Headache Medicine Volume 10 Número 2 - 2019

Editorial

► Migraine, Dizziness and Motion Sickness: Are we going in

straight lines?

Original Article

► Full Head Block for headache treatment: technical

description, indications and mechanisms

Case Report

► Alice in Wonderland Syndrome

Original Article

► “No Pain, More Gain”? Affect and Adherence to Exercise

in Migraine Patients: A Prospective Cohort Study

► Accompanying Symptoms in Vestibular Migraine

► Motion Sickness in Headache Patients

Short communication

► Histomorphometric analysis of mast cells in different

regions of human intracranial dura mater

Imagens

► Migraine with aura: MRI with perfusion aspects in the

ictal and interictal phases

Capav10n2.indd 1 22/10/19 18:16

Headache Medicine, v.10, n.2, 2019

EDITORIAL

Migraine, Dizziness and Motion Sickness: Are we going in straight lines?

Marcelo M Valença; Mario F P Peres ................................................................................................................................................ 36

ORIGINAL ARTICLE

Full Head Block for headache treatment: technical description, indications and mechanisms

Bloqueio completo da cabeça no tratamento das cefaleias: Descrição técnica, indicações e mecanismos

Bruna de Freitas Dias; Thiago Nouer Frederico; Iron Dangoni Filho; Mario Fernando Prieto Peres ...... 37-40

CASE REPORT

Alice in Wonderland Syndrome

Síndrome de Alice no País das Maravilhas

Wilson Luiz Sanvito ......................................................................................................................................................................... 41-42

ORIGINAL ARTICLE

“No Pain, More Gain”? Affect and Adherence to Exercise in Migraine Patients: A Prospective Cohort Study

“No Pain, More Gain”? Resposta Afetiva e Aderência ao Exercício em Pacientes com Migrânea: Um Estudo

Prospectivo

Arão Belitardo Oliveira; Dhiego Luigi Gringõn; Mario Fernando Prieto Peres .................................................... 43-50

Accompanying Symptoms in Vestibular Migraine

Sintomas Acompanhantes na Enxaqueca Vestibular

Aline Turbino Neves Martins da Costa; Daniel Guedes Tomedi; Camila Naegeli Caverni; Larissa Mendonça

Agessi; Rosemeire Rocha Fukue; Henrique Ballalai Ferraz; Thais Rodrigues Villa ........................................... 51-55

Motion Sickness in Headache Patients

Cinetose em pacientes com cefaleias

Marina Olivier; Sol Cavanagh; Lucas Bonamico; Francisco Gualtieri; María Teresa Goicochea ................... 56-59

SHORT COMMUNICATION

Histomorphometric analysis of mast cells in different regions of human intracranial dura mater

Análise histomorfométrica de mastócitos em diferentes regiões da dura-máter intracraniana humana

Emanuela Paz Rosas; Silvania Tavares Paz; Ana Clara de Souza Neta; Raisa Ferreira Costa; Ana Paula

Fernandes da Silva; Manuela Figueiroa Lyra de Freitas; Marcelo Moraes Valença .......................................... 60-62

IMAGENS

Migraine with aura: MRI with perfusion aspects in the ictal and interictal phases

Enxaqueca com aura: aspectos da ressonância magnética com perfusão nas fases ictal e interictal

Paulo Sergio Faro Santos; Bruno Augusto Telles ............................................................................................................... 63-64

Headache Medicine

Scientific Publication of the Brazilian Headache Societ

VOLUME 10 ∙ NUMBER 2 ∙ 2019

ISSN 2178-7468

CONTENTS

10(2).indb 1 21/10/2019 18:25:21

Headache Medicine, v.10, n.2, 2019

Headache Medicine

Scientific Publication of the Brazilian Headache Societ

Editores-chefes

Marcelo Moraes Valença

Universidade Federal de Pernambuco, Recife, PE, Brasil.

Mario Fernando Prieto Peres

Hospital Israelita Albert Einstein, IPq – HCFMUSP. São Paulo, SP, Brasil.

Editor Científic

Raimundo Pereira Silva-Néto

Universidade Federal do Piauí, Teresina, PI, Brasil.

Editor Emeritus

Wilson Luiz Sanvito

FCM Santa Casa de São Paulo, São Paulo, SP, Brasil.

Pesquisa Básica e Procedimentos

Élcio Juliato Piovesan

Universidade Federal do Paraná, Curitiba, PR, Brasil

Ensino, alunos e residentes

Yara Dadalti Fragoso – Santos, SP, Brasil.

Cefaleia na Mulher

Eliane Meire Melhado

Universidade de Catanduva, Catanduva, SP, Brasil.

Multiprossional

Juliane Prieto Peres Mercante

IPq – HCFMUSP, São Paulo, SP, Brasil.

Arão Belitardo de Oliveira

ABRACES – Associação Brasileira cefaleia em Salvas e

Enxaqueca, São Paulo, SP, Brasil

Debora Bevilaqu

a-Grossi

FMUSP – R

beirao Preto

Cefaleias Secundárias

Pedro Augusto Sampaio Rocha

Universidade Federal de Pernambuco, Recife, PE, Brasil.

Hipertensão e Hipotensão Liquórica

Ida Fortini

HC FMUSP, São Paulo, SP, Brasil.

Sandro Luís de Andrade Matas

UNIFESP, São Paulo, SP, Brasil

Cefaleias Trigêmino-Autonômicas

Maria Eduarda Nobre

Rio de Janeiro, RJ, Brasil

Cefaleia na Infância

Marco Antônio Arruda

Universidade Federal de São Paulo, SP, Brasil.

Dor orofacial

duardo Grossmann – Porto Alegre,

RS, Brasil.

Controvérsias e Expert Opinion

João José Freitas de Carvalho – Fortaleza, CE, Brasil.

Clinical Trials

Fabiola Dach

FMUSP, Ribeirão Preto, SP, Brasil

Teses

Fernando Kowacs, Porto Alegre, RS, Brasil

Imagens e Vídeos

Paulo Sérgio Faro Santos

INC, Curitiba, PR, Brasil

Advocacy

Elena Ruiz de La Torre

WHAM (World Headache Association for Migraine)

Madrid, Espanha

A revista Headache Medicine é uma publicação de propriedade da Sociedade Brasileira de Cefaleia, indexada no Latindex e no Index Scholar, publicada

pela Sociedade Brasileira de Cefaleia, www.sbcefaleia.com.br. Os manuscritos aceitos para publicação passam a pertencer à Sociedade Brasileira de

Cefaleia e não podem ser reproduzidos ou publicados, mesmo em parte, sem autorização da HM & SBCe. Os artigos e correspondências deverão ser

encaminhados para a HM através de submissão on-line, acesso pela página www.headachemedicine.com.br - Distribuição gratuita para os membros

associados, bibliotecas regionais de Medicina e faculdades de Medicina do Brasil, e sociedades congêneres

Editores Associados

CONSELHO EDITORIAL

ISSN 2178-7468

10(1).indb 2 21/10/2019 19:33:56

iii

Headache Medicine, v.10, n.2, 2019

Headache Medicine

Scientific Publication of the Brazilian Headache Societ

CONSELHO EDITORIAL

Rodrigo Noseda

Harvard Medical School, Boston, MA, EUA

Marlind Alan Stiles –

Jefferson Universtty, Philadelphia, PA, EUA

Charles Siow, Singapore

Maurice Borges Vincent, Indianapolis, IN, EUA

Michele Viana, Novara, Italia

Margarita Sanchez Del Rio, Madrid, Espanha

Sait Ashina,

Harvard Medical School, Boston, MA, EUA

Todd D Rozen,

Mayo Clinic, Jacksonville, FL, EUA

Elena Ruiz de la Torre, Espanha

Marco Lisicky, Cordoba, Argentina

Maria Teresa Goycochea, Buenos Aires, Argentina

Alex Espinoza Giacomozzi, Santiago, Chile

Joe Munoz Ceron, Bogota, Colombia

Faisal Amin, Copenhague, Dinamarca

Uwe Reuter, Berlin, Alemanha

Abouch Valenty Krymchantowski, Rio de Janeiro, RJ

Alan Chester Feitosa Jesus, Aracaju, SE

Ana Luisa Antonniazzi, Ribeirão Preto, SP

Carla da Cunha Jevoux, Rio de Janeiro, RJ

Carlos Alberto Bordini, Batatais, SP

Daniella de Araújo Oliveira, Recife, PE

Djacir D. P. Macedo, Natal, RN

Elder Machado Sarmento, Barra Mansa, RJ

Eliana Meire Melhado, Catanduva, SP

Fabíola Dach, Ribeirão Preto, SP

Fernando Kowacs, Porto Alegre, RS

Henrique Carneiro de Campos, Belo Horizonte, MG

Jano Alves de Sousa, Rio de Janeiro, RJ

João José de Freitas Carvalho, Fortaleza, CE

Luis Paulo Queiróz, Florianópolis, SC

Marcelo C. Ciciarelli, Ribeirão Preto, SP

José Geraldo Speziali, Ribeirão Preto, SP

Marcelo Rodrigues Masruha, Vitória, ES

Pedro Ferreira Moreira Filho, Rio de Janeiro, RJ

Pedro André Kowacs, Curitiba, PR

Mauro Eduardo Jurno, Barbacena, MG

Paulo Sergio Faro Santos, Curitiba, PR

Pedro Augusto Sampaio Rocha Filho, Recife, PE

Renata Silva Melo Fernandes, Recife, PE

Thais Rodrigues Villa, São Paulo, SP

Renan Domingues, Vitória, ES

Conselho Editorial Internacional

Conselho Editorial Nacional

A revista Headache Medicine é uma publicação de propriedade da Sociedade Brasileira de Cefaleia, indexada no Latindex e no Index Scholar, publicada

pela Sociedade Brasileira de Cefaleia, www.sbcefaleia.com.br. Os manuscritos aceitos para publicação passam a pertencer à Sociedade Brasileira de

Cefaleia e não podem ser reproduzidos ou publicados, mesmo em parte, sem autorização da HM & SBCe. Os artigos e correspondências deverão ser

encaminhados para a HM através de submissão on-line, acesso pela página www.headachemedicine.com.br - Distribuição gratuita para os membros

associados, bibliotecas regionais de Medicina e faculdades de Medicina do Brasil, e sociedades congêneres

ISSN 2178-7468

10(2).indb 3 21/10/2019 18:25:21

Headache Medicine, v.10, n.2, 2019

Sociedade Brasileira de Cefaleia – SBCe

filiada à International Headache Society – IH

Av. Tenente José Eduardo n° 453, sala 203

27323-240 Barra Mansa - RJ - Brasil

Fone:+55 (24) 9 8847-9980 www.sbcefaleia.com.br

secretaria@sbcefaleia.com.br

Josiane Moreira da Silva - Secretária Executiva SBCe

DIRETORIA 2018/2021

DELEGADOS

Academia Brasileira de Neurologia (ABN)

Fernando Kowacs

José Geraldo Speziali

American Headache Society (AHS)

Marcelo Cedrinho Ciciarelli

Associación Latinoamericana de Cefaleias (ASOLAC)

Carlos Alberto Bordini

European Headache Federation (EHF)

Marco Antônio Arruda

International Headache Society (IHS)

Pedro André Kowacs

Sociedade Brasileira para o Estudo da Dor (SBED)

Eduardo Grossman - José G Speziali

Responsável pelo Site

Paulo Sérgio Faro Santos

Responsável pelas Mídias Sociais

Arão Belitardo Oliveira

Comissão de Ética

Elcio Juliato Piovesan - Jano Alves de Souza

José Geraldo Speziali - Mauro Eduardo Jurno

Registro de Cefaleia no Brasil

Fernando Kowacs - Mauro Eduardo Jurno

Vanise Grassi - Élder Machado Sarmento

Liselotte Menke Barea - Luis Paulo Queiroz

Marcelo Cedrinho Ciciarelli - Mario FP Peres

Pedro Augusto Sampaio Rocha-Filho

Políticas Públicas, Institucionais e Advocacy

Patricia Machado Peixoto

COMISSÕES

Prêmios

Carlos A Bordini - Djacir Dantas de Macedo

Jano Alves de Souza - Mauro Eduardo Jurno

Pedro F Moreira Filho - Raimundo P Silva-Néto

Atividades Físicas e Fisioterapia

Cláudia Baptista Tavares - Daniela A Oliveira

Debora Bevilaqua-Grossi

Cefaleia na Infância

Marco Antonio Arruda - Thais Rodrigues Villa

Cefaleia na mulher

Eliana Meire Melhado

Dor Orofacial

Ricardo Tanus Valle

Leigos

Celia A P Roesler - Henrique Carneiro de

Campos - João José Freitas de Carvalho

Paulo Sérgio Faro Santos

Alunos Residentes

Yara Dadalti Fragoso - Diego Belandrino Swerts

Izadora Karina da Silva - Marcos Ravi Cerqueira

Ferreira Figueiredo - Caroline Folchini

Saulo Emanuel Gomes Silva - Walkyria Will-

Patrick Emanuell - Eduardo Nogueira

Psicologia

Juliane Prieto Peres Mercante - Rebeca V. A.

Vieira - Rosemeire Rocha Fukue

Procedimentos Invasivos

Cláudio Manoel Brito

Élcio Juliato Piovesan

Presidente Elder Machado Sarmento

Secretário Mario Fernando Prieto Peres

Tesoureiro Pedro Augusto Sampaio Rocha Filho

10(2).indb 4 21/10/2019 18:25:21

Headache Medicine, v.10, n.2, p.36, 2019

EDITORIAL

Migraine, Dizziness and Motion Sickness:

Are we going in straight lines?

Creative Commons (CC BY) Attribution 4.0

International.

