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Headache During a Cluster of Benign Paroxysmal Positional Vertigo Attacks Lea Pollak and Eitan Pollak Ann Otol Rhinol Laryngol published online 11 July 2014 DOI: 10.1177/0003489414539921 The online version of this article can be found at: http://aor.sagepub.com/content/early/2014/07/06/0003489414539921
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539921
research-article2014
AORXXX10.1177/0003489414539921Annals of Otology, Rhinology & LaryngologyPollak and Pollak
Article
Headache During a Cluster of Benign Paroxysmal Positional Vertigo Attacks
Annals of Otology, Rhinology & Laryngology 1–6 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0003489414539921 aor.sagepub.com
Lea Pollak, MD1, and Eitan Pollak, BA2
Abstract Objective: In view of patients’ recurrent complaints, we were interested in investigating the frequency and headache characteristics in patients during a benign paroxysmal positional vertigo (BPPV) cluster. Methods: Patients with BPPV treated at an outpatient dizziness clinic were interviewed about the presence of headache; its quality, localization, severity, time course, and aggravating and alleviating factors; and headache-related disability during their present vertigo cluster. Results: Among 152 patients with BPPV, 53 (34.8%) reported headache associated with vertigo. According to The International Classification of Headache Disorders, 8 (15%) patients could be classified as migraine without aura (1.1), 14 (26%) were classified as infrequent episodic tension-type headache associated with pericranial tenderness (2.1.1), 23 (43%) were classified as infrequent episodic tension-type headache without pericranial tenderness (2.1.2), 6 (11%) had cervicogenic headache (11.2.1), and in 2 (4%) patients, the headache could not be specified (14.2). Fifty-two age-matched BPPV patients without headache did not differ in history of headaches, BPPV history, or background diseases. The distribution of canal involvement and number of treatment maneuvers was also similar in both groups. Conclusion: Headache is frequent in BPPV. The most common is tension-type headache, followed by migraine and cervicogenic headache. Head pain seems to be an independently associated epiphenomenon of BPPV that can worsen patients’ distress. Keywords BPPV, headache
Introduction Headache can be encountered in peripheral as well as central vestibular disorders. In vestibular migraine, it constitutes one of the cardinal symptoms.1 Patients with Ménière’s disease and vestibular neuronitis can report occipital and neck pain.2 Patients with mal de debarquement syndrome— a motion triggered sensation of rocking—often develop new onset headache along with the dizziness.3 Headache presenting with central vestibular findings should always raise suspicion of a possibly life-threatening structural lesion in the posterior fossa, such as tumor or hemorrhage. The interrelation of headache and vestibular diseases has been demonstrated also during interictal periods. Vestibular abnormalities have been found not only in patients with vestibular migraine but also in patients with migraine without vertigo and chronic tension headache.4 The lifetime prevalence of migraine was found to be higher in patients with Ménière’s disease and benign paroxysmal positional vertigo (BPPV).5,6 In practice, we often meet patients with BPPV who complain about headache during the vertigo attack. This issue has garnered little attention in the literature so far. In view
of patients’ recurrent complaints, we were interested in investigating the frequency and headache characteristics in patients during a BPPV cluster.
Methods Patients diagnosed with BPPV at an outpatient dizziness clinic were asked for the occurrence of headache during the present BPPV cluster (the period of recent BPPV attacks). Those reporting headache were included in the study. Patients with secondary headaches (ie, previous trauma, tumor, metabolic, or vascular causes) were a priori excluded. Neuroimaging (brain computed tomography [CT] or magnetic resonance imaging [MRI]) was obtained in patients where the headache represented a dominant complaint, the 1
Department of Neurology, Assaf Harofeh Medical Center, affiliated with the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel 2 Haaretz Daily Newspaper,Tel Aviv, Israel Corresponding Author: Lea Pollak, MD, Kibutz Galuyot 4, 74012, Nes Ziona, Israel. Email: [email protected]
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Annals of Otology, Rhinology & Laryngology
Table 1. Characteristics in Patients With and Without Headache.
Mean age, y, mean ± SD Males/females, n Positive history of previous headaches, % First BPPV attack (vs recurrent attacks), % Posterior canal type (vs other canal types), % One treatment (vs multiple treatments), % Presence of autonomic symptoms, %
Patients With Headache (n = 53)
Patients Without Headache (n = 52)
P Value
61.2 ± 13.7 13/40 59 21 80 63 64
62.1 ± 14.2 12/40 69 29 78 58 29
NSa NSa NSa NSa NSa NSa < .001
Abbreviations: BPPV, benign paroxysmal positional vertigo; NS, statistically nonsignificant. a P ≥ .05.
