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OBJECTIVESevere traumatic brain injury (sTBI) carries significant morbidity and mortality. It remains difficult to counsel families on functional prognosis and plan research initiatives aimed at treating traumatic coma. In order to better address these problems, the authors set out to develop statistical models using retrospective data to identify admission characteristics that correlate with time until the return of consciousness, defined as the time to follow commands (TFC). These results were then used to create a TFC score, allowing for rapid identification of patients with predicted prolonged TFC.METHODSData were reviewed and collected from medical records of sTBI patients with Glasgow Coma Scale (GCS) motor subscores ≤ 5 who were admitted to Stony Brook University Hospital from January 2011 to July 2018. Data were used to calculate descriptive statistics and build binary logistic regression models to identify admission characteristics that correlated with in-hospital mortality and in-hospital command-following. A Cox proportional hazards model was used to identify admission characteristics that correlated with the length of TFC. A TFC score was developed using the significant variables identified in the Cox regression model.RESULTSThere were 402 adult patients who met the inclusion criteria for this study. The average age was 50.5 years, and 122 (30.3%) patients were women. In-hospital mortality was associated with older age, higher Injury Severity Score (ISS), higher Rotterdam score (head CT grading system), and the presence of bilateral fixed and dilated pupils (p < 0.01). In-hospital command-following was anticorrelated with age, ISS, Rotterdam score, and the presence of a single fixed and dilated pupil (p < 0.05). TFC was anticorrelated with age, ISS, Rotterdam score, and the presence of a single fixed and dilated pupil. Additionally, patients who sustained injuries from falls from standing height had a shorter average TFC. The 3 significant variables from the Cox regression model that explained the most variance were used to create a 4-point TFC score. The most significant of these characteristics were Rotterdam head CT scores, high impact traumas, and the presence of a single fixed and dilated pupil. Importantly, the presence of a single fixed and dilated pupil was correlated with longer TFC but no increase in likelihood of in-hospital mortality.CONCLUSIONSThe creation of the 4-point TFC score will allow clinicians to quickly identify patients with predicted prolonged TFC and estimate the likelihood of command-following at different times after injury. Discussions with family members should take into account the likelihood that patients will return to consciousness and survive after TBI.

Objective: Severe traumatic brain injury (sTBI) often results in disorders of consciousness. Patients emerging from coma frequently exhibit aberrant behaviors such as agitation. These non-purposeful combative behaviors can interfere with medical care. Interestingly, agitation is associated with arousal and is often among the first signs of neurological recovery. A better understanding of these behaviors may shed light on the mechanisms driving the return of consciousness in sTBI patients. This study aims to investigate the association between posttraumatic agitation and the recovery of consciousness.Methods: A retrospective chart review was conducted in 530 adult patients (29.1% female) admitted to Stony Brook University Hospital between January 2011 and December 2019 with a diagnosis of sTBI and Glasgow Coma Scale (GCS) ≤8. Agitation was defined as a Richmond Agitation Sedation Scale (RASS) > +1, or any documentation of equivalently combative and violent behaviors in daily clinical notes. The ability to follow verbal commands was used to define the recovery of consciousness and was assessed daily.Results: Of 530 total sTBI patients, 308 (58.1%) survived. Agitation was present in 169 of all patients and 162 (52.6%) of surviving patients. A total of 273 patients followed commands, and 159 of them developed agitation. Forty patients developed agitation on hospital arrival whereas 119 developed agitation later during their hospital course. Presence of in-hospital agitation positively correlated with command-following (r = 0.315, p < 0.001). The time to develop agitation and time to follow commands showed positive correlation (r = 0.485, p < 0.001). These two events occurred within 3 days in 54 (44.6%) patients, within 7 days in 81 (67.8%) patients, and within 14 days in 96 (80.2%) patients. In 71 (59.7%) patients, agitation developed before command-following; in 36 (30.2%) patients, agitation developed after command-following; in 12 (10.1%) patients, agitation developed on the same day as command-following.Conclusion: Posttraumatic agitation in comatose patients following sTBI is temporally associated with the recovery of consciousness. This behavior indicates the potential for recovery of higher neurological functioning. Further studies are required to identify neural correlates of posttraumatic agitation and recovery of consciousness after sTBI.

Background: We investigated a novel surgical approach to decompressive craniectomy (DC), the bifrontal biparietal, or “cruciate,” craniectomy, in severe pediatric traumatic brain injury (TBI). Cruciate DC was designed with a fundamentally different approach to intracranial pressure (ICP) control compared to traditional DC. Cruciate DC involves craniectomies in all 4 skull quadrants. The sagittal and coronal bone struts are disarticulated at the skull to allow the decompression of the sagittal sinus and bridging veins in addition to permitting cerebral expansion, thereby maintaining cranial compliance. Objective: To characterize ICP control with cruciate DC in pediatric TBI. Methods: We performed a retrospective review of TBI patients who underwent cruciate DC. We investigated mortality and preoperative and postoperative ICP. Group 1 underwent medical therapy prior to DC and Group 2 required immediate DC. Results: Fifteen of 18 patients survived. In Group 1, mean preoperative ICP was 18.5 mm Hg and mean postoperative ICP was 11.5 mm Hg. In Group 2, mean preoperative ICP was 27.3 mm Hg and mean postoperative ICP was 15.0 mm Hg. Conclusion: Cruciate DC was associated with lowering ICP. We observed acute drops in ICP and long-term ICP control. The floating bone struts of the cruciate DC permits the decompression of the sagittal sinus and bridging veins, with maximal relief of cerebral edema.

