Article, Neurology

The association between headache and elevated blood pressure among patients presenting to an ED

a b s t r a c t

Background: elevated blood pressure (BP) and headache have long been linked in the medical literature, although data on association are conflicting. We used previously collected data to address these related aims:

(1) using the National Hospital Ambulatory Medical Care Survey , we determined whether elevated BP is more likely in patients who present to an emergency department (ED) with headache than in patients who present with other complaints; (2) using data collected in 3 ED-based migraine clinical trials, we determined the association between improvement in headache pain and improvement in BP among patients who present to an ED with migraine and elevated BP; (3) using the data from the migraine clinical trials, we also determined if an elevated baseline BP identifies a group of patients less likely to respond to standard migraine treatment. Methods: We analyzed 2 distinct data sets. The first, NHAMCS, is a national probability sample of all US ED visits. The second is a compilation of data gathered during3 ED-based migraine randomized controlled trials. We defined elevated BP as follows: moderate elevation–systolic BP (SBP) >=150 mm Hg or Diastolic BP (DBP) >=95 mm Hg; marked elevation–SBP >=165 mm Hg or DBP >=100 mm Hg; and severe elevation–SBP >=180 mm Hg or DBP >=110 mm Hg. We report the association between headache and elevated BP in NHAMCS using odds ratios (ORs) with 95% confidence intervals (CI). We report the correlation coefficient and r2 for the association between improvement in BP and improvement in headache pain in our clinical trials data set. Finally, using our clinical trials database, we determined the influence of elevated BP at baseline on response to migraine medication by constructing a linear regression model in which the dependent variable was improvement in 0 to 10 pain score between baseline and 1 hour, and the primary predictor variable was presence or absence of elevated BP at baseline.

Results: Headache was the primary complaint in 3.7% (95% CI, 3.4-4.0%) of all US ED visits, corresponding to 4.8

million (95% CI, 4.2-5.4 million) patient visits. Among US ED patients, those with headache were more likely than patients with other chief complaints to have markedly (OR, 1.37; 95% CI, 1.16-1.61) or severely elevated BP (OR, 1.49; 95% CI, 1.17-1.90). In our clinical trials data set of patients with migraine with moderately elevated BP, there was no correlation between improvement in pain score and improvement in SBP (r = -0.07, r2 = 0, P =

.465) or DBP (r = -0.03, r2 = 0, P = .75). Similarly, there was no correlation between improvement in headache and improvement in BP among patients with migraine with markedly elevated BP (for SBP, r = -0.19, r2 = 0.04, P = .89; for DBP, r = -0.02, r2 = 0, P = .87), nor among patients with severely elevated BP (for SBP, r = 0.06, r2 = 0, P = .81; for DBP, r = 0.03, r2 = 0, P = .90). Patients with moderately elevated BP had slightly less improvement in their 0 to 10 pain score than patients with BPs below this cutoff (-0.6; 95% CI, -1.2 to -0.1; P =

.03). This was more pronounced among patients with markedly elevated BP (-0.9; 95% CI, -1.7 to -0.2). Conclusions: Although there is an association between elevated BP and headache among patients presenting to an ED, improvement in headache is not associated with improvement in BP.

(C) 2014

? Meetings at which this work has been presented: Society for Academic

Emergency Medicine, Atlanta, Georgia, May 2013.

?? Grant support: None.

? Conflicts of interest: None.

?? Author contributions: BWF conceived and designed the study. BM, JRW, and AW

abstracted data and reviewed the literature. BWF analyzed the data. BWF drafted the manuscript, and all authors contributed substantially to its revision. BWF takes responsibility for the article as a whole.

* Corresponding author at: Department of Emergency Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY, 10467. Tel.: +1 718 920 6626.

E-mail address: [email protected] (B.W. Friedman).