In these edition, Headache Medicine brings two articles about the relation of migraine with common symptoms

reported by patients, dizziness and motion sickness, leading to important management dilemmas. A nice report from

Argentina (1), researchers from Fleni Hospital in Buenos Aires showed motion sickness not only occurring unrelated to

migraine but also as a trigger of headache attacks.

Another study done by Turbino et al (2) in 143 patients diagnosed with vestibular migraine in a tertiary headache

center observed associated symptoms such as nausea, vomiting, osmophobia, tinnitus, motion sickness higher in

migraine with aura patients.

What are the lines between those symptoms? Do we have same genetic backgrounds, same underlying

mechanisms? Which brain structures are involved? Is the cerebellum, the vestibular system, thalamus, hypothalamus,

or cerebral cortex affected? Can we classify those patients in a different way? How are we going to treat headaches

with dizziness and or motion sickness?

We still have more questions than answers in this topic, hopefully more studies will come so we better understand it.

Marcelo M Valença

Mario F P Peres

REFERENCES

Olivier, M et al. Motion Sickness in Headache Patients. Headache Medicine, 2019 10(2): 56-59

Turbino, A et al. Accompanying symptoms in vestibular migraine. Headache Medicine, 2019 10(2): 51-55

10(2).indb 36 21/10/2019 18:25:21

Headache Medicine, v.10, n.2, p.37-40, 2019

ABSTRACT

RESUMO

Descritores: Bloqueios nervosos; Nervo occipital; Nervo auriculotemporal;

Nervo supraorbital; Nervo supratroclear; Nervo zigomático; Cefaleias

ORIGINAL ARTICLE

Full Head Block for headache treatment:

technical description, indications and mechanisms

Bloqueio completo da cabeça no tratamento das cefaleias:

Descrição técnica, indicações e mecanismos

Bruna de Freitas Dias

Thiago Nouer Frederico

Iron Dangoni Filho

Mario Fernando Prieto Peres

HIAE - Hospital Israelita Albert Einstein¹

FICSAE – Faculdade Israelita de Ciências e

Saúde Albert Einstein

*Correspondence

Mario F P Peres

E-mail: mariop3r3s@gmail.com

Received: June 2, 2019. Accepted:

June 8, 2019.

Creative Commons (CC BY) Attribution 4.0

International.

Headache is a most prevalent neurological condition in the world and has a

major impact on quality of life. The causes are usually multifactorial and may

have a chronic character. Headache management involves pharmacological

and non-pharmacological approach; invasive and noninvasive. Peripheral

nerve block is already a viable, safe, and effective treatment option, such as

major occipital nerve block. Full head block is a minimally invasive proposal

of peripheral pain neuromodulation for the treatment of refractory or severe

headache, mainly. The aim of this paper is to describe a technique and discuss

the role of full head block in the headache management. The proposal is

bilaterally anesthetizing the following nerves: major and minor occipital,

supraorbital, supratrochlear, zygomatic-temporal and auriculo-temporal with

local anesthetic and a corticosteroid. Many aspects should be studied: efcacy

and safety of the technique, clinical indications, professional training, need

for USG guidance, adequate dose of anesthetic and corticosteroids. In order

to further evaluate the role of peripheral blocks in headaches randomized

controlled trials are required.

Keywords: Nerve blocks; Occipital nerve; Auriculotemporal nerve; Supraorbital

nerve; Supratrochlear nerve; Zygomatic nerve; Primary headache

Cefaleias primárias são condições neurológicas prevalentes no mundo com

grande impacto na qualidade de vida. As causas são geralmente multifatoriais

e podem ter caráter crônico. O gerenciamento da dor de cabeça envolve

abordagem farmacológica e não farmacológica; invasivo e não invasivo.

O bloqueio do nervo periférico já é uma opção viável, segura e ecaz de

tratamento, como o bloqueio do nervo occipital maior. O bloqueio cefálico

completo é uma proposta minimamente invasiva da neuromodulação da

dor periférica, principalmente para o tratamento de cefaleias refratárias

ou intensas. O objetivo deste artigo é descrever uma técnica e discutir o

papel do bloqueio cefálico completo no manejo das cefaleias. A proposta é

uma anestesia local bilateraldos seguintes nervos: occipital maior e menor,

supraorbital, supratroclear, zigomático-temporal e aurículo-temporal com

anestésico local associado a corticoide. Muitos aspectos devem ser estudados:

ecácia e segurança da técnica, indicações clínicas, treinamento prossional,

necessidade de orientação por ultrassonograa, dose adequada de anestésico e

corticosteróide. Para melhor avaliação do papel dos procedimentos periféricos

nas cefaleias, ensaios clínicos randomizados e robustos são necessários.

10(2).indb 37 21/10/2019 18:25:21

Full Head Block for headache treatmen

Dias BF, et al.

Headache Medicine, v.10, n.2, p.37-40, 2019

INTRODUCTION

Headache is the most prevalent neurologic condition

in the world

. It most affects patient in productive age

and is associated with a substantial personal and societal

burden. Migraine represents the rst highest cause

of disability under 50 years of age and the second

worldwide

. Migraine, the most common primary

headache, has been found in 15,2% in Brazil

, followed

by tension-type headache (13%)

and chronic headaches

(6,9%)

. They are frequently multifactorial and have a

chronic character. Its treatment can be challenging and

involves pharmacological and non-pharmacological,

invasive and non-invasive approaches, as well as acute

and prophylactic therapy

There are now several non-invasive and invasive

options to manage headache. Peripheral nerve block

is a minimally invasive therapy and represents an

excellent alternative to conventional drugs (responsible

for a wide range of side effects due to its action on

several neurotransmitters) and to non-pharmalogical

neuromodulation, like Transcranial Magnetic Stimulation

(TMS) and Transcranial Direct Current Stimulation

(tDCS)

. The nerve block can be used in primary

(migraine, cluster headache, and nummular headache)

and secondary headaches (cervicogenic headache and

headache attributed to craniotomy), as well in cranial

neuralgias (trigeminal neuropathies, glossopharyngeal

and occipital neuralgias)

. Nerve block provides rapid

pain relief to patients and its analgesic effect often

long-lasting (sometimes for weeks to months). The

mechanism includes an interruption of neural conduction

in peripheral nerves and nerve trunks by the injection of

a local anesthetic agent (e.g., lidocaine, bupivacaine).

However, it is still incomplete understood, but is likely

secondary to effects on central pain modulation via

second order neurons in the trigeminocervical complex

Several peripheral cranial nerve targets have been

aimed in this approach. Greater occipital nerve is the

most studied peripheral nerve block, but there are

some others sites already tested, such as lesser occipital

nerve, supratrochlear nerve, supraorbital nerve and

auriculotemporal

. The procedure is fast, easy, generally

safe and well tolerated, becoming attractive for clinicians

and patients, especially for resistant headaches.

A similar procedure has been done in neurosurgical

anesthesia where all peripheral nerves are blocked

to anesthetize the scalp, the so-called scalp block

Scalp block involves regional anesthesia to the nerves

that innervate the scalp, providing analgesia for tumor

excision, epilepsy surgery and deep brain stimulation

surgery

. Full head block is different from scalp block

because of its therapeutic target and technique.

Our study aimed to describe the technique and

discuss the role of a full head block in headache

management treatment.

METHODS

The proposal of full head nerve block is to

anesthetize bilaterally greater lesser and third occipital,

supraorbital, supratrochlear, zygomatic-temporal and

auriculotemporal nerves. The techniques of each nerve

block are detailed below.

Greater occipital nerve (GON) block.

GON is located approximately two thirds of the

distance on a line drawn from the center of the mastoid

to the external occipital protuberance. GON can also

be located palpating occipital artery; because of that,

care needs to be taken to avoid intra-arterial injection.

Another option is to inject approximately 2 cm lateral to

the external occipital protuberance

Lesser occipital nerve (LON) block.

LON is located approximately one third of the way

on a line drawn from the center of the mastoid to the

greater occipital protuberance

Third occipital nerve (TON) block.

TON is located deep to the semispinalis capitis

muscle and two anatomic landmarks are used: the tip of

the mastoid process and the C3 spinous process

. The

Figure 1. Topography of the nerve’s blockage in full head block propose

10(2).indb 38 21/10/2019 18:25:22

Full Head Block for headache treatmen

Dias BF, et al.

Headache Medicine, v.10, n.2, p.37-40, 2019

third occipital nerve lies medial to great occipital nerve

and have bers communication between both, and is

blocked in the same injection of GON by the intimacy

proximity.

Auriculotemporal nerve (ATN) block

ATN is located at superior to the posterior portion

of the zygomatic bone just anterior to the ear. It follows

supercial temporal artery that can be palpated and

used as a reference for the block

Supraorbital nerve (SON) block

SON, which runs approximately 2 cm lateral to the

supratrochlear nerve, the injection can be done in this

point, or the needle can be advanced laterally through

the same puncture that was used for the STN

13,14

Supratrochlear nerve (STN) block

STN is blocked by inserting the needle just above

the eyebrow over its medial border

13,14

Zygomatic nerve (ZN) block

ZN is blocked by placing the index nger on ventral

rim of the orbit at the lateral canthus of the eye, and rmly

press against the supraorbital portion of the zygomatic

arch

12,14

POSSIBLE INDICATIONS

Full head block can be performed together with

botulinum toxin, as a bridge therapy, while waiting to

the toxin starting to work

15-17

. Refractory headache,

primary headache in pregnancy and the presence of

contraindications for other treatment’s options.

Peripheral nerve block has already been tested for

primary headache disorders like migraine prevention,

migraine acute treatment, cluster, neuralgia and tension-

type, as well as to secondary headache disorders such

posttraumatic headache, post-surgical headache

and scar related pain. It can also be considered as a

transitional treatment in chronic headaches.

LIMITATIONS

The major side effects occur due to local injection.

There are related cases of local infection, nerve damage

with later neuroma formation, hematoma, local injury to

adjacent structures and, rarely, systemic manifestations

due to absorption of local anesthetics (seizure, alteration

in consciousness and cardiac conduction effects when

high doses are used). Using small needles and aiming for

perineural sites are helpful in avoiding these side effects.

When patient has anatomic abnormalities, such as skull

defects, local infection or previous surgical scars, the

procedure is not indicated.

Assistant’s training about the location of structures,

technique and aseptic environment is necessary for

a great performance of the procedure. Studies must

be designed to identify the efcient amount of local

anesthetic, necessity of ultrasound guided

and

addition of corticosteroid (methylprednisolone or

betamethasone).

FUTURE DIRECTIONS

Thereby, clinical trials are important to assess the

role of the full head block for headache treatment. It

represents the combination of several well tolerated and

effective therapy, with a lack of side effects.

DISCUSSION

There are many examples of peripheral targeted

treatments, such as low-level laser therapy, topical

lidocaine, dry needling, electrical stimulation and

massaging

. There are other forms of inducing anesthesia

with nerve blocks, e.g., lidocaine transdermal patch

It has already been discussed through literature

about the role of peripheral nerve block on headache

management

21,22

. Peripheral nerve block can result in

rapid relief of pain and allodynia, reduce the number of

headache days and medication consumption

and its

effects may last for several weeks. Thereby, nerve block

is a viable and safe treatment option for selected groups

of headache patients, particularly those with intractable

headache.

Although there are many studies about effectiveness

of a specic nerve block

24-26

, especially greater occipital

nerve block

, there is no case report that apply full

head block for treatment of primary headache. Why

should we do a full head block? Due to: (1) distribution

nerve pain - headaches are not limited to one nerve; (2)

necessity of a complete peripheral detachment to arouse

neuromodulation; (3) acute response in headache attack;

and (4) refractory headaches to others procedures.

CONCLUSION

Considering this rational, structured scientic

evidence with blinded and sham-controlled studies is

needed to understand the action mechanism, validate

doses of the anesthetics, train professionals and establish

the efcacy of full nerve block in headache disorders.

REFERENCES

1. Feigin VL, Abajobir AA, Abate KH, Abd-Allah F, Abdulle AM,

Abera SF et al (2017) Global, regional, and national burden

of neurological disorders during 1990–2015: a systematic

analysis for the global burden of disease study 2015. Lancet

Neurol, 16:877–897.

2. Steiner TJ, Stovner LJ, Vos T, Jensen R, Katsarava Z (2018)

Migraine is rst cause of disability in under 50s: will health

politicians now take notice? J Headache Pain, 19:17.

3. Queiroz LP, Peres MFP, Piovesan EJ, Kowacs F, Ciciarelli

MC, Souza JA et al (2009) A nationwide population-based

study of migraine in Brazil. Cephalalgia, 29:642–649.

4. Queiroz LP, Peres MFP, Piovesan EJ, Kowacs F, Ciciarelli MC,

Souza JA et al (2009) A nationwide population-based study

of tension-type headache in Brazil. Headache, 49:71–78.

10(2).indb 39 21/10/2019 18:25:22

Full Head Block for headache treatmen

Dias BF, et al.

Headache Medicine, v.10, n.2, p.37-40, 2019

5. Queiroz LP, Peres MFP, Kowacs F, Piovesan EJ, Ciciarelli

MC, Souza JA et al (2008) Chronic daily headache in

Brazil: a nationwide population-based study. Cephalalgia,

28:1264–1269.

6. Pringsheim T, Davenport WJ, Mackie G, et al (2012) Canadian

Headache Society guideline for migraine prophylaxis. Can J

Neurol Sci, 39(2):S1-59.

7. Puledda F, Goadsby PJ (2017) An Update on Non-

Pharmacological Neuromodulation for the Acute and

Preventive Treatment of Migraine. Headache, 57(4):685-691.

