SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
We describe the case of a female patient with behavioral and memory disorders. A neuropsychological evaluation confirmed the absence of mental deterioration and the presence of the psychometric features of the amnesic syndrome. The clinical diagnosis was supported by MRI and histological examination.
Three patients were found to have unilateral tactile recent memory loss on examination. In two patients the loss occurred in the right hand and was accompanied by a disorder of verbal recent memory; in the third patient the loss occurred in the left hand and was not accompanied by any other disturbance in recent memory. An acute unilateral lesion, either structural or functional, in the medial temporal lobe contralateral to the tactile recent memory disturbance was the common denominator in all three cases. The proper methods for diagnosing a unilateral tactile disturbance of recent memory and other forms of fractional disorders of recent memory are discussed. Based on computerized tomography scans and behavioral and anatomical data in man and monkey, an anatomical explanation is offered to account for the syndromes of right and left unilateral tactile recent memory loss. The possible existence of other forms of fractional disturbances of recent memory and the role of the cerebral commissures in recent memory functions are discussed.
This paper investigates the memory disorder of Alzheimer-type dementia by comparing the performance of Alzheimer patients on selected memory tests with that of Korsakoff patients and healthy controls. Alzheimer patients have deficits in both primary and secondary memory, and this finding is compared with that which pharmacological studies predict would occur on the basis of cholinergic depletion. The deficits in primary memory are unlikely to be accounted for in terms of cholinergic depletion, and provide a possible explanation for the disappointing results of trials of cholinergic replacement therapy in this disorder. On the other hand, the pattern of deficit in secondary memory is entirely consistent with that expected from cholinergic depletion.
BACKGROUND: The prevalence of AD appears to vary widely in different ethnic groups. Certain risk factors for AD are well established for the general population, but there is little information regarding the relevance of these risk factors in specific ethnic groups. OBJECTIVE: The authors examined the risk of AD associated with the APOE-epsilon4 allele, the APOE-epsilon2 allele, smoking, alcohol consumption, history of hypertension, low educational level, estrogen replacement therapy, and history of head trauma with loss of consciousness among samples of white non-Hispanics (WNH) (392 AD patients, 202 normal subjects) and white Hispanics (WHIS) (188 AD patients, 84 normal controls). DESIGN: This was a case-control study of patients evaluated at an outpatient memory disorders clinic and control subjects recruited from a free memory screening offered to the community. RESULTS: Increased risk for AD was associated with the APOE-epsilon4 allele after controlling for age, education, and gender among WNH (OR = 3.5; 95% CI = 2.3 to 5.5) and WHIS (OR = 3.1; 95% CI = 1.7 to 5.8). No protective effect was conferred by the APOE-epsilon2 allele, although this relationship approached significance among WNH (p = 0.02). Low levels of education increased the risk for AD among WNH (OR = 3.1; 95% CI = 1.8 to 5.9) but not WHIS. Alcohol use and hypertension approached significance as risk factors in WNH (p < 0.05) but not WHIS. Estrogen replacement treatment approached significance as a protective factor in both ethnic groups (p < 0.05). CONCLUSIONS: Although the APOE-epsilon4 allele is a risk factor for AD among WHIS and WNH, other risk factors such as low education and hypertension appear to be important only for WNH. Risk factors for AD reported or suggested previously that were not confirmed by this study include smoking and head trauma with loss of consciousness.
Awareness of deficit was examined in 24 patients with Alzheimer's disease (AD) and their spouses (for a total of 48 participants) using performance prediction-postdiction and questionnaire discrepancy (QD) paradigms. Participants estimated their own memory performances as well the performances of spouses and of a fictional, memory-disordered patient observed on videotape. Patients overpredicted self-performances, but the extent of overestimation decreased for postdictions. Patients and caregivers accurately estimated caregiver performances but overestimated performances of the fictional patient. QD data revealed that patients underestimated their difficulties performing daily functioning tasks as compared with caregiver reports. Awareness of deficit is a complex ability, involving dissociable cognitive processes. AD patients may display intact immediate awareness of memory dysfunction but fail to incorporate incidents of memory failure into generalized self-belief systems.
