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PubMed2005

Transient global amnesia after general anesthesia.

Transient global amnesia (TGA) is an amnestic syndrome, clinically dramatic but benign in nature. The hallmark of TGA is brief inability to form new memories and recall past memories despite otherwise normal neurological function. In a significant number of patients with TGA a stressful precipitating factor can be identified. We report two cases of TGA after uneventful general anesthesia. Anesthesia per se does not appear to be a direct trigger of TGA, as our first patient had a second anesthetic the next day without recurrence of TGA. Because the presentation of TGA can be dramatic and may mimic an acute cerebral ischemic event, a thorough neurologic evaluation should be pursued.

Aged↗
PubMed1998

Effects of paeoniflorin derivatives on scopolamine-induced amnesia using a passive avoidance task in mice; structure-activity relationship.

Paeoniflorin (1) and its derivatives having in common a cage-like pinane skeleton with hemiketal-acetal system, were evaluated for their effects on memory impairment induced by scopolamine in mice using a step-down type passive avoidance task. In the test session, 1 and its derivatives were intraperitoneally (i.p.) administered at doses of 0.002, 0.01, 0.02 and 0.2 mmol/kg, and 30 min later (15 min before the experiment), scopolamine (1 mg/kg, i.p.) was given. These compounds showed dose-dependent attenuation in a dose range of 0.002-0.02 mmol/kg and also enhancement of scopolamine-induced decrease in step-down latency. The effects of these compounds, except that of 2',3',4',5'-O-tetraacetyl-3-O-methylpaeoniflorin (8), followed a bell-shaped dose response profile. 8-Debenzoyl-6-deglucosyl-3-O-methylpaeoniflorin (6) showed no significant increase in the step-down latency at all tested doses. Maximum step-down latency was obtained by 3-O-methylpaeoniflorin (3) and 2',3,3',4',5'-penta-O-methylpaeoniflorin (7) (the minimal effective dose was 0.002 mmol/kg). Relative to 3, debenzoylation, as in 8-debenzoyl-3-O-methylpaeoniflorin (4), slightly increased the latency, while deglucosylation, as in 6-deglucosyl-3-O-methylpaeoniflorin (5), significantly reduced the prolongation of latency. Removal of both glucose and benzoyl moieties resulted in the loss of activity as seen in 6. These results revealed that, in addition to the cage-like pinane skeleton, the benzoyl and the glucosyl moieties are important structural elements of the paeoniflorin skeleton as its effects on scopolamine-induced amnesia.

Amnesia↗
PubMed2001

[Effects of fluvoxamine on both the desired anxiolytic effect and the adverse motor incoordination and amnesia induced by benzodiazepines].

Fluvoxamine, a selective serotonin reuptake inhibitor, is frequently used along with benzodiazepine anxiolytics in clinics. In this study, the effects of fluvoxamine on the anxiolytic effects as well as adverse effects of benzodiazepines were examined in the light/dark box, rota-rod and passive avoidance tests using mice. Diazepam, ethyl loflazepate and its active metabolite, CM7116, were used as benzodiazepine anxiolytics. The anxiolytic effects of diazepam, ethyl loflazepate and CM7116 were potentiated by intraperitoneal treatment with fluvoxamine at 10 mg/kg, whereas only those of ethyl loflazepate were potentiated by fluvoxamine at 45 mg/kg. The motor incoordination and amnesia induced by ethyl loflazepate and CM7116 were not affected by fluvoxamine, although these adverse effects of diazepam were potentiated by fluvoxamine at 45 mg/kg. Fluvoxamine itself showed no effects in any of the tests. These results suggest that low-dose fluvoxamine potentiates the anxiolytic effects of benzodiazepines, while high-dose fluvoxamine augments the adverse effects depending on the benzodiazepine used. Consequently, when fluvoxamine is administered along with benzodiazepines, the doses of both fluvoxamine and benzodiazepines should be carefully chosen to achieve anxiolytic effects without any adverse results.

