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 32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The traditional theories according to which deprivation of the visual channel is directly responsible for every disturbance observed in children born blind or partially sighted prove to be unsatisfactory; they fail to answer why, given the same visual defect, some children develop in a healthy way while others present a typical picture of infantile psychosis. The authors put forward the following hypotheses: infantile psychosis is always both a sign of and a response to trauma, in the sense developed by Freud in Beyond the Pleasure Principle, which has struck the mother-child dual unit; the high frequency of psychotics among children born blind indicates that blindness is a particularly charged trauma. The traumatic neurosis of the parents and especially of the mother is catastrophic for the child; it is therefore necessary to understand why and how its works, how it can be avoided or dealth with. The authors present a detailed clinical description of the various possible mother-child constellations and regarding unfavourable outcomes, propose preventive measures.
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PMID:[Congenital visual deficiency: chances and difficulties of management]. 404 24

Data are reviewed on the effects of massage therapy on infants and children with various medical conditions. The infants include: premature infants, cocaine-exposed infants, HIV-exposed infants, infants parented by depressed mothers, and full-term infants without medical problems. The childhood conditions include: abuse (sexual and physical), asthma, autism, burns, cancer, developmental delays, dermatitis (psoriasis), diabetes, eating disorders (bulimia), juvenile rheumatoid arthritis, posttraumatic stress disorder, and psychiatric problems. Generally, the massage therapy has resulted in lower anxiety and stress hormones and improved clinical course. Having grandparent volunteers and parents give the therapy enhances their own wellness and provides a cost-effective treatment for the children.
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PMID:Massage therapy for infants and children. 779 May 16

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

The two principal indications of clonidine in child psychiatry are the "attention-deficit hyperactivity disorder" (ADHD) and Tourette's disorder. In the first case (ADHD), clonidine (4 to 5 micrograms/kg/day) is efficient (25 to 50% of improvement) with minimal untoward effects. The comparison between clonidine and methylphenidate (MPH) in this disease showed different actions of these two drugs on target symptoms: MPH preferentially acts in children with major attention-deficit and moderate hyperactivity whereas clonidine is more advocated in ADHD children with hyperarousal, hyperactivity and aggressivity symptoms. In Tourette's disorder, clonidine improves 30-50% of cases. Many studies have compared the efficiency of clonidine, neuroleptics and clonazepam. Clonidine is less efficient than neuroleptics such as haloperidol or fluphenazine but it is more efficient than clonazepam. Clonidine seems to be a good alternative to neuroleptics when these are not tolerated. Some authors recommend the association clonidine-clonazepam. Clonidine is very useful in Tourette's disorder associated with other syndromes such as obsessive-compulsive disorder, ADHD or withdrawal symptoms of neuroleptics. In contrast, clonidine has to be avoided in a depressive child. Clonidine in other psychiatric disorders such as infantile psychosis with hyperactivity, bipolar disorder, panic disorder, aggressivity and post-traumatic stress disorder has not been studied in children, but could be worth investigating.
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PMID:[Indications for clonidine in child psychiatry]. 827 1

Children and adolescents with developmental disorders suffer from a wide range of psychopathology. However, there are no published studies examining this subject exclusively in this population using recent diagnostic criteria. The primary purpose of this paper is to report on the diagnosis encountered in a clinical setting using DSM-III-R. The medical records of all individuals assessed in a specialized program during a 1-year period were reviewed looking at their demographic features, diagnoses, and target behaviors. Our sample consisted of 233 subjects and contained significantly more boys than girls. The most common psychiatric diagnoses were oppositional defiant disorder and attention deficit hyperactivity disorder. Pica, organic mental disorder NOS, and Autistic Disorder were more often encountered in individuals with low intellectual functioning. Depressive disorders, posttraumatic stress disorder, and developmental speech/language disorders were diagnosed more in high functioning subjects. The most common symptom was impulsivity. This retrospective study highlights the need for more rigorous examination of current diagnostic concepts and criteria in children and adolescents with developmental disorders. Prospective studies should be conducted with standardized instruments in clinics and community samples to provide more information on psychiatric disorders in this population.
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PMID:Psychopathology in children and adolescents with developmental disorders. 929 30

This review assesses the usefulness of beta-blockers in the treatment of aggression and describes the parameters for their clinical use. A Medline search using the terms "beta-blockers," "aggression," "propranolol," and "brain injury" identified relevant journal articles published in English between 1977 and 1993. Open, prospective and double-blind, placebo-controlled studies, as well as case reports, were included. Beta-blockers appear to be effective in decreasing the frequency and intensity of aggressive outbursts associated with a wide variety of conditions, such as dementias, attention-deficit disorder, personality disorders, Korsakoff's psychosis, posttraumatic stress disorder, schizophrenia, profound mental retardation, autism, and brain injury. A general discussion attempts to resolve some of the issues surrounding the possible mechanisms of beta-blocker effects, reviews the anatomic and neurochemical bases of aggression, and explores implications of the clinical use of beta-blockers.
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PMID:Beta-blockers and the treatment of aggression. 938 11

