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Twenty-Ninth International Winter-Workshop Clinical Abstracts: 29th International Winter-Workshop on Clinical, Chemical, and Biochemical Aspects of Pteridines 29 Pteridines Vol. 21, 2010, pp. 29 - 65 Abstracts Twenty-ninth International Winter-Workshop on Clinical, Chemical, and Biochemical Aspects of Pteridines Held in St.Christoph, Arlberg, Austria, February 28th - March 7th, 2010 Organized by D.Fuchs (Innsbruck), G.Reibnegger (Graz), A. Griesmacher (Innsbruck) "Mild Encephalitis" - Brain-organic Patholo- es: streptococcal infection associated autoim- gies Between Neurologic and Psychiatric mune disorder; HSV 1,2 infection associated Disease? autoimmune disorder respectively early state of systemic lupus erythematodes; undefined sys- Bechter K temic autoimmune disorder associated with Sjögren syndrom; suggestive chronic Borna- Clinic for Psychiatry and Psychotherapy II, Ulm Disease-Virus-infection. University, Bezirkskrankenhaus Günzburg, Despite some recent progress, the definition of Günzburg, Germany ME remains preliminary, on the other hand with- in the general problems of definition and catego- The term ‚mild encephalitis' (ME) (1) was pro- rization of inflammation: the established defini- posed some years ago to address a new approach tion dates back to Celsus 40 BC, modern defini- to severe psychiatric disorders with unknown eti- tions depend from the options to investigate the ology, the pathogenesis of which appeared not many aspects and factors involved. A recent defi- appropriately understood. ME means a type of nition (2) "inflammation is a complex set of inter- low level CNS inflammation possibly causing a actions among soluble factors and cells that can spectrum of psychiatric disorders in interaction arise in any tissue in response to traumatic, infec- with other contributing factors. In the meanwhile tious, post-ischaemic, toxic or autoimmune more and more findings support such view injury" appears perfect, but is not applied in clin- including recent own studies by modern CSF ical practice. Conventional histopathology diagnostics, considered the diagnostic gold stan- defines inflammation by "visible inflammatory dard in CNS-inflammation, especially acute cellular infiltrates within tissue", a limited view. It meningoencephalitis: we found in 41% of is known, that CNS-inflammation begins with an patients with affective (n=24) or schizophrenic accumulation of immune competent cells within (n=39) spectrum disorders definite CSF abnor- defined brain areas yet without visible cellular malities; in 14% intrathecal humoral immune infiltrates and such may last for longer time. An responses clearly interpreted as inflammatory; in important difference exists between acute and 10% slightly increased CSF cell counts; in 29% chronic inflammation, chronic not being clearly moderate blood CSF barrier dysfunction, in 24% defined nor in histopathology nor in the clinic, in as the only pathological sign; in 20% of affective the latter by simple time cuts. In neurology it is spectrum patients systemic inflammation, in none accepted to consider encephalitis to be chronic of the schizophrenic spectrum patients. In 6% after four weeks. In psychiatry there is little (n=4) we refined the previous differential diagno- agreement about which disorders have to be sis by the results of CSF investigation and diag- termed chronic. When adopting the neurological nosed probable ME due to various specific caus- time frame probably most psychiatric disorders Pteridines/Vol. 21/No. 2 30 Abstracts: 29th International Winter-Workshop on Clinical, Chemical, and Biochemical Aspects of Pteridines should be considered chronic. In the case of a demonstrate the dilemma in the approach to CNS neurobiological basis such as ME, we would deal inflammation in general, and even more to LLCI nearly exclusively with chronic low level neu- situations. The relationship between brain pathol- roinflammation then in psychiatry. ogy and clinical psychiatric symptoms is known What is about the symptoms of psychoses and to be weak. To better understanding causal rela- encephalitis? Classical encephalitis can cause tionships and finding better definitions we need various psychiatric syndromes, rare single cases more parameters and more refined criteria. In vivo observed may go through the range of psychiatric detection of LLCI is especially difficult. Adopting disorders within weeks, e.g. beginning with per- modern CSF-diagnostics from neurology with its sonality disturbance, progressing to affective broad background knowledge is an important but spectrum and later schizophrenic spectrum disor- only a first step to diagnose ME as a possible psy- der and only finally to organic psychoses and pos- chiatric disease. sibly backwards. The rule of non-specificity of Summing up, the present