Hypertension Journal

Show Contents

Hypertension and Its Relation to Headache and Other CraniofacialNeuralgiform Pain
  JOHTN
REVIEW ARTICLE
Hypertension and Its Relation to Headache and Other Craniofacial
Neuralgiform Pain
Vimal Kumar Paliwal1, Ravi Uniyal2, Sucharita Anand1
1Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2Department of Neurology, King GeorgeMedical University, Lucknow, Uttar Pradesh, India
Address for correspondence: Dr. Vimal Kumar Paliwal, Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226 014,Uttar Pradesh, India
Phone: +91-9415419759
E-mail: dr_vimalkpaliwal@rediffmail.com
Received: 09-11-2017; Accepted: 12-12-2017
 
ABSTRACT
Both headache and hypertension are widely prevalent in the general population. This has led to a belief that headaches havesomething to do with hypertension. However, the relationship of headache to hypertension is not a linear one. Mild and probablythe moderate chronic hypertension do not seem to produce headache. Acute rise in blood pressure leading to hypertensive crisiscan produce headache that is usually temporally related to the onset of hypertension. Acute blood pressure surge may also producehypertensive encephalopathy and posterior reversible encephalopathy syndrome, which are associated with severe headaches.Headache is also one of the cardinal features of pheochromocytoma and preeclampsia/eclampsia. Craniofacial neuralgiformpains, especially trigeminal neuralgia (TN), have also been shown to worsen with hypertension and relieved with antihypertensivemedications in a subset of patients, thereby necessitating a need to understand the relationship of hypertension to TN and possiblywith other neuralgiform pains.
Keywords:Hypertensive crisis, hypertensive encephalopathy, posterior reversible encephalopathy syndrome, trigeminal neuralgia
How to cite this article: Paliwal VK, Uniyal R, Anand S.Hypertension and its relation to headache and other craniofacialneuralgiform pain. Hypertens 2018;4(1): 26-30.
Source of support: Nil
Conflict of interest: None
 
 

Introduction

Patients who suffer from headache are anxious to know the causeof their headache. Majority of the patients relate their headacheto either a refractory error or high blood pressure. However,despite correction of hypertension and the refractory error, theycontinue to have headaches. The relationship of headache withhypertension has interested the headache specialists for nearlyone century. T.C. Janeway first suggested the causal relationship ofhypertension to headache in 1913.[1] However, the relationship ofheadache with hypertension does not appear to be linear. There aremany unanswered questions. Can mild-to-moderate hypertensionproduce headache? Does headache produce high blood pressure?Can acute rise in blood pressure produce headache? Is headacherelated to chronic hypertension? Is headache an invariablesymptom in conditions associated with acute hypertension suchas pheochromocytoma, eclampsia, and preeclampsia? Is headachea symptom of hypertensive encephalopathy or malignanthypertension? What is the possible mechanism of a hypertensive headache? Are there any specific headache characteristics that canbe attributed to hypertensive headache?

 
These are some of the questions that the researchers havetried to answer in the last century. In this review, we will take upindividual case scenarios and try to address some of these questions.

Case 1

A 40-year-old gentleman complained of low-grade continuousheadache for 1 year. He had headache few hours after waking upin the morning. His headache was bilateral, non-pulsating, notrelated to physical activity, and not associated with photophobia,phonophobia, or vomiting. He was relieved of his headache forfew hours after taking a tablet of acetaminophen, but he usuallyavoided medicines. Incidentally, during a routine physicalcheckup 6 months back, he found that his blood pressure was140/90 mmHg. Since then, he has been keeping a record of hisblood pressure, which varied from 140 to 160 mmHg systolic and80 to 95 mmHg diastolic. He had a history of episodic migraine that lately became less mild but more frequent for past 18 months.He was not adequately relieved on amitriptyline and propranolol.He came with his blood pressure record and asked whether theuse of antihypertensive medicines will relieve his headache? Thepatient was prescribed amlodipine (5 mg/day) that controlledhis blood pressure but did not relieve his headache. Gradualuptitrating the dose of amitriptyline relieved his headache.

