin. Stereotactic correlations were obtained by matching CT scan images with the true reference plane of the examination, according to an original method. This led to the diagnosis of infarction in the territory of a paramedian thalamomesencephalic artery. The amnesia probably resulted from bilateral lesions of Vicq d'Azyr's bundle. Atypical features in this case were the absence of disorder of vigilance and oculomotor disorders. This striking fact in this patient was recovery of some recognition capability contrasting with the persistence of a major evocation disorder.

Amnesia↗
PubMed1979

Long-term prognosis in transient global amnesia.

Transient global amnesia (TGA) is generally believed to be a transient ischemic attack affecting short-term memory centers. A recent three-year follow-up found a high incidence of subsequent dementia and stroke in patients with TGA. We studied the course (average, 46 months) of 32 patients with TGA and found a low rate of recurrence (12.5%), dementia (6%), or transient ischemic attacks (3%). Transient global amnesia would appear to carry a more benign prognosis than classical transient ischemic attacks.

Aged↗
PubMed1994

[Experimental techniques for developing new drugs acting on dementia (6)--Carbon monoxide-induced amnesia model in experimental animals].

Cell death, neuronal dysfunction and deterioration of memory function can be produced after carbon monoxide exposure in mice as in human. These deficiencies are developed in a delayed manner (delayed amnesia). The neurotoxicity of excitatory amino acids may be involved in this model, since dizocilpine (MK-801) fully protects against carbon monoxide-induced cell death, learning impairment and delayed amnesia. In the present paper, we described the method of carbon monoxide exposure and the characteristic of behavioral and biochemical changes after carbon monoxide exposure. These data indicate that carbon monoxide can provide an amnesic model for the investigation of memory deterioration and the development of new anti-amnesic drugs.

Amnesia↗
PubMed1993

[Learning processing in an epileptic with amnesia after memory task repetition].

We reported that some learning accomplished by an epileptic patient (YS) with organic amnesia after memory task repetition. YS's learning appeared inflexible; That was depending memory task procedural. The purpose of this paper is to investigate procedural learning processing in YS with memory disorder. We examined procedural learning in picture naming task repetition in YS and normal controls, using semantic priming paradigm. After start key press, a prime picture was displayed on the CRT display, thereafter, a target picture appeared. The subjects' task was to name the target picture aloud as rapidly and accurately as possible. In the examination, we manipulated a time interval between start key press and the prime on. Two interval conditions were used. One was the constant interval, 1010ms and another was varied interval, varied between 400ms and 1010ms. After conditioning session with constant interval, the test session with constant and varied interval was carried out. We analyzed reaction time (RT) in naming the picture targets in the test session in relation to the conditions. YS's RT in the test session with constant was shorter than in the test session with varied interval. No interval effects were found in the controls. The results indicated that previous experiment in conditioning session had larger effect on the YS's performance than the controls'. This suggests hypotheses that the learning in the patient with amnesia is tied to the specific conditions in the learning experience. The results can be explained in terms of procedural learning in YS, which is automatic processing.

Adult↗
PubMed1993

Extended temporal gradient for the retrograde and anterograde amnesia produced by ibotenate entorhinal cortex lesions in mice.

Effects of ibotenic entorhinal cortex (EC) lesions on both retrograde and anterograde amnesia in mice were assessed using two-choice discrimination tasks learned at different intervals before surgery in two eight-arm radial mazes. The results indicated that EC-lesioned mice were severely impaired in postoperative retention of discrimination problems learned 3 d or 2 weeks prior to surgery, but showed no deficit on problems learned between 4, and up to 6 weeks before surgery, as compared to sham-operated controls. When trained on a novel two-choice discrimination problem (not acquired preoperatively), experimental subjects demonstrated quite normal rates of acquisition, but were impaired in learning its reversal. Furthermore, they exhibited a faster rate of forgetting (anterograde amnesia) relative to controls over a 2-week retention interval. These results indicate that approximately 4 weeks is required before memory for a two-choice spatial discrimination problem no longer depends on the integrity of the entorhinal cortex, and suggests that, beyond this time, an EC-independent memory storage system is capable of supporting the retrieval of information. The data, together with complementary behavioral results, are discussed in the context of current theories of memory storage.

