Derivation and validation of a quantitative screening model for blunt cerebrovascular injury.

OBJECTIVE: The objective of this study was to derive and validate a new screening model using a nomogram that allows clinicians to quantify the risk of blunt cerebrovascular injury (BCVI). METHODS: In this study, the authors examined 258,935 patients from a prospectively collected nationwide Japanese database (January 2009-December 2018) who experienced blunt injury. Patients were randomly divided into training (n = 129,468) and validation (n = 129,467) cohorts. First, the authors investigated the prevalence of BCVI, which was defined as blunt injury to any intracranial vessel, the extracranial vertebral artery, the extracranial carotid (common, internal) artery, or the internal jugular vein. Then, a new arterial BCVI screening model using a nomogram was derived, based on multivariate logistic regression analysis through quantifying the association of potential predictive factors with BCVI in the training cohort. The model's discriminatory ability was validated using the area under the receiver operating characteristic curve (AUC) in the validation cohort. RESULTS: Multivariate analysis in the training cohort showed that 13 factors were significantly associated with arterial BCVI and were included in our model. These factors were 1) male sex; 2) high-energy impact; 3) hypotension on hospital arrival; 4) Glasgow Coma Scale score < 9; 5) injury to the face; 6) injury to the neck; 7) injury to the spine; 8) skull base fracture; 9) cervical spine fracture or subluxation; and those with negative associations, i.e., 10) injury to the lower-extremity region; 11) supratentorial subdural hemorrhage; 12) lumbar spine fracture or subluxation; and 13) soft tissue injury of the face. In the validation cohort, the model had an AUC of 0.83 (95% CI 0.81-0.86). When the definition of BCVI was narrowed to include only carotid (common, internal) and vertebral artery injuries, the AUC of the model in predicting these injuries was 0.89 (95% CI 0.87-0.91). CONCLUSIONS: A new screening model that incorporates an easy-to-use nomogram to quantify the risk of BCVI and assist clinicians in identifying patients who warrant additional evaluation was established.

Tau protein as a diagnostic marker for diffuse axonal injury.

BACKGROUND: Diffuse axonal injury (DAI) is difficult to identify in the early phase of traumatic brain injury (TBI) using common diagnostic methods. Tau protein is localized specifically in nerve axons. We hypothesized that serum level of tau can be a useful biomarker to diagnose DAI in the early phase of TBI. METHODS & RESULTS: We measured serum tau levels in 40 TBI patients who were suspected of DAI within 6 hours after TBI to evaluate the accuracy of the tau level as a diagnostic marker for DAI. Diagnosis of DAI was confirmed according to magnetic resonance imaging (MRI) findings. The serum tau level in the DAI group (n = 13) was significantly higher than that in the non-DAI group (n = 27) (DAI vs. non-DAI, 25.3 [0 to 99.1] pg/mL vs. 0 [0 to 44.4] pg/mL, P = 0.03)). A receiver-operating characteristic curve to evaluate the diagnostic ability of serum tau level within 6 hours for DAI showed an area under the curve of 0.690 with 74.1% for sensitivity and 69.2% for specificity. Serum tau level was not significantly higher in unfavorable outcome group (Glasgow Outcome scale [GOS] score = 1-3 at hospital discharge) compared with favorable outcome group (GOS score = 4-5) (P = 0.19). CONCLUSIONS: Tau protein may be a useful biomarker for diagnosis of DAI in the early phase of TBI.

The Tethered Effect of Vestibular Schwannoma Tumor Shrinkage Following Stereotactic Radiosurgery in Secondary Trigeminal Neuralgia.

BACKGROUND: Compression of the trigeminal nerve by vessels and tumors causes trigeminal neuralgia. However, a tethering effect, provoking an abnormal root-stretching force, has been previously reported to play a role in trigeminal nerve hyperexcitability. We report 2 patients with vestibular schwannomas treated by stereotactic radiosurgery (SRS) who presented with typical manifestations of trigeminal neuralgia after tumor shrinkage. Furthermore, we discuss the mechanisms of trigeminal neuralgia. CASE DESCRIPTION: Two patients without a history of trigeminal dysfunction, including trigeminal neuralgia, underwent SRS for vestibular schwannomas. Both patients demonstrated tumor shrinkage after transient tumor expansion following SRS. Neither patient presented with facial pain or dysesthesia at the time of peak tumor volume. However, trigeminal neuralgia occurred after tumor shrinkage. One patient underwent surgery, as the neuralgia was refractory to medical treatment; although the trigeminal nerve was adhered and tethered to the tumor, no neurovascular conflict was identified between the tumor and the nerve. We removed the tumor partially, dissecting between the nerve and the tumor, and relieved the tethered effect. Trigeminal neuralgia was relieved without medication after surgery. CONCLUSIONS: The present cases demonstrate a tethered effect of tumor shrinkage after SRS, which was considered to play a role in trigeminal neuralgia. Surgical dissection surrounding the nerve root is effective for medically resistant neuralgia, even if the tumor shrinks. Partial tumor removal is adequate in such cases, as the tumor has been controlled by radiosurgery.