Amnesia↗
PubMed1992

Protective effect of eurystatins A and B, new prolyl endopeptidase inhibitors, on scopolamine-induced amnesia in rats.

Eurystatins A and B, which are produced by Streptomyces eurythermus R353-21, potently inhibited Flavobacterium prolyl endopeptidase (PED) with IC50 values of 0.004 and 0.002 micrograms/ml, respectively, while no inhibition was observed against another 5 proteases, even at 100 micrograms/ml. The protective effect of eurystatins A and B against scopolamine (3 mg/kg, i.p.)-induced amnesia in rats was evaluated by the step-through one-trial passive avoidance method. When administered i.p. 30 min prior to the acquisition trial, both eurystatins A, at 2-8 mg/kg, and B, at 4-8 mg/kg, significantly protected rats from the amnesic effect of scopolamine without behavioral side effects.

Amino Acid Sequence↗
PubMedDate not supplied

On the role of thalamic pathology in diencephalic amnesia.

Although it is now accepted that medial diencephalic lesions can produce severe amnesia in humans, the specific nuclei and neural pathways that must be damaged to impair memory have not yet been identified. Recent studies have shown that pyrithiamine-induced thiamine deficiency (PTD) in the rat can produce a consistent pattern of pathology in the thalamus and mammillary bodies and result in permanent impairments on behavioral measures of working memory. Behavioral deficits comparable to the PTD model have been observed in rats with thalamic lesions involving lateral portions of the internal medullary lamina (the L-IML site). Such impairments are not observed following lesions of limbic-related pathways associated with the fornix, mammillary bodies, or midline thalamus. The L-IML lesion affects the mediodorsal nucleus (MDn) and both the intralaminar and paralaminar non-specific thalamic nuclei. The relationship between the non-specific thalamic nuclei and working memory is underscored by the limited behavioral effects of MDn lesions, as compared to either L-IML or PTD-induced lesions, and by anatomical analyses of PTD-related pathology, which seems to destroy the non-specific nuclei while sparing large portions of the MDn. Recent physiological studies of thalamocortical processes suggest that there are several possible mechanisms by which the non-specific nuclei might participate in memory and by which lesions in these pathways might interfere with the consolidation of memories within the cortex.

Amnesia↗
PubMed2006

Noradrenergic control of emotion-induced amnesia and hypermnesia.

Emotional memory encoding is associated with retrograde and anterograde episodic memory changes involving amnesia and hypermnesia, respectively. These effects are noradrenergic-dependent and reflect an interaction with emotional arousal and valence. Whereas anterograde amnesic effects most likely result from attentional capture by emotional arousal, retrograde amnesic and hypermnesic effects may reflect a valence-dependent filter mechanism that operates during emotional memory encoding and controls episodic memory access based upon behavioral significance. This filter mechanism may originnate in amygdala-hippocampal interactions that are modulated by both ascending locus coeruleus and descending prefrontal cortex inputs.

Amnesia↗
PubMed1985

[Transient global amnesia: study of 26 cases].

The clinical picture and investigation of 26 patients (16 males and 10 females) with diagnosis of transient global amnesia (TGA) are reported. Age ranged from 51 to 78 years at the time of TGA, which occurred mor often between 60 and 70 year-old people. Three patients presented more than one episode (3, 4 and 5). Precipitating factors were identified in 8 cases (emotional stress in 7 and physical exercise in 1). Risk factors for cerebrovascular disease were found in 13 cases, mainly hypertension (9 cases) and diabetes (3 cases). EEG was normal in 20 cases and disclosed diffuse delta waves in 2, temporal delta waves in 1 and temporal theta waves in another patient. CAT scan showed no abnormalities in 3 cases and ischemia in the vertebro-basilar system in another 2. Brain angiography was normal in 1 case and showed abnormalities in the vertebro-basilar system arteries in 3. During the follow-up period, which ranged from 1 to 84 months, no neurologic deterioration was seen. The role of risk factors for vascular diseases, epilepsy and migraine in the development of TGA is discussed.