BACKGROUND: In cognitively impaired patients without dementia, the utility of apolipoprotein E (APOE) genotyping is unclear. OBJECTIVE: To evaluate the predictive utility of the APOE epsilon4 genotype for conversion to probable Alzheimer disease (AD). DESIGN: Naturalistic, longitudinal study. SETTING: Memory disorders outpatient clinic. PATIENTS: A total of 136 patients with memory complaints were determined to have mild cognitive impairment and were evaluated every 6 months. Fifty-seven age- and sex-matched healthy controls were evaluated annually. MAIN OUTCOME MEASURES: Primary outcome measures included conversion to AD. Secondary outcome measures included change over time in Mini-Mental State Examination (MMSE) score and Selective Reminding Test (SRT) delayed recall score. RESULTS: The APOE epsilon4 allele was present in 25% of patients and 21% of healthy controls. During a mean +/- SD follow-up of 35.2 +/- 24.3 months, 35 of 136 patients converted to AD. APOE epsilon4 carrier status did not differ between converters (31%) and nonconverters to AD (23%, P = .3) and did not affect the time trend in MMSE or SRT scores in the entire sample. Four of 5 APOE epsilon4 homozygotes converted to AD compared with 7 of 29 heterozygotes (P = .02). In a Cox proportional hazards model stratified by age quartiles, after controlling for sex, education, MMSE score, and SRT delayed recall score, APOE epsilon4 increased the risk of AD in patients 70 to 85 years old (n = 57; risk ratio, 2.77; 95% confidence interval, 1.1-7.3; P = .03) but not in patients 55 to 69 years old (n = 79; P = .7). CONCLUSIONS: APOE epsilon4 carrier status was associated with conversion to AD in older outpatients after controlling for known demographic and clinical risk factors, and APOE epsilon4 homozygosity was associated with increased risk of conversion to AD. However, APOE epsilon4 carrier status by itself did not predict cognitive decline or conversion to AD, indicating that APOE genotyping in patients with mild cognitive impairment may have limited clinical applicability for prediction of outcome.
Memory performances are not constant but undergo fluctuations whose periodicity may be analyzed. Low frequency infradian rhythms (periods longer than 28 hours), circadian rhythms (periods between 20 and 28 hours) and ultradian rhythms (periods less than 20 hours) are involved in memory disorders. Paradoxical sleep represents a preferential period in which certain processes, such as the activation of the central nervous system for example, may facilitate learning process. Relations between sleep and memory lead to the discussion of the incidence of the cyclic nature of sleep (and notably the rhythm of 90 minutes' paradoxical sleep) on the daily course of cerebral activation and its effects on the variable aptitude of our capacity for remembering. The close interrelation between biological rhythms and cognition is demonstrated using two examples of mental disorders in which severe memory deficiencies are observed.
Previous investigations of memory in senile dementia of the Alzheimer's type (SDAT) have focused on verbal learning and memory. The aim of the present study was to determine whether the amnesia of SDAT is limited to verbal material. Patients with SDAT (N = 29; mean age = 69.3) and healthy normal controls (N = 41; mean age = 69.3) were given a test of facial perception and two recognition memory tasks, one for words and one for faces. The results indicate that dementia patients show a deficit in the retention of facial information. This deficit cannot be attributed to faculty initial perception or to a response bias. The verbal and facial memory deficits in SDAT appear to differ: performance on tests of verbal and facial memory is relatively independent, and substantial encoding and linguistic defects contribute to the verbal, but not the facial, memory disorder resulting in more severe impairment on tests of verbal memory. The implications of these findings for research on the neuropharmacology and pathophysiology of SDAT are discussed.
Patterns of cognitive and behavioral impairment were analyzed in patients with progressive supranuclear palsy (PSP), Parkinson's disease (PD), and senile dementia of Alzheimer's type (SDAT), matched for age, sex, manual laterality, educational level, and degree of intellectual deterioration. The scores of the three groups of patients were significantly lower than those of controls and were comparable on tests of verbal and visuospatial functions as well as global memory. Patients with SDAT could be distinguished by the severity of verbal memory disorders; patients with PSP, and to a lesser degree those with PD, by impaired performances on tests sensitive to frontal lobe dysfunction.
A 64 year-old woman experienced, at 6 weeks' interval, two episodes of encephalitis with left hemiparesis, coma and signs of meningitis. Paraclinical examinations showed lymphocytic meningitis, right temporal hypodensity at CT and high titers for herpes simplex at blood serology. The spontaneous course was favourable with almost complete recovery. A third recurrence took place 2 months later with left hemiplegia, confusion and meningism. A tentative diagnosis of herpes simplex encephalitis was confirmed by major intrathecal synthesis of herpes virus specific antibodies and by highly suggestive MRI images. Treatment with acyclovir resulted in rapid regression of motor deficit and meningism, but neuropsychological disorders regressed more slowly with persistent visuo-constructive and memory disorders. During a fourth and milder recurrence, a stereotactic temporal brain biopsy was performed, which showed lesions of encephalitis and elevated titers for HSV1 in the temporal fluid. Another course of acyclovir followed by vidarabine produced complete remission. The possibility of recurrent types of herpes simplex encephalitis is discussed.
