Introduction: Patients infected with HIV usually develop neurological complications. Seizures are amongst clinical manifestation of these neurological complications of HIV infection. We report on 150 HIV positive patients who presented with newly onset seizures. Objectives: Our objective was to evaluate the influence of HIV infection on epilepsy and particularly to look for the most common epilepsy induced complications in our context. Methodology: We recruited all patients infected with HIV and who consulted at the outpatient or admitted in the in the neurology unit of the Yaounde Central Hospital, for seizures from August 1st 2008 to December 31st 2009. All the patients were aged above 18 years, black and of Cameroonian nationality. All those who had a family history of epilepsy, as well as those with a personal history of epilepsy were excluded from the study. Results: During the period of study, we recruited 150 patients aged 38.7 ± 9.9 years and with an M/F sex ratio of 0.76. Generalized seizures were observed in 66% of patients, of whom 58% were HIV 1 positive and an average CD4 count of 65.4 ± 11.7/μl. Cerebral toxoplasmosis was the most common etiology observed in 30% of cases. Discussion: This study being hospital based must have selected the most serious patient with severe immunodeficiency. This can explain why a precise etiology was found in the majority of cases. Modi et al. (1999) found a space occupying lesion in 53%, meningitis in 22% and 25% without identifiable etiology in black South Africans. Central nervous system tuberculosis was the most frequent cause encountered in 64% of patients with etiologies. Conclusion: Seizures are one of the principal manifestations of HIV infection or its complications. Their prevalence is 9.5% in our study. Cerebral toxoplasmosis is the most frequent etiology in our study, followed by cryptococcal meningitis and tuberculous meningitis.
Cysticercosis is the most common helminthic disease of the nervous system in humans. The clinical presentation of neurocysticercosis (NCC) is nonspecifi c and can mimic a wide array of primary central nervous system (CNS) disorders, making its diagnosis a challenge especially in endemic areas. The pathophysiology of episodic CNS manifestations of NCC is not well understood. We support the hypothesis that mechanisms used by cysticerci to escape the host's immune system interfere with store-operated calcium entry (SOCE) pathways. This interference may modify brain excitability, leading to episodic manifestations like epilepsy and headaches. Recent fi ndings suggest that the store-operated calcium entry (SOCE) signaling pathway expressed in host tissues is downregulated by cysticerci ligands. SOCE regulates a vast array of cellular functions in excitable and non-excitable cells including modulation of neuronal excitability and regulation of synaptic plasticity. Inhibition of the SOCE signaling pathway alters synaptic plasticity and synchronization of cortical neuronal networks in vitro and in vivo. These modifi cations may lower seizure or headache thresholds, increasing the probability of developing these disorders. This hypothesis could be explored to improve our understanding of the mechanisms involved in episodic manifestations of NCC. If confi rmed, potential therapeutic opportunities could be expected from pharmacological modulations of specifi c proteins in the SOCE signaling pathway.
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