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PubMed2006

Reconsolidation and extinction of conditioned fear: inhibition and potentiation.

NMDA receptors are important for the acquisition, reconsolidation, and extinction of memories. NMDA receptor antagonists impair these memory processes, whereas the partial agonist D-cycloserine (DCS) potentiates both learning and extinction. Here, we used DCS and the noncompetitive NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-SH-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) to investigate the effects of enhancing and blocking NMDA receptor-mediated glutamatergic transmission on the reconsolidation and extinction of a conditioned fear memory. Either long extinction training or short memory reactivation sessions were used to preferentially engage extinction and reconsolidation processes, respectively. MK-801 blocked extinction to maintain high levels of conditioned freezing, and DCS potentiated extinction to reduce freezing, when they were administered before a long extinction training session. However, the opposite behavioral outcome was observed when the brief memory reactivation session was used: MK-801 administration impaired, whereas DCS increased, freezing, likely reflecting impairment and enhancement of reconsolidation, respectively. Finally, by using localized intracerebral infusions, we showed that the basolateral amygdala is a primary locus of action of systemically administered DCS. Thus, intrabasolateral amygdala DCS potentiated both the extinction and the reconsolidation of fear conditioning, depending on the length of the extinction/memory reactivation session. Therefore, memory reconsolidation can be both disrupted and enhanced, and extinction can be both potentiated and impaired, either to reduce or increase conditioned fear. These results have important implications for the use of reconsolidation blockade and potentiation of extinction as treatment strategies for maladaptive memory disorders.

Acoustic Stimulation↗
PubMed1985

Vasopressin: site of behavioral action and role in human mental performance.

Diminishment of endogenous vasopressin in various brain areas (dorsal and ventral hippocampus, dorsal septum) by local application of diluted anti-vasopressin serum results in attenuation of passive avoidance behavior of rats. Both post-learning or pre-retention treatment results in impaired behavior when the anti-vasopressin serum was applied in the dorsal or ventral hippocampus, whereas only pre-retention but not post-learning application of the antiserum in the dorsal septum induced behavioral impairment. Only injection of less diluted antiserum into the lateral ventricle results in attenuation of passive avoidance behavior. These results suggest that endogenous vasopressin present in these brain sites plays a functional role in brain processes related to memory and in particular in processes involved in storage and/or retrieval of information. These findings are discussed and compared with observations of vasopressin treatment on memory functions in man. The observation that some patients with memory disorders do not respond to vasopressin treatment may be due to lesions in the anatomical sites of action of vasopressin.

Animals↗
PubMed1988

The alpha-2 adrenergic agonist guanfacine improves memory in aged monkeys without sedative or hypotensive side effects: evidence for alpha-2 receptor subtypes.

The present study attempted to identify an alpha-2 agonist that could improve working memory in aged nonhuman primates without the marked hypotensive and sedative side effects produced by clonidine. Toward this end, the hypotensive, sedative, and memory-altering properties of the alpha-2 adrenergic agonists, B-HT920 and guanfacine, were compared with clonidine's effects in 9 aged rhesus monkeys. Memory capacity was assessed by a variable delay, spatial delayed response paradigm that requires the animal to remember information over short temporal intervals and to update this information on every trial. B-HT920 was found to produce a dose-response profile qualitatively similar to, but weaker than, clonidine: low doses impaired memory and began to lower blood pressure and produce sedation, while high doses improved memory. In contrast, guanfacine produced a dose-response profile opposite to that seen with clonidine: low doses improved memory without inducing hypotension or sedation, while the memory-impairing, hypotensive, and sedating properties of the drug were observed at higher doses. The potency of the 3 agonists to lower blood pressure was clonidine = B-HT920 greater than guanfacine; sedation was affected in the order clonidine greater than B-HT920 greater than guanfacine; for memory impairment, as measured by performance on the delayed response task, the rank order potency was clonidine greater than B-HT920 greater than guanfacine, while for memory improvement it was guanfacine greater than clonidine greater than B-HT920. These differences in rank order potency are consistent with the recent proposal of alpha-2 receptor subtypes, a rauwolscine-sensitive site (Rs) that binds clonidine greater than B-HT920 greater than guanfacine and a rauwolscine-insensitive site (Ri) that binds guanfacine greater than clonidine greater than B-HT920 (Boyajian and Leslie, 1987). The data suggest that the hypotensive, sedating, and memory-impairing effects of alpha-2 agonists may be due to actions at one subtype of receptor (Rs), while the memory-enhancing effects of these drugs may result from actions at another alpha-2 receptor subtype, the Ri site. The ability of low doses of guanfacine to improve memory without inducing hypotension or sedation indicates that this agonist may be an excellent candidate for treating memory disorders in man.

