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PubMed1994

Cholecystokinin-related peptides, after systemic or central administration, prevent carbon monoxide-induced amnesia in mice.

The neuroprotective actions of cholecystokinin (CCK) peptides were investigated in a mouse hypoxia model, in which the animals were successively exposed to CO gas. Working memory impairment 5 days after CO exposure was examined by using a Y-maze test; delayed amnesia was examined 7 days after CO exposure, by using a step-down type passive avoidance test. Ceruletide (1-100 micrograms/kg, given s.c. 30 min before CO exposure) significantly prevented the CO-induced impairment of performance in both tests, the improvement being correlated with the severity of hypoxia. This severity was increased by maintaining the body temperature at 38 degrees C. Ceruletide was less effective when injected immediately after a single CO exposure. The order of potency of the CCK-peptides administered systemically was: ceruletide > CCK-8S > CCK-8NS >> CCK-4. Ceruletide (0.03-0.3 micrograms/mouse) and CCK-8S (0.03-1 microgram/mouse) prevented CO-induced amnesia after i.c.v. administration. Under all experimental conditions, dizocilpine [MK-801, (+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohepten-5,10-imine maleate, 500 micrograms/kg s.c. or 10 micrograms/mouse i.c.v.] prevented completely the CO-induced amnesia. The protective effects of systemic ceruletide were blocked, partially but significantly, by the preadministration of L-364,718 (3S-(-)-N-[2,3-dihydro-1-methyl-2-oxo-S-phenyl-1H-1,4- benzodiazepine-3-yl]-1H-indole-2-carboxamide, 1-10 mg/kg i.p.), a selective CCK-A receptor antagonist. L-365,260 ([3R-(+)-2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4-benzodiazepine-3-yl] -N' - [3-methyl-phenyl]urea), a CCK-B antagonist, also decreased ceruletide-induced protection.(ABSTRACT TRUNCATED AT 250 WORDS)

Amnesia↗
PubMed1993

Transient global amnesia after cerebral angiography with iohexol.

Transient global amnesia is an unusual neurologic phenomenon that occasionally occurs after angiography, usually of the cerebral vessels. It represents a benign event, and normal function is ultimately restored, but the amnesia may be frightening for both the patient and the physician until its nature is recognized. The authors describe two cases of transient global amnesia occurring after cerebral angiography with iohexol, outline the criteria for the diagnosis and discuss the proposed mechanism of the phenomenon.

Adult↗
PubMedDate not supplied

The effect of vasopressin analog: [d(CH2)(1)5,Tyr(Me)2,delta 3Pro7]AVP on learning and memory processes in rats with experimental amnesia.

We investigated the effect of a single 2 micrograms dose of a vasopressin (AVP) analog, [d(CH2)(1)5,Tyr(Me)2,delta 3Pro7]AVP on processes of retrieval, consolidation and acquisition of conditioned reflexes in rats with experimentally induced amnesia. The investigated amnesia models were: long term ethanol intoxication, electroconvulsive shocks (ECS), and hypoxia. They all profoundly impaired the learning and memory processes in all tests used. The AVP analog-[d(CH2)(1)5,Tyr(Me)2,delta 3Pro7]AVP facilitated retrieval of passive avoidance in all amnesia models. It improved consolidation of active avoidance of rats previously treated with alcohol, but did not affect the acquisition of active avoidance. [d(CH2)(1)5,Tyr(Me)2,delta 3Pro7]AVP lack antidiuretic properties.

Alcoholism↗
PubMed1997

Effects of verapamil on electroconvulsive shock- and clonidine-induced amnesia.

The effect of the Ca2+ blocker verapamil on amnesia induced by electroconvulsive shock (ECS) or by the alpha-adrenoceptor agonist clonidine was studied in male Wistar rats trained in passive avoidance task ("step down"). Clonidine (0.1 mg/kg, i.p.) and ECS induced a pronounced amnesia, significantly reducing the percentage of rats that had acquired the task upon retention tests, given 3 h, 24 h and 7 days after training. Verapamil (10 mg/kg) administered orally for 12 days (5 days before and 7 days after training) completely abolished the ECS- or clonidine-induced amnesia. These data suggest that calcium channel blocker verapamil has a protective effect against experimentally provoked memory deficit and might be useful for the treatment of cognitive disorders.

Adrenergic alpha-Agonists↗
PubMed1997

Effects of NIK-247 on cholinesterase and scopolamine-induced amnesia.