8. Dach F, Éckeli ÁL, Ferreira Kdos S, Speciali JG (2015) Nerve

block for the treatment of headaches and cranial neuralgias

- a practical approach. Headache, 55(1):59-71.

9. Blumenfeld A, Ashkenazi A, Napchan U, et al (2013) Expert

consensus recommendations for the performance of

peripheral nerve blocks for headaches – A narrative review.

Headache, 53:437-446.

10. Dach F, Éckeli ÁL, Ferreira KS, & Speciali JG (2015)

Nerve Block for the Treatment of Headaches and Cranial

Neuralgias - A Practical Approach. Headache: The Journal

of Head and Face Pain, 55:59–71.

11. Kulikov A, Lubnin A (2018) Anesthesia for awake

craniotomy. Curr Opin Anaesthesiol, 31(5):506-510.

12. Costello TG, Cormack JR (2004) Anaesthesia for awake

craniotomy: a modern approach. J Clin Neurosci Off J

Neurosurg Soc Australas, 11(1):16-19.

13. Wahezi SE, Silva K, Shaparin N, et al (2016) Currently

Recommended TON Injectate Volumes Concomitantly

Block the GON: Clinical Implications for Managing

Cervicogenic Headache. Pain Physician, 19(7):1079-86.

14. Levin M (2010) Nerve blocks in the treatment of headache.

Neurotherapeutics, 7(2):197-203.

15. Janis JE, Barker JC, Palettas M (2017) Targeted Peripheral

Nerve-directed Onabotulinumtoxin A Injection for Effective

Long-term Therapy for Migraine Headache. Plast Reconstr

surgery Glob open, 5(3):e1270.

16. Amirlak B, Sanniec K, Pezeshk R, Chung M (2016)

Anatomical Regional Targeted (ART) BOTOX Injection

Technique: A Novel Paradigm for Migraines and

Chronic Headaches. Plast Reconstr surgery Glob open,

4(12):e1194-e1194.

17. Taylor M, Silva S, Cottrell C (2008) Botulinum toxin type-A

(BOTOX) in the treatment of occipital neuralgia: a pilot

study. Headache, 48(10):1476-1481.

18. Flamer D, Alakkad H, Soneji N, et al (2019) Comparison

of two ultrasound-guided techniques for greater occipital

nerve injections in chronic migraine: a double-blind,

randomized, controlled trial. Reg Anesth Pain Med,

44(5):595-603.

19. Piovesan EJ, Di Stani F, Kowacs PA, et al (2007) Massaging

over the greater occipital nerve reduces the intensity

of migraine attacks: evidence for inhibitory trigemino-

cervical convergence mechanisms. Arq Neuropsiquiatr,

65(3A):599-604.

20. Knezevic NN, Tverdohleb T, Nikibin F, Knezevic I, Candido

KD (2017) Management of chronic neuropathic pain with

single and compounded topical a nalgesics. Pain Manag,

7(6):537-558.

21. Giamberardino MA, Martelletti P (2015) Emerging drugs

for migraine treatment. Expert Opin Emerg Drugs,

20(1):137-147.

22. Sun-Edelstein C, Rapoport AM (2016) Update on the

Pharmacological Treatment of Chronic Migraine. Curr Pain

Headache Rep, 20(1):6.

23. Tang Y, Kang J, Zhang Y, Zhang X (2017) Inuence of greater

occipital nerve block on pain severity in migraine patients:

A systematic review and meta-analysis. Am J Emerg Med,

35(11):1750-1754.

24. Zhang H, Yang X, Lin Y, Chen L, Ye H (2018) The efcacy of

greater occipital nerve block for the treatment of migraine:

A systematic review and meta-analysis. Clin Neurol

Neurosurg, 165:129-133.

10(2).indb 40 21/10/2019 18:25:22

Headache Medicine, v.10, n.2, p.41-42, 2019

CASE REPORT

Alice in Wonderland Syndrome

Síndrome de Alice no País das Maravilhas

Wilson Luiz Sanvito

Associate Professor and Emeritus Professor

of Neurology at the Medical Sciences School

of Santa Casa in São Paulo. Assistant Étranger

of the Paris Medical School.

*Correspondence

Wilson Luiz Sanvito

E-mail: wsanvito@uol.com.br

Received: June 12, 2019. Accepted:

June 20, 2019.

Creative Commons (CC BY) Attribution 4.0

International.

At the end of my ofce

hours, I saw to a distressed

mother. Her 9-year-old daughter

presented that day during recess a

condition characterized by strange

perceptions. She reported seeing

huge and deformed people (big

noses, crooked mouths, exceedingly

long arms...). The manifestation

lasted approximately 15 minutes and

was followed by facial paleness and

an episode of mental confusion, with

verbalization of disconnected words

and incoherent phrases. Some

minutes later, the child became

drowsy and fell asleep. When her

mother arrived at the school, she

was still sleeping. When she woke

up, two hours later, she was lucid and

reported only feeling a heaviness in

her head.

During questioning, the mother

informed that since the age of

8 years, her daughter presented

headache episodes preceded

sometimes by blurry vision. The

mother is a migraineur and her

own mother, already deceased, was

also one. Nothing abnormal was

found when examining the minor

and I stated to the mother that the

episode was probably a migraine,

which during childhood can present

this kind of manifestation. In face

of the unbelief of the mother, I

requested a computed tomography

of the head and an EEG – both of

which did not show abnormalities.

I had the opportunity to follow-

up on this patient over the course

of three years. During this time,

she presented headache episodes,

not all of which were preceded

by visual manifestations. In this

case, the diagnosis was settled as

migraine with aura, consisting of a

variant called Alice in Wonderland

Syndrome.

Visual auras are the most

common and originate from the

posterior portion of the brain

(occipital lobe). The description

of a visual aura is not always easy

for the patient. The most detailed

and precise descriptions are

done through own experience, by

either doctors or other healthcare

professionals that suffer from this

sort of migraine. Data are frequently

collected from patients through the

anamnesis, in complaints during the

crises at emergency services, using

questionnaires during interviews,

and by analyzing drawings made

during the postcritical period.

All methods present limitations.

Loss of vision in half the visual

eld (hemianopsia) or in certain

points of the visual eld (negative

scotoma) are common complaints.

Scotoma can also be positive and

manifest in several ways: focused

ashes, colorful circles, the illusion

of blinking lights, eye oaters,

zigzagging lines, mosaic vision (like

a kaleidoscope)... Scotoma can have

various colors (gray, red, golden,

blue or purple), though the color

may not be specic and be more

like a very bright white. There is

also a form of negative scotoma in

which the migraineur sees objects

split in half. This condition can either

increase in size as the crises evolve

or become fragmented into smaller

parts.

Auras can be more elaborate

and present themselves as

distortions of visual gures. These

phenomena are more frequent in

children and are externalized as

perception disorders, which can

include various types of body image

distortions (macropsias, micropsias,

metamorphopsias), feelings of

derealization and depersonalization,

and changes to their perception of

time. This is the Alice in Wonderland

syndrome. In this curious syndrome,

the patient has the feeling that

10(2).indb 41 21/10/2019 18:25:22

Alice in Wonderland Syndrome

Sanvito WL, et al.

Headache Medicine, v.10, n.2, p.41-42, 2019

people are either exceedingly large (macropsias) or

disproportionally small (micropsias). This inadequacy in

size can also be perceived regarding one’s own body,

such that an individual may feel for example that one

of their limbs is gigantic. Other manifestations may

occur: distortion of their own body segments (as if

looking into a distorting mirror) or of others, feeling

of levitation or of a double personality, loss of spatial

recognition, etc. Transitory alterations in certain areas

of the brain (particularly in parietal lobe areas) seem

to be responsible for these described psychosensory

abnormalities. Auras are believed to be determined

through spreading depression, though it is not clear why

extremely elaborate auras – with important perception

disorders – are more frequent during childhood. Perhaps

the immature brain (not entirely myelinated) can be

more vulnerable to a spreading depression event.

This type of migraine is more common in children and

usually begins around the age of 8 years. The associated

manifestations, translated into elaborate auras, usually

give way during adolescence.

The Alice in Wonderland syndrome was reported

for the rst time in 1955 by the English psychiatrist

John Todd, who believed the syndrome was related to

defects in parts that form the eyes. However, it is known

now that the condition occurs due to a neural change

in perception that affects vision, feelings, touch and

even body image. The condition was initially described

as Todd’s syndrome, but as a reader and admirer of

Lewis Carroll, the psychiatrist proposed the name that

established Carroll as an author.

Though this is a polemic discussion, it seems like

migraines inuenced Lewis Carroll’s description of

some characters in the book Alice in Wonderland. The

Englishman Charles Lutwitge Dodgson (1832-1898)

adopted the name Lewis Carroll as a pseudonym to sign

his works of ction (4). This is the explanation. Lewis

Carroll was a professor, mathematician, poet, painter,

amateur photographer and deacon of the Anglican

Church. He would sign his academic publications (math

and logic) with his real name. Carroll was a curious

person that did not get along with adults and adored

young girls. He dedicated his most successful books to

a girl named Alice, daughter of dean Liddell. It seems

that Carroll loved Alice deeply, a 10-year-old girl, while

he was 32 years old. The author was also an excellent

photographer (photography was considered at the time

avant-garde art) and enjoyed photographing girls in

either revealing clothes or naked (2,3).

Regardless of Carroll’s “bilious headaches”, detailed

records from his diary (collected 20 years after they were

reported) demonstrated that he suffered from migraines

with aura. However, the book Alice in Wonderland

appeared in 1865, which according to scholars

researching his biography was before the beginning

of his migraines. Nevertheless, the subject is still under

discussion, with some believing the author had already

experienced previous migraine events.

In conclusion, I must emphasize that the Alice in

Wonderland syndrome is not a prerogative to migraine

and should be considered as a differential diagnosis

for epilepsy, use of hallucinogenic drugs (such as

LSD), consumption of hallucinogenic mushrooms,

schizophrenia, and brain tumors. The syndrome can

also occur during the initial phases of infection by the

Epstein-Barr virus in children (1).

REFERENCES

1. Bolis, V., Karadedos, Ch. et al. – Atypical manifestations

of Epstein-Barr virus in children: a diagnostic challenge. J

Pediatr (Rio J). 2016; 113-21.

2. Sanvito, W. L. - Alice no país das maravilhas. In O Mau Gênio

do Cérebro: O impacto da doença neurológica. A Girafa,

São Paulo, 2006, p. 65.

3. Sanvito, W. L. - Síndrome de Alice no país das maravilhas.

In Síndromes Neurológicas, Atheneu (4ª edição), Rio de

Janeiro, 2019, p. 15.

4. Stoffel, S. L. Lewis Carroll and Alice - New Horizons.

Thames and Hudson, London, 1997.

10(2).indb 42 21/10/2019 18:25:22

Headache Medicine, v.10, n.2, p.43-50, 2019

ABSTRACT

RESUMO

Descritores: Psicologia; Distúrbios da dor de cabeça; Estilo de vida saudável;

Comportamento Sedentário; Exercício.

ORIGINAL ARTICLE

“No Pain, More Gain”? Affect and Adherence to Exercise

in Migraine Patients: A Prospective Cohort Study

“No Pain, More Gain”? Resposta Afetiva e Aderência ao

Exercício em Pacientes com Migrânea: Um Estudo Prospectivo

Arão Belitardo Oliveira

1,2

Dhiego Luigi Gringõn

Mario Fernando Prieto Peres

2,3

Universidade Federal de São Paulo,

Departamento de Neurologia e Neurocirurgia,

Brazil.

Universidade de São Paulo, Faculdade de

Medicina, Instituto de Psiquiatria, Brazil.

Hospital Israelita Albert, Instituto do Cérebro,

Brazil.

*Correspondence

Arão Belitardo Oliveira

E-mail: araoliva@gmail.com

Received: May 15, 2019. Accepted:

May 27, 2019.

Creative Commons (CC BY) Attribution 4.0

International.

Objectives: To compare the affective and perceptual responses to a

standardized exercise session between episodic migraine patients and non-

headache persons, and its inuence on adherence to an 12-week exercise

training program. Methods: In a secondary analyses of a prospective cohort

enrolled in a clinical trial, we assessed the affective response at rest, at 15th min

of exercise, and immediately after an acute 40-min exercise session previously

the training program. All measurements were undertaken in headache-free

days. Participants were subsequently randomly assigned to a 12-week aerobic

exercise-training program, or to a waitlist. In a multiple linear regression

model, variables tested as possible predictors of adherence were body mass

index, cardiorespiratory tness, and the perceived exertion and affect scores

elicited in the previous exercise session. Results: Fifty-four participants were

analyzed for acute exercise session data (mean±SD age: 37.37±11.5; mean±SD

BMI: 26.7±4.5). Patients (N=28) and controls (N=26) showed no differences

in anthropometric characteristics and cardiorespiratory tness. Compared

to controls, migraine patients showed reduced affective response during

and after exercise, but showed no differences in perceived exertion. Twenty-

ve participants (patients: N=13; controls: N=13) concluded the 12-week

exercise-training program. Adherence was lower in migraine group (p = 0.1, d

= 0.641). Multiple linear regression analysis showed post-exercise affect score

as the only predictor variable of adherence to the exercise-training program

(β =0.405, p = 0.040). Conclusions: This study indicates that migraine patients

have lower affective response to exercise, which was associated with adherence

to the training program.

Keywords: Psychology; Headache Disorders; Healthy Lifestyle; Sedentary

Behavior; Exercise.