Adrenergic alpha-Agonists↗
PubMed1987

Bilateral paramedian thalamic artery infarcts: report of eight cases.

Eight consecutive patients with CT scan evidence of a bilateral infarct in the territory of the paramedian thalamic artery are reported. In seven cases the infarct also extended to the territory of the polar artery. The main symptoms were: disorder of vigilance which cleared in a few days, and hypersomnolence which lasted longer and in two patients was still present a year later; amnesia, detectable clinically in four patients and only with tests in two patients, which persisted in one patient for three years; changes of mood and bulimia present in five and four patients respectively; and vertical gaze paresis in five patients. Only one patient died, and in the remainder the symptoms tended to subside, but none of the patients who could be followed-up for a year returned to normal behaviour. Clinical and CT scan correlations pointed to the mammillo-thalamic tract as the structure whose damage was responsible for the memory disorders.

Adult↗
PubMedDate not supplied

Measures of visuospatial short-term memory: the Knox Cube Imitation Test and the Corsi Blocks Test compared.

The present investigation analyzes the characteristics of two tasks that have been considered as a measure of visuospatial abilities: The Knox Cube Imitation Test and the Corsi Blocks Test. The former was originally devised by Knox (1913) to diagnose mental retardation in potential immigrants to the United States, while the latter has been specifically designed to be used in neuropsychological practice by Corsi (1972). Although both tasks have been widely used in the past, there is little empirical research investigating the characteristics of these tasks from a theoretical point of view. In order to do so, we carried out two parallel experiments in which both tasks were presented in a baseline condition as well as in association with three different concurrent tasks (i.e., articulatory suppression, spatial tapping, and random generation) supposed to tap the various components of working memory. Results showed that neither of the tasks can be considered as a pure measure of visuospatial processing and that, at the same time, it is necessary to reconsider the architecture of working memory in order to suggest a more integrated functioning of the system.

Adolescent↗
PubMed2002

Verbal short-term memory in Down syndrome: a problem of memory, audition, or speech?

The current study explored three possible explanations of poor verbal short-term memory performance among individuals with Down syndrome in an attempt to determine whether the condition is associated with a fundamental verbal short-term memory deficit. The short-term memory performance of a group of 19 children and young adults with Down syndrome was contrasted with that of two control groups matched for level of receptive vocabulary. The specificity of a deficit was assessed by comparing memory for verbal and visuo-spatial information. The effect of auditory problems on performance was examined by contrasting memory for auditorily presented material with that for material presented both auditorily and visually. The influence of speech-motor difficulties was investigated by employing both a traditional recall procedure and a serial recognition procedure that reduced spoken response demands. Results confirmed that individuals with Down syndrome do show impaired verbal short-term memory performance for their level of receptive vocabulary. The findings also indicated that this deficit is specific to memory for verbal information and is not primarily caused by auditory or speech-production difficulties.

Adolescent↗
PubMed1986

[Effect of S-adenosyl-L-methionine (SAMe) on disturbances in hand movement and delayed response tasks after lesion of motor or prefrontal cortex in the monkey].

Effects of SAMe on disturbances in trained hand movement tasks or a trained delayed response task after lesion in unilateral motor cortex (hand area) or bilateral dorsolateral prefrontal cortices were studied in the monkey. Following lesion, hand movement tasks or delayed response tasks were disturbed moderately or severely for one week to several months depending on the extent of lesion or nature of task. Although treatment with small doses of SAMe (10 mg/kg/day, i.m.) had no effect, treatment with moderate doses (SAMe, 20 or 30 mg/kg, i.m.) reduced impairment and promoted recovery from both disturbances. Even in the chronic stage (76-140 days after operation), SAMe (30 mg/kg/day, i.m.) facilitated recovery from delayed response deficits. Histological findings in the acute stage after cortical lesion in rats showed that SAMe (50 mg/kg/day, s.c.) augmented infiltration of activated phagocytic macrophages in lesioned sites. Data suggest that SAMe improves recovery from behavioral and histological disturbances due to brain damages.

