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PubMedDate not supplied

Etiology of oral habits.

The pedodontic admission histories of 1600 Mexican children were analyzed, to determine general epidemiologic factors or oral habits, as well as their relationship with identifiable biopsychosociologic factors. Fifty-six percent of the children gave evidence of an oral habit, with significant predisposition among female patients, single children, subjects in poor physical health (particularly from allergies), as well as children with histories of chronic health problems. Oral habits should be considered a major health hazard because of their high incidence. Successful treatment requires a multidisciplinary approach to the basic cause of the problem.

Adolescent↗
PubMed2005

Combining Pharmacotherapy with cognitive-behavioral interventions for obsessive-compulsive disorder.

This paper reviews the evidence-based literature concerning the efficacy and effectiveness of cognitive behavior therapy (CBT), drug treatment and their combination for obsessive compulsive disorder (OCD). After a brief outline of the seminal studies, the state of the art is presented with reference to the consensual recommendations proposed in the last 10 years. Management of OCD rests on potent selective serotonin reuptake inhibitors and CBT, used separately, sequentially, or concurrently. A hierarchical model for clinical decision-making is reported. With greater severity of OCD, it is recommended to add medications. However, the response rate is still too low in many patients, and some patients remain refractory to any kind of treatment. This stresses the importance of joint efforts of psychological and biological teams to develop new treatments.

Cognitive Behavioral Therapy↗
PubMed2004

Linkage and association analysis at the serotonin transporter (SLC6A4) locus in a rigid-compulsive subset of autism.

Autism is a complex genetic neurodevelopmental disorder in which affected individuals display deficits in language, social relationships, and patterns of compulsive and stereotyped behaviors and rigidity. Linkage analysis in our dataset of 57 New England and 80 AGRE multiplex autism families reveals a multipoint heterogeneity LOD (HLOD) score of 2.74 at D17S1871 in 17q11.2. Analysis of phenotypic subsets shows an increased HLOD of 3.62 in families with compulsive behaviors and rigidity. The serotonin transporter locus (SLC6A4) maps nearby and is considered a functional candidate gene in autism and obsessive-compulsive disorder. We genotyped an insertion/deletion polymorphism in the promoter (5-HTTLPR), and seven single nucleotide polymorphisms (SNPs) across the 38-kb transcriptional unit. Transmission disequilibrium (TD) analysis reveals nominal association at a SNP in intron 5 (P = 0.02) as well as 5-HTTLPR (P = 0.01), corresponding to over-transmission of the short allele. TD analysis in the rigid-compulsive subset shows no evidence for association. Intermarker linkage disequilibrium was determined. All SNPs define a single haplotype block, while 5-HTTLPR lies 5' to this block. Three SNPs are sufficient to detect all common alleles (> or =5%) in this > 26-kb block. Analysis of haplotypes for these markers demonstrates no evidence for association to autism. These data indicate that a common allele within the coding region of SLC6A4 is not responsible for the observed linkage. However, the presence of heterogeneous disease variants within the block or the existence of a common disease-associated allele either upstream or downstream of this block is possible. In fact, such variants may well account for linkage to 17q11.2 in our families.

Autistic Disorder↗
PubMed1992

Caudate glucose metabolic rate changes with both drug and behavior therapy for obsessive-compulsive disorder.

We used positron emission tomography to investigate local cerebral metabolic rates for glucose (LCMRG1c) in patients with obsessive-compulsive disorder before and after treatment with either fluoxetine hydrochloride or behavior therapy. After treatment, LCMRG1c in the head of the right caudate nucleus, divided by that in the ipsilateral hemisphere (Cd/hem), was decreased significantly compared with pretreatment values in responders to both drug and behavior therapy. These decreases in responders were also significantly greater than right Cd/hem changes in nonresponders and normal controls, in both of whom values did not change from baseline. Percentage change in obsessive-compulsive disorder symptom ratings correlated significantly with the percent of right Cd/hem change with drug therapy and there was a trend to significance for this same correlation with behavior therapy. By lumping all responders to either treatment, right orbital cortex/hem was significantly correlated with ipsilateral Cd/hem and thalamus/hem before treatment but not after, and the differences before and after treatment were significant. A similar pattern was noted in the left hemisphere. A brain circuit involving these brain regions may mediate obsessive-compulsive disorder symptoms.

Adult↗
PubMed1986

Clomipramine: an antiobsessive drug.

In the past decade, various investigators have attempted to find new pharmacological agents for the treatment of obsessive disorders. Of these, the drug which has attracted attention and has been most promising is clomipramine. This paper attempts to review the usefulness of clomipramine in the treatment of obsessive disorder. Accidentally, it was discovered that clomipramine was effective in alleviating obsessive symptoms in depressed patients by a Spanish psychiatrist, Lopez-Ibor. Initial studies carried out mainly on patients with major depression reported that obsessive symptomatology benefited with clomipramine therapy. A number of uncontrolled and controlled studies confirmed the efficacy of this drug in obsessive neurosis. The drug improves the obsessive symptoms. Discontinuation of the drug is followed by a relapse. The efficacy, dosage, duration and side effects of treatment with clomipramine are discussed in this paper.

Anxiety↗
PubMed2006

Effects of chronic manganese exposure on cognitive and motor functioning in non-human primates.

Acute exposure to manganese is associated with complex behavioral/psychiatric signs that may include Parkinsonian motor features. However, little is known about the behavioral consequences of chronic manganese exposures. In this study, cynomolgus macaque monkeys were exposed to manganese sulfate (10-15 mg/kg/week) over an exposure period lasting 272+/-17 days. Prior to manganese exposure, animals were trained to perform tests of cognitive and motor functioning and overall behavior was assessed by ratings and by videotaped analyses. By the end of the manganese exposure period, animals developed subtle deficits in spatial working memory and had modest decreases in spontaneous activity and manual dexterity. In addition, stereotypic or compulsive-like behaviors such as compulsive grooming increased in frequency by the end of the manganese exposure period. Blood manganese levels measured at the end of the manganese exposure period ranged from 29.4 to 73.7 micro g/l (mean=55.7+/-10.8 (compared to levels of 5.1-14.2 micro g/l at baseline (mean=9.2+/-2.7)), placing them within the upper range of levels reported for human environmental, medical or occupational exposures. These results suggest that chronic exposure to levels of manganese achieved in this study may have detrimental effects on behavior, cognition and motor functioning.

Animals↗
PubMed1983

[Behavior therapy self control in chronic compulsive organismic defective habit development].

Patients with chronic compulsive organismic mishabituations, which are rather difficult to treat, can be helped by self-control methods of behavioural therapy combined with suggestive measures. The author currently regards this therapeutic approach to be superior to aversion therapy, which was occasionally used for such cases in the past. The contribution presents a scheme of therapy which can be generalized and is based on the work of Meichenbaum and Leonhard. The scheme consists of two parts containing four phases each. The actual approach and the modification necessary to tailor it to the individual case is explained by means of an example involving the treatment of psychogenic polydipsia.

Adult↗