Aged↗
PubMed2001

Neurosyphilis showing transient global amnesia-like attacks and magnetic resonance imaging abnormalities mainly in the limbic system.

We report a case of neurosyphilis with transient global amnesia (TGA)-like attacks on the first presentation. MRI abnormalities in bilateral limbic systems, including a few lesions in the basal ganglia and thalamus, were identified. Depression and dementia became apparent, accompanied by a high treponemal antibody titer and mild cortical atrophy. Antisyphilitic therapy brought about mild improvement, and the MRI abnormalities decreased.

Adult↗
PubMed2005

A patient of migraine-like headache with amnesia, pleocytosis and transient hypoperfusion of cerebral blood flow.

Pseudomigraine with pleocytosis (PMP) is an uncommon disease in Japan. The diagnostic criteria include at least one episode of transient neurological deficit accompanied or followed by migraine-like severe headache, cerebrospinal fluid (CSF) lymphocytosis, and normal neuroimaging. Both the etiology and the pathophysiology of PMP is not yet well defined. We report a 40-year-old man with a PMP-like syndrome. He came to our clinic because of severe throbbing headache and amnesia, and the examination showed CSF lymphocytosis of 23/mm3, a transient decrease of cerebral blood flow in the left thalamus. All the symptoms were completely resolved within 2 months.

Adult↗
PubMed1997

Pure amnesia caused by bilateral temporal lobe astrocytoma--case report.

A 32-year-old male presented with progressive pure amnesia caused by astrocytoma invading the bilateral medial temporal lobes. Methionine positron emission tomography demonstrated the extent of tumor invasion well. His memory impairment was partially improved by treatment for the astrocytoma. Lesion of the bilateral hippocampus causes memory impairment, but pure memory loss without other associated neurological sign or deterioration of consciousness is rare in a case of cerebral neoplasm.

Adult↗
PubMed1993

Intensity of amnesia during hypnosis is positively correlated with estimated prevalence of sexual abuse and alien abductions: implications for the false memory syndrome.

20 normal young women listened to an ambiguous story concerning a young boy who experienced fear, odd smells, and a smothering sensation during the night and skin lesions the next morning. After the Hypnotic Induction Profile (HIP) had been established, they were asked to estimate either the percentage prevalence of childhood sexual abuse or alien abduction in the general population. There were moderate (0.50) positive correlations between the subjects' estimates of prevalence and the amount of amnesia ("lost time") and indices of right-hemispheric anomalies (history of sensed presence and left-ear suppressions during a dichotic-listening task). Relevance of observations to formation of the False Memory Syndrome and to the development of nonpsychotic delusions is discussed.

Adolescent↗
PubMed1992

Triazolam-induced nocturnal bingeing with amnesia.

A combination of behavioural and cognitive adverse effects is illustrated in this case report of a recurrent triazolam-induced eating disorder. The co-occurrence of bingeing, irritability and anterograde amnesia is suggestive of a drug-induced Kleine-Levin Syndrome.

Amnesia↗
PubMed2001

Continuing cognitive impairment after isolated transient global amnesia.

Fourteen patients were investigated 3-4 days after end of their transient global amnesia (TGA) with a number of neuropsychological tests. Their performance was compared with that of a control group, matched for age, education, and profession. It was found that in spite of the common definition of TGA, impairments in both verbal and non-verbal long term memory and verbal fluency persisted and were in fact impaired to such a degree that it seemed unlikely that full recovery would have occurred within the next few days. We propose a major role of stress in the etiology and the recovery process of TGA and consider it likely that stress hormones are of major influence both in the triggering of TGA and the subsequent continuation of cognitive impairments.

Aged↗
PubMedDate not supplied

Predicting clearing of post-traumatic amnesia following closed-head injury.

