Dear editor,
I read with interest the paper of Mejia Maza and coworkers on the presence of axonal swelling and spheroids development in humans, pigs and rats with neurocysticercosis 8. Taking the advantage of a novel rat model of Taenia solium cysticercosis, the authors found not only local inflammatory changes in the brain parenchyma surrounding cysticerci, but axonal swelling with spheroid formation at a considerable distance from the parasites. From what can be understood from their work, these axons originated in neurons located near the parasites that were damaged as a result of inflammatory changes surrounding parenchymal brain cysticerci. It is possible that a sizable proportion of these damaged axons end in either the hippocampi themselves or in distant areas that further connect with hippocampi, such as the cerebral cortex and nuclei deep in the brain. This might result in partially deafferented hippocampi, which, in turn, may provide a substrate for hippocampal atrophy 1.
Hippocampal atrophy is emerging as a common complication of neurocysticercosis due to a diversity of mechanisms 3, 4. One of them, gaining adepts due to the absence of clinical or abnormal electroencephalographic activity in many cases, is the occurrence of recurrent bouts of inflammation related to the periodic release of cysticercal antigens trapped within calcified cysticerci 2, 5, 7. We have previously demonstrated that a single parenchymal brain calcification located in the occipital or the parietal lobe associates with hippocampal atrophy 6. Until now, we did not have a satisfactory explanation for the pathogenetic mechanisms involved in this remotely induced hippocampal atrophy by parasites not associated with seizures. The work of Mejia Maza and coworkers 8 opens new venues for research on these mechanisms, as damaged axons might be tracked from the parasite location (in a remote brain area) to the hippocampi.
Funding
Universidad Espíritu Santo – Ecuador.
Conflict of Interest
Nothing to disclose.
References
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