Unilateral Bone Window Cerebral Falx Incision of Bilateral Frontal Lobes Cerebral Contusion and Laceration under Neuroendoscopy and Literature Review

Background: Bilateral frontal lobes cerebral contusion and laceration is one unique brain injury in neurosurgery department. It is characteristic of recessive attacking and develops quickly. The unilateral cerebral falx incision is a new minimally invasive surgery that can solve bilateral frontal lobes cerebral contusion and laceration in one surgery. However, it has some limitations in removal of contralateral frontal hematoma and hemostasis due to the limited field of view under the microscope. The unilateral bone window cerebral falx incision of bilateral frontal lobes cerebral contusion and laceration under a neuroendoscopy can acquire a good illumination and field of view. This is beneficial to complete removal of contralateral hematoma, effective hemostasis and retaining brain tissue functions to the maximum extent. Case Presentation: The patient, a 55-year-old man, was hospitalized for “consciousness disorder by 12 h because of car accident”. Physical Examination: Coma, GCS score of E1V2M5, bilateral pupil diameter of 2 mm, presence of light response, contusion of scalp at the left top, peripheral dysphoria and bilateral Bartter syndrome negative. The patient has a history of non-traumatic cerebral stroke 3 years ago. Head CT: Longitudinal fracture of frontal parietal occipital bone, bilateral frontal lobes contusion and laceration, subarachnoid hemorrhage. Diagnosis: Bilateral frontal lobes contusion and laceration, longitudinal fracture of frontal parietal occipital bone, subarachnoid hemorrhage and hematoma of scalp. In emergency treatment, unilateral bone window cerebral falx incision of bilateral frontal lobes cerebral contusion and laceration under a neuroendoscopy was performed. The surgery has achieved satisfying effect. Discussion: This case realized the goal of removing contralateral frontal hematoma through unilateral craniotomy under a neuroendoscopy. Due to the clear field of view, it retained extracerebral layer structures of contralateral olfactory nerve protection frontotemporal completely. Moreover, this surgical technique is conducive to intraoperative recognition of pericallosal arteries and lateral fractured blood vessels. It also involves protection, which conforms to the minimally invasive philosophy. The proposed surgical technology can eliminate contralateral frontal hematoma under a good field of view. However, it is suggested not to manage with the further operation on patients who have brain swelling and difficulties in exposure of cerebral falx. These patients need to determine causes of brain swelling and choose bilateral craniectomy if necessary. Conclusions: Unilateral bone window cerebral falx incision of bilateral frontal lobes cerebral contusion and laceration under a neuroendoscopy is a new application of minimally invasive philosophy in craniocerebral injury operation. It still needs further clinical verifications and experience accumulation.

Aquaporin 4 expression and ultrastructure of the blood-brain barrier following cerebral contusion injury

This study aimed to investigate aquaporin 4 expression and the ultrastructure of the blood-brain barrier at 2-72 hours following cerebral contusion injury, and correlate these changes to the formation of brain edema. Results revealed that at 2 hours after cerebral contusion and laceration injury, aquaporin 4 expression significantly increased, brain water content and blood-brain barrier permeability increased, and the number of pinocytotic vesicles in cerebral microvascular endothelia cells increased. In addition, the mitochondrial accumulation was observed. As contusion and laceration injury became aggravated, aquaporin 4 expression continued to increase, brain water content and blood-brain barrier permeability gradually increased, brain capillary endothelial cells and astrocytes swelled, and capillary basement membrane injury gradually increased. The above changes were most apparent at 12 hours after injury, after which they gradually attenuated. Aquaporin 4 expression positively correlated with brain water content and the blood-brain barrier index. Our experimental findings indicate that increasing aquaporin 4 expression and blood-brain barrier permeability after cerebral contusion and laceration injury in humans is involved in the formation of brain edema.

Inhibition of cathepsin B protects pancreatic acinar cells against apoptosis in early pancreatic trauma in rats

Objectives:To observe the protective effect of cathepsin B inhibition against apoptosis of acinar cells in the early management of pancreatic contusion and laceration in rats,which would provide evidence of a potential early therapeutic for pancreatic contusion and laceration.Methods:Twenty-four rats were assigned to 2 groups:1)Model(n=12)with an induced pancreatic injury of severity I-II and 2)CA074-V(n=12):an induced pancreatic injury,severity I-II treated with the cathepsin B inhibitor CA074-me(0.01mg/g)by intravenous administration through the caudal vein at 5minutes post model establishment.The mice in these two groups were further randomly divided into 4 subgroups containing 3 rats each that were sacrificed for quantitation of apoptosis,immunohistochemistry of cathepsin B,and serum amylase and lipase measurements at different time points after model establishment(0,3,6,and 12hours).Results:The percentage of apoptotic pancreatic acinar cells collected from the injured tissues were much lower in the CA074-V group than the Model group at 3hours[9.25±3.94%vs.64.76±26.47%,P<0.10]and 6hours[14.71±8.22%vs.66.60±13.54%,P<0.10]post model establishment.The percentage of cathepsin B-positive pancreatic acinar cells were much lower in the CA074-V group than in the Model group at 3hours[31.07±12.02%vs.69.16±5.71%,P<0.10],6hours[24.84±0.93%vs.47.06±0.91%,P<0.10],and 12hours[28.33±9.14%vs.52.72±1.25%,P<0.10]post model establishment.Conclusions:Early cathepsin B inhibition effectively blocked acinar cell apoptosis in an experimental rat model of pancreatic contusion and laceration.