Animals↗
PubMed1995

[Familial posterior cortical atrophy with visual agnosia and Bálint's syndrome].

We report a patient of posterior cortical atrophy with progressive visual agnosia, Bálint's syndrome and dementia in which posterior cortical atrophy with similar characteristics on CT and progressive dementia were found in a sister. The patient was a 75-year-old woman who noted the onset of a progressive visual disorder at the age of 70, and whose family first noticed disoriented behavior at around the same period. Ophthalmologic examinations revealed mild cataract but no evidence of peripheral optic nerve or retinal lesions. Neuropsychological examination showed right homonymous hemianopia, visual agnosia, Bálint's syndrome, mild transcortical sensory aphasia, Gerstmann's syndrome, constructional apraxia, mild ideomotor apraxia and memory disorder. MRI showed marked dilatation of both lateral ventricles, especially the posterior horns, and severe atrophy of the occipital lobes, hippocampus, and the parahippocampal gyrus. Assessment of regional cerebral blood flow by IMP-SPECT revealed a generalized decrease in the temporo-parieto-occipital region bilaterally. The patient's sister began to show evidence of progressive dementia at 80 years of age and CT of the brain revealed marked atrophy, predominantly in the occipital lobes, similar to that of the patient. We believe this to be the first report of posterior cortical atrophy with a positive family history, suggesting the possibility of a hereditary syndrome.

Aged↗
PubMed2002

[Mild Cognitive Impairment or pre-demential Alzheimer's disease?].

The concept of Mild Cognitive Impairment (MCI) is proposed to define a state of cognition where the deficiency is greater than expected for a subject's age and socio-cultural background, but not sufficiently severe to satisfy the criteria of nosographic classifications of dementia. The concept of MCI cannot provide an etiological diagnosis but can be useful for recognizing and following patients with mild impairment. It raises the question of early diagnosis of Alzheimer's disease. The risk of progression to dementia is greater in patients with MCI, particularly those whose memory is the only domain involved - "amnesic MCI". Patients with amnesic MCI can be distinguished from those with MCI with multiple domains slightly impaired or non-amnesic MCI where only one domain (language, visual-spatial.) other than memory is involved. Depending on the type of deficiency, amnesic MCI may progress to different types of disease states. At the early stage of pure memory impairment, a distinction should be made between Alzheimer-related memory disorders and those related to another neurological conditions or the brain aging process. The question is whether the diagnosis of Alzheimer's disease can be made at this stage. Biological markers and brain imaging provide useful information, but these diagnostic tools remain imprecise and have not been validated for routine use. The process of diagnosis must therefore focus on an analysis of the cognitive impairment. The predementia phase of Alzheimer's disease is characterized by a progressive "hippocampal" decline in memory, sometimes associated with impaired execution. A careful analysis of the cognitive impairment helps identify "hippocampal amnesia syndrome" suggestive of the diagnosis of Alzheimer's disease.

Aged↗
PubMed1996

Amnesia in acute herpetic and nonherpetic encephalitis.

OBJECTIVES: To evaluate how often global amnesia syndrome is encountered as a sequel of herpes simplex virus type 1 encephalitis (HSVE) and in other types of acute encephalitides, and to evaluate whether there are qualitative differences in amnesia caused by different encephalitides. SUBJECTS: Forty-five consecutive patients with encephalitis (mean age, 40.8 years) studied prospectively within a 5-year period, 8 of whom had HSVE. There were 24 normal controls. MEASURES: Neuropsychological assessment and memory evaluation after the acute stage of encephalitis, as well as at follow-up after 27.7 +/- 18.6 months. RESULTS: Three patients (6%), including 1 with HSVE, had persistent anterc grade and retrograde memory defects, typical features of global amnesia. Twelve patients had anterograde amnesia in the first assessment. No statistically significant differences in the memory measures were found between the HSVE (n = 4) and the non-HSVE (n = 8) groups. Some patients had predominantly semantic difficulty, some had a "frontal-type" memory disorder, and in some patients rapid forgetting was the prominent feature. CONCLUSIONS: The frequency of amnesia can reliably be evaluated only in consecutive series of patients. Previous literature, mainly case reports, may give the impression that global amnesia is a common consequence of encephalitis. Our findings do not support that view. Furthermore, there are clear differences in the quality of the memory impairment between cases of acute encephalitides. Our findings suggest that amnesia as a consequence of encephalitis, even HSVE, should not be considered a uniform phenomenon.

