Calvarial fracture patterns on CT imaging predict risk of a delayed epidural hematoma following decompressive craniectomy for traumatic brain injury.

BACKGROUND AND PURPOSE: The development of a delayed epidural hematoma as a result of decompressive craniectomy represents an urgent and potentially lethal complication in traumatic brain injury. The goal of this study was to determine the incidence of delayed epidural hematoma and whether patterns of skull fractures on the preoperative CT scan could predict risk of a delayed epidural hematoma. MATERIALS AND METHODS: We retrospectively evaluated medical records and imaging studies for patients with acute traumatic brain injury who underwent a decompressive craniectomy during a 9-year period. We compared patterns of skull fractures contralateral to the side of the craniectomy with the occurrence of a postoperative delayed epidural hematoma. RESULTS: In a series of 203 patients undergoing decompressive craniectomy for acute traumatic brain injury, the incidence of a delayed epidural hematoma complication was 6% (12 of 203). All 12 patients who developed a delayed epidural hematoma had a contralateral calvarial fracture on preoperative CT at the site where the delayed epidural hematoma subsequently formed. A contralateral calvarial fracture has perfect sensitivity (100%) for subsequent development of delayed epidural hematoma in our study population. Moreover, a contralateral calvarial fracture involving 2 or more bone plates had an especially high diagnostic odds ratio of 41 for delayed epidural hematoma. CONCLUSIONS: Recognition of skull fracture patterns associated with delayed epidural hematoma following decompressive craniectomy may reduce morbidity and mortality by prompting early postoperative intervention in high-risk situations.

VEGF-A angiogenesis induces a stable neovasculature in adult murine brain.

Angiogenesis is a critical component of stroke, head injury, cerebral vascular malformation development, and brain tumor growth. An understanding of the mechanisms of adult cerebral angiogenesis is fundamental to therapeutic vessel modulation for these diseases. To study angiogenesis in the central nervous system, we injected an adenoviral vector engineered to express vascular endothelial growth factor (VEGF-A164) into adult murine striatum. Vector-infected astrocytes expressed VEGF-A164 resulting in vascular permeability, hemorrhage, and the formation of greatly enlarged "mother" vessels. Subsequently, endothelial cells and pericytes lining mother vessels proliferated and assembled into glomeruloid bodies, complex cellular arrays interspersed by small vessel lumens. As VEGF-A164 expression declined, glomeruloid bodies involuted through apoptotic processes to engender numerous small daughter vessels. Characterized by modestly enlarged lumens with prominent pericyte coverage, daughter vessels were distributed with a density greater than normal cerebral vessels. Daughter vessels remained stable and patent to 16 months and represented the final stage of VEGF-A-induced cerebral angiogenesis. Together, these findings provide a mechanistic understanding of angiogenesis in cerebral disease processes. Furthermore, the long-term stability of daughter vessels in the absence of exogenous VEGF-A164 expression suggests that VEGF-A may enable therapeutic angiogenesis in brain.

Micro-arteriovenous malformations: significant hemorrhage from small arteriovenous shunts.

OBJECTIVE: Micro-arteriovenous malformations (AVMs) represent approximately 8 to 10% of surgically treated brain AVMs. We examined the clinical presentations, radiological features, principles of surgical resection, and factors affecting outcomes for micro-AVM lesions. METHODS: Twelve patients with micro-AVMs that had been treated by surgical resection were retrospectively analyzed. The mean follow-up monitoring period was 35 months (range, 2-76 mo). Outcomes, as assessed in follow-up visits and telephone interviews (using a questionnaire), were classified according to the Glasgow Outcome Scale. RESULTS: All 12 patients presented with intracranial hemorrhage, which was intraparenchymal and superficially situated in 10 patients (83%) and intraventricular in 2 patients (17%). Hemorrhages were large (mean volume, 23 ml3; range, 1-58 ml3) and were associated with neurological deficits for 10 of 12 patients (83%). The identification of an arterialized draining vein during surgery and stereotactic angiography greatly facilitated surgical localization of the lesions. One patient (8%) developed a mild permanent deficit as a result of surgery. Although Glasgow Outcome Scale scores were excellent for all except one patient, nine patients (75%) experienced long-term neurological problems. CONCLUSION: Micro-AVMs typically present with large hemorrhages and are associated with significant neurological deficits. If a superficial clot is present, surgical resection of the lesion is strongly advocated. The ultimate clinical outcomes are determined primarily by deficits present after the initial hemorrhaging episodes.

Microarteriovenous malformations.

Microarteriovenous malformations (micro-AVMs) are a subgroup of brain AVM with a nidus diameter of less than 1 cm. Although many micro-AVMs may appear angiographically occult on cursory review, careful analysis will often reveal a subtle diagnostic feature. Micro-AVMs present with intracranial hemorrhages that are generally large and associated with significant neurologic impairment. An awareness of these lesions as a possible source of hemorrhage in a young person is critical. In general, micro-AVMs are eminently resectable lesions and patient outcome is determined primarily by the hemorrhage that brings them to medical attention.

Acute human histopathology of an intracranial aneurysm treated using Guglielmi detachable coils: case report and review of the literature.

OBJECTIVE AND IMPORTANCE: This case study provided us with the opportunity to explore the histopathological effects of Guglielmi detachable coil (GDC) therapy on the aneurysm orifice and parent vessel-aneurysm neck interface. This type of study is important to the understanding of the mechanisms of obliteration of aneurysms by GDCs. CLINICAL PRESENTATION: The patient presented with a Hunt and Hess Grade III subarachnoid hemorrhage that occurred secondary to the rupture of a small anterior communicating artery aneurysm. INTERVENTION: The aneurysm was successfully coiled without complication, but the patient died 36 hours later. We examined the gross and microscopic pathological findings of this GDC-treated anterior communicating artery aneurysm 36 hours after coiling. A discrete membrane composed of fibrin had formed completely across the aneurysm orifice, excluding the aneurysm sac from the circulation. This membrane was contiguous with the parent vessel. CONCLUSION: This case represents one of the first examples in humans of the formation of a membrane over the aneurysm orifice after GDC therapy. The formation of this membrane, shown to be composed of fibrin, was found at 36 hours after coiling, which is the earliest time frame at which membrane formation has been noted in either humans or animal models. This fibrin membrane may function both as a scaffold for subsequent endothelialization across the aneurysm neck as well as to isolate the aneurysm from the parent circulation, permitting thrombus within the aneurysm sac to mature to an endovascular scar. The factors contributing to the formation of this membrane and its clinical implications are discussed.