The inferiority complex: the Koch-Gross theory.
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Transcortical aphasia accompanied by echolalia occurs with malacias involving the postero-median part of the frontal lobe which includes the supplementary motor field of Penfield and is nourished by the anterior cerebral artery. The syndrome manifests itself in such cases even in fine detials in the same form as does in Pick's atrophy. The same also holds true for cases in which a tumour involves the region mentioned. Sentences or fragments of sentences are echolalised; tendency to perseveration is very marked. It is hardly, if at all, possible to evaluate the verbal understanding of these patients. Analysis of their behaviour supports the assumption that they have not lost the adaptation to some situations. Echolalia is often associated with forced grasping and other compulsory phenomena. Therefore, it may be interpreted as a sign of disinhibition of the acusticomotor reflex present during the development of the speech. Competition between the intentionality and the appearance of compulsory phenomena greatly depends on the general condition of the patient, particularly on the clarity of consciousness. The integrity of the postero-median part of the frontal lobe is indespensable for a normal reaction by speech to stimuli received from the sensory areas. The influence of the supplementary motor field on speech intention seems to be linked to the dominant hemisphere. In case lesions of the territory of the anterior cerebral artery and the cortico-bulbar neuron system are coexisting in the dominant hemisphere, the speech disturbance shifts to complete motor aphasia. In such cases the pathomechanism is analogous to that of the syndrome of Liepmann, i.e., right-sided hemiparesis with left-sided apraxia. So-called transcortical motor aphasia without echolalia can be caused by loss of stimuli from the sensory fields.
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BACKGROUND: To investigate whether motives for exercise participation predicted exercise dependence (ED) among endurance athletes. The rationale for the study centred upon a test of the affect regulation model utilising constructs that form part of the Self-Determination Theory as predictors of ED. It was hypothesised that non self-determined motivation, specifically external regulation, would be predictive of ED. METHODS DESIGN: correlational design, with a time gap between predictor and dependent variables. SETTINGS: competitive sports environment. PARTICIPANTS: 188 competitive endurance athletes were recruited from amateur sports clubs. INTERVENTIONS: none. MEASURES: the Behavioural Regulation in Exercise Questionnaire was administered before a training session to measure the predictor variables (motives for exercise participation), and the Running Addiction Scale was administered before a similar training session, one week later, to measure the dependent variable (ED). RESULTS: Multiple regression analysis revealed that the strongest predictor variable of ED was introjected regulation (beta=0.29, p<0.001), followed by identified regulation (beta=0.19, p<0.05). External regulation and intrinsic motivation were weak and non-significant predictors. The total variance in ED explained by the exercise participation motives was 15% (R(2)= 0.15). CONCLUSIONS: ED was predicted by motives that did not support the tenets of the affect regulation model. Results are discussed in light of the potential influence of exercise participation motives on ED and their implications for intervention strategies and diagnosis of the ED syndrome.
Compulsion is the most important symptom not only of compulsion diseases but acts as a dynamic element in relatively exceptional form of hysteria, called in this article "compulsion hysteria". Out of three patients observed by the author, one is extensively described. The fundamental structure of these patients is not that of the compulsive personality or of any other form of personality put forward by Rümke in his masterly survey of compulsive syndromes, the classic study called "Clinic and psychopathology of compulsion phenomenons". The basic personality disorder of compulsion hysteria is the hysterical personality. In the frame of this syndrome compulsion as an expedient to tyrannize other people in their surroundings. Analytically viewed, the libidinal fixation seems to be rooted between the anal phase and the oedipal phase.
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In the present study, muricide behaviour (MB) was studied in Long Evans rats in various situations. The MB pattern of each experimental group was compared, in 6 successive assays 1 hr-delayed to that of natural killer rats (NK). The percentage of NK rats was 11% in the strain used. In the 11 mg THC/kg b.w. treated naive rats, a significant additional percentage of rats (59%) became muricidal. The durations of the 3 MB phases were significantly increased as a result of an increased aggressiveness in the 1st assay but returned progressively to NK values on the 6th assay, in parallel with the physiological elimination of THC. This result indicates a true killing training in those non killer rats that became muricidal under THC. A severe magnesium deficiency induced by a 50 ppm magnesium-deficient diet induced 100% MB whereas a 150 ppm magnesium deficiency did not induce additional MB. In the severe deficiency, the MB pattern was rather similar to that of NK with the exception of the attack on the living mouse which was doubled probably because of magnesium-induced hyperexcitability responsible for a lower attack efficiency. In both 50 but also 150 ppm magnesium-deficient rats, a single injection of THC at low doses (2, 4 or 8 mg THC/kg b.w.) which is without aggressive effect in control rats, induced a 100% MB, the pattern of which was all the more severe as the magnesium deficiency was important or the THC dose higher. The pattern showed an important decrease in the two first phases and a dramatic increase in the attack on the dead mouse, suggesting that the combination of both treatments provoked severe central damage with a compulsive killing behavior. Consequently, it appears that a magnesium deficiency, even a moderate one, may aggravate the neurotoxicity of THC at low doses and, reciprocally, that low doses of THC may reveal the potential neurotoxicity of a moderate magnesium deficiency.
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BACKGROUND: Open-label trials suggested that fluvoxamine and citalopram may be effective for compulsive shopping disorder, but 2 double-blind fluvoxamine trials failed to confirm this. To test the hypothesis that citalopram is a safe, effective treatment for this disorder, we conducted a 7-week, open-label trial followed by a 9-week, double-blind, placebo-controlled discontinuation trial. METHOD: From Jan. 2001 to Jan. 2002, we enrolled adult outpatients meeting diagnostic criteria suggested in a prior study for compulsive shopping disorder and having a score of >/= 17 on the Yale-Brown Obsessive Compulsive Scale-Shopping Version (YBOCS-SV). Open-label citalopram was started at 20 mg/day and increased, absent marked response and limiting side effects, to 60 mg/day. Responders (subjects rated "much improved" or "very much improved" on the Clinical Global Impressions-Improvement scale [CGI-I] and having a >/= 50% decrease in YBOCS-SV score) were randomized to double-blind citalopram treatment at the week 7 dose or placebo for 9 weeks. RESULTS: We enrolled 24 subjects (23 women and 1 man). Mean +/- SD YBOCS-SV scores decreased significantly from 24.3 +/- 4.6 at baseline to 8.2 +/- 8.1 at week 7 (Wilcoxon signed rank: z = 4.20, p <.001). Fifteen of 24 subjects (63%) met the responder criteria. Three subjects (13%) discontinued for adverse events (1 each for headache, rash, and insomnia). Of the 15 responders who entered the double-blind treatment phase, 5 of 8 (63%) randomized to placebo relapsed (YBOCS-SV score >/= 17 and "minimally improved" or less on the CGI-I) compared with none of 7 randomized to continue taking citalopram (Fisher exact test p =.019). CONCLUSION: Citalopram appears to be a safe and effective treatment for compulsive shopping disorder. Further trials of citalopram and other selective serotonin reuptake inhibitors are warranted.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.