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At least 145 records · Page 8Linked to original sources

Clinical confirmation of the American Academy of Neurology algorithm for HIV-1-associated cognitive/motor disorder. The Dana Consortium on Therapy for HIV Dementia and Related Cognitive Disorders.

OBJECTIVE: Our goal was to put into operation the American Academy of Neurology (AAN) algorithm for the definition of minor cognitive/motor disorder and human immunodeficiency virus type 1 (HIV-1)-associated dementia complex (ADC) and examine the neuropsychological, neurologic, psychiatric, and functional deficits in affected subjects. DESIGN: Two hundred seventy-one HIV-positive men and women with CD4 count of < 200 or demonstrated cognitive impairment were recruited from three sites (Columbia University, The Johns Hopkins University, and the University of Rochester) and underwent standardized assessments. RESULTS: Sixty-five subjects met criteria for ADC (cognitive, functional, and neurologic or behavioral), 56 met criteria for minor cognitive/motor disorder, and 150 met criteria for neither. Seventy-eight subjects met neuropsychological and neurologic/behavioral criteria but did not demonstrate functional impairment. Those with ADC performed significantly worse on speeded motor and verbal memory tests and demonstrated more extrapyramidal signs and behavioral symptoms than did the other two groups. Both ADC and minor cognitive/motor disorder were independently predictive of poor physical function, after adjustment for age, gender, years of education, log (CD4 count), hemoglobin, number of HIV diagnoses and medications, and depression. CONCLUSIONS: The operationalization of AAN criteria demonstrates that it is rare to have both cognitive and functional impairment without associated neurologic and/or behavioral deficits. Functional impairment in isolation is also rare. Dementia is an independent predictor of physical function.

AIDS Dementia Complex↗

[Cognitive disorders in patients with Huntington's disease].

INTRODUCTION: Huntington s disease has been clearly recognized since 1872. It is characterized by the appearance of a motor disorder (chorea) accompanied by selective cognitive deterioration which is not interfered with by aging. DEVELOPMENT: Since the genetic defect causing it has been identified (expansion of CAG triplets on the IT 15 gene of chromosome 4) it has been possible to study families from the preclinical stage (asymptomatic persons who carried the mutation) to the stage of full development of the clinical syndrome. The behaviour disorders most often seen in these patients are depression, mania, schizophrenia, paranoia, anxiety, obsessive and obsessive compulsive disorders although other disorders may also occur. Different clinical forms of motor disorders and dementia have been reported in relation to the age of onset of the symptoms. The commonest cognitive symptoms are defects of attention, memory, planning, sequencing and visuo spatial deficits, as occurs in subcortical dementia. Our objective is to present the different clinical forms of the disorder according to the age of presentation, implication of the symptoms, severity of the genetic defect (number of CAG triplets) and to describe the study made of asymptomatic carriers so as to be able to detect incipient cognitive deterioration in these persons.

Adolescent↗

Longitudinal evaluation of cognitive disorder in Huntington's disease.

The study investigated longitudinal change in cognitive function in 87 patients with Huntington's disease (HD), using a range of neuropsychological tests, which tap mental manipulative abilities, memory, and frontal executive skills. Over a 1-year period the largest changes were noted in letter fluency, object recall, and Stroop Test performance, whereas no changes were noted over more than 3 years on the modified Wisconsin Card Sorting Test. Contrary to expectation, greater change was evident over 1 year for tasks with low compared to high cognitive demands. The differential sensitivity of tasks was attributed in part to inherent characteristics of the tests themselves: their capacity to detect minor gradations of change and their vulnerability to practice effects. However, the greater change for relatively automatic, speed-based tasks with low cognitive demands was interpreted as reflecting the evolution of HD, with a greater magnitude of change occurring in basal ganglia than cortical function. One purpose of the study was to identify tasks sensitive to the progression of HD and hence most suitable for the evaluation of therapies. Despite reaching statistical significance by virtue of the large group size, numerical differences in test scores over 1 year were very small, suggesting that the use of such tests to evaluate change in individuals or small groups of subjects would be problematic. The data highlight the slow progression of HD, the limitations of standard cognitive tests in detecting change over short periods, and the need for therapeutic studies that encompass a relatively prolonged time frame.

Adult↗

[Effectiveness of felodipine in hypertensive patients with mild cerebral cognition disorders in a randomized double-blind study].