Amnesia↗
PubMed1996

Focal retrograde amnesia: a multi-faceted disorder?

In this paper I review the recently introduced syndrome of focal retrograde amnesia-a disproportionate impairment of remote memory in the presence of normal or near normal anterograde memory. It is concluded that the modal form of the syndrome has been reliably demonstrated and that the underlying pathology involves damage to the temporal lobes and relative sparing of the hippocampal formation. A variant of the syndrome associated with parietal and occipital lobe damage is also presented. Finally, a third type of focal retrograde amnesia associated with minor brain trauma is considered to be or primarily psychogenic origin.

Amnesia, Retrograde↗
PubMedDate not supplied

Amnesia possibly associated with zolpidem administration.

Two patients experienced amnesia after taking zolpidem 5 and 10 mg. Neither patient could recall telephone conversations that took place within an hour of taking the drug. The first patient placed a call shortly after ingestion; the second took the dose, fell asleep, and was awakened by the call. Health care providers should be aware of the possibility that in some patients, sedative-hypnotic agents such as zolpidem may produce amnesia that begins a short time after ingestion and may persist into the sleep cycle. This may be particularly important in individuals who, after taking a hypnotic agent, may have to make significant decisions that they must be able to remember.

Adult↗
PubMed1997

[Isolated retrograde amnesia following viral encephalitis].

We describe a patient who presented with isolated retrograde amnesia of 2-year duration after recovery from viral encephalitis. The patient was a 29-year-old right-handed male dentist and was admitted to our hospital with a complaint of generalized convulsion. Cerebrospinal fluid (CSF) showed mononuclear pleocytosis. Neuroradiological examinations (X-ray CT, MRI and 123I-IMP SPECT) revealed no significant abnormality. Immunological method showed no specific increase of viral antibody titers. However, with a tentative diagnosis of viral encephalitis, administration of acyclovir was started. After 3 weeks he became comprehensive, and several kinds of neuropsychological tests were performed. His intelligence and immediate memory were normal, and his procedural memory of dentist was intact. On the other hand, he could not recall any information about events, both personal and public, occurred within 2 years before the onset of present illness. His autobiographical memory disorder was also demonstrated using a series of weekly comic. In isolated retrograde amnesia following viral encephalitis like this case, memory of relatively short time duration, acquired prior to the onset of present illness, tend to be disturbed.

Acyclovir↗
PubMed1998

Attenuation of ECS-induced retrograde amnesia by using an herbal formulation.

Earlier research indicated the efficacy of a complex herbal formulation in the attenuation of electroconvulsive shock (ECS)-induced amnestic deficits in rats; this study sought to ascertain whether a simplified herbal formulation (Memorin; Phyto-Pharma, India) also was effective. Rats pretreated for a fortnight with Memorin (200 mg/kg/day) or vehicle were exposed to a passive-avoidance learning paradigm in a shuttle box. The next day, the rats were administered two true or sham ECSs, 5 h apart; recall of the pre-ECS learning was reassessed on the following day. ECS was found to produce significant retrograde amnesia (p < 0.002). Memorin attenuated the ECS-induced amnesia (p = 0.00003) without influencing the ECS seizure duration. The clinical implications of these findings are discussed.

Amnesia↗
PubMed1998

An assistive device for persons with severe amnesia.

Five persons with severe amnesia were trained to use a device containing items of information relevant to daily activities. The training consisted of a procedure in which requests for information were paired with a tone, and the subject was required to access the device and respond with the answer to the request. The tone was gradually faded, with the goal of having the subject respond to a question alone. All of the subjects learned to consistently access the device and provide correct responses following a request for information. Generalization across requesters and settings in which the requests were made was also achieved. The findings are discussed in regard to the utility of exploiting the relatively well-preserved procedural memory system for rehabilitation of persons with severe amnesia.

Amnesia↗
PubMed1981

Hypothermia-induced retrograde amnesia in mature and aged rats.

