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Background Despite a proven superior efficacy of prophylactic low-molecular-weight heparin (LMWH) over unfractionated heparin (UFH) in the majority of surgical specialties, chemoprophylactic techniques after spine surgery have not been established because of the fear of epidural hematomas with LMWH. Objective To determine the efficacy of LMWH vs UFH in the prevention of venous thromboembolism (VTE) events, balanced against the risk of epidural hematoma. Methods This is the first matched cohort design that directly compares prophylactic LMWH to UFH after spine surgery for degenerative/deformity pathologies at a tertiary academic center. Prospectively collected patients receiving prophylactic LMWH and a historical cohort of patients receiving prophylactic UFH (prior to 2017) were matched in 1:1 ratio based on age ±5 yr, American Society of Anesthesiologists classification, location in the spinal column, and type of surgery. Results Of 562 patients, VTE events equaled 1.4% (n = 8): 1.4% (n = 4) with LMWH was exactly equal to 1.4% (n = 4) with UFH. Epidural hematomas reached 0.8% (n = 5): 1.4% (n = 4) with UFH vs 0.3% (n = 1) with the LMWH (P = .178). Utilizing adjusted odds ratio (ORadj), the type of chemoprophylaxis after spine surgery failed to predict VTE events. Similarly, the chemoprophylactic technique failed to predict epidural hematoma in the multivariable regression analysis, although UFH trended toward a higher complication rate (ORadj = 3.15 [0.48-20.35], P = .227). Conclusion Chemoprophylactic patterns failed to predict VTE. Although no differences in epidural hematoma rates were detected, our analysis does highlight a trend toward a safer profile with LMWH vs UFH. LMWH may be a safe alternative to UFH in spine surgery.

Physical exercise is an effective therapy for neurorehabilitation. Exercise has been shown to induce remodeling and proliferation of astrocyte. Astrocytes potentially affect the recruitment and function of neurons; they could intensify responses of neurons and bring more neurons for the process of neuroplasticity. Interactions between astrocytes, microglia and neurons modulate neuroplasticity and, subsequently, neural circuit function. These cellular interactions promote the number and function of synapses, neurogenesis, and cerebrovascular remodeling. However, the roles and crosstalk of astrocytes with neurons and microglia and any subsequent neuroplastic effects have not been studied extensively in exercise-induced settings. This article discusses the impact of physical exercise on astrocyte proliferation and highlights the interplay between astrocytes, microglia and neurons. The crosstalk between these cells may enhance neuroplasticity, leading to the neuroplastic effects of exercise.

The pathophysiology of saccular aneurysm rupture (berry aneurysm) secondary to cocaine and methamphetamine use has been classically attributed to their effects on cerebrovasculature. We conducted a literature review to determine the contribution of cocaine and methamphetamines to aneurysm formation and subarachnoid hemorrhage (SAH). Our literature search revealed the contribution to berry aneurysm by both cocaine and methamphetamines is multifactorial and includes: hemodynamic compromise, hypertensive effects, inflammation, wall stress and hypoperfusion of cerebral vasculature. The pathophysiological mechanisms by which these drugs contribute to saccular aneurysm and SAH is reviewed. We further discuss current grading scales used to measure the severity and extent of SAH in cocaine and methamphetamine users. Additionally, conflicting data regarding the specific role of cocaine and methamphetamines was retrieved. Although questions remain regarding the exact role of cocaine and methamphetamines, the evidence suggests that they do increase the probability of saccular aneurysm formation, rupture and poor patient prognosis.

Objective The onset of cardiogenic cerebral embolism is sudden, dangerous, and often has high morbidity and mortality. Improving understanding of factors contributing to outcomes of cardiogenic cerebral embolism will improve prognostic and therapeutic capabilities. Methods Through PubMed and Google Scholar, this paper examined and analyzed the factors implicated in the outcome of patients with cardiogenic cerebral embolism using the key terms 'cardiogenic cerebral embolism', 'atrial fibrillation', 'stroke related diseases', 'collateral circulation', 'emboli profile', 'epigenetic' up to 28 February 2021. Full texts of the retrieved articles were accessed. In general, in these literatures, National Institute Health of Stroke Scale (NIHSS) score ≥ 17, modified Rankin Scale (mRS) score ≥ 2, stroke recurrence, death caused by stroke are regarded as the criteria of poor prognosis. As long as one of these conditions occurs, it is judged as poor prognosis. Results Factors influencing patient outcomes including patient outcome include severity of neurological impairment, types and severity of combined heart diseases, establishment of cerebral collateral circulation, treatments, components of emboli causing cardiogenic cerebral embolism, existence and control of other system complications, distribution and expression of inflammatory immune cells and molecules in the course of cardiogenic cerebral embolism, and epigenetic changes related to disease prognosis. Conclusion Regarding to prevention and treatment of cardiogenic cerebral embolism, the related factors, such as clinical setting, emboli pathological profile, and epigenetic changes should be emphasized so that outcomes and recurrence of cardiogenic cerebral embolism can be improvised.