Objetivos: Comparar as respostas de valência afetiva e percepção do esforço

entre pessoas com migrânea e sem cefaleias durante uma sessão de exercício

padronizada e sua inuência na aderência a um programa de 12 semanas de

treinamento aeróbio. Métodos: Em análise secundária de uma coorte prospectiva

de um estudo clínico, controlado e randomizado, avaliamos a resposta afetiva

basal, no 15º minuto de exercício e imediatamente após uma sessão aguda de

exercício aeróbio previamente ao programa de treinamento aeróbio. Todas

as mensurações foram conduzidas interictalmente. Um modelo de regressão

linear múltipla testou as variáveis basais de IMC, aptidão cardiorrespiratória

e percepção do esforço e escores afetivos da sessão aguda de exercício

como preditoras de aderência ao programa. Resultados: Cinquenta e quatro

participantes foram avaliados (média±DP idade: 37,37±11,5; média±DP IMC:

26,7±4,5). Pacientes (N=28) e controles (N=26) não apresentaram diferenças

nas características antropométricas e aptidão cardiorrespiratória. Comparado

aos controles, pacientes com migrânea exibiram uma resposta afetiva reduzida

durante e após a sessão de exercício aguda, mas sem diferenças signicativa na

percepção do esforço. Vinte e cinco participantes (pacientes: N=13; controles:

N=12) concluíram o protocolo de treinamento aeróbio. Aderência foi menor no

grupo de pacientes (p = 0,1, d = 0,641). A análise de regressão mostrou a resposta

afetiva após a sessão aguda de exercício como única variável preditora de

aderência (β = 0,405, p = 0,040). Conclusão: Esse estudo sugere que pacientes

com migrânea apresentam uma resposta afetiva reduzida ao exercício, a qual

está associada a menor aderências ao programa de treinamento aeróbio.

10(2).indb 43 21/10/2019 18:25:22

Affect and Adherence to Exercise in Migraine Patients

Oliveira AB, et al.

Headache Medicine, v.10, n.2, p.43-50, 2019

INTRODUCTION

Even though regular aerobic exercise has been shown

effective for migraine prevention (1–4), as a chronic pain

condition, migraine may represent an obstacle to physical

activity participation. Epidemiological data have shown

increased risk for having migraine among individuals in

the lowest quintile of cardiorespiratory tness level (5)

and a negative association between migraine prevalence

and physical activity levels (6–10). Migraine attacks per

se can hinder physical activity participation, and physical

activity is considered a trigger factor for around 50-

60 % of patients, while 75.6 % and 84.2 % of patients

believe that moderate and vigorous exercise can

worsen attacks, respectively (11,12). Thus, the prevailing

argument to explain this negative relationship between

physical activity and migraine has been ascribed to fear-

avoidance behavior or kinesiophobia (6–12).

Alternatively, another explanation for this negative

association between physical activity and migraine

might lie in the affective response to exercise. Affective

response to exercise refers to a basic affect domain, or

the pleasure/displeasure one may feel when exercising,

and it has been established as a determinant factor of

future adherence to physical activity participation (13,14).

Its theoretical framework encompasses the rewarding,

self-reinforcing (hedonic) component of the physical

activity behavior (15–17). Exercise performed in the

positive valence is associated with higher adherence,

whereas exercise eliciting negative responses are more

likely to be discontinued (15–17). The affective response

to exercise is believed to be operationalized under the

so-called dual-mode theory (16-18). This theory proposes

a dimensional, rather than categorical, measure of affect,

which in its turn depends on whether the exercise is

performed below, at, or above the ventilatory threshold

(16-18). The ventilatory threshold represents a ventilatory

parameter that indicates the cardiometabolic turning

point marking the transition from aerobic to anaerobic

energy metabolism, above which by-products from

anaerobic metabolism (e.g., CO

, protons, etc.) build-up

in the working skeletal muscles, contributing to metabolic

acidosis, hyperventilation, limb pain, and early fatigue (16-

18). Overall, the affective response is stable and kept on

positive valence when the exercise is performed slightly

below the ventilatory threshold (or mild to moderate

exercise), it largely varies among individuals at the

ventilatory threshold (moderate exercise), and decreases

to negative valence as exercise intensity surpasses the

ventilatory threshold (e.g., vigorous exercise) (18).

Affective response to exercise has never been

assessed in migraine patients. Understanding

psychological factors related to physical activity

behavior in people with migraine has become

particularly relevant, since accumulating evidence points

to increased risk for mental and cardiovascular diseases

in this population (19–22), which in turn can be reduced

by regular physical activity (23). Thus, we wondered

whether migraine patients would exhibit altered affective

response to a single bout of exercise (i.e., acute session)

performed at the ventilatory threshold (moderate

intensity) compared to non-headache individuals, and

whether this previous measure of affect would predict

adherence to a subsequent aerobic exercise-training

program performed at the same exercise intensity. We

hypothesized that individuals with migraine would rate

lower affective scores in the exercise session compared

to non-headache individuals, and the affective response

to exercise would be positively associated with future

adherence to the exercise-training program.

METHODS

This is a prospective cohort study using secondary,

post hoc analyses of affect and perceptual measures

during an exercise session, and their inuence in

adherence to future exercise participation in a supervised

exercise training program. Data were retrieved from

patients enrolled in a clinical trial registered in the

National Institute of Health (www.ClinicalTrials.gov)

under #NCT01972607, and part of the clinical trial results

has been published elsewhere (2). The study protocol

complied with the Good Clinical Practice Principles

and the Helsinki Declaration, and was approved by the

Research Ethics Committee of the Federal University of

São Paulo/Brazil, registered under #08152011.

Participants

Participants were recruited from São Paulo

Hospital´s Headache Unit and a tertiary clinic, The

inclusion criteria were: individuals aged 20 to 60 years, of

both sexes, physically inactive (dened as ≤ 1 day/week

of leisure-time physical activity the previous 12 months),

non-headache individuals and patients with episodic

migraine (having 1-14 attacks per month), including

migraine without aura, migraine with aura, or presenting

both migraine subtypes, according to the 2nd edition of

the International Classication of Headache Disorders

(24). Exclusion criteria were: taking any prescribed

preventive medication, except abortive medication during

migraine attacks, taking dietary supplements, pregnancy,

clinical history of cardiovascular, pulmonary, metabolic,

rheumatic, musculoskeletal, and others neurological

diseases, including other headaches. All participants

had a neurological and cardiac (electrocardiographic)

examination before inclusion in study and gave signed

informed consent.

After being screened for inclusion in the study by

two headache-trained neurologists (authors RTR and

MFPP), all participants were given a headache diary and

were examined every 4 weeks (clinical visits) until the

end of the study for checking headache status (paper-

based headache diaries). Participants who self-reported

never having migraine, without any headache in the past

3 months, and did not present any headache in their

diaries, were considered as controls.

Procedures and Measures

The cardiopulmonary exercise tests, affect measures,

and the aerobic exercise-training program were

10(2).indb 44 21/10/2019 18:25:22

Affect and Adherence to Exercise in Migraine Patients

Oliveira AB, et al.

Headache Medicine, v.10, n.2, p.43-50, 2019

conducted at the Center for Studies in Psychobiology

and Exercise, a University-based center, on two

separated experimental visits. About 1-2 weeks after

the screening visit, participants were scheduled for the

cardiorespiratory tness assessment. Around a week later,

participants performed an acute, 40-min aerobic exercise

session for assessment of the affective response. Figure 1

summarizes the study’s design. All measurements were

undertaken between 8:00AM and 11:00AM, interictally. All

women were assessed within the follicular period of the

menstrual cycle for the affective response.

After the acute exercise session, researcher ABO

randomly assigned participants (simple randomization,

1:1 assignment rate) to receive a 12-week aerobic exercise-

training program or enter a waitlist. An online software

generated random numbers, previously attributed as

follows: odd numbers = exercise-training program, even

numbers = waitlist.

Cardiorespiratory Fitness Assessment

Participants underwent a maximal cardiopulmonary

exercise test on a treadmill (Centurion 300, MICROMED,

Brasília, DF, Brazil) with ramp protocol for determination

of peak oxygen uptake (VO

2Peak

), a gold-standard

measure of cardiorespiratory tness, and the ventilatory

threshold, an amply used cardiometabolic parameter of

submaximal exercise intensity. The ventilatory threshold

consist of a ventilatory indicator reecting the skeletal

muscle energy metabolism, which set the turning point

of exercise intensity above which the metabolic acidosis

from anaerobic metabolism supplementation cannot

be buffered (25). Determination criteria for VO

2Peak

consisted of meeting at least two of the following

criteria: 1) to reach the maximal age-predicted heart rate

(220-age); 2) respiratory exchange ratio > 1.1; 3) rate of

perceived exertion (RPE) ≥ 18. The ventilatory threshold

was determined adopting the ventilatory equivalents

method, dened as the stage where the rst rise in the

ventilatory equivalent of O2 (VE/VO2) occurs without

concurrent rise in the ventilatory equivalent of CO2 (VE/

VCO2) (25). Tests were conducted by a cardiologist and

exercise physiologist, not informed about participants

assignment and independent of the study.

Affective Response and Perceived Exertion

Assessment

Participants were informed that they would perform

a moderate aerobic exercise session according to the

current guidelines for exercise prescription. They were

also aware that the main goal at this visit was to assess

psychological aspects of exercise.

The exercise session consisted of 40 minutes of

moderate walking/jogging on treadmill (depending on

participant’s initial tness level), composed by 5 minutes

of warm-up, 30 minutes inside the aimed intensity, and

5 minutes of cool down period. Intensity was set at the

work rate (m.min

-1

), rate of perceived exertion (RPE),

and heart rate (HR) corresponding to the ventilatory

threshold. The HR was monitored by a heart rate

monitor(Polar® Electro, model F5, Finland) and the RPE

was assessed by the 20-point Borg’s scale (26) . The

RPE score measured at the last minute of the exercise

session was used in the analyses.

Feeling Scale (FS) was used as a measure of affect.

FS is a bipolar, Likert-type scale amply used as a broad

dimension of pleasure/displeasure (basic affect) during

exercise (27). It is composed by 11 points ranging from

+5 to -5, with anchors at zero (“Neutral”) and at each

odd integer, from “Very Good” (+5) to “Very Bad” (-5).

The affective response was assessed by two experienced

exercise physiologists (ABO, DLG), randomly assigned

(coin ipping) to conduct each experiment. FS was

employed at three time points: at rest, just before the

exercise initiates (FSREST), at the 15th minute of exercise

(FSEXE), and immediately after the exercise cessation

(FSPOST). Conversation was limited to answering

participants’ questions regarding the protocol, and

participants were not allowed to listen to music, or to

use any portable electronics. Participants experiencing

migraine attacks during the exercise sessions were

excluded from the analysis.

Aerobic Exercise-Training Protocol

Exercise sessions reproduced the acute exercise

session protocol with regard duration and intensity, and

were delivered 3 times per week. All exercise sessions

were supervised by exercise physiologists (ABO, DLG,

and MTM).

Statistical Analyses

Differences between migraine and control groups for

anthropometric variables, cardiopulmonary tness, and

adherence for the exercise-training groups were analyzed

by independent t-test. Comparisons between groups for

affective response were analyzed by repeated-measures

ANOVA,with 2 groups x 3 time points (FSREST, FSEXE, and

FSPOST); Bonferroni’s adjustments were computed for the

condence intervals of multiple pairwise comparisons. If

Figure 1. Study´s design.

10(2).indb 45 21/10/2019 18:25:23

Affect and Adherence to Exercise in Migraine Patients

Oliveira AB, et al.

Headache Medicine, v.10, n.2, p.43-50, 2019

the assumption of sphericity was violated in the repeated-

measures ANOVAs, the degrees of freedom were adjusted

by Greeenhouse-Geisser´s correction.

A multiple linear regression model was applied to

test the predictors of adherence to exercise (dependent

variable). Adherence was dened as the percentage of

attendance to the exercise protocol sessions. Predictors

variables were, body mass index (BMI), VO

2Peak

, RPE,

FSREST, FSEXE, and FSPOST. A stepwise method for

variables selection was employed in the regression

model. Analyses were computed by the SPSS software

(IBM SPSS Statistics for Windows, Version 20.0. Armonk,

NY), and graphs were designed by GraphPad Prism®

software (GraphPad Software Inc., Version 5.0, San Diego,

CA). A p < 0.05 was considered statistically signicant.

RESULTS

Participants’ ow in the study is shown in

Figure 2. Fifty-four participants (Male: N = 10, Female: N

= 44; mean±SD age: 37.37±11.5 and BMI: 26.7±4.5) were

included in the analyses. Migraine (n = 28) and control

(n = 26) groups were homogenous regarding sex, age,

BMI, cardiorespiratory tness, as well as there were no

difference between groups for the cardiorespiratory data

and work rate elicited at the ventilatory threshold (both

~ 55 % of maximal cardiorespiratory tness, and ~70 % of

maximal heart rate) (Table 1).

Figure 2. Participants’ ow in the study.

Table 1. Participants` anthropometrical, clinical, and

cardiorespiratory data.

Variables

Migraine

(N=28)

Control

(n=26)

Anthropometric Data

Sex (%)

Male 5(17.9) 5(19.2)

Female 23(82.1) 21(80.8)

Age (years) 38.6±12.4 35.9±10.5

Body Weight (kg) 72.1±16.0 69.7±11.7

Height (m) 1.62±0.08 1.63±0.08

BMI (kg/m

) 26.9±5.0 26.4±3.9

Clinical Data

Living w/ Disease (yrs) 17.6±11.1 0

Days with Headaches (/month) 9.5±6.0 0

Migraine Frequency (/month) 8.6±6.0 0

Pain Intensity (0-3) 1.58±0.3 0

Cardiopulmonary Data

At Peak

2Peak

(mL.kg.min

-2

) 31.8±6.7 32.5±7.5

HR (b.p.m) 181.7±15.1 182.8±9.5

HR (% age predicted) 100.3±6.6 99.5±4.8

WR (watts) 110.0±32.5 116.2±34.5

RPE 19.4±0.9 19.3±0.9

At the Ventilatory Threshold

(% VO

2Peak

) 55.2±9.4 55.4±7.3

HR (b.p.m) 127.7±17.7 125.1±15.6

WR (watts) 66.1±20.2 64.2±16.6

RPE 10.3±

2.5 10.1±2.3

2Peak

: Peak oxygen uptake. HR: Heart rate. WR: Work rate.

