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pressure It consists of a triad 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 a 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 causing a transmitted pressure 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 mmHg, spuriously suggesting the presence of a pheochromocytoma or renal artery stenosis In our experience, 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 Dif culty 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 making a differentiation between these two, it is useful to note that hypertensive encephalopathy is associated with a tachycardia or normal heart rate and that systolic blood pressure levels above 210 mmHg are attained only rarely in the Cushing response In relation to the third type of sympathetic hyperactivity, Pen eld described paroxysms of hypertension, intense diaphoresis, ushed skin, and mydriasis in comatose patients and attributed them to epilepsy (diencephalic seizures), although his original patient had a tumor obstructing the foramen of Munro Many similar types of attacks have been described, additional features being a slight rise in temperature just prior to the paroxysm, cyclic respirations, and shivering Often the bedsheets become soaked and the patient s forehead is covered by beads of sweat Most patients who exhibit such paroxysms are decorticate from traumatic lesions of the deep cerebral white matter or from acute hydrocephalus (the likely explanation of Pen eld s cases); in any case, they are clearly not epileptic We have conceptualized these attacks as the result of the removal of inhibitory in uences on the hypothalamus, creating, in effect, a hypersensitive decorticated autonomic nervous system The condition is perhaps analogous to overactivity of the extensor and opisthotonic posturing mechanisms that appear with little provocation in the same clinical settings Morphine and bromocriptine have been helpful in suppressing but not eliminating the attacks, and beta-adrenergic blockers reduce the hypertension and tachycardia 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 The role of direct sympathetic innervation of the heart in producing these myocardial abnormalities is unclear, but in the cases of subarachnoid hemorrhage and traumatic brain injury, the surge in circulating NE and cortisol is postulated as the cause A similar hyperadrenergic mechanism has been proposed to explain sudden death from fright, asthma, status epilepticus, and cocaine overdose Investigations by Schobel and colleagues have suggested that sustained sympathetic overactivity is responsible for the hypertension of pre-eclampsia, which may be considered in some ways as a dysautonomic state Further information on these topics is contained in the reviews by Samuels and by Ropper
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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 valid mechanism for essential hypertension requires con rmation The Effects of Thoracolumbar Sympathectomy Surgical resection of the thoracolumbar sympathetic trunk, widely used in the 1940s in the treatment of hypertension, has provided the clinician with the clearest examples of extensive injury to the peripheral sympathetic nervous system, though a similar defect had long been suspected in one type of primary orthostatic hypotension (see above) In general, bilateral thoracolumbar sympathectomy results in surprisingly few disturbances Aside from loss of sweating over the denervated areas of the body, the most pronounced abnormality is an impairment of vasomotor re exes In the upright posture, faintness and syncope are frequent because of pooling of blood in the splanchnic bed and lower extremities; although the blood pressure may fall steadily to shock levels, there is little or no pallor, nausea, vomiting, or sweating the usual accompaniments of syncope Bladder, bowel, and sexual function are preserved, though semen is sometimes ejaculated into the posterior urethra and bladder No consistent abnormalities of renal or hepatic function have been found
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