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At least 55 records · Page 3Linked to original sources
PubMed2006

Diagnosis of dementia using perfusion SPECT imaging at the patient's initial visit to a cognitive disorder clinic.

PURPOSE: This study was performed to evaluate the diagnostic accuracy of brain perfusion SPECT in patients visiting the cognitive disorder clinic for initial evaluation using 3D-SSP compared with using standard transaxial section. MATERIALS AND METHODS: Standard transaxial section displays and 3D-SSP z-score maps obtained after administration of Tc-99m ECD or I-123 IMP were randomly interpreted in 315 patients who visited initially to the cognitive disorder clinic (age 46-88 years; 162 women, 153 men). Sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic accuracy were calculated and receiver operating characteristic (ROC) analysis was performed. RESULTS: One hundred thirty-seven patients were clinically diagnosed with Alzheimer disease and 178 patients were diagnosed with other disorders and age-associated cognitive decline. Sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic accuracy calculated using standard transaxial display were 61%, 70%, 61%, 70%, and 66%, respectively, and using the 3D-SSP z-score map were 90%, 74%, 73%, 90%, and 81%, respectively. Particularly, the sensitivity value improved in mild cases compared with severe cases using 3D-SSP. Diagnostic performance with 3D-SSP was superior in both mild dementia (Az = 0.64 [section] vs 0.81 [3D-SSP], P = 0.001) and severe dementia (Az = 0.75 [section] vs 0.90 [3D-SSP], P = 0.002). CONCLUSIONS: Brain perfusion SPECT was useful for diagnosis in patients who come to the cognitive disorder clinic for initial evaluation using 3D-SSP.

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PubMed2001

[Postoperative cognitive disorders in the elderly].

TWO DISTINCT CATEGORIES: Postoperative cognitive disorders include delirium and long-term cognitive dysfunction. DELERIUM: Delirium is an acute state occurring early during the postoperative period. It may be considered as an acute cerebral insufficiency which may be consecutive both to the negative effects of aging and chronic illness on cognitive function, and to the cerebral impact of operative stress. In addition, precipitating postoperative medical factors may facilitate cerebral failure. Only a few studies have been devoted to prevention programs aimed at reducing the risk of postoperative delirium. Nevertheless, we can hypothesize that a preoperative gerontology assessment would be effective in determining risk factors of delirium in old patients and thus enable proposing individual postoperative management. LONG-TERM COGNITIVE DYSFUNCTION: The definition of this clinical picture is less precise than delirium. Long-term cognitive dysfunction corresponds to a loss of cognitive performance in the weeks and months after anesthesia. The IPOCD1 study conducted in a large cohort of elderly patients has shown that postoperative cognitive dysfunction was present in 25.8% of patients 1 week after surgery and in 9.9% 3 months after surgery. One to two years after surgery, cognitive dysfunction was observed in 10.4% of patients compared with 10.6% in a control population of non-operated patients. We would suggest that in many cases, postoperative cognitive dysfunction may result from preoperative dementia unmasked by surgery.

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PubMed1995

[Cognitive disorders in the structure of endogenous depression in old age].

31 aged inpatients (60-88 years) with major depressive episode (DSM-III-R) have been investigated in order to study the dynamics and reversion of cognitive disorders in late depression and their relation to the course and outcome of depressive phases. The dynamic evaluation was achieved by 4-times testing with HAM-D and MMSE within the phase. All patients had some cognitive disfunction at the crucial of the phase, which in most cases (90.3%) was completely reversible during the therapy. It was found that cognitive disorders were partly associated with depression and where party related to the aging processes. The degree of cognitive impairments at the crucial stage of the phase depended upon the severity (t = 0.73; p < 0.001) and complexity (t = 0.71; p < 0.001) of the depressive syndrome. It also correlated with the duration of active therapy (t = 0.53; p < 0.005) and quality of the following remission (t = 0.48; p < 0.01). The dynamic assessment of the cognitive disorders may be used for the differentiation of pure depression from the states with the beginning degenerative disease, for the prediction of the course and outcome of depression and response to the therapy.

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PubMed1997

ICD-10 mild cognitive disorder: its outcome three years later.

