Abstract

Introduction. Neurological manifestations secondary to Hymenoptera stings are rare. However, the literature describes cases of severe central and peripheral nervous system damage. Suspected pathophysiological mechanisms include hypoxic-ischemic damage, demyelination, and the direct neurotoxic effect of venoms. In this context, bee stings could be a possible atypical causative factor for Guillan–Barré syndrome and chronic inflammatory demyelinating polyneuropathy. Case report. We present the case of a 32-year-old patient who declared the presence of a bee sting two weeks before the onset of neurological manifestations (flaccid quadriparesis, predominantly distal, with paresthesia at the same level) that were initially diagnosed as a Guillain Barré syndrome. Despite the treatment with immunoglobulins in the acute phase, the worsening of the motor deficit after one month required a new course of immunoglobulins, associating corticosteroids, with initially favorable evolution. However, the presence of a new relapse after eight weeks, correlated with changes such as albumin-cytological dissociation in the examination of the cerebrospinal fluid and the appearance of active denervation on the electroneuromyography study, established the final diagnosis of chronic inflammatory demyelinating polyneuropathy. Conclusions. We consider the presented case proof of the relationship between the Hymenoptera sting and various peripheral nervous system pathologies. Inflammatory and demyelinating changes common to Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy appear to be the primary pathophysiological mechanism to explain this uncommon correlation.

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