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At least 145 records · Page 8Linked to original sources
PubMed2006

Individual differences in the propensity to approach signals vs goals promote different adaptations in the dopamine system of rats.

RATIONALE: The way an individual responds to cues associated with rewards may be a key determinant of vulnerability to compulsive behavioral disorders. OBJECTIVES: We studied individual differences in Pavlovian conditioned approach behavior and examined the expression of neurobiological markers associated with the dopaminergic system, the same neural system implicated in incentive motivational processes. METHODS: Pavlovian autoshaping procedures consisted of the brief presentation of an illuminated retractable lever (conditioned stimulus) followed by the response-independent delivery of a food pellet (unconditioned stimulus), which lead to a Pavlovian conditioned response. In situ hybridization was performed on brains obtained either following the first or last (fifth) day of training. RESULTS: Two phenotypes emerged. Sign-trackers (ST) exhibited behavior that seemed to be largely controlled by the cue that signaled impending reward delivery; whereas goal-trackers (GT) preferentially approached the location where the reward was delivered. Following a single training session, ST showed greater expression of dopamine D1 receptor mRNA relative to GT. After 5 days of training, GT exhibited greater expression levels of tyrosine hydroxylase, dopamine transporter, and dopamine D2 receptor mRNA relative to ST. CONCLUSIONS: These findings suggest that the development of approach behavior towards signals vs goal leads to distinct adaptations in the dopamine system. The sign-tracker vs goal-tracker phenotype may prove to be a valuable animal model to investigate individual differences in the way incentive salience is attributed to environmental stimuli, which may contribute to the development of addiction and other compulsive behavioral disorders.

Adaptation, Physiological↗
PubMed1990

Controlled comparisons of clomipramine and fluoxetine in the treatment of obsessive-compulsive disorder. Behavioral and biological results.

Treatment with fluoxetine hydrochloride was compared with treatment with clomipramine hydrochloride in two groups of patients with obsessive-compulsive disorder using two different experimental designs. In the first group of 11 patients with obsessive-compulsive disorder studied using a randomized, double-blind, crossover design, treatment with fluoxetine for 10 weeks was found to produce therapeutic effects similar to treatment with clomipramine for 10 weeks. There were significantly fewer total side effects reported during fluoxetine than clomipramine treatment. Drug tapering and placebo substitution in the 4-week crossover interval phase led to substantial relapses in obsessive-compulsive disorder symptoms and depression. Furthermore, responses to the second drug took as long to occur as responses to the first drug, although both drugs are thought to act by a common mechanism, serotonin uptake inhibition. A second group of 21 patients with obsessive-compulsive disorder that had been previously stabilized on clomipramine treatment with at least partial benefit were crossed over to fluoxetine treatment in a double-blind fashion. After 10 weeks of fluoxetine administration, most patients manifested behavioral rating scores of obsessive-compulsive disorder and depressive symptoms that were comparable with precrossover ratings completed during clomipramine treatment. A significant exacerbation in obsessive-compulsive disorder and depression ratings as well as a similar lag in therapeutic efficacy were also noted in this second cohort of patients with obsessive-compulsive disorder. Platelet 5-HT concentrations were reduced 95% during both clomipramine and fluoxetine treatment periods. These results suggest that fluoxetine may represent a viable alternative to clomipramine in the treatment of obsessive-compulsive disorder, although further studies with larger sample sizes are needed.

Adult↗
PubMed2005

Role of the orbital cortex and of the serotonergic system in a rat model of obsessive compulsive disorder.

The serotonergic system and the orbitofrontal cortex have been consistently implicated in the pathophysiology of obsessive compulsive disorder. Yet, the relations between these two systems and the ways they interact in producing obsessions and compulsions are poorly understood. The present study tested the hypothesis that pathology of the orbitofrontal cortex leads to a dysregulation of the serotonergic system which is manifested in compulsive behavior, using a new rat model of this disorder. In the model, 'compulsive' behavior is induced by attenuating a signal indicating that a lever-press response was effective in producing food. We found that lesion to the rat orbital cortex led to a selective increase in compulsive lever-pressing that was prevented by the serotonin re-uptake inhibitor, paroxetine, and was paralleled by an increase in the density of the striatal serotonin transporter, assessed using high affinity [3H]imipramine binding. These results suggest that the serotonergic system is involved in orbital lesion-induced compulsivity, and provide a possible account for the observed association between obsessions and compulsions and dysfunction of the orbitofrontal cortex and of the serotonergic system in obsessive compulsive disorder.

Animals↗
PubMed2001

Obsessive-compulsive-like behavioral changes in pure akinesia.