headache differed from headaches experienced in the past, the headache preceded or outlasted the vertigo attack by more than 2 weeks, or the treatment response was not satisfactory (53% of patients). The patients underwent a complete neurological examination. Tenderness of the pericranium and neck was examined by applying digital pressure over the trigger points such as the temporal and masseter muscles and the occipitonuchal area. The diagnosis of BPPV was established by a positive Dix-Hallpike or roll test.7 Following the diagnostic test, the patients were treated by an appropriate particle repositioning maneuver (Epley maneuver for posterior and anterior canal variant and barbecue treatment for horizontal canal BPPV). Patients were seen again within 1 week after the treatment. If necessary, the treatment was repeated at 3- to 7-day intervals until disappearance of nystagmus on testing. A semistructured questionnaire (available online) concerning headache quality, localization, severity, and time course was administered by the treating neurologist (L.P.). Patients were also asked about symptoms accompanying the headache, aggravating and alleviating factors, the use of analgesics, and headache-related disability. The type of headache was then classified according to The International Classification of Headache Disorders (ICHD-II).8 Fifty-two consecutive age-matched BPPV patients without headache during the present or previous BPPV clusters served as controls. The background diseases of both groups of patients were categorized according to system involvement, whereas patients with malignancies were grouped into 1 category regardless of organ involvement (cardiovascular, ocular, metabolic, rheumatologic and orthopedic, psychiatric, otolaryngological, oncological, neurological, gastrointestinal, pulmonary, and hematological diseases). The study was performed in accordance with the Declaration of Helsinki and approved by the local ethics committee. With regard to statistical methods, a paired-samples t test was applied for comparison of age in both groups of
patients. The chi-square test was applied for comparing categorical variables such as the headache and BPPV characteristics between both groups. A P value of < .05 was considered statistically significant. SPSS version 18 (SPSS Inc, Chicago, Illinois, USA) was used for the analyses.
Results Patient Characteristics Among 152 patients treated for BPPV during the years 2011 to 2012, 53 (34.8%) reported headache associated with the present BPPV cluster. Eighty percent of patients had a posterior canal type, 9% had bilateral posterior canal BPPV, and horizontal and anterior canal type of BPPV was found in 7% and 4% of patients, respectively. The mean duration of symptoms until diagnosis and treatment was 1.4 ± 1.3 months (Table 1). In the control group, 78% of patients had posterior canal BPPV, 10% bilateral posterior canal BPPV, 8% horizontal, and 4% anterior canal BPPV. The mean duration of symptoms until diagnosis and treatment was 1.2 ± 1.1 months.
Headache Characteristics The most common was a bilateral frontal pressure headache of moderate severity and intermittent course compatible with tension-type headache. The second most frequent was a unilateral pulsating headache of moderate to severe intensity with or without photophobia and phonophobia, sometimes aggravated by routine physical activity, resembling migraine headache. More than half of the patients reported autonomic symptoms such as nausea, vomiting, sweating, syncope, blurring of vision, or diarrhea. About 20% of this group of patients also had visual aura and 40% had a family history of headache. Position, for example, lying down, upward position, or certain neck movements, aggravated the headache in almost one quarter of patients. Other aggravating or alleviating factors, such as sleep or coffee deprivation, weather change, or fatigue, were relatively
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Pollak and Pollak Table 2. Headache Characteristics in Patients During a BPPV Cluster. Characteristic Quality Pressure Pulsating Stabbing Side Bilateral Unilateral Time course Intermittent Continuous Severity Mild Severe Localization Occipital Frontal Temporal Parietal Diffuse Accompanying symptoms Autonomica Anxiety Aggravating factors Position Physical activity Otherb Alleviating factors Rest Cold stimuli Physical activity Warming up the neck Use of analgesics OTC or NSAID Disability caused by headache Interruption of work or pleasure
% 84 12 4 83 17 52 48 18 61 20 33 29 15 11.5 11.5 64 13 23 9.5 11.5 9 4 2 2 45 13
Abbreviations: BPPV, benign paroxysmal positional vertigo; NSAID, nonsteroidal anti-inflammatory drug; OTC, over the counter. a ”Autonomic” refers to nausea, vomiting sweating, syncope, blurring of vision, diarrhea. b “Other” refers to sleep or coffee deprivation, weather change, or fatigue.
uncommon (11.5%). Neuroimaging (62% brain CT scan and 38% brain MRI) was performed in 53% of patients and excluded a structural lesion in all cases. Degenerative changes of the cervical spine were revealed in 2 patients with cervicogenic headache (Table 2). Forty-five percent of patients used analgesics, but only 13% reported disability caused by their headache. According to the ICHD-II, 8 (15%) patients could be classified as migraine without aura (1.1), 14 (26%) were classified as infrequent episodic tension-type headache
associated with pericranial tenderness (2.1.1), 23 (43%) were classified as infrequent episodic tension-type headache not associated with pericranial tenderness (2.1.2), 6 (11%) had cervicogenic headache (11.2.1), and in 2 (4%) patients, the headache could not be specified (14.2). The distribution of sex, history of previous headaches and BPPV, as well as number of treatments was similar among all headache types (Table 3). Migraine and cervicogenic headache were diagnosed only in women.
