Primary spinal astrocytoma is a subtype of glioma, the most common spinal cord tumor found in the intradural intramedullary compartment. Spinal astrocytomas account for 6-8% of all spinal cord tumors and are primarily low grade (World Health Organization grade I (WHO I) or WHO II). They are seen in both the adult and pediatric population with the most common presenting symptoms being back pain, sensory dysfunction, or motor dysfunction. Magnetic Resonance Imaging (MRI) with and without gadolinium is the imaging of choice, which usually reveals a hypointense T1 weighted and hyperintense T2 weighted lesion with a heterogeneous pattern of contrast enhancement. Further imaging which may aid in surgical planning includes computerized tomography, diffusion tensor imaging, and tractography. Median survival in spinal cord astrocytomas ranges widely. The factors most significantly associated with poor prognosis and shorter median survival are older age at initial diagnosis, higher grade lesion based on histology, and extent of resection. The mainstay of treatment for primary spinal cord astrocytomas is surgical resection, with the goal of preservation of neurologic function, guided by intraoperative neuromonitoring. Adjunctive radiation has been shown beneficial and may increase overall survival. The role of adjunctive chemotherapy is employed, however, its benefit has not been clearly defined. Primary spinal cord astrocytomas are rare and challenging to treat. The gold standard treatment is surgical resection. Second-line treatments include radiation and chemotherapy, although, the optimal regimen for adjunctive therapy has not yet been clearly defined.

Background and purposeThe pathogenesis of brain injury after intracerebral hemorrhage is thought to be due to mechanical damage followed by ischemic, cytotoxic, and inflammatory changes in the underlying and surrounding tissue.In recent years, there has been a greater research interest into the various inflammatory biomarkers and growth factors that are secreted during intracerebral hemorrhage. The biomarkers investigated in this study are tumor necrosis factor alpha (TNF alpha), C-reactive protein (CRP), homocysteine (Hcy), and vascular endothelial growth factor (VEGF). The aim of this study was to further investigate the effects of these biomarkers in predicting the acute severity outcome of intracerebral hemorrhage (ICH).MethodsWe conducted a retrospective chart review of patients with spontaneous ICH with TNF alpha, CRP, VEGF, and Hcy levels drawn on admission. Forty-two patients with spontaneous ICH with at least one of the above labs were included in the study. Primary outcomes included death, Glasgow Coma Scale (GCS) on admission, early neurologic decline (END), and hemorrhage size. Secondary outcomes included GCS on discharge, ICH score, functional outcome risk stratification scale of intracerebral hemorrhage (FUNC score), change in hemorrhage size, need for surgical intervention, and length of intensive care unit (ICU) stay.ResultsForty-two patients with spontaneous intracerebral hemorrhage (ICH) were analyzed, 12 patients (28.5%) required surgical intervention, and four patients (9.5%) died. Only low VEGF serum values were found to predict mortality. TNF alpha, CRP, Hcy, and VEGF levels in our patients with ICH were not found to predict early neurologic decline and were not correlated with GCS on admission, initial hemorrhage size, change in hemorrhage size, need for surgical intervention, ICH score, FUNC score, midline shift, and length of ICU stay. CRP and Hcy were elevated in 58% and 31% of patients tested, respectively. GCS on admission and ICH score were significantly associated with mortality.ConclusionAfter careful statistical review of the data obtained from this patient population, only low VEGF values were found to be a significant predictor of mortality. However, elevated CRP and Hcy levels were associated with a non-significant trend in hemorrhage size and mortality suggesting that CRP and Hcy-lowering therapies may decrease hemorrhagic stroke risk and severity.

The actions of neurons are dependent on electrochemical signal pathways mediated by neurotransmitters and create measurable electrical charges. These charges have been found to be measurable through neuroimaging technologies and now through a novel non-contact non-invasive sensor without supercooling. Identifying whether this technology can be appropriately interpreted with synchronized motor well-defined activities in vivo may allow for further clinical applications. MethodsA non-contact, non-invasive helmet constructed and modified using shielding technology with proprietary magnetic field sensors was utilized to measure the brain's electromagnetic field (EMF). Human volunteers donned helmets and were asked to perform repetitive tapping exercises in order to identify waves consistent with tapping from the left and right hemispheres. A gyroscope was utilized to ensure that measured waves were not from micro-movement but were from neuronal firing. Multiple individuals were tested to evaluate the reproducibility of tapping and commonalities between individuals ResultsRight and left-sided tapping generated discernible wave changes from baseline measurements obtained by the helmet without a subject as well as differed from when the subject was at rest. Wave patterns varied from person to person but were overall similar in each subject individually. Shielding was necessary to identify signals but EMF was identified when shielding was transitioned from around the helmet to within the helmet design. ConclusionIt is possible to measure in-vivo electromagnetic fields generated by the human brain generated by stereotyped tasks in a non-contact non-invasive manner. These waves were reliably obtained within each individual with some variability in morphology from subject to subject however were similar in each subject. Signals varied based on activity and stereotyped motor activities were identified. A helmet using shielding technology within the helmet itself was able to effectively identify EMF signals. Future analysis may focus on translating these waves into functional mapping for clinical applications.

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.

IntroductionAdvancements in neuroimaging have changed the field of medicine. Computed tomography (CT) and magnetic resonance imaging (MRI) typically produce a static image of the brain, while continuous electroencephalogram (EEG) data is limited to the cortical surface. The brain's chemical reactions produce an electric circuit that generates a magnetic field. We seek to test the ability of a non-contact sensor to measure the human brain's electromagnetic field (EMF). MethodsA lightweight, inexpensive construct was designed to hold EMF sensors to non-invasively measure the human brain's dynamic EMF. Measurements were conducted on non-clinical human volunteers. Background data without the human subjects was obtained, followed by introducing human subjects. Motionless human subject data was obtained, followed by a subject performing a task. Finally, a subject received auditory stimulation, and data was obtained. ResultsOur non-contact sensor was able to detect a difference between background activity without a human subject and the electromagnetic field of a human brain within the scalp and skull. Detectable differences in magnetic field potential were also obtained when the subject performed a task and received auditory stimulation. ConclusionIt is possible to continuously measure living human brain dynamic electromagnetic fields throughout the entire brain in a non-contact, non-invasive, continuous manner through the human scalp and skull in the standard environment. The signals are unique to the individual human and can be differentiated from background activity.