Oxidative stress in children with neurocysticercosis.

BACKGROUND

Free radicals can cause neuronal injury and play an important role in pathogenesis of neurocysticercosis. This study was done to evaluate oxidative stress (antioxidants and oxidants) in cerebrospinal fluid (CSF) of children with neurocysticercosis and to observe their correlation with the type of seizure and outcome.

METHODS

Forty consecutive confirmed cases of neurocysticercosis were evaluated for their markers of reactive oxygen species, that is, oxidants (malondialdehyde, protein carbonyl and nitrite) and antioxidant (superoxide dismutase, glutathione peroxidase, ceruloplasmin, ascorbic acid, copper and zinc) concentrations in CSF. An equal number of children, age and sex matched with an idiopathic generalized tonic-clonic seizure, were studied as controls.

RESULTS

Generalized tonic-clonic seizure (65%) was the most common presentation, and a single ring-enhancing lesion in the parietal lobe was the most common finding in cranial imaging. Oxidants such as malondialdehyde, protein carbonyl and nitrite in CSF were significantly elevated (P < 0.001), whereas antioxidants such as superoxide dismutase, glutathione peroxidase, ceruloplasmin, ascorbic acid, copper and zinc levels were significantly lower (P < 0.001) in children with neurocysticercosis than in controls. There were insignificant differences in oxidant and antioxidant value in CSF in relation to the type of seizure, number and location of lesion in cerebral cortex and antiepileptic therapy.

CONCLUSION

The significantly elevated malondialdehyde, nitrite and protein carbonyl values reflect increased oxidative stress, whereas decreased concentrations of glutathione peroxidase, ascorbic acid, zinc, copper, ceruloplasmin and superoxide dismutase point toward utilization of the antioxidants in neurocysticercosis. The observed changes in oxidants and antioxidants suggest the production of reactive oxygen species such as superoxide, hydrogen peroxides and hydroxyl radicals and their possible role in pathogenesis of neurocysticercosis.