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Recurrent Paroxysmal Positional Vertigo Related to Oral Contraceptive Treatment

April 1, 2006

By Giacomini, Pier Giorgio; Napolitano, Bianca; Alessandrini, Marco; Di Girolamo, Stefano; Magrini, Antonio

Abstract

Benign paroxysmal positional vertigo (BPPV) is a high-prevalence vestibular end-organ disorder caused by the detachment of utricular otoconia which float in the posterior or lateral semicircular canal. In the majority of cases the etiology of BPPV is unknown and it may follow viral infection, vascular disorders or head trauma. BPPV may be recurrent, with some authors demonstrating a correlation between recurrence and female gender. We report herein on ten cases (out of 289 diagnoses of BPPV) of recurrent idiopathic BPPV, occurring in healthy women receiving oral contraceptive treatment, which ceased after treatment suspension. It has been hypothesized that the impaired water and electrolyte balance, the variations of endolymphatic pH and the impairment of glucose or lipid metabolism induced by oral contraceptive treatment may cause otoconial degeneration and subsequent otoconia detachment and BPPV. The rarity of the finding (10/289) could account for the poor attention paid to the hormonal pathogenesis of BPPV.

Keywords: Canalithiasis, hormonal, oral contraceptives, positional vertigo

Introduction

Benign paroxysmal positional vertigo (BPPV) is characterized by various degrees of acute vertigo attacks that are paroxysmal and last from seconds to minutes, being elicited by changes in head position [1]. The incidence of the disease is reported to be 10 in 100 000 [2], although no general agreement exists [3]. Nevertheless, BPPV is the most frequently observed pathology in otoneurological clinical practice [1]. The average age of onset is 50-60 years, with incidence increasing with age [4], and women are more affected than men, with a 2:1 ratio [5].

The etiology of BPPV may be idiopathic, post-traumatic, post- infectious or due to vascular disorders [6], although the higher prevalence in women seems more evident in ‘idiopathic’ forms of BPPV (female/ male ratio 2-3:1) [7]. It may therefore be hypothesized that hormonal disorders in women may be involved in the genesis of some forms of BPPV of unknown etiology. The underlying pathogenetic mechanism is almost generally accepted as the detachment of otoliths from the macula utriculi and their dislocation into the semicircular canals.

The natural course of BPPV may vary. Schuknecht [8] differentiated three forms of BPPV: self-limited, recurrent and permanent, according to the type of evolution. The self-limited form is the most frequent – it subsides spontaneously within weeks or months, without a tendency of recurrence [8]; the recurrent form manifests with episodes of vertigo which recur after variable periods of remission lasting for weeks or years; and the permanent form persists continuously for more than a year and is not responsive to rehabilitative treatment.

In many cases, a diagnosis of probable or possible etiology can be formulated if BPPV occurs in patients with pathological conditions likely to provoke the detachment and/or degeneration of macular otoconia or the alteration of endolymphatic metabolism [9]. Causes of otoconia detachment include Menire’s disease, chronic otitis, blood hyperviscosity and prolonged bed rest. BPPV is fundamentally considered an idiopathic disorder as a multifactorial etiology is identified in less than 50% of patients.

As no previous remarks on this matter have been found, we report herein on ten cases of recurrent idiopathic BPPV, occurring in healthy women receiving oral contraceptive treatment, which ceased after treatment suspension.

Case presentation

Between January 2001 and January 2003, 289 patients were diagnosed as having BPPV at the outpatient clinic of the Department of Otolaryngology, University of Rome ‘Tor Vergata.’ Eighty-three patients used oral contraceptives. Among the 83 patients, 22 presented recurrent BPPV, but only in 10 patients the association of oral contraceptives treatment, recurrent BPPV and remission of symptomatology with suspension of treatment was observed.

The latter cohort consisted often young, otherwise healthy women (mean age 32 7 years, range 25-39 years). All of these patients complained of acute onset rotatory vertigo, without any obvious cause, with symptoms and paroxysmal positional nystagmus (PPN) typical for canalithiasis of the posterior semicircular canal (PSC) [10], recurrent over a period of 2-8 months and only partially responsive to ‘repositioning’ maneuvers.