RPE: Rate of perceived effort.

For the affective response to acute exercise,

repeated-measures ANOVA of FS showed a main

effect of time [F(1, 52) = 37.5; p < 0.001; η

= 0.64], a

main effect of group [F(1, 52) = 10.6; p < 0.002; η

0.41], and interaction [F(2, 104) = 5.9; p < 0.048; η

0.2] (Fig. 3a). Multiple pairwise comparisons showed

no differences between migraine and control groups

for FSREST (mean±SD = 3.5±1.9 vs 4±1.1, respectively,

p = 0.262), while there was a signicant progressive

decline from FSREST to FSPOST for both groups (Fig.

3a). The migraine group had a steeper decline, which

was signicantly lower than control group for FSEXE

(mean±SD = 2.0±1.3 vs 2.9±1.3, p < 0.031, respectively)

and FSPOST (mean±SD = 1.4±1.4 vs 2.7±1.3, p = 0.001,

respectively) (Fig. 2a). The RPE at the end of the

exercise session was not different between control and

migraine groups (mean±SD = 11.6±1.4 vs 12.4±1.4, p >

0.05, d = 0.1, respectively) (Fig. 3b).

For the adherence data, twenty-ve (migraine: n

= 13; control: n = 12) completed the exercise-training

program and were analyzed in the regression model.

There was no difference between groups for adherence

10(2).indb 46 21/10/2019 18:25:23

Affect and Adherence to Exercise in Migraine Patients

Oliveira AB, et al.

Headache Medicine, v.10, n.2, p.43-50, 2019

Although physical activity behavior is determined

by a myriad of social, cultural, and affective-cognitive

factors, the affective response to exercise is a relevant

and well-established topic in behavioral research, since it

is associated with physical activity participation, and its

public health implications in terms of management and

prevention of mental and cardiovascular diseases (14-

17). Indeed, in recognition of the relevance of affective

response on future exercise participation, current exercise

prescription guidelines have included the feeling scale as

a complementary parameter of exercise intensity (28).

We recognize that physical activity behavior is

complex, and in migraine patients, attack-related pain per

se can hinder physical activity participation and contribute

to fear-avoidance behavior/kinesiophobia (11-13). In fact,

anxiety-related processes seem to play a relevant role in

physical activity behavior in this population. For example,

in a cohort of 100 patients, Farris et al (2019) showed

that intentional avoidance of physical activity is prevalent

in up to 78 % of patients, and it positively correlates with

migraine frequency (11). Still in this study, over 70 % of

patients reported avoiding both moderate and vigorous

exercise on average 3 times per week in the previous

month, indicating that intentional avoidance constitutes

a relevant factor contributing to lower physical activity in

this population (11). In another analysis, the same group

found that physical activity avoidance is inuenced

by anxiety sensitivity, and higher anxiety score were

associated with a signicant increase in the odds of PA

avoidance at both moderate and vigorous intensities,

with stronger associations between the domains

physical concerns and vigorous exercise avoidance (up

to 7.5-fold increase) (12). Although we did not inquire our

patients about their believes/perceptions of exercise as a

trigger, or anxiety sensitivity scores, migraine frequency

or days with migraine had no correlation with adherence

Figure 3. Affective response (a) and perceived effort (b) of a 40-min. aerobic exercise session; Data are expressed as

mean±SE. *: p < 0.05 vs REST; **: p < 0.01 vs REST; #: p < 0.05 vs Control; ##: p < 0.01 vs Control; Multiple pairwise

comparisons of repeated-measure ANOVA.

to the exercise program [55.9±18.4 % vs 66.4±13.0 %,

respectively; t(23) = 1.6, p = 0.1, d = 0.64], although a large

effect size was observed.

In the whole exercise-training cohort, multiple linear

regression analysis showed FSPOST the only predictor

variable of adherence to subsequent exercise-training

program (β = 0.405, p = 0.04). Based on the adjusted R

data of our model, 12.9 % of variance in adherence was

explained by FSPOST. Also, the coefcients of this model

showed that, if all the other variables were kept constant,

every 1-point drop in the FS score resulted in 4.2 % drop

in adherence.

In order to further explore whether adherence could

be affected by migraine attacks frequency, we used

Pearson’s correlations test (as these variables presented

normal distribution) for analyses between clinical

variables and adherence in the exercise-training migraine

cohort. There were no signicant correlations between

adherence and changes in pre-post values (Δ values)

for days with migraine (r = -0.01, p = 0.981), or migraine

frequency (r = -0.18, p = 0.544) (Table 2). Neither there

were correlations between clinical and affective variables.

DISCUSSION

Our study shows for the rst time a reduced

affective response to aerobic exercise, both during

and after an acute exercise session, in individuals with

migraine compared to non-headache individuals. Also,

we provided further evidence to the idea considering the

affective response to exercise captured by the feeling

scale as a potential determinant factor of physical

activity behavior (14-17), by showing a predictive value

of post-exercise affect on future adherence to an

exercise program.

10(2).indb 47 21/10/2019 18:25:25

Affect and Adherence to Exercise in Migraine Patients

Oliveira AB, et al.

Headache Medicine, v.10, n.2, p.43-50, 2019

to the training program or affective response, and our

sample was composed by patients voluntarily interested

in exercise who did not report any attack attributed

to physical exercise (based on headache diaries data).

As such, the results found here add a new perspective

in understanding the negative relationship between

migraine and physical activity levels, which to date has

been unanimously ascribed to fear-avoidance/anxiety

mechanisms. The affect-based process contemplates the

hedonic, self-reinforcing properties of physical activity

(14-18), which are thought to be mediated by common

neurophysiological mechanisms disrupted in migraine

pathophysiology, such as monoaminergic, opioidergic,

and endocannabinoidergic signaling (2,4). Therefore, it

is likely that altered affective processes occurring during

the physical exercise session could also inuence this

negative relationship between migraine and physical

activity. This merits further investigation.

Lastly, but not least, anxiety-related processes

may eventually underlie the negative affect-exercise

adherence relationship, as anxiety sensitivity has shown

to moderate the affective response to exercise in other

clinical populations (29). Farris’s group showed that

in low-active smokers seeking treatment for smoking

cessation, anxiety sensitivity negatively associated with

physical activity enjoyment scale (PACES) and correlated

with anxiety and mood in the 1-mile walk test (29). The

authors ponder that anxiety sensitivity may attenuate

positive physical feelings (enjoyable feelings) elicited by

physical activity, exacerbate the forcasting of negative

affective and physical outcomes, resulting in affective

states that contribute to avoidance behavior (29).

With regard the exercise intensity and its implication

on the affect-adherence relationship, a consistent line

of evidence suggests a negative association between

vigorous exercise and long-term adherence to physical

activity (14-18). These authors criticize the “no pain, no

gain” pop culture, arguing that in terms of public health,

pursuing higher exercise intensity may be detrimental

for assuring long-term adherence to physical activity

participation. Exercise performed at the ventilatory

threshold, as used here, prevents the build-up of by-

products and metabolites from anaerobic metabolism,

and hence hyperventilation, limb pain, and early fatigue

(19). It also promotes cardiorespiratory tness and is

a standardized cardiometabolic parameter of exercise

intensity. Nonetheless, affective response at this intensity

largely varies in the population (19). On the other hand, as

vigorous exercise may also promote specic therapeutic

effects, recent work has aimed at manipulating exercise

prescription in order to conceive vigorous exercise with

positive affect, and hence, promote long-term adherence

to high intensity exercise (30). These authors have

employed repeated, short high-intensity bouts of exercise

(also known as high intensity interval training, or “HIIT”)

(30). In the context of migraine, data from clinical trials

have shown preventive effects with either moderate (i.e.,

at the ventilatory threshold) (2-4), or vigorous exercise

performed as HIIT (≥ 90% of maximal HR) (31). In the later

study, vigorous exercise performed with the HIIT approach

promoted superior clinical effects on migraine frequency,

cardiorespiratory tness, and retinal blood vessels dilation,

suggesting greater clinical and cardiovascular effects

compared to moderate exercise (31). Because to date

there is no study comparing long-term adherence between

vigorous vs moderate exercise in migraine patients, these

data underscore the need for further studies aiming at

investigating psychological and physiological outcomes

from different exercise prescriptions in migraine trials,

and developing new strategies to increase the affective

component of physical activity.

The affective response and adherence to exercise

should be further investigated in people with migraine.

As outlined by Farris et al (2019), clinicians should aim at

managing the subjective appraisal of bodily sensations

by incorporating psychoeducation strategies to reinforce

the clinical benets of regular physical activity (2-3),

adjusting current exercise prescriptions frames to t

gradual exposure approaches (i.e., desensitization),

and by comparing beliefs of migraine trigger effects of

physical activity with objective data (12). We propose

for the newbie patient that is physically inactive or low-

active (i.e., those not meeting the minimum amount

of physical activity recommended by health and

exercise guidelines), practitioners should preconize a

reduced session time for aerobic exercise (e.g., up to

Table 2. Correlations between adherence and migraine clinical data.

Adherence to

Exercise

Migraine Days

Migraine

Frequency

Δ Migraine Days

Δ Migraine

Frequency

Adherence

- -

Migraine Days

r -.35 -

p .23

Migraine Frequency

r -.37 .86 -

p .20 <.001

Δ Migraine Days

r -.00 .36 .30 -

p .98 .22 .31

Δ Migraine Frequency

r -.18 .17 .20 .88 -

p .54 .57 .49 <.001

10(2).indb 48 21/10/2019 18:25:25

Affect and Adherence to Exercise in Migraine Patients

Oliveira AB, et al.

Headache Medicine, v.10, n.2, p.43-50, 2019

20 minutes), with gradual, progressive load increment

until targeted perceptual (e.g., keep between 11 and 13

on 20-point Borg´s scale, the verbal anchors “Light” and

“Somewhat hard”, respectively), affective (e.g., no lower

than +1 on feeling scale, the verbal anchor “Good”), and

cardiovascular parameters (e.g., not above ventilatory

threshold, or ~70 % of maximal age-predicted HR). Other

exercise prescription approaches (e.g., HIIT) should be

also tested in this population to establish safe, enjoyable,

and realistic exercise routines that assure adherence.

One should be aware of several limitations in this

study while interpreting these ndings. This study found

a large effect size for the affect variables outcome, but

the small sample size yielded underpowered data (β =

0.73), and limit extrapolation from the regression model.

From clinical practice, we perceive that migraine patients

interested in participating in studies with physical exercise

represent a minority of this population, and this may

constitute selection bias. Additionally, based on headache

diaries checking, physical activity was not a trigger

among the patients of this study, most participants were

women, and there were some restrictive inclusion criteria.

All these factors limit the generalizability of our results.

Importantly, the expectation towards improvement in

headaches through exercise training might have rendered

patients more motivated than control individuals. Yet,

if this was true, our results would be underestimated.

Another limitation concerns to performance bias, as

the experimenters that conducted the exercise sessions

were not blinded to participants’ conditions. This could

have resulted in unequal attention delivered by the

experimenters to the participants, inuencing the affect

scores. Lastly, although the exercise protocol tried to

reproduce a regular aerobic exercise session, it is not

possible to exclude the inuence of factors related to the

laboratory/experimental settings.

The strengths of this study are the prospective design,

the use of gold-standard measure of cardiorespiratory

tness, and standardized exercise testing and prescription

based on ventilatory threshold, which allowed us to

compare subjective psychological parameters in response

to an objective, physiologic stimulus.

CONCLUSIONS

In conclusion, the affective response to an aerobic

exercise of equivalent physiological intensity is reduced in

migraine patients compared to non-headache individuals,

and predicted adherence to future participation in an

exercise-training program. Interventions with physical

activity/exercise should adopt the feeling scale as a

complementary parameter of exercise intensity and

exploit activities that elicit higher affective responses.

REFERENCES

1. Amin FM, Aristeidou S, Baraldi C, Czapinska-Ciepiela EK,

Ariadni DD, di Lenola D, et al. The association between

migraine and physical exercise. The journal of headache and

pain [Internet]. 2018;19(1):83.

2. Oliveira AB, Ribeiro RT, Mello MT, Tuk S, Peres MFP.

Anandamide Is Related to Clinical and Cardiorespiratory

Benets of Aerobic Exercise Training in Migraine Patients:

A Randomized Controlled Clinical Trial. Cannabis and

Cannabinoid Research [Internet]. 2019 Feb 28;can.2018.0057.

3. Peres M, Mercante J, Belitardo de Oliveira A. Non-

Pharmacological Treatment for Primary Headaches

Prevention and Lifestyle Changes in a Low-Income

Community of Brazil: A Randomized Clinical Trial. Headache:

The Journal of Head and Face Pain. 2019;59(1):86–96.

4. Oliveira AB, Bachi ALL, Ribeiro RT, Mello MT, Vaisberg M,

Peres MFP. Exercise-Induced Change in Plasma IL-12p70

Is Linked to Migraine Prevention and Anxiolytic Effects in

Treatment-Naïve Women: A Randomized Controlled Trial.

NeuroImmunoModulation. 2017;24(6):293–299.