The Time Course of Headache In 33 out of 48 (69%) patients (in 5 patients, the information could not be reliably obtained), the headache started simultaneously with the vertigo attack, whereas in 4 (8%) patients, the headache preceded the vertigo attack, and in 11 (23%) patients, it followed the onset of vertigo by several days. In 48% of patients, the headache resolved with particle repositioning treatment, in 48%, it outlasted the vertigo attack by 1 to 14 days, and 4% of patients reported spontaneous resolution of the headache before treatment was administered. Among patients with recurrent BPPV, 46% reported headache only with the last BPPV attack, whereas 54% suffered from headaches also during all previous vertigo periods.
History of Previous Headaches Among 24 out of 53 (41%) patients with BPPV clusterrelated headache and no previous headache history, 75% experienced a tension-type headache during the vertigo attack, 15% experienced migraine, and 10% of patients had a cervicogenic headache. Twenty-nine out of 53 (59%) patients with BPPV-related headache also had a previous history of headaches: 13 (45%) migraine, 12 (41%) tension headache, and 4 (14%) cervicogenic headache. Fifty-seven percent reported that the BPPV-associated headache resembled their previous headaches with a concordance of 61.5% for migraine, 50% for tension headache, and 50% for cervicogenic headache (P = .98). In 43% of patients, the vertigo-associated headache did not resemble their former headaches.
BPPV Patients With and Without Headache Patients with BPPV with and without headache did not differ in the frequency of history of headaches, duration of symptoms, or the history of previous BPPV attacks (Table 1). The distribution of canal involvement and the number of particle repositioning maneuvers applied was similar in both groups. However, autonomic symptoms were encountered more often in the headache group (36%) than in the control group (29%) (P = .0004). Both groups of patients were comparable for the history of background diseases.
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Annals of Otology, Rhinology & Laryngology
Table 3. Type of Headache in BPPV Patients According to ICHD-II. ICHD-II Code
Type of Headache Patients No. (out of 53) % Males/females History of headache First vs recurrent BPPV clusters One vs multiple treatments
1.1
2.1.1
Migraine Without Aura
2.1.2
Infrequent Episodic Infrequent Episodic Tension-Type Tension-Type Headache With Headache Without Pericranial Tenderness Pericranial Tenderness
11.2.1
14.2
Cervicogenic Headache
Nonspecified Headache
P Value
8 15 0/8 5 2/6
14 26 5/9 9 4/10
23 43 7/15 10 4/19
6 11 0/6 3 1/5
2 4 1/1 1 1/1
NSa NSa NSa
5/3
12/2
13/10
4/2
1/1
NSa
Abbreviations: BPPV, benign paroxysmal positional vertigo; ICHD-II, The International Classification of Headache Disorders; NS, statistically nonsignificant. a P ≥ .05.
Discussion Our study showed that headache was quite frequent and occurred in about one third of patients during a BPPV cluster. The time course of headaches corresponded to that of the vertigo attack and more than half of the patients suffered from headache with every BPPV attack. The headache was predominantly moderate and did not constitute the main complaint nor did it cause disability. The most frequent was a tension-type headache, followed by migraine and cervicogenic headache. In about half of the patients, the tension and cervicogenic headaches resembled their previous headaches, whereas migraine recurred during the vertigo attack in 65% of migraineurs. Patients with BPPV with and without headache were comparable with respect to headache history, background diseases, BPPV characteristics, and treatment response. Autonomic symptoms were more frequent in the headache group and might be thus at least partly attributable to migraine itself. It seems therefore that headache is a genuine and independent symptom in BPPV. The pathophysiology of tension headache is poorly understood.9 Frequent tension-type headaches are presumably due to limbic pain modulation and not by input from pericranial and neck muscles, as believed previously.10 The functional relations between labyrinthine sensory input and behavioral and autonomic systems have been clinically recognized and also confirmed by anatomical studies.11-15 The pericranial muscle tenderness observed in a part of patients with tension headache has been thought to result from sensitization of the second-order neurons in the trigeminal nucleus.16,17 Trigeminal and vestibular reciprocal relationships have been well established in the past and were
assumed to influence the vestibular control of eye and head movements by complementary sensory information from the face, in addition to that from the neck.18 Taken together, vestibular connections with the limbic and trigeminal nervous system might be responsible for the pathogenesis of tension headache during a BPPV attack. The association of BPPV and the history of migraine have been previously reported. Migraine was found to be 3 times more common in patients with BPPV than in the general population in 1 study,6 whereas others reported independence of migraine and BPPV.19 However, the occurrence of migraine during a BPPV cluster has not been investigated until now, to the best of our knowledge. The current concept of migraine pathophysiology refers to the neurovascular model where aminergic brainstem nuclei influence sensory inputs, cranial blood vessels, and nociceptive modulation.20 In vestibular migraine, vestibular