ABSTRACT
Autism is a severe neurodevelopmental disorder that is typically diagnosed by 3 years of age. Core symptoms of autism include profound deficits in social interaction and communication, restricted interests, stereotyped responses, and other repetitive patterns of behavior. Other abnormalities include mental retardation and comorbid epilepsy. These symptoms underscore the consequences of genetic inheritance for brain function and behavior. The etiology of autism may involve an interaction between genetic susceptibility (mediated by multiple genes) and environmental factors influencing brain development.
Subject(s)
Autistic Disorder/etiology , Autistic Disorder/genetics , Brain Diseases/etiology , Developmental Disabilities/etiology , Brain Diseases/genetics , Child, Preschool , Developmental Disabilities/genetics , Environment , Genetic Predisposition to Disease , HumansABSTRACT
The world population is aging The frontier between physiological and pathological brain aging is somewhat unclear. Pathological aging can cause both mild cognitive impairments and dementias (vascular and Alzheimer). It is important to understand brain aging in order to identify risk factors and develop protective measures. Proper lifetime brain protection could improve quality of life in old age.
Subject(s)
Aging/psychology , Brain/physiopathology , Population Dynamics , Aged , Aged, 80 and over/psychology , Aging/physiology , Brain/growth & development , Cognition Disorders/epidemiology , Cognition Disorders/etiology , Cognition Disorders/prevention & control , Dementia/epidemiology , Dementia/etiology , Dementia/prevention & control , Female , Humans , Male , Psychology , RiskABSTRACT
The adult brain has more plasticity than previously believed. Neurogenesis, growth and branching of dendrites, and remodeling of synaptic contacts in different regions of the brain occur continuously. Numerous studies have reported a decrease in neuroplasticity in depressed patients and/or in animals subjected to stress and to different models of depression. This has led to the proposal of a new approach to the pathophysiology of depression: depression could be the result of the decrease in neuroplasticity in brain structures involved in the control of mood. This new approach to the pathophysiology of depression can lead to better understanding of, or the proposal of more solid hypotheses about, some issues such as the impact of genetics and environmental factors on the occurrence of depressive episodes, the increased risk of depression in patients with somatic diseases in which there are alterations of neuroplasticity, or the increased risk of depressive relapse in depressed patients in partial remission in whom we suspect that neuroplasticity is only partially restored. These observations have also led to the proposal of new hypotheses concerning the mode of action of antidepressant drugs. In this regard, tianeptine is of particular interest. Tianeptine's pharmacological and clinical properties have been extensively studied. Tianeptine has specific neurotrophic properties, and its antidepressant properties have been well demonstrated. Tianeptine provides early relief of anxious symptoms without sedation in depressed patients. The acceptability and safety profiles of tianeptine are appreciated by both physicians and patients; for instance, tianeptine does not induce sexual dysfunction, nausea, or weight gain. It is of interest to focus on what we already know about tianeptine's pharmacological and clinical properties, and to create mechanistic hypotheses about the similarities and differences observed in clinical practice between tianeptine and other antidepressants.
Subject(s)
Antidepressive Agents/pharmacology , Antidepressive Agents/therapeutic use , Depressive Disorder/physiopathology , Depressive Disorder/therapy , Neuronal Plasticity/drug effects , Anti-Anxiety Agents/adverse effects , Anti-Anxiety Agents/pharmacology , Anti-Anxiety Agents/therapeutic use , Antidepressive Agents/adverse effects , HumansSubject(s)
Humans , Male , Female , Economic Development , Population , Population Dynamics , Population Forecast , Public Health , Budgets , Cause of Death , Demography , Fecundity Rate , Fertility , Gross Domestic Product , Infant Mortality , Longevity , Maternal Mortality , Mental Disorders/epidemiology , Neurologic Manifestations , Tuberculosis/epidemiologyABSTRACT
Em um estudo aberto multicêntrico, 154 esquizofrênicos (DSM-III - R) com um escore total > 60 na PANSS foram tratados durante 7 meses com a risperidona depois de um período de "wash-out". As doses foram aumentadas até 3 mg duas vezes por dia na primeira semana e de forma flexível, de acordo com a ICG, a dose podia ser aumentada até 16 mg/dia no final do primeiro mês. A partir daí, foi recomendado manter-se dose estável nos próximos 6 meses do tratamento. Os parâmetros de eficácia foram: ICG aplicada mensalmente e PANSS aplicada nos meses 1, 4 e 7. A segurança da risperidona foi avaliada por meio de exame físico, testes laboratoriais, ECG e sinais vitais (PS,PD e FC). As reaçoes adversas foram registradas em todas as visitas do estudo, os sintomas extrapiramidais (SEP) foram avaliados segundo a Extrapyramidal Symptom Rating Scale (ESRS) e também ICG para gravidade de parkinsonismo e discinesia. Cerca de 77 porcento dos pacientes completaram o estudo e em apenas 9 porcento o térmico precoce foi atribuído a falta de eficácia. De uma maneira geral, a risperidona foi eficaz (diminuiçao da sintomatologia > 20 porcento) em cerca de 70 porcento dos pacientes. As reaçoes adversas mais freqüentes foram insônia (14,1 porcento ) e ganho de peso (10,9 porcento). A risperidona nao causou nenhuma alteraçao importante nos testes laboratoriais realizados antes do início e no final do tratamento. Durante o período de tratamento houve uma diminuiçao dos SEP apesar de ter havido um aumento da dose média diária. Isto foi atribuído à tolerância. A dose ótima foi de 6 a 8 mg/dia, contudo, para alguns pacientes mais pode ser necessário se aumentar a dose. Em conclusao, nossos dados sugerem que a risperidona é um medicamento seguro, tem um rápido início de açao e na dose média de 6 a 8 mg/dia foi eficaz tanto em sintomas positivos como negativos; a resposta terapêutica tende a aumentar ao longo do tratamento enquanto que os SEP, além de poucos, mant6em-se estáveis ou tendem a diminuir.
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Antipsychotic Agents/therapeutic use , Risperidone/therapeutic use , Psychotic Disorders/drug therapy , Antipsychotic Agents/adverse effects , Brazil , Patient Dropouts , Basal Ganglia Diseases/drug therapy , Multicenter Studies as Topic , Psychotic Disorders , Risperidone/adverse effects , Schizophrenia/drug therapyABSTRACT
Os autores estudaram 29 pacientes esquizofrênicos crônicos e hospitalizados, sob tratamento com neurolépticos por via oral, nos quais esta medicaçäo foi substituída por decanoato de haloperidol, por via intramuscular aplicada a cada quatro semanas. Os pacientes foram avaliados, antes, durante e após o tratamento, através da BPRS, escala clínica global e escala de efeitos colaterais de BORDELEAU. A grande maioria dos pacientes recebeu 100mg IM cada quatro semanas, equivalente, aproximadamente, a 20 vezes a dose diária de haloperidol ou dose correspondente de outro neuroléptico. Concluíram que o decanoato de haloperidol, administrado nestas condiçöes, mostrou-se um medicamento seguro e eficaz, tornando-se uma opçäo prática e confortável para o tratamento de manutençäo de esquizofrênicos crônicos