5. Hagen K, Wisløff U, Ellingsen Ø, Stovner L, Linde M.

Headache and peak oxygen uptake: The HUNT3 study.

Cephalalgia. 2016;36(5):437–44.

6. Varkey E, Hagen K, Zwart J, Linde M. Physical activity and

headache: results from the Nord-Trøndelag Health Study

(HUNT). Cephalalgia : an international journal of headache.

2008 Dec;28(12):1292–7.

7. Hagen K, Åsberg AN, Stovner L, Linde M, Zwart JA, Winsvold

BS, et al. Lifestyle factors and risk of migraine and tension-

type headache. Follow-up data from the Nord-Trøndelag

Health Surveys 1995–1997 and 2006–2008. Cephalalgia.

2018;0(0):1–8.

8. Le H, Tfelt-hansen P, Skytthe A et al. Association between

migraine , lifestyle and socioeconomic factors : a population-

based cross-sectional study. Journal of Headache and Pain.

2011;12:157–72.

9. Molarius A, Tegelberg A, Ohrvik J. Socio-economic factors,

lifestyle, and headache disorders - a population-based study

in Sweden. Headache. 2008;48(10):1426–37.

10. Queiroz LP, Peres M, Piovesan E, Kowacs F, Ciciarelli M,

Souza J, et al. A nationwide population-based study of

migraine in Brazil. Cephalalgia : an international journal of

headache. 2009 Jun;29(6):642–9.

11. Farris SG, Thomas JG, Abrantes AM, Lipton RB, Burr

EK, Godley FA, et al. Anxiety sensitivity and intentional

avoidance of physical activity in women with probable

migraine. Cephalalgia. 2019;1(0):1–5.

12. 12. Farris SG, Thomas JG, Abrantes AM, Godley FA, Roth JL,

Lipton RB, et al. Intentional avoidance of physical activity in

women with migraine. Cephalalgia Reports. 2018;1:1–8.

13. Benatto MT, Bevilaqua-Grossi D, Carvalho GF, Bragatto MM,

Pinheiro CF, Straceri LS, et al. Kinesiophobia Is Associated

with Migraine. Pain Medicine. 2019;20(4):846–51.

14. Ekkekakis P, Partt G, Petruzzello SJ. The Pleasure and

Displeasure People Feel When they Exercise at Different

Intensities. Sports Medicine [Internet]. 2011;41(8):641–71.

15. Ekkekakis P. People have feelings! Exercise psychology in

paradigmatic transition. Current Opinion in Psychology

[Internet]. 2017;16:84–8.

16. Rhodes RE, Kates A. Can the Affective Response to Exercise

Predict Future Motives and Physical Activity Behavior?

A Systematic Review of Published Evidence. Annals of

Behavioral Medicine. 2015;49(5):715–31.

17. Williams DM. Exercise, affect, and adherence: an integrated

model and a case for self-paced exercise. Journal of sport &

exercise psychology. 2008 Oct;30(5):471–96.

18. Ekkekakis P, Hall EE, Petruzzello SJ. Variation and

homogeneity in affective responses to physical activity

of varying intensities: an alternative perspective on dose-

response based on evolutionary considerations. Journal of

sports sciences. 2005;23(5):477–500.

19. Kurth T, Winter A, Eliassen A, Dushkes R, Mukamal K,

Rimm E, et al. Migraine and risk of cardiovascular disease

in women: prospective cohort study. BMJ. 2016;353:i2610.

20. Mahmoud AN, Mentias A, Elgendy AY, Qazi A, Barakat

AF, Saad M, et al. Migraine and the risk of cardiovascular

and cerebrovascular events: a meta-analysis of 16 cohort

10(2).indb 49 21/10/2019 18:25:25

Affect and Adherence to Exercise in Migraine Patients

Oliveira AB, et al.

Headache Medicine, v.10, n.2, p.43-50, 2019

studies including 1 152 407 subjects. BMJ Open [Internet].

2018;8(3):e020498.

21. Peres M, Mercante J, Tobo P, Kamei H, Bigal M. Anxiety and

depression symptoms and migraine: a symptom-based

approach research. Journal of Headache and Pain. 2017;18:1–

22. Mercante J, Peres M, Bernik A. Primary headaches in patients

with generalized anxiety disorder. Journal of Headache and

Pain. 2011;12(3):331–8.

23. Pedersen BK, Saltin B. Exercise as medicine – evidence

for prescribing exercise as therapy in 26 different chronic

diseases. Scandinavian Journal of Medicine and Science in

Sports. 2015;25(Suppl 3):1–72.

24. Headache Classication Sub-Committee of the International

Headache Society. The International Classication of

Headache Disorders. Cephalagia, 2004, 24:9-160.

25. Balady GJ, Arena R, Sietsema K, Myers J, Coke L, Fletcher

GF, et al. Clinician’s guide to cardiopulmonary exercise

testing in adults: A scientic statement from the American

heart association. Circulation. 2010 Jul 13;122(2):191–225.

26. Borg GA. Psychophysical bases of perceived exertion. Med

Sci Sports Exerc. 1982;14(5):377-81.

27. Hardy C, Rejeski W. Not what, but how one feels: the

measurement of affect during exercise. Journal of sport &

exercise psychology. 1989;11:304–17.

28. American College of Sports Medicine’s Guidelines for

Exercise Testing and Prescription. 9th ed. Philadelphia,

PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2014.

456.

29. Farris SG, Legasse AJ, Uebelacker LA, Brown RA, Price LH,

Abrantes AM. Anxiety Sensitivity is Associated with Lower

Enjoyment and an Anxiogenic Response to Physical Activity

in Smokers. Cognitive Therapy and Research [Internet].

2018;0(0):1–10.

30. Zenko Z, Ekkekakis P, Ariely D. Can You Have Your Vigorous

Exercise and Enjoy It Too? Ramping Intensity Down

Increases Postexercise, Remembered, and Forecasted

Pleasure. Journal of Sport and Exercise Psychology

[Internet]. 2016;38(2):149–59.

31. Hanssen H, Minghetti A, Magon S, Rossmeissl A, Rasenack

M, Papadopoulou A, et al. Effects of different endurance

exercise modalities on migraine days and cerebrovascular

health in episodic migraineurs: A randomized controlled

trial. Scandinavian Journal of Medicine and Science in

Sports. 2018;8(3):1103–12.

10(2).indb 50 21/10/2019 18:25:25

Headache Medicine, v.10, n.2, p.51-55, 2019

ABSTRACT

RESUMO

Descritores: Enxaqueca com aura; Enxaqueca sem aura; Vertigem; Distúrbios

vestibulares; Tontura.

ORIGINAL ARTICLE

Accompanying Symptoms in Vestibular Migraine

Sintomas Acompanhantes na Enxaqueca Vestibular

Aline Turbino Neves Martins da Costa

Daniel Guedes Tomedi

Camila Naegeli Caverni

Larissa Mendonça Agessi

Rosemeire Rocha Fukue

Henrique Ballalai Ferraz

Thais Rodrigues Villa

Universidade Federal de São Paulo

*Correspondence

Aline Turbino Neves Martins da Costa

E-mail: alineturbino@gmail.com

Received: May 6, 2019.

Accepted: May 17, 2019.

Creative Commons (CC BY) Attribution 4.0

International.

Objective: The aim of this study was to classify the patients with vestibular

migraine into the subgroups with and without aura, and to evaluate the occurrence

of the accompanying symptoms of migraine in each subgroup. Methods: A

prospective study performed at a tertiary center of vestibular migraine, with

patients fullling denitive diagnostic criteria for vestibular migraine through

International Classication of Headache Disorders ICHD-3 β. Patients were

stratied in the subtypes with and without aura, and the accompanying symptoms

were veried in each subgroup. Results: A total of 143 patients were included,

124 women and 19 men (86% and 13%, respectively). The mean age of onset of

migraine in the patients ranged from 4 to 71 years (SD: 16.0) with a mean of 23

years, and an average headache frequency of 17 days per month (SD: 19.6), with a

visual analog scale mean of 7.45 (SD: 1.88). Of the 143 patients evaluated, 101 (70%)

had ICHD-3 β criteria for the diagnosis of migraine with aura. In patients with the

migraine subgroup with aura, we found a higher relative risk for nausea 2,78 (CI:

0.15-1.0; p0.04), vomiting, 2.65 (CI: 1.26-5.55; p0.009), phonophobia 3,546 (1,647-

7,637, p0,001), osmophobia 3,016 (1,219-7,462, p0,014), kinesiophobia, 2,391 (1,128-

5,071, p, 021), tinnitus 2,275 (1,062-4,873, 032), aural fullness 3,934 (1,519 - 10,192,

p0,003), motion sickness associated with dizziness 3,924 (1,415 - 10,881, p0,006).

Conclusion: In our center, migraine with aura was the most frequent subtype

of migraine in patients with vestibular migraine. During the head attacks, some

associated symptoms were more likely to occur in the aura subgroup, among them:

nausea, vomiting, phonophobia, osmophobia, kinesiophobia, tinnitus, aural fullness

and motion sickness accompanied by dizziness. In our sample, vestibular migraine

associated with migraine with aura showed a higher risk of associated symptoms,

suggesting that this subgroup is more severe, and with a more disabling disease.

Keywords: Migraine with aura; Migraine without aura; Vertigo; Vestibular

disorders; Dizziness.

Objetivo: O objetivo deste estudo foi classicar os pacientes com enxaqueca

vestibular nos subgrupos com e sem aura e avaliar a ocorrência dos sintomas

associados à enxaqueca em cada subgrupo. Métodos: Estudo prospectivo

realizado em um centro terciário de enxaqueca vestibular, com pacientes

preenchendo critérios diagnósticos denitivos para enxaqueca vestibular por

meio da Classicação Internacional de Distúrbios da Dor de Cabeça ICHD-3 β.

Os pacientes foram estraticados nos subtipos com e sem aura, e os sintomas

associados foram vericados em cada subgrupo. Resultados: Foram incluídos 143

pacientes, 124 mulheres e 19 homens (86% e 13%, respectivamente). A idade média

de início da enxaqueca nos pacientes variou de 4 a 71 anos (DP: 16,0), com média

de 23 anos e frequência média de cefaleia de 17 dias por mês (DP: 19,6), com média

da escala visual analógica de 7,45 (DP: 1,88). Dos 143 pacientes avaliados, 101 (70%)

apresentavam critérios ICHD-3 β para o diagnóstico de enxaqueca com aura. Nos

pacientes com subgrupo de enxaqueca com aura, encontramos maior risco relativo

de náusea 2,78 (IC: 0,15-1,0; p0,04), vômitos 2,65 (IC: 1,26-5,55; p0,009), fonofobia

3.546 ( 1.647-7.637, p0.001), osmofobia 3.016 (1.219-7.462, p0.014), cinesiofobia,

2.391 (1.128-5.071, p, 021), zumbido 2.275 (1.062-4.873, 032), plenitude auricular

3.934 (1.519 - 10.192, p0.003), enjoo de movimento associado a tontura 3.924

(1.415 - 10.881, p0.006). Conclusão: Em nosso centro, a enxaqueca com aura foi

o subtipo mais frequente de enxaqueca em pacientes com enxaqueca vestibular.

Durante os ataques na cabeça, alguns sintomas associados apresentaram maior

probabilidade de ocorrer no subgrupo aura, entre eles: náusea, vômito, fonofobia,

osmofobia, cinesiofobia, zumbido, plenitude aural e enjoo acompanhados de

tontura. Em nossa amostra, a enxaqueca vestibular associada à enxaqueca com

aura apresentou maior risco de sintomas associados, sugerindo que esse subgrupo

é mais grave e com uma doença mais incapacitante.

10(2).indb 51 21/10/2019 18:25:25

Accompanying Symptoms in Vestibular Migraine

Costa ATNM, et al.

Headache Medicine, v.10, n.2, p.51-55, 2019

INTRODUCTION

Vestibular migraine (VM) is one of the variants of

migraine, with vestibular symptoms (VS) beyond the

typical disease model, with a lifetime prevalence of 1%.

It is the most common cause of episodic vertigo and the

second most frequent cause of vertigo in general.

Studies on vertigo and dizziness showed a

prevalence of 4% to 51.7% among patients with migraine.

A tertiary neuro-otology center studied the epidemiology

of vestibular disorders and their clinical form and found

28.2% of patients with VM.

Many authors have already demonstrated the

association between migraine and vestibular symptoms,

which are three times more common in the migraine

population.

The International Headache Society (IHS) has

included in an appendix, in 2013, the third edition of the

International Classication of Headache Disorders a rst

step towards the identication of new entities.

5,6

(Table 1)

The accompanying symptoms are part of the

diagnostic criteria for both migraine and vestibular

migraine and may be responsible together with

vestibular symptoms for the signicant impact on

patients’ quality of life.

METHODS

A prospective study carried out in a tertiary VM

outpatient clinic at the Federal University of São

Paulo, from Jan 2014 to July 2016, by a neurologist

specialized in headache, where demographic data

was collected, as diagnosis of the migraine subtypes

and accompanying symptoms.

We evaluated 198 patients with vestibular symptoms

and headache, and 55 patients were excluded. All

patients included had diagnostic criteria for denitive VM

by ICHD-3β, and the neurological and otoneurological

examination of these patients was normal.

We excluded 55 patients, where dizziness could

be attributed to systemic causes, or to patients with

neurological diseases (epilepsy, stroke) and vestibular,

as well as those who used ototoxic medications, chronic

alcoholics, patients with a history of drug addiction,

previous history of otologic diseases (antecedent of

repeated ear infections, ear trauma) and cranial injuries.