Mature (10-month-old) and aged (25-month-old) rats were trained on a passive avoidance task. Following training, rats in each age group were exposed to a hypothermia treatment, restraint alone, or no treatment. The hypothermia treatment involved immersing the mature rats in 4 degrees C water for 12 min and immersing the aged rats in 1 degrees C water for 12 min. This treatment reduced the body temperature of both age groups to an equivalent temperature (22 degrees C). Following immersion, the body temperature of the aged rats continued to decline to a lower level and recovered at a slower rate than the mature rat's temperatures. When all rats were tested 24 hr after training for retention of the avoidance task, mature rats performed better than aged rats when trained with the same shock intensity. Increasing the shock duration for the aged rats eliminated the performance differences on the passive avoidance task between ages. Rats exposed to hypothermia showed poorer retention of the task (i.e., retrograde amnesia) than all control conditions. However, no age differences in the degree of amnesia induced by the hypothermia treatment were apparent once age groups were equated on the intensity of the amnesic agent (hypothermia) and degree of initial learning.

Aging↗
PubMed1995

The effects of ascorbic acid and oxiracetam on scopolamine-induced amnesia in a habituation test in aged mice.

The effects of a nootropic drug, oxiracetam (50-100-200 mg/kg ip), and a potent antioxidant agent, ascorbic acid (62.5-125-250 mg/kg ip), administered alone or in combination, were investigated on scopolamine-induced amnesia in a mouse habituation test. The light-dark aversion test was selected and was carried out in aged mice. Habituation to the test box occurred over a 3-day period, control mice showing a significant between-day increase in the time spent in the dark box, but not in the number of transitions. On Day 4, following post-trial administration over a 3-day period of oxiracetam (50-100 and 200 mg/kg ip) or ascorbic acid (62.5-125 and 250 mg/kg ip), a significant between-day increase in the time spent in the black area, but not in the number of transitions, was found. The combination of oxiracetam (100 mg/kg ip) with ascorbic acid (125 mg/kg ip) produced a similar pattern of results. The acute administration of scopolamine (0.25 mg/kg ip) to mice treated over a 3-day period with vehicle disrupted the habituation response. In mice that had received the 3-day treatment with oxiracetam or ascorbic acid or its combination, scopolamine failed to alter significantly the learning pattern. In conclusion, these data demonstrate that ascorbic acid, alone or in combination with oxiracetam, may prevent experimentally induced amnesia in aged mice.

Aging↗
PubMed1986

Reversal of scopolamine-induced amnesia of passive avoidance by pre- and post-training naloxone.

In a series of five experiments, the modulating role of naloxone on a scopolamine-induced retention deficit in a passive avoidance paradigm was investigated in mice. Scopolamine, but not methyl scopolamine (1 and 3 mg/kg), induced an amnesia as measured by latency and duration parameters. Naloxone (0.3, 1, 3, and 10 mg/kg) injected prior to training attenuated the retention deficit with a peak of activity at 3 mg/kg. The effect of naloxone could be antagonized with morphine (1, 3, and 10 mg/kg), demonstrating the opioid specificity of the naloxone effect. Post-training administration of naloxone (3 mg/kg) as a single or as a split dose also attenuated the scopolamine-induced amnesia. Control experiments indicated that neither an increase in pain sensitivity (pre-training naloxone) nor an induced aversive state (post-training naloxone) appear to be responsible for the influence of naloxone on the scopolamine-induced retention deficit. These results extend previous findings implicating a cholinergic-opioid interaction in memory processes. A possible mechanism for this interaction involving the septo-hippocampal cholinergic pathway is discussed.

Animals↗
PubMed1996

Nefiracetam (DM-9384) reverses apomorphine-induced amnesia of a passive avoidance response: delayed emergence of the memory retention effects.

