Sinus Headache and Migraine

Educational Objectives

The goal of this program is to improve the diagnosis and treatment of headaches. After hearing and assimilating this program, the clinician will be better able to:

1. Diagnose disorders that account for sinus headaches.

2. Discuss various theories and data supporting the high prevalence of migraine headaches in patients with sinus headaches.

Summary

Undiagnosed migraine sufferers often receive diagnosis of sinus and/or tension headaches: according to study by Lipton et al (2001), ≈14.6 million undiagnosed migraineurs in United States; diagnosis of “other” in 26%, tension-type headache (TTH) 32%, and sinus headache ≈44%

Sinus headache and migraine: study by Schreiber et al, 2004 — 2991 enrolled patients evaluated for International Headache Society (IHS) diagnosis of migraine; of patients who thought they had sinus headaches, 80% had IHS diagnosis of migraine with or without aura; another 8% had diagnosis of probable migraine; hence 88% of those thought to have sinus headache probably had migraine

Proposed mechanisms: possible interrelationship between sinus headache, rhinitis, paranasal anatomic abnormalities, and headache and/or migraine; activation of cranial parasympathetic nerves — study looking at ipsilateral autonomic symptoms in migraine patients (Obermann, 2007) found that cranial parasympathetic symptoms very common in patients with migraine headache; in many cases, more common in men than in women; interestingly, cluster headaches, with cranial autonomic symptoms, also more common in men than in women; activation of trigeminal nerve may result in reflex activation of cranial parasympathetic nerves, leading to autonomic symptoms; allergic and nonallergic rhinitis and chronic rhinosinusitis and mucosal contact points — sinuses and nares richly innervated by V1 and V2 distributions of trigeminal nerve; ethmoidal and nasopalatine main sensory nerves; they project to spinal nucleus of trigeminal nucleus; in intranasal study, Wolff took electrode and stimulated various parts within nares and paranasal sinuses and looked at areas of referred pain; different locations referred pain to common locations seen typically with migraine headaches; various mucosal contact points could activate trigeminal nociceptors and promote pain; theory of vacuum phenomena — occlusion of osteomeatal complex of maxillary sinus creates vacuum which could produce pain; peripheral release of inflammatory mediators — most likely hypothesis; histamines, prostaglandins, leukotrienes, or neuropeptides could activate peripheral nociceptors, either within nares or at dural level; propensity to activate mast cells in atopic individuals could, in theory, produce pain; theorized pathogenesis — various allergens bind to IgG antibodies bound to mast cells; mast cells release histamine, interleukins, and other inflammatory mediators; activation of trigeminal nerve, leading to release of various neuropeptides, eg, substance P, calcitonin gene-related peptide, neurokinin A; dilation of blood vessels occurs; every expansion and contraction of arteries, pulsatile pain similar to migraine produced; parasympathetic reflex then leads to release of variety of other chemicals from parasympathetic fibers, causing rhinorrhea and other symptoms

3 types of rhinitis: allergic — known exposure to allergen causes rhinitis symptoms; nonallergic — rhinitis symptoms present but allergy testing negative; patients often have nonallergic triggers, similar to triggers for migraine, eg, perfumes, cigarette smoke, diesel fumes, solvents, paint fumes; mixed — includes patients with allergic triggers and nonallergic symptoms

Study by Ku et al, 2006 — prevalence of migraine in patients with allergic rhinitis ≈35%, compared to ≈5% in primary care nonrhinitis group (highly statistically significant difference)

Allergy and migraine: mast cell degranulation occurs during migraine attack; plasma histamine levels increased in migraine patients both during ictal and interictal time periods, suggesting that histamine release could be part of migraine attack; intravenous allergen challenge in rats can induce plasma protein extravasation within dura, which can later be blocked by antihistamines; Alpay et al, 2010 — double-blind randomized controlled trial; IgG food testing on all migraine patients to find foods patients allergic to; randomized to diet that included or excluded these foods; frequency of migraine compared to baseline decreased by ≈25% in group that avoided these foods, whereas it remained same in group that received provocative diet; Migraine, Allergy and Rhinitis Study (MARS) — conducted in 3 outpatient allergy practice sites in Cincinnati, OH; 536 patients with allergic rhinitis underwent structured verbal headache diagnostic interview; all patients assigned migraine diagnosis based on International Classification of Headache Disorders (ICHD) criteria for migraine by headache specialists blinded to rhinitis diagnosis; all underwent allergy testing with 20 allergens indigenous to Cincinnati area; prevalence of migraine differed by whether patients received immunotherapy and based on age; age-immunotherapy interaction, ie, immunotherapy group had decreased prevalence of migraine at younger age as compared to nonimmunotherapy group; in older age groups, immunotherapy associated with higher prevalence of migraine, in contrast to lower prevalence of migraine in nonimmunotherapy group; self-reported frequency of migraine suggested that immunotherapy may be preventive for migraine attacks in younger patients; stratified analysis by age, in patients <45 yr of age and >45 yr of age showed this effect only in patients in younger age group; population data show atopy more prevalent in younger age group and peaks at age 22 yr; highly atopic individuals (³65% positive allergy tests) seemed to report higher frequency of migraine, especially in those <45 yr of age

Headache attributed to rhinosinusitis: defined by IHS as frontal headache accompanied by pain in face, ears, or teeth; clinical, endoscopic, computerized tomographic or magnetic resonance imaging evidence of acute-on-chronic sinusitis; headache and facial pain develop simultaneously with acute onset of symptoms; symptoms must resolve after successful treatment of infection; in American Academy of Otolaryngology criteria for rhinosinusitis, purulence in nasal cavity on endoscopic examination major criterion, headache minor criterion; facial pain, nasal obstruction, and headache decreased postoperatively in patients who underwent surgery for chronic rhinosinusitis (Bhattacharyya, 2004)

