Linzey JR, Wilson TJ, Sullivan SE, Thompson BG, Pandey AS. Frontal Sinus Breach During Routine Frontal Craniotomy Significantly Increases Risk of Surgical Site Infection: 10-Year Retrospective Analysis. Neurosurgery. 2017;0(0):1-8. doi:10.1093/neuros/nyx046.
Frontotemporal craniotomies are at particular risk for breaching the frontal sinus, especially when the patient has a large frontal sinus or the surgeon is attempting to expose anterior communicating (ACOM) artery aneurysms. Frontal sinus breach (FSB) has the potential to cause postoperative complications due to the introduction of microflora from the frontal sinus into the sterile environment of the intracranial compartment.
In this retrospective study, the authors are attempting to determine if FSB is a risk factor for developing cranial surgical site infections in patients undergoing craniotomies for clip ligation of anterior circulation aneurysms. They hypothesized that the surgical site infection (SSI) rate for craniotomies with an FSB would be significantly higher than for craniotomies without an FSB, given the contamination of the intracranial compartment during FSB. This study included 862 patients undergoing 910 craniotomies. Primary outcome of interest was occurrence of a cranial surgical site infection. Of the 910 craniotomies, 141 (15.5%) involved FSB. Of those involving FSB, 22 (15.6%) developed a cranial surgical site infection, compared to only 56 of the 769 without FSB (7.3%). Cranial surgical site infection requiring reoperation was much more likely in patients with FSB compared to those without a breach (7.8% vs 1.6%). Patients with FSBs had 2 times the odds of developing a cranial surgical site infection as those without FSB. The authors overall infection rate of 8.6% for craniotomies is comparable with other published data. In addition, the length of surgical procedure was associated with increased risk of infection, which supports previously published data. As expected, longer procedures were also more common in patients with FSB compared to those without, as those with FSB will require repair of such defects, thus adding procedural time.
Important to look at the bone windows on the postoperative CT to evaluate the integrity of the frontal sinus in patients having undergone frontal craniotomy.
6 Tables
Tung EL, McTaggart RA, Baird GL, et al. Rethinking Thrombolysis in Cerebral Infarction 2b. Stroke. 2017;48(9):2488-2493. doi:10.1161/STROKEAHA.117.017182.
Mechanical thrombectomy (MT) has become the standard of care, along with intravenous tissue-type plasminogen activator, for patients with emergent large vessel occlusion in the anterior circulation. The thrombolysis in cerebral infarction (TICI) scale is a widely used scoring system to evaluate the degree of reperfusion achieved after MT. While it seems intuitive that higher rates of recanalization are associated with improved patient outcomes, there currently exists a lack of consensus regarding the optimal variant of TICI scale. Variations include the original TICI scale (oTICI), the modified TICI (mTICI), and a more recently proposed 6-step grading criteria (mTICI 2c).
Initially, TICI grade 2a or better recanalization was considered successful. More recently, the threshold for successful recanalization has been considered as TICI 2b. However, several recent studies have found that patients who were treated with MT for an anterior circulation emergent large vessel occlusion with oTICI 3, mTICI 2c, or mTICI 3 grades of reperfusion had significantly superior clinical outcomes compared with patients with oTICI 2b and mTICI 2b reperfusion. These findings suggest that there may be value in distinguishing the TICI 2b classification from classifications corresponding to higher reperfusion when evaluating reperfusion after MT.
The purpose of this study was to evaluate differences in early neurological improvement and independence at 90 days using the original TICI, modified TICI, and modified TICI with 2c scales.
This was a retrospective review of 129 consecutive patients with middle cerebral artery, M1 segment or intracranial internal carotid artery occlusions. Patient angiograms were graded by 2 experienced readers by percentage recanalization. This was then categorized into original TICI, modified TICI (mTICI), and mTICI with TICI 2c (mTICI 2c) grading scales.
The mTICI 2c scale is as follows: 0/1 is no or minimal reperfusion; 2a is partial filling <50% territory; 2b is partial filling >50% territory and 2c is near complete perfusion except slow flow or few distal cortical emboli. Grade 3 is complete perfusion.
A significant difference in early neurological improvement was observed between 2b and 3 as well as between 2b and 2c under the mTICI 2c grading scale. Similarly, a significant difference in functional independence was observed between 2b and 3, as well as between 2b and 2c under the mTICI 2c scale. The difference in early neurological improvement or functional independence between 2b and 3 for the original TICI and mTICI scales was not significant. When combining the 2c and 3 groups under the mTICI 2c scale, there were significant differences between 2b and 2c/3 in regard to both early neurological improvement and independence.
