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At least 19 recordsLinked to original sources
PubMed1992

[Obsessive-compulsive behavior (arithmomania). Atrophy of the caudate nuclei].

We report the case of a 56-year-old woman who died after a 2.5 years progressive course of behavioral disorders associating severe obsessive-compulsive counting with disinhibition. Neuropathological examination showed severe gliosis of the caudate nuclei whereas the lentiform nuclei and frontal cortex were not involved. In contrast with previous reports, this case lacked psychic akinesia which is usually combined with obsessive-compulsive behavior. It is a further illustration of how subcortical lesions can produce a frontal like syndrome. It suggests a fundamental role of the caudate nuclei in the control of behavior.

Atrophy↗
PubMed1977

Development of a state measure of obsessive compulsive behavior.

The Reaction Inventory-Interference was developed to identify obsessional thoughts and compulsive acts, which interfere with an individual's daily activities. The 50 items in the inventory were administered to 172 Ss. On the basis of item test correlations, 40 items were retained for subsequent analyses. The estimate of internal consistency for the 40 item inventory was .95. The correlation between the 40-item inventory and the "symptom" score on the Leyton Obsessional Inventory was .66. Factor analysis of the 40-item inventory yielded nine factors.

Compulsive Behavior↗
PubMed1991

Platelet 3H-imipramine binding sites in obsessive-compulsive behavior.

Several studies indicate a serotonergic dysfunction in patients with obsessive-compulsive disorder (OCD). We examined serotonergic function in OCD by determining platelet 3H-impiramine binding sites in patients with OCD during a drug-free baseline period as well as normal control volunteers. The maximum number of binding sites (Bmax) and apparent dissociation constant (Kd) was determined using 3H-imipramine (IMI) as the binding ligand. We observed that the mean 3H-IMI binding Bmax (fmol/mg protein) determined in 24 patients with OCD was not significantly different from that in 23 normal control subjects. There were no significant differences in the Kd between patients with OCD and normal control subjects. Our results are thus similar to those reported by Insel et al (1985) and Black et al (1990), who observed no significant differences in platelet 3H-IMI binding between OCD patients and controls; but different from those reported by Weizmann et al (1986), who observed decreased 3H-IMI Bmax in OCD patients. The discrepancy in the results is not clear, but may be related to several factors. Our results thus indicate that any abnormality in serotonergic function present in patients with OCD is not related to imipramine binding sites in the platelets. However, the possibility that there may be an abnormal platelet serotonin uptake or other serotonergic function in OCD cannot be ruled out.

Adult↗
PubMed1992

Serotonergic function in obsessive-compulsive disorder. Behavioral and neuroendocrine responses to oral m-chlorophenylpiperazine and fenfluramine in patients and healthy volunteers.

To evaluate serotonergic (5-hydroxytryptamine) function in obsessive-compulsive disorder, behavioral and neuroendocrine responses to m-chlorophenylpiperazine (m-CPP; 0.5 mg/kg orally) and fenfluramine hydrochloride (60 mg orally) were examined in 20 patients and 10 healthy controls under double-blind, placebo-controlled conditions. Following m-CPP, but not fenfluramine or placebo, 55% (11/20) of the patients with obsessive-compulsive disorder experienced a transient exacerbation of obsessive-compulsive disorder. Prolactin response was blunted in patients following m-CPP but not following fenfluramine. Patients with greater behavioral response to m-CPP had smaller prolactin responses. Cortisol response to m-CPP and fenfluramine did not significantly differ between the groups. Behavioral and neuroendocrine responses appeared divergent. This does not suggest simply upregulation or downregulation of 5-hydroxytryptamine receptors, but rather complex mechanisms involving multiple neurotransmitter and neuromodulator systems.

Administration, Oral↗
PubMed1991

Noradrenergic function in obsessive-compulsive disorder: behavioral and neuroendocrine responses to clonidine and comparison to healthy controls.