 
26 Hypertension Journal, January-March, Vol 4, 2018

Hypertension, headache and other craniofacial pains Paliwal, et al.

Headache Attributable to Mild-to-Moderate Chronic
Hypertension


This case scenario is not uncommon in the headache specialtyclinics. Most headache experts believe that mild chronichypertension (140-159/90-99 mmHg) and moderate chronichypertension (160-179/100-109 mmHg) does not produceheadache. The evidence came from the studies on ambulatory bloodpressure monitoring in patients with headache.[2,3] They found thatthe patient's mean blood pressure values during headache periodsand headache-free periods were not significantly different. Theblood pressure values 1 h before onset were not different fromblood pressure values at the time of onset of headache, therebysuggesting that even if the blood pressure was high in a subgroupof patients during headache periods, it was not the headache thatproduced hypertension. More importantly, they also found thatthe maximal blood pressure recordings in majority of these patientswere outside their headache periods. The above patient sufferedfrom tension-type headache that gradually evolved in frequencyfrom his usual migraine attacks (transformed migraine).

Based on these observations, international classificationof headache disorder 3rd edition suggests that the mild andmoderate hypertension may not cause headache.[4] However,since 30% of patients with headache in the above study hadmoderate hypertension, the relationship of headache secondaryto moderate chronic hypertension is still controversial.

Case 2

A 46-year-old gentleman complained of mild dyspnea on exertion,swelling over feet for 1 week, and acute severe, bilateral, and pulsatingheadache for 2 days. Headache was associated with occasionalvomiting but without photophobia and phonophobia. The patientexperienced exacerbation of headache on physical activity. Hewas a chronic smoker, tobacco chewer, and chronic alcoholic. Hewas not a known hypertensive or diabetic. He had headaches veryoccasionally in the past. On examination, he had blood pressure of190/130 mmHg, high jugular venous pressure, and tachypnea onsupine position, mild pedal edema, and mild hepatomegaly. Hischest auscultation revealed S3 gallop,Electrocardiogram (EKG)showed the left ventricular hypertrophy with strain pattern, normaltroponin I levels, and a two-dimensional echo was suggestive of signsof hypertensive heart failure. His fundus examination and a cranialcomputed tomography (CT) were also normal. He was admittedand started on the infusion of sodium nitroprusside that graduallyreduced his blood pressure to 140/80 mmHg over 1 day that alsopromptly relieved his headache and features of heart failure.

 
Headache Attributable to Acute Arterial Hypertension
Without Hypertensive Encephalopathy


ICHD 3rd edition classifies headache attributable to hypertensionwith blood pressure ≥180 mmHg systolic and ≥120 mmHg diastolicwith appearance of headache in temporal relation to rise in bloodpressure with/without relief from headache with reduction in bloodpressure and without evidence of pheochromocytoma, eclampsia/preeclampsia, or any other conditions that could better explainthe headache as headache attributable to arterial hypertension(10.3). When these hypertensive surges are not associated withend-organ damage like hypertensive encephalopathy, ICHD3rd edition refers these as headache attributable to hypertensive crisiswithout hypertensive encephalopathy (10.3.2).[4] The short-lastingheadaches are reported with acute blood pressure surges in theabsence of evidence of pheochromocytoma.[5] These hypertensiveattacks are also referred to as hypertensive urgencies where it maypresent with headache, epistaxis, and psychomotor agitation withoutevidence of end-organ damage secondary to hypertension.[6,7]

What is the Mechanism of Hypertension-related Headache?