Background A major challenge during endoscopic transsphenoidal surgery is adequate intraoperative hemostasis. The Aquamantys® is a relatively new bipolar sealing device which uses radiofrequency energy and saline. This promotes hemostasis while decreasing charring and thermal spread. In this paper, we describe our experience with the Aquamantys® Mini EVS 3.4 Epidural Vein Sealer Bipolar Electrocautery System (Medtronic Advanced Energy, Portsmouth, NH, USA) during endoscopic surgery for tumors of the skull base with particular attention to ergonomic benefits and technical nuances. Methods We conducted a retrospective review of all patients undergoing endoscopic surgery for skull base tumors from September 2012 to June 2016 at our institution. All procedures used the Aquamantys® system. 45 cases were identified. Results Successful hemostasis was achieved in all cases with an average estimated blood loss (EBL) of 46 mL (Range 10–250). There were no intraoperative complications. The single-shaft design allowed for excellent manipulation compared to pistol-grip bipolar forceps. The thermal energy provided excellent radial coverage without extensive penetration into viable pituitary tissue. Conclusion To our knowledge, this is the largest series documenting the use of the Aquamantys® system in skull base surgery. The device is easily mobile and highly effective within the endonasal corridor and should be a tool in the repertoire of the endoneurosurgeon. Randomized control trials would be useful in comparing EBL between the Aquamantys® and standard bipolar electrocautery.

The authors present a case of intraspinal malignant psammomatous melanotic schwannoma (PMS) not associated with Carney complex and review all reported cases not associated with this syndrome. The focus of this review paper is on the characteristics of the malignant progression of PMS. A 54-year-old man had a history of squamous cell carcinoma of the neck and tonsillar carcinoma. The patient’s serial CT scanning study showed a mass in the left C-5 foramen. On presentation he was neurologically intact. After 18 months, the patient developed radiating pain down the left arm with decreased sensation. MRI of the cervical spine showed an enhancing 2.1 × 1.5 × 1.9-cm mass in the left C5–6 foramen. A C5–6 hemilaminectomy was performed with gross-total removal of the tumor. At 3 months postoperatively, the patient developed new-onset pain and weakness. MRI showed a dumbbell-shaped mass in the left C-7 foramen. MRI of the pelvis showed a 1.4 × 1.0-cm lesion on the right ischium and a 1.1 × 2.8-cm lesion on the right inferior pubic ramus. Anterior cervical discectomy of C5–6 and C6–7 with corpectomy of C-6 with subtotal resection of the tumor was completed. PMS should not be considered a benign tumor because in 41.1% of patients, including the patient in this report, the tumor progresses to malignancy. Long-term follow-up is needed in these patients. New surgical treatment plans should be considered.

Modulation of ischemic cell death can be accomplished via a multitude of mechanisms, such as quenching radical species, providing alternative energy sources, or altering glutamate excitation. Transient cerebral ischemia will induce apoptotic cell death selectively to hippocampal cornus ammon's field 1 of the hippocampus (CA1) pyramidal cells, while neighboring CA3 and dentate neurons are spared. Poly MVA is a dietary supplement based on the nontoxic chemotherapeutic lipoic acid-palladium complex (LAPd). LAPd is a liquid crystal that works in cancer cells by transferring excess electrons from membrane fatty acids to DNA via the mitochondria. Therefore, by its structural nature and action as a redox shuttle, it can both quench radicals as well as provide energy to the mitochondria. To understand the role of LAPd in regulating ischemic cell death, we studied Poly MVA. Male Mongolian gerbils were subjected to 5 min of bilateral carotid artery occlusion under a controlled temperature environment (37.0-38.0 degrees C). Animals were injected with physiological saline or either 30, 50, or 70 mg/kg of Poly MVA every 24 h beginning immediately after the occlusion until being sacrificed on experimental day 4. Damage was evaluated by analyzing nesting behavior and conducting blinded measures of viable CA1 lengths. All Poly MVA treatment dosages significantly (p < 0.05) reduced hippocampal CA1 damage by 72 h. Nesting scores were significantly improved after 30 and 50 mg/kg treatment but not 70 mg/kg. While nesting is usually a very accurate indicator of morphological damage, the 70 mg/kg-treated animals demonstrated excessive energy, thus ignoring the nesting material. While numerous routes offer varying degrees of CA1 neuronal survival after transient global ischemia, only the LAPd complex, which quenches radicals and provides energy to stabilize the mitochondria, offers such significant protection. Thus, the administration of Poly MVA may be a potent neuroprotective agent for victims of transient ischemic attack (TIA), cardiac arrest, anesthetic accidents, or drowning.

The present study utilized the administration of the mitochondrial toxin, 3-nitropropionic acid (3-NP), to mimic the pathology associated with Huntington's disease (HD). 3-NP causes striatal cell degeneration via the inhibition of succinate dehydrogenase. There is growing evidence suggesting the role of apoptosis in 3-NP cell death. TUNEL staining, DNA fragmentation, and changes in bcl-2 mRNA levels have been associated with this metabolic impairment. We wish to further elucidate the apoptotic cascade in this model of HD pathogenesis. 3-NP was administered to rats intraperitoneally at 20mg/kg/day for up to 3 days. At 3 days, characteristic behavioral and morphological effects became evident. While cell death did not become apparent within the first 3 days, there were changes in the levels of apoptotic regulatory proteins and translocation of cytochrome c. Within 24 h after 3-NP administration there were elevations in both bcl-xl and bax. However, bcl-xl protein levels quickly returned to control levels while bax levels continued to increase, resulting in a detrimental bax/bcl-xl ratio. Bax has been demonstrated to facilitate cytochrome c release by forming mitochondrial pores. We saw cytochrome c translocate from the mitochondria to the cytosol approximately 24 h after initial 3-NP administration when compared to saline-injected controls. This evidence generated using the 3-NP degeneration model may help elucidate the apoptotic cascade associated with HD neurodegeneration.