Acute Disease↗
PubMed1996

Failure to recall (but not to remember): pure transient amnesia during nonconvulsive status epilepticus.

We report a patient with a generalized frontal-predominant nonconvulsive status epilepticus without clinically apparent altered consciousness. The patient was examined and EEG performed during and after the episode. Severe retrograde and anterograde amnesia during the seizure, contrasting with a preservation of ongoing memories formation that could be assessed only after its resolution, suggests a transient disconnection of access to stored representations. This unusual memory disorder is both clinically and electrographically dissimilar to other reported cases of transient epileptic amnesia. Although the patient probably had numerous episodes previously, there was no history of overt seizure.

Adult↗
PubMed2005

Allocentric and egocentric spatial impairments in a case of topographical disorientation.

We describe a patient with a topographical disorientation after a stroke of the right mediotemporooccipital lobe including the parahippocampal cortex (PHC). Clinical observations and neuropsychological testing reveal an impairment of allocentric spatial representations as well as impairments of visuospatial learning and memory. These findings are in accordance with the well-known function of the PHC in topographical disorientation. As a new finding, results from oculomotor tasks show additional impairments of the egocentric spatial coordinate frame suggesting that in topographical disorientation due to a lesion of the right mediotemporooccipital lobe not only allocentric but also egocentric visuospatial functions are disturbed.

Aged↗
PubMed1993

Psychomimetic reactions after neurolept and propofol anaesthesia.

The purpose of this study was to compare the frequency of psychomimetic reactions after 24 h and 3 months following total intravenous anaesthesia with propofol and neurolept anaesthesia. Forty otherwise healthy female patients were randomly divided into two groups. All were undergoing elective gynaecological laparotomy for non-malignant disease. Nineteen patients were anaesthetized with droperidol, fentanyl, pancuronium, N2O/O2. Twenty patients received total intravenous anaesthesia with propofol, fentanyl and pancuronium. Twenty-four hours after the anaesthesia the patients were interviewed about their subjective experiences of anaesthesia and recovery. Three months after the operation the patients were sent a questionnaire concerning ability to work, sleep and memory disorders. After 24 h the anaesthesia was judged as good by 18 patients receiving propofol and 13 patients receiving NLA (n.s.). The recovery was judged as good by 16 patients in the propofol group and six patients in the NLA group (P < 0.05). Locked-in feelings were reported by one patient in the propofol group and ten patients in the NLA group (P < 0.01). Impairment of memory was reported by one patient in the propofol group and seven patients in the NLA group (P < 0.01). A questionnaire used after 3 months was answered by 18 patients in the propofol group and 17 patients in the NLA group. There were few complaints, and no differences were found between the two groups. In conclusion, total intravenous anaesthesia with propofol seems more acceptable than anaesthesia with neurolept as judged by the patients 24 h after anaesthesia. There were no differences between the two groups concerning psychomimetic reactions 3 months after anaesthesia.

Adult↗
PubMed2006

Intranasal insulin improves memory in humans: superiority of insulin aspart.

There is compelling evidence that intranasal administration of regular human insulin (RH-I) improves memory in humans. Owing to the reduced tendency of its molecules to form hexamers, the rapid-acting insulin analog insulin aspart (ASP-I) is more rapidly absorbed than RH-I after subcutaneous administration. Since after intranasal insulin administration, ASP-I may also be expected to access the brain, we examined whether intranasal ASP-I has stronger beneficial effects on declarative memory than RH-I in humans. Acute (40 IU) and long-term (4 x 40 IU/day over 8 weeks) effects of intranasally administered ASP-I, RH-I, and placebo on declarative memory (word lists) were assessed in 36 healthy men in a between-subject design. Plasma insulin and glucose levels were not affected. After 8 weeks of treatment, however, word list recall was improved compared to placebo in both the ASP-I (p<0.01) and the RH-I groups (p<0.05). ASP-I-treated subjects performed even better than those of the RH-I-treated group (p<0.05). Our results indicate that insulin-induced memory improvement can be enhanced by using ASP-I. This finding may be especially relevant for a potential clinical administration of intranasal insulin in the treatment of memory disorders like Alzheimer's disease.

Administration, Intranasal↗