All patients were receiving oral contraceptive therapy: five patients were taking ethinylestradiol/ drospirenone, three were taking ethinylestradiol/levonorgestrel and two ethinylestradiol/ gestodene, for a period of 6-36 months.

The otoneurological examination consisted of:

(1) Obtaining an accurate history.

(2) Pure tone and impedance audiometry.

(3) Vestibular examination with assessment of spontaneous and evoked nystagmus by infrared videonystagmoscopic observation and electronystagmographic recording. The assessment of evoked nystagmus consisted of eliciting nystagmus by head positioning, such as the Dix-Hallpike maneuver [10] for diagnosis of canalithiasis of the PSC and the McClure maneuver [11] for diagnosis of canalithiasis of the lateral semicircular canal.

Table I. Population profile.

(4) During the follow-up period patients were instructed not to avoid movements that may elicit vertigo. Upon the occurrence of relapsing vertigo, the patients were asked to record it and undergo re-examination as soon as possible at the outpatient clinic. The relapses were then defined on the basis of the signs and symptoms recorded.

Hearing was normal in all patients and no patient had a history of labyrinthine or neurological pathology.

The Dix-Hallpike maneuver elicited rotatory vertigo, with intense neurovegetative symptoms, and a nystagmus pattern characteristic of BPPV of the PSC canal in all ten patients (six cases to the left, four cases to the right side). The patients were treated with the Epley repositioning maneuver [12] and rechecked for the presence of vertigo and/or nystagmus after 3 days, 1 month and 3 months.

On the 3-day check-up, all patients reported a subsiding of positional vertigo after the repositioning maneuver, but typical BPPV and PPN were still present after performing the Dix-Hallpike maneuver. At the 1-month check-up, the patients experienced relapses (1-3 episodes) of BPPV with a symptom-free interval of 10-20 days; at the 2-month check-up, all patients experienced at least one episode of BPPV per month. Due to personal previous anecdotical observations of spontaneous resolution of BPPV after discontinuing contraceptive therapy for unrelated causes (unpublished data), all patients were required to discontinue hormonal treatment and monthly examinations were carried out for the next 6 months.

In all cases, the recurrence of BPPV subsided after suspension of oral contraceptives. At the 6-month follow-up no recurrences were reported by patients and no PPN was observed for 6 months after the first episode (Table I).

Discussion

The recurrence of BPPV has been addressed marginally by different authors. Published papers concerning the long-term outcome of different therapeutic strategies report a varied rate of recurrence, which is mainly related to methodological differences between the studies (sample size, follow-up period, type of study, method of analysis). Considering studies with long-term follow-up periods, in which the recurrence rate is determined prospectively, we conclude that the rate of recurrence of BPPV is high, and may exceed 40% [13- 15]. Regarding the factors that may influence a relapse of disease, Dornhoffer and Colvin [16] observed a significant correlation between recurrent BPPV episodes and concomitant Meniere’s disease, while Beynon and colleagues [13] demonstrated a correlation between female gender and recurrent BPPV.

The evaluation of recurrence can also be based on clinical history, identifying elements that characterize the pathologic condition and help solve the etiologic problem. One of the aspects less studied, but certainly fundamental, is the catabolism of otoliths and the genesis of endolabyrinthic bodies of a different nature.

Various hormonal triggers may be released in the premenstrual syndrome, during pregnancy, in premenopausal syndromes and by the use of oral contraceptives [17], which have been associated with neurological symptoms including vertigo. Specifically, the use of oral contraceptives may have multiple metabolic effects. The mechanisms presumed responsible for premenstrual hormonemediated vestibular impairment [18] are as follows:

(1) A sudden fall in blood estrogens and progesterone levels, with a peak in blood aldosterone concentration and subsequent variations of endolymph/perilymph pressures, due to impaired water and electrolyte balance.

(2) secondary hypothyroidism.

(3) Blood hyperviscosity.