symptoms were related to interactions between pain and vestibular pathways.21 Vestibular nuclei project to the dorsal raphe nucleus, magnus raphe nucleus, locus ceruleus, and lateral tegmentum and can activate monoaminergic pathways involved in migraine.22,23 Benign paroxysmal positional vertigo might therefore be a vestibular trigger for activation of the pain receptors in the brainstem that activate the trigeminovascular system. Cervicogenic headache is a referred pain from the cervical spine to the frontal, parietal, and orbital regions.24,25 The pain is typically triggered by neck movements or sustained awkward head posture or by external pressure on the occiput. According to the ICHD-II, the diagnosis of cervicogenic headache requires the presence of a cervical lesion, but it occurs usually without any cervical abnormality other than commonly found in the general population such as
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Pollak and Pollak degenerative spine disease.26 In contrast to tension headache with pericranial tenderness, it is usually unilateral. The presumed mechanism involves convergence between cervical and trigeminal afferents in the trigeminocervical nucleus.27 Patients with BPPV tend to avoid head movements to prevent vertigo, which leads to increased tone of the cervical muscles and might lower the threshold of the cervical pain afferents. In all patients with headache referred for a brain CT or MRI, a structural lesion was excluded. In view of our previous clinical experience and the findings in this study, we believe that only a minority of BPPV patients who complain about headache during their vertigo attack need further investigation. Neuroimaging should be performed in patients where the headache represents a dominant complaint, if the neurological examination reveals other than BPPV findings or in cases of unexplained treatment failure. The limitation of the study consists of the subjective perception of pain (headache) and the possible presence of confounding factors such as anxiety, depression, or coincidental pain triggers other than vertigo. The headache classification is based on reported symptoms and lacks any objective assessment measures. Moreover, some types of headache might not strictly correspond with a distinct headache subtype and certain overlap is possible, such as tension-type headache with pericranial tenderness and cervicogenic headache.
Conclusion Headache is frequent in BPPV and should be considered to represent a genuine symptom associated with the entity. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
Supplementary Material Supplementary material for this article is available on the AOR website at http://aor.sagepub.com/supplemental.
References 1. Radtke A, von Brevern M, Neuhauser H, Hottenrott T, Lempert T. Vestibular migraine. Long-term follow-up of clin-
ical symptoms and vestibule-cochlear findings. Neurology. 2012;79:1607-1614. 2. Eklund S. Headache in Meniere’s disease. Auris Nasus Larynx. 1999;26:427-433. 3. Cha YH, Cui Y. Rocking dizziness and headache: a two-way street. Cephalalgia. 2013;33:1160-1169. 4. Boldingh MI, Ljøstad U, Mygland A, Monstad P. Comparison of interictal vestibular dysfunction in vestibular migraine vs migraine without vertigo. Headache. 2013;53:1123-1133. 5. Radtke A, Lempert T, Gresty MA, et al. Migraine and Ménière’s disease. Is there a link? Neurology. 2002;59: 1700-1704. 6. Uneri A. Migraine and benign paroxysmal positional vertigo: an outcome study of 476 patients. Ear Nose Throat J. 2004;83:814-815. 7. Parnes LS, Agrawal SK, Atlas J. Diagnosis and management of benign paroxysmal positional vertigo (BPPV). CMAJ. 2003;169:681-693. 8. Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders. Cephalalgia. 2004;24(suppl 1): 9-160. 9. Lipchik GL, Holroyd KA, France CR, et al. Central and peripheral mechanisms in chronic tension-type headache. Pain. 1996;64:467-475. 10. Holroyd KA. Behavioral and psychologic aspects of the pathophysiology and management of tension-type headache. Curr Pain and Headache Rep. 2002;6:401-407. 11. Smith PF, Zheng Y, Horii A. Does vestibular damage cause cognitive dysfunction in humans? J Vestib Res. 2005;15: 1-9. 12. Pollak L, Klein C, Rafael S, Vera K, Rabey JM. Anxiety in the first attack of vertigo. Otolaryngol Head Neck Surg. 2003;128:829-834. 13. Metts BA, Kaufman GD, Perachio AA. Polysynaptic inputs to vestibular efferent neurons as revealed by viral transneuronal tracing. Exp Brain Res. 2006;172:261-274. 14. Halberstadt AL, Balaban CD. Serotonergic and nonserotonergic neurons in the dorsal raphe nucleus send collateralized projections to both the vestibular nuclei and the central amygdaloid nucleus. Neuroscience. 2006;140:1067-1077. 15. Markia B, Kovács ZI, Palkovits M. Projections from the vestibular nuclei to the hypothalamic paraventricular nucleus: morphological evidence for the existence of a vestibular stress pathway in the rat brain. Brain Struct Funct. 2008;213: 239-245. 16. Bernstein R. Central sensitization and headache. In: Olesen J, Tfelt-Hansen P, Welch KMA, eds. The Headaches. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2000: 125-136. 17. Olesen J, Schoenen J. Synthesis of tension-type headache mechanisms. In: Olesen J, Tfelt-Hansen P, Welch KMA, eds. The Headaches. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2000:615-618. 18. Buisseret-Delmas C, Compoint C, Delfini C, Buisseret P. Organisation of reciprocal connections between trigeminal and vestibular nuclei in the rat. J Com Neurol. 1999;409:53-68.
