Neurocysticercosis is a neglected and usually poverty‐related disease of high public importance. The mechanisms by which the calcified lesions cause epilepsy are not known, but have been attributed to residual perilesional gliosis or an inflammatory process. This case shows that an inflammatory response to a calcified granuloma may be associated with the development of epilepsy. The increase in glutamate and kinin B1 (pro‐epileptogenic) receptors added by reduced expression of kinin B2 (anti‐epileptogenic) receptors may explain the chronic epileptogenesis associated with the lesion, corroborating the hypothesis of inflammatory mechanisms involved in the pathophysiology of epilepsy in these patients.

ObjectiveWe report a case of biopsy-proven giant cell arteritis after an initial presentation of area postrema syndrome.MethodsA 65-year-old man was evaluated using MRI, temporal artery biopsy, and ultrasound.ResultsThe patient presented with refractory nausea, vomiting, and hiccups that caused weight loss without any other neurologic or clinical symptoms. His MRI scan 15 days later revealed a hyperintense sign on the area postrema with no abnormal diffusion or contrast enhancement, compatible with isolated area postrema syndrome. An extensive workup for inflammation and other etiologies including neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody disorder, and multiple sclerosis (MS) showed negative results. The patient responded to treatment with methylprednisolone. Two months after the initial clinical manifestation, the patient developed fatigue, headache, and scalp tenderness. He was diagnosed with giant cell arteritis after ultrasonography and biopsy were performed. He responded well to oral glucocorticoids and had only 1 relapse during tapering. He has not had arteritic ischemic optic neuropathy or any new episodes of area postrema syndrome.DiscussionThis case demonstrates the importance of expanding the differential diagnosis in patients with area postrema syndrome and no other signs of NMOSD.

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Introduction: Bickerstaff encephalitis is a rare disease and considered a spectrum of the Guillain Barré syndrome. We present a case report of subacute onset of gait impairment, impaired consciousness, ophthalmoplegia, respiratory dysfunction and severe dysautonomia with atypical and diffuse brainstem and diencephalic white matter abnormalities, a positive seric GQ1B and neurological recovery after two cycles of immunoglobulin and plasmapheresis. The aim is to describe an atypical case of Bickerstaff encephalitis. Case report: A 30-year-old man was admitted with a ten days history of vertigo, dysphagia, bilateral ptosis and tetraparesis with brachial predominance. His examination showed appendicular ataxia, tetraparesis, ophthalmoplegia and ptosis. Due to the clinical presentation, we started treatment with immunoglobulin but he evolved with need of mechanical ventilation and had two cardiac arrests due to severe dysautonomia. His lumbar puncture showed no albuminocytologic dissociation. His magnetic resonance imaging showed nonspecific foci signal hyperintensities on FLAIR (Fluid-Attenuated Inversion Recovery) in cerebellum, hippocampus and globus pallidus. His serum GQ1B testing was positive, confirming the initial clinical hypothesis of Bickerstaff encephalitis. He was submitted to plasmapheresis and a second cycle of immunoglobulin, with complete clinical recovery six months after. Conclusion: We described a case of atypical Bickerstaff encephalitis, highlighting the importance of recognizing atypical clinical patterns for an appropriate treatment.