Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5526_Библиотеки_им_академика_М_И_Перельмана.pdf
72
6. Headache Classication Subcommittee of the International Headache Society. The international classication of headache disorders: 2nd edition. Cephalalgia. 2004;24(1):9–160.
7. Napthali K, Koloski N, Talley NJ.Abdominal migraine. Cephalalgia. 2016;36(10):980–6.
8. Drossman DA, Corazziari E, Delvaux M, Spiller R, Talley NJ, Thompson WG, Whitehead
WE. Rome III: The functional gastrointestinal disorders. 3rd ed. McLean: Degnon
Associates; 2006.
9. Irwin S, Barmherzig R, Gelfand A.Recurrent gastrointestinal disturbance: abdominal migraine
and cyclic vomiting syndrome. Curr Neurol Neurosci Rep. 2017;17(3):21.
10. Korterink J, Devanarayana NM, Rajindrajith S, Vlieger A, Benninga MA.Childhood functional abdominal pain: mechanisms and management. Nat Rev Gastroenterol Hepatol.
2015;12(3):159–71.
11. Bentley D, Katachburian A, Brostoff J.Abdominal migraine and food sensitivity in children.
Clin Allergy. 1984;14(5):499–500.
12. Özge A, Öksüz N, Ayta S, Uluduz D, Yıldırım V, Toros F, Taşdelen B.Atopic disorders
are more common in childhood migraine and correlated headache phenotype. Pediatr Int.
2014;56(6):868–72.
13. Egger J, Carter CM, Wilson J, Turner MW, Soothill JF.Is migraine food allergy? A doubleblind controlled trial of oligoantigenic diet treatment. Lancet. 1983;322(8355):865–9.
14. Bentley D, Kehely A, al-Bayaty M, Michie CA.Abdominal migraine as a cause of vomiting in
children: a clinician’s view. J Pediatr Gastroenterol Nutr. 1995;21:S49–51.
15. Goadsby PJ.Pathophysiology of migraine. Ann Indian Acad Neurol. 2012;15:S15–22.
16. Loewendorf AI, Matynia A, Saribekyan H, Gross N, Csete M, Harrington M.Roads less traveled: sexual dimorphism and mast cell contributions to migraine pathology. Front Immunol.
2016;7:140.
17. D’Andrea G.Pathogenesis of chronic migraine: the role of neuromodulators. J Headache Pain.
2015;16(S1):A38.
18. Good PA.Neurologic investigations of childhood abdominal migraine: a combined electrophysiologic approach to diagnosis. J Pediatr Gastroenterol Nutr. 1995;21(Suppl 1):S44–8.
19. Tan V, Sahami AR, Peebles R, Shaw RJ.Abdominal migraine and treatment with intravenous
valproic acid. Psychosomatics. 2006;47(4):353–5.
20. Jones AL, Roberts RC, Colvin DW, Rubin GL, Coughtrie MW.Reduced platelet phenolsulphotransferase activity towards dopamine and 5-hydroxytryptamine in migraine. Eur J Clin
Pharmacol. 1995;49(1):109–14.
21. Gibb C, Glover V, Gilbertson NB, Bentley D, Sandler M.Platelet phenolsulphotransferase
activity and ‘abdominal migraine’. Arch Dis Child. 1988;63(12):1500–1.
22. McFerron BA, Waseem S.Chronic recurrent abdominal pain. Pediatr Rev. 2012;33(11):509–17.
23. Amin MA, Manna RM, Nahin S, Hawlader MDH.Abdominal migraine with acute watery
diarrhea and dehydration: successful treatment with Valproic acid in a pediatric case. Clin Case
Rep. 2024;12(3):e8703.
24. Drossman DA.Functional gastrointestinal disorders: history, pathophysiology, clinical features and Rome IV.Gastroenterology. 2016;150:1262–79.
25. Drossman DA, Hasler WL.Rome IV-functional GI disorders: disorders of gut-brain interaction. Gastroenterology. 2016;150(6):1257–61.
26. Roberts JE, deShazo RD.Abdominal migraine, another cause of abdominal pain in adults. Am
J Med. 2012;125:1135–9.
27. Abu-Arafeh I, Russell G.Prevalence and clinical features of abdominal migraine compared
with those of migraine headache. Arch Dis Child. 1995;72(5):413–7.
28. Mortimer MJ, Kay J, Jaron A.Clinical epidemiology of childhood abdominal migraine in an
urban general practice. Dev Med Child Neurol. 1993;35(3):243–8.
29. Dignan F, Abu-Arafeh I, Russell G.The prognosis of childhood abdominal migraine. Arch Dis
Child. 2001;84(5):415–8.