It is important to note that the effect of oral contraceptives on vestibular function has not been addressed precisely and seems somehow controversial. The episodic occurrence of vertigo, not better specified, has been described in patients taking these drugs [1921], as well as the absence of negative effects of oral contraceptives on otologic disorders [22]. Furthermore, apart from impacting on the estrogenemia/ progestenemia, oral contraceptives can also induce hyperlipidemia type IV [2\3] and hyperinsulinism with a reduced glucose tolerance [24], similarly to what happens during the ‘premenstrual state’.

Referring to our observations on recurrent and persisting BPPV in young women during contraceptive therapy, it should be emphasized that each systemic disease or condition capable of causing otoconia dislodgement with a partial functional lesion could be responsible for BPPV [9].

Otoconia detachment and formation of highdensity mineralized particles in the semicircular canals are considered the main causes of BPPV, even though the chemical composition of such particles is currently unknown [25]. It has been reported that pH variations and/ or ion deficiencies in the endolymph may alter the structure of the otoconia [26]. A deficit in endolymphatic calcium supply has been suggested to explain senile otoconial demineralization [27,28]; in fact, a possible pathogenesis seems to be related to impaired calcium homeostasis, frequently associated with menopausal hormonal deficiencies or changes. This hypothesis would suggest a higher prevalence of senile otoconial degeneration in females, currently not yet confirmed by histological studies [29].

In the ten described cases of BPPV related to contraceptives assumption, different pathogenetic hormone-mediated mechanisms might be hypothesized:

(1) The variation of endolymphatic pressure, due to alterations of water and electrolyte balance with chronic hydrops, could cause degeneration of the fibers anchoring the otoconia.

(2) Variations of endolymphatic pH, due to a secondary hyperaldosteronism, could cause otoconial degeneration.

(3) A vascular affection of otoconia and macula, due to a secondary impairment of glucose or lipid metabolism, could cause otoconia or otoconial membrane degeneration.

These mechanisms could explain how the mentioned BPPV, recurrent and responsive to the suspension of hormonal treatment, could occur. The rarity of the finding (10/289) could account for the poor attention paid to the hormonal pathogenesis of BPPV.

In conclusion, the effect of hormones on vestibular function appears not completely explored [30], but is worthy of further investigation to clarify clinical entities such as the cases of BPPV reported herein.

References

1. Strupp M, Arbusow V. Acute vestibulopathy. Curr Opin Neurol 2001;14:11-20.

2. Mizukoshi K, Watanabe Y, Shojaku H, Okubo J, Watanabe I. Epidemiological studies on benign paroxysmal positional vertigo in Japan. Acta Otolaryngol Suppl 1988;447:67-72.

3. Froehling DA, Silverstein MD, Mohr DN, Beatty CW, Offord KP, Ballard DJ. Benign positional vertigo: incidence and prognosis in a population-based study in Olmsted County, Minnesota. Mayo Clin Proc 1991;66:596-601.

4. Katsarkas A. Electronystagmographic (ENG) findings in paroxysmal positional vertigo (PPV) as a sign of vestibular dysfunction. Acta Otolaryngol 1991;1H:193-200.

5. Baloh RW, Honrubia V, Jacobson K. Benign positional vertigo: clinical and oculographic features in 240 cases. Neurology 1987;37:371-378.

6. Baloh RW, Jacobson K, Honrubia V. Horizontal semicircular canal variant of benign positional vertigo. Neurology 1994;43: 2542- 2549.

7. Katsarkas A. Benign paroxysmal positional vertigo (BPPV): idiopathic versus post-traumatic. Acta Otolaryngol 1999;119: 745- 749.

8. Schuknecht HF. Cupololithiasis. Adv Otorhinolaryngol 1973; 20:434-443.

9. Karlberg M, Hall K, Quicken N, Hinson J, Halmagyi GM. What inner ear diseases cause benign paroxysmal positional vertigo? Acta Otolaryngol 2000;120:380-385.

10. Dix MR, Hallpike CS. Pathology, symptomatology and diagnosis of certain common disorders of the vestibular system. Ann Otol Rhinol Laryngol 1952;61:987-1016.

