Wilson JR, Tetreault LA, Kim J, et al. State of the Art in Degenerative Cervical Myelopathy: An Update on Current Clinical Evidence. Neurosurgery. 2017;80(3S):S33-S45. doi:10.1093/neuros/nyw083.
Degenerative cervical myelopathy (DCM) is used to describe myelopathy resulting from degenerative pathology in the cervical spine including spondylosis, degenerative disc disease, ossification of the posterior longitudinal ligament (OPLL), and ossification of the ligamentum flavum. The authors provide a wide-ranging overview of the state of the art in degenerative cervical myelopathy, with a focus on updating the spine surgeon on the current evidence surrounding pathophysiology, natural history, imaging, outcome measures, and outcome prediction tools. They also provide an overview of the evidence for surgical vs. non–operative management, and a summary of the literature regarding the most commonly used approaches to the cervical spine.
The pathophysiology of DCM includes both static and dynamic factors. Static factors result from congenital stenosis or acquired stenosis secondary to spondylosis and disc degeneration. Dynamic factors relate to exacerbation of spinal cord compression seen with physiological and, in the setting of degenerative subluxation, pathological motion of the cervical spine. In addition to physical compression, there is a reduction in blood supply leading to ischemia within the cord. Pathological features of DCM include gray and white matter degeneration, anterior horn cell loss, cystic cavitation, and Wallerian degeneration of the posterior columns adjacent to the site of compression.
There is also likely a secondary cascade of neuro–inflammation consisting of microglia activation and macrophage recruitment which occurs at the site of mechanical compression within the spinal cord. In the non–compressed non–myelopathic spinal cord, the blood-spinal cord-barrier is isolated from the peripheral immune system; however, chronic compression renders the cord susceptible to cell infiltration that may be involved in neural degeneration.
Regarding imaging predictors of outcome, there is low-level evidence suggesting that a greater number of high signal intensity (SI) segments on T2-weighted images, low SI change on T1WI, combined T1/T2 SI, are predictors of worse outcomes. In contrast, SI grade on T2WI, compression ratio and canal diameter are not predictive of surgical outcomes. Explanations for these findings include might include: (1) a high SI on T2WI reflects a broad spectrum of histological changes (edema, demyelination or ischemia, or necrosis, myelomalacia, and cavitation) and a wide range of recuperative potentials and (2) multilevel SI, combined T1/T2 SI are all indicative of severe damage that may be irreversible even after surgical decompression.
2 tables, 1 schematic
Much, much more to this review, so highly recommended
Choi D, Bilsky M, Fehlings M, Fisher C, Gokaslan Z. Spine Oncology—Metastatic Spine Tumors. Neurosurgery. 2017;80(3S):S131-S137. doi:10.1093/neuros/nyw084.
There have been several recent advances that contribute to better outcomes for spine metastatic disease. This review covers a wide range of topics related to current and future treatment of metastatic disease. Understanding the factors that influence duration of survival and quality of life can help doctors and patients to make appropriate treatment decisions, and genetic subtyping, novel immunotherapies, and advances in radiation techniques have allowed personalized treatment for patient benefit. Advances in surgical techniques permit minimally invasive augmentation of vertebral body integrity without resorting to larger open surgeries, and thereby decrease pain and allow rapid recovery from surgery. Percutaneous cement augmentation, vertebral body stenting or support, and percutaneous instrumentation have increased the accessibility of surgical treatments to patients with poorer prognosis. New materials and devices for spine reconstruction can make surgery easier, and radiolucent materials permit more effective radiation treatments and radiological surveillance after surgery.
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Levitt MR, Hlubek RJ, Moon K, et al. Incidence and predictors of dural venous sinus pressure gradient in idiopathic intracranial hypertension and non-idiopathic intracranial hypertension headache patients: results from 164 cerebral venograms. J Neurosurg. 2017;126(2):347-353. doi:10.3171/2015.12.JNS152033.
This is an important paper given the recent interest in venous stenosis as a cause of IIH.
