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OLARU, Natalia; DRAGAN, Diana; VATAMAN, Anatolie; CHIOSA, Vitalie. Epilepsy associated with cerebral toxoplasmosis. In: MedEspera: the 10th Intern. Medical Congress for Stud. and Young Doctors, 24-27 April 2024: abstract book. Chișinău, 2024, p. 191. ISBN 978-9975-3544-2-4. |
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Introduction. Parasitic infections of the central nervous system (CNS) are an acquired cause of epileptic seizures and epilepsy in countries with low and medium economic incomes, including the Republic of Moldova. Cerebral toxoplasmosis is caused by the intracellular protozoan parasite, Toxoplasma gondii, which forms brain cysts, especially in immunocompromised patients. Parasite proliferation and microglia produce a modulation in the expression of pro-inflammatory genes, with the establishment of chronic latent infection. The latest studies show that toxoplasmosisinduced structural damage in the brain parenchyma and recurrent inflammation interfere with GABAergic signaling, which is mainly responsible for the occurrence of epileptic seizures, using it as a carbon source for parasite metabolism and facilitating parasite dissemination. Aim of study. Evaluation of neurological manifestations, seizure semiology, electrophysiological and neuroimaging changes in epilepsy caused by cerebral toxoplasmosis, and the neurobiological mechanisms involved in epileptogenesis. Methods and materials. The study included 11 patients with cerebral toxoplasmosis and epileptic seizures. The diagnosis was established based on the clinical manifestations, serological tests analysis, electrophysiological (EEG) and neuroimaging examination. Results. In the study 8 patients were HIV positive, stage C3 and 1 patient suffered from congenital toxoplasmosis. Typical seizure semiology showed focal onset: clonic 54.2%, tonic, cognitive and focal to bilateral tonic-clonic. EEG abnormalities was found in 39.2 % as focal slowing and focal epileptiform discharges. All patients performed neuroimaging, which identified cystic lesions in affected areas of CNS: frontal and temporal lobes, basal ganglia, thalami, periventricular regions and cerebellar white matter. Conclusion. Toxoplasmosis is a frequent opportunistic infection in immunocompromised patients, a late complication of HIV infection and usually occurs in patients with CD4-T-cell counts below 200/mm3.The clinical manifestations and epileptic seizures caused by cerebral toxoplasmosis are polymorphic and depends on the number and location of the cysts, and also on the host's immune response. epileptic seizures and epilepsy in countries with low an d medium economic incomes, including the Republic of Moldova. Cerebral toxoplasmosis is caused by the intracellular protozoan parasite, Toxoplasma gondii, which forms brain cysts, especially in immunocompromised patients. Parasite proliferation and microglia produce a modulation in the ex pression of pro-inflammatory genes, with the establishment of chronic latent infection. The latest studies show that toxoplasmosisinduced structural damage in the brain parenchyma and recurrent inflammation interfere with GABAergic signaling, which is mainly responsible for the occur rence of epileptic seizures, using it as a carbon source for parasite metabolism and faci litating parasite dissemination. Aim of study. Evaluation of neurological manifestations, seizure semiolo gy, electrophysiological and neuroimaging changes in epilepsy caused by cerebral toxopla smosis, and the neurobiological mechanisms involved in epileptogenesis. Methods and materials. The study included 11 patients with cerebral toxoplasmosis an d epileptic seizures. The diagnosis was established based on the clini cal manifestations, serological tests analysis, electrophysiological (EEG) and neuroimaging exami nation. Results. In the study 8 patients were HIV positive, stage C3 and 1 patie nt suffered from congenital toxoplasmosis. Typical seizure semiology showed focal ons et: clonic 54.2%, tonic, cognitive and focal to bilateral tonic-clonic. EEG abnormalities was foun d in 39.2 % as focal slowing and focal epileptiform discharges. All patients performed neuroimagi ng, which identified cystic lesions in affected areas of CNS: frontal and temporal lobes, basal ganglia, thalami, periventricular regions and cerebellar white matter. Conclusion. Toxoplasmosis is a frequent opportunistic infection in im munocompromised patients, a late complication of HIV infection and usually occurs in pa tients with CD4-T-cell counts below 200/mm3.The clinical manifestations and epileptic seizures cau sed by cerebral toxoplasmosis are polymorphic and depends on the number and location of the cys ts, and also on the host's immune response. |
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