Mucosal contact point headaches: criteria include evidence that mucosal contact points exist and relief obtained with topical lidocaine or within 7 days after surgical correction; retrospective study of refractory or transformed migraine patients with mucosal contact points who all improved with topical anesthesia; study found that headache days decreased from 17.7 to 7.7 postoperatively; headache severity decreased; headache disability improved

Pathophysiology of rhinologic headaches: mucosal contact points; chronic sinusitis or frank infections of sinuses; vacuum phenomenon; these could directly activate trigeminal afferents leading to headache; other ways in which sinusitis and/or rhinitis could modulate headache or migraine include aggravation of obstructive sleep apnea (nasal steroids can decrease frequency of apneic episodes), insomnia, and depression; 2- or 3-hit theory — migraine nervous system; atopy occurs in ≈20% of population; some people born with or develop anatomic abnormalities; presence of >1 of these phenomena leads to different type of phenotype than typically seen; V1 distribution of trigeminal nerve not only trigger site for migraine; other branches of trigeminal nerve might be involved

Questions and Answers

Nonallergic rhinitis same as vasomotor rhinitis? no; nonallergic rhinitis consists of 2 subtypes, ie, vasomotor rhinitis and nonallergic rhinitis with nasal eosinophilia

Allergy and migraine: mast cell degranulation occurs during migraine attack; plasma histamine levels increased in migraine patients during both ictal and interictal time periods, suggesting that histamine release could be part of migraine attack; intravenous allergen challenge in rats can induce plasma protein extravasation within dura, which can later be blocked by antihistamines

Readings

Alpay K et al: Diet restriction in migraine, based on IgG against foods: a clinical double-blind, randomised, cross-over trial. Cephalalgia 30:829, 2010; Bhattacharyya N: Symptom outcomes after endoscopic sinus surgery for chronic rhinosinusitis. Arch Otolaryngol Head Neck Surg 130:329, 2004; Bisdorff AR: Management of vestibular migraine. Ther Adv Neurol Disord 4:183, 2011; Calhoun AH et al: The point prevalence of dizziness or vertigo in migraine and factors that influence presentation. Headache 51:1388, 2011; Cohen JM et al: Migraine and vestibular symptoms identifying clinical features that predict “vestibular migraine”. Headache 51:1393, 2011; Fasunla AF et al: ­Migraine-associated vertigo: a review of the pathophysiology and differential diagnosis. Int J Neurosci Dec 1, 2011 [Epub ahead of print]; Ku M et al: Prevalence of migraine headaches in patients with allergic rhinitis. Ann Allergy Asthma Immunol 97:226, 2006; Kurth T et al: Migraine and stroke: a complex association with clinical implications. Lancet Neurol 11:92, 2012; Liem MK et al: CADASIL and migraine: a narrative review. Cephalalgia 30:1284, 2010; Lipton RB et al: Migraine diagnosis and treatment: results from the American Migraine Study II. Headache 41:638, 2001; Mandell DM et al: Vessel wall MRI to differentiate between reversible cerebral vasoconstriction syndrome and central nervous system vasculitis: preliminary results. Stroke Dec 8, 2011 [Epub ahead of print]; Martin VT et al: Allergy and immunotherapy: are they related to migraine headache? Headache 51:8, 2011; Mathias CJ et al: Postural tachycardia ­syndrome-current experience and concepts. Nat Rev Neurol 8:22, 2011; Obermann M et al: Prevalence of trigeminal autonomic symptoms in migraine: a population-based study. Cephalalgia 27:504, 2007; Rubin DI, Cheshire WP: Evaluation of “dizziness” in the neurology office. Semin Neurol 31:29, 2011; Sadek AR et al: Posterior reversible encephalopathy syndrome: a case following reversible cerebral vasoconstriction syndrome masquerading as subarachnoid haemorrhage. Acta Neurochir (Wien) Jan 12, 2012 [Epub ahead of print]; Scarupa MD et al: Rhinitis and rhinologic headaches. Allergy Asthma Proc 25:101, 2004; Sousa A et al: ­Long-term ­follow-up of patients with postural tachycardia syndrome. Clin Auton Res Dec 22, 2011 [Epub ahead of print]; Schreiber CP et al: Prevalence of migraine in patients with a history of self-reported or physician-diagnosed “sinus” headache. Arch Intern Med 164:1769, 2004. Zhang H et al: Reversible cerebral vasoconstriction syndrome and subarachnoid hemorrhage: which occurs first? Intern Med 51:135, 2012.

Disclosures

In adherence to ACCME Standards for Commercial Support, ­Audio-Digest requires all faculty and members of the planning committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial interest. For this program, the following has been disclosed: Dr. Martin has received grants from GlaxoSmithKline, is a consultant and speaker for Allergan, is a speaker for Zogenix, and is a consultant for Nautilus, Nupath, and MAPP. The planning committee reported nothing to disclose.

Acknowledgements

Dr. Martin was recorded at the 25th Annual Practicing Physician’s Approach to the Difficult Headache Patient, held February 17-20, 2012, in Rancho Mirage, CA, and sponsored by Diamond Headache Clinic Research and Educational Foundation, Diamond Inpatient Headache Unit at Saint Joseph Hospital, Rosalind Franklin University of Medicine and Science. To learn more about CME meetings presented and jointly sponsored by Diamond Headache Clinic Research and Educational Foundation, Diamond Inpatient Headache Unit at Saint Joseph Hospital, Rosalind Franklin University of Medicine and Science, and Resurrection Health Care, visit www.­dhc-fdn.org. The ­Audio-Digest Foundation thanks the speaker and the sponsors for their cooperation in the production of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

OT451601

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.

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