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19. Von Brevern M, Radtke A, Lezius F, et al. Epidemiology of benign paroxysmal positional vertigo: a population based study. J Neurol Neurosurg Psychiatry. 2007;78:710-715. 20. Tfelt-Hansen PC, Koehler PJ. One hundred years of migraine research: major clinical and scientific observations from 1910-2012. Headache. 2011;51:752-758. 21. Furman JM, Marcus DA, Balaban CD. Migraineous vertigo: development of a pathogenetic model and structured diagnostic interview. Curr Opin Neurol. 2003;16:5-13. 22. Dalkara T, Zervas NT, Moskowitz MA. From spreading depression to the trigeminovascular system. Neurol Sci. 2006;27(suppl 2):S86-S90. 23. Cui Y, Li QH, Yamada H, Watanabe Y, Kataoka Y. Chronic degeneration of dorsal raphe serotoninergic neurons modu-
lates cortical spreading depression: a possible pathophysiology of migraine. J Neurosci Res. 2013;91:734-744. 24. Bogduk N, Govind J. Cervicogenic headache: an assessment of the evidence on clinical diagnosis, invasive tests, and treatment. Lancet Neurol. 2009;8:959-968. 25. Vincent MB. Cervicogenic headache: a review comparison with migraine, tension-type headache, and whiplash. Curr Pain Headache Rep. 2010;14:238-243. 26. Coskun O, Ucler S, Karakurum B, et al. Magnetic resonance imaging of patients with cervicogenic headache. Cephalalgia. 2003;23:842-845. 27. Bovim G. Cervicogenic headache, migraine, and tension type headache. Pressure-pain threshold measurements. Pain. 1992;51:169-185.
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Headache During a Cluster of Benign Paroxysmal Positional Vertigo Attacks Lea Pollak and Eitan Pollak Ann Otol Rhinol Laryngol published online 11 July 2014 DOI: 10.1177/0003489414539921 The online version of this article can be found at: http://aor.sagepub.com/content/early/2014/07/06/0003489414539921
Published by: http://www.sagepublications.com
Additional services and information for Annals of Otology, Rhinology & Laryngology can be found at: Email Alerts: http://aor.sagepub.com/cgi/alerts Subscriptions: http://aor.sagepub.com/subscriptions Reprints: http://www.sagepub.com/journalsReprints.nav Permissions: http://www.sagepub.com/journalsPermissions.nav
>> OnlineFirst Version of Record - Jul 11, 2014 What is This?
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539921
research-article2014
AORXXX10.1177/0003489414539921Annals of Otology, Rhinology & LaryngologyPollak and Pollak
Article
Headache During a Cluster of Benign Paroxysmal Positional Vertigo Attacks
Annals of Otology, Rhinology & Laryngology 1–6 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0003489414539921 aor.sagepub.com
Lea Pollak, MD1, and Eitan Pollak, BA2
Abstract Objective: In view of patients’ recurrent complaints, we were interested in investigating the frequency and headache characteristics in patients during a benign paroxysmal positional vertigo (BPPV) cluster. Methods: Patients with BPPV treated at an outpatient dizziness clinic were interviewed about the presence of headache; its quality, localization, severity, time course, and aggravating and alleviating factors; and headache-related disability during their present vertigo cluster. Results: Among 152 patients with BPPV, 53 (34.8%) reported headache associated with vertigo. According to The International Classification of Headache Disorders, 8 (15%) patients could be classified as migraine without aura (1.1), 14 (26%) were classified as infrequent episodic tension-type headache associated with pericranial tenderness (2.1.1), 23 (43%) were classified as infrequent episodic tension-type headache without pericranial tenderness (2.1.2), 6 (11%) had cervicogenic headache (11.2.1), and in 2 (4%) patients, the headache could not be specified (14.2). Fifty-two age-matched BPPV patients without headache did not differ in history of headaches, BPPV history, or background diseases. The distribution of canal involvement and number of treatment maneuvers was also similar in both groups. Conclusion: Headache is frequent in BPPV. The most common is tension-type headache, followed by migraine and cervicogenic headache. Head pain seems to be an independently associated epiphenomenon of BPPV that can worsen patients’ distress. Keywords BPPV, headache
Introduction Headache can be encountered in peripheral as well as central vestibular disorders. In vestibular migraine, it constitutes one of the cardinal symptoms.1 Patients with Ménière’s disease and vestibular neuronitis can report occipital and neck pain.2 Patients with mal de debarquement syndrome— a motion triggered sensation of rocking—often develop new onset headache along with the dizziness.3 Headache presenting with central vestibular findings should always raise suspicion of a possibly life-threatening structural lesion in the posterior fossa, such as tumor or hemorrhage. The interrelation of headache and vestibular diseases has been demonstrated also during interictal periods. Vestibular abnormalities have been found not only in patients with vestibular migraine but also in patients with migraine without vertigo and chronic tension headache.4 The lifetime prevalence of migraine was found to be higher in patients with Ménière’s disease and benign paroxysmal positional vertigo (BPPV).5,6 In practice, we often meet patients with BPPV who complain about headache during the vertigo attack. This issue has garnered little attention in the literature so far. In view
of patients’ recurrent complaints, we were interested in investigating the frequency and headache characteristics in patients during a BPPV cluster.
