ABSTRACT
Astrocyte activation indicated by increased S100B is considered a potential pathogenic factor for schizophrenia. To investigate the relationship between astrocyte activation and cognitive performance, S100B serum concentration, memory performance, and psychopathology were assessed in 40 first-episode and 35 chronic schizophrenia patients upon admission and after four weeks of treatment. Chronic schizophrenia patients with high S100B were impaired concerning verbal memory performance (AVLT, Auditory Verbal Learning Test) compared to chronic and first-episode patients with low S100B levels. The findings support the hypothesis that astrocyte activation might contribute to the development of cognitive dysfunction in schizophrenia.
Subject(s)
Memory Disorders/blood , Memory Disorders/etiology , Nerve Growth Factors/blood , S100 Proteins/blood , Schizophrenia/complications , Adult , Chronic Disease , Female , Humans , Male , Neuropsychological Tests , S100 Calcium Binding Protein beta Subunit , Schizophrenia/blood , Verbal Learning/physiology , Young AdultABSTRACT
This report is about a 40-year-old man suffering from fluctuating catatonia as main symptom of long-lasting paraneoplastic encephalitis caused by a testicular neoplasm. With recurrence of a neoplasm initially diagnosed as seminoma after a 7-year symptom-free interval the patient suddenly developed various neurological and psychopathological symptoms including seizures, autonomic dysregulation, continuous anterograde short-term amnesia and predominantly a long-lasting complex catatonic syndrome with on-off phenomena. Repeated MRI scans of the brain showed no pathology; brain FDG-PET scans indicated a hypometabolism of the frontal cortex and the left temporal lobe. Eventually a paraneoplastic encephalitis was diagnosed. Repeated resections of tumour recurrences and plasmapheresis moderately alleviated catatonic symptoms. Haloperidol and lorazepam effectively relieved catatonic symptoms in contrast to various atypical antipsychotic drugs and diazepam. A series of 12 electroconvulsive treatments (ECT) temporarily improved residual catatonic symptoms such as catalepsy, stupor and mutism. Further neoplasm recurrences, however, reinforced catatonia until the tumour was successfully treated and the patient fully recovered. This case report illustrates the potential but also the limitations of various therapeutic approaches in organic catatonia due to paraneoplastic encephalitis.
