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Query: UMLS:C0004352 (autism)
 32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Symptoms are the verbal and nonverbal communicative expressions of experience. At any one time, the symptom is dependent on structural changes, genetic variations, metabolic abnormalities, immunopathic and other disorders, and the totality of social, economic, and situational experience. Complaints of pain may vary with time depending on the interaction of these features in a manner not directly related to the intensity of a noxious stimulus.
J Autism Child Schizophr 1975 Mar
PMID:Factors in the diagnosis and treatment of chronic pain. 23 77

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

If the aims of defense and coping are considered, it can be concluded that essentially the different kinds of defense should serve to cope with reality. They intend either to inhibit the pressure of the unconscious drives and emotions or to bring them in tracks which are better to overlook. Or they tend unconsciously to reduce the demands of the surroundings and/or to make it possible to use former patterns of coping, as e.g. in regression and transference, or to reduce the cognitive and emotional reception of it, as in autism. Whereas those defense mechanisms, which preponderantly serve to deal with the drives and emotions, may lead to a better coping with the given situation, those defense mechanisms, however, which mostly serve to a reduction of the perception of the environment or to a decrease of expectations of the surroundings, are not increasing the coping capacities with a really given situation. But also when defense is rigid or excessive, which can, if a certain genetic predisposition is given, also be visible in autoimmune-processes, the coping with reality is more difficult. Thereby it is, however, to consider that a rigid defense diminishes the danger of ego-fragmentation and, especially when a psychotherapy is done, leads with the time on this way to a better coping with the outside reality and the inner possibilities. In serious terminal diseases a defense, which permits an active life, seems to have a better prognosis than a resignated acceptation of the illness, which originates in the activity of the superego. Heavy pain-syndromes in diseases which are not life-menacing can apparently be dealt with the better the more the concerned people succeed to turn the anxiety which is little related to objects in object-related fear. With that potencies of the ego are free which otherwise would have to be invested in the defense of anxieties.
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PMID:[The ego--defense mechanisms and coping]. 266 14

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

Children's mental disorders are frequent, often chronic, and precursors of adult dysfunction. Most of the 9 million children with mental disorders go untreated. The successful treatment of childhood disorders represents a major public health concern. Although no cure is available for any condition, effective treatments exist. These include psychotherapies, such as behavioral treatment, parental therapy, family therapy, and medications. Mood disorders may respond to psychotherapeutic and pharmacological treatments. Anxiety disorders have been found to respond to medication and psychotherapeutic interventions. Hyperactivity disorders benefit greatly from stimulant medications, as do conduct disorders. Combining medication with behavioral treatment provides optimal efficacy in hyperactive children. Favorable outcomes in conduct disorders are also obtained from psychotherapeutic interventions with parents and children. In autism, the most severely handicapping childhood disorder, treatment can reduce disturbance to a level that enables the child to remain in the home rather than being placed in an institutional setting. The motor and phonic tics of tourette's disorder can be controlled with medication. Symptoms of post-traumatic stress disorder can be improved through psychotherapeutic treatments. There is an array of therapeutic interventions that can bring meaningful relief to children with serious, chronic mental disorders. Their successful application is a wise investment, given the pain, long-term disadvantages, and financial costs associated with untreated childhood behavioral and emotional disorders.
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PMID:Treatment of psychiatric disorders in children and adolescents. 808 82

Trisomy 17 has never been reported in a live birth. We present a case of mosaic trisomy 17 in a male presenting with mental retardation, seizures, attention deficit hyperactivity and autistic disorders, hearing loss, growth retardation, microcephaly, and minor anomalies. Although peripheral blood lymphocyte chromosomes were normal, trisomy 17 was present in the skin fibroblasts. The percentage of abnormal cells appears to have increased from 18% in an initial skin biopsy at age 3 years 8 months to 80% at age 8 years 8 months. Molecular analysis using 13 highly polymorphic markers spanning the length of chromosome 17 demonstrated the extra chromosome 17 in the skin to be of paternal origin. Three alleles were never seen in the trisomic cell line, suggesting that the extra chromosome arose through a mitotic duplication error after conception. Uniparental disomy was excluded in the euploid blood sample. Although Smith-Magenis syndrome involves a deletion of proximal 17p, some of the clinical features of this mosaic trisomy 17 patient, such as decreased REM sleep and increased tolerance to pain, are suggestive of phenotypic features observed in Smith-Magenis syndrome. We speculate that there are dosage-sensitive genes located in 17p11.2 that produce these phenotypes for either deficiencies or over-expression of their gene products.
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PMID:A clinical and molecular study of mosaicism for trisomy 17. 855 63

