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A 31-year old man with chicken-pox encephalitis presented with a cerebellar syndrome and disorders of memory. The latter consisted of severe anterograde amnesia with normal retrograde memory, without confabulation or anosognosia. This suggested that the hippocampus was involved, probably functionally, since the outcome was rapidly favourable and the MRI was normal.
INTRODUCTION: Cerebrovascular disease can cause different memory disorders depending on the area of the brain involved. More specifically, ischemic lesions in the frontal region can be associated to short-term verbal memory disorders. PATIENTS AND METHODS: Two groups of subjects were studied, 10 of whom were patients who presented a frontal cerebral infarction and 10 healthy controls. They were administered a memory task involving word recognition. While they were performing the task the electrical activity of their brains was recorded in order to examine event-related potentials (ERP). RESULTS: The patients' performance of the task was poorer than that of the healthy control subjects. Likewise, while the latter displayed a predominantly frontal distribution of ERPs, in the patients the frontal activity diminished and was seen to be chiefly temporoparietooccipital. CONCLUSIONS: These findings allow important conclusions to be drawn about the characteristics of the memory disorder presented by these patients.
Despite increasing research into the severe effects of childhood memory disorders, there is currently a paucity of evidence available to inform the design of appropriate rehabilitation strategies. Indeed, within the paediatric literature there is no model that links specific memory disorders with hypotheses for appropriate rehabilitation strategies. This paper introduces a series of intervention hypotheses based on an examination of the strengths and weaknesses associated with each type of childhood memory disorder, including short-term phonological, visuo-spatial, central executive and long-term semantic and episodic memory. Guidance is provided for integrating the hypotheses within practical rehabilitation strategies and case studies are described to examine a number of the hypotheses.
The impact of advanced brain imaging procedures in the field of human memory disorder is reviewed, with particular emphasis on current and potential applications that may impact upon the diagnosis and management of memory-disordered patients. While both advanced structural, resting physiological and functional physiological brain imaging procedures have been applied to conditions where memory disorder is a major feature, the specific implications of research findings for diagnosis and treatment in routine clinical practice remain tentative and promising, but not yet substantive enough to inform clinical decisions to a significant degree. In terms of diagnostic applications, several promising areas include dementia, epilepsy, and transient amnesic states. In the case of applications in treatment settings, advanced brain imaging procedures may help to monitor neural correlates of spontaneous recovery or progression of memory function, and may also help in the planning and monitoring of therapeutic intervention.
Brain lesions cause memory to break down in several distinct ways in people. First, cortical lesions cause disturbances in short-term memory. Second, other cortical lesions disturb the retrieval of previously well-established semantic and episodic memories. Third, frontal cortex dysfunction seems to be related to a memory syndrome caused by a breakdown in the ability to plan and carry out elaborative processing. Fourth, and most explored, is the amnesic syndrome(s), caused by limbic system or diencephalic lesions. Other less-studied forms of memory breakdown almost certainly exist and some memory syndromes are compounded from these more basic deficits. Appropriate assessment of memory disorders must take this heterogeneity and complexity into account, and is important not only for clinical purposes but also to gain further insight into the precise nature of the different kinds of breakdown. The major theoretical and clinical requirements that such assessment procedures must meet are outlined.
To answer the questions, where are the lesions responsible for memory disorders located in "normal" aged individuals and how can they be distinguished from those of organic diseases such as Alzheimer's, is not easy, and no currently available parameters enable us to differentiate qualitatively between the lesions in the normal aged brain susceptible to cause memory deficiencies from the more plentiful ones found in Alzheimer's disease. Perhaps it is merely a problem of technical difficulties. Indeed, interpreting the findings reported in the literature is difficult because, for a long time, certain elementary precautions were not taken in the determination of anatomic-clinical correlations. In addition, morphologists and biologists were unaware of the delayed expression of the neuropathological symptoms, the frequency of diseases capable of causing memory disorders, the importance of familial support, the frequency of false dementia, and the influence of the population evaluated: only prospective studies, clinical then neuropathological, will avoid these problems, but it is very difficult to study "benign" memory disorders in aging. Theoretical difficulties are rooted in the definition of "normalcy" in the adult and especially in the aged. Today, the tendency is towards the use of statistical criteria. Should a continuous approach to normality (the whole group is considered as a homogeneous populations) be used or a discontinuous one, more genetic, like that of Gallen and Gambino, distinguishing between several populations, normal and pathological? Neuropathologists and some clinicians prefer the latter.
