[Speech training and training of daily activities of a child with aphasia following a cognition disorder].
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BACKGROUND: Cognitive impairment may be part of the endophenotype of bipolar disorder (BP), but little is known about patterns and severity of impairment in BP subgroups and their relation to depression. The same applies to deficits in emotion processing known to be present in BP. METHOD: To explore the relationship between depression and impairment in cognition and emotion processing and the differences between BP subgroups, we assessed 36 (25 BP I and 11 BP II) patients using a cognitive battery and a facial emotion recognition task. RESULTS: BP patients were impaired compared to published norms on memory, naming and executive measures (Binomial Single Proportion tests, p<0.05). Cognitive performance was largely unrelated to depression ratings. Surprise recognition was the only emotion processing impairment in BP patients compared to controls (patients' recognition score 75% v. controls' 89%, p=0.024). Patients with higher depression ratings were more impaired in recognizing expressions of anger (t23=2.21, p=0.037). BP II patients were more impaired than BP I patients in IQ, memory and executive measures (Mann-Whitney tests, p<0.05). Depression severity or exposure to medication or electroconvulsive therapy (ECT) did not explain these differences. CONCLUSIONS: We confirm cognitive impairment and an isolated facial emotion processing deficit in BP patients and suggest that these deficits are largely unrelated to depressive symptoms. Our study also provides evidence that cognitive deficits are more severe and pervasive in BP II patients, suggesting that recurrent depressive episodes, rather than mania, may have a more detrimental and lasting effect on cognition.
The fragile X syndrome is one of the main etiologies of mental retardation in human beings. Some of its specific cognitive and language disturbances are nowadays well known. Disturbances of behavior are frequent. They are akin to psychotic manifestations and are mainly described in terms of autistic syndromes. The question of the possible links between autism and the fragile X syndrome is being discussed since 1980. The authors give a synthetic and critic overview of the studies reporting on the frequency of co-occurrence of these syndromes and offer some reflexion on the true questions at stakes in the debate. They emphasize the determining role of future clinical research in autism in order to objectively contribute to the progression of knowledge in this field.
OBJECTIVE: In a previous randomized controlled study, the authors reported significant beneficial effects of cognitive therapy for relapse prevention in bipolar disorder patients up to 1 year. This study reports additional 18-month follow-up data and presents an overview of the effect of therapy over 30 months. METHOD: Patients with DSM-IV bipolar I disorder (N=103) suffering from frequent relapses were randomly assigned into a cognitive therapy plus medication group or a control condition of medication only. Independent raters, who were blind to patient group status, assessed patients at 6-month intervals. RESULTS: Over 30 months, the cognitive therapy group had significantly better outcome in terms of time to relapse. However, the effect of relapse prevention was mainly in the first year. The cognitive therapy group also spent 110 fewer days (95% CI=32 to 189) in bipolar episodes out of a total of 900 for the whole 30 months and 54 fewer days (95% CI=3 to 105) in bipolar episodes out of a total of 450 for the last 18 months. Multivariate analyses of variance showed that over the last 18 months, the cognitive therapy group exhibited significantly better mood ratings, social functioning, coping with bipolar prodromes, and dysfunctional goal attainment cognition. CONCLUSIONS: Patients in the cognitive therapy group had significantly fewer days in bipolar episodes after the effect of medication compliance was controlled. However, the results showed that cognitive therapy had no significant effect in relapse reduction over the last 18 months of the study period. Further studies should explore the effect of booster sessions or maintenance therapy.
A 68 year old man developed progressive cognitive impairment with an akinetic-rigid syndrome which was atypically responsive to levodopa. The patient died after 18 months and the postmortem examination showed typical Lewy bodies in the substantia nigra and pale bodies in the cortex which were unlabelled by ubiquitin antibodies. This case is particular by the neuropathological examination (no immunoreactivity to antibodies against ubiquitin) and by the abnormal response to treatment (dystonia). These two aspects are discussed.
