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PubMed2005

Increased incidence of jugular valve insufficiency in patients with transient global amnesia.

OBJECTIVE: While transient global amnesia (TGA) is a clinically well defined disorder, its etiology is poorly understood. Cerebral venous hypertension and subsequent damage to hippocampal and diencephalic structures are among the discussed hypothetical causes. Using a direct method for the study of retrograde flow during a Valsalva maneuver, we determined whether jugular valve insufficiency contributes to cerebral venous hypertension in patients with TGA. METHODS: Jugular valve closure was assessed by duplex sonography in 20 patients with TGA and 20 age and gender matched controls. The diagnosis of valvular insufficiency was made on the basis of recently established criteria. RESULTS: Valvular insufficiency (either left or right-sided, or bilateral) was identified in 85% of patients with TGA,and in 45% of controls (p = 0.008). All patients with involuntary Valsalva episodes immediately prior to TGA developed valvular insufficiency (n = 8; p = 0.13 compared with patients who did not recall such an event). The mean duration of the insufficiency jet did not differ significantly between patients with TGA (3.26 s) and controls (2.78 s; p = 0.315). However, patients with TGA who experienced a trigger event were characterized by significantly longer insufficiency reflux times (3.84 s) than those without (2.55 s; p = 0.03). CONCLUSIONS: TGA is associated with an increase in the prevalence of jugular insufficiency. Valvular insufficiency may lead to increased venous pressure transmission during a Valsalva maneuver and thus contribute to venous ischemia in TGA. The association of valvular insufficiency and longer reflux times with the occurrence of a trigger event further suggests that cerebral venous congestion is an important etiological factor in transient global amnesia.

Aged↗

PubMed2003

A case of germinoma in the septum pellucidum manifesting as amnesia and hemiparesis.

BACKGROUND: We report a rare case of germinoma mainly located in the septum pellucidum. CASE DESCRIPTION: A 19-year-old man presented with germinoma located in the septum pellucidum manifesting as amnesia and right hemiparesis. Magnetic resonance imaging demonstrated a heterogeneously enhanced mass in the septum pellucidum and abnormal T2-weighted signals in the left basal ganglia. An anterior transcallosal approach was performed to remove the mass in the septum pellucidum. The histological diagnosis was germinoma. Radiotherapy and chemotherapy were given. He was discharged with slight amnesia and right hemipareis. INTERPRETATION: Intracranial germinoma can arise from the septum pellucidum.

Adult↗

PubMed1993

Inhibiting synthesis of the putative retrograde messenger nitric oxide results in amnesia in a passive avoidance task in the chick.

It has been hypothesized that nitric oxide (NO) may act as a 'retrograde messenger' in the CNS, mediating intersynaptic communication in the context of neural plasticity during memory formation. To test this hypothesis the effects of the competitive NO synthase inhibitor N-nitro-L-arginine (NARG) on memory retention has been studied in a one-trial passive avoidance task in the day-old chick. Intracerebral injections before training into the intermediate medial hyperstriatum ventrale (IMHV), an area that is of crucial importance in learning in the chick, produced amnesia in this task when tested at various time points from 30 min to 24 h after training. Time- and dose dependencies of NARG when injected i.p. or i.c. were evaluated. Injection into one IMHV alone (left or right) proved to be sufficient to produce amnesia. Diffusion of NARG into the untreated hemisphere was ruled out by injecting it with L-arginine, which competes with NARG and prevents inhibition of NO synthase. Additional tests showed that the amnestic effect is not due to state-dependent learning, nor to interference of the drug with general motor ability or motivation.

Amnesia↗

PubMed1994

Behavioral evidence for a modulating role of sigma ligands in memory processes. I. Attenuation of dizocilpine (MK-801)-induced amnesia.