Twenty-two patients who underwent surgery for ruptured aneurysm of the anterior communicating artery were investigated by a battery of neuropsychological tests, including memory evaluation tests. According to the results obtained at these tests the patients were divided into three groups: 1) 7 patients had no memory disorders; 2) 10 patients presented with memory disorders affecting memory; their complaints concerned behavior, and the memory deficit was discovered at neuropsychological examination; 3) 5 patients presented with an obvious amnesic syndrome, and the tests confirmed a severe learning deficit and a severe forgetting while recognition remained normal in 4 patients. Age, residual lesions at CT and electrophysiological signs of focalization correlated well with the residual neuropsychological disorders. Leaving aside quantitative aspects, the memory deficits observed in the second and third groups seemed to be qualitatively different and might correspond to different anatomical and functional sequelae.
OBJECTIVES: To compare patient characteristics and family perceptions of patient function at one urban and one rural memory disorders clinic. DESIGN: Secondary, cross-sectional data analyses of an extant clinical database. SETTING/PARTICIPANTS: First time visits (n = 956) at two memory disorders clinics. MEASUREMENTS: Patient and family-member demographics and assessment results for the Mini-Mental State Examination (MMSE), instrumental activities of daily living (IADLs), activities of daily living (ADLs), the Memory Change and Personality Change components of the Blessed Dementia Rating Scale, and the Revised Memory and Behavior Problems Checklist. RESULTS: In both clinics, patients and family members were more likely female. The typical urban clinic patient was significantly more likely to be living in a facility and more educated than the typical rural patient. Urban and rural patients did not show significant differences in age- and education-adjusted MMSE scores or raw ADL/IADL ratings, but the urban family members reported more memory problems, twice as many personality changes, more-frequent behavior problems, and more adverse reactions to problems. CONCLUSION: Physicians who practice in both urban and rural areas can anticipate differences between patients, and their families, who seek a diagnosis of memory disorders. Our most important finding is that despite similarities in reported functional abilities, urban families appear to be more sensitive to and more distressed by patients' cognitive and behavioral symptoms than rural families. These differences may reflect different underlying needs, and should be explored in further research.
Early referral for specialist assessment is becoming more common with memory disorders and dementia: the mean Mini-Mental State Examination (MMSE) score of new patients at our clinic rose from 18.7 to 20.7 between 1986 and 1990. The clinical diagnosis of mild to moderate dementia has been recognized to be difficult, but several studies have reported cross-sectional diagnosis. We examined the number of visits required to establish a clinical diagnosis of dementia in the first 125 patients attending a Memory Disorders Clinic who had at least two visits (six months apart) and the stability of the diagnoses. Just under half of the patients required at least two visits to establish the clinical diagnosis. The MMSE was not a good guide to the number of visits required but the diagnosis at the first visit remained stable in all patients who scored < or = 10/30. Sixteen per cent of patients interchanged between the categories of Alzheimer's, mixed and vascular dementias. Possible age-associated memory impairment progressed to dementia in six of eight cases, and depression to dementia in three cases. The diagnosis of mild to moderate dementia should not be restricted to a cross-sectional approach, but should involve serial clinical, psychological and affective assessments.
The proportion of patients consulting pluridisciplinary memory clinics who present anxiety disorders varies with recruitment and referral practices but often exceeded 10p.100. Most of these subjects have an anxiety trait or stress-related generalized anxiety, often triggered by diagnosis of Alzheimer's disease in a close friend or relation. The consultant should play special attention to analyzing the complaint in order to disclose difficulties in attention, true "loss of memory" events, and any recent traumatic events. The psychometric examination is generally normal or evidences discrete frontal dysfunction. Other diagnoses should be ruled out: associated depression, iatrogenic effect, alcoholism, anxiety as a sign of a somatic disease. Management may include drugs, usually on a short term regimen. Short-term psychotherapy or group therapy may be helpful.