Nefiracetam is a novel pyrrolidone derivative which attenuates scopolamine-induced learning and post-training consolidation deficits. Given that apomorphine inhibits passive avoidance retention when given during training or in a defined 10-12h post-training period, we evaluated the ability of nefiracetam to attenuate amnesia induced by dopaminergic agonism. A step-down passive avoidance paradigm was employed and nefiracetam (3 mg/kg) and apomorphine (0.5 mg/kg) were given alone or in combination during training and at the 10-12h post-training period of consolidation. Co-administration of nefiracetam and apomorphine during training or 10h thereafter produced no significant anti-amnesic effect. However, administration of nefiracetam during training completely reversed the amnesia induced by apomorphine at the 10h post-training time and the converse was also true. These effects were not mediated by a dopaminergic mechanism as nefiracetam, at millimolar concentrations, failed to displace either [3H]SCH 23390 or [3H]spiperone binding from D1 or D2 dopamine receptor subtypes, respectively. It is suggested that nefiracetam augments molecular processes in the early stages of events which ultimately lead to consolidation of memory.

Animals↗
PubMed2004

Dose-finding study of intravenous midazolam for sedation and amnesia during spinal anesthesia in patients premedicated with intramuscular midazolam.

PURPOSE: We investigated the effective and safe dose of intravenous midazolam for sedation and amnesia during spinal anesthesia in patients premedicated with intramuscular midazolam. METHODS: One hundred and eighty patients aged 20-50 years scheduled for spinal anesthesia received midazolam 0.06 mg.kg(-1) and atropine 0.01 mg.kg(-1) intramuscularly 15 min before entering the operating room. Spinal anesthesia was performed with 0.5% hyperbaric tetracaine. Five minutes after starting surgery, midazolam 0 (control group), 0.01, 0.02, 0.03, 0.04, or 0.05 mg.kg(-1) was intravenously administered (30 patients each). Blood pressure, heart rate, respiratory rate, percutaneous oxygen saturation (S(p)(O)(2)), verbal response, eyelash reflex, and involuntary body movement were measured every 5 min for 30 min. Memory during surgery was also investigated. RESULTS: The number of the patients with loss of verbal response, with loss of eyelash reflex, and with no memory during surgery were significantly larger in the groups receiving midazolam >or=0.03 mg.kg(-1), >or=0.04 mg.kg(-1), and >or=0.02 mg.kg(-1), respectively. The decrease in blood pressure or increase in respiratory rate with decrease in S(p)(O)(2) was significantly larger in the groups receiving midazolam >or=0.03 mg.kg(-1) or 0.05 mg.kg(-1), respectively. CONCLUSION: For sedation and amnesia of the patients aged 20-50 years in spinal anesthesia with about 1 h duration receiving intramuscular midazolam 0.06 mg.kg(-1) as a premedication, intravenous midazolam 0.02 mg.kg(-1) might be effective and safe.

Adult↗
PubMed1978

ADH and related peptides: effect of pre- or posttraining treatment on puromycin amnesia.

The peptide Z-Pro-Leu-Gly-NH2 attenuated puromycin-induced amnesia in mice when administered 5 days prior to training, while arginine vasopressin, lysine vasopressin and cyclo(Leu-Gly), were effective when given 24 hr before training. The activity of all peptides to inhibit puromycin-induced amnesia decreased as the interval after training and before peptide administration increased, suggesting that the peptides influence memory processes rather than generalized arousal mechanisms.

Animals↗
PubMed1981

Reversal of guanethidine- and diethyldithiocarbamate-induced amnesia by peripherally-administered catecholamines.

The effect of peripherally-administered catecholamines on guanethidine- and diethyldithiocarbamate-induced amnesia of a PA training in mice was investigated. The amnesic effect of guanethidine could be blocked with 50 mg/kg DA, or 0.75 mg/kg NE when given either before, immediately, or 10 min after but not 90 min following PA. Epinephrine or a lower dose of DA could be attenuate the guanethidine-induced amnesia. The amnesic effect of diethyldithiocarbamate could be blocked with 50 mg/kg DA, 0.75 mg/kg NE or 0.5 mg/kg E when given either before, immediately or 10 ming after but not 90 min following PA. The amnesic effects of these compounds were interpreted in terms of their peripheral antiadrenergic actions.

Animals↗