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ObjectiveTo detail the scope and nature of financial conflicts of interest (COIs) between neurologists and the pharmaceutical and medical device industries (Industry) using the Centers for Medicare and Medicaid Services Open Payments (OP) database, with a focus on trends from 2013 to 2016.MethodsPayments from Industry to US neurologists were categorized into research payments, general (nonresearch) payments, and value of ownership in Industry. We performed descriptive analyses to detail the scope and nature of these relationships and trends over time.ResultsAt least 9,505 neurologists received at least one payment from Industry each year. From 2013 to 2016, 1.6 million payments totaled $354 million, of which 99.5% of payments and 85.6% of payment value were for general/nonresearch-related payments. Most neurologists (between 65% and 80%) received less than $1,000 per year, but over 200 neurologists each received more than $100,000 during some years. Several received over $1 million. General payments are increasing, research payments are steady, and neurologists' ownership and investments are decreasing.ConclusionsNeurologists have extensive financial relationships with Industry, though this is driven by a well-paid minority. As a profession, we must work to establish firm rules to manage these potential COIs, ensuring that relationships with Industry yield synergistic advances while minimizing bias and maintaining public trust.

Brain death has been accepted as a legal definition of death in most countries, but practices for determining brain death vary widely. One source of variation is in the use of ancillary tests to assist in the diagnosis of brain death. Through case-based discussions with 3 experts from 3 continents, this article discusses selected aspects of brain death, with a focus on the use of ancillary tests. In particular, we explore the following questions: Are ancillary tests necessary, or is the clinical examination sufficient? What ancillary tests are preferred, and under which circumstances? Are ancillary tests required when the primary mechanism of injury is brainstem injury? Should the family's wishes play a role in the need for ancillary tests? The same case-based questions were posed to the rest of our readership in an online survey, the preliminary results of which are also presented.

Objective: To determine the safety of domperidone in the treatment of nausea associated with dihydroergotamine (DHE) infusion and headache. Methods: We audited our use of domperidone for the inpatient management of nausea, focusing on known safety concerns, particularly potential cardiac arrhythmias. Results: We reviewed 103 consecutive admissions of 90 patients admitted for IV DHE by infusion. Most admissions were to treat chronic migraine with (n = 53) or without (n = 46) aura. Domperidone was administered in 85 of 103 encounters and was well-tolerated at doses up to 80 mg/d. A significant side effect, akathisia, was observed in one patient. Baseline ECG with corrected QT interval (QTc) was obtained on all patients. Repeat ECG after domperidone was obtained in 21 patients, whose baseline characteristics did not differ from the group as a whole. ECG was interpreted blindly by a cardiac electrophysiologist. QTc did not differ before and after domperidone administration (Wilcoxon signed-rank test, median [interquartile range] 435.0 [410.5–453.0] at admission and 427.0 [399.0–452.5] after domperidone; p = 0.15). In combination with other antiemetics, domperidone was effective in treating nausea such that no patients had refractory nausea severe enough to limit DHE dose. Conclusions: This retrospective audit demonstrates that domperidone is safe in the treatment of nausea associated with inpatient DHE infusion and headache. While larger prospective trials are necessary to confirm these results and assess efficacy, current evidence and clinical experience suggests that domperidone is safe and useful for nausea and headache management. Classification of evidence: This study provides Class IV evidence that for patients with headache undergoing DHE infusion, domperidone is safe and effective in the treatment of nausea.

I read with interest Llinas et al.1's article that discussed burnout and resiliency. I appreciate the authors' emphasis on the primacy of systemic changes to address the problem, such as increasing opportunities for recognition and rewarding activities.

In the article “BOLD cerebrovascular reactivity as a novel marker for crossed cerebellar diaschisis,” Sebok et al. reported similar sensitivity of blood oxygen level–dependent cerebrovascular reactivity (BOLD-CVR) in detecting crossed cerebellar diaschisis (CCD) as compared to (15O)-H2O-PET in 25 participants with symptomatic unilateral cerebrovascular steno-occlusive disease and reported that those with CCD had poorer baseline neurologic performance and 3-month neurologic outcome. In response, Reidler et al. question whether CCD was the cause of consequence of poor outcomes, noting that it may be an epiphenomenon of large-volume supratentorial strokes and citing conflicting evidence in the literature about independent association of CCD with post-stroke outcomes. They suggest accounting for lesion volume and distribution in the analyses. In their reply, Niftrik et al. agree that their finding of worse outcome in those with CCD should be cautiously interpreted and investigated in follow-up studies, but argue that supratentorial stroke volume is an inexact measurement, although stroke location would be helpful to examine. They clarify their finding of impaired supratentorial BOLD-CVR in the group with CCD and opine that hemodynamic changes may cause CCD rather than just functional disruption.