The potentiating effect of low doses of sigma ligands on the N-methyl-D-aspartate (NMDA)-induced excitation of pyramidal CA3 dorsal hippocampal neurons has recently been reported. In the present study, we investigated behavioral effects relevant to these findings in the experimental amnesia induced by the non-competitive NMDA antagonist, dizocilpine (MK-801), in mice. At doses below 1 mg/kg s.c., the sigma ligands, 1,3-di-(2-tolyl)guanidine (DTG), (+)-SKF 10,047, and (+)-pentazocine, but not their (-)-isomers, significantly decreased MK-801 (100 microgram/kg s.c.)-induced impairment of spontaneous alternation performances in 8-min sessions of a Y-maze exploration, an index of spatial working memory, without affecting the concomitant hyperlocomotion. The effect of DTG (100 micrograms/kg s.c.) was completely antagonized by the simultaneous administration of BMY 14802 (10 mg/kg i.p.) and NE-100 (1 mg/kg i.p.), two putative sigma antagonists, which had no effect by themselves. In long-term memory tests (step-down and step-through types of passive avoidance, elevated plus-maze), DTG exhibited a significant attenuation of MK-801-induced amnesia, at doses of 10 and 100 micrograms/kg s.c. In all tests of short- and long-term memory, the effects exhibited by the sigma ligands tested had a bell-shaped curve; no effect was seen at 1 mg/kg. DTG did not affect the impairment of alternation induced by CPP (5 mg/kg i.p.): the modulation may selectively target the blockade of NMDA receptor-associated ion channels. Moreover, DTG (1-1000 micrograms/kg) did not affect the impairment induced by scopolamine (1 mg/kg i.p.) or diazepam (4 mg/kg i.p.), but significantly prevented the impairment induced by mecamylamine (10 mg/kg i.p.). These results suggest that the potentiating effect of sigma ligands on NMDA receptor-mediated glutamatergic neurotransmission, already demonstrated electrophysiologically, may have some relevance to learning and memory processes in the hippocampus. A similar modulation may also affect cholinergic nicotinic systems.

Amnesia↗

PubMed1988

Reversal of alcohol-induced amnesia by the benzodiazepine inverse agonist Ro 15-4513.

We investigated the effects of benzodiazepine inverse agonists on ethanol-induced amnesia using a passive avoidance task. Pretraining treatment of mice with ethanol significantly impaired the passive avoidance response: there was a significant reduction in the % retention and step-down latency. The benzodiazepine inverse agonists, Ro 15-4513 and beta-CCM, significantly increased the % retention and prolonged the step-down latencies in mice treated with ethanol, but FG 7142 did not. The anti-amnesic effects of Ro 15-4513 were completely antagonized by co-administration of Ro 15-1788, a benzodiazepine antagonist. These results suggest that the anti-amnesic effect of Ro 15-4513 on alcohol-induced amnesia is mediated by benzodiazepine receptors.

Amnesia↗

PubMed1994

Intrahippocampal, but not intra-amygdala, infusion of an inhibitor of heme oxygenase causes retrograde amnesia in the rat.

Zinc protoporhyrin-9 (ZnPP) is an inhibitor of heme oxygenase, the enzyme involved in the biosynthesis of carbon monoxide (CO). CO regulates the activity of glutamatergic synapses and has been proposed to play a role in the early phases of long-term potentiation. The present paper reports on the effect of ZnPP on memory of inhibitory avoidance and of habituation to a novel environment. The bilateral infusion of ZnPP (2 micrograms/side) into the dorsal hippocampus caused amnesia for the inhibitory avoidance task when given before training or 0 or 30 min, but not 60 or 100 min, after training. The immediate post-training intrahippocampal infusion of ZnPP also caused amnesia for the habituation task. The immediate post-training intra-amygdala infusion of ZnPP had no effect on retention of the avoidance task. The data are consistent with the hypotheses that memory involves long-term potentiation initiated at the time of training in the hippocampus, and that hippocampal but not amygdala long-term potentiation may be regulated by CO.

Amnesia, Retrograde↗

PubMed1995

Effects of dynorphin A-(1-13) on carbon monoxide-induced delayed amnesia in mice studied in a step-down type passive avoidance task.

The effects of dynorphin A-(1-13) on carbon monoxide (CO)-induced amnesia in mice were investigated using a step-down type passive avoidance task. Memory deficiency occurred in mice when training commenced 7 days after CO exposure although it was not produced 1 day after CO exposure. The median step-down latency in the retention test of the CO-exposed group was significantly shorter than that of the control group. Administration of dynorphin A-(1-13) (1.5 nmol/mouse i.c.v.) 15 min before the first training session prolonged the step-down latency in the CO-exposed group. Dynorphin A-(1-13) administered immediately after the first training session or administered 15 min before the retention test also prolonged the step-down latency in the CO-exposed group. To determine whether this effect of dynorphin A-(1-13) was mediated via kappa-opioid receptors, we attempted to block its action using a kappa-opioid receptor antagonist (nor-binaltorphimine). Nor-binaltorphimine (5.44 nmol/mouse i.c.v.) blocked the effect of dynorphin A-(1-13) on delayed amnesia. However, dynorphin A-(1-13) (0.5, 1.5 and 5.0 nmol/mouse) did not facilitate the acquisition of memory in normal mice. These results suggest that dynorphin A-(1-13) modulates the kappa-opioid receptor-mediated opioid neuronal system, and that it ameliorates the disruptive effect of CO on acquisition, consolidation and/or recall of memory.

