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INTRODUCTION: Global amnesia (AG) is a dysfunction of memory, in which there is a sudden incapacity to remember recent events and assimilate new information. The aetiology is currently under discussion. The main hypotheses under consideration are an ischemic mechanism and an epileptic mechanism. OBJECTIVE: To study the cerebral blood flow in patients with temporary global amnesia (AGT) or permanent global amnesia (AGP) using functional neuroimaging techniques. MATERIAL AND METHODS: Four patients were studied. Two had severe alterations of fixation memory which had been present for months. The other two had a sudden loss of recent memory, although space-person orientation and immediate memory remained normal. In all cases the cerebral blood flow (FSC), was assessed by single photon emission tomography (SPECT), using Tc-HMPAO as the radio tracer. RESULTS: We describe 4 patients, 2 men and 2 women aged between 42 and 64.2 with AGT and the others with AGP. On SPECT there was temporal hypoperfusion in all 4 patients. In 2 cases there was associated parietal hypoperfusion and in 1 case there was frontal hypoperfusion. CONCLUSIONS: These findings suggest that AGT and AGP are of vascular origin and that SPECT is a useful diagnostic technique in patients with AG.
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In this article we review the existing evidence on the memory impact of age EEG oscillations discharges. Original developmental equation provides reliable descriptors of brain electrical activity in people 21 to 83 years old. The magnitude of the deviations increases with clinical severity. Different levels of neurological manifestations are characterized by distinctive profiles of recognized pathological values of brain electrical features. Computerized personality profile of some of these levels can be achieved with high accuracy. Such classification, providing objective markers of cerebrovascular brain dysfunctions, may be a useful adjunct to differential diagnosis, which relies primarily on subjective clinical impressions.
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The hypothesis that neurotoxins may play a role in neurodegenerative disorders remains an elusive one, given that epidemiologic studies often provide conflicting results. Although these conflicting results may result from methodological differences within and between studies, the complexity of chemical disruption of the central nervous system cannot be ignored in attempts to evaluate this hypothesis in different neurodegenerative disorders. Spencer provides a detailed review of the complex processes involved in defining the neurotoxic potential of naturally occurring and synthetic agents. Even concepts such as exposure and dose, as often reported in studies attempting to evaluate the risk imparted by a potential compound, can be deceptive. For example, although dose reflects "that amount of chemical transferred to the exposed subject", factors such as time and concentration in the organism, the ability to access the central nervous system, and how a compound reaches the central nervous system (routes of administration) or secondarily affects other organ systems leading to central nervous system disruption are clearly important to the concept of neurotoxic risk in neurodegenerative disorders. These factors would appear to explain the observed disagreements between studies using animal or neuronal models of neurotoxicity and population-based studies in humans. The importance of these factors and how a potential neurotoxin is investigated are clearly seen in the data on AD and aluminum. In contrast, the impact of MTPT on the central nervous system is more direct and compelling. Added complexity in the study of neurotoxins in human neurodegeneration is derived from data showing that agents may have additive, potentiating, synergistic, or antagonistic effects. Therefore, data from studies evaluating EMF risks could be readily confounded by the presence or absence of heavy metals (eg, arc welding). Other factors that may conceal neurotoxic causes for a given disorder focus on additional features such as genetic predispositions, physiologic changes that occur in aging, and even nutritional status that can support or hinder the affect of a given agent on the central nervous system. Finally, many studies that investigate exposure risk do not readily incorporate the five criteria proposed by Schaumburg for establishing causation. For example, if we apply Schaumburg's first criterion, epidemiologic studies often determines the presence of an agent through history, yet they cannot readily confirm exposure based on environmental or clinical chemical analyses to fulfill this criterion for causation. Additional limitations in research design along with the populations and methods that are sued to study neurotoxins in human neurodegenerative disorders often fail to meet other criteria such as linking the severity and onset with duration and exposure level. Therefore, although studies of agents such as MTPT provide compelling models of neurotoxins and neurodegeneration in humans, disorders such as ALS, PD, and particularly AD will require additional effort if research is to determine the contribution (presence or absence) of neurotoxins to these neurologic disorders.
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Magnetic resonance based volumetric measures of hippocampal formation, amygdala (A), caudate nucleus (CN), normalised for total intracranial volume (TIV), were analysed in relation to measures of cognitive deterioration and specific features of memory functions in 18 patients with probable Alzheimer's disease. Neuropsychological examination included the mini mental state examination (MMSE), the Mattis dementia rating scale (DRS), tests of executive functions, assessment of language abilities and praxis, the Wechsler memory scale (WMS), the California verbal learning test (CVLT) and the Grober and Buschke test. The volume of the hippocampal formation (HF/TIV) was correlated with specific memory variables: memory quotient and paired associates of the WMS; intrusions and discriminability at recognition for the Grober and Buschke test. By contrast, except for intrusions, no correlations were found between memory variables and the volume of amygdala (A/TIV). No correlations were found between the volume of caudate nuclei (CN/TIV) and any neuropsychological score. The volume of the hippocampal formation was therefore selectively related to quantitative and qualitative aspects of memory performance in patients with probable Alzheimer's disease.
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INTRODUCTION: For the past few years, in the field of psychiatric disorders, measurements of subjective quality of life are integrated as an important criterion of judgment. The use of standardized questionnaires, based on the patients point of view has become widespread. However, in schizophrenic patients, cognitive impairement, and notably memory, is often advanced as a limit to the use of the self-reported questionnaires. METHODS: In this preliminary study, we investigated in 53 schizophrenic patients, the impact of memory impairment, specifically the episodic memory, on quality of life, taking into account confounding socio-demographic and clinical factors. The memory was assessed using the BEM 84. The patient's subjective quality of life was assessed by the self-reported questionnaire S-QoL. RESULTS: No correlation was found between memory efficiency and quality of life level: patients with severe and non-severe impairment scored all the S-QoL domains similarly. DISCUSSION: However, the majority of schizophrenic patients could be considered as deficient on a wide assortment of neuropsychological evaluations, in particular in the attention and executive functions. The influence of the whole cognitive impairment of life must be confirmed.