To evaluate noradrenergic (NE) function in obsessive-compulsive disorder (OCD), behavioral, physiological, and neuroendocrine responses to the alpha 2-adrenergic agonist clonidine were examined in 18 patients with OCD and 10 healthy subjects. Subjects received single i.v. doses of 2 micrograms/kg of clonidine administered under double-blind, placebo-controlled, random-assignment conditions. Following clonidine, but not following placebo, patients transiently experienced a significant reduction of obsessions and compulsions. Significant drowsiness and a reduction in anxiety were also noted, but the antiobsessional effect appeared independent of the soporific and antianxiety effects. Growth hormone (GH), cortisol, and 3-methoxy-4-hydroxyphenylglycol responses to clonidine did not differentiate patients from healthy controls. Blood pressure and pulse in response to clonidine did not differ between groups. Improvement in OCD symptoms after clonidine significantly correlated with GH response to clonidine, suggesting specific noradrenergic mediation. This finding lends only partial support for a primary defect of noradrenergic function in OCD.

Adolescent↗
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↗
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↗
PubMed1979

Exposure therapy for phobias and obsessive-compulsive disorders.

When abnormal fears or excessively compulsive behavior begin to rule a person's life, the consequences can be devastating to both patient and family. But three quarters of cooperative patients can be restored to normal functioning through a form of therapy based on exposing the patient continually to the stimuli that evoke symptoms until they can be tolerated and the phobic or compulsive behavior dissipates.

Adult↗
PubMed1991

How to recognize the signs of sexual addiction. Asking the right questions may uncover serious problems.

The sexual addiction model enables physicians to understand the self-destructive behavior of patients whose actions may otherwise appear inexplicable. When a person is preoccupied with sex and continues to engage in compulsive sexual activity despite adverse consequences (eg, loss of marriage, job, health, freedom), he or she is a sex addict. Treatment allows sex addicts to stop their compulsive behavior and improve their relationships. Preferred treatment includes professional counseling and attendance at self-help programs based on the Alcoholics Anonymous model. Partners of sex addicts, whose coaddiction may manifest itself through various physical symptoms, depression, or compulsions, can benefit from the same treatment approach.

Adult↗
PubMed1992

Differential response of seven subjects with autistic disorder to clomipramine and desipramine.

OBJECTIVE: Clomipramine, a serotonin reuptake blocker that has unique antiobsessional properties, was hypothesized to have a different effect from that of desipramine, a tricyclic antidepressant with selective adrenergic effects, for the stereotyped, repetitive behaviors in autism. METHOD: Seven subjects, ages 6-18 years, with autistic disorder completed a 10-week double-blind, crossover trial of clomipramine and desipramine following a 2-week single-blind, placebo phase. RESULTS: Clomipramine was superior to desipramine and placebo, as indicated by standardized ratings of autism and anger as well as ratings of repetitive and compulsive behaviors. Clomipramine and desipramine were equally superior to placebo for ratings of hyperactivity. Parents of all seven subjects elected to have their children continue to take clomipramine after the study. CONCLUSIONS: Clomipramine and desipramine are differentially effective in treating the obsessive-compulsive and core symptoms in autistic disorder. Biological links between compulsions and stereotyped, repetitive behaviors in autistic disorder should be explored.

Adolescent↗
PubMed1992

[Case report: anorexia nervosa in a 10-year-old boy].

A 10-year-old boy was admitted to the Children's Hospital with a 7-month history of disturbed eating behavior and a recent rapid weight loss: During the 24-day hospital stay the boy displayed a characteristic anorectic eating pattern, hyperactivity, anxiety, depression and compulsive behavior. Discharge followed a 4-kg weight gain. During the subsequent 12 months of outpatient care weight gain and eating behavior normalized. The boy's premorbid personality was described as compulsive and difficult. Although his intelligence was above average the boy had spelling problems and inadequate verbal skills. A change to a college-preparatory school and contact with a family with a vegetarian way of life probably precipitated the acute illness.

Anorexia Nervosa↗
PubMed2026

Sequential rTMS for MDD and OCD in a patient with left parietal perinatal ischemic infarct: a case report.

