The Tangled History of Brain–Heart Pathways in Acute Brain Injury

  
By Eelco F. M. Wijdicks
First Online: 02 March 2021

When we try to reconstruct the complex discovery of heart–brain pathways, we find it has been moving from bench to bedside and back. Perhaps a good moment to start is around the turn of the century with Cushing, who among other European researchers, found that when intracranial pressure (ICP) rapidly increases, there are “Kussmaul-Tenner” spasms (extensor rigidity), bladder and bowel incontinence, apnea, and a “prominent vagus effect,” by which he meant bradycardia and eventually asystole. But the ICP must rise quickly above the mean blood pressure for this to occur. (Detailed results were published in a number of manuscripts [1,2,3,4]). In 1928, Heymans further refined Cushing’s findings by showing that an initial, hypertension-associated tachycardia occurred just before the onset of bradycardia [5]. This bradycardic response with hypertension became known as the Cushing reflex. We now understand this pattern as a state of sympathetic activation secondary to medullary hypoxia mediated by depolarization of rostral ventrolateral medulla (RVLM) presynaptic neurons [6].

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