Pure akinesia is a disorder characterized by profound freezing in the absence of rigidity or tremor that is not improved by levodopa therapy. We report two cases of pure akinesia who developed obsessive-compulsive-disorder- (OCD-) like behavior during their illness. Although the pathophysiological mechanism underlying freezing is unclear, the coexistence of pure akinesia and OCD-like behavior suggests that both symptoms have a common pathological basis in these two cases, presumably damage to the pallidum.

Journal Article↗
PubMed1992

Behavior therapy for obsessive compulsive disorder.

Behavior therapy for OCD with exposure and response prevention is effective in reducing obsessions and rituals in at least half of those suffering this disabling disorder. Office-based sessions in which patients participate actively in designing exposure and response prevention homework are usually sufficient. Therapist assistance is sometimes needed for those who fail to perform these assignments on their own. Poor compliance, severe comorbid conditions, and CNS-depressing drugs can interfere with behavior therapy. Techniques to manage these difficulties, including modifications of behavior treatment and the use of serotonin reuptake inhibiting drugs, can increase substantially the number of patients responsive to behavior therapy.

Adaptation, Psychological↗
PubMed1996

Self-restraint and self-injury: occurrence and motivational significance.

The occurrence of self-restraint was examined in a sample of 99 adults with severe or profound mental retardation who exhibited self-injury. Results showed that 46% of the sample exhibited self-restraint. A significantly higher occurrence of compulsive behaviors was found for subjects who engaged in self-injury and self-restraint when compared to self-injury subjects without self-restraint. To determine the motivational significance of self-restraint, we assessed the response to brief interruption of this behavior. Subjects who engaged in self-restraint responded more negatively to response interruption than did control subjects. These preliminary findings support the hypothesis that self-injury may be related to a compulsive behavior disorder in some individuals who self-restrain.

Adolescent↗
PubMed1995

Improvement of right hemispheric functions in a child with Gilles de la Tourette's syndrome by weak electromagnetic fields.

Gilles de la Tourette's syndrome (GTS) is a chronic, familial neuropsychiatric disorder of unknown etiology characterized clinically by the occurrence of motor and vocal tics and by the presence of a variety of neurobehavioral and neurocognitive abnormalities including hyperactivity, self-multilatory behavior, obsessive-compulsive behavior, learning disabilities, and conduct disorder. On the basis of neuropsychological assessments it has been suggested that GTS is associated with greater right than left hemispheric dysfunction which accounts for decrements in visuospatial, visuoconstructional and visuomotor skills in these patients. Recent case studies have demonstrated that extracranial application of electromagnetic fields (EMFs) in the picotesla (pT) range intensity improves visuospatial and visuoperceptive functions in patients with neurodegenerative disorders including Parkinson's disease, multiple sclerosis and Alzheimer's disease. I now present a 6 1/2 year old boy with GTS in whom this treatment modality produced, in addition to symptomatic behavioral improvement, also improvement in visuoconstructional and visuomotor skills as evidenced on various drawing tasks particularly copy of the Rey-Osterrieth Complex Figure, a task which is especially vulnerable to right hemispheric functions. These findings suggest that pT range EMFs may be useful for the treatment of GTS and related disorders and also reverse some of the cognitive impairments associated with the disease which are related to right hemispheric dysfunction and which contribute to learning disabilities in these patients.

Brain↗
PubMed1997

Reversal of a visuoconstructional disorder by weak electromagnetic fields in a child with Tourette's syndrome.

Tourette's syndrome (TS), a chronic familial neuropsychiatric disorder of unknown etiology, is characterized clinically by the occurrence of motor and vocal tics and by the presence of a variety of neurobehavioral and neurocognitive abnormalities including hyperactivity, self-mutilatory behavior, obsessive-compulsive behavior, learning disabilities, and conduct disorder. Cognitive deficits related to right hemispheric dysfunction are common in TS patients accounting for decrements in visuospatial, visuoconstructional and visuomotor skills. An 11 year old boy with a 5 years history of TS exhibited during a routine neuropsychological assessment an unusual visuoconstructional disorder which previously has been observed in dyslexic children. Specifically, when instructed to draw a bicycle from memory, he drew spontaneously a design executed from the perspective of a bird's eye view. After receiving a 20 minute treatment session with picotesla range electromagnetic fields (EMFs) applied extracranially, this visuocontructional disorder was spontaneously reversed and he drew an elaborate and detailed bicycle positioned in profile. A placebo EMF treatment, which was administered prior to magnetic therapy, had no effect on this child's visuoconstructional disorder. During the ensuing week there was a marked reduction in the child's hyperactive behavior with attentuation of motor tics. Spontaneous drawing of a bicycle a week after the administration of magnetic therapy was executed in profile although some elements were presented from a bird's eye view. This case demonstrates the potential impact of treatment with picotesla EMFs in reversing specific cognitive deficits in TS related to right posterior hemispheric dysfunction.

Brain Diseases↗
PubMed1979

Fatal intoxication from 3,4-methylenedioxyamphetamine.