OBJECTIVE: The aims were to (i) report the outcome of mild cognitive disorder (MCD) 3.6 years after initial interview and diagnosis; (ii) identify predictors of new cases of MCD. The hypotheses were that (i) persons with MCD are more likely to develop dementia than those without MCD; (ii) symptoms of anxiety or depression predict MCD caseness at follow-up. DESIGN: Longitudinal cohort study. SETTING: Community of elderly people (age 70-97 years). PARTICIPANTS: 612 of 897 elderly subjects (mean 76 years) were reinterviewed. Of the 36 MCD cases originally identified, 25 were available at follow-up. 24 incident cases of MCD were identified. MAIN OUTCOME MEASURES: ICD-10 dementia, DSM-III-R dementia, ICD-10 mild cognitive disorder diagnoses made by the Canberra Interview for the Elderly, tests of anxiety, depression, neuroticism and cognitive performance. MAIN RESULTS: Of the original 25 MCD cases available at follow-up, two had a diagnosis of MCD, and three had a diagnosis of both ICD-10 and DSM-III-R dementia. The prevalence of MCD and DSM-III-R dementia at follow-up was no greater for MCD cases diagnosed at initial interview than in normal subjects at initial interview. There was, however, an increased prevalence of ICD-10 dementia among original MCD cases. At initial interview and at follow-up MCD cases were more anxious and depressed but had similar cognitive performance to normals. For incident cases of MCD the only significant predictor was age. CONCLUSIONS: MCD cannot be seen to be a specific forerunner of dementia. Those with a diagnosis of MCD are distinguished more by their anxiety, depression and neuroticism than by their cognitive deficits.

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PubMed1999

Drug-induced cognition disorders in the elderly: incidence, prevention and management.

The aetiology of cognitive impairment is multifactorial; however, drugs are an important cause of delirium and dementia. Several factors may increase the risk of drug-induced cognition disorders in the elderly including imbalances in neurotransmitters (e.g. acetylcholine), age-related alterations in pharmacokinetics and pharmacodynamics, and high levels of medication use. Nearly any drug can cause cognitive impairment in susceptible individuals; however, certain classes are more commonly implicated. Benzodiazepines, opioids, anticholinergics, and tricyclic antidepressants are probably the worst offenders. Older antihypertensive agents (reserpine, clonidine) have negative effects on cognition; however, large clinical trials in the elderly indicate that commonly used agents [e.g. thiazide diuretics, calcium antagonists (amiodipine, diltiazem), ACE inhibitors (captopril, enalapril) and beta-blockers (atenolol)] have minimal effects on cognition. Newer antidepressants such as selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors (SSRIs) and reversible inhibitors of monoamine oxidase A have not been shown to have negative effects on cognition. Although some drugs have shown low risk for causing cognition disorders in research studies, risk may be increased in frail older adults taking several medications and each case should be reviewed carefully. Identification of drug-induced cognitive impairment is crucial to early detection and resolution of symptoms. Preventive strategies directed at avoiding high risk medications when possible, appropriately adjusting doses based on age-related changes and close follow-up may prevent these conditions.

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PubMed2001

Future trends in the treatment of cognitive disorders.

This review provides an overview of the different types of cognitive disorders, with special emphasis on the description on Alzheimer's disease, as statistical data indicate that it is the major cause of dementia or cognitive decline. The factors responsible for biochemical changes at the cellular level and the different therapies available for the treatment of cognitive disorders are described. Recent advances, including the elucidation of biochemical changes at the molecular level and different approaches to treat the disease, are also briefly reviewed. (c) 2001 Prous Science. All rights reserved.

Journal Article↗
PubMed1999

The physiological approach: functional architecture of working memory and disordered cognition in schizophrenia.

The method of single-cell recording in awake behaving monkeys as they perform behavioral tasks is perhaps the most powerful approach to understanding the neural basis of behavior. In contrast to cellular analyses in vitro, e.g., in slice preparations, the in vivo approach allows direct correlation of cellular activity and specific processes as they are isolated by behavioral paradigms. As brain mechanisms are studied under natural conditions, inferences about the dynamic basis of information processing are direct. Limitations of this approach include the inability to unequivocally identify the cell under investigation, though location by cytoarchitectonic area and cortical depth is possible. Neurophysiological studies have not only given a dynamic view of neural processing "on line" but have allowed investigators to examine fundamental issues about normal brain function and dementia. Here I illustrate some of these issues and the power of single cell physiology to address them. Before doing so, it should be patently obvious that recording one cell at a time is a technical necessity and in no way should be taken to imply that any behavior is dependent on a single cell. Rather the neuron investigated is a representative of a cohort of cells acting in aggregate.

