• Hanfeng Chen, Ziqi Xu, and Yuan Yuan.
• Medicine (Baltimore). 2020 Jul 31; 99 (31): e21522.

RationalePosterior reversible encephalopathy syndrome (PRES) and reversible cerebral vasoconstriction syndrome (RCVS) are separate clinical entities with distinct pathophysiological features. But in some special conditions PRES and RCVS can occur simultaneously.Patient ConcernsWe report the unique case of a 40-year-old female presented with crescendo headache, blurred vision, and recurrent generalized tonic-clonic seizure. She had a minor neck injury 1 week before but attracted no more attention. Neurological tests on admission yielded a Glasgow Coma Scale score of 13. No obvious focal neurological deficit apart from positive signs of meningeal irritation was presented.DiagnosesXanthochromia and hemorrhagic cerebrospinal fluid with pleocytosis was found on lumbar puncture. Cranial computed tomography was negative but magnetic resonance imaging demonstrated bilateral areas of vasogenic edema in the parieto-occipital lobes and cerebellum consistent with PRES. An incidental subacute spinal subdural hematoma extending from the level of C6 to T1 was depicted by spinal magnetic resonance imaging, presumably as a complication of negligible neck trauma. Spinal digital subtraction angiography showed no evidence of spinal aneurysm, arteriovenous malformation, or dural arteriovenous fistula. Cerebral digital subtraction angiography showed segmental narrowing and dilatation of vessels, a potential feature of RCVS, involving the circle of Willis and their branches.InterventionsThe patient was treated with nimodipine for vasodilation and other symptomatic therapies. The spinal subdural hematoma was not warranted for surgical intervention and managed with simple analgesics.OutcomesThe patient experienced a dramatic improvement in neurological symptoms and was discharged without sequelae. Follow-up imaging showed complete resolution of all radiological changes.LessonsClinician should be aware of spinal subdural hematoma as the potential trigger in development of PRES and RCVS. We speculate that endothelial dysfunction and vascular tone dysregulation may be implicated to play the major pathophysiologic role.

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