[Human science. Cognition. 5. Cognition disorders: cognition as a behavior standard].
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Cognitive impairment is a frequent manifestation of advanced human immunodeficiency virus (HIV) infection. The response to antiretroviral medication is often partial and poorly sustained. Recent studies suggest that free radical production within the CNS and neuronal apoptosis may play important roles in the pathogenesis of HIV dementia. We conducted a randomized double-blind, placebo-controlled trial using a parallel group, 2 x 2 factorial design evaluating deprenyl, a monoamine oxidase B inhibitor and putative anti-apoptotic agent, and thioctic acid, an antioxidant, in 36 patients with HIV-associated cognitive impairment. Both deprenyl and thioctic acid were well tolerated with few adverse events. Deprenyl recipients showed significant improvement on tests of verbal memory compared with patients not taking deprenyl. Thioctic acid treatment did not improve cognitive function. These results suggest that deprenyl treatment is associated with cognitive improvement in subjects with mild HIV-associated cognitive impairment, whereas thioctic acid has no benefit. A larger efficacy trial is needed to assess the long-term effect of deprenyl on cognitive performance in patients with HIV infection.
Cognitive impairment is a common and disabling complication of advanced HIV infection. Antiretroviral agents are the only proven therapies currently used for the treatment of HIV dementia, but the response to these agents is frequently unsatisfactory, short-lived, or complicated by intolerable side effects. We hypothesized that OPC-14117, a lipophilic antioxidant that acts to scavenge superoxide anion radicals, might ameliorate the toxic interactions between HIV infected macrophages and neurons. We conducted a double-blind, placebo-controlled, randomized clinical trial to assess the safety and tolerability of OPC-14117 240 mg per day. All 30 patients enrolled (15 per group) had cognitive impairment based on performance on neuropsychological tests. The primary outcome was tolerability of the study drug as measured by the proportion of subjects able to complete the study on their assigned dosage of experimental medication. Overall OPC-14117 was as well tolerated as placebo. Five subjects withdrew because of adverse experiences (two placebo, three OPC-14117). The OPC-14117-treated group had better scores on a clinical global impression scale, compared with the placebo group. There were trends toward improvement in the cognitive test scores; however, these changes were not statistically significant. These results demonstrate that this antioxidant intervention is well tolerated in cognitively impaired patients with advanced HIV infection, and suggest that a larger efficacy trial to assess the impact of OPC-14117 on cognitive performance is warranted.
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Cognitive disorders affect thinking and perceptual processes and the acquisition of knowledge and new information. They have an enormous societal impact because special educational resources are required, and independent living often cannot be achieved. Learning problems may lead to behavioral disorders in the home and community. The pathogenesis of most mild and moderate cognitive disorders is poorly understood. Severe cognitive impairment is usually accompanied by somatic abnormalities, and an etiology can be identified in many cases. Specific treatments are available for disorders such as cogenital hypothyroidism, some metabolic acidurias, and congenital toxoplasmosis. Other disorders affecting cognition such as fetal alcohol syndrome, maternal cocaine and heroin exposure, HIV encephalopathy, and prematurity require aggressive prevention and education to reduce their occurrence. The recent advances in molecular genetics offer a faster and better method of diagnosing fragile X syndrome, now recognized as the most common inheritable cause of mental retardation. In the future, DNA analysis may elucidate the basis of many other cognitive disorders.
This study investigated the occurrence of cognitive disorders 1 and 6 months after stroke in a cohort of patients with a first-ever stroke. In addition, it was investigated whether age, sex and level of education are risk factors for vascular cognitive disorders. Memory, simple speed, cognitive flexibility and overall cognitive functioning were examined in 139 patients at 1 and 6 months post-stroke. Inclusion criteria on admission were first cerebral stroke, age>/=40, no other neurological or psychiatric disorders and ability to communicate. Mean age was 69.3 years (S.D.=12.3). Patients were compared with a healthy control group matched for age, sex and level of education. A large group of patients who, at 1 month after stroke, scored below the cutoff on cognitive domains, scored above the cutoff on most of these cognitive domains at 6 months. For overall cognitive functioning, 16 out of 39, for memory, 13 out of 26 and for cognitive flexibility, 15 out of 49 patients, who at 1 month scored below the cutoff, scored above the cutoff at 6 months. Simple speed did not change; 12 patients scored above the cutoff and 7 patients scored below the cutoff at 6 months after stroke. Speaking in terms of improvement or deterioration, most people remained stable on the four cognitive domains (ranging from 37.6% to 83.5%), and a substantial group improved (ranging from 12.9% to 52.1%). Older and female patients had more cognitive disturbances. Overall, the conclusion is that the prognosis of cognitive functioning after stroke is general favourable, especially in younger patients.