A. C. Atalar et al.
7 Episodic Syndromes That May BeAssociated withMigraine: Abdominal Migraine
30. Kunishi Y, Iwata Y, Ota M, Matsubayashi M, Kanno M, Kuboi Y, Yoshie K, Kato Y.Abdominal
migraine in a middle-aged woman. Intern Med. 2016;55(19):2793.
31. Hershey AD.Current approaches to the diagnosis and management of paediatric migraine.
Lancet Neurol. 2010;9(2):190–204.
32. Baglioni V, Bozza F, Beatrice A, Cameli N, Colacino Cinnante EM, Lentini G, Faedda N,
Natalucci G, Guidetti V.Non-pharmacological treatments in paediatric migraine. J Clin Med.
2024;13(5):1278.
33. Hershey AD.Pediatric headache. Continuum (Minneap Minn). 2015;21(4 Headache):1132–45.
34. Puledda F, de Boer I, Messina R, Garcia-Azorin D, Portes Souza MN, Al-Karagholi MA,
de Dhaem OB, Tassorelli C, May A.Worldwide availability of medications for migraine
and tension-type headache: a survey of the international headache society. Cephalalgia.
2024;44(11):3331024241297688.
35. Tsai M, Monkul Nery ES, Kerr L, Khanna R, Komori M, Dennehy EB, Wilbraham D, Winner
P.Pharmacokinetics, safety, and tolerability of lasmiditan in pediatric patients with migraine.
Clin Pharmacokinet. 2021;60(6):819–28.
36. Loh NR, Whitehouse WP, Howells R.What is new in migraine management in children and
young people? Arch Dis Child. 2022;107(12):1067–72.
73
Chapter 8
Episodic Syndromes That May
BeAssociated withMigraine: Benign
Paroxysmal Vertigo
TiagoGomes De Paula andThaisRodrigesVilla
8.1 Introduction
Benign paroxysmal positional vertigo (BPPV) is one of the most common causes of
episodic vertigo, and its relationship with vestibular migraine (VM) has generated
increasing interest in clinical practice and research. VM, in turn, is one of the main
causes of episodic vertigo, often underdiagnosed despite its high prevalence among
migraine patients [1, 2]. The overlap between BPPV and VM creates a diagnostic
challenge, as both share similar vestibular symptoms, such as dizziness and vertigo,
complicating appropriate clinical management [1, 2]. In this chapter, we will discuss the pathophysiology, diagnosis, and treatment of BPPV in the context of VM,
with an emphasis on practical approaches and controlling this condition.
8.2 Pathophysiology ofVestibular Migraine andBPPV
The pathophysiology of VM is not yet fully elucidated, but it is believed to involve
a complex interaction between the trigeminal and vestibular systems. Studies show
that the trigeminal nucleus has reciprocal connections with the vestibular nuclei,
and this interaction can generate vestibular symptoms during migraine attacks [3,
4]. Additionally, the involvement of neurotransmitters such as serotonin and norepi-
nephrine is proposed as one of the mechanisms contributing to vestibular dysregulation in migraine patients [3].
VM is characterized by episodes of vertigo associated with migraine, with vestibular symptoms that can last from minutes to hours, often accompanied by other
symptoms such as photophobia, phonophobia, and nausea [1, 3]. BPPV, on the other
T. Gomes De Paula · T. R. Villa (*)
Headache Center Brasil, São Paulo, Brazil
Switzerland AG 2026
D. Uludüz et al. (eds.), Rare Causes of Headache Disorders, Headache,
https://doi.org/10.1007/978-3-032-10242-3_8
75© The Author(s), under exclusive license to Springer Nature
76
T. Gomes De Paula and T. R. Villa
hand, is caused by the displacement of otoliths within the semicircular canals of the
inner ear, resulting in short episodes of vertigo, typically triggered by changes in
head position [2, 5]. BPPV is often associated with migraine, and the risk of recurrence is higher in patients who have both VM and BPPV [1, 6].
The overlap between VM and BPPV occurs because both conditions share similar vestibular mechanisms, such as hyperexcitability of the vestibular nuclei. This
may explain why some patients present symptoms of both conditions simultaneously [4, 6]. It is important to remember that migraine patients exhibit greater vestibular sensitivity, contributing to the frequency and severity of vertigo episodes [3].
Studies suggest that VM may affect vestibular pathways at multiple levels,
involving mechanisms such as activation of the vestibular nuclei by the trigeminal
nucleus [3, 5]. In BPPV, activation of these same circuits may also trigger vertigo,
leading to signicant overlap between the two conditions [2, 5]. The interaction
between the trigeminal and vestibular systems seems to be the convergence point
between VM and BPPV, especially in patients with chronic migraine [5].
