Subthalamic nucleus (STN) deep brain stimulation (DBS) is currently the main surgical procedure for medically refractory Parkinson's disease. The benefit of intra-operative microelectrode recording (MER) for the purpose of neurophysiological localization and mapping of the STN continues to be debated.A retrospective review of the charts and operative reports of all patients receiving STN DBS implantation for Parkinson's disease at our institution from January 2004 to March 2011 was done.Data from 43 of 44 patients with Parkinson's disease treated with STN DBS were reviewed. The average number of tracts on the left was 2.4, versus 2.3 on the right. The average dorsal and ventral anatomical boundaries of the STN based on Schaltenbrand's Stereotactic Atlas were estimated to be at -5.0 mm above and +1.4 mm below target respectively. The average dorsal and ventral boundaries of the STN using MER were -2.6 mm above and +2.0 mm below target respectively. The average dorsal-ventral distance of the STN as predicted by Stereotactic Atlas was 6.4 mm, compared to 4.6 mm as determined by MER. MER demonstrated the average dorsal and ventral boundaries on the left side were -2.6 mm and +2.2 mm from target respectively, while the average dorsal and ventral boundaries on the right side were -2.5 mm and +1.8 mm from target respectively with MER.MER in STN DBS surgery demonstrated measurable difference between stereotactic atlas/MRI STN target and neurophysiologic STN localization.
Abstract Background Trauma-induced coagulopathy in traumatic brain injury (TBI) remains associated with high rates of complications, unfavorable outcomes, and mortality. The underlying mechanisms are largely unknown. Embedded in the prospective multinational Collaborative European Neurotrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) study, coagulation profiles beyond standard conventional coagulation assays were assessed in patients with isolated TBI within the very early hours of injury. Methods Results from blood samples (citrate/EDTA) obtained on hospital admission were matched with clinical and routine laboratory data of patients with TBI captured in the CENTER-TBI central database. To minimize confounding factors, patients with strictly isolated TBI (iTBI) ( n = 88) were selected and stratified for coagulopathy by routine international normalized ratio (INR): (1) INR < 1.2 and (2) INR ≥ 1.2. An INR > 1.2 has been well adopted over time as a threshold to define trauma-related coagulopathy in general trauma populations. The following parameters were evaluated: quick’s value, activated partial thromboplastin time, fibrinogen, thrombin time, antithrombin, coagulation factor activity of factors V, VIII, IX, and XIII, protein C and S, plasminogen, D-dimer, fibrinolysis-regulating parameters (thrombin activatable fibrinolysis inhibitor, plasminogen activator inhibitor 1, antiplasmin), thrombin generation, and fibrin monomers. Results Patients with iTBI with INR ≥ 1.2 ( n = 16) had a high incidence of progressive intracranial hemorrhage associated with increased mortality and unfavorable outcome compared with patients with INR < 1.2 ( n = 72). Activity of coagulation factors V, VIII, IX, and XIII dropped on average by 15–20% between the groups whereas protein C and S levels dropped by 20%. With an elevated INR, thrombin generation decreased, as reflected by lower peak height and endogenous thrombin potential (ETP), whereas the amount of fibrin monomers increased. Plasminogen activity significantly decreased from 89% in patients with INR < 1.2 to 76% in patients with INR ≥ 1.2. Moreover, D-dimer levels significantly increased from a mean of 943 mg/L in patients with INR < 1.2 to 1,301 mg/L in patients with INR ≥ 1.2. Conclusions This more in-depth analysis beyond routine conventional coagulation assays suggests a counterbalanced regulation of coagulation and fibrinolysis in patients with iTBI with hemostatic abnormalities. We observed distinct patterns involving key pathways of the highly complex and dynamic coagulation system that offer windows of opportunity for further research. Whether the changes observed on factor levels may be relevant and explain the worse outcome or the more severe brain injuries by themselves remains speculative.
Neurocognitive problems associated with posttraumatic stress disorder (PTSD) can interact with impairment resulting from traumatic brain injury (TBI).We aimed to identify neurocognitive problems associated with probable PTSD following TBI in a civilian sample.The study is part of the CENTER-TBI project (Collaborative European Neurotrauma Effectiveness Research) that aims to better characterize TBI. For this cross-sectional study, we included patients of all severities aged over 15, and a Glasgow Outcome Score Extended (GOSE) above 3. Participants were assessed at six months post-injury on the PTSD Checklist-5 (PCL-5), the Trail Making Test (TMT), the Rey Auditory Verbal Learning Test (RAVLT) and the Cambridge Neuropsychological Test Automated Battery (CANTAB). Primary analysis was a complete case analysis. Regression analyses were performed to investigate the association between the PCL-5 and cognition.Of the 1134 participants included in the complete case analysis, 13.5% screened positive for PTSD. Probable PTSD was significantly associated with higher TMT-(B-A) (OR = 1.35, 95% CI: 1.14-1.60, p < .001) and lower RAVLT-delayed recall scores (OR = 0.74, 95% CI: 0.61-0.91, p = .004) after controlling for age, sex, psychiatric history, baseline Glasgow Coma Scale and education.Poorer performance on cognitive tests assessing task switching and, to a lesser extent, delayed verbal recall is associated with probable PTSD in civilians who have suffered TBI.
