Daou B, Chalouhi N, Starke RM, et al. Clipping of previously coiled cerebral aneurysms: efficacy, safety, and predictors in a cohort of 111 patients. J Neurosurg. 2016;125(December):1-7. doi:10.3171/2015.10.JNS151544.
This retrospective cohort study evaluated the efficacy and safety of microsurgical clipping in the treatment of recurrent, previously coiled cerebral aneurysms and to identify risk factors that can affect the outcomes of this procedure. The mean patient age was 50.5 years, the mean aneurysm size was 7 mm, and 97.3% of aneurysms were in the anterior circulation. Complete aneurysm occlusion, as assessed by intraoperative angiography, was achieved in 97.3% of aneurysms (108 of 111 patients). Among patients, 1.8% had a recurrence after clipping. Retreatment was required in 4.5% of patients after clipping. Major complications were observed in 8% of patients and mortality in 2.7%. Ninety percent of patients had a good clinical outcome. Aneurysm size and location in the posterior circulation were significantly associated with higher complications. All 3 patients who had coil extraction experienced a postoperative stroke.
They conclude that surgical clipping is an appropriate treatment strategy for the management of recurrent cerebral aneurysms after endovascular coiling. Direct clipping of the aneurysm neck is feasible in most cases of recurrent, previously coiled cerebral aneurysms. Coil extraction should not regularly be attempted because it is associated with high morbidity. In other words, when direct clipping is not possible because of coil loops extending into the aneurysm neck, or with transmural calcification and scarring, other techniques such as wrapping should be considered.
Serrone JC, Tackla RD, Gozal YM, et al. Aneurysm growth and de novo aneurysms during aneurysm surveillance. J Neurosurg. 2016;125(6):1374-1382. doi:10.3171/2015.12.JNS151552.
Over an 11.5-year period, the authors recommended surveillance imaging to 192 patients with 234 unruptured intracranial aneurysms. The incidence of unruptured intracranial aneurysm growth and de novo aneurysm …
Domino JS, Baek J, Meurer WJ, et al. Emerging temporal trends in tissue plasminogen activator use. Neurology. 2016;87(21):2184-2191. doi:10.1212/WNL.0000000000003349.
Mexican Americans (MA) have an increased stroke burden when compared to their non-Hispanic white (NHW) counterparts, including increased stroke incidence and poorer neurologic, functional, and cognitive outcomes.
The authors explored the temporal trends in tissue plasminogen activator (tPA) administration for acute ischemic stroke (AIS) in a biethnic community without an academic medical center. Cases of AIS were identified from 7 hospitals in the Brain Attack Surveillance in Corpus Christi (BASIC) project, a population-based surveillance study from 2000-2012. There were 5,277 AIS cases identified from 4,589 individuals. tPA use was steady at 2% and began increasing in 2006, reaching 11% in subsequent years. Although ethnicity did not modify the temporal trend, Mexican Americans were less likely to receive tPA than non- Hispanic whites due to emerging ethnic differences in later years. The results suggest that increases in tPA use were greater in higher severity patients compared to lower severity patients, and a gap between MAs and NHWs in tPA administration may be emerging. The authors conclude that as physician experience with tPA and its use in community settings increases, follow-up studies should continue to explore temporal trends in tPA as well as identify possible strategies to improve tPA use in MAs.
2 Figures (graphs), 2 Tables
Goldstein LB. IV tPA for acute ischemic stroke. Neurology. 2016;87(21):2178-2179. doi:10.1212/WNL.0000000000003366.
In this editorial on the Domino et al. paper, Dr. Goldstein notes that there were considerable barriers that slowed IV tPA adoption after it was approved by the FDA in 1996. Eight years after FDA approval, IV tPA was being given to only 1%–2% of stroke patients. Transformation of the structure and organization of stroke care delivery were needed, and in part led to …
Akoudad S, Wolters FJ, Viswanathan A, et al. Association of Cerebral Microbleeds With Cognitive Decline and Dementia. JAMA Neurol. 2016;73(8):934. doi:10.1001/jamaneurol.2016.1017.
The authors wanted to determine whether microbleed count and location were associated with an increased risk for cognitive impairment and dementia. They evaluated a prospective population-based study set in the general community, and assessed the presence, number, and location of microbleeds at baseline (August 2005 to December 2011) on brain MRI in 4841 participants 45 years or older. Trained research physicians, blinded to clinical data, reviewed the MRs. Cerebral microbleeds were defined as small, round to ovoid areas of focal signal loss on T2- weighted images. Participants underwent neuropsychological testing at 2 time points approximately 6 years apart, and were also followed up for incident dementia. 3257 participants underwent baseline and follow-up cognitive testing. Microbleed prevalence was 15.3%. The presence of more than 4 microbleeds was associated with cognitive decline. The presence of microbleeds was associated with an increased risk for dementia after adjustment for age, sex, and educational level, including Alzheimer dementia.