The authors conclude that higher levels of recanalization after MT for emergent large vessel occlusion results in greater early neurological improvement and functional independence. They also show that to discern this greater degree of early neurological improvement and functional outcome, a TICI scale which incorporates the TICI 2c grade is needed. They challenge mTICI 2b as the cutoff for successful recanalization, and endorse the adoption of the mTICI scale that includes the TICI 2c grade.
2 Figures, 4 Tables
Villanueva-Meyer JE, Mabray MC, Cha S. Current Clinical Brain Tumor Imaging. Neurosurgery. 2017;81(3):1-19. doi:10.1093/neuros/nyx103.
This very good review provides an overview of current MRI methods routinely employed in the care of the brain tumor patients. The authors focus on advanced techniques including diffusion, perfusion, spectroscopy, tractography, and functional MRI as they pertain to noninvasive characterization of brain tumors and pretreatment evaluation. There are also very informative sections on treatment response, including pseudoprogression and pseudoresponse, and longer-term complications such as stroke-like migraine attacks after radiation therapy (SMART).
12 Figures
Mack MJ, Acker MA, GelijnsAC, et al. Effect of Cerebral Embolic Protection Devices on CNS Infarction in Surgical Aortic Valve Replacement. JAMA. 2017;318(6):536. doi:10.1001/jama.2017.9479.
This was a randomized clinical trial of patients with calcific aortic stenosis undergoing surgical aortic valve replacement (SAVR) at 18 North American centers between March 2015 and July 2016. The interventions evaluated were the use of 1 of 2 cerebral embolic protection devices (n = 118) for suction-based extraction which was the CardioGard (CardioGard) device, extracting both particulate and gaseous emboli and n = 133 for intra-aortic filtration device which was the Embol-X device, (Edwards Lifesciences) vs a standard aortic cannula (control; n = 132) at the time of SAVR. The primary end point was freedom from clinical or radiographic CNS infarction at 7 days after the procedure. Secondary end points included a composite of mortality, clinical ischemic stroke, and acute kidney injury within 30 days after surgery; delirium; mortality; serious adverse events; and neurocognition.
Among 383 randomized patients (mean age, 73.9 years), the rate of freedom from CNS infarction at 7 days was 32.0% with suction-based extraction vs 33.3%with control and 25.6% with intra-aortic filtration vs 32.4% with control. The 30-day composite end point was not significantly different between suction-based extraction and control (21.4% vs 24.2%, respectively) nor between intra-aortic filtration and control (33.3% vs 23.7%). There were no significant differences in mortality (3.4% for suction-based extraction vs 1.7% for control; and 2.3% for intra-aortic filtration vs 1.5% for control) or clinical stroke (5.1% for suction-based extraction vs 5.8% for control; and 8.3% for intra-aortic filtration vs 6.1% for control).
They conclude that among patients undergoing SAVR, cerebral embolic protection devices compared with a standard aortic cannula did not significantly reduce the risk of CNS infarction at 7 days. Nearly 69% of patients who underwent SAVR experienced clinical or radiographic stroke. However, the majority of these events were only detectable by postoperative diffusion-weighted MRI, with just 9% of patients exhibiting clinical findings. Neither the number of MRI lesions nor total lesion volume differed between patients receiving either of the cerebral embolic protection devices and the patients in the control group.
3 Figures (charts and graphs) and 2 Tables
Liu H, MacMillian EL, Jutzeler CR, et al. Assessing structure and function of myelin in cervical spondylotic myelopathy. Neurology. 2017;89(6):602-610. doi:10.1212/WNL.0000000000004197.
In cervical spondylotic myelopathy, routine MRI outcomes, such as maximal spinal cord compression (MSCC) and the presence of signal intensity changes, are not always sensitive to identify clinically relevant pathologies (i.e., those warranting surgical intervention). This is a significant problem because an estimated 20%–25% of otherwise healthy individuals will present with some form of compression, not all of which requires intervention. The authors assessed the extent of demyelination in cervical spondylotic myelopathy (CSM) using myelin water imaging (MWI) and electrophysiologic techniques. Myelin water fraction (MWF), which measures water trapped between myelin bilayers, was defined as the fractional signal with T2 less than 35ms. MWF was calculated for each voxel to produce a MWF map. For each study participant, the average MWF in the whole cord and dorsal column were calculated.
MWF as a surrogate marker of myelin has previously been demonstrated in postmortem combined MRI and histologic studies. Consistent with these ex-vivo observations, MWF is sensitive to changes in patient populations commonly associated with demyelination in the CNS, including multiple sclerosis, phenylketonuria, and schizophrenia. MWI operates on the principle that the MR signal from water trapped between myelin bilayers can be extracted from the total MR signal based on a characteristic short T2 relaxation time. The ratio of myelin water signal relative to the total signal is termed myelin water fraction (MWF).
