Abstract

Dear Editor,
I read with interest a unique case published by Ahmad et al. [1] in the most recent issue of the Sudanese Journal of Pediatrics, highlighting a case of neurocysticercosis (NCC) induced dystonia in a pediatric patient. In the article, the authors mentioned a hypothesis regarding the pathophysiology of NCC-related movement disorders. It is stated that an inflammatory reaction around the cyst in conjunction with edema and meningeal irritation propagates movement disorders such as dystonia, as seen in this case. While this is undoubtedly an explanation regarding the mechanism of NCC and other movement disorders, dystonia specifically has a vascular component to its pathophysiology [2,3].

Dystonia, a rare manifestation seen in NCC as pointed out by the authors, may be attributed to vascular mechanisms, which involve the perforating branches of the middle cerebral artery, leading to blood-brain barrier dysfunction, cerebral ischemia, and increased levels of excitatory neurotransmitters, as observed in altered glycemic states [4]. This hypothesis could partially explain the fact that most cases of chorea and dystonia reported in the literature had small cystic lesions without edema or distortion of the nearby structures by pressure. Although this case is an exception, given that the brain magnetic resonance imaging showed ring-enhancing lesions within the basal ganglia and cortex with peri lesional edema, the proposed mechanism remains the same. Given that movement disorders only occur in approximately 3% of individuals with NCC, further research is needed to elicit the mechanisms of other individual movement disorder mechanisms associated with NCC [4,5].

Key words: Neurocysticercosis; Dystonia; Movement disorders; Chorea; Middle cerebral artery.