The ability to predict the resolution of post-traumatic amnesia (PTA) early in the course of acute rehabilitation was studied in a sample of 98 closed-head injury (CHI) patients admitted for acute rehabilitation. The subjects' age, length of coma, time post-injury and Orientation Group Monitoring System (OGMS) subscale and aggregate scores were evaluated for the ability to predict if and when a patient would clear PTA. The results indicated that the combination of time post-injury and week one OGMS aggregate score provided the best prediction of whether and when PTA would clear. A shorter time from injury to acute rehabilitation was a positive prognostic indicator, accounting for more variance than either age or duration of coma. Whereas the aggregate OGMS score was a better indicator than any of the subscale scores, the results also suggested that specific aspects of cognition have differential predictive power, which may derive from different types of injury to the brain. Although the prediction model was statistically significant, its practical significance was limited. In particular, the high base rate for clearing PTA, 83.7%, attenuated the potential for differential prediction. Finally, this study provided additional support for the construct validity of the OGMS as a measure of cognitive function during the acute phase of recovery from CHI.

Adolescent↗
PubMedDate not supplied

Post-traumatic amnesia and Glasgow Coma Scale related to outcome in survivors in a consecutive series of patients with severe closed-head injury.

A consecutive series of 93 severe closed-head injury (SCHI) patients, discharged from hospital in a conscious state, were rated on the Glasgow Outcome Scale at 6 and 12 months post-injury. Patients were included in this study if they had a period of post-traumatic amnesia (PTA) exceeding 24 h. Approximately 80% of patients had made a good recovery by 12 months post-injury; a better outcome than has been found in studies using the presence of coma during the first 6 h post-admission to hospital to define severe head injury. When analysed individually, duration of PTA and Glasgow Coma Scale scores on admission to hospital were both strongly correlated with outcome. Only duration of PTA, however, contributed significantly to outcome variance when potential outcome predictors were assessed using a stepwise multiple regression analysis. The definition of severe head injury, the higher than usual incidence of good recovery in the present study, and the relationship between injury severity and outcome are discussed.

Adolescent↗
PubMedDate not supplied

Measuring post-traumatic amnesia (PTA): an historical review.

The duration of post-traumatic amnesia (PTA), which is the period following brain injury when patients are disoriented and impaired in the acquisition of new information, has been used as a behavioural indicator of the severity of injury. This paper reviews earlier retrospective and more recently developed prospective methods of assessing the duration of PTA. Prospective assessment that commences before the resolution of PTA overcomes the possible over- or underestimation of the duration of PTA inherent in methods that assess PTA retrospectively by clinical interview.

Amnesia↗
PubMedDate not supplied

Post-coma disturbance and post-traumatic amnesia as nonlinear predictors of cognitive outcome following severe closed head injury: findings from the Westmead Head Injury Project.

This study sought to identify combinations of early neurological variables which best predict cognitive outcome 12 months after severe head injury. At the time of admission patients were assessed on seven neurological indices. Twelve months later a battery of neuropsychological tests examining recent memory functioning and speed of information processing was administered. Recent memory functioning was best predicted by a combination of post-coma disturbance (PCD; i.e. the duration of post-traumatic amnesia, PTA, minus the duration of coma) and presence of subarachnoid haemorrhage (multiple r = 0.54, p < 0.001). Speed of information processing was best predicted by the duration of PTA (r = 0.35, p < 0.01). However, these conclusions were based on square root transformation of PCD and PTA variables. The success of this transformation in assisting prediction confirms suggestions that the relationship between PTA and cognitive outcome is nonlinear.

Adolescent↗
PubMedDate not supplied

The Children's Orientation and Amnesia Test: educational status is a moderator variable in tracking recovery from TBI.

The Children's Orientation and Amnesia Test (COAT) is an objective, standardized means of assessing cognitive functioning in children and adolescents who are in the early stages of recovery from traumatic brain injury. The COAT is composed of 16 items that assess general orientation, temporal orientation, and memory. This study was designed to determine if children who are receiving special education services perform more poorly on the COAT than children who are in the regular classroom. It was found that children receiving special services performed significantly more poorly, and 13% of them were classified in the impaired range, as compared to 3% of the students in the regular classroom. The results provide important reference data for interpreting COAT scores of children with traumatic brain injuries who have either premorbid learning disabilities or other special service needs.

Adolescent↗