The dopaminergic system, and in particular the dopamine D2 receptor, has been implicated in reward mechanisms. The net effect of neurotransmitter interaction at the mesolimbic brain region induces "reward" when dopamine (DA) is released from the neuron at the nucleus accumbens and interacts with a dopamine D2 receptor. "The reward cascade" involves the release of serotonin, which in turn at the hypothalmus stimulates enkephalin, which in turn inhibits GABA at the substania nigra, which in turn fine tunes the amount of DA released at the nucleus accumbens or "reward site." It is well known that under normal conditions in the reward site DA works to maintain our normal drives. In fact, DA has become to be known as the "pleasure molecule" and/or the "antistress molecule." When DA is released into the synapse, it stimulates a number a DA receptors (D1-D5) which results in increased feelings of well-being and stress reduction. A consensus of the literature suggests that when there is a dysfunction in the brain reward cascade, which could be caused by certain genetic variants (polygenic), especially in the DA system causing a hypodopaminergic trait, the brain of that person requires a DA fix to feel good. This trait leads to multiple drug-seeking behavior. This is so because alcohol, cocaine, heroin, marijuana, nicotine, and glucose all cause activation and neuronal release of brain DA, which could heal the abnormal cravings. Certainly after ten years of study we could say with confidence that carriers of the DAD2 receptor A1 allele have compromised D2 receptors. Therefore lack of D2 receptors causes individuals to have a high risk for multiple addictive, impulsive and compulsive behavioral propensities, such as severe alcoholism, cocaine, heroin, marijuana and nicotine use, glucose bingeing, pathological gambling, sex addiction, ADHD, Tourette's Syndrome, autism, chronic violence, posttraumatic stress disorder, schizoid/avoidant cluster, conduct disorder and antisocial behavior. In order to explain the breakdown of the reward cascade due to both multiple genes and environmental stimuli (pleiotropism) and resultant aberrant behaviors, Blum united this hypodopaminergic trait under the rubric of a reward deficiency syndrome.
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PMID:Reward deficiency syndrome: a biogenetic model for the diagnosis and treatment of impulsive, addictive, and compulsive behaviors. 1128 Sep 26

Aniracetam is a pyrrolidinone-type cognition enhancer that has been clinically used in the treatment of behavioral and psychological symptoms of dementia following stroke and in Alzheimer's disease. New discoveries in the behavioral pharmacology, biochemistry and pharmacokinetics of aniracetam provided new indications for this drug in the treatment of various CNS disorders or disease states. This article reviews these new findings and describes the effects of aniracetam in various rodent models of mental function impairment or cerebral dysfunction. Also, several metabolites of aniracetam have been reported to affect learning and memory in animals. It is, therefore, conceivable that major metabolites of aniracetam contribute to its pharmacological effects. The animal models, used in pharmacological evaluation of aniracetam included models of hypoattention, hypovigilance-arousal, impulsiveness, hyperactivity, fear and anxiety, depression, impaired rapid-eye movement sleep, disturbed temporal regulation, behavioral performance, and bladder hyperactivity. These are models of clinical disorders or symptoms that may include personality disorders, anxiety, depression, posttraumatic stress disorder, attention-deficit/hyperactivity disorder, autism, negative symptoms of schizophrenia, and sleep disorders. At present, there is no convincing evidence that promising effects of aniracetam in the animal models will guarantee its clinical efficacy. It is conceivable, however, that clinical trials will demonstrate beneficial effects of aniracetam in the above listed disease states. New findings regarding the mechanism of action of aniracetam, its central target sites, and its effects on signal transduction are also discussed in this review article.
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PMID:Aniracetam: its novel therapeutic potential in cerebral dysfunctional disorders based on recent pharmacological discoveries. 1207 May 27

Although the exact nature of sleep disturbances present in children with psychiatric disorders has not been studied extensively, it is apparent that children with significant emotional and behavioral problems are more likely to experience sleep difficulties. Children with sleep-related issues that are limited to bedtime can be managed effectively with specific cognitive-behavioral interventions. Children with more pervasive anxiety (eg, PTSD or OCD, mood disorders such as major depression or bipolar disorder, or neurodevelopmental disabilities such as autism) require a more exhaustive evaluation, and most of them also need sleep problems to be managed by sleep professionals using combinations of psychotherapeutic and pharmacologic approaches.
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PMID:Sleep in children with psychiatric disorders. 1500 82

Magnetic resonance imaging (MRI) has opened a new window to the brain. Measuring hippocampal volume with MRI has provided important information about several neuropsychiatric disorders. We reviewed the literature and selected all English-language, human subject, data-driven papers on hippocampal volumetry, yielding a database of 423 records. Smaller hippocampal volumes have been reported in epilepsy, Alzheimer's disease, dementia, mild cognitive impairment, the aged, traumatic brain injury, cardiac arrest, Parkinson's disease, Huntington's disease, Cushing's disease, herpes simplex encephalitis, Turner's syndrome, Down's syndrome, survivors of low birth weight, schizophrenia, major depression, posttraumatic stress disorder, chronic alcoholism, borderline personality disorder, obsessive-compulsive disorder, and antisocial personality disorder. Significantly larger hippocampal volumes have been correlated with autism and children with fragile X syndrome. Preservation of hippocampal volume has been reported in congenital hyperplasia, children with fetal alcohol syndrome, anorexia nervosa, attention-deficit and hyperactivity disorder, bipolar disorder, and panic disorder. Possible mechanisms of hippocampal volume loss in neuropsychiatric disorders are discussed.
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PMID:MR-based in vivo hippocampal volumetrics: 2. Findings in neuropsychiatric disorders. 1535 39


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