INTRODUCTION: Platelets have been implicated in memory disorders but this has not been investigated in patients with immune or idiopathic thrombocytopenia (ITP). ITP is an autoimmune disorder in which autoantibodies bring about platelet destruction. We previously reported a group of ITP patients who manifested TIA-like syndrome and gradual memory loss leading to dementia: platelet microparticles (PMP), a marker of platelet activation, were often elevated, suggesting that procoagulant PMP released from stimulated platelets contributed to thrombosis in small vessels. We have expanded on those studies to better define the clinical, laboratory, and radiologic characteristics of this syndrome. MATERIALS AND METHODS: Twenty ITP patients with this syndrome were studied in comparison to twenty-three ITP patients without it (patient controls). Clinical and laboratory features were compared and radiologic images were analyzed. Factors influencing the rate of progression to advanced dementia were also investigated. RESULTS AND CONCLUSION: Recurring dizzy or weak spells, TIA-like syndrome, recent memory loss, and cognitive impairment were common initial complaints. In some, these symptoms progressed rapidly to dementia but was indolent in others. Progression was faster in those with splenectomy and higher platelet counts. MRI showed enhanced signal in subcortical, periventricular areas, consistent with ischemic small vessel disease. Compared to patient controls, bleeding was less frequent and platelet activation (increased PMP, CD62p) was more frequent in the study group. Thrombotic complications may occur in ITP, manifested as TIA-like syndrome or memory loss due to ischemic small vessel disease, progressing to vascular dementia. Memory disturbances associated with platelet disorders warrants further investigation.
Our previous research with intra-cerebral event-related potentials in conjunction with an original Memory Workload Paradigm has shown that significant load effects for the N4 latency were found only for both amygdalae and the left posterior hippocampus as well as for both anterior neo-cortical regions of the temporal gyri. These same structures are also affected in Alzheimer's Disease. Therefore, based on our previous intra-cerebral findings, our present research was to use our novel Memory Workload Paradigm in conjunction with surface ERPs as neurophysiological markers to tap cerebral regions and functions involved in memory disorders pertaining to early Alzheimer's Disease as opposed to normal memory processes in age-matched normal control subjects. Moreover, the Mangina-Test which measures varying degrees of 'Analytical-Specific Visual Perception' was individually administered to all patients and controls in separate sessions. Results indicate that for the early Alzheimer's Disease group, a significant main effect for memory load was found for the P400 amplitude (F(3,30)=4.52, P<0.02) which was absent in the normal group. In particular, the P400 amplitude was significantly higher on posterior head regions for patients with early Alzheimer's Disease as opposed to age-matched normal subjects (F(7,140)=3.54, P<0.03) which distinguished both groups (F(1,20)=6. 13, P<0.03). For the P400 latency, a significant memory load effect was present only for the normal group (F(3,30)=11.26, P<0.01). The Mangina-Test performance clearly differentiated both groups (F(1, 19)=105.85, P<0.001). The present data provide the first valuable evidence that ERPs to our novel Memory Workload Paradigm are sensitive neurophysiological diagnostic markers which delineate the early clinical brain irregularities underlying early Alzheimer's Disease as opposed to the normal memory processes of age-matched normal subjects. In addition, their use could be valuable for the objective clinical follow-up of therapeutic interventions in early Alzheimer's Disease.
The neuropsychological characteristics of a patient with a bilateral thalamic infarct in the posterior communicating artery territory due to basilar artery thrombosis are described. MRI examination showed bilateral thalamic acute ischemic lesions in the zone anterior to the tuberothalamic branches. In the cognitive exploration, the patient showed verbal and visual memory disorders, impairment of the executive functions including inability to generate and make decisions and behavioural disorders including lack of inhibition, euphoria, and occasional aggressiveness. Two months later the patient had improved in the neuropsychological test scores but still suffered from severe recent memory loss, and certain behavioural disorders including lack of inhibition and euphoria. Other cases on thalamic infarcts with cognitive and behavioural impairments due to disconnection of the front subcortical pathways have been described in the literature.