Reduced delivery of glucose and oxygen during brain ischemia can cause energy failure (ATP depletion), which can in turn trigger processes leading to cell death. Glucose can support glycolytic ATP production even in the absence of oxygen, and it would seem to follow that increased glucose in the residual blood flow to ischemic brain should increase cell survival. This was tested experimentally in a rat model of ischemia/reperfusion by Pulsinelli et al1 several decades ago. Glucose had a striking effect, but in the direction opposite to what might be expected: rats in which circulating blood glucose was increased by intravenous infusion had far more extensive brain injury and mortality compared with normoglycemic rats. This experiment has subsequently been revisited dozens of times, using different animal species, stroke models, glucose concentrations, timing of glucose elevations, and permutations of these factors. The net result is one of the most robust in all of stroke research: hyperglycemia almost always exacerbates brain injury.2,3 Clinical experience mirrors the animal literature in these respects, because both retrospective studies and patient registries show a striking correlation between elevated admission glucose concentrations and poor outcomes.4 Hyperglycemia is similarly associated with increased hemorrhage formation and poor outcome in patients treated with tissue plasminogen activator.5–7 Random blood glucose levels are ≈4.4 to 6.1 mmol/L in both humans and rodents, with rodents being the species most commonly used for experimental stroke. The definition of hyperglycemia varies somewhat in stroke studies, ranging from 6.1 to >10 mmol/L glucose. Using these definitions, hyperglycemia is found at presentation in 30% to 60% of all patients with stroke.8,9 Some of these patients are diabetic, but acute, poststroke hyperglycemia is a sympathomimetic stress response in most. Despite the frequency of hyperglycemia in stroke and >30 …

I applaud the Brain Death Working Group for working toward uniform standards for determination of brain death.1

I read with interest the article by Hocker et al.1 I took care of a 45-year-old man several years ago with neurotropic squamous cell carcinoma of the oropharynx (T2N0M0). His brother and paternal uncle had testicular cancer, and his mother had breast cancer. Three months after his initial resection, he developed neuropathic pain of the tongue, and MRI showed tumor recurrence. Two weeks later, he developed classic Miller-Fisher syndrome with mild ophthalmoparesis, ataxia, areflexia, elevated CSF protein, and an elevated anti-Gq1b. He was treated with IV immunoglobulin and did well. Two weeks later, he underwent repeat surgery. In the days following this, he developed neuropathic pain in the right shoulder that persisted for a month and was followed by atrophy and weakness in several right arm muscles. Clinical and electrodiagnostic testing confirmed a diagnosis of brachial neuritis.

Objective:The mechanism of hypoglycorrhachia—low CSF glucose—in meningitis remains unknown. We sought to evaluate the relative contribution of CSF inflammation vs microorganisms (bacteria and fungi) in lowering CSF glucose levels.Methods:We retrospectively categorized CSF profiles into microbial and aseptic meningitis and analyzed CSF leukocyte count, glucose, and protein concentrations. We assessed the relationship between these markers using multivariate and stratified linear regression analysis for initial and repeated CSF sampling. We also calculated the receiver operating characteristics of CSF glucose and CSF-to-serum glucose ratios to presumptively diagnose microbial meningitis.Results:We found that increasing levels of CSF inflammation were associated with decreased CSF glucose levels in the microbial but not aseptic category. Moreover, elevated CSF protein levels correlated more strongly than the leukocyte count with low CSF glucose levels on initial (R2= 36%,p< 0.001) and repeated CSF sampling (R2= 46%,p< 0.001). Hypoglycorrhachia (Conclusions:The main driver of hypoglycorrhachia appears to be a combination of microbial meningitis with moderate to high degrees of CSF inflammation and proteins, suggesting that the presence of microorganisms capable of catabolizing glucose is a determinant of hypoglycorrhachia in meningitis. A major notable exception is neurosarcoidosis. Low CSF glucose and CSF-to-serum glucose ratios are useful markers for the diagnosis of microbial meningitis.