Background: Coronavirus 2019 (COVID19) has impacted acute stroke (AS) care with several reports globally showing drops in AS volumes during the pandemic. We studied the impact of COVID19 on AS and transient ischemic attack (TIA) care in a health system serving Southeast Michigan as we rolled out a policy aimed at limiting admissions and transfers. Methods: In this retrospective study conducted at 2 hospitals, we included consecutive patients presenting to the emergency department (ED) for whom a Stroke Alert (SA) was activated during the period 3/20 to 5/20/20 (COVID) and a similar period in 2019 (pre-COVID). We compared demographics, time metrics, and discharge outcomes. Results: 264 patients were seen pre-COVID compared to 121 during COVID (p Conclusion: There was greater than 50% reduction in stroke admissions during the COVID19 pandemic which is consistent with other reports. Although patients were managed more quickly, they tended to have more severe strokes, fewer stroke mimic diagnoses, and worse outcomes compared to patients treated in the pre-COVID period.

This review of the literature will focus on the indications, surgical techniques, and outcomes for expandable transforaminal lumbar interbody fusion (TLIF), anterior lumbar interbody fusion (ALIF), and lateral lumbar interbody fusion (LLIF) operations. The expandable TLIF cage has become a workhorse for common degenerative pathology, whereas expandable ALIF cages carry the promise of greater lordotic correction while evading the diseased posterior elements. Expandable LLIF cages call upon minimally invasive techniques for a retroperitoneal, transpsoas approach to the disc space, obviating the need for an access surgeon and decreasing risk of injury to the critical neurovascular structures. Nuances between expandable and static cages for all 3 TLIF, ALIF, and LLIF operations are discussed in this review.

Although foreign medical graduates (FMGs) have been essential to the US physician workforce, the increasing competitiveness has made it progressively challenging for FMGs to match in US neurosurgery programs. We describe geographic origins and characteristics associated with successful match into US neurosurgery training programs.Retrospective review of AANS membership data (2007-2017). Scopus was used to collect bibliometrics.From 2009 neurosurgical residents, 165 (8.2%) were FMGs. Most were male (n = 148; 89.6%) with a median age of 34.0 years. Top six feeder countries (TFC) included India (13.9%; n = 23), Lebanon and Pakistan (9.1%; n = 15), Caribbean Region (7.2%; n = 12), Mexico (6.67%; n = 11), and Greece (3.6%; n = 6). Compared to FMGs from non-top feeder countries (NTFC), TFC FMGs had higher H-indices (2 vs 4, p = 0.049), greater number of publications (2 vs 5, p = 0.04), were more likely to have an MBBS/MBBCh (n = 38 vs n = 17, p = 0.03), and had twice as many candidates from major feeder medical schools that successfully matched into a US neurosurgery program (n = 43 vs NTFC = 20, p 0.001). NTFC FMGs were almost 3-times more likely to match at an affiliated neurosurgery program (8 vs TFC = 3, p = 0.03), while TFC FMGs were 1.5-times more likely to match at an NIH Top-40 program (33 vs NTFC = 21, p = 0.03).TFC graduates have higher bibliometrics, frequently come from major feeder schools, and have greater match success at a broader selection of programs and NIH top-40 programs. Future studies characterizing FMG country and medical school origins may enable foreign students to geographically target institutions of interest and could allow US programs to better evaluate foreign training environments.

Key points Muscle-derived neurotrophic factors may offer therapeutic promise for treating neuromuscular diseases. We report that a muscle-derived neurotrophic factor, BDNF, rescues synaptic and muscle function in a muscle-type specific manner in mice modelling Kennedy's disease (KD). We also find that BDNF rescues select molecular mechanisms in slow and fast muscle that may underlie the improved cellular function. We also report for the first time that expression of BDNF, but not other members of the neurotrophin family, is perturbed in muscle from patients with KD. Given that muscle BDNF had divergent therapeutic effects that depended on muscle type, a combination of neurotrophic factors may optimally rescue neuromuscular function via effects on both pre- and postsynaptic function, in the face of disease. Abstract Deficits in muscle brain-derived neurotrophic factor (BDNF) correlate with neuromuscular deficits in mouse models of Kennedy's disease (KD), suggesting that restoring muscle BDNF might restore function. To test this possibility, transgenic mice expressing human BDNF in skeletal muscle were crossed with '97Q' KD mice. We found that muscle BDNF slowed disease, doubling the time between symptom onset and endstage. BDNF also improved expression of genes in muscle known to play key roles in neuromuscular function, including counteracting the expression of neonatal isoforms induced by disease. Intriguingly, BDNF's ameliorative effects differed between muscle types: synaptic strength was rescued only in slow-twitch muscle, while contractile strength was improved only in fast-twitch muscle. In sum, muscle BDNF slows disease progression, rescuing select cellular and molecular mechanisms that depend on fibre type. Muscle BDNF expression was also affected in KD patients, reinforcing its translational and therapeutic potential for treating this disorder.