The aim of this work was to perform a scoping systematic review on the animal literature surrounding mean arterial blood pressure (MAP) and functional outcomes post-acute spinal cord injury (ASCI). We performed a systematic review of the literature by searching: MEDLINE, BIOSIS, EMBASE, Global Health, SCOPUS, and Cochrane Library from inception to January 2015. We also performed a hand search of various published meeting proceedings. Through a two-step review process, using two independent reviewers, we selected articles for the final review based on pre-defined inclusion/exclusion criteria. Ten studies were included within the final systematic review. A variety of animal models were used within these studies. All included studies had some objective means of documenting functional outcome post-manipulation of the MAP. Four studies could be considered to be "positive studies," showing some neurological improvement or beneficial effect to having the blood pressure manipulated. Two studies displayed worse functional outcomes secondary to episodes of hypotension. Four studies failed to demonstrate a relationship between MAP and functional outcome within the animal models. This review concludes that, within the animal literature, there is insufficient evidence to draw a conclusion about the effect of MAP on neurological outcome in animal models of ASCI.
In patients with severe brain injury, withdrawal of life-sustaining measures (WLSM) is common in intensive care units (ICU). WLSM constitutes a dilemma: instituting WLSM too early could result in death despite the possibility of an acceptable functional outcome, whereas delaying WLSM could unnecessarily burden patients, families, clinicians, and hospital resources. We aimed to describe the occurrence and timing of WLSM, and factors associated with timing of WLSM in European ICUs in patients with traumatic brain injury (TBI). The CENTER-TBI Study is a prospective multi-center cohort study. For the current study, patients with traumatic brain injury (TBI) admitted to the ICU and aged 16 or older were included. Occurrence and timing of WLSM were documented. For the analyses, we dichotomized timing of WLSM in early (< 72 h after injury) versus later (≥ 72 h after injury) based on recent guideline recommendations. We assessed factors associated with initiating WLSM early versus later, including geographic region, center, patient, injury, and treatment characteristics with univariable and multivariable (mixed effects) logistic regression. A total of 2022 patients aged 16 or older were admitted to the ICU. ICU mortality was 13% (n = 267). Of these, 229 (86%) patients died after WLSM, and were included in the analyses. The occurrence of WLSM varied between regions ranging from 0% in Eastern Europe to 96% in Northern Europe. In 51% of the patients, WLSM was early. Patients in the early WLSM group had a lower maximum therapy intensity level (TIL) score than patients in the later WLSM group (median of 5 versus 10) The strongest independent variables associated with early WLSM were one unreactive pupil (odds ratio (OR) 4.0, 95% confidence interval (CI) 1.3–12.4) or two unreactive pupils (OR 5.8, CI 2.6–13.1) compared to two reactive pupils, and an Injury Severity Score (ISS) if over 41 (OR per point above 41 = 1.1, CI 1.0–1.1). Timing of WLSM was not significantly associated with region or center. WLSM occurs early in half of the patients, mostly in patients with severe TBI affecting brainstem reflexes who were severely injured. We found no regional or center influences in timing of WLSM. Whether WLSM is always appropriate or may contribute to a self-fulfilling prophecy requires further research and argues for reluctance to institute WLSM early in case of any doubt on prognosis.
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Introduction: Ketamine, an N-methyl D-aspartate (NMDA) receptor antagonist, carries potential benefit in patients with neurological illness. The cerebrovascular/cerebral blood flow (CBF) response to ketamine has been poorly outlined in the literature. Methods: We performed a systematic review of the literature on the cerebrovascular/CBF effects of ketamine in both animal and human subjects. Results: We identified 38 animal studies, and 20 human studies. Within the animal studies, a variety of different models were utilized with the majority focusing changes in global CBF or regional cerebral blood flow (rCBF). Overall, ketamine led to an increase in either global CBF or rCBF, with a vasodilatory effect in medium cerebral vessels. With the human studies a total of 379 patients, 107 of which were control subjects, were studied. Most studies focused on either 131Xe CT or PET imaging with ketamine administration. There was a trend to an increase in global CBF and rCBF with ketamine administration. Conclusions: Animal models indicate an increase in global CBF and rCBF with ketamine administration. Human studies display an Oxford 2b, GRADE C, level of evidence to support an increase in global CBF and rCBF with ketamine administration in both healthy volunteers and elective surgical patients without neurological illness.
The quantification and objective documentation of autonomic dysfunction in traumatic brain injury (TBI) is neither well studied nor extensively validated. Most of the descriptions of autonomic dysfunction in the literature are in the form of vague non-specific clinical manifestations. Few studies propose the use of objective measures of assessing the extent of autonomic dysfunction to link them to the outcome of TBI. Our goal was to perform a scoping systematic review of the literature on the objective documentation of autonomic dysfunction in terms of functional and physiological variables to be linked to outcome of TBI. PubMed/MEDLINE®, BIOSIS, Scopus, Embase, Cochrane Libraries, and Global Health databases were searched. Two reviewers independently screened the results. Full texts for citations passing this initial screen were obtained. Inclusion and exclusion criteria were applied to each article to obtain final articles for review. The initial search yielded 2619 citations. Of 69 articles selected for final review, 14 were chosen based on the inclusion and exclusion criteria and are included in the results of this article. 9 of these articles assessed autonomic dysfunction using functional variables and 7 assessed autonomic dysfunction using physiological variables. Some studies included both functional and physiological variables. Of the nine studies linking autonomic dysfunction to functional variables, nine included heart rate variability (HRV), three included baroreflex sensitivity (BRS), and two included blood pressure variability (BPV). A total of 2714 adult patients were studied. Although the nature of association between autonomic dysfunction and outcome is unclear, the objective quantification of autonomic dysfunction seems to be associated with global patient outcome and other neurophysiological measures. Further studies are needed to validate its use and explore the underlying molecular mechanisms of the described associations.
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