The treatment of memory disorders, such as the gradual weakening of memory with age, the ravages of Alzheimer's disease and the cognitive deficits in various forms of mental retardation, may greatly benefit from a better understanding of the molecular and cellular mechanisms of memory formation. There is increasing interest in the possibility of pharmacologically enhancing learning and memory even in the absence of specific anatomically evident pathology. Substantial evidence in experimental systems ranging from molluscs to humans indicates that the cAMP response element binding protein (CREB) is a core component of the molecular switch that converts short- to long-term memory. Recent studies have greatly strengthened and refined our understanding of the role of CREB in learning and memory in mammals, in addition to providing greater insight into the molecular mechanisms of CREB regulation and function. This involvement of CREB and the upstream signalling pathways leading to its activation in learning-associated plasticity makes them attractive targets for drugs aimed at improving memory function, in both diseased and healthy individuals. However, CREB and its close relatives cAMP response element modulator and activating transcription factor-1 are ubiquitous proteins with several critical functions. This creates hurdles that the authors believe may limit the usefulness of CREB per se as a target for the development of memory-enhancing drugs, and focus on components of the upstream signalling pathways or on specific downstream targets will be required.
Medial temporal lobe atrophy determined by temporal lobe oriented computed tomography (CT), 1 year before death, is strongly associated with histopathologically confirmed Alzheimer's disease (AD). The aim of this study was to assess the diagnostic accuracy of medial temporal lobe measurement for the diagnosis of AD in patients referred to a memory disorders clinic, especially those at an early stage of the disease. CT oriented to the temporal lobe was performed in 333 subjects aged 41-93 years consecutively recruited in a Memory Disorders Clinic: 124 had probable AD, Mini Mental State score (MMS) = 17 (8); 50 possible AD [MMS = 21 (5)]; and 119 patients had miscellaneous memory disorders [MMS = 22 (7): frontotemporal lobe dementia, subcortical dementia, cortical Lewy body disease, vascular dementia, Korsakoff syndrome, focal atrophy, etc.]. There were also 19 anxious/depressed patients [MMS = 29 (1)] with normal performance on memory tests, and 21 controls. The minimum width of the medial temporal lobe was measured. The best cut-off to distinguish AD patients from non-AD patients was 11.5 mm, in agreement with data in the literature. At this threshold, 84% of probable AD patients had a positive test and 90% of controls and anxious/depressed patients had a negative test. For the diagnosis of probable AD, sensitivity of the measurement was 0.81, specificity 0.95, predictive positive value 0.99, predictive negative value 0.45, and diagnostic accuracy 0.83. The test was positive in half the possible AD patients, and half those with miscellaneous memory disorders. It was negative in all anxious/depressed patients. Therefore, temporal lobe oriented CT might be a valuable tool for assessment of medial temporal lobe atrophy in AD routine practice.
OBJECTIVE: To investigate the effect of TMCZCJ on the blood rheology in hypostasis rats due to stagnation of the liver-qi and on the learning-memory disorder in cerebral ischemia-reperfusion mice. METHOD: The models of hypostasis due to stagnation of the liver-qi were made by combining irritation with hypodemic injected adrenalin and ice-bath in rats, and the models of learning-memory disorder were made by repeatedly ligating-reperfusing the bilateral carotid in mice. The hypostasis rats and learning-memory disorder mice were perorally administrated TMCZCJ(7.7, 15.4 g.kg-1) once a day, for fourteen consecutive days. RESULT: TMCZCJ can significantly reduce plasma viscosity, blood viscosity and reduced viscosity in hypostasis rats. It can also improve the latent learning-memory capability and memory gain-repetition ability in water-maze for cerebral ischemia-reperfusion mice. CONCLUSION: TMCZCJ can improve remarkably blood rheology in hypostasis rats and learning-memory disorder in cerebral ischemia-reperfusion mice.
