[Obsessional-compulsive phenomena in parkinsonism (author's transl)].
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An uncontrolled clinical study was carried out to evaluate the therapeutic efficacy of clomipramine (Anafranil, Geigy Pharmacueticals) in a group of twenty obsessive-compulsive neurotic patients. Clomipramine proved to be extremely useful in alleviating obsessive-compulsive neurosis as well as phobia. This finding was not secondary to the improvement in anxiety or depression which occurred, as the degree of improvement in obsessive symptoms far exceeded the improvement in the other symptoms.
The clinical presentation and natural history of Gilles de la Tourette syndrome (TS) are reviewed. The waxing and waning of symptoms, the rostrocaudal progression of areas of motor involvement, complex stereotypies, and the familial aggregation of TS and chronic multiple tics are suggestions of underlying neurochemical disturbance; whereas attentional problems, impulsivity and obsessive-compulsive behaviors create interesting links with other disorders. The most robust metabolic findings are the lowered CSF HVA in many TS patients, and the positive response of symptoms to dopamine blockers and clonidine particularly, which would be consistent with dopamine receptor hypersensitivity and possible noradrenergic-dopaminergic interactions in TS. However, no definitive account of patho-physiology or genetic contributions to the disorder is yet available.
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African Americans with obessive-compulsive disorder are underrepresented in behavioral treatment outcome studies. This paper consists of a clinical discussion of issues arising during the treatment with exposure plus response prevention of two African-American women with obessive-compulsive disorder. Clinical issues, such as excessive shame, insanity fears, and a sense of uniqueness, complicated the treatment process. However, both clients made significant improvement as assessed by behavioral testing, target ratings and the Yale-Brown Obsessive-Compulsive Scale.
Exposure therapy with response prevention is regarded as the most effective treatment in obsessive compulsive disorder. This procedure has been applied in outpatients as well as inpatients.
The efficacy of contemporary cognitive therapy for obsessive-compulsive disorder (OCD) has only recently been investigated. The current study compares exposure and response prevention (ERP) and cognitive behavior therapy (CBT) delivered in an individual format. Participants were randomly assigned to the 12 consecutive-week CBT or ERP treatment. Based on 59 treatment completers, there was no significant difference in YBOCS scores between CBT and ERP at post-treatment or at 3-month follow-up. A higher percentage of CBT participants obtained recovered status at post-treatment (67%) and at follow-up (76%), compared to ERP participants (59% and 58%, respectively), but the difference was not significant. Effect sizes (ESs) were used to compare the results of the current study with a previous study conducted at our center that utilized group CBT and ERP treatments, as well as other controlled trials that have compared CBT and ERP. The significance of these results is discussed and a comparison is made with the existing literature.
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.
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In children and adolescents motor/vocal tics and obsessive-compulsive behavior are known to be closely related. Thereby, a continuum of symptoms ranging from single tics to a mixed picture of tics/rituals/obsessive-compulsive traits to clinically relevant obsessions and compulsions could be described. As neurobiological substrates dysfunctions in corresponding cortico-striato-thalamocortical circuits (sensorimotor circuit in tic symptomatology, orbitofrontal circuit in obsessive-compulsive behavior) were postulated. For both disturbances behavioral therapy can be used to improve control mechanisms to counterregulate tics and obsessive-compulsive behavior, respectively, and psychopharmacological agents can be administered to compensate dysbalances in neurotransmitter systems. In case of a mixed symptomatologic picture it is necessary to include interventions for both pols of the symptom-continuum in the therapeutic programme to achieve extensive improvement as a basis for a further positive development of the patient.
The distribution of obsessive compulsive symptoms was compared in 16 individuals with primary obsessive compulsive disorder (OCD) and 16 individuals with Gilles de la Tourette syndrome (GTS) and associated obsessive compulsive behaviors (OCB). The two groups showed significant differences in the distribution of OC symptomatology. Furthermore, those OCD probands who shared a similar symptom profile with GTS individuals all had a positive family history of OCD. All of the other OCD probands were isolated cases. Implications of this finding on the etiology and pathogenesis of the two disorders are discussed.
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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.
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A controversy exists over whether or not the results of randomized controlled trials (RCTs) are generalizable to routine clinical practice. The present study examines the effectiveness of cognitive-behavior therapy (CBT) for obsessive-compulsive disorder (OCD) in a private practice setting. Twenty-six consecutive clients referred to a private anxiety disorders specialty clinic began treatment for OCD. Of the 19 (73%) clients who completed treatment, 84% were treatment responders. Clients, treatment, and outcome of the present study are compared with those of representative RCTs, and it is concluded that there are more similarities than differences. It is concluded that CBT can be effectively delivered in routine clinical practice.
OBJECTIVES: An autism susceptibility locus (AUTS1, MIM#608636) has been identified in chromosome 7q31. NrCAM is a candidate gene for AUTS1 because it is expressed in the brain and encodes a receptor involved in nervous system development. Polymorphisms in NrCAM have been reported to be associated with autism susceptibility and with substance abuse, implicating NrCAM in reward circuitry. Self-stimulatory, perseverative behavior in autism might be due to defects in reward circuitry. In addition, models of drug addiction have also borrowed from models of obsessive-compulsive behavior designed to reduce anxiety. Thus, our goals were to replicate previous associations of NrCAM with autism, making use of a large cohort, and to clarify whether NrCAM was associated with a specific endophenotype of autism in the repetitive behaviors and stereotyped interests domains. METHODS: We genotyped six NrCAM single nucleotide polymorphisms in 352 families and we tested for association between these polymorphisms and autism in the entire cohort and in two subsets, one with severe obsessive-compulsive behaviors and one with pronounced self-stimulatory behaviors. RESULTS: We found no association between single nucleotide polymorphisms of NrCAM and autism in our large cohort, or in the severe obsessive-compulsive behavior and self-stimulatory behavior subsets. However, we observed a significant overtransmission (21 transmitted vs 6 nontransmitted, chi2=12.054, P=0.0005) of the haplotype G-G-A-G-C-A of rs722519-rs1269622-rs405945-rs6958498-rs401433-rs439587 in the severe obsessive-compulsive behavior subset, likely driven by the G-C haplotype of rs6958498-rs401433, which itself showed significant overtransmission (31 transmitted vs 13 nontransmitted, chi2=8.844, P=0.003). CONCLUSIONS: Overtransmission of particular haplotypes of NrCAM, that may relate to the expression level of NrCAM in the brain, appeared to be associated with autism in the severe obsessive-compulsive behavior subset.