Methods Patients diagnosed with BPPV at an outpatient dizziness clinic were asked for the occurrence of headache during the present BPPV cluster (the period of recent BPPV attacks). Those reporting headache were included in the study. Patients with secondary headaches (ie, previous trauma, tumor, metabolic, or vascular causes) were a priori excluded. Neuroimaging (brain computed tomography [CT] or magnetic resonance imaging [MRI]) was obtained in patients where the headache represented a dominant complaint, the 1
Department of Neurology, Assaf Harofeh Medical Center, affiliated with the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel 2 Haaretz Daily Newspaper,Tel Aviv, Israel Corresponding Author: Lea Pollak, MD, Kibutz Galuyot 4, 74012, Nes Ziona, Israel. Email: [email protected]
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Table 1. Characteristics in Patients With and Without Headache.
Mean age, y, mean ± SD Males/females, n Positive history of previous headaches, % First BPPV attack (vs recurrent attacks), % Posterior canal type (vs other canal types), % One treatment (vs multiple treatments), % Presence of autonomic symptoms, %
Patients With Headache (n = 53)
Patients Without Headache (n = 52)
P Value
61.2 ± 13.7 13/40 59 21 80 63 64
62.1 ± 14.2 12/40 69 29 78 58 29
NSa NSa NSa NSa NSa NSa < .001
Abbreviations: BPPV, benign paroxysmal positional vertigo; NS, statistically nonsignificant. a P ≥ .05.
headache differed from headaches experienced in the past, the headache preceded or outlasted the vertigo attack by more than 2 weeks, or the treatment response was not satisfactory (53% of patients). The patients underwent a complete neurological examination. Tenderness of the pericranium and neck was examined by applying digital pressure over the trigger points such as the temporal and masseter muscles and the occipitonuchal area. The diagnosis of BPPV was established by a positive Dix-Hallpike or roll test.7 Following the diagnostic test, the patients were treated by an appropriate particle repositioning maneuver (Epley maneuver for posterior and anterior canal variant and barbecue treatment for horizontal canal BPPV). Patients were seen again within 1 week after the treatment. If necessary, the treatment was repeated at 3- to 7-day intervals until disappearance of nystagmus on testing. A semistructured questionnaire (available online) concerning headache quality, localization, severity, and time course was administered by the treating neurologist (L.P.). Patients were also asked about symptoms accompanying the headache, aggravating and alleviating factors, the use of analgesics, and headache-related disability. The type of headache was then classified according to The International Classification of Headache Disorders (ICHD-II).8 Fifty-two consecutive age-matched BPPV patients without headache during the present or previous BPPV clusters served as controls. The background diseases of both groups of patients were categorized according to system involvement, whereas patients with malignancies were grouped into 1 category regardless of organ involvement (cardiovascular, ocular, metabolic, rheumatologic and orthopedic, psychiatric, otolaryngological, oncological, neurological, gastrointestinal, pulmonary, and hematological diseases). The study was performed in accordance with the Declaration of Helsinki and approved by the local ethics committee. With regard to statistical methods, a paired-samples t test was applied for comparison of age in both groups of
patients. The chi-square test was applied for comparing categorical variables such as the headache and BPPV characteristics between both groups. A P value of < .05 was considered statistically significant. SPSS version 18 (SPSS Inc, Chicago, Illinois, USA) was used for the analyses.
Results Patient Characteristics Among 152 patients treated for BPPV during the years 2011 to 2012, 53 (34.8%) reported headache associated with the present BPPV cluster. Eighty percent of patients had a posterior canal type, 9% had bilateral posterior canal BPPV, and horizontal and anterior canal type of BPPV was found in 7% and 4% of patients, respectively. The mean duration of symptoms until diagnosis and treatment was 1.4 ± 1.3 months (Table 1). In the control group, 78% of patients had posterior canal BPPV, 10% bilateral posterior canal BPPV, 8% horizontal, and 4% anterior canal BPPV. The mean duration of symptoms until diagnosis and treatment was 1.2 ± 1.1 months.
