Background:Spinal dural arteriovenous fistulas (DAVFs) are rare lesions that lead to venous congestion and ischemic injury resulting in neurologic deterioration. Here we present a patient diagnosed with glioblastoma multiforme (GBM) who became symptomatic from a spinal DAVF after a diagnostic high-volume lumbar puncture (LP).Case Description:When a 72-year-old female developed partial seizures in her left upper extremity without other focal neurological deficits, she underwent a magnetic resonance imaging (MRI) scan of the brain. The MRI revealed a right frontal/posterior corpus callosal lesion. She next had a MR-guided high-volume LP. A GBM was diagnosed following a biopsy. Postoperatively, after the LP, she was noted to have bilateral deltoid and bilateral 4/5 lower extremity weakness, with diffuse hyperreflexia. The MRI and magnetic resonance angiogram (MRA) of the cervical spine demonstrated a large venous varix at the C5-C6 level within the left neural foramen. She underwent successful complete embolization of two thyrocervical branches with direct communication to an enlarged anterior spinal artery. One month later, her neurological examination returned to baseline; she was walking independently with only 4+/5 residual weakness in her left lower extremity.Conclusions:Here we report a patient with a cranial GBM and an incidental cervical spinal C5-C6 DAVF that became symptomatic after a high-volume LP. It is possible that the high-volume LP increased vascular congestion, thus precipitating the onset of cervical myelopathy.

Antiplatelet medications are the mainstay for secondary stroke treatment. Aspirin, clopidogrel, and aspirin-dipyridamole are commonly used antiplatelet medications. Other antiplatelet medications such as ticagrelor and prasugrel have been majorly used in cardiovascular or neuro-interventional specialties. Recent studies have paved a way to their use in secondary stroke prevention. In this review, we have briefly discussed the pharmacology of ticagrelor, published literature in cardiology and stroke trials, use of ticagrelor among patients with ischemic strokes, and compared its efficacy, limitations and side-effects with other antiplatelet medications.

A 55-year-old male with a past medical history significant for anxiety (on fluvoxamine 100 mg daily for the past year), obstructive sleep apnea and intermittent use of pseudoephedrine as needed for congestion (last dose was 5 days prior to admission) presented to our tertiary care emergency department with a thunderclap headache (TCH) and sudden anterograde amnesia. At 7 days prior his admission, the patient was evaluated by his dentist for a toothache that was attributed to a possible infected tooth and was subsequently treated with amoxicillin-clavulanate. Then 3 days later, he presented to an emergency department (ED) with a severe holocranial TCH and was found to be hypertensive. A non-contrast computed tomography (NCCT) of his brain did not show any acute intracranial abnormalities. A CT angiogram (CTA) of the head and neck was also unremarkable. His headache was attributed to elevated blood pressure coupled with his recent history of a toothache and he was discharged from the ED on metoprolol. Despite medical management

Introduction : Arteriovenous malformations (AVM) are rare congenital malformations in the brain, often presenting with cerebral hemorrhage. Unruptured AVMs usually remain asymptomatic, or they can present with headache, seizure, or focal neurological deficits. “Arterial steal” is one of the mechanisms which can lead to focal neurological deficits. The idea of vascular steal through high flow shunting within brain AVMs is not a new concept. There is, however, debate about whether the vascular steal phenomenon indeed exists empirically. In a study focused on vascular reserve in patients with cerebral AVMs (utilizing acetazolamide augmentation and perfusion CT methods), decreased hemodynamic reserve was noted in 27% of parenchymal regions of interest close to the AVM and in 17% of parenchymal regions of interest far from the AVM. Other imaging modalities have shown abnormal blood regulation around AVM however there exists a level of discordance between various modalities which questions whether vascular steal exists in vivo. We present an ischemic stroke caused by “arterial steal” phenomenon. Methods : Case report Results : 63‐year‐old male with past medical history of seizure, hypertension presented with confusion and dysarthria for 3 weeks. On exam he was found to have right upper quadrantanopia. CT head without contrast and MRI of brain revealed an evolving infarct in the left posterior cerebral artery (PCA) territory. CT angiogram showed possible occlusion in the left PCA P2 segment which correlated to the previously described stroke and in addition showed evidence of left thalamic AVM. Evaluation for cardioembolic or atheroembolic sources was unrevealing. A diagnostic cerebral angiogram showed a 1.3 mm AVM fed through anterior choroidal branches as well as posterior choroidal branches through left posterior communicating artery. There was delayed filling in the left PCA territory likely due to steal phenomenon which might be the etiology of the stroke. Conclusions : In our case, as demonstrated on angiogram, vascular steal phenomenon through high flow shunting of AVM is the likely explanation for the ischemic stroke.

Introduction : Delayed cerebral ischemia (DCI) and cerebral infarction (CI) due to vasospasm is a major cause of death and disability after aneurysmal subarachnoid hemorrhage (aSAH). Transluminal balloon angioplasty (BA) and super‐selective intra‐arterial (IA) infusion of vasodilators are considered for refractory vasospasm. We examined the safety and efficacy of repeated daily IA treatment in vasospasm. Methods : We reviewed records a single center of vasospasm treatment for aSAH from 2016 through 2019. Primary endpoints were rate of cerebral infarctions and safety related to daily treatments. Secondary endpoints were mortality and favorable clinical outcome at hospital discharge defined as modified Rankin scale of scores 0–2. Results : Of 426 patients with SAH, 197 were aneurysmal with 79 with DCI. Forty‐five out of 79 underwent IA treatment, of which 14 underwent 1 or 2 treatments (Group 1) and 31 underwent ≥3 treatments (Group2). Incidence of CI were similar (Group 1: 42.8%; Group 2: 54.8%, p = 0.45) Good clinical outcomes at discharge were seen in 36% in Group 1 and 16% in Group 2 (p = 0.15). Mortality was 7% in group 1 and 26% in group 2 (p = 0.17). Conclusions : Complications including vessel dissection, systemic hypotension and seizures did not increase with repeated treatments. CI was not noted to differ, but the outcomes were worse in group 2 which may relate to severity of SAH rather than DCI.