BACKGROUND: Cognitive impairment without dementia is commonly observed in ageing populations. The present study aims to describe types of impairment and evolution over a one-year period. METHOD: Three hundred and ninety-seven normal French elderly persons demonstrating recent, observable change in cognitive performance were examined annually using a computerised cognitive examination. RESULTS: Five subtypes were differentiated by cluster analysis. Two of the groups were predicted by logistic regression to be at high risk of senile dementia. Of 16 incident cases of senile dementia diagnosed in the following year, 13 were found to have derived from these two groups. The typology was also found to be useful in the description of age-associated memory impairment. CONCLUSIONS: Subclinical cognitive impairment was found to not constitute a unitary phenomenon and heterogeneous subgroups could be differentiated. The concept of 'normality' in elderly cohorts is reconsidered in the light of these findings.
The cognitive (executive) ability of patients with Parkinson's-disease (PD) deteriorates gradually during the progression of the disease. Fluency of speech, word finding, working memory, ability to plan the future and flexibility decline. Cognitive disturbance was found to be proportional with the speech, posture, gait and balance problems and can not be influenced by L-dopa substitution. Apart the dorsal and ventral mesolimbic dopaminergic systems the coerulo-cortical noradrenergic, serotoninergic and cholinergic systems are also impaired in PD. Subcortical dementia in PD can also be explained by the functional disability of dorsolateral and anterior cingular circuits. Attention deficit can be explained by the dopamine depletion of cingular cortex. Cortical Lewy bodies, neurofibrillary tangles, neurit plaques and additional vascular pathology should also play a role in cognitive impairment of PD. In several systemic degenerative diseases associating with Parkinson's syndrome (PS) i.e. progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), multiple system atrophy (MSA) dementia can be detected with various severity, therefore the question arises concerning the correlation between cognitive disability and PS. Parkinson syndrome can also develop in frontotemporal dementias (FTD), Alzheimer's disease and cortical Lewy body disease (CLBD) but no correlation exists between motor disability and severity of dementia. In CLBD dementia can be the initial symptom in 18% of cases but PS can also preceeds the dementia. In PSP profound depletion of other monoaminergic neurotransmitter system was also reported. In FTDs associated with PS degeneration of substantia nigra, locus coeruleus and basal nucleus of Meynert has been reported with increased number of neurofibrillary tangles. In patients with vascular PS (VP) there is generally no tremor and rigidity, but pseudobulbar palsy, dementia, gate disturbance, incontinency appears; L-dopa treatment is generally ineffective. In VP no cellular loss can be found within the substantia nigra, but leukoaraiosis, lacunae in the white matter and basal ganglia are commonly demonstrated.
In this study, 24 patients with subacute schizophrenic or schizoaffective psychoses were treated with "Integrated Psychological Therapy for Schizophrenic Patients" (IPT, Roder et al. 1988) and compared with 21 subacute schizophrenic or schizoaffective patients treated with sociotherapy, in respect of cognitive changes. Each therapy was administered at 8 sessions weekly for a period of 6 weeks. Advantages of the cognitively oriented therapy (IPT) appeared significantly greater with regard to interference and short-time memory improvement, and tendentially in respect to overinclusion. Neither type of therapy seems to affect schizophrenic concretism. Cognitive disorders, as reported by the patients themselves, show some remission with both forms of therapy. At 6 and 12 weeks after completion of therapy, differences between the two groups on these measures became insignificant. The findings suggest a quicker reduction of cognitive disorders by IPT in comparison with sociotherapy.