The symptoms of MDA intoxication exhibited by the decedent prior to death closely mimic those of acute amphetamine poisoning: profuse sweating, violent and irrational behavior, and stereotypically compulsive behavior. Therefore, if amphetamines are not detected in specimens from a person displaying classic symptoms of amphetamine poisoning, hallucinogenic amphetamine derivatives may be considered. In the case described, a divided dose of 850 mg of MDA ingested within 2 h and 15 min was sufficient to cause the death of a 24-year-old male, 4 h after the final dose. While the methaqualone may have contributed to the demise of the decedent, the authors think that the MDA itself was sufficient to cause death. Results of limited recovery studies of MDA extraction from blood and elution from TLC plates supported the observations of Cimbura [13]. Approximately 85% of MDA is extracted by the method described and its elution from TLC plates is quantitative. This case points out once again the dangers of false advertising in the illicit market. The decedent, himself a dealer in the illicit drug market, and all present at the party believed the ingested white powder to be a mixture of morphine, LSD, and amphetamine, hence MDA. They were totally unfamiliar with 3,4-methylenedioxyamphetamine, MDA.

3,4-Methylenedioxyamphetamine↗
PubMed1980

Gilles de la Tourette syndrome: clinical and family study of 50 cases.

Fifty patients with Tourette syndrome were evaluated; data included family history, clinical characteristics, response to haloperidol, and side effects during haloperidol therapy. Sixteen patients had a family history of Tourette syndrome, and another 16 had a family history of tics. Twenty-four families had more than 2 members with Tourette syndrome or tics. There was no preponderance of families with a Jewish, Eastern European background in this sample. Thirty-four patients had obsessive-compulsive behavior. Among the 50 patients there was a high frequency of sleep disturbance, learning disability, self-destructive behavior, inappropriate sexual activity, and antisocial behavior. Family history was significantly related to the occurrence of sleep disturbance, obsessive-compulsive behavior, haloperidol response, and the frequency of side effects caused by haloperidol. The precise mode of genetic transmission in familial Tourette syndrome remains to be determined.

Female↗
PubMed1989

Obsessive-compulsive disorder in mentally retarded patients.

Of 283 mildly to profoundly retarded patients, 10 (3.5%) presented with compulsive behavior that significantly interfered with their daily functioning. Compulsions occurred in the context of obvious cerebral dysfunction and in the absence of anxiety or "ego-dystonic" qualities. The interrater reliability of the differential diagnosis between compulsions, stereotypies, and other repetitive behaviors was good (kappa = .82). A severity rating scale for the compulsive behavior yielded total scores with good interrater reliability (intraclass correlation coefficient = .82). Single items that described observable behaviors had good reliability, while inner resistance and subjective distress were not reliably assessed and contributed little to the total score. The authors suggest that the DSM-III-R diagnosis of obsessive-compulsive disorder be considered in mentally retarded patients, despite the absence of recognizable ego dystonic characteristics. Emphasis should be on the behavioral, externally observable components of the disorder, rather than on inner conflicts and anxiety. Such a diagnostic approach may also benefit nonretarded compulsive patients.

Adolescent↗
PubMed2004

Behavioral differences among subjects with Prader-Willi syndrome and type I or type II deletion and maternal disomy.

OBJECTIVE: To determine whether phenotypic differences exist among individuals with Prader-Willi syndrome with either type I or type II deletions of chromosome 15 or maternal disomy 15 leading to a better understanding of cause and pathophysiology of this classical genetic syndrome. METHODS: We analyzed clinical, anthropometric, and behavioral data in 12 individuals (5 men, 7 women; mean age: 25.9 +/- 8.8 years) with PWS and a type I (TI) deletion, 14 individuals (6 men, 8 women; mean age: 19.6 +/- 6.5 years) with PWS and a type II (TII) deletion, and 21 individuals (10 men, 11 women; mean age: 23.6 +/- 9.2 years) with PWS and maternal disomy 15 (UPD). The deletion type was determined by genotyping of DNA markers between proximal chromosome 15 breakpoints BP1 and BP2. TI deletions are approximately 500 kb larger than TII deletions. Several validated psychological and behavioral tests were used to assess phenotypic characteristics of individuals with PWS representing the 3 genetic subtypes. RESULTS: Significant differences were found between the 2 deletion groups and those with UPD in multiple psychological and behavioral tests, but no differences were observed in other clinical or anthropometric data studied. Adaptive behavior scores were generally worse in individuals with PWS and the TI deletion, and specific obsessive-compulsive behaviors were more evident in the TI individuals compared with those with UPD. Individuals with PWS with TI deletions also had poorer reading and math skills as well as visual-motor integration. CONCLUSIONS: Our study indicates that individuals with TI deletion generally have more behavioral and psychological problems than individuals with the TII deletion or UPD. Four recently identified genes have been identified in the chromosome region between BP1 and BP2 with 1 of the genes (NIPA-1) expressed in mouse brain tissue but not thought to be imprinted. It may be important for brain development or function. These genes are deleted in individuals with TI deletion and are implicated in compulsive behavior and lower intellectual ability in individuals with TI versus TII.

