Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between May-October 1989, physicians selected 50 mothers of low socioeconomic and educational background with Down Syndrome (DS) children who attended the Genetic Clinic at the Institute of Child Health and Hospital for Children in Madras, India for a study to evaluate their knowledge, attitude, and practices. The study consisted of a preevaluation, education and genetic counseling, and reevaluation at 3 months. Only 18% of the mothers knew that their children had DS. Physicians had diagnosed it at birth in these cases. Most mothers (62%) came to the hospital because they had noticed developmental delay. Most (64%) did not know what caused DS. 36% believed DS occurred due to various prenatal events including poor diet, weakness, injury, abortifacients, abdominal pain, vomiting, and long birth intervals. Family tended to blame the mothers for the child's disability which evoked social and emotional problems. When 52% learned of their children's handicap, they suffered depression. 80% did not know that their children required special care. Once learning this, however, most mothers (88%) wanted either themselves or someone else to care for their children. 96% breast fed their children and weaned them properly. 90% of the children had received immunizations. After genetic counseling and health education, all mothers understood their children's condition. 75% worked with their children at home doing passive exercises and developing their vocabulary. The rearing practices of the DS children were the same as those of the normal children. The mothers learned via the health education and genetic counseling that family planning and amniocentesis could prevent the birth of a DS child. The health education and genetic counseling program improved mothers knowledge, attitude, and practices toward child-rearing practices of DS children. This program can be duplicated among poor and illiterate parents in rural areas.
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PMID:KAP study on mothers of children with Down syndrome. 183 90

The EURODEM re-analyses of 11 case-control studies of Alzheimer's disease imply that familial aggregation of dementia, Down's syndrome, and parkinsonism occurs more frequently in Alzheimer's disease than in matched controls. Prior history of head trauma, hypothyroidism, and depression also occurs in higher frequency among patients with Alzheimer's disease. Exposure to a series of other medical conditions and environmental toxins was not significant. The association between Alzheimer's disease and maternal age remains unclear.
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PMID:The EURODEM collaborative re-analysis of case-control studies of Alzheimer's disease: implications for clinical research and practice. 191 70

A 21-year-old young man with Down's syndrome presented with depressive symptoms and intermittent features of a Parkinsonian like syndrome. After treatment with amitriptyline for 18 months he slowly improved and almost regained his former personality. Neither imaging procedures nor clinical features were able to establish a definitive cause of this patient's depression. There was no evidence of either neurodegenerative or premature aging processes. Discussion focused on increasing clinicians' awareness of frequently undiagnosed but treatable depressive disorders within the Down's syndrome population.
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PMID:Differential diagnosis and treatment of depressive features in Down's syndrome: a case illustration. 214 93

Many conditions in clinical neurology may be responsive to pyridoxine as a therapeutic agent. The current difficulty is in trying to isolate the conditions that are most likely to respond. Treating seizures is a major part of a neurologic practice. Our current therapeutic agents are only partially successful and limited by multiple side effects. One problem is that patients often have to take these agents for an entire lifetime, further raising the risk of toxicity. If pyridoxine supplementation can improve the efficacy of currently used medications, it will be gladly accepted into our therapeutic arsenal. Headache, chronic pain, and depression all appear to run together in many of our patients. The observations that serotonin deficiency is a common thread between them and that pyridoxine can raise serotonin levels open a wide range of therapeutic options. Small studies have been carried out with mixed success. Comparison with amitriptyline in the treatment of headache appears to show about equal efficacy, although side effects would be expected to be more of a problem with the amitriptyline. Behavioral disorders are relatively common and continue to be a major problem, disrupting the lives of the patients and their families. Current treatments are not acceptable to most people because of the risk of side effects with long-term usage. If, as Dr. Feingold suggests, many of these problems are caused by "toxic" exposures to chemicals that are pyridoxine antagonists, supplementation at early ages may reduce the incidence of hyperactivity and aggressive behavior. This raises the question of safety. Is pyridoxine safe for long-term use in large segments of the population, including children? The studies on children with Down's syndrome and autism, utilizing much higher doses than are used for other therapeutic purposes, seem to indicate relative safety if carefully monitored. Studies involving large population groups with carpal tunnel syndrome, all adults, using 100-150 mg/day have shown minimal or no toxicity in five- to 10-year studies. Women self-medicating for PMS taking 500 to 5000 mg/day have shown peripheral neuropathy within one to three years. It would appear from this retrospective analysis that pyridoxine is safe at doses of 100 mg/day or less in adults. In children there is not enough data to make any sort of suggestion. Because the major neurologic complication is a peripheral neuropathy and the causes of this condition are myriad, pyridoxine may cause neuropathy only in patients with a pre-existing susceptibility to this condition.
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PMID:Vitamin B6 in clinical neurology. 216 44

