Chordoma is a low-grade notochordal tumor of the skull base, mobile spine and sacrum which behaves malignantly and confers a poor prognosis despite indolent growth patterns. These tumors often present late in the disease course, tend to encapsulate adjacent neurovascular anatomy, seed resection cavities, recur locally and respond poorly to radiotherapy and conventional chemotherapy, all of which make chordomas challenging to treat. Extent of surgical resection and adequacy of surgical margins are the most important prognostic factors and thus patients with chordoma should be cared for by a highly experienced, multi-disciplinary surgical team in a quaternary center. Ongoing research into the molecular pathophysiology of chordoma has led to the discovery of several pathways that may serve as potential targets for molecular therapy, including a multitude of receptor tyrosine kinases (e.g., platelet-derived growth factor receptor [PDGFR], epidermal growth factor receptor [EGFR]), downstream cascades (e.g., phosphoinositide 3-kinase [PI3K]/protein kinase B [Akt]/mechanistic target of rapamycin [mTOR]), brachyury—a transcription factor expressed ubiquitously in chordoma but not in other tissues—and the fibroblast growth factor [FGF]/mitogen-activated protein kinase kinase [MEK]/extracellular signal-regulated kinase [ERK] pathway. In this review article, the pathophysiology, diagnosis and modern treatment paradigms of chordoma will be discussed with an emphasis on the ongoing research and advances in the field that may lead to improved outcomes for patients with this challenging disease.

Background: A minimally invasive approach to the L2-S1 disc spaces through a single, left-sided, retroperitoneal oblique corridor has been previously described. However, the size of this corridor varies, limiting access to the disc space in certain patients. Here, the authors retrospectively reviewed lumbar spine magnetic resonance imaging (MRI) in 300 patients to better define the size and variability of the retroperitoneal oblique corridor. Methods: Lumbar spine MRI from 300 patients was reviewed. The size of the retroperitoneal oblique corridor from L2-S1 was measured. It was defined as the (1) distance between the medial aspect of the aorta and the lateral aspect of the psoas muscle from L2-L5 and (2) the distance between the midpoint of the L5-S1 disc and the medial aspect of the nearest major vessel on the left at L5-S1. In addition, the rostral-caudal location of the iliac bifurcation was measured. Results: The size of the retroperitoneal oblique corridor at L2/3, L3/4, L4/5, and L5/S1 was, respectively, 17.3 ± 6.4 mm, 16.2 ± 6.3 mm, 14.8 ± 7.8 cm, and 13.0 ± 8.3 mm. The incidence of corridor size <1 cm at L2/3, L3/4, L4/5, and L5/S1 was 10.3%, 16.0%, 30.0%, and 39.3%, respectively. The iliac bifurcation was most commonly found behind the L4 vertebral body (n = 158, 52.67%) followed by the L4/5 disc space (n = 74, 24.67%). Conclusion: The size of the retroperitoneal oblique corridor diminishes in a rostral-caudal direction, often limiting access to the L4/5 and L5/S1 disc spaces.

Background: Deep brain stimulation (DBS) lead edema can be a serious, although rare, complication in the postoperative period. Of the few cases that have been reported, the range of presentation has been 33 h–120 days after surgery. Case Description: We report a case of a 75-year-old male with a history of Parkinson’s disease who underwent bilateral placement of subthalamic nucleus DBS leads that resulted in symptomatic, left-sided lead edema 6 h after surgery, which is the earliest reported case. Conclusions: DBS lead edema is noted to be a self-limiting phenomenon. It is critical to recognize the possibility of lead edema as a cause of postoperative encephalopathy even in the acute phase after surgery. Although it is important to rule out other causes of postoperative changes in the patient examination, the recognition of lead edema can help to avoid extraneous diagnostic tests or DBS lead revision or removal.

Background: Spinal cord stimulation (SCS) is a well-established treatment modality for chronic pain. Thoracic radiculopathy has been reported as a complication of SCS paddle lead implantation by several authors and commonly presents as abdominal pain. Methods: We performed a search of all patients who underwent either placement of a new epidural paddle lead electrode or revision of an epidural paddle lead electrode for SCS in the thoracic region from January 2017 to January 2018. We then investigated all cases of immediate postoperative abdominal pain. Results: We identified 7 patients who had immediate postoperative abdominal pain among 86 cases of epidural SCS procedures. Most patients were discharged on postoperative days 1–3. No patients required revisions or removals of their SCS for any reason. Conclusions: We conclude that the etiology of immediate postoperative abdominal pain after thoracic paddle lead implantation for SCS is most likely thoracic radiculopathy. We hypothesize that small, transient epidural hematomas could be the cause of this thoracic radiculopathy. We argue that all patients with immediate postoperative abdominal pain and no other neurologic deficits after thoracic paddle lead implantation for SCS should first be treated conservatively with observation and pain management.

Objectives A significant number of chronic pain patients rely on spinal cord stimulation (SCS) for treatment of their intractable pain. A screening trial using percutaneous electrodes is an integral step for predicting a successful treatment course with a permanent SCS system. Most of these trials are performed in an outpatient ambulatory surgical center and some in the office setting. However, there are select patients who are considered poor candidates for percutaneous trials. We present the initial report of patients who have received surgical implantation of permanent paddle-leads for SCS trials at our institution and show that this was a safe and effective alternative for our patients who could not undergo percutaneous trials. Methods We retrospectively reviewed the hospital charts of 12 patients who underwent permanent surgically-implanted paddle-lead trials from 2014 to 2017. Success was considered positive with a 50% reduction in pain rating. If positive, patients were brought back to the operating room to have the implanted leads connected to an internalized pulse generator. Results All 12 patients met the criteria for a successful trial. Only one patient had his SCS system surgically removed after nine months. None of our patients reported or returned with paddle-lead migrations or infections. Conclusions We report that surgically-implanted paddle-lead trials were a safe and effective alternative to percutaneous trials in our patients who were deemed poor candidates for percutaneous trials. No complications occurred and all of our patients received a second surgery for internalization of the SCS system. Patients who have previously failed percutaneous trials may be false-negatives to SCS.

Metastasis of systemic neoplasms to the spine is common; however, the metastasis of primary spinal cord tumors to other regions in the body is an infrequent occurrence.