Depressed skull fracture compressing eloquent cortex causing focal neurologic deficits.

BACKGROUND: Depressed skull fractures are typically the consequence of high-impact injuries with inward buckling of the cranium. The majority of depressed skull fractures are managed conservatively in the absence of dural violation, sinus involvement, significant underlying hematoma, depressed fragment greater than 1 cm, wound infection, or gross wound contamination. Even in the presence of any of the aforementioned criteria, cranioplasty is typically considered an urgent procedure rather than a neurosurgical emergency. Rarely, a depressed fracture fragment can cause focal neurologic deficit(s) due to direct compression of the underlying eloquent cortex. CASE DESCRIPTION: A 40-year-old male presented to the emergency department after a mechanical fall with a left central facial nerve palsy, left hemiplegia, left hemianesthesia, and fixed right gaze deviation. The neurologic deficits observed were attributed to a combination of blunt force trauma to the head (i.e., coup-contrecoup injury) and the depressed fracture fragment compressing the underlying eloquent cortex. He underwent emergent cranioplasty with fragment elevation within 2 hours of the traumatic injury. At 6-month follow-up, he regained full neurologic function without any residual deficits. CONCLUSIONS: Our experience highlights a rare indication for emergent cranioplasty with an excellent functional outcome attributable to immediate fracture elevation and decompression of eloquent cortex.

Spinal Intradural Arachnoid Cysts in Adults: An Institutional Experience and Literature Review.

BACKGROUND: Adult spinal intradural arachnoid cysts are rare pathologic entities with an unclear etiopathogenesis. These lesions can be dichotomized into primary (idiopathic) or secondary (related to inflammation, intradural surgery, or trauma) etiologies. Limited series have depicted optimal management strategies and clinical outcomes. OBJECTIVE: To illustrate our experience with spinal intradural arachnoid cysts and to present a literature review of surgically treated cysts to elucidate the clinical and anatomic differences between etiologies. METHODS: Institutional review revealed 29 patients. Various data were extracted from the medical record. Initial and follow-up symptomatologies of the surgical cohort were compared. The literature review included case series describing cysts managed surgically. RESULTS: From patients treated surgically at our institution (22), there was a significant reduction in thoracic back pain postoperatively ( P = .034). A literature review yielded 271 additional cases. Overall, primary and secondary lesions accounted for 254 and 39 cases, respectively. Cysts of secondary origin were more likely localized ventral to the spinal cord ( P = .013). The rate of symptomatic improvement after surgical intervention for primary cysts was more than double than that of secondary cysts ( P < .001). Compared with primary etiologies, the rates of radiographic progression ( P = .032) and repeat surgery ( P = .041) were each more than double for secondary cysts. CONCLUSION: Surgical intervention for spinal intradural arachnoid cysts improves thoracic back pain. The literature supports surgical intervention for symptomatic primary spinal intradural arachnoid cysts with improved clinical outcomes. Surgery should be cautiously considered for secondary cysts given worse outcomes.

Supratentorial cortical ependymoma: A systematic literature review and case illustration.

Cortical ependymomas are currently not considered a subgroup of supratentorial ependymomas; however, there is a growing body of literature investigating the natural history of these lesions compared to supratentorial ependymomas. We performed a systematic literature review of cortical ependymomas with a focus on the natural history, clinical characteristics, and clinical outcomes of these lesions as compared to supratentorial ependymomas. Our search revealed 153 unique cases of cortical ependymomas. The mean age on presentation was 21.2 years. Males and females comprised 58.8% (90/153) and 41.2% (63/153) of cases, respectively. The most common presenting symptom was seizure activity occurring in 44.4% of the cohort (68/153). The recently recognized C11orf95-RELA fusion was identified in 13.7% of the cohort (21/153) and 95.5% of cases (21/22) reporting molecular characterization. World Health Organization grades 2 and 3 were reported in 52.3% (79/151) and 47.7% (72/151) of cases, respectively. The frontal lobe was involved in the majority of cases (54.9%, 84/153). Gross total resection was achieved in 80.4% of cases (123/153). Tumor recurrence was identified in 27.7% of cases (39/141). Mean clinical follow-up was 41.3 months. Mean overall survival of patients who expired was 27.4 months whereas mean progression-free survival was 15.0 months. Comparatively, cortical ependymomas with C11orf95-RELA fusions and supratentorial ependymomas with C11orf95 RELA fusions exhibited differing clinical outcomes. Further studies with larger sample sizes are necessary to investigate the significance of RELA fusions on survival in cortical ependymomas and to determine whether cortical ependymomas with C11orf95-RELA fusions should be classified as a distinct entity.

Neutrophil Count on Admission Predicts Acute Symptomatic Hydrocephalus After Aneurysmal Subarachnoid Hemorrhage.

OBJECTIVE: To investigate the association between immunologic counts on admission and acute symptomatic hydrocephalus after aneurysmal subarachnoid hemorrhage (aSAH). METHODS: We conducted a retrospective analysis of 143 consecutive patients with aSAH. Patient demographics, clinical parameters, laboratory values, and radiographic imaging were obtained. Univariate and multivariate logistic regression analyses were performed to investigate parameters independently associated with acute symptomatic hydrocephalus. Receiver operating characteristic (ROC) curve analysis determined the best threshold value of neutrophil count to differentiate patients with and without hydrocephalus. RESULTS: Overall, acute symptomatic hydrocephalus developed in 39.16% of patients. In an adjusted multivariate logistic regression model, Hunt and Hess grade 4-5 (odds ratio [OR]: 16.052, 95% confidence interval [CI]: 1.188-216.983; P = 0.037), modified Fisher score 3-4 (OR: 10.107, 95% CI: 1.715-59.572; P = 0.011), intraventricular hemorrhage (OR: 4.578, 95% CI: 1.417-14.788; P = 0.011), neutrophil count (OR: 1.183, 95% CI: 1.033-1.354; P = 0.015), and prior ischemic stroke (OR: 7.003, 95% CI: 1.293-37.929; P = 0.024) were significantly associated with hydrocephalus. ROC analysis for neutrophil count confirmed an acceptable area under the curve (AUC 0.780, 95% CI: 0.701-0.859; P < 0.001). The best threshold value of neutrophil count to predict hydrocephalus was ≥9.80 × 103/mL. Overall, 81.25% of patients who developed shunt dependence had a neutrophil count ≥9.80 × 103/mL on admission (P = 0.003). CONCLUSIONS: Neutrophil count ≥9.80 × 103/mL on admission predicts acute symptomatic hydrocephalus after aSAH in an adjusted multivariate logistic regression model. Moreover, shunt dependence was associated with higher neutrophil counts.

Corticosteroid-Induced Regression of Glioblastoma: A Radiographic Conundrum.

Corticosteroid-induced regression of lesion contrast enhancement on imaging studies is most commonly appreciated with primary central nervous system lymphoma; however, although exceedingly rare, a limited number of primary and metastatic intracranial lesions have been reported to exhibit similar radiographic changes subsequent to corticosteroid therapy. To date, there have been six cases of glioblastoma reported to exhibit such changes. Lesion transformation on repeat imaging after the initiation of steroids represents a diagnostic dilemma for clinicians when attempting to differentiate between a diagnosis of glioblastoma and lymphoma. Stereotactic biopsy may be inadvertently postponed due to high clinical suspicion for steroid-induced cytotoxicity traditionally seen with lymphomatous cells. To highlight this radiographic conundrum, we present a rare case of corticosteroid-induced regression of glioblastoma and discuss the relevant literature. To our knowledge, this is the first case report to describe the molecular profile of a glioblastoma that underwent corticosteroid-induced regression.