Background

Elevated Blood pressure and headache have long been linked in the medical literature [1], although data on association are conflicting. International guidelines stipulate that headache should be attributed to elevated BP if the systolic BP (SBP) rises rapidly to 180 mm Hg or higher, or if the diastolic BP rises to 120 mm Hg or higher, and if the headache resolves with normalization of BP [2]. This guideline statement is supported by ambulatory BP-monitoring studies in Hypertensive patients, which demonstrate that, in general,

http://dx.doi.org/10.1016/j.ajem.2014.05.017

0735-6757/(C) 2014

routine headache is not preceded by atypical fluctuations in BP [3,4]. Left unclear by these data is the role of elevated BP in headaches of sufficient intensity to warrant a visit to a medical provider, a not uncommon scenario; and the question of how to manage patients with both an acute headache, such as migraine, and elevated BP.

To help guide in the care of these patients, we used previously collected data to address these related aims: (1) using the National Hospital Ambulatory Medical Care Survey , a national database, we determined how frequently patients with headache present to an emergency department (ED) with elevated BP, and if elevated BP is more likely in patients who present to an ED with headache than in patients who present with other complaints; (2) using data collected in the course of 3 ED-based migraine clinical trials, we determined if there is an association between improvement in headache pain and improvement in BP among patients who present to an ED with migraine and elevated BP; (3) using the data from these 3 migraine clinical trials, we determined if an elevated baseline BP identifies a group of patients less likely to respond to standard migraine treatment.

Methods

Overview: Using 2 distinct databases, we assessed the relationship between headache and elevated BP among patients presenting to an ED. In the first database, a national probability sample designed to be representative of all US ED visits, we determined: (1) The frequency of elevated BP among patients presenting to EDs across the United States with headache, (2) the association between headache and elevated BP among all ED patients, and (3) ED treatment patterns with regard to elevated BP among headache patients. In the second analysis, we used data gathered during 3 ED-based migraine Randomized controlled trials to determine: (1) Whether improvement of headache in migraine research subjects with elevated BP is associated with improvement in BP and (2) whether elevated BP at baseline is associated with more refractory headaches. The Albert Einstein College of Medicine Institutional Review Board reviewed this study administratively and exempted it from further review.

Databases

The NHAMCS is a publically available data set collected and distributed by the National Center for Health Statistics. It is available at http://www.cdc.gov/nchs/ahcd.htm. Using a 4- stage probability sampling method, trained data extractors identify randomly selected ED visits at randomly selected emergency service areas from randomly selected hospitals from randomly selected regions of the United States. Trained analysts extract from the medical record the patient’s socio- demographic characteristics, characteristics of the patient’s chief complaint, presenting vital signs, workup, and treatment. We used the 2010 data set, which was the most current data set at the time of our analysis.
  • During the years 2005 to 2013, we completed 3 ED-based migraine randomized comparative efficacy trials in which patients presenting to 1 of 4 EDs with an acute migraine headache were treated with intravenous (IV) metoclopramide [5-7]. These migraine clinical trials used nearly identical inclusion and exclusion criteria and enrolled patients with nearly identical sociodemographic characteristics. Therefore, we felt it reasonable to combine the data from these similar studies into 1 data set for the purpose of this analysis. In each of these RCTs, research subjects had BP and pain scores assessed at baseline and 1 hour later. In the first study, an examination of the efficacy of dexamethasone, all subjects received metoclo- pramide (20 mg IV) + diphenhydramine (25 mg IV). Half of the subjects also received dexamethasone (10 mg IV), whereas the other half received IV placebo. This study was a negative
  • study–there were no differences between study arms in primary or secondary outcomes. The second study was a metoclopramide dose-finding study. ED patients with migraine were randomized to receive 10, 20, or 40 mg of IV metoclo- pramide. In this study, all research subjects also received diphenhydramine (25 mg IV). This study too was a negative study. The third study was a randomized comparison of metoclopramide (10 mg IV) vs. ketorolac (30 mg IV) vs. valproate (100 mg IV). To minimize heterogeneity in our BP analysis, we only used the data of research subjects treated with metoclopramide. We felt that including the data from those subjects randomized to ketorolac or valproate would introduce too much heterogeneity into our BP analysis.