The authors reviewed 164 cerebral venograms with manometry in 155 patients performed for headache between January 2008 and May 2015. Patient demographics, headache etiology, intracranial pressure (ICP) measurements, and radiographic and manometric results were recorded. Cerebral venous pressure gradient (CVPG) was defined as a difference ≥ 8 mm Hg by venographic manometry. The overall incidence of CVPG was 25.6% (42 of 164 procedures); 35.4% (34 of 96 procedures) in IIH patients and 11.8% (8 of 68 procedures) in non-IIH patients. CVPG was seen in 8.3% (n = 5) of the procedures in the 60 patients with a preexisting shunt and in 0% (n= 0) of the 11 procedures in the 77 patients with normal ICP. Dural venous sinus abnormalities were demonstrated by MR in 73 (65.2%) of these cases. A diagnosis of IIH was a significant positive predictor of CVPG. Normal ICP and previous CSF shunting were significant negative predictors, and noninvasive imaging results were not helpful for screening. Noninvasive imaging can reveal dural venous sinus abnormalities, although these may represent normal anatomical variants in up to 31% of cases. While there is a good correlation between headache and dural venous sinus abnormalities on noninvasive imaging such as CT venography or MR venography, the results of this paper dispute that such imaging should be used as a screening tool to determine whether patients should undergo invasive cerebral venography. Their results suggest that noninvasive imaging may not accurately predict CVPG: the PPV was < 50%, and multivariate analyses failed to demonstrate noninvasive imaging as a significant predictor of CVPG. 20.5% of 39 patients in this cohort with CVPG had anatomically normal venous sinuses on noninvasive imaging.
The authors propose a treatment algorithm in patients with headache in whom IIH is suspected, which includes lumbar puncture. In those patients with elevated ICP without a preexisting CSF shunt, cerebral venography and manometry should be performed to rule out CVPG. Routine noninvasive cerebrovascular imaging may not be predictive of CVPG (although cranial imaging is still recommended to rule out secondary causes of intracranial hypertension), so they do not routinely perform CTV or MRV prior to venography.
1 figure, 2 tables
Alperin N, Loftus JR, Bagci AM, et al. Magnetic resonance imaging–based measures predictive of short-term surgical outcome in patients with Chiari malformation Type I: a pilot study. J Neurosurg Spine. 2017;26(1):28-38. doi:10.3171/2016.5.SPINE1621.
This study identifies quantitative imaging-based measures in patients with Chiari malformation Type I (CM-I) that are associated with positive outcomes after suboccipital decompression with duraplasty. Fifteen patients in whom CM-I was newly diagnosed underwent MRI preoperatively and 3 months postoperatively. More than 20 previously described morphological and physiological parameters were derived to assess quantitatively the impact of surgery. Postsurgical clinical outcomes were assessed in 2 ways, based on resolution of the patient’s chief complaint and using a modified Chicago Chiari Outcome Scale (CCOS). The strongest physiological parameter predictive of outcome was the preoperative maximal cord displacement in the upper cervical region during the cardiac cycle, which was significantly larger in the favorable-outcome subcohorts for both outcome types. The mean cord displacement of the patients who had a positive outcome in the modified Chicago Chiari Outcome Scale and the chief-complaint approaches were 329 and 278 μm, respectively, significantly above the mean values in the patients whose chief complaint did not improve (199 and 183 μm, respectively) and well above the normative value of 174 μm, previously measured in control subjects. The authors also note that the measurement of cord displacement is derived from the transverse cine phase-contrast scan commonly performed to visualize and/or measure craniospinal CSF flow at the upper-cervical region. Therefore, this important indicator can be readily available as part of a routine clinical MRI scan for the diagnosis of CM-I.
They conclude that physiological measures were stronger predictors of outcome than the morphological measures in patients with CM-I. Maximal cord displacement and intracranial volume change during the cardiac cycle together with a measure that reflects the cerebral venous drainage pathway emerged as likely predictors of decompression outcome in patients with CM-I.
3 figures, 5 tables
van der Kleij LA, De Vis JB, Olivot J, et al. Magnetic Resonance Imaging and Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage. Stroke. 2017;48(1):239-245. doi:10.1161/STROKEAHA.116.011707.