The strengths of this study, according to the authors, is the longitudinal population based design with a large sample size, the use of an extensive neuropsychological test battery, and the virtually complete screening for incident dementia. Limitations include multiple statistical tests, increasing the chance of type I errors. Second, selection bias may have influenced the results, because healthier people without subjective memory complaints were more likely to receive follow-up cognitive testing. Most importantly perhaps, the microbleed number may not reflect the true biological number because microbleed detection strongly depends on technical imaging methods used. T2W images were used, and as we know, SWI is far superior for the detection of these lesions.
Manoso MW, Moore TA, Agel J, Bellabarba C, Bransford RJ. Floating
Austein F, Riedel C, Kerby T, et al. Comparison of Perfusion CT Software to Predict the Final Infarct Volume After Thrombectomy. Stroke. 2016 doi:10.1161/STROKEAHA.116.013147.
The purpose of the study was to determine the accuracy of different commercial perfusion CT software packages to predict the final infarct volume (FIV) after mechanical thrombectomy. Packages evaluated included 1) Philips Brain CT Perfusion Package, Philips Healthcare, The Netherlands, 2) Siemens (Syngo Volume Perfusion CT Neuro, Siemens Healthcare, Erlangen, Germany, and 3) RAPID (iSchemaView Inc, Menlo Park, CA). CTP data from 147 mechanically recanalized acute ischemic stroke patients were postprocessed. Ischemic core and final infarct volume were compared about thrombolysis in cerebral infarction (TICI) score and time interval to reperfusion. Final infarct volume was measured at follow-up imaging between days 1 and 8 after stroke. Significant differences were found between the packages about over- and underestimation of the ischemic core, with RAPID best-predicting hypoperfusion volume in nonsuccessfully recanalized patients. They conclude that this software package overestimated the final infarct volume to a significantly lower degree and estimated a malignant mismatch profile less often than other software.
Tan BYQ, Wan-Yee K, Paliwal P, et al. Good Intracranial Collaterals Trump Poor Alberta Stroke Program Early CT Score for Intravenous Thrombolysis in Anterior Circulation Acute Ischemic Stroke. Stroke. 2016 doi:10.1161/STROKEAHA.116.013879.
As a nice background and reference to describe the various collateral scoring systems, see: Yeo et al, Assessment of Intracranial Collaterals on CT Angiography in Anterior Circulation Acute Ischemic Stroke, AJNR 2015.
The authors evaluated the prognostic effect of the collateral circulation in patients with thrombolysed acute ischemic stroke who have large early infarct sizes as indicated by low ASPECTS score. They stratified patients using ASPECTS into 2 groups: large volume infarcts (ASPECTS≤ 7 points) and small volume infarcts (ASPECTS 8–10). They also evaluated a third group …
Saber H, Silver B, Santillan A, Azarpazhooh MR, Misra V, Behrouz R. Role of emergent chest radiography in evaluation of hyperacute stroke. Neurology. 2016;87(8):782–785. doi:10.1212/WNL.0000000000002964.
Despite evidence supporting the prompt administration of IV rtPA, fewer than one-third of acute ischemic stroke patients receive this medication within the target window of 60 minutes or less. Patient and technical factors often contribute to delays in the so-called door-to-needle time or the period from hospital presentation to initiation of treatment. Given this background, the authors compared features of patients who had a CXR done before IV thrombolytics with those who did not. Rates of cardiopulmonary adverse events, intubation, and in-hospital mortality were also compared. Logistic regression analysis was performed to evaluate the association of CXR performance with door-to-needle time greater than or equal to 60 minutes. In the cohort of 615 patients, 243 had CXR done before IV thrombolytics. Patients with CXR before treatment had significantly higher admission neurologic deficit and initial respiratory rates. Patients with CXR done before treatment had longer mean door-to-needle times than those without pretreatment radiography (75.8 vs 58.3 minutes). The performance of CXR before IV thrombolytics prolongs door-to-needle time in acute ischemic stroke patients. CXR before treatment should be reserved for situations wherein acute cardiopulmonary conditions would otherwise preclude the administration of IV thrombolytics.
Banwell B. Pediatric multiple sclerosis. Neurology. 2016;87(8):822–826. doi:10.1212/WNL.0000000000003014.
This is the 2015 Sydney Carter Award Lecture in which Dr. Banwell summarizes the learning curve and milestones achieved in pediatric multiple sclerosis care and research to date.
