Spontaneous vertebral subdural hematoma (SDH) is very rare. due to hyperacute

Spontaneous vertebral subdural hematoma (SDH) is very rare. due to hyperacute stage of SDH. After hematoma evacuation her symptoms gradually improved. We suggest that spinal cord evaluation should be considered in patients with headache who have ICVS although intracranial hemorrhage would not be visible in brain images. Keywords: Spinal subdural hematoma Subarachnoid hemorrhage Intracranial GSK1070916 vasospasm Headache INTRODUCTION Intracranial vasospasm (ICVS) can be caused by any situation that brings about bleeding into the cerebral subarachnoid space such as traumatic subarachnoid hemorrhage (SAH) cerebral tumoral bleeding or rupture of vascular malformations but the rupture of cerebral aneurysms within the basal cistern is most commonly associated with ICVS [1]. Moreover migraine taking vasoactive drugs (cocaine pseudoephedrine immunosuppressants or selective serotonin reuptake inhibitors) or the postpartum period can also cause ICVS and tend to induce vasospasm most often without intracranial bleeding [2]. Because ICVS leads to cerebral ischemia that can cause devastating neurological deterioration in some cases it is important that ICVS be detected and its cause be identified as early as possible [1]. Acute spontaneous spinal subdural hematoma (SDH) is very rare. However it often results in serious complications hence appropriate therapeutic approaches and rapid diagnosis are needed [3 4 ICVS associated with spontaneous spinal SDH has also been reported very rarely [4]. Here we firstly report a case of ICVS without intracranial hemorrhage that was caused by acute spontaneous spinal SDH. CASE A 41-year-old woman was admitted to our hospital with a complaint of severe headache. She had headache for 3 years and expressed it as throbbing pain in both temporal regions accompanied by nausea. This pain was exacerbated by physical activity and under sunlight. Symptoms tended to occur once in 1~2 months lasted for 1~3 days and then vanished. Weekly before admission to your medical center her headaches symptoms were not the same as those before. She experienced a twinge it the proper posterior throat for the very first time and consequently experienced severe discomfort in the complete mind but no nausea throwing up or fever. She was accepted towards the neurology division of another medical center and underwent computerized tomography (CT) angiography 2 times after the headaches developed; simply no bleeding was observed however multifocal vasospasms of intracranial arteries had been exposed (Fig. 1A B). She was identified as having status migrainosus; therefore steroid pulse therapy with dental beta-blockers and nonsteroidal anti-inflammatory drugs received to relieve headaches. Nevertheless her symptoms did not improve but rather worsened. Several hours before admission to our hospital she started GSK1070916 complaining of nausea and vomiting as well as very sharp tearing pain in the neck and back. According to the analysis of a cerebrospinal fluid (CSF) specimen that was obtained via lumbar puncture in an outside hospital 3 days after symptom onset the levels of white blood cells (WBC) protein and glucose were 4/μl 62 mg/dl and 46 mg/dl respectively. Other CSF profiles were not provided. She had a history of hypertension and her blood pressure was well controlled with regular antihypertensive medication. She SMARCB1 denied any history of auto-immune or cerebrovascular diseases. There was also no special family history of migraine or autoimmune disease. On admission to our hospital her blood pressure was 195/114 mmHg; pulse 60 beats/min; respiration 20 breaths/min; and body temperature 36.6 Mental status was alert and oriented. Cranial GSK1070916 nerve examination and motor and sensory functions were normal. No pathologic reflexes GSK1070916 were found yet neck stiffness was suspected. According to the routine blood tests the only abnormality was that the WBC count was increased to 18000/μl. In the blood coagulation test prothrombin time-international normalized ratio and activated partial thromboplastin time were 0.99 s GSK1070916 (normal range 0 s) and 28 s (normal range 20 s) respectively;.