[Approach to a schizophrenic patient with obsessive behavior].
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Compulsive Behavior↗
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[Male anorectic behavior. Obsession with ponderal identity. Nosologic and therapeutic considerations].
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Adolescent↗
[Obsessive behavior and thoughts in patients with myasthenia gravis].
230 patients with myasthenia gravis were investigated by a german questionnaire, the HAMBURGER-ZWANGS-INVENTAR, in order to quantify their obsessive and compulsive behaviour. Compared to normals, myasthenic patients show higher scores on the compulsion-subscales of the inventory. The most significant differences appeared on the orderliness-subscale. On the other hand ratings of obsessive behaviour are significantly lower than in the normal population. Especially (auto)aggressive ruminations do hardly occur in myasthenia, which is a remarkable fact in this autoaggressive immunological disease. Compulsive behaviour cannot be interpretated as clinical compulsive disorder, caused by myasthenia. Questionnaire replies rather indicate one aspect of the way of coping with the disease and its treatment.
Activities of Daily Living↗
Altered serotonin activity in anorexia nervosa after long-term weight restoration. Does elevated cerebrospinal fluid 5-hydroxyindoleacetic acid level correlate with rigid and obsessive behavior?
To avoid the confounding influences of malnutrition or weight loss, we studied patients with anorexia nervosa at normal weight and stable dietary intake. Compared with 15 controls, 17 long-term weight-restored anorectic subjects had elevated concentrations of cerebrospinal fluid 5-hydroxyindoleacetic acid, the major serotonin metabolite, whereas levels of cerebrospinal fluid homovanillic acid, the major dopamine metabolite, were normal. Elevated levels of cerebrospinal fluid 5-hydroxyindoleacetic acid may indicate increased serotonin activity. Such activity could contribute to pathological feeding behavior. Most importantly, this study raises the question as to whether increased cerebrospinal fluid 5-hydroxyindoleacetic acid levels are associated with overly inhibited, anxious, or obsessive traits.
Adult↗
[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↗
Kanner's syndrome or early-onset psychosis: a taxonomic analysis of 142 cases.
Case history data on 142 psychotic children were obtained using the Rimland Diagnostic Check List. A particular variety of the method known as numerical taxonomy was used to classify the children into subgroups on the basis of responses on the Check List. A comparison was made between a classification of Kanner's syndrome vs. "no Kanner's syndrome" and a classification using random classes as starting points. The "best" classification of the data was one in which 2 classes were obtained, one containing all the Kanner's syndrome children plus other early-onset, nonrelating psychotic children and the other containing children with later onset and more varied symptoms. Those attributes which significantly differentiated between the classes both in the "best" classification and in the Kanner's syndrome classification were extracted. A distinction between Kanner children and other similar children was found only for 3 specific behaviors: obsessive desire for sameness, islets of special ability, and skillful manipulation of small objects.
Adolescent↗
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↗
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↗
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↗
[Obsessive-compulsive behavior and progressive supranuclear palsy].
A case of progressive supranuclear palsy characterized by a loss of self-activation and a compulsive behaviour of the obsessive type is reported. The pathological examination was remarkable for the intensity of pallidal lesions and their diffusion to both the external and internal segments. While the loss of self-activation seemed to result from a damaged cortico-subcortical circuit forming a limbic loop, the compulsive behaviour of the obsessive type may have resulted from the interruption of a frontal-caudal-pallidal-luysian circuit.
Globus Pallidus↗
Adolescence and eating disorder: the obsessive-compulsive syndrome.