    Measures

    National Hospital Ambulatory Medical Care Survey

    We used the following measures reported in NHAMCS:

    • Reason for visit. NHAMCS reports up to 3 reasons for visit for each patient visit. We considered patients to have presented to the ED for headache if their primary stated reason for visit was one of the following: (i) headache, pain in the head; (ii) migraine; or (iii) sinus problems (pain and pressure). We included sinus problems (pain and pressure) within our headache categorization because it is clear that many patients with migraine headache consider their headaches to be attributable to sinus disease [8]. Because we did not wish to include patients presenting primarily with rhinorrhea and congestion, we did not include patients whose primary chief complaint was one of the following: (i) sinus problems (unmodified); (ii) sinus problems (sinus inflammation, infec- tion); or (iii) sinus problems (sinus congestion). Similarly, we did not include patients whose secondary or tertiary reason for visit was headache because we did not wish to include patients who presented primarily for a febrile illness that included headache as one of a constellation of symptoms. In one of our analyses, we compare patients with headache to those patients who presented to the ED for management of abdominal pain. For the abdominal pain analysis, we used the following reason for visit codes: (i) stomach and abdominal pain, cramps, and spasms, including gastric pain; (ii) abdominal pain, cramps, spasms not otherwise specified (NOS), including abdominal discomfort, gas pain, and intestinal colic; (iii) lower abdominal pain, cramps, spasms, including Right lower quadrant pain, left lower quadrant pain, and inguinal pain; (iv) upper abdominal pain, cramps, spasms, including Epigastric pain, left upper quadrant pain, pain in umbilical region, and right upper quadrant pain.

    • Systolic BP (SBP). This was the patient’s presenting SBP.
    • Diastolic BP (DBP). This was the patient’s presenting DBP.
    • Antihypertensive medication was defined to include any of the following: agents for Hypertensive emergencies; angiotensin- converting enzyme inhibitors; anti-adrenergic agents, periph- erally acting; anti-adrenergic agents, centrally acting; anti- anginal agents; ?-adrenergic blocking agents; calcium channel blocking agents; diuretics; peripheral vasodilators; antihyper- tensive combinations; Angiotensin II inhibitors; and vasopres- sin antagonists

    5) We included the following covariates in the regression model described below:

    • Age in years. This was a continuous value
    • Sex. Reported as male or female
    • Race/ethnicity. Reported as Hispanic, non-Hispanic white, non-

    Hispanic black, or non-Hispanic other

    • Geographic region. Reported as northeast, midwest, southeast, west

    triage acuity. Reported as nonurgent, semiurgent, urgent, emergent, immediate.

    Clinical trials data set

    We extracted the following information from each of our data sets.

    • Pain score. Each research subject was asked to describe their headache intensity at baseline and again 60 minutes later using a 0 to 10 verbal integer scale, on which 0 signified no pain and 10 signified the worst pain imaginable.

    • SBP and DBP. Using an automated sphygmomanometer, research associates specifically trained to measure BP assessed it at baseline and again 60 minutes later.

      Analysis

      Definition of hypertension

      We reviewed the medical literature to determine standardized or evidence-based definitions for moderate and severe acute elevations in BP. We were unable to identify definitions that met these criteria. We therefore created the following definitions for this analysis:

      • Moderately elevated acute BP: SBP >=150 mm Hg or DBP >=95 mm Hg
      • Markedly elevated acute BP: SBP >=165 mm Hg or DBP >=100 mm Hg
      • Severely elevated acute BP: SBP >=180 mm Hg or DBP >=110 mm Hg.

        National Hospital Ambulatory Medical Care Survey

        In NHAMCS, each patient visit is assigned a weight, which incorporates the 4-stage sampling strategy and missing data. Representative national data can be calculated using this weight. Using the complex samples module from SPSS v. 21, we calculated the frequency, with 95% CI, of elevated BP among patients presenting with a chief complaint of headache; the OR, with 95% CI, of elevated BP among patients who presented for headache vs. those who presented for anything else; and the frequency, with 95% CI, of receipt of antihypertensive medications for each level of elevated BP. We performed a second analysis, in which we compared the frequency of elevated BP among those patients who presented with headache vs. those patients who presented with a chief complaint of abdominal pain. We identified abdominal pain as an appropriate comparator group because abdominal pain, like headache, can be caused by many different benign or malignant process and is often associated with nausea, vomiting, and anorexia, which may result in dehydration and lower BP. The frequency of elevated BP among patients with headache vs. patients with abdominal pain is also reported as ORs with 95% CI. Finally, to account for the influence of Sociodemographic variables and severity of illness on the relationship between chief complaint and BP, we built a logistic regression model in which we included chief complaint (headache or not headache) as the primary predictor variable and elevated BP (yes or no) as the dependent variable as well as the following covariates: age as a continuous value in years, sex, geographic region (northeast, midwest, southeast, and west), race/ ethnicity (Hispanic, non-Hispanic white, non-Hispanic black, and non-Hispanic other), and the patient’s triage urgency using a 5-tiered system (nonurgent, semiurgent, urgent, emergent, and immediate).

