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https://www.novapublishers.com/catalog/product_info.php?products_id=38720Idiopathic Intracranial Hypertension May be Caused by Reactivation of Latent Cerebral Toxoplasmosis Due to Various Medications and Biologic Substances (pp. 273-336)
Authors: (Joseph Prandota,Dept.of Social Pediatrics,University Medical School,Wroclaw,Poland)
Abstract:
Idiopathic intracranial hypertension (IIH) presents with headaches associated with an increased cerebrospinal fluid pressure. Recently, we have demonstrated that recurrent headaches in non-HIV-infected subjects were due to acquired cerebral toxoplasmosis (CT). The aim of this chapter was therefore to focus on the pathomechanisms that may lead to reactivation of latent CT and manifest as IIH. Literature informations and other data cited in this work were selected to illustrate that various medications and biologic substances may affect latent CNS T. gondii infection/ inflammation intensity and/or host defense mechanisms (the production of NO, cytokines, tryptophan degradation by indoleamine 2,3-dioxygenase (IDO), mechanisms mediated by an IFN- responsive gene family, limiting the availability of intracellular iron to T. gondii, production of reactive oxygen/nitrogen species) and cause choroid plexitis and/or vasculitis. Examples of such triggers revealing IIH and accompanying disturbances of IFN--mediated immune responses that control T. gondii include: minocycline (decreased NO, iNOS, TNF-, IFN-; IL-1, PGE2, COX-2 expression, activity (?), increased TNF- and IL-6), retinoids (decreased NO synthesis, iNOS-2, TNF-; increased IFN-, IL-2, TGF-1, IL-12), nitrofurantoin (hyperproduction of ROS; redox reactions regulate IDO and tryptophan metabolism), muronabad CD3 (increased NO, TNF-, IFN-, IL-2, IL-6, IL-8). These irregularities could markedly impair host defense mechanisms important for immune control of the parasite, and finally reactivate latent CNS T. gondii infection. Therefore, in subjects with IIH, pseudotumor cerebri and/or aseptic meningitis, test(s) for T. gondii infection should be seriously taken into consideration. It seems that headaches and meningitis are clinical manifestations of the Jarisch-Herxheimer reaction in CT.
Intracranial Hypertension seems fairly common in ME. Thoughts?