definition of ME psychiatric symptoms holds for various organic remains preliminary, but appears advantageous to causes including encephalitis. Non-classical the alternative of further neglecting the preva- inflammation (classical i. fits acute but does not lence of LLCI situations, which may not rarely fully cover chronic i.) is now more and more rec- causally underlie psychiatric disorders. We pro- ognized to exist though yet lacking clear defini- pose to diagnose ME in severe psychiatric disor- tions. Just recently one new term was proposed ders (schizophrenic or affective spectrum) with that is 'parainflammation', describing chronic the following CSF-findings: probable ME with inflammation with preferential fibrosis (3). Low oligoclonal bands exclusively detected within level CNS- respectively neuro-inflammation CSF not in parallel in blood, or with intrathecal (LLCI) is now often mentioned but lacks clear production of specific immunglobulin subclasses definition. One good exception is the categoriza- (IgA or IgG or IgM or combined); possible ME tion of microgliaactivation in four grades, repre- with exclusive blood-CSF-barrier-dysfunction senting one important aspect of neuro-inflamma- (for details see (6)). tion though not always indicating inflammation (4); the lower grades proposed (1+2) would well References: match with what here is termed LLCI and ME 1 Bechter K. Mild encephalitis underlying psy- respectively. chiatric disorder - A reconsideration and Refined definitions are not an academic point hypothesis exemplified on Borna disease. but are important for clinic and research. The Neurol Psych Brain Res 2001;9:55-70 unmet problem is demonstrated for example with 2 Nathan C. Points of control in inflammation. the many open questions regarding the role of Nature 2002;420:846-52 HIV-brain-infection for related psychiatric distur- 3 Medzhitov R. Origin and physiological roles bances. When taking a strict definition of HIV- of inflammation. Nature 2008;454:428-35 Encephalitis (HIV-E), HIV-E includes the post- 4 Raivich G, Bohatschek M, Kloss CU, Werner mortem finding of three classical inflammatory A, Jones LL, Kreutzberg GW. Neuroglial acti- foci; then postmortem diagnosis matches relative- vation repertoire in the injured brain: graded ly well with clinical HIV-E-diagnosis (5). response, molecular mechanisms and cues to However, LLCI is present in non-HIV-E cases physiological function. Brain Res Brain Res postmortem frequently and associated with vari- Rev 1999;30:77-105 ous psychiatric syndromes, including cognitive 5 Cherner M, Cysique L, Heaton RK, Marcotte decline or psychosis. Even more critical in such TD, Ellis RJ, Masliah E, Grant I. definition of HIV-E, not only from a practical but "Neuropathologic confirmation of definitional especially from a theoretical point of view is, that criteria for human immunodeficiency virus- non-HIV-E cases may present up to two classical associated neurocognitive disorders. J inflammatory foci within the brain which remain Neurovirol 2007;13:23-8. non-diagnostic for HIV-E. Such examples 6 Bechter K, Reiber H, Herzog S, Fuchs D, Pteridines/Vol. 21/No. 2 Abstracts: 29th International Winter-Workshop on Clinical, Chemical, and Biochemical Aspects of Pteridines 31 Tumani H, Maxeiner HG. Cerebrospinal fluid higher ATP content in vari-ous brain areas sug- analysis in affective and schizophrenic spec- gesting that their antioxidative mechanisms seem trum disorders: Identification of subgroups to be less pronounced (GR, GPX, GST) than with immune responses and blood-CSF barri- those of adult rats, while the GSSG content is er dysfunction. J Psychiatric Res 2010:44:321- higher in juvenile rats. The application of 30. Haloperidol to adult rats seems to lead to a reduc- tion of antioxidative mechanisms in various brain areas. There is also evidence that Haloperidol Oxidative and Antioxidative Mechanisms in affects ATP. In juvenile rats, Haloperidol seems to Juvenile and Adult Rats after Application of have rather little influence on antioxidative mech- Haloperidol anisms. While our results show that Haloperidol does Berger M, Clement HW, Heiser P, Sommer O, not directly influence radical concentration in Hoinkes A, Schulz E both young and old rats, there is evidence that Haloperidol clearly has noticeable, age-related University Hospital Freiburg, Department Child effects on radical formation occurring on the level & Adolescent Psychiatry, and University Hospital of radical detoxification mechanisms. Freiburg, Department General & Visceral Surgery, Freiburg, Germany Expression of Indoleamine 2,3-dioxygenase-2 Tardive dyskinesia which is presumed to be (IDO2) at the Human Feto-Maternal Interface connected with elevated oxidative stress, is described as a typical side effect of Haloperidol. Blaschitz
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