Dr. Banwell notes that the available MS diagnostic criteria proposed by Poser in 1983 specifically excluded the diagnosis of MS in persons younger than ten years, and did not formally comment on MS in youth. Further complicating the diagnosis and care of pediatric patients with MS is …
Mossa-Basha M, de Havenon A, Becker KJ, et al. Added Value of Vessel Wall Magnetic Resonance Imaging in the Differentiation of Moyamoya Vasculopathies in a Non-Asian Cohort. Stroke. 2016;47(7):1782–1788. doi:10.1161/STROKEAHA.116.013320.
Moyamoya vasculopathy is divided into moyamoya disease (MMD) and moyamoya syndrome (MMS). This is a steno-occlusive process of the carotid termini, proximal middle cerebral artery, and anterior cerebral artery with development of compensatory collaterals. If patients have a well-recognized associated condition, then it is called moyamoya syndrome, whereas those patients with no known associated risk factors are said to have moyamoya disease. By definition, the pathognomic arteriographic findings are bilateral in moyamoya disease (although severity can vary between sides). Patients with unilateral findings have moyamoya syndrome, even if they have no other associated risk factors. MMS may arise secondary to many underlying disease processes, including sickle cell anemia, NF1, radiation therapy, congenital syndromes, intracranial atherosclerotic disease (A-MMS), and vasculitis (V-MMS). Making a correct and specific diagnosis will alter management, since MMD is treated by surgical revascularization, whereas the SAMMPRIS trial showed that aggressive medical management is the first-line therapy for a patient with high-grade (70%–99%) atherosclerotic stenosis. In this study, 10 atherosclerotic disease related MMS patients, 3 vasculitis disease related MMS patients, and 8 moyamoya disease patients with 38 affected carotid segments were evaluated with vessel wall MR. The most common vessel wall MRI findings for moyamoya disease were nonenhancing, nonremodeling lesions without T2 heterogeneity; for A-MMS eccentric, remodeling, and T2 heterogeneous lesions with mild/moderate and homogeneous / heterogeneous enhancement; and for V-MMS concentric lesions with homogeneous, moderate enhancement. There was an 11% inter-reader agreement for diagnosis on luminal imaging when compared with 82% for luminal imaging + vessel wall MRI. They conclude that vessel wall MRI improves diagnostic accuracy and diagnostic confidence in the differentiation of MMD from …
Gondi V, Yock TI, Mehta MP. Proton therapy for paediatric CNS tumours — improving treatment-related outcomes. Nat Rev Neurol. 2016;12(6):334–345. doi:10.1038/nrneurol.2016.70.
In this review, the authors provide an introduction to the types of pediatric CNS tumors for which proton therapy can be considered, and discuss the evidence that proton therapy limits toxicities and improves quality of life for patients. As you no doubt remember from your residency, a proton has a defined maximum penetration depth, called the Bragg peak, at which the majority of its energy is released over a few millimeters. The Bragg peak is determined by the energy of a proton, and can be shortened to match the distal edge of the target by placement of customized tissue-equivalent material in the beam path. Before reaching the Bragg peak, a proton loses only a small amount of its energy, so delivers a lower ‘entrance’ dose than does conventional X‑ray therapy. Beyond the Bragg peak, a proton has no energy, so delivers no ‘exit’ dose. The improvement in dose distribution achieved with proton therapy can meaningfully affect the risk of long-term radiotherapy effects, such as secondary malignancy, cognitive toxicity, endocrinopathy, hearing loss and vasculopathic effects. Despite its higher up front costs, proton therapy has been shown to be more cost effective than X ray therapy owing to the dramatic reduction in the excess costs of managing long-term toxicities. Keep in mind that randomized trials of proton ther¬apy versus X ray therapy are unlikely due to the rarity of the diseases involved and the ethical issues surrounding the enrollment of children into trials in which one arm is asso¬ciated with a greater likelihood of toxicity. Uncertainty about the biological effects of proton therapy on certain healthy tissue and the relative inaccessibility of proton therapy, especially in developing nations, pose important …
Cavalcanti DD, Preul MC, Kalani MYS, Spetzler RF. Microsurgical anatomy of safe entry zones to the brainstem. J Neurosurg. 2016;124(5):1359–1376. doi:10.3171/2015.4.JNS141945.