Headache Characteristics The most common was a bilateral frontal pressure headache of moderate severity and intermittent course compatible with tension-type headache. The second most frequent was a unilateral pulsating headache of moderate to severe intensity with or without photophobia and phonophobia, sometimes aggravated by routine physical activity, resembling migraine headache. More than half of the patients reported autonomic symptoms such as nausea, vomiting, sweating, syncope, blurring of vision, or diarrhea. About 20% of this group of patients also had visual aura and 40% had a family history of headache. Position, for example, lying down, upward position, or certain neck movements, aggravated the headache in almost one quarter of patients. Other aggravating or alleviating factors, such as sleep or coffee deprivation, weather change, or fatigue, were relatively
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Pollak and Pollak Table 2. Headache Characteristics in Patients During a BPPV Cluster. Characteristic Quality Pressure Pulsating Stabbing Side Bilateral Unilateral Time course Intermittent Continuous Severity Mild Severe Localization Occipital Frontal Temporal Parietal Diffuse Accompanying symptoms Autonomica Anxiety Aggravating factors Position Physical activity Otherb Alleviating factors Rest Cold stimuli Physical activity Warming up the neck Use of analgesics OTC or NSAID Disability caused by headache Interruption of work or pleasure
% 84 12 4 83 17 52 48 18 61 20 33 29 15 11.5 11.5 64 13 23 9.5 11.5 9 4 2 2 45 13
Abbreviations: BPPV, benign paroxysmal positional vertigo; NSAID, nonsteroidal anti-inflammatory drug; OTC, over the counter. a ”Autonomic” refers to nausea, vomiting sweating, syncope, blurring of vision, diarrhea. b “Other” refers to sleep or coffee deprivation, weather change, or fatigue.
uncommon (11.5%). Neuroimaging (62% brain CT scan and 38% brain MRI) was performed in 53% of patients and excluded a structural lesion in all cases. Degenerative changes of the cervical spine were revealed in 2 patients with cervicogenic headache (Table 2). Forty-five percent of patients used analgesics, but only 13% reported disability caused by their headache. According to the ICHD-II, 8 (15%) patients could be classified as migraine without aura (1.1), 14 (26%) were classified as infrequent episodic tension-type headache
associated with pericranial tenderness (2.1.1), 23 (43%) were classified as infrequent episodic tension-type headache not associated with pericranial tenderness (2.1.2), 6 (11%) had cervicogenic headache (11.2.1), and in 2 (4%) patients, the headache could not be specified (14.2). The distribution of sex, history of previous headaches and BPPV, as well as number of treatments was similar among all headache types (Table 3). Migraine and cervicogenic headache were diagnosed only in women.
The Time Course of Headache In 33 out of 48 (69%) patients (in 5 patients, the information could not be reliably obtained), the headache started simultaneously with the vertigo attack, whereas in 4 (8%) patients, the headache preceded the vertigo attack, and in 11 (23%) patients, it followed the onset of vertigo by several days. In 48% of patients, the headache resolved with particle repositioning treatment, in 48%, it outlasted the vertigo attack by 1 to 14 days, and 4% of patients reported spontaneous resolution of the headache before treatment was administered. Among patients with recurrent BPPV, 46% reported headache only with the last BPPV attack, whereas 54% suffered from headaches also during all previous vertigo periods.
History of Previous Headaches Among 24 out of 53 (41%) patients with BPPV clusterrelated headache and no previous headache history, 75% experienced a tension-type headache during the vertigo attack, 15% experienced migraine, and 10% of patients had a cervicogenic headache. Twenty-nine out of 53 (59%) patients with BPPV-related headache also had a previous history of headaches: 13 (45%) migraine, 12 (41%) tension headache, and 4 (14%) cervicogenic headache. Fifty-seven percent reported that the BPPV-associated headache resembled their previous headaches with a concordance of 61.5% for migraine, 50% for tension headache, and 50% for cervicogenic headache (P = .98). In 43% of patients, the vertigo-associated headache did not resemble their former headaches.
BPPV Patients With and Without Headache Patients with BPPV with and without headache did not differ in the frequency of history of headaches, duration of symptoms, or the history of previous BPPV attacks (Table 1). The distribution of canal involvement and the number of particle repositioning maneuvers applied was similar in both groups. However, autonomic symptoms were encountered more often in the headache group (36%) than in the control group (29%) (P = .0004). Both groups of patients were comparable for the history of background diseases.