Animals↗
PubMed2000

[Amyotrophic lateral sclerosis manifesting as cognitive disorders. Value of brain perfusion scintigraphic tomography in intensive care].

BACKGROUND: Cognitive disorders have been described in amyotrophic lateral sclerosis, but usually after the diagnosis has ben established. CASE REPORT: A 57-year-old man was intubated for acute respiratory distress subsequent to pneumonia and diaphragm palsy. He had a 2-year history of drug-resistant depression and deterioration of cognitive functions. A pyramidal syndrome associated with biopsy-proven chronic neurogenic atrophy led to the diagnosis of amyotrophic lateral sclerosis. The electromyogram did not contribute to diagnosis. Brain MRI only evidenced moderate bilateral frontal-temporal atrophy. Brain SPECT demonstrated major perfusion defects in the frontal lobes. DISCUSSION: This patient had amyotrophic lateral sclerosis and frontal-temporal dementia with an unusually late onset clinical presentation: cognitive disorder was the inaugural sign. Brain SPECT and muscle biopsy enabled us to identify the cortical and peripheral motor neurone involvement in this uncooperative intensive care patient totally dependent on mechanical ventilation.

Biopsy↗
PubMed2002

Cognitive disorders: diagnosis and treatment.

During the last half century, medical developments have expedited an increase of life expectancy all over the world. Owing to this extension of life, some pathological processes that formerly were considered to exhibit low prevalence now have become top priorities for public health programs. Among these pathological processes, cognitive diseases stand out, the two most frequent being Alzheimer's disease and cognitive disorders of vascular etiology, for which humans are at increased risk beyond age 65. We studied 120 adults with cognitive disorders representing a variety of etiologies. We performed a comparative statistical study between members of this group of patients and a group of general patients by means of different neurophysiological examinations: acoustically evoked potentials, P300, brain electrical activity mapping both in the resting state and under complex stimulation, and Doppler ultrasonographic extracranial and transcranial assessment. The comparative study between both populations revealed significant differences in results of the various tests. Neurotransmitter equilibrium (dopamine, acetylcholine, gamma-aminobutyric acid [GABA], etc.) in the areas of the cerebral cortex related to cognitive disorders is essential in the diagnosis and treatment of these diseases.

Adult↗
PubMedDate not supplied

[Neurophysiologic evaluation of cognitive disorders in patients with epilepsy].

Aiming to evaluate cognitive disorders in patients with epilepsy examinations were performed using WB scale and event related potentials (ERP) as well as in the control group of healthy volunteers. The study involved 12 patients with epilepsy aging from 15 to 65 years and duration of the disease from 5 to 21 years, 8 males and 4 females: 9 patients received monotherapy and 3 polytherapy. Auditory ERP were studied by averaging 128 expected responses. Recording electrodes were placed by the 10-20 system at sites Fz, C3, Cz, C4, Pz, P4. After recording of the repeated responses the determination of latency of P-300 wave and N2-P3 amplitude were performed. Prolongation of latency of P-300 wave and increased amplitude were recorded in patients with polytherapy and longer duration of the disease. It has been concluded that in patients with chronic epilepsy treated by polytrauma there are changes of the basic characteristics of the parameters of of the cognitive evoked responses.

Adolescent↗
PubMed2003

Corticobasal degeneration as a cognitive disorder.

The presence of cognitive impairment in corticobasal degeneration (CBD) is now widely recognised. Our review of the literature reveals that, although the pattern and severity of neuropsychological impairments can be highly variable across patients, several general trends can be identified. The most characteristic impairments are limb apraxia (usually ideomotor), constructional and visuospatial difficulties, acalculia, frontal dysfunction, and nonfluent aphasia. The limb apraxia is associated with deficits in drawing, copying, and handwriting, but there is emerging evidence that the problems with handwriting are not due exclusively to the apraxia. The findings with respect to episodic memory are more variable, but when there is impairment in this area, it tends to be milder than that seen in Alzheimer's disease. Semantic memory functioning appears relatively preserved but has been poorly studied. Problems with speech are common, and may be due to dysarthria or buccofacial apraxia. Aphasia, although initially considered rare, is in fact a common accompaniment of CBD, may be the presenting feature, and is typically nonfluent in type. More systematic investigation of the clinical and neuropathological overlap between progressive nonfluent aphasia (generally considered to be a form of frontotemporal dementia) and CBD is needed.

