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PubMed2003

Transient partial amnesia complicating cardiac and peripheral arteriography with nonionic contrast medium.

The aim of this study was to present a case of disruption of the blood-brain barrier during the coronary and lower extremity angiographies with radiological and clinical findings. This condition was secondary to intraarterial use of a nonionic, monomeric contrast medium. A total of 450 cc contrast media was used. Computed tomography examination showed contrast enhancement of the right occipital and frontoparietal cortical regions, which returned to normal one day after. The patient also fully recovered from the neurological symptoms within 24 h. We discussed the possible mechanism for blood-brain barrier disruption in this case.

Amnesia↗
PubMed2003

Preserved memory traces within diencephalic amnesia.

A male patient with bilateral thalamic lesions (medio-ventral nuclei) was investigated. Despite explicit memory impairments his lexical ability was normal. We recorded magnetic field changes (magnetoencephalography, MEG) during the performance of an animate/inanimate discrimination task in which some words where repeated after long delays. Normally, repeated items are classified significantly faster than their first presentations which is accomplished by an unconscious process called priming. The patient did not show any behavioural evidence of priming but the physiological data indicated preservation of this robust form of memory. Brain activation associated with repetitions was attenuated at early stages. The activity difference was posteriorly distributed which is consistent with previous reports about repetition priming. The present study indicated that the bilateral thalamic lesions of our patient disconnected the information processing stream between the primed information and the behavioural response.

Amnesia↗
PubMed1987

Reversal of scopolamine-induced amnesia and alterations in energy metabolism by the nootropic piracetam: implications regarding identification of brain structures involved in consolidation of memory traces.

Pretreatment with scopolamine, 3 mg/kg, prevented the acquisition of a passive avoidance task in rats. These amnesic effects of scopolamine could largely be overcome by treatment with 100 mg/kg of the nootropic drug piracetam. In order to identify the brain structures involved, the effects of these drugs on regional energy metabolism were measured throughout the brain, utilizing Sokoloff's 2-deoxyglucose autoradiographic procedures. Scopolamine, 3 mg/kg, reduced glucose utilization in several areas of the cerebral cortex. These effects were largest in the parietal and temporal cortices. Other areas affected included the sensorimotor and cingulate cortices, the ventral and lateral thalamus, and the dendritic neuropil of the CA1, CA2, and CA3 regions of the hippocampus. The regional depressions in glucose metabolism observed following scopolamine treatment in the rat had some resemblance to depressions in glucose metabolism reported for Alzheimer's disease patients in positron emission tomography studies. Piracetam, 100 mg/kg, did not alter the energy metabolism of any of the 41 brain regions examined. However, this dose of piracetam completely reversed the scopolamine-induced depressions in the hippocampus. Piracetam partially but significantly reversed the scopolamine effects in the cingulate cortex. It is concluded that the data provide support for the hippocampal-cholinergic theory of memory as originally formulated by Meyers and Domino in 1964 and give insight into the mechanisms by which nootropics work.

Amnesia↗
PubMed1988

Diencephalic amnesia: a reorientation towards tracts?

The principal thalamic and hypothalamic structures implicated in mnemonic information processing are the mediodorsal nucleus of the thalamus, the pulvinar, anterior thalamus, and laterodorsal nucleus, the mamillary body, and the mamillothalamic tract and internal medullary lamina. Determining the contribution of an individual region in memory is quite difficult as it is nearly impossible to find a circumscribed damage of only one region. On the contrary, some illnesses affecting primarily the diencephalon, such as Korsakoff's disease, tend to involve several structures together. Furthermore, even when cases with similar circumscribed diencephalic damage can be found, these will not necessarily demonstrate the same outcome on the behavioral level. Therefore, the role or contribution of individual memory-related diencephalic structures has to be inferred by comparing a number of cases and by then extracting distinct features common to a given group. Such an approach revealed that the contributions of the two fiber systems mentioned above, mamillothalamic tract and internal medullary lamina, might be more important in processing information long-term than had been acknowledged previously and might be more important than that of the nuclear masses mentioned, especially of the mediodorsal thalamus. This outcome underlines the view that emphasizing interactions between brain regions rather than single static masses will provide a more realistic picture of how the nervous system acts in information processing.

Amnesia↗
PubMed1996

Reversion of beta 25-35-amyloid peptide-induced amnesia by NMDA receptor-associated glycine site agonists.

The effects of D-cycloserine (DCS), a N-methyl-D-aspartate receptor-associated glycine site agonist, and milacemide (MIL), a glycine prodrug, were examined on learning impairments induced by administration of beta 25-35-amyloid peptide (3 nmol i.c.v.). Mice were examined for spontaneous alternation and step-down passive avoidance, 7 and 14 days after beta 25-35, respectively. The beta 25-35-induced deficits were reversed by DCS, 1-30 mg/kg i.p., or MIL, 3-100 mg/kg i.p., each drug being ineffective on control mice behaviours. These observations strengthen the therapeutic potential of glycine site agonists against the memory impairments induced by beta-amyloid peptides.

Acetamides↗