Amnesia↗

PubMed1984

Amnesia in a patient with bilateral lesions to the thalamus.

A case of anterograde amnesia is described in a 38-yr-old man with bilateral thalamic lesions. The patient appeared to have suffered no general intellectual loss and performed normally on standard memory tasks involving immediate recall of new material. There was, however, consistent impairment in recalling material, verbal and non-verbal, over delays as brief as a few seconds. Impairment was especially marked on tests involving free recall and partial cueing procedures; recognition memory was also impaired. Premorbid memory tested normally and susceptibility to interference was less than in other organic amnesics. Various interpretations of the patient's amnesia were considered but a deficit at the initial stages of information processing appeared to be indicated.

Adult↗

PubMed1990

Frontal hypermetabolism and thalamic hypometabolism in a patient with abnormal orienting and retrosplenial amnesia.

A patient with verbal amnesia and a propensity to direct his attention to the right following a retrosplenial area lesion was studied with positron emission tomography using [F-18] fluorodeoxyglucose. These studies showed that the left thalamus was hypometabolic, and the anterior 2/3 of the left hemisphere was hypermetabolic when compared with the right. There were no significant differences seen in the medial temporal lobes. Based on this study, it is posited that interruption of hippocampal input into the anterior thalamus was responsible for the amnesia, and the left frontal hyperactivity was associated with the propensity to attend contralaterally.

Adult↗

PubMed1992

Right motor neglect associated with dynamic aphasia, loss of drive and amnesia: case report and cerebral blood flow study.

A 30-year-old right-handed man had right motor neglect, amnesia, aphasia and loss of drive following bilateral thalamic and subthalamic infarctions. Serial resting cerebral blood flow (CBF) measurements with either Xenon 133 inhalation or positron emission tomography at 1, 8 and 10 months post-onset showed a widespread and long-lasting low CBF in the cortex. An additional CBF measurement, during motor tasks, showed a marked interhemispheric asymmetry in the pattern of activation: whereas left hand movement resulted in a CBF increase in contralateral superior rolandic and prerolandic areas, no significant regional CBF changes were seen during right hand movement, despite recovery from motor neglect. This loss of CBF increase in cortical motor and premotor areas during voluntary movement of the previously neglected side points to a disruption of cortico-subcortical pathways subserving motor activation. The pathophysiology of aphasia, loss of drive and amnesia as well as their relationships to motor neglect, may also be discussed on the basis of thalamo-cortical disconnections.

Adult↗

PubMed1995

Focal retrograde amnesia following closed head injury: a case study and theoretical account.

In this paper we present data from a closed head injury patient who presents a striking example of what Kapur (Cortex 29, 217-234, 1993) has termed " focal retrograde amnesia". The patient, D.H., is unable to recollect any autobiographical incidents from the pre-morbid period, although he is able to provide personal and public information from this period. The data are discussed in relation to other reported instances of focal retrograde amnesia and a preliminary theoretical account is offered.

Adult↗

PubMed1982

Variations in amnesia with intravenous diazepam.

Volunteer senior students who had not previously received a benzodiazepine were employed to determine whether amnesia induced by the intravenous administration of diazepam remained constant. Profoundness of amnesia was tested 24 hours after drug administration following a first and second exposure to the drug. The two experiences were set 28 days apart. The study showed that recall of events in the immediate post-drug administration period was likely to be less impaired following a second exposure to diazepam than following the first. It also revealed that recall of visual stimuli was significantly better than recall of cutaneous-tactile stimuli. The clinical implications of these findings are discussed.

Amnesia↗

PubMed1975

Retrograde amnesia induced by hypoxia and electroconvulsive shock in two rat strains.

Hypoxia or electroconvulsive shock (ECS) was administered to two strains of rats following one trial passive avoidance training. ECS produced retrograde amnesia in the Blue Spruce Farms Long Evans hooded rat when administered within 10 sec after training and in the Charles River albino rat when administered within 75 sec after training. Hypoxia was effective in producing retrograde amnesia when administered up to 40 min after training in the hooded rat but only when administered between 20 and 30 min after training in the albino rat. The importance of strain variability is discussed.

Amnesia↗

PubMed1983

Transient aversion and long-lasting amnesia following cycloheximide injection in the rat.