11. McClure JA. Horizontal canal BPV. Am J Otolaryngol 1985; 14:30-35.

12. Epley JM Caveats in particle repositioning for treatment of canalithiasis (BPPV). Otolaryngol Head Neck Surg 1997; 8:68-76.

13. Beynon GJ, Baguley DM, da Cruz MJ. Recurrence of symptoms following treatment of posterior semicircular canal benign paroxysmal positional vertigo with a particle repositioning maneuver. J Otolaryngol 2000;29:2-6.

14. Hain TC, Helminski JO, Reis IL, Uddin MK. Vibration does not improve results of the canalith repositioning procedure. Arch Otolaryngol Head Neck Surg 2000;126;617-622.

15. Nunez RA, Cass SP, Furman JM. Short- and long-term outcomes of canalith repositioning for benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 2000;122: 647-652.

16. Dornhoffer JL, Colvin GB. Benign paroxysmal positional vertigo and canalith repositioning: clinical correlations. Am J Otol 2000;21:230-233.

17. Rubin W. Biochemical evaluation of the patient with dizziness. Semin Hearing 1989;10:151-159.

18. Andrews JC, Ator GA, Honrubia V. The exacerbation of symptoms in Meniere’s disease during the premenstrual period. Arch Otolaryngol Head Neck Surg 1992; 118:74-78.

19. Rybak LP. Metabolic disorders of the vestibular system. Otolaryngol Head Neck Surg 1995;112:129-132.

20. Egarter C, Huber J, Leikermoser R, Haidbauer R, Pusch H, Fischl F, Putz M. Tibolone versus conjugated estrogens and sequential progestogen in the treatment of climateric complaints. Maturitas 1996;23:55-62.

21. Brill K, Schnitker J, Albring M. Long-term experience with low dose oral contraceptives. Gynecol Endocrinol 1990;4: 227-286.

22. Vessey M, Painter R. Oral contraception and ear disease: findings in a large cohort study. Contraception 2001;63: 61-63.

23. Stone NJ, Levy RJ. The hyperlipidemias and coronary artery disease. Dis Mon 1972;(Aug):3-35.

24. Godsland IF, Crook D, Wynn V. Low-dose oral contraceptives and carbohydrate metabolism. Am J Obstet Gynecol 1990;163:348-353.

25. Thalmann R, Ignatova E, Kachar B, Ornitz D, Thalmanna I. Development and maintenance of otoconia. Biochemical considerations. Ann N Y Acad Sci 2001;942:162-178.

26. Erway LC, Purichia NA, Netzler ER. Genes, manganese, and zinc in formation of otoconia: labeling, recovery, and maternal effects. Scanning Electron Microsc 1986;4: 1681-1694.

27. Lim DJ. Otoconia in health and disease: a review. Ann Otol Rhinol Laryngol 1983;112(Suppl):12-24.

28. Ross MD, Peacor D, Johnsson LG, Allard LF. Observations on normal and degenerating human otoconia. Ann Otol 1976; 85:310-326.

29. Johnsson LG, Rouse RC, Wright CG, Henry PJ, Hawkins JE Jr. Pathology of neuroepithelial suprastructures of the human inner ear. Am J Otolaryngol 1982;3:77-90.

30. Seemungal BM, Gresty MA, Bronstein AM. The endocrine system, vertigo and balance. Curr Opin Neurol 2001;14: 27-34.

PIER GIORGIO GIACOMINI, BIANCA NAPOLITANO, MARCO ALESSANDRINI, STEFANO DI GIROLAMO, & ANTONIO MAGRINI

Department of Otolaryngology, University of Rome ‘Tor Vergata’, Rome, Italy

(Received 2 March 2005; revised 25 October 2005; accepted 28 October 2005)

Correspondence: P. G. Giacomini, Department of Otolaryngology, Policlinico ‘Tor Vergata’, Viale Oxford 81, 1-00133 Rome, Italy. Tel: +39 06 20902925. Fax: +39 06 20902921. E-mail: digirolamo@med.uniroma2.it or bnapolitano@inwind.it

Copyright Taylor & Francis Ltd. Jan 2006




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