Somatosensory evoked potentials (SSEPs) and MWI were acquired in 14 patients with CSM and 18 age-matched healthy controls. MWI was performed on a 3.0T whole body scanner. Myelin water fraction was extracted for the dorsal columns and whole cord. SSEPs and MWF were also compared with conventional MRI outcomes, including T2 signal intensity, compression ratio, maximum spinal cord compression (MSCC), and maximum canal compromise (MCC).
Group analysis showed marked differences in T2 signal intensity, compression ratio, maximum spinal cord compression, and maximum canal compromise between healthy controls and patients with CSM. There were no group differences In MWF and SSEP latencies. However, patients with CSM with pathologic SSEPs exhibited reduction in MWF. MWF was also correlated with SSEP latencies.
An important outcome of the study was that conventional CSM diagnosis alone yielded no obvious differences in neurophysiologic or myelin water imaging measures. Consistent with previous literature, approximately 60% of patients with CSM in our study presented with pathologic SSEPs. An equal number and approximately half of healthy controls also demonstrated pathologic SSEPs. Myelin water fraction values in healthy controls were comparable to previous studies and not different from patients with CSM on a group level. In contrast to healthy controls, pathologic SSEP classification in individual patients with CSM was associated with reduced myelin water fraction. In pragmatic terms, this means that microstructural changes in white matter become evident in clinically obvious CSM symptoms (e.g., clumsiness) that are also accompanied by objective measures of spinal cord pathology (e.g., impaired SSEPs).
4 Figures, 1 Table
Lewis A, Greer D. Current controversies in brain death determination. Nat Rev Neurol. 2017;13(8):505-509. doi:10.1038/nrneurol.2017.72.
In this article, the authors examine four prominent controversial brain death cases from 2013–2016. They review current controversies, including protocol variability, recognition of the American Academy of Neurology (AAN) criteria for brain death as an accepted medical standard, and management of objections to discontinuation of organ support after determination of brain death. Brain death remains conceptually and legally valid, and it is vital that these issues are solved.
The American Academy of Neurology (AAN) published criteria for determination of brain death in adults in 1995, and updated them in 2010. These guidelines require identification of the brain injury etiology; confirmation of normal hemodynamics and absence of complicating factors such as pharmaceuticals or laboratory abnormalities that could affect the clinical examination; and demonstration that a patient is comatose, lacks brainstem reflexes, and cannot breathe spontaneously. If a portion of the neurological examination is medically contraindicated, an ancillary test such as an EEG or angiogram can be used to confirm lack of brain activity or blood flow to the brain.
While the AAN guidelines are considered to be the bedrock of brain death determination throughout the USA and in many countries around the world, institutional protocols deviate from the AAN guidelines both nationally and internationally in terms of prerequisites, examiner qualifications, ancillary testing, and apnea testing. In addition, some countries adhere to the UK philosophy that determination of death by neurological criteria requires brainstem death rather than whole-brain death.
Reports of recovery from brain death damage the credibility of brain death determinations. When reporting about brain death, the media often provide misinformation to the general public, suggesting that recovery from brain death is possible. The Quality Standards Subcommittee of the AAN conducted a literature search of MEDLINE and Embase from 1996 to 2009 before publishing the 2010 brain death criteria and they confirmed that no recovery of neurological function had been observed after determination of brain death on the basis of the 1995 AAN criteria. Nonetheless, they noted reports of brain death mimics, including Guillain–Barré syndrome, organosphosphate poisoning, high cervical spine injury, lidocaine toxicity, baclofen overdose, and delayed neuromuscular blockade clearance, from which recovery could inappropriately be deemed ‘recovery from brain death’.
Frisoni GB, Boccardi M, Barkhof F, et al. Strategic roadmap for an early diagnosis of Alzheimer’s disease based on biomarkers. Lancet Neurol. 2017;16(8):661-676. doi:10.1016/S1474-4422(17)30159-X.
