Biomedical subjects
M Czygan
Publications and source records attributed to M Czygan.
Borna disease virus in human brains with a rare form of hippocampal degeneration but not in brains of patients with common neuropsychiatric disorders.
To estimate the frequency of persistent Borna disease virus (BDV) infections of the human central nervous system and to determine which neuropsychiatric disorders might be associated with this viral infection, reverse transcription-nested polymerase chain reaction was used to screen a large collection of autopsy brain samples for the presence of BDV-specific nucleic acids. The presence of BDV RNA was found in 3 brains of persons with psychiatric symptoms and prominent hippocampal degeneration previously reported to be positive by others. However, no BDV RNA was detected in 86 randomly collected brains from persons with various psychiatric disorders, including schizophrenia, affective disorders, and Alzheimer's disease, or from suicide victims or in 52 brains from healthy controls. Furthermore, no BDV-RNA was detected in 16 surgical brain samples from persons with epilepsy-associated hippocampal sclerosis. These results indicate that life-long persistent BDV infections are rare in humans and that such infections may be associated with certain forms of hippocampal degeneration.
[Borna disease virus and psychiatric diseases. Fact or artefact?].
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No Borna disease virus-specific RNA detected in blood from psychiatric patients in different regions of Germany. The Bornavirus Study Group.
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IgG-antibodies to CNS proteins in patients with multiple sclerosis.
The CSF and sera of 185 patients with multiple sclerosis (MS), 130 patients with other inflammatory diseases of the CNS (OID) and 50 patients with spinal disc syndrome (controls) were investigated for IgG-antibodies to CNS proteins by SDS-PAGE and immunoblotting and by isoelectric focusing combined with affinity blotting. IgG-antibodies to CNS proteins in serum (immunoblotting) were detected in 18 patients with MS (10%), in 29 patients with OID (22%) and in four controls (8%). Intrathecal synthesis of IgG-antibodies to CNS proteins was demonstrated in 11 patients with MS (6%), in 37 patients with OID (28%) and in none of the controls. In 4/11 patients with MS intrathecally produced antibodies were shown to be specific for glial fibrillary acidic protein (GFAP). Of patients with MS, 180 displayed oligoclonal IgG-bands in the CSF. Specificity of these bands for CNS proteins was demonstrated only in 2/180 specimens (1%). These findings indicate, that in most patients with MS oligoclonal IgG-bands in the CSF do not contain relevant amounts of antibodies to CNS proteins.
[Intrathecal IgG synthesis: when is determination of oligoclonal bands necessary?].
Two quantitative methods of determining the intrathecal synthesis of IgG were tested for their usefulness in deciding about the necessity of further investigations of oligoclonal bands (OCB) in the CSF. For this purpose, in 2003 patients with various neurological diseases the intrathecal synthesis of IgG was determined by Reiber's formula and by the IgG index, as well as by the demonstration of OCB by isoelectric focusing (IEF). While OCB could be detected in no patient with an IgG index < 0.45, these bands were always demonstrated in patients with an index > 0.80. Even though arrange of 0.45-0.8 OCB was only detected in 268/1316 patients (20.4%), in 190/268 samples (70.8%) OCB were the only criterion for intrathecal synthesis of IgG. Calculation of intrathecal synthesis of IgG by Reiber's formula was less helpful in deciding about the necessity for IEF. Even though they had no intrathecal synthesis of IgG, as calculated by Reiber's formula, 189/1472 patients (12.8%) had OCB in the CSF. OCB were always detected if local production of IgG was > 12%. In patients with a severe damage of the blood-CSF barrier, calculation of the IgG index gave more false-positive results than calculations using Reiber's formula.
Guillain-Barré syndrome following streptokinase therapy.
Clinical and laboratory data from a patient with Guillain-Barré syndrome indicated a probable etiological correlation of polyradiculitis to the intravenous administration of streptokinase. Oligoclonal IgG bands in the cerebrospinal fluid and serum were shown to be specific for streptokinase. Serum titers of streptokinase were elevated 64-fold for IgG, 16-fold for IgM, and 4-fold for IgA compared to controls. Clinical symptoms of Guillain-Barré syndrome are thought to result from streptokinase antibody complex mediated damage to the local blood-nerve barrier. The pathogenic relevance of autoantibodies to albumin and proteins of the central and peripheral nervous systems, occurring early after onset of symptoms, remains to be determined.