8.3 Case Study
A 36-year-old female patient sought care at Headache Center Brasil in São Paulo
with a history of dizziness episodes that began at the age of 15, associated with
nausea, aural fullness, and tinnitus. At 25, her symptoms worsened and became
daily. Later, she developed headaches with photophobia, phonophobia, and
visual aura.
At the age of 32, the patient was diagnosed with BPPV and VM after DixHallpike maneuvers showed typical nystagmus and imaging exams revealed no
abnormalities. Previous treatments with propranolol, unarizine, amitriptyline, and
venlafaxine were ineffective in controlling the disease. Treatments such as amitriptyline and venlafaxine initially led to a slight reduction in crises; however, this
improvement was neither sustained nor progressive, and the crises remained frequent, signicantly impacting her quality of life. At admission, the patient had a
severe disability level (Migraine disability assessment schedule (MIDAS) IV, severe
disability).
At the age of 36, she started treatment with botulinum toxin, showing signicant
improvement after the rst cycle and progressive improvement in subsequent cycles.
After eight cycles of botulinum toxin treatment, the patient experienced a marked reduction in the frequency and intensity of vertigo episodes, with progressive disease control.
Her quality of life improved considerably, reecting the success of the treatment.
In view of this case, we initiated treatment with botulinum toxin, which demonstrated signicant improvement after the rst cycle and progressive improvement in
subsequent cycles. After eight cycles of treatment with botulinum toxin, the patient
showed a marked reduction in the frequency and intensity of vertigo episodes, with
progressive control of the disease. Her quality of life improved considerably, reecting the success of the treatment.
8 Episodic Syndromes That May Be Associated with Migraine: Benign…
77
8.4 Case Discussion
The case presented here highlights the complexity of the differential diagnosis
between BPPV and VM.Both present with vestibular symptoms such as vertigo,
which can lead to inaccurate or incomplete initial diagnoses. The patient experienced years of disabling symptoms until the coexistence of the two conditions was
specied.
Diagnostic Key: The clinical history and careful listening to the patient about
her migraine symptoms were crucial to conrm the combined diagnosis [2,
4, 7, 8].
Clinical Dilemma: The delay in recognizing VM in patients initially presented
with BPPV alone reects the need for greater vigilance and clearer protocols
to differentiate the two conditions, especially in patients with a history of
migraine [6, 8].
8.5 Clinical Management
This case demonstrates the efcacy of treatment with botulinum toxin in a patient
refractory to conventional therapies, such as propranolol, unarizine, amitriptyline,
and venlafaxine.
First Line: Repositioning maneuvers in isolated cases of BPPV, with the Epley and
Semont maneuvers, continue to be the mainstay of management.
Vestibular Migraine: Preventive treatment with beta-blockers and anticonvulsants is
often used, but the lack of response in cases such as our patient’s reinforces the
importance of considering alternatives such as botulinum toxin and anti-CGRP
(calcitonin gene-related peptide) monoclonal antibodies [9].
Vestibular Rehabilitation: A multimodal approach combining vestibular rehabilita-
tion and drug prophylaxis can maximize outcomes [2, 7, 8, 10].
8.6 Clinical Aspects andQuality ofLife
The delay in introducing effective treatments, such as botulinum toxin, questions
current clinical practices. Why are proven therapies reserved for refractory cases,
when they could benet patients soon after initial therapy has failed? The signicant
improvement in patient quality of life after the introduction of botulinum toxin
highlights its importance in the therapeutic armamentarium [8, 11].
78
T. Gomes De Paula and T. R. Villa
8.7 Diagnosis
The diagnosis of BPPV in the context of vestibular migraine requires a thorough
evaluation, as both conditions can present overlapping symptoms. For BPPV, the
classic diagnosis involves performing repositioning maneuvers, such as the DixHallpike maneuver, which induces characteristic nystagmus in patients with the
canalicular form of BPPV [1, 3]. For VM, the diagnostic criteria established by the
International Headache Society and the Bárány Society require that the patient presents vestibular symptoms of moderate to severe intensity, associated with migraine
features such as headache, photophobia, phonophobia, and/or aura [5, 7, 10, 12].
In patients with VM, vestibular and audiometric tests are often normal, but may
reveal abnormalities during vertigo episodes, making it essential to differentiate
positional vertigo from spontaneous vertigo that occurs in VM [1]. The duration of
episodes can range from a few minutes to several hours, and vestibular symptoms
may precede, accompany, or follow the headache episode [1, 5]. Additionally, imaging tests, such as magnetic resonance imaging (MRI), are generally used to rule out
other neurological conditions that may be associated [10]. Evaluation using questionnaires like the Dizziness Handicap Inventory can also help quantify the impact
of dizziness and assist in the decision to intensify treatment [8].