        Clinical trials data set

        For analysis of our clinical trial data, we calculated 1-hour improvement in headache as baseline headache score minus 1-hour headache score. We calculated 1-hour improvement in SBP as baseline SBP minus 1-hour SBP, and similarly for DBP. We calculated the correlation between these continuous data using Pearson r, reported the r2 and P value, and plotted the individual values using a scatterplot. To determine the influence of elevated BP on improve- ment in headache, we constructed a linear regression model in which

        presence of elevated BP was considered the primary predictor variable, the improvement in headache score was the dependent variable, and 4 dummy variables were created to account for the various doses of IV metoclopramide and the adjuvant therapy used in each of the trials. The influence of elevated BP on the improvement in pain score is reported with 95% CI.

        Results

        In 2010, there were 129.8 million (95% CI, 116.0-143.7 million) patient visits to US EDs. Headache was the primary complaint in 3.7% (95% CI, 3.4-4.0%) of these visits, corresponding to 4.8 million (95% CI, 4.2-5.4 million) patient visits.

        Of patients who presented to the ED with a primary complaint of headache, 23.9% (95% CI, 21.4-26.7%) had moderately elevated BP (SBP >=150 mm Hg or a DBP >=95 mm Hg) vs 22.3% (95% CI, 21.3-

        23.3%) of the nonheadache population. Among the patients with headache, 14.9% (95% CI, 13.0-17.1%) had markedly elevated BP (SBP

        >=165 mm Hg or DBP >=100 mm Hg) vs 11.4% (95% CI, 10.7-12.0%) of

        the nonheadache population. Similarly, 7.0% (5.6-8.7%) had severely elevated BP (SBP >=180 mm Hg or DBP >=110 mm Hg) vs 4.8% (4.4- 5.2%) of the nonheadache population. Odds ratios are presented in Table. The association between headache and elevated BP did not change substantially when we changed the comparison group from all nonheadache visits to abdominal pain visits nor when we performed a logistic regression model controlling for triage acuity and socio- demographic characteristics, in which those with a chief complaint of headache were compared to all other chief complaints (Table).

        Among patients who presented to the ED primarily for headache with moderately elevated BP, 21.7% (16.1-28.6%) were treated with an antihypertensive agent, vs 31.0% (22.4-41.0%) with markedly elevated BP, and 41.1% (27.9-55.8%) with severely elevated BP.

        In the RCT data set, 659 of 664 enrolled research subjects had baseline BPs recorded. Of these, 17% (112) met our criteria for moderately elevated BP, 60 (9.1%) met our criteria for markedly elevated BP, and 21 (3%) met our criteria for severely elevated BP.

        Among those with moderately elevated BP, there was no correlation between improvement in pain score and improvement in SBP (r = -0.07, r2 = 0, P = .465) or DBP (r = -0.03, r2 = 0, P =

        .75) (Fig. 1A and B). Similarly, among patients with markedly elevated BP, there was no correlation between improvement in headache and improvement in SBP (r = -0.19, r2 = 0.04, P = .89) or DBP (r = – 0.02, r2 = 0, P = .87) (Fig. 2A and B), nor among patients with severely elevated BP, for SBP (r = 0.06, r2 = 0, P = .81) or DBP (r = 0.03, r2 = 0, P = .90) (Fig. 3A and B).