The mechanism of headache by acute rise in blood pressure is notprecisely known. It is believed that with the acute rise in bloodpressure, the cerebral autoregulation comes into play to maintaincerebral perfusion and neurological functions. When the bloodpressure is high but amenable to cerebral autoregulation, theneurological functions remain intact, but there is vasoconstrictionof small cerebral arterioles (site of cerebral autoregulation).Therefore, the increased vascular resistance that is producedby cerebral small arteries and arterioles results in the increasedtransmural pressure in the large cerebral arteries that mainlyoccupy the base of the brain largely in the posterior fossa. Thecervical nerve roots supply these arterial walls and the stretchingof the walls of these arteries due to increased transmural pressureproduces a referred pain to occipital and neck region. Thatpossibly also explains the reason of occipital/nuchal headachessecondary to hypertension. However, these headaches can beglobal or frontal as seen in children with acute hypertension.

Are there any Specific Characteristics of Hypertensionrelated
Headache?


The ICHD 3rd edition recommends that the headacheoccurring secondary to hypertensive crisis without hypertensiveencephalopathy (10.3.2) has to be bilateral, pulsating quality, andit exacerbates with physical activity. The case 2 described aboveshowed all these characteristics. People have also describedbioccipital headaches, but headache can be generalized or frontalespecially in children. Nuchal headaches and headaches on wakingup in the morning or headaches causing early morning awakeningare also described as features of hypertensive headaches.[5,8,9]

Case 3

A 72-year-old gentleman presented with headache, altered behaviorwith irrelevant talks, episodes of loss of recent memory, social disinhibition, imbalance, and altered sleep-wake cycles for 12 days.His headache was bilateral occipital, nuchal, and throbbing and usedto exacerbate on walking and bending forward and was associatedwith vomiting at the peak intensity of headache. He was a knownhypertensive (on amlodipine 5 mg daily) with poor complianceon drugs. On examination, he was confused. His blood pressurewas 200/130 mmHg, with tachycardia, episodic diaphoresis,and episodes of extreme anxiety. Rest of the neurological andsystemic examination was normal. His fundus showed signs ofearly papilledema. His cranial magnetic resonance imaging (MRI)showed bilateral (right>left) occipital white matter hyperintensityon T2-weighted and fluid-attenuated inversion recovery images[Figure 1] with punctate hemorrhages on susceptibility-weightedimages. He was promptly treated with IV sodium nitroprussideinfusion that reduced his blood pressure to 150/90 mmHg within24 h. He completely recovered from headache and the highermental dysfunction. A repeat MRI scan showed near completeresolution of posterior white matter hyperintensities [Figure 1].

Hypertension Journal, January-March, Vol 4, 2018 27

Paliwal, et al. Hypertension, headache and other craniofacial pains

Headache Attributable to Hypertensive Encephalopathy

ICHD 3rd edition refers headaches that are temporally relatedto high blood pressure ≥ 180/120 mmHg and encephalopathy(confusion, lethargy, seizures, or visual abnormalities) as "headacheattributable to hypertensive encephalopathy (10.3.3). Additionalfeatures required are relief from headache with recovery fromhypertensive encephalopathy and, in addition, two of three headachecharacteristics - diffuse pain, throbbing character, and aggravation ofheadache on physical activity. When these patients have characteristicMRI picture as shown in Figure 1, the condition is called "posteriorreversible encephalopathy syndrome (PRES)." Unlike hypertensivecrisis without hypertensive encephalopathy, the blood pressure hererises beyond the range of cerebral autoregulation. Hence, failureof cerebral autoregulation results in cerebral hyperperfusion andvasogenic cerebral edema. Poor sympathetic innervation of posteriorcirculation results in predominant posterior predilection of vasogenicedema. Headache may be present in up to 50% of patients withPRES. Patients with chronic hypertension can also have papilledema,thereby referring the condition as "malignant hypertension." Thosewithout history of chronic hypertension may develop hypertensiveencephalopathy with < 180/120 mmHg of blood pressure. Theexamples of such conditions are pheochromocytoma and eclampsia.