The effects of NIK-247 on cholinesterase, scopolamine-induced amnesia and spontaneous movement were examined and compared with those of the well-known cholinesterase inhibitors tacrine and E-2020. NIK-247, tacrine and E-2020 all strongly inhibited acetylcholinesterase (AChE) in human red blood cells (IC50s = 1.0 x 10(-6), 2.9 x 10(-7) and 3.7 x 10(-8) M, respectively). In addition, NIK-247 and tacrine, but not E-2020, strongly inhibited butyrylcholinestrase (BuChE) in human serum. All three drugs produced mixed inhibition of AChE activity. Moreover, the inhibitory effect of NIK-247 on AChE was reversible. All compounds at 0.1-1 mg/kg p.o. significantly improved the amnesia induced by scopolamine (0.5 mg/kg s.c.) in rats performing a passive avoidance task. The three compounds at 1 and 3 mg/kg p.o. did not significantly decrease spontaneous movement by rats. These findings suggest that NIK-247 at a low dose (0.1-1 mg/kg p.o.) improves scopolamine-induced amnesia but does not affect spontaneous movement. The findings suggest that NIK-247 may be a useful drug for the treatment of Alzheimer's disease.

Acetylcholinesterase↗
PubMed1997

Mesograde amnesia during the sleep onset transition: replication and electrophysiological correlates.

The present study was designed to explore mechanisms of amnesia for meaningful auditory material presented during the sleep onset transition. Thirty undergraduate subjects (17 female, 13 male) were presented with auditory stimuli in an oddball paradigm until sleep onset. Subjects were allowed to accumulate either 30 seconds or 10 minutes of sleep, then awakened and tested on free recall and recognition memory for the meaningful stimuli. After 10 minutes of sleep, but not after 30 seconds of sleep, subjects had profound amnesia on free recall for stimuli presented in the 4-minute window prior to sleep onset. Increased beta electroencephalograph (EEG) power during the sleep period correlated positively with recall of stimuli in the 4-minute presleep window. Event-related potential recordings provided suggestive evidence that subjects continued to process the auditory stimuli to some extent during the sleep onset transition. When allowed to sleep for 10 minutes, subjects evidenced a mixed anterograde and retrograde amnesia for auditory stimuli presented in the 4-minute window prior to sleep onset. The results are discussed in terms of stimulus encoding, consolidation, and retrieval.

Acoustic Stimulation↗
PubMed1997

Evaluation of pre-ECS antihypertensive drug administration in the attenuation of ECS-induced retrograde amnesia.

Two once-daily electroconvulsive shocks (ECS) produced retrograde amnesia in rats trained on a Hebb-Williams maze; Verapamil (12.5 mg/kg, i.p.) or felodipine (10 mg/kg, p.o.) administered half an hour before each ECS attenuated this ECS-induced amnesia. Hence, these drugs may hold promise for the containment of amnesia induced by electroconvulsive therapy (ECT). Speculatively, one or more of several mechanisms may be involved: cerebral vasodilatation, enhancement of cholinergic tone, and inhibition of calcium-mediated impairment of neuronal function. These drugs may also act by attenuating the systolic surge in blood pressure during ECT, thereby decreasing edema due to cerebral hyperperfusion, as well as decreasing the possible transfer of potentially neurotoxic macromolecules through a putative breach in the blood-brain barrier.

Amnesia, Retrograde↗
PubMed1998

[Treatment of patients with psychogenic amnesia with the help of therapeutic anamnesis].

Psychogenic (dissociative) amnesia is a psychiatric disorder characterised by a sudden loss of memory which is too extensive to be explained by ordinary forgetfulness, but which has no organic disease or explanation. Psychogenic amnesia is categorised among the dissociative disorders in DSM-IV and ICD-10 and begins suddenly, usually after severe psychosocial stress. The prognosis is good with complete recovery, and there is seldom relapse. This article describes a man, 45 years of age, who developed severe depression and amnesia following a very troublesome divorce. He did not talk, he communicated by signs and gestures, and he isolated himself in his mother's home. After being admitted to a psychiatric ward he became anorectic and developed erosive eoesophagitis/gastroduodenitis. Initially he was given perfenazin (Trilafon) 24 mg/day. The psychiatric treatment produced no results for the first three weeks, but the patient gradually recovered when the therapist and the patient recapitulated the conflicts associated with the divorce, using documents from the patient's lawyer as a guide. This method is called "therapeutic anamnesis" and is similar in many ways to psychiatric treatment of post-traumatic stress reactions.

Amnesia↗
PubMed1998

[FLAIR images of mild head trauma with transient amnesia].

