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Background: The emergence of neurologic symptoms after carotid revascularization is not uncommon and typically caused by perioperative ischemic stroke or hyperperfusion. Postoperative vasculopathy, including reversible cerebral vasoconstriction syndrome (RCVS) is a rare complication of carotid intervention and may be an under-identified cause of neurologic deficit after revascularization. We report a case of reversible postoperative vasculopathy following carotid revascularization as well as its management. Case Presentation: A 74 year old right-handed woman presented to the emergency department with sudden onset left arm weakness and episodic shaking while hypotensive. Computed tomography angiography revealed total occlusion of her right internal carotid artery. Transcranial Doppler monitoring demonstrated active embolic events in her right middle cerebral artery raising concern for continued stump embolization. She underwent carotid revascularization with carotid endarterectomy, mechanical thrombectomy, and carotid angioplasty and initially did well postoperatively. On postoperative day 5, she developed a fixed right gaze and left hemiparesis. Computed tomography revealed new right frontal lobe and basal ganglia infarcts, and angiography showed new right internal carotid, middle cerebral, and anterior cerebral artery vasoconstriction consistent with postoperative vasculopathy. Despite treatment with pressure augmentation and vasodilator therapy, her symptoms persisted resulting in left hemiplegia at discharge. Discussion: This case highlights postoperative vasculopathy (including RCVS) as a rare potential complication after carotid revascularization that should be considered in a patient with persistent acute neurologic symptoms. Information regarding incidence and predisposing risk factors is limited. Multiple diagnostic and therapeutic modalities may be necessary in the recognition and treatment of postoperative vasculopathy.

Introduction: SARS-Coronavirus-2 infection leading to COVID-19 disease presents most often with respiratory failure. The systemic inflammatory response of SARS-CoV-2 along with the hypercoagulable state that the infection elicits can lead to acute thrombotic complications including ischemic stroke. We present 3 cases of patients with COVID-19 disease who presented with varying degrees of vascular thrombosis. Cases: Cases 1 and 2 presented as cerebral ischemic strokes without respiratory failure. Given their exposure risks, they were both tested for COVID-19 disease. Case 2 ultimately developed respiratory failure and pulmonary embolism. Cases 2 and 3 were found to have simultaneous arterial and venous thromboembolism (ischemic stroke and pulmonary embolism) as well as positive antiphospholipid antibodies. Conclusion: Our case series highlight the presence of hypercoagulability as an important mechanism in patients with COVID-19 disease with and without respiratory failure. Despite arterial and venous thromboembolic events, antiphospholipid and hypercoagulable panels in the acute phase can be difficult to interpret in the context of acute phase response and utilization of thrombolytics. SARS-CoV-2 testing in patients presenting with stroke symptoms may be useful in communities with a high case burden or patients with a history of exposure.

Background and Purpose: The association between SARS-CoV-2 infection and stroke remains unknown. We aimed to compare the characteristics of stroke patients who were hospitalized with Coronavirus Disease 2019 (COVID-19) based on the timing of stroke diagnosis. Methods: We performed a retrospective analysis of adult patients in a health system registry of COVID-19 who were hospitalized and had imaging-confirmed acute stroke during hospitalization. Baseline characteristics and hospital outcomes were collected and analyzed. Results: Out of 882 COVID-19 patients who were hospitalized between March 9 to May 17, 2020, 14 patients (2% of all COVID-19 patients and 21% of those who underwent imaging) presented with stroke or developed stroke during hospitalization. Eleven had acute ischemic stroke (AIS) and 3 had acute hemorrhagic stroke. Six patients (43%) presented to the hospital with acute stroke symptoms and were found to have SARS-CoV-2. Compared to patients who presented with AIS, more patients with AIS during hospitalization were male, of older age, had pneumonia and acute respiratory distress syndrome, were severely ill, and had high inflammatory and thrombotic markers (including C reactive protein, D dimer, ferritin, and fibrinogen). Among all patients, hospital mortality was high (50%) and the majority of patients who were discharged had poor neurological outcome. Conclusions: A distinction should be made between patients who present with acute stroke with concurrent SARS-CoV-2 infection and those who develop stroke as a complication of severe COVID-19. It is likely that a subset of stroke patients will incidentally test positive for the virus given the widespread pandemic.

Purpose: Acute symptomatic seizures (ASyS) are common in critically ill patients. It is unknown how ASyS affect posthospitalization self-reported health compared to patients with established epilepsy. Methods: This is a retrospective cohort study from 2010 to 2018. Patients were identified by an institutional epilepsy database (Ebase). Patient-reported outcome measures (PROMs) were completed as part of standard of care and included the number of seizures in the prior 4 weeks, Liverpool Seizure Severity Scale (LSSS) ictal score, quality of life in epilepsy (QOLIE)-10, Patient Health Questionnaire-9 scales, and the PROM Information System Global Health (PROMIS-GH) scale. Mixed-effects models were created to adjust for age, sex, and race and to examine score trajectory over the 1 year after baseline. Results: A total of 15 311 established epilepsy patients and 317 patients with ASyS were identified. When compared to patients with epilepsy, patients with ASyS were older, mostly male, more often black, and had worse baseline scores on the QOLIE-10 ( P < .001), PROMIS-GH Physical Health ( P = .037), and LSSS Ictal ( P = .006) scales. Patient-Reported Outcomes Measurement Information System Mental and Physical Health T-scores were worse than the general population (T-score = 50) for patients with both ASyS (44 and 42.5, respectively) and epilepsy (44.2 and 44.6, respectively). After adjusting for age, sex, and race, patients with ASyS reported 38% fewer seizures ( P = .006) yet worse QOLIE-10 score ( P = .034). We found that scores improved over time for all PROMs except for PROMIS-GH Mental Health. Conclusion: Compared to patients with epilepsy, patients with ASyS had fewer seizures but worse epilepsy-specific quality of life. Independent of group status, scores generally improved over time.