A recent study showed that 90-day case fatality for aneurysmal subarachnoid hemorrhage (aSAH) is 30%. Determinants of functional outcome after aSAH may include the severity of the initial hemorrhage, rebleeding of the aneurysm, and cerebral ischemia. Ischemia can be divided into (1) acute ischemia at the time of bleeding when intracranial pressure rises and cerebral perfusion pressure drops, (2) procedure-related ischemia from endovascular or neurosurgical treatment of the aneurysm, and (3) delayed cerebral ischemia (DCI), which can occur between days 4 and 14 after the hemorrhage. In this systematic review and meta-analysis the authors analyzed (1) the proportion of patients with MRI-DWI lesions within 72 hours after aSAH, both before and after aneurysm treatment; (2) determinants of MRI-DWI lesions within 72 hours after aSAH; (3) analyzed the proportion of patients with MRI DWI lesions between 72 hours and 21 days after aSAH; (4) investigated the predictive value of MRI-DWI lesions within 72 hours for the development of DCI; and 5) investigated whether MRI-DWI can be used for the diagnosis of DCI in patients with clinical deterioration. The search strategy yielded a total of 7299 articles, of which 13 were included with 522 SAH patients. Six studies fulfilled the criteria for high-quality studies.
If you look at DWI lesions between 72 hours and 21 days, these were assessed in 8 studies and reported in 173 out of 346 patients (47%). The 95% prediction interval was 20% to 76%. The study with the lowest proportion of DWI lesions only included patients with a good clinical condition on admission (H&H I–II). In none of the studies was a lesion defined as a hyperintense b1000-signal on DWI with a corresponding low ADC signal. One high-quality study with 61 patients performed MRI within 72 hours and at a median follow-up time of 7 days from ictus. Twelve patients were lost to follow-up. New DWI lesions were observed in 25 of 49 patients (51%).
If you look at the predictive value of MRI-DWI lesions within 72 hours for the development of DCI, there was a single high-quality study with 85 patients, clinical deterioration because of DCI developed in 6 out of 7 patients with DWI lesions within 72 hours and in 8 out of 78 patients without DWI lesions within 72 hours. The positive predictive value of pretreatment DWI lesions within 72 hours for developing clinical deterioration because of DCI was 86% and the negative predictive value was 90%.
The authors found that the proportion of patients with MRI-DWI lesions, both pretreatment within 72 hours and between 72 hours and 21 days after ictus, differed widely between studies. They put forth potential future research questions such as (1) Does imaging performed within hours after DCI onset confirm the ischemic mechanism of clinical deterioration?; (2) What is the additional value of arterial spin labeling and perfusion weighted imaging besides DWI?; (3) Are MRI-DWI lesions on admission risk factors for developing procedure-related ischemia from endovascular or neurosurgical treatment of the aneurysm?; and (4) Are MRI-DWI lesions on admission associated with functional outcome in SAH patients who do not develop complications in the first 3 weeks after the hemorrhage?
Rebello LC, Bouslama M, Haussen DC, et al. Endovascular Treatment for Patients With Acute Stroke Who Have a Large Ischemic Core and Large Mismatch Imaging Profile. JAMA Neurol. 2017;74(1):34. doi:10.1001/jamaneurol.2016.3954.
Definitions: Parenchymal hematoma type 1 is defined as hemorrhage in less than 30% of the infarcted area, with some mild mass effect. In parenchymal hematoma type 2, hemorrhage is seen in more than 30% of the infarcted area, and there is significant mass effect.
The authors analyzed where patients with large baseline ischemic cores on CTP and a mismatch imaging profile benefited from endovascular therapy for acute ischemic stroke. Inclusion criteria were intracranial internal carotid artery and/or proximal middle cerebral artery (M1 and/or M2) occlusion on CTA; time from last known normal to treatment of less than 12 hours; imaging screening using CTP with the automated RAPID software, version 4.5.0 (iSchemaView); baseline ischemic cores on CTP (regional cerebral blood flow [rCBF], <30%) greater than 50mL; and absolute mismatch volume (Tmax, >6 seconds per lesion; rCBF, <30%) greater than 40 mL with involvement of eloquent areas (sensorimotor, language, spatial attention, or visual functions).