One of the biggest challenges in the differential diagnosis between VM and
BPPV is the similarity of vestibular symptoms, such as movement-triggered vertigo. In some cases, BPPV may be diagnosed initially, but over time, the development of migraine symptoms or refractoriness to treatment indicates the concomitant
presence of VM [3, 4].
8.8 Treatment
The management of BPPV and VM depends on controlling vestibular symptoms
and appropriate prophylaxis. BPPV is classically treated with repositioning maneuvers, such as the Epley and Semont maneuvers, which have a high success rate in
repositioning otoliths [3, 6, 12, 13]. However, in patients with BPPV and VM, clini-
cal approaches may be more complex, requiring a combination of prophylactic
therapies for migraine and specic treatments for vestibular symptoms [2, 4, 7, 10].
In VM, prophylactic therapy includes the use of beta-blockers (such as propranolol), calcium channel blockers (such as unarizine), anticonvulsants (such as topiramate and valproic acid), and tricyclic antidepressants (such as amitriptyline) [2, 3,
10, 12]. However, in refractory cases, botulinum toxin and anti-CGRPs have
emerged as effective alternatives, signicantly reducing the intensity of episodes
and migraine-related disability [1, 4, 9].
Recently, monoclonal antibodies against CGRP (calcitonin gene-related peptide), such as galcanezumab, have shown efcacy in the prophylactic treatment of
8 Episodic Syndromes That May Be Associated with Migraine: Benign…
79
chronic migraine, including cases of vestibular migraine. Galcanezumab works by
blocking the CGRP receptor [9].
In cases refractory to medications, botulinum toxin is an effective option. Studies
have shown that patients who fail treatment with conventional medications, such as
propranolol and topiramate, experience signicant improvement with botulinum
toxin, both in reducing headache crises and vestibular symptoms [8, 12]. Liu etal.
highlighted that patients who failed rst-line medication were more likely to benet
from botulinum toxin [8].
Vestibular rehabilitation is another valuable tool for improving balance and
reducing vertigo symptoms in patients with VM and BPPV, improving patients’
quality of life [3]. The multimodal approach, which combines vestibular rehabilitation with the use of prophylactic medications, has shown superior results in controlling symptoms [2, 7, 8, 10].
8.9 Conclusion
The overlap between BPPV and VM often coexists, challenging physicians and
complicating proper diagnosis and management. Repositioning maneuvers are
effective in BPPV, but in patients with concomitant VM, management requires a
more comprehensive approach. Botulinum toxin has proven to be a valuable therapy
in refractory cases, providing signicant symptomatic relief. Early recognition of
the severity of symptoms and intensication of treatment, when necessary, are crucial to improving patients’ quality of life.
References
1. Yollu U, Uluduz DU, Yilmaz M, Yener HM, Akil F, Kuzu B, Kara E, Hayir D, Ceylan D,
Korkut N. Vestibular migraine screening in a migraine-diagnosed patient population, and
assessment of vestibulocochlear function. Clin Otolaryngol. 2017;42(2):225–33. https://doi.
org/10.1111/coa.12699. Epub 2016 Aug 1.
2. Dieterich M, Obermann M, Celebisoy N.Vestibular migraine: the most frequent entity of episodic vertigo. J Neurol. 2016;263(Suppl 1):S82–9.
Epub 2016 Apr 15. PMID: 27083888; PMCID: PMC4833782.
3. Görür K, Gür H, İsmi O, Özcan C, Vayisoğlu Y. The effectiveness of propranolol, unarizine, amitriptyline and botulinum toxin in vestibular migraine complaints and prophylaxis: a
non-randomized controlled study. Braz J Otorhinolaryngol. 2022;88(6):975–81. https://doi.
org/10.1016/j.bjorl.2021.02.005. Epub 2021 Mar 7. PMID: 33722518; PMCID: PMC9615515.
4. Benjamin T, Gillard D, Abouzari M, Djalilian HR, Sharon JD. Vestibular and auditory
manifestations of migraine. Curr Opin Neurol. 2022;35(1):84–9. https://doi.org/10.1097/
CO.0000000000001024. PMID: 34864754; PMCID: PMC8755616.
5. Barbosa F, Villa TR.Vestibular migraine: diagnosis challenges and need for targeted treatment.
Arq Neuropsiquiatr. 2016;74(5):416–22.
https://doi.org/10.1007/s00415- 015- 7905- 2.
https://doi.org/10.1590/0004- 282X20160037.