Vascular cognitive impairment (VCI) was proposed as an umbrella term to include subjects affected with any degree of cognitive impairment resulting from cerebrovascular disease (CVD), ranging from mild cognitive impairment (MCI) to vascular dementia. VCI may or may not exclude the host of "focal" circumscribed impairments of specialized functions such as language (aphasia), intentional gesture (apraxia), or categorical recognition (agnosia), among others, that may result from a stroke. Therefore, there are no universally accepted diagnostic criteria for VCI. We conclude that this concept could be more useful if it were to be limited to cases of vascular MCI without dementia, by analogy with the concept of amnestic MCI, currently considered the earliest clinically diagnosable stage of Alzheimer disease (AD). In agreement with our view,the Canadian Study on Health and Aging successfully implemented a restricted definition of VCI, excluding cases of dementia (i.e., vascular cognitive impairment no dementia, VCI-ND). The Canadian definition and diagnostic criteria could be utilized for future studies of VCI. This definition excludes isolated impairments of specialized cognitive functions. Vascular dementia (VaD): The main problem of this diagnostic category stems from the currently accepted definition of dementia that requires memory loss as the sine qua non for the diagnosis. This may result in over-sampling of patients with AD worsened by stroke (AD+CVD). This problem was minimized in controlled clinical trials of VaD by excluding patients with a prior diagnosis of AD, those with pre-existing memory loss before the index stroke, and those with amnestic MCI. We propose a definition of dementia in VaD based on presence of abnormal executive control function, severe enough to interfere with social or occupational functioning. Vascular cognitive disorder (VCD): This term, proposed by Sachdev [P. Sachdev, Vascular cognitive disorder. Int J Geriat Psychiatry 14 (1999)402-403.] would become the global diagnostic category for cognitive impairment of vascular origin, ranging from VCI to VaD. It would include specific disease entities such as post-stroke VCI, post-stroke VaD, CADASIL, Binswanger disease, and AD plus CVD. This category explicitly excludes isolated cognitive dysfunctions such as those mentioned above.
We report here on a survey conducted in Addis Ababa between September and December of 1994 to estimate the prevalence and socio-demographic correlates of schizophrenia, schizoaffective, and severe cognitive disorders. An Amharic version of the CIDI was used to collect data from a random community sample of 1420 individuals aged 15 and above. Weighted lifetime and one-month prevalence were 0.4% and 0.3%, for schizophrenia, and 0.5% and 0.4% for schizoaffective disorders, respectively. The prevalence of severe cognitive disorders was found to be 2.6%. Multivariate logistic analysis showed that the risk of lifetime psychosis (schizophrenia, schizoaffective, bipolar disorders, and depressive episodes with psychotic symptoms) was significantly higher in the age group 25-44 years compared to the reference age group of 15-24 years: adjusted Odds Ratio and 95% confidence interval, OR (95% CI) = 2.41 (1.01, 5.74); it was also significantly higher in the never married group compared to those married: OR (95% CI) = 3.01 (1.08, 8.42). The risk was significantly lower in the employed compared to the unemployed: OR (95% CI) = 0.42 (0.18, 1.00). There was a statistically significant trend of increasing risk of severe cognitive disorders with increasing age. The trend was in the reverse direction for educational status, the risk decreasing significantly with increasing educational attainment.
Transient cognitive disorders (delirium and pseudodelirium) are highly prevalent among the elderly, especially those with brain damage. Delirium is a common feature of physical illness or drug intoxication in elderly patients and requires prompt medical attention. While potentially reversible, delirium may herald death. Pseudodelirium may be induced by psychosocial stress or accompany a functional mental disorder. Transient cognitive disorders must not be confused with dementia, a chronic syndrome. The author discusses clinical features, etiology, pathogenesis, diagnosis, and treatment of delirium and related transient disorders of cognition in the elderly.
Cognitive disorders of schizophrenics as well as subjects with affective psychosis were studied with the aid of 10 tests. Differences between schizophrenics and patients with affective psychosis could hardly be detected. Subgroup differences within the two broad diagnostic categories are pointing to the importance of the severity of illness. However, some differences between two small samples (N = 9) carefully matched with regard to several relevant aspects - especially concerning the severity of disorder - show that the diagnostic category is not wholly unimportant. Judged on the basis of these differences, there are probably no deficits of a fundamentally different nature; the assumption of divergent cognitive styles or defence mechanisms considering comparable basic deficits seems more plausible.
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