BACKGROUND AND OBJECTIVE: Cognitive impairment occurs more frequently in hypertensives than in normotensive individuals. Early signs of cognitive impairment are predictors of dementia in late life. Felodipine is capable of almost normalizing plasma viscosity, which is elevated in most of hypertensive patients, thus improving microcirculation. The aim of this study was to evaluate whether this hemorheologic property of felodipine in addition to its blood pressure lowering effect can improve cognitive performance in hypertensive patients. PATIENTS AND METHODS: Randomized, double-blind comparison between felodipine 10 mg and hydrochlorothiazide 50 mg amiloride 5 mg (HCT/amiloride) in patients 50-70 years of age with impaired cognitive function (c.l. test 1-2 points) and with resting blood pressure values of diastolic > 95 and < or = 115 mmHg and/or systolic > 160 and < or = 210 mmHg. Blood pressure measurements and evaluation of total short term storage capacity were done at the beginning and after 12 weeks of treatment. RESULTS: 31 patients (14 felodipine and 17 HCT/amiloride) were included in the per protocol analysis. Blood pressure values at the beginning and after 12 weeks of treatment were (mmHg): for felodipine systolic 168 +/- 4 and 150 +/- 6 (p < 0.01), diastolic 108 +/- 3 and 88 +/- 4 (p < 0.001). For amiloride/HCT systolic 173 +/- 8 and 150 +/- 10 (p < 0.01), diastolic 105 +/- 5 and 88 +/- 5 (p < 0.001). Short term storage capacity improved by 15 +/- 6 bits during felodipine treatment (p < 0.001) and by 9 +/- 9 bits during amiloride/HCT treatment (p < 0.05). Thus cognitive improvement was superior by 67% in the felodipine group compared to amiloride/HCT (p < 0.05). CONCLUSION: In this study a pronounced improvement of mental performance occurred in patients treated with felodipine. Since the cognitive gain was significantly superior to amiloride/HCT treatment there must be an additional blood pressure-independent effect of felodipine, such as enhancing microcirculation. Whether these properties possibly counteract the development of dementia in hypertensives has to be evaluated in long term studies in more patients.

Aged↗

Diagnosis and management of memory loss and cognitive disorders among elderly persons.

Memory loss and other cognitive dysfunctions, although common in elderly persons, are not universal features of old age. Instead they herald the presence of various neuropsychiatric diseases, which are first recognized as syndromes. The two most common neuropsychiatric syndromes, dementia and delirium, produce global changes in cognition and other capacities. They are differentiated by the patient's level of consciousness, which is impaired in delirium but intact in dementia. Delirium is generally reversible and often indicates serious physical illness. Although dementia is occasionally reversible, the mainstays of its management and treatment are palliative. Comorbid psychiatric symptoms are common in patients with both delirium or dementia, and their recognition and treatment constitute an important task for the geropsychiatrist. The differential diagnosis of primary dementing illness and other psychiatric illnesses such as depression is complex, because symptoms of the two kinds of disorders often coexist and common pathogenetic mechanisms may underlie both syndromes.

Aged↗

[Cognitive disorders in schizophrenic patients. A controlled study].

In a controlled study, the cognitive functions measured by different association tests in a group of 40 schizophrenic inpatients (ICD 295.1+.3+.6) were compared to those of a control group that was matched according to age, sex and IQ. The results indicate that the basic cognitive functions of schizophrenic patients do not differ significantly from those of a control group in the lower-order tasks. In more complex and higher-order tasks, however, schizophrenic patients show a tendency to prefer less obvious associations (overinclusion) and to reject conventional associations (overexclusion). The results are discussed in the context of current literature as a lack of the cognitive organizing principle and its effects on rehabilitation, creativity and art in schizophrenic patients.

Adult↗

Effects of N-propargyl-1-(R)aminoindan (rasagiline) in models of motor and cognition disorders.

N-propargyl-1-(R)aminoindan (rasagiline) is a new and selective irreversible MAO-B inhibitor, currently being considered as the mesylate salt for potential therapy in certain neurological disorders. It has been studied in animal models of cognition and motor dysfunction. Its ability to restore normal motor activity was determined in models of acute drug-induced dopaminergic dysfunction: Its effects in improving cognition and memory deficits was studied in adult and senescent rats that had been exposed to prolonged hypoxia, then subjected to the passive and active avoidance tests. In alpha-methyl-p-tyrosine (alpha-MpT)-induced hypokinesia (100-120 mg/kg, i.p.) pretreatment with rasagiline at 2.5 mg/kg i.p. restored motor activity to control level. But pretreatment with reserpine abolished the protective effect of rasagiline. Rasagiline at 0.5 mg/kg/day was protective against alpha-MpT also in hypoxia-lesioned rats. In haloperidol-induced catalepsy in rats (1.5 mg/kg, s.c.) or mice (4-6 mg/kg s.c.), rasagiline improved recovery of normal locomotion, gait and coordination at 0.4-2.4 mg/kg i.p. and 1.8-1.5 mg/kg i.p., respectively. In amphetamine-induced stereotypy (0.6 mg/kg s.c., rasagiline potentiated this effect at 1.5 mg/kg i.p. In hypoxia-induced impairment of memory and learning, rasagiline at 0.32-0.5 mg/kg/day per os improved performance of adult rats in passive and active avoidance, and of senescent rats in active avoidance. Selegiline was either ineffective or less effective at equivalent doses. Racemic N-propargyl-1-aminoindan (AGN-1135), besides being of lower potency, had a different dose-dependency than rasagiline in antagonizing haloperidol-induced catalepsy or alpha-MpT-induced hypokinesia. 1-(R)aminoindan ((R)AI), a metabolite of rasagiline, in relatively high doses produced effects that were distinct in certain respects from those of rasagiline.

Aging↗