        As demonstrated in Figs. 1 to 3, there was a reduction in BP between baseline and 1 hour of 10 to 30 mm Hg regardless of improvement in pain score. Because pain improvement was not driving this reduction, we sought alternative explanations. Specifi- cally, we determined whether baseline BP was associated with improvement in BP among patients with elevated BP. Indeed, baseline SBP did explain some of the variability in improvement in SBP (r = 0.36, r2 = 0.13, P b .01) and similarly with baseline DBP (r = 0.57, r2 = 0.33, P b .01) (Fig. 4A and B). The most plausible explanation for these observations is regression of abnormal values to values that more closely approximate population means.

        After adjusting for investigational medication, the presence of elevated BP at baseline had a small, but statistically significant, downward trend on pain relief. Patients with moderately elevated BP had slightly less improvement in their 0 to 10 pain score than patients with BPs below this cutoff (- 0.6; 95% CI, – 1.2 to – 0.1, P =

        .03). This effect was more pronounced among patients with markedly elevated BP (- 0.9; 95% CI, – 1.7 to – 0.2). Because only 21 patients had severely elevated BP, we did not repeat this analysis for those data.

        Table

        Odds (OR, 95% CI) of patients with headache having elevated BP at triage vs patients with other chief complaints

        Blood pressure Headache vs any other chief complaint Headache vs abdominal pain Headache vs any other chief complaint, controlling

        for triage acuity and sociodemographic characteristics

        Moderately elevated

        (SBP >=150 mm Hg or DBP >=95 mm Hg)

        Markedly elevated

        (SBP >=165 mm Hg or DBP >=100 mm Hg)

        Severely elevated

        (SBP >= 180 mm Hg or DBP >=110 mm Hg)

        1.10 (0.95-1.27) 1.06 (0.87-1.28) 1.27 (1.09-1.48)

        1.37 (1.16-1.61) 1.25 (1.01-1.55) 1.63 (1.38-1.93)

        1.49 (1.17-1.90) 1.57 (1.12-2.20) 1.87 (1.46-2.41)

        Limitations

        Limitations of working with NHAMCS have been well described previously [9]. Primary among these is the use of data that were

        Fig. 1. A, Improvement in SBP vs improvement in pain score over 1 hour among patients with migraine with SBP >=150 mm Hg or DBP >=95 mm Hg. The relationship between these variables is plotted as a line with 95% CI. B, Improvement in DBP vs improvement in pain score over 1 hour among patients with migraine with SBP >=150 mm Hg or DBP >=95 mm Hg. The relationship between these variables is plotted as a line with 95% CI.

        collected not for research purposes, but for clinical care. Stated reasons for visit may not have captured the patient’s true concern. Reliability and accuracy of the listed BP are unknown. Nevertheless, we do not believe there are systematic errors in these variables that would affect our results. Some data suggest that elevated BPs at triage tend to regress to the mean during subsequent ED course [10,11].

        Fig. 2. A, Improvement in SBP vs improvement in pain score over 1 hour among patients with migraine with SBP >=165 mm Hg or DBP >=100 mm Hg. The relationship between these variables is plotted as a line with 95% CI. B, Improvement in DBP vs improvement in pain score over 1 hour among patients with migraine with SBP >=165 mm Hg or DBP >=100 mm Hg. The relationship between these variables is plotted as a line with 95% CI.

        Fig. 3. A, Improvement in SBP vs improvement in pain score over 1 hour among patients with migraine with SBP >=180 mm Hg or DBP >=110 mm Hg. The relationship between these variables is plotted as a line with 95% CI. B, Improvement in DBP vs improvement in pain score over 1 hour among patients with migraine with SBP >=180 mm Hg or DBP >=110 mm Hg. The relationship between these variables is plotted as a line with 95% CI.

        Thus, the triage BP may not accurately reflect the BP 20 minutes later. This is a limitation that cannot be addressed using NHAMCS data. Finally, NHAMCS does not record data on a patient’s history of hypertension. Thus, we cannot know how many of these patients with elevated BP had hypertension or were being treated with antihypertensives.