Audiometric examination and computerized cranial

tomography were performed, before inclusion of the

patients. Patients with low-frequency sensorineural

hearing loss were excluded, as well as patients with

ischemic lesions in neuroimaging

Regarding statistics, we rst characterized the

sample collected by calculating frequencies and

percentages or means and standard deviations. Patients

were then divided into migraine without aura and

migraine with aura and the rates and the percentages

were obtained for each group.

The groups were compared with respect to the

follow-up symptoms, using the chi-square test

and,

if necessary, the Fisher’s exact test.

. Odds ratios (OR)

and respective 95% condence intervals (95% CI) were

also calculated.

The statistical package used was Minitab, version 18.

This research was approved by the Ethics

Committee of the University and the patients completed

the Informed Consent Term.

RESULTS

Of the 198 patients evaluated, 55 were excluded with

a denitive diagnosis of VM. Thus, the group consisted of

124 women and 19 men (86% and 13%, respectively). The

mean age of onset of migraine in patients ranged from 4

to 71 years, with a mean of 23 years (SD16), with a mean

frequency of 17 days of headache per month (SD10.8). Of

the 143 patients with VM, 101 (70%) had ICHD-3 β criteria

for migraine with aura (MA) and 29% (42) for migraine

without aura (MWO) (Table 2).

As for the type of aura, 87 (86%) patients presented

visual aura, 31 (30%), sensory aura and 3 (2.9%), motor

aura (Table 3).

Concerning pain intensity assessed by visual analog

scale (VAS), a mean of 7.45 (SD1.88) was obtained.

During VM crises, we evaluated some accompanying

symptoms in the subgroups of migraine with and without

aura. The symptoms were more frequent in VM with aura.

Definite V

At least ve episodes with vestibular symptoms of a

moderate or severe intensity, lasting 5 minutes to 72

hours.

Current or previous history of migraine with or without

aura according to the International Classication of

Headache Disorders (ICHD).

One or more migraine features with at least 50% of the

vestibular episodes:

- Headache with at least two of the following

characteristics: one-sided location, pulsating quality,

moderate or severe pain intensity, aggravation by

routine physical activity;

- Photophobia and phonophobia;

- Visual aura.

Not better accounted for by another vestibular or ICHD

diagnosis.

Table 1. VM diagnostic criteria - ICHD-B β diagnosis

Photophobia, phonophobia, nausea, and vomiting

are present in the diagnostic criteria of VM and should

accompany at least 50% of the episodes of dizziness.

5-6

The association of VM with subtypes of migraine,

migraine with and without aura, and its association with

accompanying symptoms has not been consistently

analyzed in the literature.

OBJECTIVE

To classify the patients with denitive diagnosis of

VM in the subtypes of migraine with and without aura

and to evaluate the accompanying symptoms of each

subgroup.

10(2).indb 52 21/10/2019 18:25:25

Accompanying Symptoms in Vestibular Migraine

Costa ATNM, et al.

Headache Medicine, v.10, n.2, p.51-55, 2019

In the MA subgroup we found a higher relative risk

for: nausea 2,788 (1,020 - 7,623, p0,040); vomiting 2,655

(1,269-5,557, p0.009); phonophobia 3,546 (1,647 - 7,637,

p = 0.001), osmophobia 3,016 (1,219 - 7,462, p = 0,014),

kinesiophobia 2,391 (1,128 - 5,071, p = 0,021), tinnitus

4,273 (1,215 - 15,049, p = 3,934 (1,519-10,192, p = 0.003),

motion sickness associated with dizziness 3,924 (1,415-

10,881, p = 0.006) (Table 4).

Table 3. Frequency distribution of the variable Type of

aura

Type of aura

Yes No

n % n %

Visual aura 87 86,14 14 13,86

Sensory Aura 31 30,69 70 69,31

Motor aura 3 2,97 98 97,03

Others 2 1,98 99 98,02

n: number of patients.

Variable N Mean SD

Age (years) 143 37.83 17.66

Age at headache onset

(years)

143 23.13 16.08

Pain duration (hours) 143 15.43 9.92

Pain frequency (days/

month)

143 17.52 10.82

Daily headache (months) 143 13.53 19.68

Pain intensity (VAS) 143 7.45 1.88

Sex

Female Male

86.71% 13.29%

Aura

with aura without aura

70.63% 29.37%

Table 2. Demographic and clinical characteristics of

patients with migraine

SD: standard deviation, VAS: visual analog scale.

Table 4. Joint frequency distribution between patient characteristics and VM and migraine groups with aura and

without aura, p-value of the chi-square test, odds ratio and respective 95% condence interval.

Variables

Without aura With aura

P Value Odds ratio

Confidenc

interval

n % n %

Nausea 33 78,57 92 91,02 0,040 2,788 1,020 7,623

Vomiting 17 40,48 65 64,36 0,009 2,655 1,269 5,557

Phonophobia 13 30,95 101 61,39 0,001 3,546 1,647 7,637

Photophobia 14 33,33 51 50,50 0,060 2,040 0,963 4,322

Osmophobia 7 16,67 38 37,62 0,014 3,016 1,219 7,462

Kinesiophobia 14 33,33 55 54,46 0,021 2,391 1,128 5,071

Tinnitus 3 7,14 25 24,75 0,016 4,273 1,215 15,049

Headache 25 59,52 75 74,26 0,080 1,962 0,917 4,197

Aural fullness 6 14,29 40 39,60 0,003 3,934 1,519 10,192

Hearing loss 5 11,90 18 17,82 0,380 1,605 0,554 4,650

Motion sickness + headache 6 14,29 30 29,70 0,053 2,535 0,967 6,647

Motion sickness + dizziness 5 11,90 35 34,65 0,006 3,924 1,415 10,881

Motion sickness 6 14,29 29 28,71 0,068 2,417 0,920 6,348

Source: the author

DISCUSSION

The migraine association with aura and MV remains

controversial. In the study by Calhoun et al.

, which

aimed to determine and characterize the prevalence

of dizziness in migraine, 425 patients were evaluated,

of which 28% had MA. The prevalence of dizziness was

twice as high (24.5% vs 12.1%) in migraine with aura

compared to migraine without aura (P <0.01). Prevalence

also increased with age (P <0.05).

Another study

evaluated the prevalence of vertigo,

dizziness, and VM over the years in patients diagnosed

with migraine, comparing them with a control group.

Both groups were assessed for symptoms of dizziness

and vertigo.

The study included 327 patients diagnosed with

migraine with and without aura and 324 controls with no

history of a frequent headache. 199 (60.9%) patients had

migraine with aura (MA), 128 (39.1%) migraine without

aura (MWA).

Patients of the MA subgroup had, more frequently,

vertigo symptoms/dizziness than those with MWA. Of

the 199 patients in the MA subgroup, 19 (14.84%) always

reported vertigo symptoms/dizziness associated with

headache, than those of the MWA 19 subgroup (9.55%)

reported. Patients in the MA subgroup had a higher

association with dizziness and vertigo (P <0001).

In Neuhauser’s study

, 4869 patients were evaluated

on the epidemiology of MV in the general population. In

this sample 33 patients had VM, being 36% MA and 64%

MWA, and after regression analysis of migraine with aura,

it was not a risk factor for VM.

In the study by Cohen et al,(12), they identied

predictive factors of the VM of the 147 individuals, 100

(68%) were women and 47 (32%) men aged 15 to 92

years (mean age 45 years). Of the 147 evaluated, 57

(39%) had migraine with aura and 90 (61%) had no aura;

10(2).indb 53 21/10/2019 18:25:25

Accompanying Symptoms in Vestibular Migraine

Costa ATNM, et al.

Headache Medicine, v.10, n.2, p.51-55, 2019

of the subgroup with aura 21 (37%) were male and 36

(63%) female. A signicant difference was observed

in the subgroups of migraine patients with vestibular

symptoms: sensitivity to bright lights occurred in 74% of

the subgroup with aura and 43% in the subgroup without

aura (p <0001), motion sickness (51% with aura and 39%

without aura) and climate changes (54% with aura and

31% without aura), the differences approached but did

not reach signicance (P = 0.08 and .07, respectively).

To investigate the clinical features of multiple

diseases that involved vertigo/dizziness, Esch et al.

investigated 122 patients, and only 16 were diagnosed

with VM, where the accompanying symptoms were

evaluated. Of the patients, 7 (44%) had aura, 16 (100%)

reported nausea, 7 (44%) vomiting, 11 (69%) photophobia

and 11 (69%) phonophobia, as well as asymmetric hearing

loss in 12 (75%) and tinnitus in 2 (13%).

A study published in the Neurology Journal

VM, its clinical evolution and cochlear dysfunctions in a

9-year follow-up, followed 61 patients with the diagnosis.

The accompanying symptoms were assessed at baseline

and followed-up after nine years.

The most frequent accompanying symptoms at the

initial evaluation were photophobia in 59% of the patients

and phonophobia in 54%, during the 9-year follow-up,

these symptoms were 80% and 77%, respectively.

During VM crises, cochlear symptoms appeared

in 49% of the patients, tinnitus in 33%, auditory

symptoms (tinnitus symmetrical, aural fullness) in

26% and hearing difculty in 26%. Initially, 18% of the

patients reported aura and, during follow-up, 44% of

the patients reported symptoms.

This study followed patients with a denitive

diagnosis of VM for nine years, their accompanying and

cochlear symptoms both at admission and during follow-

up, showed worsening of symptoms also in the interictal

period. It was possible to observe the appearance of aura

during the patients’ follow-up of the patients. The author

of the publication suggests that the worsening of the

evolution of symptoms, including in the interictal period,

may be associated with a progressive deterioration of

the vestibular system caused by the disease.

In our sample, patients with VM diagnosis of the

aura subgroup had a higher chance of presenting nausea,

vomiting, phonophobia, osmophobia, kinesiophobia,

tinnitus, auricular fullness and motion sickness associated

with dizziness. Photophobia, headache, hearing loss,

headache-associated kinesis, and isolated kinesis were

not associated with the MA subgroup.

There are, to date, no other studies correlating the

odds ratio of the accompanying symptoms between the

VM and the subgroups of migraine.

We must emphasize the signicant size of this

sample, and that this is a tertiary research center of VM.

All patients were diagnosed by a neurologist specialized

in headache and vestibular symptoms and met the

criteria of VM according to ICHD-3 β.

Although there was no statistical difference

between the groups (migraine with or without aura

regarding vestibular symptoms), they appeared three

times more in the subgroup with aura. However, because

of the size of our sample, it may not be possible to state

that having aura is a risk factor for developing vestibular

symptoms. Thus, studies with larger populations should

be carried out.

It is still relevant to note that, in the aura subgroup,

the accompanying symptoms had a higher relative

risk ratio for several accompanying symptoms, which

demonstrates the greater severity and a more debilitating

condition for this association of diagnoses.

Leão’s cortical spreading depression

in migraine

with aura and neuronal hyperexcitability exacerbate the

trigeminal activation process, thus causing neurogenic

inammation. This could contribute to the activation and

sustained sensitization of this process, as well as cause

reversible vasospasm of the internal auditory artery,

responsible for vestibular symptoms, both during VM

crises, and could also be responsible for damages in this

pathway, which could justify vestibular symptoms, even

during the interictal period.

16,17

CONCLUSION

Patients with vestibular migraine and migraine

with aura, when compared to patients with VM and

migraine without aura, present a higher relative risk

of having accompanying symptoms such as nausea,

vomiting, phonophobia, osmophobia, kinesiophobia,

tinnitus, auricular fullness, and motion sickness

associated with dizziness.

Detailed anamnesis and the active search for the

presence of aura, during the initial assessment and

also during the evolution of the patient with VM, are

necessary, in order to diagnose vestibular symptoms.

Diagnosing this subgroup with aura, where the

accompanying symptoms are more frequent, makes

them a group of patients with a more severe disease

and with a worse prognosis.

REFERENCES

1. Stolte B, Holle D, Naegel S, Diener HC, Obermann M.

Vestibular migraine. Cephalalgia. 2015 Mar;35(3):262-70.

doi: 10.1177/0333102414535113.

2. Dieterich M, Obermann M, Celebisoy N. Vestibular migraine:

the most frequent entity of episodic vertigo. J Neurol.

2016;263: 82-9. doi: 10.1007/s00415-015-7905-2

3. Cho SJ, Kim BK, Kim BS et al. Vestibular migraine in

multicenter neurology clinics to the appendix criteria in

the third beta edition of the International Classication of

headache disorders. Cephalalgia. 2016;36(5):454-462. doi:

10.1177/0333102415597890.

4. Guerra-Jiménez G, Arenas Rodríguez A, Falcón González

JC, Pérez Plasencia D, Ramos Macías Á. Epidemiología de

los trastornos vestibulares en la consulta de otoneurología.

Acta Otorrinolaringol Esp. 2017;68(6):317-22. doi 10.1016/j.

otorri.2017.01.007.

5. Headache Classication Committee of the International

Headache Society (IHS).The International Classication of

Headache Disorders, 3rd edition (beta version). Cephalalgia.

2013 Jul;33(9):629-808. doi: 10.1177/0333102413485658.

6. Lempert T, Olesen J, Furman J, Waterston J, Seemungal

B, Carey J, et al. Vestibular migraine: diagnostic criteria. J

Vestib Res. 2012;22(4):167-72. doi: 10.3233/VES-2012-0453.

7. Bussab WO, Morettin PA. Estatística Básica. 8. ed. São

Paulo: Editora Saraiva, 2013.

10(2).indb 54 21/10/2019 18:25:25

Accompanying Symptoms in Vestibular Migraine

Costa ATNM, et al.

Headache Medicine, v.10, n.2, p.51-55, 2019

8. Pagano M, Gauvreau K. Princípios de Bioestatística. São

Paulo. Editora Pioneira Thomson Learning, 2004.