Adult↗
PubMedDate not supplied

[Clozapine-induced obsessive-compulsive disorder: a case report].

Since 1992 it has been reported that obsessive-compulsive behavior may emerge in patients treated with clozapine. We would like to report a case of obsessive-compulsive behavior emerging after initiation of treatment with clozapine in a 22-year-old man with a diagnosis of schizoaffective disorder that was successfully treated with fluoxetine.

Adult↗
PubMed1999

OCD-Like behaviors caused by a neuropotentiating transgene targeted to cortical and limbic D1+ neurons.

To study the behavioral role of neurons containing the D1 dopamine receptor (D1+), we have used a genetic neurostimulatory approach. We generated transgenic mice that express an intracellular form of cholera toxin (CT), a neuropotentiating enzyme that chronically activates stimulatory G-protein (Gs) signal transduction and cAMP synthesis, under the control of the D1 promoter. Because the D1 promoter, like other CNS-expressed promoters, confers transgene expression that is regionally restricted to different D1+ CNS subsets in different transgenic lines, we observed distinct but related psychomotor disorders in different D1CT-expressing founders. In a D1CT line in which transgene expression was restricted to the following D1+ CNS regions-the piriform cortex layer II, layers II-III of somatosensory cortical areas, and the intercalated nucleus of the amygdala-D1CT mice showed normal CNS and D1+ neural architecture but increased cAMP content in whole extracts of the piriform and somatosensory cortex. These mice also exhibited a constellation of compulsive behavioral abnormalities that strongly resembled human cortical-limbic-induced compulsive disorders such as obsessive-compulsive disorder (OCD). These compulsive behaviors included episodes of perseverance or repetition of any and all normal behaviors, repetitive nonaggressive biting of siblings during grooming, and repetitive leaping. These results suggest that chronic potentiation of cortical and limbic D1+ neurons thought to induce glutamatergic output to the striatum causes behaviors reminiscent of those in human cortical-limbic-induced compulsive disorders.

Aggression↗
PubMed2006

Behavioral inhibition and obsessive-compulsive disorder.

Behavioral inhibition is frequently cited as a vulnerability factor for development of anxiety. However, few studies have examined the unique relationship between behavioral inhibition and obsessive-compulsive disorder (OCD). Therefore, the current study addressed the relationship between behavioral inhibition and OCD in a number of ways. In a large unselected student sample, frequency of current OC symptoms was significantly correlated with retrospective self-reports of total levels of childhood behavioral inhibition. In addition, frequency of current OC symptoms was also significantly correlated with both social and nonsocial components of behavioral inhibition. Further, there was evidence for a unique relationship between behavioral inhibition and OC symptoms beyond the relationship of behavioral inhibition and social anxiety. In addition, results showed that reports of childhood levels of behavioral inhibition significantly predicted levels of OCD symptoms in adulthood. Finally, preliminary evidence suggested that behavioral inhibition may be more strongly associated with some types of OC symptoms than others, and that overprotective parenting may moderate the impact of behavioral inhibition on OC symptoms. The current findings suggest the utility of additional research examining the role of behavioral inhibition in the etiology of OCD.

Adult↗
PubMed1993

Is Tourette syndrome a cause of sudden infant death syndrome and childhood obstructive sleep apnea?

The cause of sudden infant death syndrome (SIDS) is unknown. Sleep-related impairment of respiratory control and arousal are postulated; hyperdopaminergic and hyposerotonergic dysfunction may contribute to events leading to infant apnea and SIDS. Psychosocial adversity and impulsive and compulsive behaviors characterize some families of SIDS victims. Tourette syndrome (TS) is a common hereditary neurobehavioral disorder characterized by the frequent presence of impulsive and compulsive behaviors. Sleep disorders are common and include sleep apnea and abnormal arousal. Hyperdopaminergic and hyposerotonergic abnormalities are postulated to contribute to the pathophysiology of the disorder. The following is a report of the presence of incidents of infant apnea and SIDS in families in which TS was present. In an additional TS family, a child had obstructive sleep apnea syndrome (OSAS). Results of a preliminary survey suggest that TS gene carriers are at increased risk of life-threatening apneas of infancy and that the prevalence of SIDS in such families may be 2 to 5 times the prevalence in the general population. The presence in some pedigrees of sleep apnea in children and adults suggest that in some instances disorders of sleep-related ventilatory control and arousal occurring throughout the life-span share common pathophysiological mechanisms.

Child↗