Neurol Sci (2004) 25:S132–S134 DOI 10.1007/s10072-004-0271-y H E A D A C H E S A N D C E R E B R O VA S C U L A R D I S E A S E
P. Cortelli • D. Grimaldi • P. Guaraldi • G. Pierangeli
Headache and hypertension
Abstract Headache is generally regarded as a symptom of high blood pressure in spite of conflicting opinions on the association of headache and arterial hypertension. Most studies have shown that mild chronic hypertension and headache are not associated and this demonstration needs to be implemented in clinical practice. Whether moderate hypertension predisposes to headache remains controversial, but there is little evidence that it does. Headaches caused by significant disturbances in arterial pressure are included in the section “Headache attributed to adisorders of homeostasis” (code 10.3) of the 2nd edition of the International Classification of Headache disorders. Key words Headache • Arterial pressure • Hypertension
P. Cortelli () • D. Grimaldi • P. Guaraldi Dipartimento di Neuroscienze Università di Modena Via Del Pozzo 71, I-41100 Modena, Italy e-mail:
[email protected] G. Pierangeli Dipartimento di Scienze Neurologiche Università di Bologna, Bologna, Italy
An association between hypertension and headache was first proposed by Janeway in 1913 [1]. Many studies were subsequently done and conflicting results have emerged from investigations into the relationship between headache and arterial blood pressure. Bulpitt et al. observed that 31% of patients with untreated severe hypertension complained of headache compared with 15% of treated hypertensive patients and controls without hypertension [2]. Cooper et al., in a sample of 11 710 hypertensive patients, reported that headache was a common symptom related to high blood pressure levels [3]. Rasmussen, in a Swedish population-based study, observed that women with migraine showed significantly higher diastolic blood pressure than those without migraine [4]. By contrast, in another population-based study, Walters found no differences in systolic and diastolic blood pressure levels when individuals with headache were compared with individuals who had not had a headache in the previous year [5]. Two hundred consecutive patients with hypertension were studied by Stewart in 1953, with 96 of them aware of their blood pressure status. Among the people aware of their hypertensive status, 71 (74%) complained of headache, whereas among the 104 people who were not aware of their blood pressure status, only 17 (16%) complained of headache. Stewart concluded that once people become aware of their hypertension diagnosis, the frequency of reported headache increases [6]. Using data from the 1960–1962 United States Health Examination Survey of Adults, Weiss observed no differences in the occurrence of headache among 6672 normotensive and hypertensive people who were not aware of their blood pressure status [7]. Bensenor et al., using 24-hour ambulatory blood pressure monitoring, did not demonstrate any difference in blood pressure levels between women with and without chronic daily headache [8]. More recently, Hansson et al. [9] concluded that the incidence of headache can be reduced by antihypertensive treatment, in a study using data from seven randomised, double-blind, placebo-controlled trials.
P. Cortelli et al.: Headache and hypertension
However, many studies question the role of angiotensin II receptor antagonist in migraine prophylaxis and 50% of patients in this study were also randomised to aspirin or were using beta-blockers which are both drugs used for migraine prophylaxis [10]. Wiehe et al. evaluated the association between headache and hypertension in a sample of 1174 individuals aged over 17 years, representative of inhabitants of Porto Alegre, Brazil. Headache over their lifetimes or in the last year, defined as episodic and chronic tension type headache, was not associated with hypertension. Individuals with optimal or normal blood pressure complained of migraine more frequently than the participants with high-normal blood pressure or hypertension [11]. Enough data are now available to conclude that mild (140–159/90–99 mmHg) or moderate (160–179/100–109 mmHg) chronic arterial hypertension does not appear to cause headache. Whether moderate hypertension predisposes to headache remains controversial. Headaches caused by significant disturbances in arterial pressure are included in the section “Headache attributed to disorders of homeostasis” (code 10.3) of the 2nd edition of the International Classification of Headache disorders [12] which considers that hypertension due to the following can cause headache: pheochromocytoma, malignant hypertension, preeclampsia and eclampsia and acute pressor response to exogenous agents. Headaches due to severe hypertension are usually a bioccipital throbbing but can be generalised or a frontal throbbing (especially in children). The headache is often present in the morning on awakening. The diastolic blood pressure is usually elevated to 120 mmHg or higher.
10.3.1 “Headache attributed to pheochromocytoma” The most common symptom of pheochromocytoma is a rapid-onset headache that is reported by up to 92% of patients. The headache, which lasts less than an hour in 70% of cases, is bilateral, severe and throbbing, and may be associated with nausea in 50% of cases. Some patients may not get headaches even with blood pressures as high as 260/100 mmHg. Hypertension, which is paroxysmal in 50% and sustained in 50%, is found in 90% of patients. Paroxysmal hypertension may show elevations to 300/160 mmHg. Symptoms and signs of adrenergic stimulation are common with sweating, palpitations and tachycardia each reported by about 70% of patients. Anxiety, dizziness, abdominal pain, chest pain, weight loss, heat intolerance, nausea/vomiting, pallor (less often flushing), syncope, and orthostatic hypotension may also occur. Many patients have spells lasting between 15 and 60 minutes occurring from several times per day to once or twice a year. Paroxysms can begin spontaneously or be triggered by physical exertion, certain medications, emotional stress,
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changes in posture and increases in intraabdominal pressure. Laboratory and imaging studies are required to establish diagnosis. A 24-hour urine collection reveals elevations and sensitivity for diagnosis as follows: metanephrine and normetanephrine, up to 98%; vanillymandelic acid, 60–% to 70%; and total catecholamines, 60% to 79%. MRI of the abdomen, pelvis, chest and neck is almost 100% sensitive in detecting pheochromocytomas; CT scans have a sensitivity of 95% and specificity of 65% for detection of adrenal tumours. Scintigraphic imaging with I-131 metaiodobenzylguadnidine has a sensitivity of 88% and specificity of 99%. Indications include evaluation of extraadrenal, recurrent, or metastatic pheochromocytomas or those with silent adrenal masses and borderline catecholamine levels. The hypertension due to pheochromocytoma is treated first with slow upward titration of an alpha-blocker (e.g., prazosin, terazosin and phenoxybenzamine) and later addition of a betablocker for rate control after full alpha-blockade. A combination drug such as labetalol can sometimes be useful. Direct vasodilators, calcium channel blockers, and angiotensin-converting enzyme inhibitors are sometimes used cautiously when the hypertension is resistant to initial therapy. Surgical removal can be curative, especially in benign tumours.
