It is unusual for a journal focused on tropical medicine to feature a predominance of articles addressing neurologic conditions. In general, one must review numerous tables of content in tropical medicine publications to accumulate enough ‘neurologic literature’ to fill an afternoon’s reading. So it was a real treat to open the February issue of AJTMH.
For those who are not particularly familiar with the recent advances that neuroimaging have facilitated in our understanding of the pathophysiology of cerebral malaria, an editorial by Hoffman and Wassmer1 lay the groundwork as they discuss the role of increased intracranial pressure in cerebral malaria deaths and the identification of reversible cerebral vasoconstriction syndrome in cerebral malaria in a 21 year old man returning from a holiday in Kenya.2 From Zambia, Potchen et al.3 report their work using one of the few 1.5T MRIs available in a malaria endemic region to explore the pathogenic mechanisms that might be driving malaria-induced cerebral edema. Surprisingly, blood brain barrier breakdown, long thought to be a principal contributor to cerebral malaria mortality, was not seen in this Zambian cohort. The increasing availability of neuroimaging in tropical settings is highlighted several times in this AJTMH issue including in the imaging highlights section which shows the MRI findings of metronidazole-associated encephalopathy.
The ever-present conundrum of whether or not to administer agents to kill parasites living in the CNS versus giving steroids to control inflammation and hoping for the best is another major theme. Linking human and animal studies, Prociv and Turner4 offer an interesting article on the subarachnoid phase of neuroangiostrongyliasis—the number one cause of eosinophilic meningitis worldwide. Early treatment is key—and initiating anthelminthics after CNS invasion occurs may well do more harm than good. We learn that adverse neurologic events during mass distribution of ivermectin for onchocerciasis control which has previously been attributed to co-infection with Loa Loa (and hence another example of the nervous system’s intolerance for killing in situ parasites), may actually be due to an mdr-1 gene polymorphism that allows toxic levels of ivermectin to accumulate in the brain.5 And Garvey et al. utilize advanced neuroimaging in conjunction with sera test in their work with neurocysticercosis in rural Peru.6
Twelve of the 45 articles in the February issue of AJTMH are neurologic—happy reading!
1. Hoffmann A, Wassmer SC. New Syndromes Identified by Neuroimaging during Cerebral Malaria. Am J Trop Med Hyg 2018;98:349-350.
2. Yamamoto K, Kato Y, Shinohara K, et al. Case Report: Reversible Cerebral Vasoconstriction Syndrome in Cerebral Malaria. Am J Trop Med Hyg 2018;98:505-507.
3. Potchen MJ, Kampondeni SD, Seydel KB, et al. 1.5 Tesla Magnetic Resonance Imaging to Investigate Potential Etiologies of Brain Swelling in Pediatric Cerebral Malaria. Am J Trop Med Hyg 2018;98:497-504.
4. Prociv P, Turner M. Neuroangiostrongyliasis: The “Subarachnoid Phase” and Its Implications for Anthelminthic Therapy. Am J Trop Med Hyg 2018;98:353-359.
5. Chandler RE. Serious Neurological Adverse Events after Ivermectin-Do They Occur beyond the Indication of Onchocerciasis? Am J Trop Med Hyg 2018;98:382-388.
6. Garvey BT, Moyano LM, Ayvar V, et al. Neurocysticercosis among People Living Near Pigs Heavily Infected with Cysticercosis in Rural Endemic Peru. Am J Trop Med Hyg 2018;98:558-564.