학술논문
The neurocardiac axis in traumatic brain injury--an endless pathophysiological hot spot
Document Type
Academic Journal
Source
Journal of Hypertension Research. Oct-Dec 2020, Vol. 7 Issue 4, p124, 7 p.
Subject
Language
English
Abstract
Introduction Traumatic brain injury (TBI) continues to be one of the leading causes of mortality and disability in young adults [1-3]. Through high healthcare costs, this so-called 'silent epidemic' represents [...]
Traumatic brain injury (TBI) continues to be one of the leading causes of morbidity and mortality worldwide. Depending on the type of traumatic mechanical forces that act on the skull, primary polymorphic injuries may occur due to the direct impact. Secondary injuries are usually rapidly induced in the acute phase after the initial hit and are represented by neuroinflammation, cerebral edema, or ischemia. As in every acute stress condition, sympathetic activation is the primary and central pathophysiological alteration after TBI, being responsible for the more significant part of the systemic organ damage, systemic inflammation, and finally for the poor outcome. Massive catecholamine release translates into massive peripheral vasoconstriction and raised systemic vascular resistance, an entity frequently recognized as 'neurogenic hypertension'. Catecholamine cardiotoxicity may induce stress cardiomyopathy, characterized by myocytolysis or contraction band necrosis, induced by accelerated myocardial necrosis in a hypercontracted state. If stress cardiomyopathy was reported to occur simultaneously with a stressful event, like TBI, another similar entity named neurogenic stunned myocardium was described to arise secondary to the primary neurologic pathology. A reversible microcirculatory dysfunction has also been identified. Considering the rationale of beta-blocker use in patients with concomitant TBI and stress cardiomyopathy, further homogenous trials are needed to establish benefits and safety. Keywords: trauma brain injury, intracranial hypertension, heart-brain axis, neurogenic hypertension, catecholamine, stress cardiomyopathy, Takotsubo, neurogenic stunned myocardium.
Traumatic brain injury (TBI) continues to be one of the leading causes of morbidity and mortality worldwide. Depending on the type of traumatic mechanical forces that act on the skull, primary polymorphic injuries may occur due to the direct impact. Secondary injuries are usually rapidly induced in the acute phase after the initial hit and are represented by neuroinflammation, cerebral edema, or ischemia. As in every acute stress condition, sympathetic activation is the primary and central pathophysiological alteration after TBI, being responsible for the more significant part of the systemic organ damage, systemic inflammation, and finally for the poor outcome. Massive catecholamine release translates into massive peripheral vasoconstriction and raised systemic vascular resistance, an entity frequently recognized as 'neurogenic hypertension'. Catecholamine cardiotoxicity may induce stress cardiomyopathy, characterized by myocytolysis or contraction band necrosis, induced by accelerated myocardial necrosis in a hypercontracted state. If stress cardiomyopathy was reported to occur simultaneously with a stressful event, like TBI, another similar entity named neurogenic stunned myocardium was described to arise secondary to the primary neurologic pathology. A reversible microcirculatory dysfunction has also been identified. Considering the rationale of beta-blocker use in patients with concomitant TBI and stress cardiomyopathy, further homogenous trials are needed to establish benefits and safety. Keywords: trauma brain injury, intracranial hypertension, heart-brain axis, neurogenic hypertension, catecholamine, stress cardiomyopathy, Takotsubo, neurogenic stunned myocardium.