Anterior cervical discectomy and fusion (ACDF) is a very common surgery performed globally. Although a few cases of expectorating screws or extrusion of screws into the gastrointestinal tract through esophageal perforations have previously been reported, there has not been a case reporting pharyngeal perforation and entire cervical construct extrusion in the literature to date. In this report the authors present the first case involving the extrusion of an entire cervical construct via a tear in the posterior pharyngeal wall. An 81-year-old woman presented to the emergency department (ED) with a complaint of significant cervical pain 5 days after a fall due to a syncopal event. Radiological findings showed severe anterior subluxation of C-2 on C-3 with no spinal cord signal change noted. She underwent ACDF at the C2–3 level utilizing a polyetheretherketone (PEEK) cage, allograft, autograft, and a nontranslational plate with a locking apparatus and expanding screws. The screw placement was satisfactory on postoperative radiography and the Grade II spondylolisthesis of C-2 on C-3 was reduced appropriately with the surgery. The postoperative radiographs obtained demonstrated good instrumentation placement. Three and a half years later the patient returned to the ED having expectorated the entire anterior cervical construct. A CT scan demonstrated the C-2 and C-3 vertebral bodies to be fused posteriorly with an anterior erosive defect within the vertebral bodies and the anterior fusion hardware at the C2–3 level no longer identified. The fiberoptic laryngoscopy demonstrated a 1 × 1 cm area over the importation of the hypopharynx, above the glotic area. The Gastrografin swallowing test ruled out any esophageal tear or fistula and confirmed the presence of a large ulcer on the posterior wall of the oropharynx. To the best of the authors' knowledge, this is the first ever reported case of a tear in the posterior pharyngeal wall along with extrusion of the entire cervical construct after ACDF. This case demonstrates a rare but potentially serious complication of ACDF. Based on the available literature, each case requires separate and distinct treatment from the others.

A rare complication of cervical spine decompression is acute paralysis following the procedure. This neurologic deficit is thought to be due to reperfusion injury of a chronically ischemic spinal cord and is referred to as "white cord syndrome" given the pathognomonic finding of hyperintensity on T2-weighted MRI. Three prior cases have been reported. We present a case of transient quadriplegia following posterior cervical decompression.A 41-year-old male with cervical spondylotic myelopathy presented with bilateral progressive upper extremity weakness, hyperreflexia, and cervical spine MRI showing severe cord compression at C1 and partial hyperintense signal. Intraoperatively, after C1 bony decompression and without perceptible technical cause, the patient experienced a complete loss of both somatosensory evoked potentials (SSEPs) and motor evoked potentials (MEPs) with an eventual return to baseline prior to completing the operation.The patient awoke from surgery with acute quadriplegia without perceptible technical cause (intraoperative compression or evident anatomic compromise). An immediate postoperative MRI revealed a more pronounced hyperintensity in the central cervical cord on T2-weighted sequences. Treatment with increased mean arterial pressure (MAP) therapy and dexamethasone resulted in the patient regaining some movement over a period of hours and full strength over a period of months.The mechanism of acute weakness following cervical spine decompression in the absence of perceptible technical cause is not fully understood, but current theory suggests that a reperfusion injury is most likely the cause. It remains a diagnosis of exclusion. Familiarity with this potential postoperative complication can aid in appropriate postoperative therapy with early diagnosis and intervention leading to restored spinal cord function and excellent prognosis.

A systematic PubMed and Google Scholar search for studies related to the anatomy, history, surgical approaches, complications, and diseases of the superior sagittal sinus was performed. The purpose of this review is to elucidate some of the more recent advances of our understanding of this structure. One of the earliest anatomical landmarks to be described, the superior sagittal sinus (SSS, sinus sagittalis superior (Latin); "sagittalis" Latin for 'arrow' and "sinus" Latin for 'recess, bend, or bay') has been defined and redefined by the likes of Vesalius and Cushing. A review of the various methods of approaching pathology of the SSS is discussed, as well as the historical discovery of these methods. Disease states that were emphasized include invasion of the SSS by meningioma, as well as thrombosis and vascular malformations.

Intracranial germ cell tumors are uncommon and account for only 0.3–3.4% of all intracranial tumors. Teratomas are a subset of these neoplasms, and their finding in brain structures is exceptionally rare, and occurrence within the skull base is quite novel. The authors report the case of a 57-year-old male patient who presented with vision changes, incontinence, ataxia, and altered mental status of 1 week's duration. Imaging revealed a large intrasellar mass with suprasellar extension, involvement of the ventricular system, and marked hydrocephalus with the enlargement of the lateral and third ventricles. The patient underwent a pterional craniotomy/transsylvian approach for resection of the mass. Postoperative histological examination of the resected mass was confirmatory for a mature cystic teratoma. This was followed by radiotherapy, stereotactic radiosurgery, and adjuvant radiotherapy. At the most recent followup, approximately 4 years later, the patient is doing well with improved vision since the operation. This report highlights our experience with a teratoma in a very unusual location, and we review the relevant literature.

