Depressed Skull Fractures Overlying Dural Venous Sinuses: Management Modalities and Review of Literature.

AIM: To characterize the sociodemographic, clinical and radiological findings of patients with depressed skull fractures overlying cranial dural sinuses that we have faced in our institute. In addition, to explore the indications and choices for the surgical and nonsurgical management of such cases, and assess outcomes in these two treatment groups. MATERIAL AND METHODS: We prospectively followed up a cohort of 34 patients with fractures over dural venous sinuses from January 2013 to December 2017. Twelve (35.1%) were simple depressed fractures (SDFs) and 22 (64.7%) were compound depressed fractures (CDFs). Eighteen patients (52.9%) were treated surgically, and 16 (47.1%) were treated conservatively. RESULTS: The mean age was 20.8 years. Thirty-two of the patients were males (94.12%). The mean time from trauma until hospital arrival was 3.8 hours, and the mean admission Glasgow Coma Score (GCS) was 13.7. Direct trauma was the most common mode of injury. Funduscopy was performed in 16 patients (47.1%), and magnetic resonance venography (MRV) in four patients (11.8%). Twenty-four patients (70.59%) had the fracture overlying the superior sagittal sinus (SSS). The mean length of hospital stay was five days, and the mean follow-up duration was 6.8 months. Twenty-eight patients (82.35%) had a good recovery. CONCLUSION: The majority of SDFs and some CDFs overlying dural sinuses can be managed safely without major surgical intervention. Conservation should be favored when the sinus is patent, dura intact, and bone displacement is insignificant in neurologically intact patients with an apparently clean wound. Otherwise, surgery should be considered. We also propose including a funduscopic examination and venogram as parts of the initial trauma work-up for these patients.

Expression and activation of STAT family proteins in cerebral arteriovenous malformations.

OBJECTIVE: Cerebral arteriovenous malformations (AVMs) do not seem to be static congenital vascular malformations but rather are dynamically changing pathologies. In this work, we investigated the expression and possible activation of different signal transducers and activators of transcription (STAT) family members in AVM nidus. METHODS: Immunohistochemical analysis was conducted on 25 AVM specimens from 24 patients using antibodies against STATs 1, 3, 5, and 6 as well as their phosphorylated forms. Analysis was also undertaken to determine if there is any correlation between STAT activation and different clinical parameters of AVM patients. RESULTS: Our studies revealed that both STATs 1 and 3 were highly expressed in cerebral AVM, mainly in the endothelium of AVM blood vessels and perivascular infiltrating inflammatory cells within the nidus. STAT3 showed the most intense level of expression within the endothelium and perivascular infiltrating inflammatory cells. It was intensely expressed in the endothelium of 25 (100%) specimens and in the infiltrating inflammatory cells of 24 (96%) specimens. The expression of the phospho-STATs 1 and 3 was also high in the endothelium and perivascular infiltrating inflammatory cells indicating activation of STATs 1 and 3 in AVM. We could not find any significant effect of hemorrhage or preoperative embolization, or other clinical parameters, on the activation of STATs 1 and 3 in cerebral AVMs. CONCLUSION: We obtained evidence for significant overexpression and activation of both STATs 1 and 3 in cerebral AVM, thus suggesting an important role for these proteins in mediating the pathophysiology of cerebral AVM.

Activation of nuclear factor κB in cerebral arteriovenous malformations.

BACKGROUND: Cerebral arteriovenous malformations (AVMs) do not seem to be static congenital vascular malformations, but rather are dynamically changing pathologies. It is well-known from clinical situations that these AVMs can enlarge or shrink. Nuclear factor κB (NF-κB) is a nuclear transcription factor that regulates a number of physiological processes, such as inflammation, apoptosis, and cellular growth. OBJECTIVE: To analyze phosphorylation of NF-κB and related molecules in cerebral AVM specimens. METHODS: We examined 19 specimens of cerebral AVMs from 18 patients. Immunohistochemical analysis was performed using an NF-κB p65 (C22B4) rabbit monoclonal antibody, the phosphorylated form of NF-κB (PNF-κB) p65 (Ser276) rabbit antibody, and an IκBα mouse monoclonal antibody. RESULTS: Expression of NF-κB was mainly confined to the endothelial lining and the infiltrating inflammatory cells in the perivascular regions. PNF-κB showed the highest level of expression in both endothelial cells and perivascular infiltrating cells. PNF-κB was intensely expressed in the endothelium and perivascular infiltrating cells of 15 specimens (78.9%). NF-κB and IκB were also expressed in endothelial cells and perivascular infiltrating inflammatory cells, but at lower levels than PNF-κB. Immunohistochemical studies revealed that PNF-κB was mainly concentrated in the nuclei of endothelial and infiltrating inflammatory cells. On the contrary, expression of both NF-κB and IκB was mainly concentrated in the cytoplasm of endothelial and inflammatory cells. CONCLUSION: We detected activation of NF-κB in the endothelium and perivascular infiltrating inflammatory cells within the cerebral AVM nidus, suggesting a role in the pathophysiology of cerebral AVM.