Headache Attributable to Pheochromocytoma (10.3.1)

Pheochromocytoma produces episodic short-lasting headachesdue to episodic surge in blood pressure. It usually producesother signs of enhanced adrenergic drive such as palpitation,anxiety, sweating, and pallor. If the acute rise in blood pressureproduces symptoms of hypertensive encephalopathy, then thediagnosis of headache is coded as 10.3.3 (headache attributable tohypertensive encephalopathy). The most important characteristicis episodic short duration of headache that usually lasts < 1 h.[10]The headache is usually very severe, occipital, or may be frontalespecially in children, throbbing with increase in headache onexertion. The accompanying symptoms may be facial flushing, tremors, impending doom with severe anxiety, abdominal andchest discomfort, dyspnea, and vomiting.[11] Diagnosis requiresdemonstration of high urinary excretion of catecholamines orcatecholamine metabolites in a 24-h urinary sample. Abdominal CTscan demonstrates adrenal masses. Medical management requiresadequate sympathetic blockade by alpha-blockers followed bybeta-blockers. Definitive treatment is the excision of adrenalmasses. The features of adrenergic drive and headache usuallyresolve with the definitive treatment of pheochromocytoma

 
Headache Attributable to Eclampsia/Preeclampsia (10.3.4)

Headache is not unusual in pregnancy, and it is very commonto have a mild heaviness of head with other tension-type likeheadache characteristics. However, if the headache is severe,occurring for the 1st time in pregnancy, or with the recent changein character and severity and with new found high blood pressure,then these headaches should be considered as a cardinal features ofpreeclampsia.[12] It is important to identify such headaches becausemajority of patients will have headache prior to the onset of seizures.For ICHD 3rd edition diagnosis of "headache attributable topreeclampsia/eclampsia (10.3.4)," headache should appear duringpregnancy or postpartum period (up to 4 weeks) in a woman withdiagnosis of preeclampsia or eclampsia, and there should either betemporal correlation of occurrence of headache with preeclampsia/eclampsia or relief of headache in the postpartum state.

Case 4

A 45-year-old female complained of brief episodes of electricshock-like pain on the left side of face (V2 and V3 distribution)for 1 month. These episodes ranged from few seconds to2 min. Chewing, talking, and touching the face on affectedarea precipitated these pain attacks. She had 10-15 such painattacks daily. Incidentally, she was found to have hypertensionduring the evaluation of these pain attacks. Her neurologicalexamination was normal. Her cranial MRI revealed anteriorinferior cerebellar artery loop abutting the trigeminal nerve root[Figure 2]. She was started on amlodipine 5 mg and atenolol50 mg. Her blood pressure was normal on the subsequent visits.Interestingly, her pain episodes also disappeared. She continuedto remain normotensive and pain free for past 1 year.

Craniofacial Neuralgiform Pain And Hypertension

Among craniofacial neuralgiform pains, trigeminal neuralgia (TN)has been shown to have some association with hypertension. Thephenomenon of TNs worsening/precipitating by hypertensioncan possibly be explained by the fact that hypertension canlead to increase tortuosity of blood vessels.[13] Most patientswith TN show compression of trigeminal nerve root entry zoneby a tortuous blood vessel. This compression leads to focaldemyelination and ephaptic transmission with in the nerve fibers,thereby producing the typical symptomatology.[14] Uncontrolledhypertension may increase the blood vessel tortuosity, therebyworsening the compression and aggravation of symptoms. The reverse is probably responsible for amelioration of pain attackswith antihypertensive medications.

 
28 Hypertension Journal, January-March, Vol 4, 2018

Hypertension, headache and other craniofacial pains Paliwal, et al.

