Subjective cognitive concerns not related to objective impairment in patients with somatic symptom and related disorders.

OBJECTIVES: Patients with Somatic Symptom and Related Disorders (SSRD) report subjective cognitive concerns, and research indicates that they show objective cognitive impairment. This study explored the value of subjective concerns flagging objective impairment. Furthermore, we investigated whether coping moderated this relationship, and the role of depressive symptomatology. METHOD: In a cross-sectional design, objective impairment was measured with an extensive neuropsychological assessment; subjective concerns with the Cognitive Failure Questionnaire; coping styles with the Coping Inventory of Stressful Situations; and symptoms of depression with the Patient Health Questionnaire- 9. RESULTS: The results show that subjective concerns are of limited value in signaling objective impairment in patients with SSRD. Regression analyses performed on data from 225 patients showed that symptoms of depression (ß = .32) were the main predictor of subjective concerns, which were unrelated to objective impairment. Coping was not a moderator, but patients with emotion-oriented coping styles had more subjective concerns (ß=.40), and conversely, patients with avoidance- and/or task-oriented coping styles had less (respectively, ß=-.27 and ß=-.24). CONCLUSIONS: These results align with the Somatosensory Amplification Theory; patients with SSRD may amplify benign cognitive failures and experience them as intrusive, noxious, and more intense. In patients with SSRD, subjective cognitive concerns are more related to psychological constructs (symptoms of depression and coping styles) than to objective impairment.

Does homocarnosine mediate the dyskinetic movements induced by gaba-transaminase inhibitors.

Unilateral application of gamma-aminobutyric acid (GABA) antagonists on the motor cortex of conscious rats produces myoclonic movements. Paradoxically, the same behaviour can be observed with high concentrations of some GABA-transaminase (GABA-T) inhibitors. Since the GABA conjugate homocarnosine is increased in the brain following GABA-T inhibition and since homocarnosine is known to displace [3H]-GABA from its binding sites at high concentration, we investigated whether homocarnosine might explain the dyskinetic movements produced by these GABA-T inhibitors. We found that homocarnosine produces dyskinesia similar to that observed with GABA antagonists and GABA-T inhibitors when applied directly to the cortex. However, this property of homocarnosine is unlikely to be the basis of the dyskinetic effect of GABA-T inhibitors since we found no relationship between brain homocarnosine levels and the appearance of abnormal movements following GABA-T inhibition.

An analysis of the cortical and striatal involvement in dyskinesia induced in rats by intracerebral injection of GABA-transaminase inhibitors and picrotoxin.

Unilateral intrastriatal injection of various substances induces a characteristic dyskinetic syndrome in rats. These substances include picrotoxin as well as a series of irreversible GABA-transaminase inhibitors. Using the degree of enzyme inhibition in various brain areas as a measure of drug distribution following intrastriatal administration of gamma-acetylenic GABA and gamma-vinyl GABA, there was found considerable retrodiffusion via the needle tract to the overlying cortex. Topical application of gamma-acetylenic GABA and gamma-vinyl GABA to the cortical surface overlying the striatum produced a high incidence of identical dyskinesias without any evidence of diffusion of drugs to the striatum. The cortically induced movements could be duplicated by picrotoxin application to a defined cortical area. These findings suggest that interference with gabaergic function in the striatum is not necessary for the production of the dyskinetic syndrome and that this syndrome may be a cortically induced phenomenon.

Mapping of dyskinetic movements induced by local application of picrotoxin or (+)-gamma-acetylenic GABA on the rat motor cortex.

Unilateral application of picrotoxin or (+)-gamma-acetylenic GABA ((+)GAG) on the cortex of rats produces a characteristic dyskinetic syndrome. Using stereotaxic coordinates, the cortical localization of these abnormal movements was mapped and found to be similar to that previously described after electrical stimulation of these cortical areas: Abnormal movements of the head and forelimb were produced by picrotoxin of (+)GAG applied to sites more anteriorly and of the hindlimb more posteriorly. The degree enzyme inhibition following application of (+)GAG was used to demonstrate a very limited degree of drug diffusion. These results suggest that interferences with GABAergic function in well-defined cortical areas may play a role in dyskinetic movement disorders.