Case report: A vertebral bone spur as an etiology for spinal cord herniation: case presentation, surgical technique, and review of the literature.

Objective: The pathophysiology of idiopathic spinal cord herniation remains unknown. However, several different factors have been postulated, such as congenital causes (ventral dura mater duplication, preexisting pseudomeningocele, or other congenital dural defects), inflammation, remote spinal trauma, or thoracic disc herniation. Herein, the diagnosis and surgical treatment of a patient with spinal cord herniation caused by an intraspinal bone spur is presented along with a relevant literature review. Case presentation: A 56-year-old male patient presented with a non-traumatic Brown-Sequard syndrome persisting for over 1 year. A magnetic resonance imaging of the spinal axis revealed a ventral spinal cord displacement in the level of T 6/7. A supplementary thin-sliced computed tomography of the spine revealed a bone spur at the same level. For neurosurgical intervention, T 6 and T 7 laminectomy was performed. The cranial and caudal end of the right paramedian ventral dural defect was visualized and enlarged. Following extradural spinal cord mobilization by denticulate ligament transection, the spinal cord was finally released. The spinal cord was rotated and the ventral closure of the dural defect was performed by continuous suture. The patient recovered from surgery without additional deficits. The patient's postoperative gait, sensory, and motor function deficits improved, and further neurological deterioration was prevented. Conclusion: Since the first description of spinal cord herniation by Wortzman et al. in 1974, approximately 260 cases have been reported in the literature. In addition to other causes, intraspinal bone spur is a possible cause of spinal cord herniation.

Case report: Interdisciplinary treatment of complex C1/C2 fractures in a patient with concomitant three-vessel coronary artery disease requiring bypass surgery.

Background: Acute myocardial infarction (MI) frequently leads to consciousness disturbance following hemodynamic collapse. Therefore, MI can occur together with upper cervical spine trauma. Herein, we report the successful treatment of complex C1/C2 fractures in a patient with concomitant three-vessel coronary artery disease (CAD). Case presentation: A 70-year-old patient presented in our emergency outpatient clinic after a hemodynamic collapse without neurological deficits or heart-related complaints. Computed tomography (CT) scan of the cervical spine revealed a dislocated odontoid fracture Anderson and D'Alonzo type II and an unstable Gehweiler type III injury (Jefferson's fracture). An intradiploic arachnoid cyst in the posterior wall of the posterior fossa was a coincident radiological finding. Furthermore, coronary angiography confirmed three-vessel CAD with high-grade coronary artery stenosis. Indication for upper cervical spine surgery and bypass surgery was given. An interdisciplinary team of neurosurgeons, cardiothoracic surgeons and anesthesiologists evaluated the patient's case to develop the most suitable therapy concept and alternative strategies. Finally, in first step, C1-C2 fusion was performed by Harms technique under general anesthesia with x-ray guidance, spinal neuronavigation, Doppler ultrasound and cardiopulmonary monitoring. Cardiothoracic surgeons were on standby. One month later bypass surgery was performed uneventfully. Follow-up CT scan of cervical spine revealed intraosseous screw positioning and beginning fusion of the fractures. The patient did not develop neurological deficits and recovered completely from both surgeries. Conclusions: Treating complex C1/C2 fractures with concomitant severe CAD requiring treatment is challenging and carries a high risk of complications. To our knowledge, the literature does not provide any guidelines regarding therapy of this constellation. To receive upper cervical spine stability and to prevent both, spinal cord injury and cardiovascular complications, an individual approach is required. Interdisciplinary cooperation to determine optimal therapeutic algorithms is needed.

Surgical management of choroid plexus papilloma of the cerebellopontine and cerebellomedullary angle: classification and strategy.

Choroid plexus papillomas (CPPs) are primary neuroectodermal neoplasms that usually arise in the fourth ventricle in adults. In this study, we present 12 patients with CPP arising from the cerebellopontine angle (CPP-CPA) and/or of the cerebellomedullary angle (CPP-CMA) that were treated in our department. Patients who underwent surgery for the treatment for CPP-CPA/CMA from January 2004 to March 2020 were identified by a computer search of their files from the Department of Neurosurgery, Tübingen. CPPs were classified according to their location into type 1 (tumor portion only in the CPA,), type 2 (tumor portions only in the CMA), and type 3 (tumor portions both in the CPA and CMA). Patients were evaluated for initial symptoms, previous therapies in other hospitals, extent of tumor resection, recurrence rate, and complications by reviewing patient documents. Of approximately 1500 CPA lesions, which were surgically treated in our department in the last 16 years, 12 patients (mean age 42 ± 19 years) were found to have CPP-CPA/CMA. Five were male, and seven were female patients. Gross total resection was achieved in nine cases, and a subtotal resection was attained in three cases. Tumor recurrence in the same location after the first surgery in our hospital was observed in 2 patients after 15 and 40 months of follow-up, and in another patient, distant metastases (C3/4 and L3 levels) were observed. Surgical removal of CPP is the treatment of choice, but additional therapeutic options may be necessary in case of remnant tumor portions, recurrence, or malignant transformation.

Paradigm-shift: radiological changes in the asymptomatic iNPH-patient to be: an observational study.

BACKGROUND: Many radiological signs are known for the diagnosis of idiopathic normal pressure hydrocephalus (iNPH). However, there is little information about these signs in the pre-symptomatic phase. For pathophysiological investigative purposes we conducted a descriptive image analysis study on pre-symptomatic patients. METHODS: Patients that had contact with either the neurological or neurosurgical department of the university hospital Tuebingen from 2010 through 2016 with magnetic resonance images > 3 years before onset of symptoms, were included. The date of onset and severity of symptoms, date of first imaging and birth date were recorded. Evan's index (EI), width of the third ventricle (3VW), tight high convexity (THC), Sylvian fissure, extent of white matter hyperintensities and aqueductal flow were assessed in images before and around symptom onset. RESULTS: Ten patients were included. In all ten patients the first symptom was gait disturbance. Nine of ten pre-symptomatic images showed classic signs for iNPH. EI showed a significant increase between the pre-symptomatic and symptomatic phase. 3VW showed a trend for increase without significance. THC changed back and forth over time within some patients. CONCLUSIONS: In accordance with the scarce literature available, radiological changes are present at least 3 years before onset of iNPH-symptoms. EI seems to be a robust measure for pre-symptomatic radiological changes. Extrapolating the data, the development of iNPH typical changes might be an insidious process and the development of THC might be a variable and non-linear process. Further studies with larger sample sizes are necessary to put these findings into the pathophysiological perspective for the development of iNPH.