A newly advanced MRI pulse sequence, the FLAIR (fluid-attenuated inversion recovery) imaging, in which a long TE spin echo sequence is used with suppression of the CSF with an inversion pulse, displays the CSF space as a no signal intensity area. We examined 45 cases of mild head trauma with posttraumatic amnesia by FLAIR images and could detect some findings which could not be detected by CT scan and conventional MR images. These findings could be detected in many patients with long post-traumatic amnesia (over 2 hours), but they could not be detected in patients with short posttraumatic amnesia (within 30 mins). These findings existed surrounding lateral ventricles and we classified them into 3 types: type 1 is anterior horn of lateral ventricle, type 2 is the base of frontal lobe, type 3 is cerebral deep white matter. Some of them were examined again by FLAIR images a month later, and these findings had disappeared. We suspect that these lesions were brain edema or mild contusion without hemorrhage.

Adolescent↗
PubMed1955

Studies in traumatic amnesia.

Retrograde amnesia is for a period of time, usually for a fraction of a minute in simple concussion, and not loss of memory for an event. The length of time for which there is no recollection is not directly related to the duration of coma but can be for days or even weeks. It is characterized by inability of restoration of memory for the period in question. Any retrograde amnesia of more than a day's duration results from trauma only if the trauma is severe enough to cause prolonged coma, usually weeks. It should be under suspicion of being due pathologically to more than concussion. Careful attention should be given to the possibility of hysteria or malingering as a factor.

Amnesia↗
PubMed1983

Alleviation of infantile amnesia in rats by means of a pharmacological contextual state.

Although a number of studies have demonstrated that the relatively rapid rate of forgetting in young rats (i.e., infantile amnesia) can be alleviated by various reminder treatments, the possibility of enhancing retention by other procedures seems largely unexplored. Given the putative importance of contextual cues as sources of memory retrieval, this experiment examined whether the presence of a distinctive pharmacological state at training and testing could override infantile amnesia. Weanling rats were given pentobarbital or saline prior to Pavlovian fear-conditioning. When tested 1 week later, subjects in the same-state drug condition showed better retention than the same-state saline group. This finding extends previous work on memory recovery in young animals by demonstrating alleviation of infantile amnesia without a re-exposure to the CS or UCS during the retention interval.

Animals↗
PubMed1986

Alleviation of infantile amnesia in rats by internal and external contextual cues.

A previous study [Richardson, R., Riccio, D.C., and Jonke, T. (1983). Alleviation of infantile amnesia in rats by means of a pharmacological contextual state. Devel. Psychobiol., 16:511-518] found that ontogenetic forgetting ("infantile amnesia") in rats was attenuated by a "contextual matching" manipulation: Subjects trained in a distinct pharmacological state and tested in that state retained learned fear better than saline controls. To determine whether improved retention could be obtained with salient but nonpharmacological contexts, two experiments were conducted employing fear conditioning in preweanling rats. In Experiment 1, an internal context (illness induced by lithium chloride) present at training and testing reduced infantile forgetting. In Experiment 2, matching an exteroceptive context (home nest shavings) at training and testing was also found to be sufficient to alleviate infantile amnesia. In both experiments, retention was not improved in controls exposed to the context at training only or testing only, indicating that the contextual effect is not on acquisition or retrieval processes per se. These findings provide indirect support for views that emphasize the role of contextual cues in retrieval (Spear, 1978). In addition, they indicate that contextual matching is not limited to a state dependent drug, but may include a wide range of "distinctive" stimuli.

Animals↗
PubMed2001

Severe Amnesia in Epilepsy: Causes, Anatomopsychological Considerations, and Treatment.

Severe amnesia in epileptic patients is a catastrophic condition that may be due to different etiologies. Because of the striking findings and thorough neuropsychological studies of Patient H.M., the literature has focused on postsurgical occurrence of such memory impairment, with much less emphasis on other causes. Here we summarize, for comparison, the history of H.M. We report five patients with pronounced memory loss who had extensive neuropsychological and electroencephalographic testing. MRI was also performed in four of the patients, MRI volumetric measurements of amygdala and hippocampal formation in three, and measurements of entorhinal cortex in two. The amnesia occurred after head trauma in one patient, following encephalitis in one, after partial status epilepticus in two, and after unilateral surgical resection in a woman with bilateral lesions. On the basis of these studies it was impossible to distinguish the role of recurrent temporal lobe epileptic seizures as distinct from underlying lesions in the genesis and course of the memory loss. We review here the anatomical substrate, neuropsychological, and other investigations and the etiological factors leading to the amnesia in these patients, together with current concepts regarding possible causes of such severe memory dysfunction. In patients with this degree of severity of memory deficit, temporal resection in an attempt to control seizures did not lead to a measurable increase in memory problems. It also, however, did not bring about worthwhile improvement in seizure control.