Major depressive disorder (MDD) commonly co-occurs with obsessive-compulsive disorder (OCD), resulting in greater symptom severity, functional impairment, and suboptimal response to standard pharmacologic and psychotherapeutic interventions. These challenges underscore the need for neuromodulation strategies to target distinct neural networks implicated in mood regulation and compulsivity. This report describes outcomes of high-frequency (HF) repetitive transcranial magnetic stimulation (rTMS) of the left dorsolateral prefrontal cortex (DLPFC), and low-frequency (LF) rTMS of the right orbitofrontal cortex (OFC), in a patient with comorbid MDD, OCD, and a left parietal perinatal ischemic infarct. Over the course of treatment, serial psychometric assessments demonstrated progressive reductions in frequency and intensity of depressive symptoms, anxiety, and obsessive-compulsive behaviors, measured via Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder 7-Item Scale (GAD-7), and Yale-Brown Obsessive-Compulsive Scale (Y-BOCS). This case adds to the growing body of literature demonstrating efficacy of DLPFC and OFC stimulation for depression and OCD. Further large-scale, blinded, and randomized trials are warranted to examine the efficacy of sequential DLPFC and OFC stimulation for comorbid MDD and OCD compared with single-site DLPFC stimulation.

dorsolateral prefrontal cortex (DLPFC)↗
PubMedDate not supplied

Oxytocin in obsessive compulsive disorder.

A double-blind, placebo-controlled study with syntocinon (oxytocin) was carried out in 12 patients, nine females and three males with obsessive compulsive disorder (OCD). Patients were treated by intranasal administration of oxytocin spray (18 IU per day) or placebo. No reductions in the number of obsessions or compulsive behaviors were observed in either treatment group. To evaluate whether a higher dosage would exert more beneficial effects, two additional patients were treated with a threefold higher dosage of oxytocin using an open design. In one patient a slight reduction in the number of checking rituals was observed, whereas in the other patient virtually no effect was observed. The results of this study do not support the hypothesis that oxytocin might be a potential anticompulsive agent.

Adult↗
PubMed1976

On the supersensitivity of dopamine receptors, induced by neuroleptics.

Different neuroleptics caused dopamine receptor blockade (antagonism against methylphenidate-induced compulsive gnawing) for varying lengths of time. When the receptor blockade had expired, supersensitivity to dopamine agonists (occurrence of apomorphine-induced compulsive gnawing and enhancement of methylphenidate-induced gnawing) developed and persisted for varying periods of time. The degree and duration of supersensitivity was related to the degree and duration of the preceding receptor blockade. Inhibition of catecholamine or 5-HT synthesis had no influence on development of supersensitivity. Stimulation with a dopamine agonist, apomorphine, during the period of the development of supersensitivity did not modify the enhanced receptor supersensitivity. A cholinergic-dopaminergic balance was shown to be involved in the manifestation of compulsive behavior during the supersensitivity phase. Tolerance to the dopamine antagonistic effect of a neuroleptic also developed after a single neuroleptic treatment, most likely due to increased sensitivity of the receptors for the dopamine agonist. It is concluded, that the dopamine receptor blockade induced by a single dose of a neuroleptic agent is a dynamic phenomenon which in the course of time is replaced by an increased sensitivity of the receptors to dopamine agonists. Noradrenergic or 5-HT neuron systems do not seem to be involved in the neuroleptic-induced supersensitivity, whereas a dopaminergic-cholinergic balance is operative in the supersensitivity situation.

Animals↗
PubMed1992

Dental treatment of patients with Gilles de la Tourette's syndrome.

Gilles de la Tourette's syndrome, a familial neurologic disorder with onset in early life, is characterized by chronic intermittent motor and vocal tics. Many of the orofacial tics and compulsive behaviors seen in this disorder may cause destructive oral lesions. The medications used in treating the syndrome may adversely interact with dental therapeutic agents, frequently cause hyposalivation associated with the development of dental caries and periodontal disease, and may produce tardive dyskinesia with buccolingual choreiform movements. The oral signs and symptoms associated with the syndrome are reviewed, and modifications in dental treatment on the basis of the patient's behavioral alterations, and current drug therapy are suggested.

Bruxism↗