The purpose of this study was to examine the role of perceived parenting stress and parental depression on marital intimacy between parents of handicapped children versus developmentally normal children, and to investigate discrepancies between husbands' and wives' reports of marital intimacy. The parents of 31 autistic children, 31 Down Syndrome children and 62 developmentally normal children, matched for both mental and chronological age were studied. Results indicated significantly greater stress and depression, as well as lower marital intimacy for mothers of autistic children than mothers of normal children, and significantly greater stress than mothers of Down Syndrome children who fell somewhere between other groups of parents in all three measures. Fathers of autistic children experienced significantly higher parenting stress than the other groups, as well as lower marital intimacy but there were no differences amongst fathers on measures of depression. Low scores on subscales of identity and compatibility for mothers implying low self esteem contributed significantly to the lowered perception of marital intimacy. Implications for intervention, based on these findings, are discussed.
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PMID:Marital intimacy in parents of exceptional children. 252 93

Twenty-four patients with Down syndrome and leukemia were studied. A strong male predominance (79%) was found. Age ranged between 18 months and 15 years (mean: 5 6/12); 54% of the patients were less than 4 years of age at the time of diagnosis. A preleukemic phase was noted in 6/24 patients. This phase, characterized essentially by thrombocytopenia, lasted from 2-8 months. Patients with preleukemia had unusual blast cell morphology and involvement of more than one cell line (dyserythropoiesis, hypolobulated megakaryocytes) and were probably M7 leukemias. All patients demonstrated severe methotrexate toxicity at standard methotrexate doses. Toxicity, manifesting as mouth ulcerations and bone marrow depression was seen regardless of the route of administration (oral, intrathecal or intravenous). A 30%-50% reduction of the standard dose was tolerated. Methotrexate absorption and clearance were studied in two patients and were found to be normal. We postulate that the observed toxicity of methotrexate may be due to a gene dosage effect for enzymes known to be on chromosome 21 and intervening in purine metabolism. Increased purine synthesis implies greater tetrahydrofolic acid demands and therefore greater sensitivity to an antifolate agent.
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PMID:Down syndrome and leukemia: unusual clinical aspects and unexpected methotrexate sensitivity. 295 83

In a child with Down's syndrome (DS) and her sibling, host immune responses were evaluated under experimental gingivitis conditions. The children live in the same environment under identical conditions. In the DS child an earlier and more extensive gingival inflammation than in her sibling had been observed. Investigation of nonspecific host defense mechanisms revealed identical results in both children for the phagocytosis and intracellular killing of Candida albicans by polymorphonuclear leukocytes in crevicular washings (CR-PMNs), in blood (PB-PMNs) and blood monocytes. Furthermore, CR- and PB-PMNs were able to secrete identical amounts of hydrogen peroxide upon stimulation. The chemotactic response of PB-PMNs in the DS child was impaired, however. The results of the studies performed on parameters of specific host defense mechanisms showed low blastogenic responses to phytohemagglutinin (PHA) and pokeweed (PWM) by lymphocytes of the DS child as compared with her sibling. Also a lack of immune regulation leading to prolonged helper/inducer cell activation on a local (gingival) and circulation level and a less pronounced T-cell depression in PB were shown. Together, these differences observed in specific and nonspecific host response mechanisms may be responsible for the earlier and more extensive gingival inflammation found in the DS child.
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PMID:Nonspecific and specific immune responses in a child with Down's syndrome and her sibling. A case report. 296 46

The occurrence of anxiety or depression, experience of social support and feelings about the family situation were evaluated in 13 mothers of children of primary school age with Down's syndrome (DS). The results were compared with those obtained in a group of 13 females engaged in taking care of these children and assisting their families. Questionnaires were used to assess feelings of depression or anxiety (Hospital Anxiety and Depression Scale), to evaluate social support (Interview Schedule for Social Interaction) and the family situation (Family Adaptability and Cohesion Evaluation Scale). A semi-structured interview with the mothers was also conducted. The results indicated that negative feelings at the birth of a child with DS had almost invariably changed in a positive direction. Experience of depression or anxiety was uncommon. Social and emotional contacts were quantitatively normal, although more empathy was often desired. The families were relatively often described as enmeshed and controlled, but the experience of the family situation was generally positive.
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PMID:Mothers of primary school children with Down's syndrome. How do they experience their situation? 297 64