The relationship of TN and hypertension has been assessed in fewstudies but with ambiguous results.[15,16] Recently, a population-basedstudy clearly demonstrated significantly higher risk of developing TNin hypertensive patients.[17] Many authors have shown pain attacksof TN improving with antihypertensive medicines [Table 1].[18-21]However, a systematic and a relatively large-scale study is required tobring up a clear relationship of TN with hypertension.[22]

Antihypertensive Medicines Causing Headache

A systematic review on antihypertensive drugs effect on headacheshows that the antihypertensive medicines reduce headache, butthe effect is dependent on the class of medicines.[23] However,some antihypertensive medicines may produce headache as aside effect. These medicines include angiotensin-convertingenzyme inhibitors, angiotensin receptor blockers II, calciumchannel blockers, alpha-blockers, and direct vasodilators.The likely mechanism is their common property to produceintracranial vasodilatation. The headache is generally mild andmay improve with cold pack, hot bath, breathing exercises, orregular physical exercises. If the headache is severe and frequent,then there is a need to change the antihypertensive medication.

Headache And Ischemic Stroke

Headache may be a presenting feature of cerebellar infarcts.However, headache has been documented in other strokes. In arecent meta-analysis, 27% of patients with ischemic stroke hadheadaches.[24] The headache was associated with female sex,younger age, cerebellar stroke, history of migraine, and bloodpressure < 120/80 mm of Hg. The pathophysiology of headache in ischemic stroke could be distention or distortion of blood vessels,thereby stimulating the intracranial nociceptive afferents, arterialdissection (intracranial and extracranial), and involvement oftrigeminal vascular and cervical vascular systems.[25]

 
Hypertension and Its Relation to Headache and Other CraniofacialNeuralgiform Pain
Figure 1: (a) Cranial magnetic resonance imaging (MRI) fluidattenuatedinversion recovery image showing predominant parietooccipitalwhite matter hyperintensity that showed near completeresolution on a follow-up MRI (b)

Hypertension and Its Relation to Headache and Other CraniofacialNeuralgiform Pain
Figure 2: Axial images of fast imaging employing steady-stateacquisition sequence show the left anterior inferior cerebellar arteryloop (straight arrow) abutting trigeminal nerve root (curved arrow)

Table 1: Published case reports of trigeminal neuralgia that improved with antihypertensive therapy
Hypertension and Its Relation to Headache and Other CraniofacialNeuralgiform Pain

Hypertension Journal, January-March, Vol 4, 2018 29

Paliwal, et al. Hypertension, headache and other craniofacial pains

Conclusion

Hypertension may produce headache in certain circumstances.Acute rise in blood pressure in hypertension naive or chronichypertensive patients may produce headache in temporalrelation to rise in blood pressure. Hypertension when very severemay break the boundary of cerebral autoregulation and produceshypertensive encephalopathy and other organ dysfunctions inaddition to acute headaches. Certain hypertensive emergenciessuch as pheochromocytoma and eclampsia/preeclampsia haveheadache as an initial and a cardinal feature that sometimes isa reason for the diagnosis of these conditions. Cranial and facialneuralgiform pains, especially TN, are now shown to have someassociation with hypertension at least in a subset of patients, buttheir relationship needs to be established in the future studies.

REFERENCES
  1. Janeway TC. A clinical study of hypertensive cardio-vasculardisease. Arch Intern Med 1913;12:755-98.
  2. Gus M, Fuchs FD, Pimentel M, Rosa D, Melo AG, Moreira LB,et al. Behavior of ambulatory blood pressure surroundingepisodes of headache in mildly hypertensive patients. ArchIntern Med 2001;161:252-5.
  3. Kruszewski P, Bieniaszewski L, Neubauer J, Krupa-Wojciechowska B. Headache in patients with mild to moderatehypertension is generally not associated with simultaneousblood pressure elevation. J Hypertens 2000;18:437-44.
  4. Headache Classification Committee of the International HeadacheSociety (IHS) the International classification of HeadacheDisorders, 3rd edition. Cephalalgia 2018;38:1-211.
  5. Dodick DW. Recurrent short-lasting headache associated withparoxysmal hypertension: A clonidine-responsive syndrome.Cephalalgia 2000;20:509-14.
  6. Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin P.Hypertensive urgencies and emergencies. Prevalence andclinical presentation. Hypertension 1996;27:144-7.
  7. Weiss NS. Relation of high blood pressure to headache,epistaxis, and selected other symptoms. The United States healthexamination survey of adults. N Engl J Med 1972;287:631-3.
  8. Spierings EL. Acute and chronic hypertensive headache andhypertensive encephalopathy. Cephalalgia 2002;22:313-6.
  9. Cortelli P, Grimaldi D, Guaraldi P, Pierangeli G. Headache andhypertension. Neurol Sci 2004;25 Suppl 3:S132-4.
  10. Lance JW, Hinterberger H. Symptoms of pheochromocytoma,with particular reference to headache, correlated withcatecholamine production. Arch Neurol 1976;33:281-8.