Aphasia↗
PubMed1999

The role of norepinephrine in the pathophysiology of cognitive disorders: potential applications to the treatment of cognitive dysfunction in schizophrenia and Alzheimer's disease.

The role of noradrenergic neurotransmission in normal cognitive functions has been extensively investigated, however, the involvement of noradrenergic functions in the cognitive impairment associated with schizophrenia and Alzheimer's disease has not been as intensively considered. The limited ability of atypical antipsychotics to treat the cognitive impairment of schizophrenia, and cholinomimetics to treat the cognitive impairment of Alzheimer's disease, may be related to the influence of a multiplicity of neurotransmitter abnormalities including noradrenergic dysfunction, which these treatments do not address. The evidence of noradrenergic dysfunction occurring concomitantly with dopamine dysfunction in schizophrenia and acetylcholine dysfunction in Alzheimer's disease supports therapeutic approaches using noradrenergic drugs in combination with neuroleptics and cholinesterase inhibitors, respectively, to enhance the treatment of cognitive impairment. Given the results of animal and human studies, it appears that alpha-2A agonists may be the optimal choice for this purpose.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1994

Cognitive disorders and negative symptoms as correlates of motivational deficits in psychotic patients.

The problem of a possible lack of motivation to perform cognitive tasks, which is often encountered in psychotic patients, has been approached from the perspective of the 'energetics' of cognition (Hockey et al. 1986) and from the broader clinical context of psychosis as an 'amotivational syndrome' and its related negative symptoms. The presence of motivational deficits was investigated in a group of psychotic in-patients (N = 73, and 40 had schizophrenia) compared with a control group of non-psychotic psychiatric in-patients (N = 23). The motivational deficit was operationalized in terms of Sanders's (1983) cognitive-energetic model as a large effect of 'time-on-task' during a simple, monotonous reaction test. Significantly more psychotic patients than control patients showed evidence of this type of motivational deficit. The deficit appeared to be related with negative but not with positive symptoms of psychosis. Furthermore, the deficit was shown to be related to the cognitive disorders of psychosis, which have been amply documented in the literature, i.e. disorders of vigilance, verbal memory and distractibility. These results suggest that the cognitive disorders of psychosis are not of a 'computational' but of an 'energetical', i.e. motivational nature.

Adolescent↗
PubMed2002

[Alcohol-induced cognitive disorder: alcohol dementia].

Cognitive impairment is frequently observed in patients with alcohol misuse or alcohol addiction. Multiple cognitive functions are reduced in these patients. Frontal lobe functions, as planning, abstract thinking, set shifting or continuous performance are most frequently affected. Alcohol amnestic syndrome, alcohol dementia and the Wernicke-Korsakow-Syndrome constitute distinct entities. Alcohol dementia follows the diagnostic criteria of dementia with clear evidence for alcohol abuse or alcohol addiction. The diagnostic procedure of alcohol-induced cognitive impairment includes medical history, physical and neuropsychiatric examinations; laboratory examinations, neuropsychological assessment, brain imaging and electroencephalographic recordings. At the moment, there are no established treatment options for alcohol-induced cognitive impairment. Some evidence is provided that nootropics might be of benefit. Alcohol abstinence is a most important step. Psychosocial interventions are essential to support the patients in their daily activities.

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PubMed2003

Plants with traditional uses and activities, relevant to the management of Alzheimer's disease and other cognitive disorders.

In traditional practices of medicine, numerous plants have been used to treat cognitive disorders, including neurodegenerative diseases such as Alzheimer's disease (AD) and other memory related disorders. An ethnopharmacological approach has provided leads to identifying potential new drugs from plant sources, including those for memory disorders. There are numerous drugs available in Western medicine that have been directly isolated from plants, or are derived from templates of compounds from plant sources. For example, some alkaloids from plant sources have been investigated for their potential in AD therapy, and are now in clinical use (e.g. galantamine from Galanthus nivalis L. is used in the United Kingdom). Various other plant species have shown favourable effects in AD, or pharmacological activities indicating the potential for use in AD therapy. This article reviews some of the plants and their active constituents that have been used in traditional medicine, including Ayurvedic, Chinese, European and Japanese medicine, for their reputed cognitive-enhancing and antidementia effects. Plants and their constituents with pharmacological activities that may be relevant to the treatment of cognitive disorders, including enhancement of cholinergic function in the central nervous system, anti-cholinesterase (anti-ChE), antiinflammatory, antioxidant and oestrogenic effects, are discussed.

Alkaloids↗