Cerebrospinal fluid filtration in a case of schizophrenia related to "subclinical" Borna disease virus encephalitis

Citation
K. Bechter et al., Cerebrospinal fluid filtration in a case of schizophrenia related to "subclinical" Borna disease virus encephalitis, KEY T BRAIN, 1999, pp. 19-35
Citations number
49
Categorie Soggetti
Current Book Contents
ISSN journal
09341420
Year of publication
1999
Pages
19 - 35
Database
ISI
SICI code
0934-1420(1999):<19:CFFIAC>2.0.ZU;2-J
Abstract
Schizophrenia may represent a clinical syndrome caused by various etiologie s and through various pathogenetic pathways. Recent studies suggest viruses to be a more important cause of schizophrenia than previously thought. Bor na disease virus (BDV) causes meningoencephalitis or behaviour abnormalitie s in a broad range of animals, and accumulating data suggest a causal role of BDV for human neuropsychiatric disorders including schizophrenia. Howeve r, it is difficult to establish causality in the clinical situation. We add ressed this problem by detailed investigations over the long term in a sugg estive single case. Furthermore, we hypothesized a therapeutic effect of ce rebrospinal fluid filtration (CSFF) in such case comparable to that in ther apy resistant postinfectious Guillain-Barre syndrome (GBS). A variety of signs and findings in a 28 years old man indicated a subclinic al BDV encephalitis being responsible for DSM-IV recent onset schizophrenia , mainly: elevating BDV specific serum ab's, elevated CSF proteins, slow al pha-waves and dysrhythmia in EEG on admission (no gross neurologic abnormal ities). Positive schizophrenic symptoms improved under psychopharmaca medic ation but not the primary negative symptoms. Therefore the patient was trea ted by CSFF in two filtration series, each over five days. Outcome was moni tored by a battery of assessments and tests. Negative schizophrenic symptoms were rapidly improved under CSFF, in parall el neurological soft signs, performance in attention tests and EEG; this wa s similar in time pattern as GBS symptoms improve under CSFF. Clinical stat us and test performance remained on an improved level after CSFF (p < 0.05) and improved further spontaneously over the long-term (8 months inpatient, 11 months outpatient observation) to full remission. We conclude, that eve probably observed the natural course of a mild or 'su bclinical' BDV-encephalitis-related schizophrenia, which could be ameliorat ed by psychopharmaca and CSFF. Removing yet partially defined toxic factors , similar to chat found in GBS, from cerebrospinal fluid may explain clinic al improvement under CSFF. 'Subclinical' encephalitis by BDV or other virus es may more frequently underly schizophrenic symptoms than previously detec ted. Our observation indicates a novel pathogenetic principle in a case of schizophrenia.