80
6. Mahrous MM.Vestibular migraine and benign paroxysmal positional vertigo, close presentation dilemma. Acta Otolaryngol. 2020;140(9):741–4. https://doi.org/10.1080/00016489.202
0.1770857. Epub 2020 Jun 18.
7. Kim SK, Hong SM, Park IS, Choi HG.Association between migraine and benign paroxysmal positional vertigo among adults in South Korea. JAMA Otolaryngol Head Neck Surg.
2019;145(4):307–12. https://doi.org/10.1001/jamaoto.2018.4016. PMID: 30676633; PMCID:
PMC6481427.
8. Liu YF, Macias D, Donaldson L, Dornhoffer JR, Rizk HG.Pharmacotherapy failure and progression to botulinum toxin injection in vestibular migraine. J Laryngol Otol. 2020;134(7):586–91.
https://doi.org/10.1017/S002221512000095X. Epub 2020 Jul 27.
9. Sharon JD, Krauter R, Chae R, Gardi A, Hum M, Allen I, Levin M.A placebo controlled,
randomized clinical trial of galcanezumab for vestibular migraine: the INVESTMENT study.
Headache. 2024;64(10):1264–72. https://doi.org/10.1111/head.14835. Epub ahead of print.
10. Agessi LM, Villa TR.Vestibular migraine with visual aura and olfactory hallucination in children:
two case reports. Neuropediatrics. 2018;49(6):414–6.
Epub 2018 Oct 10.
11. Surmeli R, Surmeli M, Yalcin AD, Sahin Yilmaz AA, Erden Habesoglu T, Gunay G.Vestibular
migraine: Onabotulinum toxin effectivity, prospective-randomized study. Clin Neurol
Neurosurg. 2025;254:108949. https://doi.org/10.1016/j.clineuro.2025.108949. Epub
2025 May 4.
12. Salmito MC, Duarte JA, Morganti LOG, Brandão PVC, Nakao BH, Villa TR, Ganança
FF.Prophylactic treatment of vestibular migraine. Braz J Otorhinolaryngol. 2017;83(4):404–10.
https://doi.org/10.1016/j.bjorl.2016.04.022. Epub 2016 Jun 2. PMID: 27320656; PMCID:
PMC9442697.
13. Chen J, Zhang S, Cui K, Liu C.Risk factors for benign paroxysmal positional vertigo recurrence: a systematic review and meta-analysis. J Neurol. 2021;268(11):4117–27. https://doi.
org/10.1007/s00415- 020- 10175- 0. Epub 2020 Aug 24.
T. Gomes De Paula and T. R. Villa
https://doi.org/10.1055/s- 0038- 1673642.
Part II
Trigeminal Autonomic
Cephalalgias (TACs)
Chapter 9
Short-Lasting Unilateral Neuralgiform
Headache Attacks withConjunctival
Injection andTearing (SUNCT)
UtkuTopbaş , NevraÖksüz , andAynurÖzge
9.1 Introduction
Short-lasting unilateral neuralgiform headache attacks with conjunctival injection
and tearing (SUNCT) is one of the rare headache syndromes included in the primary
trigeminal autonomic cephalalgias group, according to the International
Classication of Headache Disorders, 3rd edition1 (ICHD-3) [1]. Its prevalence was
found to be 6.6 per 100,000 [2]. The typical age of onset is between 40 and 60years
and cases between 3 and 88years have been reported [3]. The prevalence of SUNCT
between men and women is similar with recent case series [4].
The pathophysiology of SUNCT is not fully understood. The anatomical structures responsible for SUNCT are the hypothalamus, trigeminovascular complex
(TCC), and the cranial autonomic system [5]. Afferent bers are responsible for
extracranial and intracranial pain synapse with the TCC.The second order neurons
of the TCC synapse with the thalamus and pain matrix to produce pain. TCC is
known to synapse with the ipsilateral superior salivatory nucleus (SSN). Therefore,
it modulates the SSN during pain and is responsible for ipsilateral cranial autonomic symptoms via the sphenopalatine ganglion [6]. The hypothalamus is known
to have a pain-modulating effect on the TCC.In the pathogenesis of SUNCT, pain
occurs continuously at regular intervals due to the central disinhibition of the hypothalamus on the TCC [6].
U. Topbaş · N. Öksüz (*) · A. Özge
Mersin State Hospital, Mersin, Turkey
Switzerland AG 2026
D. Uludüz et al. (eds.), Rare Causes of Headache Disorders, Headache,
https://doi.org/10.1007/978-3-032-10242-3_9
83© The Author(s), under exclusive license to Springer Nature