Rats were first trained to press a bar for water reinforcement. The day after reaching criterion, the animals received a subcutaneous injection of cycloheximide (CXM-2.5 mg/kg) or saline, 15 minutes before a single punishment (P) session where bar pressing was followed by a strong inescapable footshock (CXM-P and saline-P groups). No punishment was given to control groups (CXM-NP and saline-NP groups). Retention for this learning experience was tested 24 hr, one week or two weeks later. Performances of the control groups were similar at the three retention intervals although some CXM-induced aversion appeared at 24 hr. The saline-P groups always demonstrated good retention of prior aversive experience. By contrast, a long-lasting CXM-induced amnesia was apparent among the CXM-P groups. This deficit is not easily explained by nonspecific effects of the drug such as altered motor activity or motivational changes. Moreover, CXM-induced amnesia seems to be the result of impaired memory formation rather than impaired memory retrieval.

Amnesia↗

PubMed1986

Hypothermia-induced anterograde amnesia and its reversal in rats trained on a T-maze escape task.

Previous studies have demonstrated anterograde amnesia (AA) and its reversal in rats trained on passive avoidance tasks. The present investigation was conducted to determine whether induction and/or reversal of AA is limited to inhibitory learning tasks or whether these phenomena can be illustrated in behavioral situations involving choice. Accordingly, in Experiment 1, rats were trained on a T-maze escape task as either hypothermic (28 degrees C) or normothermic. Twenty-four hours later half of each acquisition group was tested as either hypothermic or normothermic. Results indicated a stern retention decrement for animals trained at a lower body temperature and tested as normothermic. However, this prograde memory deficit was attenuated when animals were recooled shortly prior to testing. In an attempt to extend the phenomenon of memory recovery observed in Experiment 1, Experiment 2 examined whether pretest injections of d-amphetamine (0.5 mg/kg), a purported amnesia-attenuating agent, could lessen the AA induced by hypothermia. Amphetamine, at least at the dose used, did not reduce the memory impairment. Results are interpreted in terms of the state dependent nature of memory.

Amnesia↗

PubMed1995

Concussion-induced retrograde amnesia in rats.

Three experiments were conducted to investigate the characteristics of retrograde amnesia (RA) induced by concussion in rats. In Experiment 1, rats receiving experimental concussion shortly after training in a single punishment trial exhibited severe forgetting on a retention test 48 h later. In the second experiment, rats receiving a concussion within 6 h after training showed severe RA, while those receiving concussion one day to five days after training exhibited progressively weaker amnesia. In Experiment 3, amnesic animals in one group received pretest noncontingent foot shock as a reminder treatment. This pretest cue significantly increased the cross-through latency, thus indicating a reduction in the memory deficit resulting from concussion. These results suggest that experimental concussion can be an effective method to induce retrograde memory loss in rats; that the RA caused by concussion is time-dependent; and that concussion-induced RA can be alleviated by a pretest cue indicating that the underlying mechanism of concussion-induced RA is more likely to be a retrieval deficit than a consolidation failure.

Amnesia, Retrograde↗

PubMedDate not supplied

Reversal of ECS-induced amnesia by post-ECS injections of amphetamine.

Water deprived rats were trained to drink from a water spout within an apparatus on each of 2 days. On the third day, passive avoidance of the spout was induced by giving the animal a 0.3 sec, 5 mA footshock after 1 lick at the spout. A test for retention of the avoidance learning was given 48 hr following training. ECS administered through cortical electrodes at 15 sec following the footshcok impaired retention. The amnesia was attenuated when amphetamine (1 mg/kg) was injected immediately but not at 6 hr following the ECS. In a second experiment, attentuation of amnesia by amphetamine was not found when the ECS occured at 4 sec instead of 15 sec following the footshock. The results are interpreted in terms of reactivation by amphetamine of a consolidation process that was interrupted by ECS.

Amnesia↗

PubMed1976

Cycloheximide-induced amnesia for taste aversion memory in rats.

Male hooded rats were conditioned in one trial to avoid saccharin by pairing saccharin drinking with an intragastric injection of LiC1. A 24 hr water-saccharin preference test showed that conditioned rats exhibited a very low preference for saccharin whereas rats injected intraventricularly with cycloheximide (CXM, 400 mug) 5, 7, or 9 hr before training exhibited a greatly increased saccharin preference which differed significantly from NaC1 injected controls. This 24 hr amnesia was found to be dependent upon the time of administration of CXM, since injection at 1, 3 or 17 hr before training did not confer amnesia. The nature of the task, a control measure and a control experiment indicate that the CXM-induced change in saccharin preference at 24 hr is not due to a CXM-induced aversion, nor a loss in drinking ability nor an inability to retrieve information whilst under the influence of CXM.

Amnesia↗