The Cushing response, reflex, triad, or “reaction,” as Cushing described it, occurs as a result of an abrupt increase in intracranial pressure. It consists of hypertension, bradycardia, and slow, irregular breathing elicited by the stimulation of mechanically sensitive regions in the paramedian caudal medulla (Hoff and Reis). Similar pressure-sensitive areas in the upper cervical spinal cord are also implicated in the Cushing response when intraspinal pressure is raised abruptly; a ventral medullary vasodepressor area that acts in the opposite manner has been found in animals. The proximate cause of the Cushing response is probably from mechanical distortion of the lower brainstem, either from a mass in the posterior fossa or, more often, from a large mass in one of the hemispheres or a subarachnoid hemorrhage that elevates the pressure within the fourth ventricle. Often, only the hypertensive component of the reaction occurs, with the systolic blood pressure reaching levels of 200 mm Hg, spuriously suggesting the presence of a pheochromocytoma or renal artery stenosis. The most severe instances of this type of centrally provoked hypertensive syndrome have occurred in children with cerebellar tumors who presented with headache and extreme systolic hypertension. Difficulty may arise in differentiating this response from hypertensive encephalopathy, especially from cases that derive from renovascular hypertension, which may likewise be accompanied by headache and papilledema. In differentiating these two, it is useful to note that primary hypertensive encephalopathy is associated with a tachycardia or normal heart rate and that systolic blood pressure levels above 210 mm Hg are attained only rarely in the Cushing response.
During episodes of intense sympathetic discharge of any type, there are alterations in the ECG, mainly in the ST segments and T waves; in extreme cases, evidence of myocardial damage can be observed. Both direct sympathetic innervation of the heart and the surge in circulating NE and cortisol are the cause of these findings. A similar hyperadrenergic mechanism has been proposed to explain sudden death from fright, asthma, status epilepticus, and cocaine overdose. Investigations by Schobel and colleagues had suggested that sustained sympathetic overactivity is responsible for the hypertension of preeclampsia, which may be considered in some ways as a dysautonomic state but this may be an oversimplification. Further information on these topics is contained in Chap. 34 and in the reviews by Samuels and Ropper.
A role has also been inferred for the ventrolateral medullary pressor centers in the maintenance of essential hypertension. Geiger and colleagues removed a looped branch of the posteroinferior cerebellar artery that had been apposed to the ventral surface of the medulla in 8 patients who had intractable essential hypertension; they found that 7 improved. Vascular decompression of cranial nerves has proved to be a credible therapeutic measure for hemifacial spasm and some cases of vertigo and trigeminal neuralgia, as discussed in Chap. 4, but the notion of vascular compression of the ventral medulla as a mechanism for typical essential hypertension requires confirmation before being accepted.
The Effects of Thoracolumbar Sympathectomy