10.3.2 “Headache attributed to hypertensive crisis without hypertensive encephalopathy” This is a headache associated with a hypertensive crisis (>160/120 mmHg) without clinical features of hypertensive encephalopathy. Usually, the headache is bilateral, pulsating and precipitated by physical activity and resolves within an hour after normalisation of blood pressure. Vasopressor toxins and medications have to be ruled out as causative factors.
10.3.3. “Headache attributed to hypertensive encephalopathy” Hypertensive encephalopathy is an acute cerebral syndrome due to sudden, severe hypertension. The rate and extent of the rise in blood pressure are the most important factors in the development of this condition. In those with chronic hypertension, hypertensive encephalopathy may not result unless the blood pressure is 250/150 mmHg or higher. A previously normotensive person may develop the encephalopathy with a lower elevation (160/100 mmHg). The presenting symptoms can be headache, nausea and vomiting. Complaints of blurred or dim vision, scintillating scotoma or visual loss may also be reported. Anxiety, agitation and then decreased levels of consciousness and
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sometimes seizures can follow. Papilledema and focal neurologic deficits can be present.
10.3.4 “Headache attributed to pre-eclampsia”; 10.3.5 “Headache attributed to eclampsia” Preeclampsia occurs in up to 7% of pregnancies and eclampsia is found in up to 0.3%. The criteria for preeclampsia include the following: proteinuria of more than 300 mg/day or two spot urines with more than 1 g protein/l collected more than 6 hours apart; oedema; hypertension persistently higher than 140/90 or relative hypertension with a rise over a first-trimester baseline blood pressure of at least 30 mmHg systolic or 15 mmHg diastolic; onset after the 20th week of gestation up to 48 hours post partum. Eclampsia occurs with the additional complications of seizures or coma. As many as 45% of cases of eclampsia have an onset post partum, with a mean of 6 days and up to 4 weeks. Risk factors for preeclampsia in primigravida are prepregnancy hypertension, obesity, multiple abortions or miscarriages, and cigarette smoking. The incidence of pregnancy-induced hypertension is greater in first or multiple pregnancies and in younger and older women.
10.3.’6 “Headache attributed to acute pressor response to an exogenous agent” A sudden severe headache can occur due to a rapid increase in blood pressure when patients taking monoamine oxidase inhibitors drink red wine or eat foods such as cheese, chicken livers, or pickled herring, which have a high tyramine content, or also take sympathomimetic medications such as pseudoephedrine. Use of illicit drugs with sympathomimetic actions such as
P. Cortelli et al.: Headache and hypertension
cocaine, methamphetamine and methylenedioxymethamphetamine (“ecstasy”) can also cause acute hypertension (sometimes leading to strokes) and headache.
References 1. Janeway TC (1913) A clinical study of hypertensive cardiovascular disease. Arch Intern Med 12:755–798 2. Bulpitt CJ, Dollery CT, Carne S (1976) Change in symptoms of hypertensive patients after referral to hospital clinic. Br Heart J 38(2):121–128 3. Cooper WD, Glover DR, Hormbrey JM, Kimber GR (1989) Headache and blood pressure: evidence of a dose relationship. J Human Hypertens 3(1):41–44 4. Rasmussen BK, Jensen R, Schroll M, Olesen J (1991) Epidemiology of headache in a general population – a prevalence study. J Clin Epidemiol 44(11):1147–1157 5. Walters WE (1971) Headache and blood pressure in the community. Br Med J 1(741):142–143 6. Stewart McD G (1953) Headache and hypertension. Lancet 1:1261–1266 7. Weiss NS (1972) Relation of high blood pressure to headache, epistaxis, and selected other symptoms. The United States Health Examination Survey of Adults. N Engl J Med 287(13):631–633 8. Bensenor IJ, Lotufo PA, Mion D, Martins MA (2002) Blood pressure behaviour in chronic daily headache. Cephalalgia 22(3):190–194 9. Hansson L, Smith DH, Reeves R, Lapuerta P (2000) Headache in mild-to-moderate hypertension and its reduction by irbesartan therapy. Arch Intern Med 160(11):1654–1658 10. Bensenor IJ, Lotufo PA (2001) Headache, hypertension, and irbesartan therapy. Arch Intern Med 161(5):775–776 11. Wiehe M, Fuchs SC, Moreira LB, Moraes RS, Fuchs FD (2002) Migraine is more frequent in individuals with optimal and normal blood pressure: a population-based study. J Hypertens 20(7):1303–1306 12. The International Classification of Headache Disorders, 2nd Edn. (2004) Cephalalgia 24[Suppl 1]:107–113
