Amezinium Metilsulfate

Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by recurrent thunderclap headaches with reversible cerebral vasoconstriction, and often precipitated by the postpartum state and vasoactive medications. We describe a case of a patient with RCVS induced by amezinium metilsulfate, a sympathomimetic drug, in whom magnetic resonance angiography (MRA) initially revealed diffusely dilated cerebral arteries.

A 34-year-old woman was prescribed amezinium metilsulfate for hypotension. Twelve days later, she suffered from abrupt severe headaches and was referred to our department. She had no neurological deficits; however, MRA revealed diffusely dilated anterior, middle, and posterior cerebral arteries with vasoconstriction. She was tentatively diagnosed with RCVS and successfully treated with verapamil for headache. Nevertheless, follow-up MRAs disclosed widespread segmental vasoconstriction that resolved in two months.

Diffuse cerebrovascular dilation has not been addressed but may be associated with RCVS pathophysiology. In addition, physicians should bear in mind that amezinium metilsulfate can potentially induce RCVS.

In January, 2011, a 78-year-old man was referred to us with syncope and persistent hiccups. He had had nausea and continuous hiccups 9 days earlier, and had fainted while visiting a local clinic. At our hospital, he had an immediate reduction in systolic blood pressure of 40 mm Hg and loss of consciousness after standing up after lying in a supine position for 5 min. Neurological evaluation showed a right hypoglossal nerve palsy, but MRI of the brain and spinal cord and cerebrospinal fl uid were normal. Chest radiography, gastroendoscopy, ECG, and echocardiography showed no abnormalities. Metoclopramide was prescribed for hiccups and amezinium metilsulphate for orthostatic hypotension. He was discharged because his symptoms improved. 2 weeks later he developed muscle weakness, and after 3 days could not walk. On readmission, he had dysarthria and dysphagia. Ophthalmoscopy showed no abnormalities. He had severe muscle weakness in his upper and lower limbs. CSF white blood cell count was 78 μL (99% lymphocytes) and protein concentration 1·03 g/L. MRI of the brain showed lesions in the medulla oblongata. We suspected acute disseminated encephalomyelitis, herpes simplex virus encephalitis, or neuromyelitis optica (NMO) spectrum disorder, and he was given methylprednisolone pulse therapy (1 g per day) and acyclovir 1500 mg per day. Despite treatment, his muscle weakness worsened. 1 week after completion of methylprednisolone pulse therapy, he had dyspnoea. Arterial blood gas fi ndings were unremarkable while on 2 L oxygen, so we planned MRI of the spinal cord the same day. His blood saturation level started decreasing, while he was in the