 
  1. Mannelli M, Ianni L, Cilotti A, Conti A. Pheochromocytomain Italy: A multicentric retrospective study. Eur J Endocrinol1999;141:619-24.
  2. Franchesca FT, Robbins M. Clinical features and prognosisof headache in preeclampsia and eclampsia. Neurology2016;86:SI5.013.
  3. Hiroki M, Miyashita K, Oda M. Tortuosity of the white mattermedullary arterioles is related to the severity of hypertension.Cerebrovasc Dis 2002;13:242-50.
  4. Love S, Coakham HB. Trigeminal neuralgia: Pathology andpathogenesis. Brain 2001;124:2347-60.
  5. Teruel A, Ram S, Kumar SK, Hariri S, Clark GT. Prevalence ofhypertension in patients with trigeminal neuralgia. J HeadachePain 2009;10:199-201.
  6. Siqueira SR, Teixeira MJ, Siqueira JT. Clinical characteristics ofpatients with trigeminal neuralgia referred to neurosurgery. EurJ Dent 2009;3:207-12.
  7. Pan SL, Yen MF, Chiu YH, Chen LS, Chen HH. Increased riskof trigeminal neuralgia after hypertension: A population-basedstudy. Neurology 2011;77:1605-10.
  8. Uniyal R, Paliwal VK, Kumar N, Malhotra HS, Garg RK,Neyaz Z, et al. Teaching neuroimages: Amlodipine-responsivetrigeminal neuralgia: An alibi for vascular compression theory.Neurology 2017;89:e20.
  9. Lanzino G, Giordan E. Reader response: Teaching neuroimages:Amlodipine-responsive trigeminal neuralgia: An alibi forvascular compression theory. Neurology 2018;90:248.
  10. Conforti R, Parlato RS, De Paulis D, Cirillo M, Marrone V,Cirillo S, et al. Trigeminal neuralgia and persistent trigeminalartery. Neurol Sci 2012;33:1455-8.
  11. Sahin S, Kilinc Y, Karan NB, Ayrikcil S, Yilmaz D. Trigeminalneuralgia in a patient with vascular loop triggered byhypertension. J Anesth Crit Care Open Access 2017;9:335.
  12. Uniyal R, Paliwal VK, Malhotra HS, Garg RK, Kumar N. Authorresponse: Teaching neuroimages: Amlodipine-responsivetrigeminal neuralgia: An alibi for vascular compression theory.Neurology 2018;90:248.
  13. Webb AJ, Rothwell PM. The effect of antihypertensive treatmenton headache and blood pressure variability in randomizedcontrolled trials: A systematic review. J Neurol 2012;259:1781-7.
  14. Trentschert S, Wimmer R, Greisenegger S, Lang W, Lalouschek W.Headache at stroke onset in 2196 patients with ischemic stroke ortransient ischemic attack. Stroke 2005;36:e1-3.
  15. Kumral E, Bogousslavsky J, Van Melle G, Regli F, Pierre P.Headache at stroke onset: The Lausanne stroke registry. J NeurolNeurosurg Psychiatry 1995;58:490-2.

 
30 Hypertension Journal, January-March, Vol 4, 2018