6.8: Arterial hypertension

In cases of vascular hypertension unassociated with cerebral changes, Sutherland and Wolff (1940) likened the headaches to migraine attacks and stated that dilation of extracranial arteries is responsible for the pain. Although paroxysmal hypertension appears to be a sufficient mechanism of vascular headache, the relationship between chronic hypertension and headache remains unsettled. For many years, an occipital headache, present on awakening and disappearing as the day progressed, was regarded as the characteristic symptomatic expression of essential hypertension (Platt, 1950). However, according to Waters (1971), hypertension per se is an uncommon cause of headache. Despite the contentions of Sutherland and Wolff (1940), the mechanisms by which hypertension may precipitate vascular headache apparently vary. Stewart (1955) found that headache was significantly more frequent in patients who knew they were hypertensive than among those who did not know, suggesting an anxiety factor. It seems clear that waking headache (but not necessarily occipital) is more common in untreated than in treated hypertensive patients or in untreated control subjects (Bulpitt et al., 1976). In addition, the headache improves more often when the systolic blood pressure is reduced by 60 mm Hg than when it is reduced by only 35 mm Hg. On the other hand, Badran et al. (1970) found that headache was statistically more common in hypertensive patients only when their diastolic pressure exceeded 140 mm Hg.

In chronically hypertensive patients, the relationship between cerebral blood flow and mean arterial pressure is altered in that the range of blood pressure over which autoregulatory responses maintain constant cerebral blood flow is higher (Strandgaard et al., 1973), and there is evidence that this phenomenon occurs primarily at the level of the small resistance cerebral arteries (Stromberg and Fox, 1972). This shift in cerebral autoregulation may be caused by damaged small arterial walls or it may be a central nervous system response to hypertension. Since the shift is quite variable among hypertensive patients, the compensatory vascular response may be causally related to hypertensive headache, although there are no data to support this possibility.

It has been estimated that headache occurs in 75% of patients with hypertensive encephalopathy (Clarke and Murphy, 1956). The headaches associated with hypertensive encephalopathy are similar to those produced by intracranial tumors and may be produced by cerebral edema (Dalessio, 1980). In this setting, there initially is marked vasoconstriction of cerebral vessels leading to ischemia and localized edema. Associated focal or massive cerebral hemorrhage may also play a role in the production of severe headache in such patients. In hypertensive encephalopathy, the ophthalmoscopic changes are crucial to the diagnosis which is further substantiated when neurologic symptoms and signs as well as urinary changes and elevation of the serum urea nitrogen are found to be present. In some instances, hypertensive encephalopathy produces optic disc swelling that is indistinguishable from that produced by intracranial mass lesions. This topic is covered in elsewhere.

Patients with pheochromocytoma may develop a severe vascular headache (Bridgwater and Starling, 1982). Thomas et al. (1966) reviewed the histories of 100 patients with proven pheochromocytoma seen at the Mayo Clinic and found that episodic headache was present in 80%. It was usually of rapid onset, bilateral, severe, throbbing, and associated with nausea in about half of the cases. The headache usually lasted less than 1 hour and was accompanied by other symptoms of catecholamine release in 90% of patients. Paroxysms of hypertension often accompany the headache in this disorder (Gitlow and Mendlowitz, 1961). Measurements taken during headache range from 200/100 to 300/160 mm Hg; however, comparable elevations may be seen in those patients without headache. Patients with sustained hypertension are far less likely to experience headache than those with paroxysmal elevations of blood pressure. Attempts to relate the occurrence and severity of headache to the type of catecholamine secreted by the tumor have been unsuccessful (Lance and Hinterberger, 1976).

 

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