Traumatic brain injury (TBI) survivors frequently suffer from life-long deficits in cognitive functions and a reduced quality of life. Axonal injury, observed in most severe TBI patients, results in accumulation of amyloid precursor protein (APP). Post-injury enzymatic cleavage of APP can generate amyloid-β (Aβ) peptides, a hallmark finding in Alzheimer’s disease (AD). At autopsy, brains of AD and a subset of TBI victims display some similarities including accumulation of Aβ peptides and neurofibrillary tangles of hyperphosphorylated tau proteins. Most epidemiological evidence suggests a link between TBI and AD, implying that TBI has neurodegenerative sequelae. Aβ peptides and tau may be used as biomarkers in interstitial fluid (ISF) using cerebral microdialysis and/or cerebrospinal fluid (CSF) following clinical TBI. In the present review, the available clinical and experimental literature on Aβ peptides and tau as potential biomarkers following TBI is comprehensively analyzed. Elevated CSF and ISF tau protein levels have been observed following severe TBI and suggested to correlate with clinical outcome. Although Aβ peptides are produced by normal neuronal metabolism, high levels of long and/or fibrillary Aβ peptides may be neurotoxic. Increased CSF and/or ISF Aβ levels post-injury may be related to neuronal activity and/or the presence of axonal injury. The heterogeneity of animal models, clinical cohorts, analytical techniques and the complexity of TBI in available studies make the clinical value of tau and Aβ as biomarkers uncertain at present. Additionally, the link between early post-injury changes in tau and Aβ peptides and the future risk of developing AD remains unclear. Future studies using e.g. rapid biomarker sampling combined with enhanced analytical techniques and/or novel pharmacological tools could provide additional information on the importance of Aβ peptides and tau protein in both the acute pathophysiology and long-term consequences of TBI.

Tsitsopoulos PP, Tobieson L, Enblad P, Marklund N. Clinical outcome following surgical treatment for bilateral cerebellar infarction.Acta Neurol Scand: 2011: 123: 345–351.© 2010 John Wiley & Sons A/S. Objectives – To analyze the initial clinical and radiological findings, the surgical treatment, and the clinical outcome following surgical decompression in patients with space-occupying bilateral cerebellar infarction. Materials and Methods – Ten patients with expansive bilateral cerebellar infarction and decreased level of consciousness were operated with suboccipital craniectomy, removal of the infarcted tissue, and placement of external ventricular drainage. Long-term outcome was assessed using the modified Rankin scale (mRS). Results – Mean Glasgow coma scale (GCS) score before surgery was 8.9 ± 3.3 and improved to 12.6 ± 3.6 at discharge. At the long-term follow-up (median 57.6 months), six patients had a favorable outcome (mRS 1.3 ± 0.8). Four patients, all with an associated brain stem infarct, had a poor outcome. Conclusions – In the absence of brain stem infarcts, surgical treatment resulted in a favorable clinical outcome and should be considered a treatment option for patients with expansive bilateral cerebellar infarction.

Simulation-based learning (SBL) is an essential adjunct to modern surgical education. Our study aimed to evaluate the educational benefit and motivational impact of a pilot practical neurosurgical module. 38 clinical medical students from several EU Medical Schools attended an international surgical course focused on teaching and learning basic surgical skills. We designed a pilot neurosurgical workshop instructing students to insert an intracranial pressure bolt using an ex vivo pig model. Each delegate was assessed by two consultant neurosurgeons using a validated assessment tool. Structured questionnaires were distributed on completion of the module. Delegate performance increased (p < 0.001) with no difference in performance improvement across year of study (p = 0.676) or medical school (p = 0.647). All delegates perceived this workshop as a potential addition to their education (median 5/5, IQR = 0), and indicated that the course provided motivational value towards a neurosurgical career (median 4/5, IQR = 1), with no difference seen between year of study or medical school (p > 0.05). Our pilot neurosurgical workshop demonstrated the educational value of practical SBL learning for motivating students towards a surgical career. Homogeneous views across year of study and medical school underline the value of developing a unified strategy to develop and standardise undergraduate surgical teaching with a practical focus.

OBJECTIVE: Degenerative cervical spondylotic myelopathy (CSM) is a major cause of spinal cord dysfunction with an unpredictable prognosis. Βiomarkers reflecting pathophysiological processes in CSM have been insufficiently investigated. It was hypothesized that preoperative cerebrospinal fluid (CSF) biomarker levels are altered in patients with CSM and correlate with neurological status and outcome. METHODS: CSF biomarkers from patients with CSM and controls were analyzed with immunoassays. Spinal cord changes were evaluated with MRI. The American Spinal Cord Injury Association Impairment Scale, the Japanese Orthopaedic Association Cervical Myelopathy Evaluation Questionnaire (JOACMEQ), and the EQ-5D questionnaire were applied prior to and 3 months after surgery. A p value < 0.05 was considered statistically significant. RESULTS: Twenty consecutive CSM patients with a mean age of 67.7 ± 13 years and 63 controls with a mean age of 65.2 ± 14.5 years (p > 0.05) were included in the study. In the CSM subjects, CSF neurofilament light subunit (NF-L) and glial fibrillary acidic protein (GFAP) concentrations were higher (p < 0.05), whereas fatty acid–binding protein 3 (FABP3), soluble amyloid precursor proteins (sAPPα and sAPPβ), and amyloid β (Aβ) peptide (Aβ38, Aβ40, and Aβ42) concentrations were lower than in controls (p < 0.05). Aβ peptide levels correlated positively with symptom duration. Preoperative JOACMEQ lower extremity function and CSF NF-L levels correlated positively, and the JOACMEQ bladder function correlated negatively with sAPPα and sAPPβ (p < 0.05). CSF NF-L and FABP3 levels were higher in patients with improved outcome (EQ-5D visual analog scale difference > 20). CONCLUSIONS: CSF biomarkers of glial and axonal damage, inflammation, and synaptic changes are altered in symptomatic CSM patients, indicating that axonal injury, astroglial activation, and Aβ dysmetabolism may be present in these individuals. These findings reflect CSM pathophysiology and may aid in prognostication. However, future studies including larger patient cohorts, postoperative biomarker data and imaging, and longer follow-up times are required to validate the present findings.