doi: 10.1161/CIRCULATIONAHA.105.598706
(Circulation. 2006;113:e164-e165.)
© 2006 American Heart Association, Inc.
Correspondence |
Letter Regarding Article by Law et al, "Headaches and the Treatment of Blood Pressure: Results From a Meta-Analysis of 94 Randomized Placebo-Controlled Trials With 24 000 Participants"
Hypertension Unit, Heart Institute (InCor), University of Sao Paulo, Sao Paulo, Brazil
School of Medicine, University of Sao Paulo, Sao Paulo, Brazil
Is headache a cause or a consequence of hypertension? This apparently simple dilemma has not been answered over the last 100 years. All previous studies addressing this issue had important limitations, which left this as a medical impasse. The same seems to occur in a recent publication by Law et al1 in Circulation. After a judicious selection of 94 randomized trials with 4 classes of blood pressure–lowering drugs at fixed doses, the authors concluded that all classes reduce the prevalence of headache by one third, suggesting that high blood pressure is a cause of headache. Despite the robust study design, important points remain to be mentioned. First, the observation that blood pressure–lowering drugs prevent migraine is a well-established characteristic of many classes of antihypertensive drugs.2 Therefore, it is very likely that people in the interventional arm of the study would have fewer headaches than those in placebo arm. Second, none of the selected studies were designed to specifically evaluate the relationship between headache and hypertension; therefore, secondary analyses must be made with caution, because detailed information about the pattern of headache and its relationship with hypertension was completely absent in the majority of these trials. Previous studies showed no significant differences in blood pressure values before or during headache when 24-hour ambulatory blood pressure measurements were compared in patients with and without headache.3,4 Eventually, to improve our search for a cause-effect relation between headache and hypertension, it would be more appropriate to test the effects of analgesics on blood pressure. An interesting approach was explored recently in a randomized Brazilian study involving 100 patients who were helped in an emergency department.5 The authors compared symptomatic, chronic hypertensive patients’ therapeutic responses to symptomatic medication (dipyrone or diazepan) or an antihypertensive drug (captopril). The number of patients treated with a symptomatic drug who reached discharge criteria (patients reporting no symptoms, systolic pressure <180 mm Hg, and diastolic pressure <110 mm Hg) was similar to that of patients treated with antihypertensive drugs. These results no longer support the idea that headache could be a cause of high blood pressure and not a consequence, as suggested by Law et al.1 People with hypertension need treatment for hypertension, and people with headache need treatment for their headaches with prophylactic drugs, which could include antihypertensive drugs with prophylactic properties, or analgesics. Most of the time, analgesics would be a better, cheaper, and probably safer option.
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Dr Lotufo received grants from Bristol-Myers Squibb because of participation in the Clarity Study in 2003–2004 (enrollment of participants). The other authors report no conflicts.
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 Top References Acknowledgments References |
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1. Law M, Morris JK, Jordan R, Wald N. Headaches and the treatment of blood pressure: results from a meta-analysis of 94 randomized placebo-controlled trials with 24 000 participants. Circulation. 2005; 112: 2301–2306.
2. Bensenor IM, Lotufo PA. Headache, hypertension, and irbesartan therapy. Arch Intern Med. 2001; 161: 775–776.
3. Gus M, Fuchs FD, Pimentel M, Rosa D, Melo AG, Moreira LB. Behavior of ambulatory blood pressure surrounding episodes of headache in mildly hypertensive patients. Arch Intern Med. 2001; 161: 252–255.
4. Bensenor IJ, Lotufo PA, Mion D Jr, Martins MA. Blood pressure behaviour in chronic daily headache. Cephalalgia. 2002; 22: 190–194.[CrossRef][Medline] [Order article via Infotrieve]
5. Lima SG, Nascimento LS, Santos Filho CN, Albuquerque M de F, Victor EG. Systemic hypertension at emergency units: the use of symptomatic drugs as choice for management. Arg Bras Cardiol. 2005; 85: 115–123.