In this matched case-control study of 28 pairs of patients, endovascular therapy was significantly associated with a favorable shift in the overall distribution of 90-day modified Rankin Scale scores, higher rates of independent outcomes (90-day modified Rankin Scale scores of 0-2, 25%vs 0%), and smaller final infarct volumes (87 vs 242 mL). Endovascular therapy was also associated with numerically lower rates of parenchymal hematoma type 2, hemicraniectomy, and 90-day mortality. None of the 12 intervention patients and 1 of the 12 control patients (8%) developed a parenchymal hematoma type 2.
They conclude that endovascular therapy appears to benefit patients with large ischemic cores and large mismatch profiles. This benefit likely becomes less pronounced with increasing age. This study has potentially important implications to the current practice standards considering that the recently published pooled analysis of the 5 major thrombectomy trials failed to demonstrate a treatment benefit in patients with ASPECT scores of 5 or less.
Apra C, Kotbi O, Turc G, et al. Presentation and management of lateral sinus thrombosis following posterior fossa surgery. J Neurosurg. 2017;126(1):8-16. doi:10.3171/2015.11.JNS151881.
There are no guidelines for the management of postoperative lateral sinus thrombosis following posterior fossa surgery. This study was a retrospective single center analysis of adult patients who underwent surgical removal of a posterior fossa space-occupying lesion with available postoperative imaging. Postoperative lateral sinus thrombosis was defined as T2* hypointensity within the venous sinus and/or a filling defect on postcontrast MRI or CT scan.
Among 180 patients, 12 (6.7%) were found to have lateral sinus thrombosis on postoperative imaging, none of whom were symptomatic. Unadjusted risk factors for postoperative lateral sinus thrombosis were a history of deep venous thrombosis, oral contraceptive pill use, midline surgical approach, and surgical exposure of the sinus. Postoperative complications occurred in 56.2% of patients (9 of 16) who received treatment-dose curative anticoagulant therapy and in 27% of patients (45 of 164) who did not. None of the 12 cases of postoperative lateral sinus thrombosis identified here were symptomatic. The most common symptom for spontaneous cerebral vein or sinus thrombosis is headaches, reported in 70% of cases, but during the postoperative period this symptom is both common and nonspecific. This good tolerance is quite different when compared to patients with spontaneous lateral sinus thrombosis. They conclude that postoperative lateral sinus thrombosis following posterior fossa surgery for a space-occupying lesion is asymptomatic and well tolerated in adults. The authors propose that well-tolerated postoperative lateral sinus thrombosis following posterior fossa surgery in asymptomatic patients should be followed conservatively, without systematic introduction of anticoagulant therapy, together with close clinical and radiological follow-up to identify early any thrombosis-linked complications.
1 figure, 3 tables
Kim DY, Son JP, Yeon JY, et al. Infarct Pattern and Collateral Status in Adult Moyamoya Disease. Stroke. 2017;48(1):111-116. doi:10.1161/STROKEAHA.116.014529.
The present study aimed to explore the mechanism of ischemic stroke in patients with MMD. They evaluated the infarct pattern and collateral status, using MRI in patients with MMD. They investigated the acute infarct pattern on DWI, microembolic signals on transcranial Doppler monitoring, and collateral status using DSC MR perfusion–based collateral map to estimate the role of embolic and hemodynamic mechanisms.
A total of 67 hemispheres (31 patients with bilateral and 5 patients with unilateral MMD) were analyzed. Most patients (83.7%) showed embolic pattern and rarely a deep (9.3%) or hemodynamic infarct pattern (7.0%) on DWI. Most cases (86%) showed good collateral status, and few patients with acute infarcts of embolic pattern showed poor collateral status (n=7). They conclude that in adult MMD patients, embolic phenomenon played an important role in ischemic stroke. Therapeutic strategies against thromboembolism, as well as collateral enhancing strategies targeting improvement of hemodynamic status or increased washout of emboli, are warranted.
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