Biomarkers of functional impairment, neuronal loss, and protein deposition that can be assessed by neuroimaging (ie, MRI and PET) or CSF analysis are increasingly being used to diagnose Alzheimer’s disease in research studies and specialist clinical settings. However, the validation of the clinical usefulness of these biomarkers is incomplete, and that is hampering reimbursement for these tests by health insurance providers, their widespread clinical implementation, and improvements in quality of health care. The authors have developed a strategic five-phase roadmap to foster the clinical validation of biomarkers in Alzheimer’s disease, adapted from the approach for cancer biomarkers. Sufficient evidence of analytical validity (phase 1 of a structured framework adapted from oncology) is available for all biomarkers, but their clinical validity (phases 2 and 3) and clinical utility (phases 4 and 5) are incomplete. To complete these phases, research priorities include the standardization of the readout of these assays and thresholds for normality, the evaluation of their performance in detecting early disease, the development of diagnostic algorithms comprising combinations of biomarkers, and the development of clinical guidelines for the use of biomarkers in qualified memory clinics.
Efforts to standardize and validate biomarkers have varied. Some biomarkers are the subject of one or more initiatives aimed at standardization or utility analysis, but others are less well investigated. For example, despite ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) PET being widely regarded as a useful biomarker for the early detection of Alzheimer’s disease, there is no structured program aimed at standardizing the readout of cortical hypometabolism measured in this way. The systematic assessment of Alzheimer’s disease biomarkers in representative populations is particularly relevant to their implementation in routine clinical practice. The highly selected patients included in the assessment of biomarkers in the initial phases of their development might not be representative of real-world populations (eg, with regard to comorbidities, socioeconomic status, or education), such that biomarkers might yield notably different results in research settings from those in clinical settings. No data are yet available on changes in health outcomes (disability, mortality, morbidity, or quality of life) attributable to the use of Alzheimer’s disease biomarkers, which is due partly to the lack of treatments able to delay disease progression, access to which is likely to depend on fulfilment of biomarker-supported criteria. Biomarker validation is further hampered by the lack of a consistent methodological framework.
The inconsistent evidence on the usefulness of biomarkers for Alzheimer’s disease has led to their exclusion from most evidence-based guidelines. Importantly, the development of clinical guidelines is a lengthy procedure and does not provide ready means for criteria to be easily updated as evidence accumulates. The practice parameters from the American Academy of Neurology for the diagnosis of dementia, which are now over a decade old, state that there is not enough evidence to support or refute the use of PET, CSF, or other biomarkers for the diagnosis of Alzheimer’s disease. The European guidelines, which were last updated in 2012, state that, in clinical practice, CT and MRI should be used to exclude (usually non-degenerative) causes of dementia (class I evidence) and that biomarkers should be used to confirm diagnosis only in selected cases. The evidence for ¹⁸F-FDG PET and CSF biomarkers is rated as class II and class III, respectively, for discriminating between Alzheimer’s disease, frontotemporal lobar degeneration, and dementia with Lewy bodies. The only biomarker recommended by the Alzheimer’s Association and the Amyloid Imaging Task Force to aid a specific diagnosis of Alzheimer’s disease is amyloid PET, which is very expensive. In the face of inconsistent or lacking guidelines, clinicians might base the use of biomarkers on practical considerations that reflect resources and experience, rather than on clinical and evidence-based considerations. In one study, the choice of neuroimaging technique (CT, MRI, or ¹⁸F-FDG PET) in the workup of dementia was driven as much by test availability, physicians’ familiarity with the technology, and waiting time for patients as by the clinically relevant parameters, such as the patient’s age, severity of cognitive impairment, or the diagnostic question (eg, clinical suspicion of cerebrovascular disease). If multiple means of determining the same pathology are available, financial considerations can take precedence over other factors.
5 tables including one panel on take home messages
Bear JJ, Gelfand AA, Goadsby PJ, Bass N. Occipital headaches and neuroimaging in children. Neurology. 2017;89(5):469-474. doi:10.1212/WNL.0000000000004186.
The authors investigated the common thinking, as reinforced by the International Classification of Headache Disorders, 3rd edition, that occipital headaches in children are rare and suggestive of serious intracranial pathology.
They performed a retrospective chart review cohort study of all patients <18 years of age referred to a university child neurology clinic for headache in 2009. Patients were stratified by headache location: solely occipital, occipital plus other area(s) of head pain, or no occipital involvement. Children with abnormal neurologic examinations were excluded. They assessed location as a predictor of whether neuroimaging was ordered and whether intracranial pathology was found. 308 patients were included with a median age was 12 years and 57% were female. Headaches were solely occipital in7% and occipital-plus in 14%. Patients with occipital head pain were more likely to undergo neuroimaging than those without occipital involvement. Occipital pain alone or with other locations was not significantly associated with radiographic evidence of clinically significant intracranial pathology. This lack of association was true whether the reported headaches were solely occipital or involved the occipital location along with other pain locations. In fact, among the 4 patients in the cohort with serious intracranial pathology, none reported occipital pain.
1 Figure, 4 Tables