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The authors present a critical overview of the multiple studies of cognitive functions of patients with obsessive compulsive disorder. First are mentioned some correlations between neurological diseases and obsessive compulsive disorder. Then, the authors analyse the results obtained by the patients in WAIS, in the tactual perception memory test, in visual memory and orientation and in verbal memory. Verbal behaviour, performances in sensory perception tests, motor performances, attention and, lastly, troubles in information processing are reviewed. With these results, the authors try to develop the relevant theories about the mechanisms in obsessive compulsive disorder: dysfunction of the dominant hemisphere and abnormality of the serotoninergic system.
OBJECTIVES: To find a correlation between chronic nonrheumatic atrial fibrillation (CNRAF) and cognitive impairment in a group of older, nondemented patients. SETTING: Acute Care Unit for the Elderly, Poliambulanza Hospital, Brescia (Italy). METHODS: Two hundred fifty-five hospital in-patients older than 70 years (42 with CNRAF and 213 controls with normal sinus rhythm) were assessed by complete clinical history, physical examination, ECG, serum albumin levels, APACHE II score, mental status (Mini-Mental State Exam [MMSE] and Geriatric Depression Score [GDS]), functional status (Barthel Index and instrumental activities of daily living [IADL]), number of prescribed drugs, and comorbidity (Charlson Index). RESULTS: The group of patients with CNRAF had MMSE scores significantly lower than that of the reference group with normal sinus rhythm. Chronic nonrheumatic atrial fibrillation retained an independent relation to cognitive impairment also after adjusting for those variables associated with mental decline in univariate models (GDS, IADL, and APACHE II scores). CONCLUSIONS: The results of this study support the relationship between nonrheumatic atrial fibrillation and impaired cognitive function. Independent of etiopathogenetic mechanisms (thromboembolic or hemodynamic hypotheses), prevention of cognitive impairment in older persons should take into account the treatment of atrial fibrillation and its consequences.
While diagnostic criteria and epidemiologic results are available for dementia, reliable quantitative information on mild cognitive impairment is rare. The distinction between mild cognitive impairment, effects of normal ageing and dementia can be difficult to establish. Conceptual problems notwithstanding, a growing number of patients with dementia and with mild cognitive impairment can be safely predicted. Reduced quality of life on the part of patients and their families, growing demand for care and increasing costs of illness will prove the socioeconomic relevance of dementia.
There seems to be an anatomic correspondence between pathways of monoamine-containing neurons and the brainstem and diencephalic lesions associated with Korsakoff's psychosis. In 25 patients with Korsakoff's disease, we found that CSF levels of metabolites of norepinephrine, dopamine, and serotonin were significantly lower than in controls. Norepinephrine metabolite levels were reduced more consistently and extensively than those of dopamine and serotonin. The 25 patients had circumscribed cognitive deficits, but were not demented. We argue that norepinephrine-containing neurons are selectively damaged in Korsakoff's psychosis and that lesions of brain monoamine-containing neurons cause specific cognitive impairments, not global dementia.
In order to evaluate the relationship between exposure to aluminum and cognitive functions, a group of 50 aluminum welders underwent to the following neuropsychological tests: Wechsler Memory Scale, Color-Word Test and Raven Progressives Matrices test. The results of the tests showed a reduction of memory, of concentration and a slight reduction of attention. The authors conclude that aluminum exposure leads cognitive changes.
The syndrome of mild cognitive impairment (MCI) is heterogeneous in terms of aetiology, psychopathology, and prognosis. It is characterised by cognitive deterioration significantly exceeding the decline attributable to aging but not reaching the severity of dementia. The prevalence of MCI is estimated to be 17% in the population over 65 years old. At neuropathological examination, a large proportion of patients with mild cognitive impairment, particularly of the amnestic type, show typical features of Alzheimer's disease. The former progresses to dementia at an annual rate of 10% to 15%. In some cases, however, there is stable impairment or remission. The neurodegenerative process of Alzheimer's disease can be demonstrated in at least some patients using volumetric magnetic resonance imaging, 18-FDG positron emission tomography, or biochemical markers in the cerebrospinal fluid. It is not yet known whether patients with mild cognitive impairment or at least those with predementia Alzheimer's disease can benefit from currently available symptomatic treatments. Patients with early-stage Alzheimer's are an important target group for treatment interventions aiming at slowing the neurodegenerative process.
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