        During the migraine clinical trials, we did not collect data regarding diagnosed history of hypertension, previous BPs, or use of antihypertensive medications. It is likely that patients with elevated BP included some with diagnosed hypertension taking multiple antihypertensives and others who had never been diagnosed with hypertension. Similarly, the normal BP group likely contained patients with a history of hypertension who were well controlled on antihypertensives. It may be that we have lumped distinct popula- tions. However, especially in an ED population, relying on markers of health care access to split groups of patients may result in a socioeconomic categorization more than a categorization based on biological phenomena.

        Fig. 4. A, Baseline SBP vs improvement in SBP between baseline and 1 hour among patients with migraine with SBP >=150 mm Hg or DBP >=95 mm Hg. The relationship between these variables is plotted as a line with 95% CI. The most likely explanation for the association depicted here is regression of abnormal systolic blood pressure values towards the population mean. B, Baseline DBP vs improvement in DBP between baseline and 1 hour among patients with migraine with SBP >=150 mm Hg or DBP >=95 mm Hg. The relationship between these variables is plotted as a line with 95% CI. The most likely explanation for the association depicted here is regression of abnormal diastolic blood pressure values towards the population mean.

        Discussion

        In this article, we used 2 complimentary databases to explore the relationship between elevated BP and headache among patients presenting to an ED. The NHAMCS, a national probability sample database, provided a wealth of data regarding ED practice across the country. Our migraine clinical trial database provided prospectively gathered data using a standardized methodology and validated instruments. Using these databases, we found that (1) elevated BP is common among ED patients who present with a chief complaint of headache; (2) ED patients with headache are more likely to have elevated BP than are ED patients with other chief complaints; (3) only a minority of patients who present to an ED with headache and elevated BP are treated with antihypertensive agents; (4) among patients who present to an ED with migraine and an elevated BP, there is no correlation between improvement in headache and improvement in

        SBP or DBP; and (5) among patients who present to an ED with migraine, elevated BP at baseline is associated with less headache relief. The NHAMCS data demonstrate that markedly and severely elevated

        BP is more common among patients who present to an ED with headache than among patients who present to an ED for any chief complaint other than headache or among those who present specifically for abdominal pain. Some have attributed elevated triage BPs among ED headache patients to pain or anxiety, confounding factors that may drive both the elevated BP and the need for an ED visit [12]. However, our data demonstrate that BP is higher among patients with headache even when compared to other ED patients and that this relationship is directly related to degree of BP elevation. Therefore, one can have more confidence that the association is in fact genuine and not confounded by psychological distress, a finding reflected in the work of Tanabe et al [13], who compared ED BPs to home BPs in a cohort of patients, and found that the elevation of ED BP above home BP could not be explained by pain or psychological distress. However, the directionality of this association between BP and headache, and the causal pathway are still unknown–one may hypothesize that elevated BP is causing headache, although it is just as likely that headache is causing elevated BP. Alternatively, the relationship may be confounded by a third variable we have not considered.

        The NHAMCS data also demonstrate that even marked elevations of BP in patients with headache usually are not treated with antihypertensive medications. However, the higher the BP, the more likely the patient is to receive an antihypertensive. Forty percent of headache patients who presented with SBP >=180 mm Hg or DBP

        >=110 mm Hg were treated with an antihypertensive, although 60% were not. Heterogeneity in clinical practice reflects uncertainty. Until high-quality clinical trial data are available, it will remain unclear how best to manage these patients. Some clinicians treat patients with acutely elevated BP with antihypertensives with the goal of prevent- ing morbidity or mortality. In our migraine clinical trials, we did not observe any BP-related adverse outcomes [5,6,7], lending some support to the practice of not treating elevated BP with antihyper- tensive in patients who present to an ED with migraine.

        Much to our surprise, among patients with migraine and elevated blood pressure, we did not identify an association between improve- ment in blood pressure and improvement in headache. An often- quoted aphorism in emergency medicine is that if one treats the pain, the blood pressure will improve–an observation that may rely on regression of abnormal values to the population mean. As depicted in Figs. 1, 2, and 3, among patients with elevated BP, there was a general improvement in BP of 10 to 30 mm Hg. Regression to the mean is a more likely explanation for this improvement than an association with relief of pain. Therefore, a therapeutic strategy aimed solely at lowering BP is unlikely to improve the headache.