Background: Refractory status epilepticus is often treated with third-line therapy, such as pentobarbital coma. However, its use is limited by side effects. Recognizing and preventing major and minor adverse effects of prolonged pentobarbital coma may increase good outcomes. This study retrospectively reviewed direct and indirect medical and surgical pentobarbital coma. Methods: Retrospective chart review of all patients with refractory status epilepticus treated with pentobarbital over a 1 year period at a large tertiary care center. We collected baseline data, EEG data, and complications that were observed. Results: Overall, nine patients [median age 46.4 (IQR 21.7, 75.5) years] were induced with pentobarbital coma median 11 (IQR 3, 33) days after seizure onset for a median of 9 (IQR 3.5, 45.4) days. A total of four to eight concurrent antiepileptics were tried prior to the pentobarbital coma. Phenobarbital, due to recurrence of seizures on weaning pentobarbital coma, was required in seven patients. Observed complications included peripheral neuropathy (77.8%), cerebral atrophy (33.3%), volume overload (44.4%), renal/metabolic (77.8%), gastrointestinal (66.6%), endocrine (55.6%), cardiac/hemodynamic/vascular (77.8%), respiratory (100%), and infectious (77.8%). The number of complications trended with duration of induced coma but was nonsignificant. Median ICU length of stay was 40 (IQR 28, 97.5) days. Overall, five patients were able to follow commands after a median 37 (IQR 25.5, 90) days from coma onset. There were eight patients that were discharged from hospital with three remaining in a prolonged unresponsive state. There was one patient that died prior to discharge. Conclusions: This study highlights the high morbidity in patients with refractory status epilepticus requiring pentobarbital coma. Anticipating and addressing the indirect and direct complications in prolonged pentobarbital coma may improve survival and functional outcomes in patients with refractory status epilepticus.

Ictal bradyarrhythmias are rare episodes occurring in patients with or without a past cardiac history. These episodes go unnoticed unless the patient is monitored on simultaneous video-electroencephalogram and 1-lead electrocardiogram. Recognizing ictal bradyarrhythmias is important, since episodes may predispose patients to sudden, unexplained death in epilepsy. We present 2 cases of ictal asystole in patients with right temporal lobe epilepsy. The first patient had seizures refractory to medical therapy and received a pacemaker. The seizures in the second patient responded well to antiepileptic medication, and a pacemaker was deferred. These cases highlight the differing cardiovascular treatment options for ictal asystole.

Objective: Creutzfeldt–Jakob disease is a rapidly progressive spongiform encephalopathy. The E200K mutation is found in a majority of genetically transmitted Creutzfeldt–Jakob disease cases. Methods: We describe the case and associated neuroimaging of an E200K-129M gene-mutation-related fatal spongiform encephalopathy with resultant clinical insomnia and thalamic changes. Results: A 46-year-old Caucasian male presented with, who was well until 2 months prior to admission, a rapidly progressive dementia followed by a change in personality with auditory and visual hallucinations. His wife noted progressively worsening jerking and other limb movements and that he kept his eyes open overnight and was “awake” at all hours. Magnetic resonance imaging, electroencephalogram and initial cerebrospinal fluid analysis were essentially non-diagnostic. Positron emission topography revealed severe bilateral thalamic hypometabolism. Posthumous cerebrospinal fluid analysis revealed abnormal PrP 27-30 protein. Autopsy confirmed prion disease and presence of the E200K-129M mutation. Conclusion: This report highlights that positron emission topography imaging may help diagnose E200K-129M mutation-related spongiform encephalopathy. In cases of non-diagnostic magnetic resonance imaging, electroencephalogram and cerebrospinal fluid studies, early positron emission topography may help in the workup of rapidly progressive dementia.

Objective: Apnea test is required as part of the brain death examination. The duration of the apnea test is variable but typically requires 8–10 min. Prolonged apnea tests have been reported in the setting of hypothermia. Here, we describe a case of prolonged duration of apnea test secondary to a phenomenon called cardiac ventilation. Methods: The patient presented in coma with brainstem areflexia after having an intracerebral hemorrhage resulting in subfalcine, central, uncal, and tonsillar herniations. Confounding variables were excluded. Brain death testing was performed, and she was found to have brainstem areflexia. Pre-requisites for apnea test were then met. Results: Apnea testing, however, was prolonged at 110 min. When reconnected to ventilator, it was noted that she had small (30–35 cc) tidal volumes at a rate of her heart rate without respiratory effort. Ancillary testing with four-vessel cerebral angiogram confirmed cerebral circulatory arrest. Conclusions: To our knowledge, this is the longest reported case of apnea testing during brain death testing. Variables known to cause a delay in the rise of carbon dioxide (PaCO2) levels were excluded. We suspect the hyperdynamic cardiac state caused cardiac ventilations resulting in slow increase in carbon dioxide levels.