Background: Measurement of optic nerve sheath diameter (ONSD) using ocular ultrasonography has shown a promise in predicting increased intracranial pressure (ICP). However, this method is dependent on operator technique and equipment availability. We propose an alternative method of measuring ONSD and Marshall score grading by utilizing initial computed tomography (CT) head obtained on admission. We believe that such a technique could help predict patients requiring an invasive ICP monitor on admission. Methods: Patients were retrospectively selected from the neurosurgery database of a level II trauma center. Control patients originated from a database of nontraumatic brain injury (TBI) patients with a negative CT head and no intracranial pathology. Study subjects included patients aged 18–90 years, who sustained a severe TBI requiring placement of an ICP monitor on admission. All patients had a non-contrast CT head before the placement of an ICP monitor. Patients receiving any intervention for decreasing suspected elevated ICPs and those with any documented orbital fractures before ICP monitor placement were excluded from the study. All measurements were performed by at least of two independent assessors. Results: A total of 242 patients were reviewed, of which 204 (100 control and 104 intervention) met inclusion criteria for this study. T he average age in the control group was 49.1 ± 22.9 years old while the average age of the intervention group was 36.9 ± 15.1 years (P < 0.0001). The average Glasgow Coma Scale was 7 in the intervention group. The average ONSD of the control group was 5.73 ± 0.58 mm compared to 6.76 ± 0.83 mm in the intervention group (P < 0.0001). Linear regression analysis demonstrated a statistically significant correlation between ONSD and opening ICP (r = 0.40, P < 0.001) and peak ICP (r = 0.31, P < 0.0001). An ONSD 6.0 mm + Marshall score 3 on initial CT head demonstrated a 92.5% sensitivity, 92.6% specificity, and 96.1% positive predictive value for developing an ICP 20 mmHg during hospitalization. Conclusion: Utilizing ONSD in combination with Marshall score grading on initial CT head is a strong predictor of elevated ICP. These criteria can be used in future studies to develop more objective criteria to guide ICP monitor placement.

Introduction Traumatic brain injury (TBI) results in primary and secondary brain injuries. Secondary brain injury can lead to cerebral edema resulting in increased intracranial pressure (ICP) secondary to the rigid encasement of the skull. Increased ICP leads to decreased cerebral perfusion pressure which leads to cerebral ischemia. Refractory intracranial hypertension (RICH) occurs when ICP remains elevated despite first-tier therapies such as head elevation, straightening of the neck, analgesia, sedation, paralytics, cerebrospinal fluid (CSF) drainage, mannitol and/or hypertonic saline administration. If unresponsive to these measures, second-tier therapies such as hypothermia, barbiturate infusion, and/or surgery are employed. Methods This was a retrospective review of patients admitted at Arrowhead Regional Medical Center from 2008 to 2019 for severe TBI who developed RICH requiring placement into a pentobarbital-induced coma with therapeutic hypothermia. Primary endpoints included mortality, good recovery which was designated at Glasgow outcome scale (GOS) of 4 or 5, and improvement in ICP (goal is <20 mmHg). Secondary endpoints included complications, length of intensive care unit (ICU) stay, length of hospital stay, length of pentobarbital coma, length of hypothermia, need for vasopressors, and decompressive surgery versus no decompressive surgery. Results Our study included 18 patients placed in pentobarbital coma with hypothermia for RICH. The overall mortality rate in our study was 50%; with 60% mortality in pentobarbital/hypothermia only group, and 46% mortality in surgery plus pentobarbital/hypothermia group. Maximum ICP prior to pentobarbital/hypothermia was significantly lower in patients who had a prior decompressive craniectomy than in patients who were placed into pentobarbital/hypothermia protocol first (28.3 vs 35.4, p<0.0238). ICP was significantly reduced at 4 hours, 8 hours, 12 hours, 24 hours, and 48 hours after pentobarbital and hypothermia treatment. Initial ICP and maximum ICP prior to pentobarbital/hypothermia was significantly correlated with mortality (p=0.022 and p=0.026). Patients with an ICP>25 mmHg prior to pentobarbital/hypothermia initiation had an increased risk of mortality (p=0.0455). There was no statistically significant difference in mean ICP after 24 hours after pentobarbital/hypothermia protocol in survivors vs non-survivors. Increased time to reach 33°C was associated with increased mortality (r=0.47, p=0.047); with a 10.5-fold increase in mortality for >7 hours (OR 10.5, p=0.039).

Pathophysiological mechanisms and cascades take place after a mild traumatic brain injury (mTBI) that can cause long-term sequelae, including chronic traumatic encephalopathy in patients with multiple concurrent TBIs. As diagnostic imaging has become more advanced, microanatomical changes present after mTBI may now be more readily visible. In this narrative review, the authors discuss emerging diagnostics and findings in mTBI through advanced imaging, electroencephalograms, neurophysiologic processes, Q2 biochemical markers, and clinical tissue tests in an effort to help osteopathic physicians to understand, diagnose, and manage the pathophysiology behind mTBI, which is increasingly prevalent in the United States.

Background: Surgical outcome prediction has assisted physicians in discussing surgical intervention or expectant management. While increasing pituitary tumor size would seem to be associated with increasing challenge of removal and associated complications, that relationship has not been borne in the literature. Methods: We performed a retrospective review of a consecutive cohort of pituitary surgeries completed at our institution. Data included age at the time of surgery, presenting symptoms and Glasgow Coma scale (GCS), GCS at discharge or 7 days postoperatively, GCS at 6 months, adenoma size, imaging characteristics of the tumor and brain before resection, postoperative complications, the presence of preoperative hydrocephalus, brainstem compression, and patient mortality. Results: Patients with giant adenomas were more likely to present with a cranial nerve palsy (P = 0.019), altered mental status (P = 0.0001), hydrocephalus (P = 0.002), and mass effect on the brainstem (P = 0.020). Patients who experienced a postoperative decline in mental status were more likely to present with altered mental (P = 0.006), had an increased prevalence of mass effect on the brainstem (P = 0.005), and were more likely to have either an ischemic stroke (P = 0.0001) and vasospasms or new intraparenchymal hemorrhage (P = 0.013). Conclusion: The results of this study demonstrate that postoperative mental status declines after pituitary adenoma resection can be directly related to brainstem compression and further surgical irritation of the surrounding vasculature. The intraoperative irritation can be multifactorial and may result as the decompressed brain structures assume their anatomical position.