In this image rich paper, the authors examined 13 safe entry zones on the brainstem (previously described in the literature) and used cadaveric dissections to evaluate the main surgical approaches currently employed to manage intrinsic brainstem lesions. Through dissection images of these approaches, they demonstrate what can be seen on the brainstem through each of these surgical corridors and delineate the safe entry zones provided by each approach. The approaches described include three midbrain regions (anterior mesencephalic zone, lateral mesencephalic sulcus, intercollicular region), 6 pontine zones (peritrigeminal zone, supratrigeminal zone, lateral pontine zone, supracollicular zone, infracollicular zone, median sulcus of the fourth ventricle), and 4 medullary zones (anterolateral and posterior median sulci of the medulla, olivary zone, and lateral medullary zone). In addition to the surface anatomy, the paper describes the general surgical approaches to the regions, including Orbitozygomatic, Subtemporal, Subtemporal Transtentorial, Anterior Petrosectomy, Suboccipital Telovelar, Median Supracerebellar Infratentorial, Extreme Lateral Supracerebellar Infratentorial, Retrosigmoid, Far Lateral, and Retrolabyrinthine.
13 illustrations and 2 tables.
Close to all a Neuroradiologist needs to know about surgical approaches to the brainstem, and then some.
Drazin D, Nuño M, Patil CG, Yan K, Liu JC, Acosta FL. Emergency room resource utilization by patients with low-back pain. J Neurosurg Spine. 2016;24(5):686–693. doi:10.3171/2015.7.SPINE14133.
The authors conducted a retrospective analysis of patients with LBP discharged from hospitals according to the Nationwide Inpatient Sample (NIS) between 1998 and 2007. A majority (65%) of patients discharged from hospitals in the US from 1998 to 2007 with a primary diagnosis of LBP were admitted through the ER, with more patients being admitted via this route each year (183,151 patients). These patients were less likely to be discharged directly home …
- Anderson MA, Burda JE, Ren Y, et al. Astrocyte scar formation aids central nervous system axon regeneration. Nature. 2016;532(7598):195–200. doi:10.1038/nature17623.
This is an important paper to be aware of: Astrocytic scars have been regarded as barriers to central nervous system axon regrowth since around 1952. Through an impressive set of experiments, the authors show that using three genetically targeted loss-of-function manipulations in adult mice that prevent scar formation or stop scar forming astrocytes all failed to result in spontaneous regrowth of transected corticospinal, sensory or serotonergic axons through severe spinal cord injury (SCI) lesions. Specifically, they 1) prevented astrocyte scar formation, 2) attenuating scar-forming astrocytes, and 3) ablated chronic astrocytic scars (using genetically targeted diphtheria toxin receptor and ultra-low doses of diphtheria toxin). They conclude that these experiments show that contrary to the prevailing dogma, astrocytic scar formation is not a principal cause for the failure of injured mature CNS axons to regrow across severe CNS lesions. In fact, scar-forming astrocytes permit and support robust amounts of appropriately stimulated CNS axon regeneration. These findings have obvious important implications for CNS repair strategies.
- Liddelow SA, Barres BA. Regeneration: Not everything is scary about a glial scar. Nature. 2016;532(14 April):182–183. doi:10.1038/nature17318.
This is an Editorial that goes along with the previous paper by Anderson et al. How do we reconcile previous experiments showing scar is bad with this current information? One potential answer is that other inhibitory cell types such as fibroblasts and pericytes, also contribute to the glial scar. Other studies have identified different types of reactive astrocyte. Perhaps in the previous studies different types of injury produced different types of reactive astrocyte, some being inhibitory and others not so much. They conclude that “ in spite of long-held beliefs to the contrary, reactive astrocytes may not …
- Chen Z, Zheng Y, Yuan Y, et al. Modic Changes and Disc Degeneration Caused by Inoculation of Propionibacterium acnes inside Intervertebral Discs of Rabbits: A Pilot Study. Biomed Res Int. 2016;2016:9612437. doi:10.1155/2016/9612437.
Wild-type strain of P. acnes isolated from a patient associated with Modic change and disc degeneration was inoculated into the intervertebral discs of rabbits (n=8). S. aureus was injected into the discs to establish a model of discitis as a comparison. A standard strain of P. acnes was inoculated as the control. MRI and histological change were evaluated. MRI was performed before and every two weeks after the inoculation until the end of follow-up at the eighth week. Both the P. acnes-inoculated and S. aureus-inoculated rabbits showed hyperintense signals at endplates and hypointense signals at nucleus pulposus on T2WI. However, P. acnes only resulted in moderate disc degeneration and endplates rupture in histological examination. They conclude that compared to S. aureus, the pathological change caused by P. acnes would be considered as Modic-I change and disc degeneration rather than a discitis.
They are of the opinion that the presented data satisfied the first, second, and third criteria of Koch’s Postulates and they extrapolate that P. acnes has a strong connection with Modic change and disc degeneration. 3 figures with histopathology.
In case you had forgotten Koch’s postulates:
- The pathogen must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms.
- The pathogen must be isolated from a diseased host and grown in pure culture.
- The cultured microorganism should cause the disease when introduced into a healthy organism.
- The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent.
- Hall SS, Dougherty RF, Reiss AL. Profiles