Dubai Police Medical Services, Dubai, United Arab Emirates
To the Editor:
Although Law et al1 show that blood pressure–lowering drugs prevent a significant proportion of headaches, the causal relation between hypertension and headache remains ambiguous. The statistically significant inverse relation between blood pressure—both systolic and diastolic—and nonmigrainous headache in the largest cross-sectional study2 indicates that there is a third critical, idiosyncratic, perfusion-related variable between hypertension and headache. Despite the general perception, migraine is not a pan-trigeminal disorder.3,4 In humans, pain and temperature fibers from only the ophthalmic area descend to the lower limit of the first cervical spinal segment; this long-held view, although controversial, is supported by sectional studies at and below the obex for severe trigeminal neuralgia. Additionally, photophobia of migraine is a reflex that involves the ophthalmic nerve. Finally, ipsilateral migraine aura or headache has never been reported after enucleation or evisceration of the eye.4 Headache, migrainous or nonmigrainous, primarily involves the ophthalmic division of the trigeminal nerve.
A nexus between migraine, autonomic dysfunction, and intraocular pressure (IOP) has been proposed recently.4 Autonomic hypofunction prevails in migraine patients and can underlie sudden ocular choroidal congestion in diverse stressful clinical circumstances; mechanical deformation of the corneoscleral envelope might generate both the scintillating scotoma and the headache of migraine.4 Remarkably, a higher blood pressure is correlated with a higher IOP.5 The tamponade function of IOP maintains ocular integrity; a higher IOP limits ocular choroidal hyperperfusion and possibly prevents the development of headache at relatively higher levels of blood pressure. Every physiological function has an upper threshold; the tamponade effect of rising IOP is probably overwhelmed in severe or malignant hypertension, hypertensive encephalopathy, and pheochromocytoma-related surges of blood pressure.
The common action by which migraine prophylactic agents prevent attacks likely involves a lowering of the IOP; propranolol, atenolol, metoprolol, nadolol, clonidine, flunarizine, verapamil, diuretics, and angiotensin-converting enzyme inhibitors lower IOP.4,5 Intriguingly, the prophylactic effect of migraine-preventing agents is not predictable or dose-dependent. Lowering IOP beyond a certain critical threshold, which varies for every individual, can aggravate the tendency to develop ocular choroidal congestion and mechanical deformation of the pressure-sensitive ophthalmic nerve fibers of the iris and the chamber angle.
Rather than being a simple function of blood pressure, headache in hypertension patients appears to be the outcome of a complex interaction between autonomic function, choroidal perfusion, and IOP, the many trait- and state-dependent factors that determine the mechanical properties of the corneoscleral envelope, and the endogenous pain-control mechanism.
Disclosures
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None.
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TopReferencesAcknowledgments References |
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1. Law M, Morris JK, Jordan R, Wald N. Headaches and the treatment of blood pressure: results from a meta-analysis of 94 randomized placebo-controlled trials with 24 000 participants. Circulation. 2005; 112: 2301–2306.
2. Hagen K, Stovner LJ, Vatten L, Holmen J, Zwart J-A, Bovim G. Blood pressure and risk of headache: a prospective study of 22 685 adults in Norway. J Neurol Neurosurg Psychiatry. 2002; 72: 463–466.
3. Gupta VK. Lamotrigine, migraine aura and headache: tightening the Gordian knot of primary headache? J Neurol Neurosurg Psychiatry. November 27, 2005. Available at: http://jnnp.bmjjournals.com/cgi/eletters/76/12/1730#764. Accessed January 25, 2006.
4. Gupta VK. Migrainous scintillating scotoma and headache is ocular in origin: a new hypothesis. Med Hypotheses. 2006; 66: 454–460.[CrossRef][Medline] [Order article via Infotrieve]
5. Klein BE, Klein R, Knudtson MD. Intraocular pressure and systemic blood pressure: longitudinal perspective: the Beaver Dam Eye Study. Br J Ophthalmol. 2005; 89: 284–287.
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