        Although improvement in BP was not associated with improvement in headache among patients with elevated BP, a higher baseline BP was associated with worse Pain outcomes. Migraineurs with elevated BP reported less improvement on a 0 to 10 pain scale than migraineurs without elevated BP. This phenomenon was more striking among patients with higher baseline BP elevations. However, even among patients with higher BPs, the difference in outcomes falls below standard thresholds for minimum clinically significant difference [14].

        Therefore, the clinical impact of this finding is unlikely to be substantial. It is clear that antihypertensives prevent headache in outpatient populations [15]. On the basis of our data, it seems less likely that antihypertensives will benefit patients with migraine acutely.

        The relationship between BP and pain is complex. Since initial reports of an association between chronic Severe hypertension and headache [1], there have been countless attempts to understand this association more completely. There are robust outpatient data demonstrating that antihypertensive agents, regardless of class, prevent headache, thereby suggesting that lowering BP itself can prevent headache [15]. On the other hand, some population data and laboratory work suggest that chronic hypertension and acutely elevated BP moderate nociception, a phenomenon named hyperten- sion-associated hypalgesia [16]. We do not have a ready explanation for the association between high BP and headache we discovered in the NHAMCS data. For all those patients who ask us, “Is my high BP causing my headache?” we can only answer “maybe.”

        In conclusion, while there is an association between elevated blood pressure and headache among patients presenting to an emergency department, it is not clear how best to manage these patients.

        References

        1. Janeway TC. A clinical study of hypertensive cardiovascular disease. Arch Intern Med 1913;12:755-98.
        2. The international classification of headache disorders, 3rd edition (beta version). Cephalalgia 2013;33:629-808.
        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;161:252-5.
        4. Kruszewski P, Bieniaszewski L, Neubauer J, Krupa-Wojciechowska B. Headache in patients with mild to moderate hypertension is generally not associated with simultaneous blood pressure elevation. J Hypertens 2000;18:437-44.
        5. Friedman BW, Greenwald P, Bania TC, et al. Randomized trial of IV dexamethasone for acute migraine in the emergency department. Neurology 2007;69:2038-44.
        6. Friedman BW, Mulvey L, Esses D, et al. Metoclopramide for acute migraine: a dose-

          finding randomized clinical trial. Ann Emerg Med 2011;57:475-482 e1.

          Friedman BW, Garber L, Yoon A, et al. Randomized trial of IV valproate vs metoclopramide vs ketorolac for acute migraine. Neurology 2014;82:976-83.

        7. Eross E, Dodick D, Eross M. The Sinus, Allergy and Migraine Study (SAMS). Headache 2007;47:213-24.
        8. McNaughton CD, Self WH, Pines JM. Annals of Emergency Medicine Journal Club. Observational health services studies using nationwide administrative data sets: understanding strengths and limitations of the National Hospital Ambulatory Medical Care Survey: answers to the May 2013 Journal Club questions. Ann Emerg Med 2013;62:425-30.
        9. Pitts SR, Adams RP. Emergency department hypertension and regression to the mean. Ann Emerg Med 1998;31:214-8.
        10. Cienki JJ, Deluca LA, Feaster DJ. Course of untreated high blood pressure in the emergency department. West J Emerg Med 2011;12:421-5.
        11. Denny CJ, Schull MJ. Headache and facial pain. In: Tintinalli JE, Strapcyznski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, editors. Tintinalli’s emergency medicine: a comprehensive study guide. 7th ed. New York: McGraw Hill; 2011.
        12. Tanabe P, Persell SD, Adams JG, McCormick JC, Martinovich Z, Baker DW. Increased blood pressure in the emergency department: pain, anxiety, or undiagnosed hypertension? Ann Emerg Med 2008;51:221-9.
        13. Todd KH, Funk JP. The minimum clinically important difference in physician- assigned visual analog pain scores. Acad Emerg Med 1996;3:142-6.
        14. 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;112:2301-6.
        15. Ghione S. Hypertension-associated hypalgesia. Evidence in experimental animals and humans, pathophysiological mechanisms, and potential clinical conse- quences. Hypertension 1996;28:494-504.