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Table 3. Type of Headache in BPPV Patients According to ICHD-II. ICHD-II Code
Type of Headache Patients No. (out of 53) % Males/females History of headache First vs recurrent BPPV clusters One vs multiple treatments
1.1
2.1.1
Migraine Without Aura
2.1.2
Infrequent Episodic Infrequent Episodic Tension-Type Tension-Type Headache With Headache Without Pericranial Tenderness Pericranial Tenderness
11.2.1
14.2
Cervicogenic Headache
Nonspecified Headache
P Value
8 15 0/8 5 2/6
14 26 5/9 9 4/10
23 43 7/15 10 4/19
6 11 0/6 3 1/5
2 4 1/1 1 1/1
NSa NSa NSa
5/3
12/2
13/10
4/2
1/1
NSa
Abbreviations: BPPV, benign paroxysmal positional vertigo; ICHD-II, The International Classification of Headache Disorders; NS, statistically nonsignificant. a P ≥ .05.
Discussion Our study showed that headache was quite frequent and occurred in about one third of patients during a BPPV cluster. The time course of headaches corresponded to that of the vertigo attack and more than half of the patients suffered from headache with every BPPV attack. The headache was predominantly moderate and did not constitute the main complaint nor did it cause disability. The most frequent was a tension-type headache, followed by migraine and cervicogenic headache. In about half of the patients, the tension and cervicogenic headaches resembled their previous headaches, whereas migraine recurred during the vertigo attack in 65% of migraineurs. Patients with BPPV with and without headache were comparable with respect to headache history, background diseases, BPPV characteristics, and treatment response. Autonomic symptoms were more frequent in the headache group and might be thus at least partly attributable to migraine itself. It seems therefore that headache is a genuine and independent symptom in BPPV. The pathophysiology of tension headache is poorly understood.9 Frequent tension-type headaches are presumably due to limbic pain modulation and not by input from pericranial and neck muscles, as believed previously.10 The functional relations between labyrinthine sensory input and behavioral and autonomic systems have been clinically recognized and also confirmed by anatomical studies.11-15 The pericranial muscle tenderness observed in a part of patients with tension headache has been thought to result from sensitization of the second-order neurons in the trigeminal nucleus.16,17 Trigeminal and vestibular reciprocal relationships have been well established in the past and were
assumed to influence the vestibular control of eye and head movements by complementary sensory information from the face, in addition to that from the neck.18 Taken together, vestibular connections with the limbic and trigeminal nervous system might be responsible for the pathogenesis of tension headache during a BPPV attack. The association of BPPV and the history of migraine have been previously reported. Migraine was found to be 3 times more common in patients with BPPV than in the general population in 1 study,6 whereas others reported independence of migraine and BPPV.19 However, the occurrence of migraine during a BPPV cluster has not been investigated until now, to the best of our knowledge. The current concept of migraine pathophysiology refers to the neurovascular model where aminergic brainstem nuclei influence sensory inputs, cranial blood vessels, and nociceptive modulation.20 In vestibular migraine, vestibular symptoms were related to interactions between pain and vestibular pathways.21 Vestibular nuclei project to the dorsal raphe nucleus, magnus raphe nucleus, locus ceruleus, and lateral tegmentum and can activate monoaminergic pathways involved in migraine.22,23 Benign paroxysmal positional vertigo might therefore be a vestibular trigger for activation of the pain receptors in the brainstem that activate the trigeminovascular system. Cervicogenic headache is a referred pain from the cervical spine to the frontal, parietal, and orbital regions.24,25 The pain is typically triggered by neck movements or sustained awkward head posture or by external pressure on the occiput. According to the ICHD-II, the diagnosis of cervicogenic headache requires the presence of a cervical lesion, but it occurs usually without any cervical abnormality other than commonly found in the general population such as
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Pollak and Pollak degenerative spine disease.26 In contrast to tension headache with pericranial tenderness, it is usually unilateral. The presumed mechanism involves convergence between cervical and trigeminal afferents in the trigeminocervical nucleus.27 Patients with BPPV tend to avoid head movements to prevent vertigo, which leads to increased tone of the cervical muscles and might lower the threshold of the cervical pain afferents. In all patients with headache referred for a brain CT or MRI, a structural lesion was excluded. In view of our previous clinical experience and the findings in this study, we believe that only a minority of BPPV patients who complain about headache during their vertigo attack need further investigation. Neuroimaging should be performed in patients where the headache represents a dominant complaint, if the neurological examination reveals other than BPPV findings or in cases of unexplained treatment failure. The limitation of the study consists of the subjective perception of pain (headache) and the possible presence of confounding factors such as anxiety, depression, or coincidental pain triggers other than vertigo. The headache classification is based on reported symptoms and lacks any objective assessment measures. Moreover, some types of headache might not strictly correspond with a distinct headache subtype and certain overlap is possible, such as tension-type headache with pericranial tenderness and cervicogenic headache.
Conclusion Headache is frequent in BPPV and should be considered to represent a genuine symptom associated with the entity. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
Supplementary Material Supplementary material for this article is available on the AOR website at http://aor.sagepub.com/supplemental.
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