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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Two cases of electroconvulsive therapy (ECT) in adolescence are presented and the literature on the use of ECT in childhood and adolescence is reviewed. ECT was effective in children and adolescents with bipolar disorder and depression. Inadequate information exists to make a judgment regarding schizophrenia, delirium, and anorexia nervosa. ECT is not effective in autism and chronic organic brain syndromes. Complications cited include organicity and seizures in the period immediately after ECT, anxiety reactions, and disinhibition. Long-term memory deficit or cognitive impairment has not been found, although further research to rule out residual impairment is needed.
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PMID:A review of ECT for children and adolescents. 222 48

There are some evidences to propose blood platelets as a model of bioaminergic neurons. Similarities between platelets and neurons are particularly important with respect to serotonin metabolism but now it is possible to extend this model to other neurotransmitters such as dopamine, GABA, glutamate... The reason for these similarities may be due to the common embryonic origin of these two very different cell types. Some changes of platelet functions are observed in psychiatric syndromes. For example: serotonin uptake, bioamine storage, enzymatic activities are modified in different types of depression and schizophrenia, infantile autism, neurologic diseases (migraine, chorea, Down syndrom). Furthermore, psychotropic drugs also alter the platelet functions. Recently, the discovery of neuro-endocrine disorders in psychiatric diseases has led to the proposal of platelets as a model in neuro-endocrinology. Some arguments can be developed to support this hypothesis. In biological psychiatry, the platelet model seems actually useful essentially in the classification of psychiatric diseases, the management of treatments and the study of new psychotropic drugs. However methodologic difficulties still presently limit the development of this model.
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PMID:[Blood platelets: neuronal model in psychiatric disorders]. 286 6

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 clinical spectrum of autism spans a broad range of functions, but the core symptoms remain the same regardless of the intelligence of the child: the autistic type of social deficit that ranges from a lack of inclination to relate to extreme difficulty with the mechanics of social interactions, a global communication deficit that involves both verbal and nonverbal modes, and a severe cognitive deficit involving concept formation (abstraction) that is combined with an exceptional memory for factual information. These symptoms may vary dramatically in severity, but the basic deficits are identifiable regardless of IQ. Under-recognition of autism is a major problem at all IQs, but especially in patients with IQs above 50. No drugs have been found to significantly improve the core deficits in autism. Antipsychotics should be avoided except for short-term use. Antidepressants, anxiolytics, and anticonvulsants are important in the treatment of depression, affective modulation, situation-related stress, and seizures. Intensive social skills training is assuming a prominent role in behavior modification programs, and success with higher-functioning autistic children suggests that outcome can be improved by intensive training. The neurobiology of autism has also undergone dramatic changes. The psychogenic theories of etiology have been completely invalidated. Autism is now considered to be a neurological disorder resulting from an error in brain development. The precise location and nature of this deficit are still being actively debated and investigated. One theory emphasizes a dysfunction of the limbic system that results in an impairment in the acquisition of information. A second theory proposes a primary role for dysfunction of the cortical association network responsible for the processing of information.
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PMID:New perspectives in autism, Part II: The differential diagnosis and neurobiology of autism. 306 39

The role of cognition in child development is reviewed with respect to the role of cognitive processing and cognitive deficits. Cognitive processing is discussed with respect to the self-system; the effects of psychosocial experiences; risk, vulnerability and protective mechanisms; vulnerability to depression; aetiology and treatment of depression. Cognitive deficits are discussed with respect to the socio-emotional consequences of language delay and reading difficulties; hyperkinetic/attentional deficit syndromes; schizophrenia; and autism. It is concluded that the ways in which we appraise our life circumstances and the ways in which we react to experiences of all kinds are greatly influenced by how we think about ourselves and our environment. Biases and distortions in such cognitive processing may be associated with social and emotional malfunction. These biases may derive from earlier experiences, from intensive temperamental styles, or from deficits in the ability to process incoming information. The further study of cognitive processing and cognitive deficits is likely to be rewarding and helpful for clinical practice.
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PMID:The role of cognition in child development and disorder. 356 6

Developmental psychopathology constitutes a research strategy that is concerned with questions about continuities and discontinuities over time (the developmental perspective) and over the span of behavioural variation (the psychopathological perspective). The utility of this approach is discussed in relation to childhood depression, autism and schizophrenia, and the effects of adverse life experiences.
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PMID:Child psychiatry: the interface between clinical and developmental research. 396 Oct 41

Due to asymmetry of brain neurotransmitters and differential hemispheric information processing modes, it is suggested that the excessive use of one information processing mode could engender a state of brain reactivity whose neurochemical correlates would be either a rise in melatonin or beta-endorphin in systemic circulation. Since melatonin and beta-endorphin have opposite effects on lung-mediated regulation of prostaglandins, it is further suggested that the pulmonary inactivation of prostaglandin E1 would either be increased or inhibited. Low levels of PGE1 would engender high levels of PGE2 whose effects would explain the findings in schizophrenics of: 'reducing' pattern of visual evoked response, cerebral atrophy, and viral and autoimmune phenomena. The primacy of the disordered cognitive style in leading up to the immunological, biochemical and neuropathological processes is stressed. Implications of this model for understanding depression, anxiety and phobic disorders, autism, attention deficit disorder, obesity, alcoholism, smoking, drug addiction, sexual deviations, and certain psychosomatic and psychophysiological disorders are suggested.
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PMID:How information processing mode could affect prostaglandin E1 metabolism and lung inactivation: relevance of hemispheric specialization, neurotransmitter asymmetry and brain reactivity. 614 17

This is a report on recent developments in pediatric psychopharmacology: new drugs and new applications for established drugs. The drugs reviewed include imipramine, amitryptiline, lithium, piracetam, propranolol, tryptophan, clonidine, pyridoxine and fenfluramine. Putative indications include prepubertal depression, school phobia, anorexia nervosa, explosive-aggressive behavior, learning disabilities, attention deficit disorder (hyperactivity), Tourette's syndrome, autism, and the Lesch-Nyhan syndrome. Some of the information presented in this report must be regarded as "preliminary," and caution is advised in its interpretation and application.
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PMID:New developments in pediatric psychopharmacology. 635 89

Investigated the association between various depression assessment methods in 38 adults with mild or moderate mental retardation, half of whom had relatively high and the other half had relatively low depression screening scores. Measures included a standard psychiatric interview (Diagnostic Interview for Children and Adolescents), an informant rating scale (Reiss Screen for Maladaptive Behavior), and a self-report measure (Self-Report Depression Questionnaire). Association between measures was generally low, yielding discordant classification results. Potential reasons for these discrepancies were offered, and implications for clinical and research assessment of mood disorders in mental retardation were discussed.
J Autism Dev Disord 1994 Jun
PMID:A comparison of assessment methods for depression in mental retardation. 805 Sep 84


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