Diet clearly influences neurotransmission. This can be important in grossly undernourished children. It can also be important in children in whom normal homeostatic mechanisms governing food intake are bypassed. Subtle differences in behavior can occur with physiologic variation in food intake. Components of foods can also be used as drugs. Starvation can impair neuronal maturation and can have lasting effects upon behavior and intellectual performance. The extent of starvation's impact upon the brain depends upon whether undernutrition occurred during a critical phase in brain development. Short-term fasting has small, but significant, effects upon intellectual performance. Even when gross malnutrition is not present, subtle changes in diet may modulate brain function. Tryptophan, tyrosine, and choline in the diet are used as precursors for neuronal synthesis of serotonin, dopamine and norepinephrine, and acetylcholine, respectively. It is likely that the brain's sensitivity to certain components of the diet exists to permit monitoring of food intake by the central nervous system. Tryptophan, tyrosine, and choline may be useful in treatment of humans with sleep disorders, pain depression, mania, hypertension, shock, or dyskinesias. Other components of the diet that may affect behavior include food additives, sugar, and caffeine. Food additives may exacerbate hyperactive symptoms in a small proportion of children with attention deficit disorder. Given that there is little potential for harm and that there is a subpopulation that may respond, a trial of a diet that contains no food additives may be a valid diagnostic approach for children with attention deficit disorder who do not respond to stimulant therapy or for children for whom stimulant therapy is not desired. Refined sugar has been blamed for many behavioral abnormalities. Subtle effects of carbohydrate upon behavior have been reported, but the existing data do not support the hypothesis that sucrose or fructose exert special effects upon neurotransmission. Caffeine is easily detected as a stimulant by humans, but it has little effect upon cognitive function. Administration of large doses of vitamins has no beneficial effect in most humans with schizophrenia, attention deficit disorder, autism, Down's syndrome, or drug addiction. Large doses of niacinamide may even be harmful, as they may cause hepatic damage.
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PMID:Dietary influences on neurotransmission. 302 51

The prevalence of severe dementia in the United States is about 1.3 million cases, of which at least 50 to 60% are of the Alzheimer type. Severe dementia of the Alzheimer type is found rarely in a clearly dominant pattern, although often one or more relatives are affected. Down's syndrome in adults is often associated with Alzheimer changes. The diagnosis is a clinicopathological one; there is a considerable error rate in the clinical diagnosis early in the course of the disease, especially in regard to dementia in depression. The differential diagnosis involves a great many disorders, including multi-infarct dementia, tumors, subdural hematomas, and others. Physiological aspects of Alzheimer's disease include a diffusely slow electroencephalogram, reduced cerebral blood flow, and particular patterns noted on positron emission tomographic scanning. The latter technique has also demonstrated that oxygen extraction is normal in Alzheimer's disease, thus excluding ischemia from possible pathogenetic factors. Morphological changes, that is, the presence of plaques and tangles, are widely distributed in neocortex, paleocortex, and many deep gray areas down through the pontine tegmentum, but largely exclude the basal ganglia, thalamus, and substantia nigra. Numerous plaques without neocortical tangles are found in many demented persons older than 75 years. A severe loss of large neocortical neurons is characteristic of the disease. The chemical nature of the paired helical filaments that make up the neurofibrillary tangle has not yet been ascertained. Neurons are markedly deficient in the basal forebrain nuclei, and this deficiency may account for the severe diminution of choline acetyltransferase and acetylcholine in the neocortex and paleocortex. Muscarinic cholinergic receptors are present in normal amounts. Norepinephrine is reduced in some cases, and somatostatin in most. Substance P is low in severe cases. The etiology of the disorder is unknown and the role of aluminum is disputed. Management of patients with Alzheimer's disease is difficult, and neuroleptics are to be used with great caution because of their side effects. Substrate therapy has not been effective; physostigmine improves memory but is not suitable for general use. Trophic factors, gangliosides, and aluminum chelation are being investigated for use in pharmacological intervention.
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PMID:Senile dementia of the Alzheimer type. 613 75


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