MR imaging of the brain, performed in 86 normal subjects and 113 patients with objective memory disorder or dementia, demonstrated white- and gray-matter areas of high signal intensity on long TR images (short and long TE). Hyperintensities were analyzed with respect to size (on a scale of 0-3) and location: lesions were periventricular, subcortical, or cortical. The patients with memory disorder and dementia were categorized as having probable/possible Alzheimer disease, a combination of Alzheimer disease and multiinfarct cognitive disorder, or multiinfarct cognitive disorder alone on the basis of clinically determined Hachinski ischemic scores. Significant correlations were found between age and scores for periventricular lesions (r = .40, p less than .0005) and subcortical lesions (r = .39, p less than .0005) in normal subjects. Correlations were also found between the Hachinski ischemic score and scores for periventricular lesions (r = .21, p less than .01), subcortical lesions (r = .27, p less than .0002), and cortical lesions (r = .32, p less than .0005) in subjects with memory disorder/dementia. Comparing multiinfarct cognitive disorder, Alzheimer disease, and normal groups, the mean scores for periventricular lesions were 12.0 +/- 4.6, 7.6 +/- 4.8, and 3.4 +/- 2.6, while mean scores for subcortical lesions were 10.8 +/- 12.2, 4.1 +/- 6.4, and 0.8 +/- 1.2, respectively. Periventricular lesions were present in 99-100% of patients with Alzheimer disease and multiinfarct cognitive disorder. On the other hand, subcortical lesions, which were identified in 100% of patients with multiinfarct cognitive disorder, were present in only about half of the patients with Alzheimer disease. Thus, scores for both periventricular and subcortical lesions are positively correlated with age and risk factors for cerebrovascular disease and also are significantly increased in the presence of objective memory disorder or dementia. These results imply that in the subject groups considered here, elderly patients with vascular dementia are most likely to have severe white-matter abnormalities on MR scans. The score for subcortical lesions appears to be more helpful than the score for periventricular lesions in distinguishing vascular dementia from Alzheimer disease and normal aging, so that a patient with prominent subcortical white-matter abnormalities is more likely to have a diagnosis of vascular than degenerative dementia.
Time disorientation is a common feature of anterograde memory disorder caused by brain illness. This observation suggests that the subjective time constructions used to organize events are strongly dependent upon memory storage processes. This study evaluated one prominent cognitive theory of time estimation from the point of view of organic memory disorder. A severely amnesic subject and 10 unimpaired subjects were asked to estimate time intervals using methods gleaned from the cognitive study of subjective time estimation. Results strongly suggest that the ability to remember new information is required in order to maintain an accurate time perspective. The time context for this subject essentially resided in the past, roughly corresponding to the time of her original brain surgery for a dermoid cyst near the third ventricle. Her ability to estimate time intervals and general time perspective was constrained by her impoverished store of knowledge for personal experiences.
INTRODUCTION: Normal aging is characterised by alterations affecting the cognitive functions. In 1958 Kral coined the term 'benign senescent forgetfulness' to designate a memory disorder that is different from those that occur during normal aging. In 1986, a group of researchers at the National Institute of Mental Health and other centres proposed a novel neuropsychological entity called age-related memory disorder. The determination of the prevalence, progression and risk factors of this condition currently represents an important challenge for the scientific community. AIMS: To establish the rate of prevalence and to identify some of the risk factors involved in age-related memory disorders. SUBJECTS AND METHODS: The universe consisted of all the patients over 50 years of age from a health district (234 individuals); the diagnostic criteria were applied to the whole sample. In addition to the patients, a control group was also chosen in order to be able to establish a correlation with selected risk factors. RESULTS AND CONCLUSIONS: The prevalence rate was found to be 39.7%, of which 38.7% were males and 40.4% were females. It was also observed that the impairment was greater as the patient's age and the length of the disease history increased. As far as risk factors are concerned, it was observed that smoking and psychosocial characteristics constitute predisposing factors, while this was not the case for arterial hypertension, a history of dementia and the satisfaction of basic needs.
The effects of exifone (ADLONE), hexahydro-2,3,4,3',4',5'-benzophenone, were tested in two models of memory in the mouse: habituation of exploratory activity and antagonism of amnesia induced by scopolamine in a passive avoidance task. In the first model, mice which had received exifone (128 and 256 mg/kg IP) 30 minutes before a 3 minute exposure to a staircase exploratory test showed a more marked decrease in exploratory activity in the same apparatus 24 hours later (habituation) than a control group indicating improved memory. Similar results were obtained with piracetam (512 mg/kg, IP). In the second model exifone (512 mg/kg PO), administered 60 minutes before both the learning and retention trials of a standard step-through passive avoidance, task partially antagonized the amnesia induced by 10 mg/kg scopolamine IP administered immediately after the learning trial. Similar results were obtained with piracetam (800 mg/kg PO). Taken together these results suggest that exifone facilitates memory function in simple rodent models in a manner consistent with its supposed therapeutic effects in man.