Hypertension affects more than a quarter of the world's adult population.
Essential, or primary, or idiopathic hypertension is historically defined as a rise in blood pressure (BP) without any known causes, which still accounts for ≈95% of all hypertension 1).
Ever since the identification of hypertension in 1872, researchers have struggled to find its cause(s) with only minor successes 2).
Whereas multiple risk factors for hypertension, including genetic variations, obesity, insulin resistance, high alcohol intake, and stress, have been identified, primary causes for hypertension remain elusive. Also, the predictive factors for its development are unclear 3) 4) 5).
Despite medical advancements, no underlying cause can be found in more than 9 out of 10 patients with hypertension. Although elevated sympathetic nervous activity contributes to the development of hypertension, the mechanism by which this occurs remains poorly understood 6).
The so-called Cushing reflex has been suggested to explain arterial hypertension. According to this mechanism, hypoperfusion of the rostral ventrolateral medulla induces sympathetic nervous system activation and a pressor response. The pressor response then increases perfusion of a primary brain area regulating sympathetic activity, but in doing so heightens systemic blood pressure. The initial hypoperfusion could arise as a result of narrowed vertebral arteries—evident as high resistance and low flow in these arteries. Although systemic hypertension might lead via remodeling to a narrowing of vertebral arteries, it has been suggested that hypertension is the result of narrowed vertebral arteries rather than the cause 7).
There are anatomical and physiological evidences that the ventrolateral (VL) region of the medulla plays an important role in blood pressure regulation and that dysfunction at this level may generate hypertension (HT). Vascular compression by a megadolicho-artery from the vertebrobasilar arterial system at the root entry/exit zone (REZ) of the glossopharyngeal (IXth) and vagal (Xth) cranial nerves (CNs) and the adjacent VL aspect of the medulla has been postulated as a causal factor for HT from neurogenic origin. The first attempts at microvascular decompression (MVD) of the IX-Xth CNs together with the neighbouring VL brainstem was revealed promising.
Established criteria for indication of MVD as an aetiological treatment of apparent essential HT are still needed 8).
Renovascular disease is a well-described cause of hypertension, which is caused by the increase in renin secretion with subsequent increase in angiotensin and aldosterone but is found to be a primary cause in a minority of cases 9).
Hypertension is refractory to treatment in ≤20% to 30% of cases despite the availability of numerous classes of antihypertensives, and finding primary cause could improve treatment of refractory hypertension 10)..
Elevated blood pressure (BP), which presents in approximately 80 % of patients with acute intracerebral hemorrhage (ICH), is associated with increased risk of poor outcome.
Volume expansion and hypertension are widely used for the hemodynamic management of patients with subarachnoid hemorrhage to prevent delayed cerebral ischemia.
Given the suggestion of possible worse neurobehavioral outcome with augmented blood pressure (ABP), a larger trial to determine the optimal blood pressure management in this patient population is warranted (ClinTrials.gov NCT01414894.) 16).
Lenticulostriate artery are particularly susceptible to damage from hypertension. They may either rupture, producing an intracerebral hemorrhage that is initially centered in the region they supply, or become occluded producing a lacunar infarct in the tissue they supply.