INTRODUCTION: Bilateral thalamic tumours are very rare and have been recently identified as a subgroup of thalamic neoplasms due to their characteristic clinical presentation, with behavioural and memory disorders and without sensory or motor changes. We describe a patient who presented with mood and behaviour changes due to a bilateral thalamic glioma, discuss the literature related to these rare neoplasms and review the anatomical bases of their particular clinical presentation. CASE REPORT: A 67-year-old woman consulted because of behavioural changes and frequent forgetfulness. Neurological examination was normal except from a deficit in the retention of words and numbers. MR images revealed bilateral thalamic swelling by a isointense in T1, hyperintense in T2 and protonic density mass that did not enhance. The tumour was diagnosed as an astrocytoma by stereotactic biopsy. She continued to deteriorate and a year after diagnosis she was bedridden and with a severe dementia. CONCLUSION: Bithalamic tumors, as other lesions that affect the thalamus bilaterally, characteristically present with mood and behaviour changes and memory impairment.
During the past 10 years numerous investigations concerned with the neuropsychological, neuropathological and etiological factors involved in alcoholic Korsakoff's syndrome have been published. The neuropsychological research has focused on the patients' anterograde and retrograde amnesias, and several theories based upon current models of human information processing have been advanced as partial explanations of the amnesic syndrome. While neuropathological investigations have continued to implicate midline diencephalic structures in the chronic symptoms of this disorder, some very recent studies have begun to assess the role of neurotransmitters in the patients' memory disorders. The etiology of the disorder also appears to be more complex than once believed. Animal studies demonstrating the neurotoxicity of alcohol have suggested that the patients' severe memory deficits may be due to an interaction of malnutrition and the toxic effects of alcohol. Behavioral investigations reporting that non-Korsakoff alcoholics have memory deficits qualitatively similar to those of Korsakoff patients support the idea that Korsakoff's syndrome is not acute but may develop slowly during decades of alcohol abuse.
This study investigated the hypothesis that memory disordered patients suffer of an exalted forgetting rate from long-term memory within the first few minutes following acquisition. For this purpose, we administered to groups of Alzheimer's (AD), Multi-infarct demented (MID), pure amnesic and age-matched normal controls a test involving immediate and 15-min delayed word-list recall and a modified version of the Huppert and Piercy's procedure (1978) assessing yes/no Recognition for pictures at 90 sec, 10 min, 1 hr and 24 hr delay intervals. Results showed an abnormal immediate/delayed performance decline for the word-list recall in AD and pure amnesic patients. In the same period, however, their Recognition score in the Huppert and Piercy's procedure decayed at normal rate. In the following intervals (1 hr and 24 hr), both groups disclosed abnormal forgetting slopes. Vascular demented patients, by contrast, disclosed fully normal forgetting rates both on the word-list recall and on the Huppert and Piercy's procedure. These findings are discussed in the light of cognitive mechanisms and neuroanatomical structures presumably underlying memory consolidation.
Neuropsychological studies of memory disorders have played a prominent role in the development of theories of memory. To test and refine such theories in future, it will be advantageous to include research that utilizes physiological measures of the neural events responsible for memory. Measures of the electrical activity of the brain in the form of event-related potentials (ERPs) provide one source of such information. Recent results suggest that these real-time measures reflect relevant encoding and retrieval operations. In particular, distinct electrical responses have been associated with recollective processing of words and with priming of visual word-form. This source of evidence can thus enrich our understanding of both the cognitive structure and neural substrates of human memory.
INTRODUCTION: Thalamic infarcts in paramedian artery territory are seen fairly frequently owing to certain peculiarities of the vascularization of the thalamus. However, clinical diagnosis is usually difficult because of the many varieties and peculiarities of the symptomatology. MATERIAL AND METHODS: We present a review of twelve cases of bilateral paramedian infarcts of the thalamus seen in our Department of Neurology and in a private surgery. We analyze the symptoms and their relationship to the neuro-radiological findings. Finally we compare our observations with the descriptions published by other authors and seek and anatomo-functional relationship for each of the symptoms and signs observed. RESULTS: The usual clinical outline in our patients included disorders of consciousness, different types of oculomotor disorders and cerebellar symptoms, mainly of gait. Other less common findings were memory disorders and abnormal movements. In no case were there sensory changes and pyramidal signs were rare in the absence of significant extra-thalamic lesions. CONCLUSIONS: Our findings, although generally comparable to those described in the literature consulted, were somewhat different with regard to cerebellar symptoms and the absence of sensory and pyramidal signs. We also emphasize the marked differences seen between the individual patients in our series. A good knowledge of the possible clinical variants of these lesions is necessary for a correct initial diagnostic approach in the study of these patients.