Persistent neurogenesis exists in the subventricular zone (SVZ) of the ventricles and the subgranular zone (SGZ) of the dentate gyrus of the hippocampus in the adult mammalian brain. Adult endogenous neurogenesis not only plays an important role in the normal brain function, but also has important significance in the repair and treatment of brain injury or brain diseases. This article reviews the process of adult endogenous neurogenesis and its application in the repair of traumatic brain injury (TBI) or ischemic stroke, and discusses the strategies of activating adult endogenous neurogenesis to repair brain injury and its practical significance in promoting functional recovery after brain injury.
Adult ; Animals ; Humans ; Brain/physiopathology* ; Hippocampus/physiopathology* ; Mammals/physiology* ; Neurogenesis/physiology* ; Brain Hemorrhage, Traumatic/therapy* ; Ischemic Stroke/therapy* ; Recovery of Function ; Spinal Cord/physiopathology*

PURPOSETraumatic brain injury (TBI) is a leading cause of death and disability. Intracranial hemorrhage (ICH) secondary to TBI is associated with a high risk of coagulopathy which leads to increasing risk of hemorrhage growth and higher mortality rate. Therefore, antifibrinolytic agents such as tranexamic acid (TA) might reduce traumatic ICH. The aim of the present study was to investigate the extent of ICH growth after TA administration in TBI patients.

METHODSThis single-blind randomized controlled trial was conducted on patients with traumatic ICH (with less than 30 ml) referring to the emergency department of Vali-Asr Hospital, Arak, Iran in 2014. Patients, based on the inclusion and exclusion criteria, were divided into intervention and control groups (40 patients each). All patients received a conservative treatment for ICH, as well as either intravenous TA or placebo. The extent of ICH growth as the primary outcome was measured by brain CT scan after 48 h.

RESULTSAlthough brain CT scan showed a significant increase in hemorrhage volume in both groups after 48 h, it was significantly less in the TA group than in the control group (p = 0.04). The mean total hemorrhage expansion was (1.7 ± 9.7) ml and (4.3 ± 12.9) ml in TA and placebo groups, respectively (p < 0.001).

CONCLUSIONIt has been established that TA, as an effective hospital-based treatment for acute TBI, could reduce ICH growth. Larger studies are needed to compare the effectiveness of different doses.

Adult ; Antifibrinolytic Agents ; therapeutic use ; Brain Injuries, Traumatic ; diagnostic imaging ; drug therapy ; Cerebral Hemorrhage, Traumatic ; drug therapy ; Female ; Humans ; Male ; Middle Aged ; Single-Blind Method ; Tomography, X-Ray Computed ; Tranexamic Acid ; therapeutic use

Progressive hemorrhagic injury (PHI) can be divided into coagulopathy-related PHI and normal coagu- lation PHI. Coagulation disorders after traumatic brain injuries can be included in trauma-induced coagulopathy (TIC). Some studies showed that TIC is associated with PHI and increases the rates of disability and mortality. In this review, we discussed some mechanisms in TIC, which is of great importance in the development of PHI, including tissue factor (TF) hypothesis, protein C pathway and thrombocytopenia. The main mechanism in the relation of TIC to PHI is hypocoagulability. We also reviewed some coagulopathy parameters and proposed some possible risk factors, predictors and therapies.
Blood Coagulation Disorders ; epidemiology ; etiology ; Brain Injuries, Traumatic ; complications ; Cerebral Hemorrhage ; epidemiology ; etiology ; therapy ; Fibrin Fibrinogen Degradation Products ; analysis ; Humans ; Incidence ; Protein C ; physiology ; Risk Factors ; Thromboplastin ; physiology

Adolescent ; Adult ; Brain Hemorrhage, Traumatic ; complications ; etiology ; Craniocerebral Trauma ; complications ; diagnostic imaging ; Hearing Loss, Sensorineural ; diagnosis ; etiology ; physiopathology ; therapy ; Humans ; Male ; Radiography

After the spontaneous relief of initial symptoms by traumatic carotid-cavernous fistula (CCF), paradoxical worsening of patient's condition can be followed. We present a case of a 60-yr-old man whose audible bruit from a traumatic CCF had completely disappeared. A few days later, however, the patient had spontaneous intracerebral hematoma with cortical venous drainage. Complete obliteration of the fistula was achieved after embolization. When initial audible bruit in traumatic CCF disappears suddenly, cerebral angiography should be performed to differentiate venous hypertension by the hemodynamic changes of the cavernous sinus channels from spontaneous resolution of CCF.
Brain/pathology ; Carotid Arteries/pathology ; Carotid-Cavernous Sinus Fistula/*complications/*pathology/therapy ; Cerebral Angiography/methods ; Cerebral Hemorrhage, Traumatic/*etiology/therapy ; Humans ; Male ; Middle Aged ; Research Support, Non-U.S. Gov't ; Tomography, X-Ray Computed/methods