Journal Article↗
PubMed1980

Extended retrograde amnesia gradients: peripheral epinephrine and frontal cortex stimulation.

This experiment examined the possibility that hormonal responses to training may increase the susceptibility of memory to an amnestic agent. As long as one week after training, rats that received a subcutaneous epinephrine injection shortly before electrical stimulation of frontal cortex exhibited amnesia on later retention tests. These findings suggest that retrograde amnesia gradients may reflect, in part, maximum susceptibility to amnesia shortly after training because the effects on memory of an amnestic agent are potentiated by the neuroendocrine response to training.

Animals↗
PubMed1982

Time-dependent recovery from electroconvulsive shock-induced amnesia.

To examine time-dependent recovery from ECS-induced amnesia, 44 hooded rats were trained to leverpress for food. On treatment day the first leverpress was followed by footshock and ECS or sham ECS (SECS). Animals in both treatment conditions then experienced a 10-min extinction session either 1 or 3 days following treatment. For both the 1-day and 3-day delay ECS groups, the latencies to the first response during extinction were lower than the latencies of the corresponding SECS groups. When extinction followed treatment by 1 day, the ECS rats also made more responses during the test than the SECS rats; however, when tested 3 days after treatment, the ECS and SECS groups did not differ on extinction response rate. In this operant setting, therefore, time-dependent recovery from amnesia can be demonstrated with response rate as the amnesia measure. In addition, since both groups of SECS animals exhibited significant interrelationships of measures following treatment and the same measures were not associated in the ECS groups, it was hypothesized that the proactive effects of ECS include a reduction in the stability of performance.

Animals↗
PubMed1982

Pre-test epinephrine injections reverse DDC-induced retrograde amnesia.

The effects of pre-test systemic administration of epinephrine on DDC-induced retrograde amnesia (RA) for discriminated Pavlovian fear-conditioning were examined in rats. Epinephrine reversed RA with the optimal dosage being 0.05 mg/kg. Apparently, the effect was specifically reversal of amnesia since (a) performance was restored to control levels, but no higher, and (b) sensitization and activity-related artifacts were minimized. These results are consistent with those showing reversal of RA by pre-test administration of hormones or catecholamine agonists. That is, they suggest that amnesia is due to a retrieval deficit rather than to failure of memory storage. Results are discussed in terms of epinephrine-induced modulation of storage and retrieval processes through central and peripheral mechanisms.

Animals↗
PubMed1984

A pilot study of lorazepam-induced amnesia with cis-platinum-containing chemotherapy.

Eighteen patients with advanced epithelial ovarian cancer were given 36 courses of cis-platinum-containing chemotherapy at Cedars-Sinai Medical Center. Patients were given lorazepam (Ativan) prior to chemotherapy. Amnesia for the day of chemotherapy was reported in 29 courses. Lack of recall for the chemotherapy infusion and the subsequent 8 hr or greater was reported in 33 of the 36 courses. In two courses, no amnesia effects were noted. No serious side effects of lorazepam therapy occurred and all patients believed that the amnesic effect was beneficial during chemotherapy. Lorazepam (Ativan) appears to be a safe medication to induce amnesia for cis-platinum chemotherapy and deserves further study to determine its effect on anticipatory vomiting, nausea and vomiting, and patient compliance with continued chemotherapy.

Adult↗
PubMed1981

Amnesia due to beta-antagonists in a passive avoidance task in the chick.

The beta-adrenergic antagonists sotalol, nadolol and timolol (which act at both beta 1- and beta 2-receptors) induce amnesia in the domestic chick when given systemically after a one trial passive avoidance task. State dependent learning and effects on performance at test (e.g. interference with recall) almost certainly do not cause the observed amnesia. All three effective beta-antagonists induce amnesia only when injected within a limited period after training, suggesting effects on memory formation. Sotalol differs markedly from nadolol and timolol in: (a) showing a sharp and markedly earlier loss of effectiveness as administration is moved to progressively later times after training (25-30 min rather than 40-50 min), (b) producing when given after training a delayed and gradual loss of retention rather an immediate and rapid loss. These differences seem not to reflect a lesser effectiveness of sotalol, nor a greater delay in the onset of its action, but instead qualitative differences in effects on memory formation.

Adrenergic alpha-Antagonists↗