Spontaneous Cortical Spreading Depression and Intracranial Pressure Following Acute Subdural Hematoma in a Rat
Acute subdural hemorrhage (ASDH) is a frequent and devastating consequence of traumatic brain injury. Tissue damage develops rapidly and makes treatment even more difficult. Management of increased intracranial pressure (ICP) due to extravasated blood vol
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Abstract Acute subdural hemorrhage (ASDH) is a frequent and devastating consequence of traumatic brain injury. Tissue damage develops rapidly and makes treatment even more difficult. Management of increased intracranial pressure (ICP) due to extravasated blood volume and brain swelling is often insufficient to control all adverse effects of ASDH. In addition to sheer volume, spontaneously triggered cortical spreading depression (CSD) that leads to cell death following ischemia or trauma may contribute to injury development after ASDH. Therefore, we explored the occurrence of CSD by tissue impedance (IMP) measurement in a rat model subjected to ASDH. IMP and intraventricular and mean arterial pressure were monitored before (baseline), during (blood infusion), and after ASDH for 3 h. Tissue impedance increased by around 203% of baseline during subdural infusion of 300 ml of autologous, venous blood and dropped back to baseline within 22 min. Fifty-six minutes after the start of ASDH a cluster of four short-lasting (3–3.5 min; 140–160% of baseline) IMP increases started that reflected spontaneous CSDs. This pattern presumes that CSD occurs early after ASDH and therefore may contribute to the rapid lesion development in this disease. Keywords Cortical spreading depolarization • Acute subdural hematoma • Ischemia • Brain injury • Rat
B. Alessandri (), J.S. Tretzel, A. Heimann, and O. Kempski Institute for Neurosurgical Pathophysiology, University Medicine of the Johannes Gutenberg-University Mainz, D-55131 Mainz, Germany e-mail: [email protected]
Introduction Cortical spreading depression (CSD) is an electrophysiological phenomenon that was first described experimentally by Leão [14]. He found that spontaneous cortical activity is depressed for several minutes following electrical or mechanical stimulation and that this phenomenon spreads from the origin of stimulation. In uninjured tissue CSD is transient. Leão [15] also reported CSD following global ischemia. Since then CSD has been described in various animal models of human diseases [11, 20, 22, 25] and recently also in human patients [5, 7, 9]. Massive disturbance of ionic homeostasis is a basic reaction of CSD. These shifts lead to cell swelling and shrinkage of the extracellular space. Restoration of normal conditions is energy-dependent and the brain copes with vasodilatation [14]. Under pathophysiological conditions (e.g., focal ischemia), however, inverse hemodynamic reactions are observed in regions with pre-existing compromised blood flow. In this case gradients of cerebral blood flow (CBF), oxygen and glucose exist that allow initial persistent, anoxic depolarization in the ischemic core to become a transient depolarization in the surrounding tissue, with reduced CBF and energy supply and a CSD in healthy tissue [12, 16–18, 21]. Consequently, vasoconstriction and increased energy demand lead to cell death in the peri-ischemic area around the core, thereby expanding the injury. Such a chain of events may also play a crucial role in lesio
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