Although it is widely recognized that eating disorders primarily begin during the adolescent period, the centrality of obsessive-compulsive symptomatology and dynamisms and their relationship to adolescent conflict and development has not been generally accepted or understood. Social pressures toward conformity with the ideal of feminine thinness, which are especially influential during the adolescent period, combine with obsessive-compulsive predispositions to produce eating disorder symptoms and patterns of behavior. Obsessive preoccupation with images of food as well as ruminative calorie counting, and ritualistic behavior regarding food, use of laxatives, and vomiting, together with an underlying focus on control, undoing and other obsessive-compulsive defenses, and a sado-masochistic orientation to the body all point to an essential obsessive-compulsive disorder. The presence of dysphoric affect and the erratic success of antidepressant medication with eating disorder patients has led to a belief in an underlying affective disorder. However, careful assessment of eleven studies presenting differential diagnostic data regarding anorexia nervosa reveals that noneating related obsessive-compulsive patterns and symptoms are second overall in incidence to depressive patterns and symptoms. With critical re-evaluation of data presented, the obsessive-compulsive condition equals or supersedes the depressive one in many samples. Moreover, given the intense achievement orientation of persons with obsessive-compulsive illness, along with other psychodynamic factors, depressive symptoms could well be considered a secondary breakdown effect. If the all-pervasive obsessive-compulsive nature of eating-related symptomatology discussed here is taken into consideration, depressive symptoms must be considered either secondary or incidental. As patients with eating disorders are notoriously secretive and oftentimes misleading about their symptoms and themselves, a diagnostic assessment of such patients in intensive treatment at a long-term hospital facility was carried out. Compared with a control group randomly selected from the remainder of the hospital patient population, obsessive-compulsive manifestations of rumination, ritualistic behavior, excessive cleanliness, excessive orderliness, perfectionism, miserliness, rigidity, and scrupulousness and self-righteousness were all significantly associated with the eating disorder patient group. The current eating disorder picture, therefore, appears to be a modern form of obsessive-compulsive illness beginning during the adolescent period.
Adolescent↗
L-tryptophan in neuropsychiatric disorders: a review.
Animal data indicate that serotonin (5-HT) is a major neurotransmitter involved in the control of numerous central nervous system functions including mood, aggression, pain, anxiety, sleep, memory, eating behavior, addictive behavior, temperature control, endocrine regulation, and motor behavior. Moreover, there is evidence that abnormalities of 5-HT functions are related to the pathophysiology of diverse neurological conditions including Parkinson's disease, tardive dyskinesia, akathisia, dystonia, Huntington's disease, familial tremor, restless legs syndrome, myoclonus, Gilles de la Tourette's syndrome, multiple sclerosis, sleep disorders, and dementia. The psychiatric disorders of schizophrenia, mania, depression, aggressive and self-injurious behavior, obsessive compulsive disorder, seasonal affective disorder, substance abuse, hypersexuality, anxiety disorders, bulimia, childhood hyperactivity, and behavioral disorders in geriatric patients have been linked to impaired central 5-HT functions. Tryptophan, the natural amino acid precursor in 5-HT biosynthesis, increases 5-HT synthesis in the brain and, therefore, may stimulate 5-HT release and function. Since it is a natural constituent of the diet, tryptophan should have low toxicity and produce few side effects. Based on these advantages, dietary tryptophan supplementation has been used in the management of neuropsychiatric disorders with variable success. This review summarizes current clinical use of tryptophan supplementation in neuropsychiatric disorders.
Dopamine↗
Serotonergic and noradrenergic sensitivity in obsessive-compulsive disorder: behavioral findings.
Six of eight patients with obsessive-compulsive disorder had an exacerbation of symptoms when given m-chlorophenylpiperazine. Fenfluramine and placebo produced mild improvement. Six patients given intravenous clonidine experienced marked reduction in obsessions. Implications for serotonergic and noradrenergic hypotheses of obsessive-compulsive disorder are discussed.
Adult↗
[Multiple tics and Gilles de la Tourette syndrome].
Tic disorders are frequent in childhood, varying from transient motor tics over multiple chronic tic disorders to full-blown Gilles de la Tourette syndrome (GTS). GTS is genetically determined. In affected families, relatives of the patient(s) with GTS may show minor symptoms only. The clinical picture is extremely variable, extending from the well known motor tics over complex compulsive obsessive behavior to purely sensory tics. The optimal treatment today is the use of dopamine antagonists.
Antipsychotic Agents↗
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↗
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↗
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↗
Drug versus behavioral treatment of obsessive-compulsive disorder.
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Behavior Therapy↗