An evolutionary diagram that takes into account the development of personality and its structuring or restructuring was developed thanks to a better understanding of autistic disorders from a psychodynamic point of view through long term psychoanalytic treatment of autistic children. This grid is organised around the major stages of the formation of the bodily ego which autistic children helped us understand better. The construction of space and the capacities of cognitive instrumentation are logically within this line of structuring. These major stages are defined: the first is the "successful" autistic state; the second is the stage where the primary skin is recovered (feeling of a circular envelope); the third is the symbiotic phase which includes vertical splitting then horizontal splitting of the image of the body; finally, the fourth is the phase of individuation/separation into a whole body. At each stage the following are assessed: state of the image of the body, of the gaze, of language, of writing, the autistic symptoms, emotional-relational manifestations, exploration of space and objects, recognition in time, the aggressive behaviours, reactivity to pain and to immune states (somatic and psychosomatic manifestations).
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PMID:[Clinical guide scale for the developmental stages of treated autism]. 865 99

We measured CSF levels of beta-endorphin, an opioid hormone, in 19 patients with infantile autism and in 3 patients with Rett syndrome, and compared them with control values. In infantile autism, CSF levels of beta-endorphin did not differ significantly from those of age-matched controls. There was no significant correlation between CSF levels and clinical symptoms, including self-injurious behavior, pain insensitivity, and stereotyped movement. However, CSF levels of beta-endorphin were significantly higher in the patients with Rett syndrome than in the control (p < .05). Data suggest that neurons containing beta-endorphin may not be involved in patients with infantile autism. Thus, there is no relationship between dysfunction of brain opioid and autism.
J Autism Dev Disord 1997 Apr
PMID:CSF beta-endorphin levels in patients with infantile autism. 910 66

Neuropsychiatric diseases viewed as multifaceted expression of a dysfunctional brain in which atypical responses are evoked by various sensory inputs. Disease entities have traditionally been classified according to the predominant manifestation ( ) without regard to the overlapping features of many of the diseases (+/-). Thus, mild to moderate pain, mood, cognitive, and neurosomatic symptoms are frequently present in chronic fatigue syndrome (CFS) patients. Fibromyalgia syndrome (FMS) is listed as an example of a predominantly chronic pain syndrome. Affect (mood) disorders include depression (Depress.), anxiety, panic reactions, blunted affect, mania, etc. Schizophrenia (Schizo.) is listed as an example of a major cognitive psychosis. Autism as well as various forms of dementia would be included in this category. Irritable bowel syndrome (IBS) is an example of a neurosomatic disease.
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PMID:Stealth viruses as neuropathogens. 1015 Jan 89

Autism can be considered as an early general developmental disorder, characterized by problems of social interaction, problems of verbal and non verbal communication, and behavioral or ideational stereotypes. However, within autism we observe a clinical heterogeneity of autistic disorders which suggests the possibility of autistic subtypes. Several authors hypothesize an analgesia among autistic children; this analgesia may be related to self-mutilation found among autistics. The current research had two objectives: 1) to develop and validate evaluation tools for measuring aggression directed towards the self (Yale-Paris Self-Injurious Behavior Scale: YAPA SIB) and pain reactivity (Pre-Linguistic Behavioral Pain Reactivity Scale: PLBPRS); instruments appropriate for autistics and capable of showing different behavioral sub-types; 2) to study in 80 autistic children pain reactivity, self-injurious behavior, and their relation in different observational situations. The results show that the scales of self-injurious behavior and pain reactivity have good discriminative capacity, good test-retest reliability, and good validity. The results suggest additionally that the apparent decreased pain reactivity observed in autistics does not derive from a real analgesia but from a different mode of pain expression related to difficulties with verbal communication, body representation and certain cognitive disorders (learning disorders, problems representing sensations and emotions, problems establishing cause-effect relationships). Additionally, there is a significant relationship between certain self-injurious behaviors and the apparent reduced pain reactivity. Interpretations of this result are presented and the possible role of stress in autism is discussed.
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PMID:[Study of the relationships between self-injurious behavior and pain reactivity in infantile autism]. 1037 Aug 85


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