9. Calhoun AH, Ford S, Pruitt AP, Fisher KG. The point

prevalence of dizziness or vertigo in migraine – and factors

that inuence presentation. Headache: The Journal of

Head and Face Pain. 2011;51(9):1388-1392. doi:10.1111/j.1526-

4610.2011.01970.x

10. Vuković V, Plavec D, Galinović I, Lovrenčić-Huzjan A, Budišić M,

Demarin V. Prevalence of vertigo, dizziness, and migrainous

vertigo in patients with migraine. Headache: The Journal

of Head and Face Pain. 2007 Nov-Dec;47(10):1427-35. doi:

10.1111/j.1526-4610.2007.00939.x

11. Neuhauser HK, Radtke A, von Brevern M, Feldmann M, Lezius

F, Ziese T, et al. Migrainous vertigo: prevalence and impact on

quality of life. Neurology. 2006;67(6):1028-1033. doi: 10.1212/01.

wnl.0000237539.09942.06

12. Cohen JM, Bigal ME, Newman LC. Migraine and vestibular

symptoms - identifying clinical features that predict

“Vestibular Migraine”. Headache: The Journal of Head

and Face Pain. 2008;51(9):1393-1397. doi: 10.1111/j.1526-

4610.2011.01934.x

13. van Esch BF, van Wensen E, van der Zaag-Loonen HJ,

van Benthem PPG, van Leeuwen R. Clinical characteristics

of benign recurrent vestibulopathy: clearly distinctive

from vestibular migraine and Meniere’s disease?

Otol Neurotol. 2017;38(9):e357-e363. doi: 10.1097/

MAO.0000000000001553

14. Andrea R, von Brevern M, Neuhause H, et al. Vestibular

migraine: long-term follow-up of clinical symptoms and

vestibulo-cochlear ndings. Neurology. 2012;79(15):1607-

14. doi: 10.1212/WNL.0b013e31826e264f.

15. Noseda R, Burstein R. Migraine pathophysiology:

anatomy of the trigeminovascular pathway and

associated neurological symptoms, cortical spreading

depression, sensitization, and modulation of pain.

Pain. 2013 Dec;154 Suppl 1:S44-53. doi: 10.1016/j.

pain.2013.07.021.

16. Vass Z, Steyger PS, Hordichok AJ, Trune DR, Jancsó

G, Nuttall AL. Capsaicin stimulation of the cochlea and

electric stimulation of the trigeminal ganglion mediate

vascular permeability in cochlear and vertebro-basilar

arteries: a potential cause of inner ear dysfunction in

headache. Neuroscience. 2001;103(1):189-201. doi: 10.1016/

S0306- 4522(00)00521- 2.

17. Vass Z, Dai CF, Steyger PS, Jancsó G, Trune DR,

Nuttall AL. Co-localization of the vanilloid capsaicin

receptor and substance P in sensory nerve bers

innervating cochlear and vertebro-basilar arteries.

Neuroscience. 2004;124(4):919-27. doi: 10.1016/j.

neuroscience.2003.12.030.

10(2).indb 55 21/10/2019 18:25:26

Headache Medicine, v.10, n.2, p.56-59, 2019

RESUMO

ABSTRACT

Keywords: Individual susceptibility, Motion sensitivity, Motion sickness,

Migraine.

ORIGINAL ARTICLE

Motion Sickness in Headache Patients

Cinetose em pacientes com cefaleias

Marina Olivier

Sol Cavanagh

Lucas Bonamico

Francisco Gualtieri

María Teresa Goicochea

cción Cefaleas. Sector Dolor.

Departamento

de Neurología.

Argentina

Sección Neurootología. Departamento de

Neurología.

Argentina

*Correspondence

rina Olivier

E-mail: marinaolivier@hotmail.com

Received: June 5, 2019. Accepted:

June 12, 2019.

Creative Commons (CC BY) Attribution 4.0

International.

Introdução: Dor de cabeça é uma das razões mais frequentes de consultas

em neurologia. Alguns pacientes com dor de cabeça relatam intolerância à

mobilização passiva, associada a tontura, náusea, vômito, conhecida como

cinetose. Esses sintomas são causados por um conito entre os sistemas: visual,

vestibular e somatossensitivo. Objetivo: Determinar a prevalência de cinetose

em pacientes consultados por dor de cabeça. Método: Estudo transversal,

retrospectivo e descritivo. Foram incluídos pacientes com idade superior

a 18 anos, consultados para dor de cabeça na Clínica de Dor de Cabeça, do

Hospital Fleni, Buenos Aires, Argentina, no período de 2 de janeiro a 30 de

junho de 2017, por meio de entrevista estruturada. Resultados: Do total de 266

pacientes: 62 (23,3%) apresentaram cinetose (idade média de 41,5 anos; 80,6%

eram mulheres), 14 descreveram-na apenas na infância e 48 persistiram com

sintomas até o momento da consulta. Entre os pacientes com dor de cabeça

e cinetose 52 (83,9%) apresentaram enxaqueca, 7 pacientes apresentaram

cefaléia tensional, 2 cefaleia em salvas. A prevalência de enxaqueca foi maior

naqueles que relataram cinetose apenas na infância em comparação aos que

continuaram com ela (85,7 vs. 56,2%, p = 0,045), 12,5% dos pacientes com

cinetose atual relataram isso como um gatilho para enxaqueca. 204 pacientes

não apresentaram cinetose (76,7%). Conclusão: Consideramos que em

pacientes com dor de cabeça é importante identicar a cinetose, pois pode ser

limitante e também desencadear uma enxaqueca. Seu diagnóstico e tratamento

melhorariam a qualidade de vida de nossos pacientes.

Descritores: Susceptibilidade individual, Sensibilidade a movimentos, Cinetose,

Enxaqueca.

Introduction: Headache is one of the most frequent consultations in neurology.

Some patients with headache report intolerance to passive mobilization,

associated with dizziness, nausea, vomiting, known as motion sickness. These

symptoms are caused by a conict between the systems: visual, vestibular and

somatosensitive. Objective: To determine the prevalence of motion sickness in

patients who consult due to headache. Method: Cross-sectional, retrospective

and descriptive study. It included patients over 18 years of age, who consulted

for headache at the Headache Clinic, during the period from January 2 to June

30, 2017, through a structured interview. Results: Of a total of 266 patients:

62 (23.30%) presented motion sickness (mean age 41.5 years; 80.6% were

women). 14 described motion sickness only in childhood and 48 persisted with

symptoms until the time of consultation. Among the patients with headache

and motion sickness 52 (83.87%) presented migraine; 7 patients presented

tension headaches; 2 in salvos; 1 undetermined The prevalence of migraine was

higher in those who reported motion sickness only in childhood compared to

those who continued with motion sickness (85.7 vs. 56.25%, p = 0.045), 12.5%

of patients with current motion sickness reported it as a migraine trigger, 204

patients did not have motion sickness (76.7%). Conclusion: We consider that

in patients with headache it is important to identify motion sickness as it can

be limiting and also be a migraine trigger. Its diagnosis and treatment would

improve the quality of life of our patients.

10(2).indb 56 21/10/2019 18:25:26

Motion Sickness in Headache Patients

Olivier M, et al.

Headache Medicine, v.10, n.2, p.56-59, 2019

INTRODUCTION

Headache is one of the most frequent causes for

consultations in neurology. Headache represents a broad

and heterogeneous group of clinical entities; being

tension-type headache the most prevalent in the general

population; followed by migraine.

Migraine prevalence varies between 10-16%, with

female predominance of 3/1; representing a signicant

socio-economic and personal impact (1). It is among

the ten most prevalent disorders and is classied as the

second cause of disability of all diseases worldwide (2).

Migraine is characterized by recurrent attacks of moderate

to severe pain, of pulsatile characteristic, associated

with photophobia or, phonophobia, nausea and / or

vomiting, which sometimes becomes incapacitating for

the individual’s daily life, in both social and labor aspects.

Some patients who consult for headache also report

intolerance to passive mobilization; known as motion

sickness. More than two thousand years ago Hippocrates

observed that “…. Sailing in the sea caused movement

disorder ... (Reason and Brand, 1975), The term “nausea”

derives from the Greek root “Naus” which means a ship

(3). Motion sickness is a syndrome present in healthy

subjects, triggered by passive movement (car trips,

trains, airplanes, ships) or by the illusion of movement

(environmental movement surrounding it; exposure to

3D movies, virtual reality). Active movement of the head

during a trip in a means of transport (passive movement)

can cause or worsen it (3).

This syndrome is characterized by a group of signs

and symptoms, among which are mentioned, dizziness,

nausea, vomiting, drowsiness, yawns, irritability, paleness,

bradycardia, palpitations, ataxic gait, arterial hypotension,

apathy, headache. (4). The severity of symptoms varies

according to individual susceptibility and the intensity of

the stimulus to which the subject is exposed. Increased

susceptibility has been suggested in women, the

menstrual cycle being implicated as a trigger; In addition

to some evidence of genetic contribution, variables such

as anxiety or fear and sleep deprivation may contribute;

reason why the prevalence described in the literature is

very variable (1-90%) (5). Susceptibility begins around 6

or 7 years of age; with a peak between 9 and 10 years;

which implies that hormonal changes per se would not

have a direct effect. These symptoms are caused by

incongruous sensory interactions; a conict between the

visual, vestibular and somatosensitive systems. Before

an acute trigger the symptoms last for hours to a day

after the stimulus is suspended; If the stimulus continues,

such as a boat trip, relief occurs by central adaptation

(habituation) in approximately 3 days.

OBJECTIVES

The primary objectives of this study were to

determine the prevalence of motion sickness in patients

who consulted a neurology service due to headache;

and identify what type of headache is most frequently

associated with motion sickness. Secondary objectives,

to determine the severity of motion sickness and identify

motion sickness as a possible migraine trigger.

METHODS

A cross-sectional, retrospective and descriptive

study was carried out; which included patients over 18

years of age, who consulted for headache as the primary

complaint in the Headache Section of Pain Clinic, Hospital

Fleni, Buenos Aires, Argentina, during the period from

January 2 to June 30, 2017. A structured questionnaire

was used for the interview and the data were analyzed.

Headache diagnoses were made applying the

criteria of the International Classication of Headache

Disorders, 2013. Motion sickness was classied using the

Motion sickness susceptibility questionnaire short-form

(MSSQ-Short) (6) according to the stimulus that triggers

the symptom in Mild: terrestrial trigger , Moderate:

acquatic trigger; Severe: aerial and visual trigger.

The STATA v13 program was used. Quantitative

data were expressed in means +/- SD or numbers and

their percentages. Normality was evaluated according to

asymmetry, kurtosis and Z test. For the comparison of

proportions, a non-parametric Wilcoxon rank-sum test

was used.

Study approved by the Research and Ethics

Committee, given the exception of taking informed

consent.

RESULTS

Of a total of 266 patients who consulted Fleni Hospital

due to headache, 62 (23.3%) presented motion sickness,

mean age was 41.5 years; 80.6% were women. Of which

14 patients described motion sickness exclusively during

childhood and 48 patients reported persisting with the

symptoms until the time of consultation (Graph 1). The

latter were classied according to the intensity of motion

sickness in: mild 64.5%; moderate 16.7% and severe 18.8%.

From the group of patients with headache and

motion sickness; 52 (83.9%) met diagnostic criteria

for migraine (62.9% episodic, 9.7% with aura and 11.3%

chronic); 11.3% of patients had tension headache; 3.2%

cluster headache and 1.6% headache of undetermined

characteristic (Graph 2).

The prevalence of migraine was higher in those

patients who reported motion sickness only in childhood

compared to those who continued with motion sickness

(85.7 vs. 56.2%, p = 0.045). 12.5% of patients with current

motion sickness reported it as a migraine trigger.

204 patients did not have motion sickness (76.7%);

the average age was 43.5 years; and 81.8% were women.

83.33% presented migraine (67.6% episodic; 17.6%

chronic; 14.7% with aura), 9.3% had tension headache,

2.9% cluster headache, 1.5% had undetermined headaches

and 2% cranial neuralgia (Graph 3).

DISCUSSION

Reports in the literature describes the association

between migraine and motion sickness may reache up

to 50%; also 20% of patients with tensión-type headache

10(2).indb 57 21/10/2019 18:25:26

Motion Sickness in Headache Patients

Olivier M, et al.

Headache Medicine, v.10, n.2, p.56-59, 2019

also experience motion sickness (7). Our study revealed a

prevalence of motion sickness in patients with headache

of 23.3%; of these, 84% suffered some type of migraine;

and 11% had tension headache; 12.5% reported motion

sickness as a trigger for a migraine attacks.

Motion sickness not only interferes with long-

distance trips such as pleasure trips; but also in those of

short distance, such as daily transfers to work, activities

such as going to a shopping, supermarket or cinema.

It affects both adults and children. At present, the use

of mobile devices during the trips, possibly facilitates

the increase of this symptom; since performing active

movements during a passive movement favors its

presentation.

Given that it is a frequent condition, which can

become disabling and even trigger a migraine attack, it

must be taken into account in the medical consultation,

in order to indicate the appropriate treatment, both non-

pharmacological and pharmacological (scopolamine,

promethazine, anti-histamines). Rizatriptan was studied

as a preventive treatment (prior to the exposure of stimuli)

of motion sickness (8) showing clinical improvement.

A group of patients identied motion sickness

as a trigger for a migraine attacks. This information

could be useful to evaluate the clinical behavior of the

migraine attacks, so recognizing it may be helpful in its

managament.

CONCLUSION

Motion sickness is an important issue in migraine

management, causing limitations in daily life activities.

In rst consultations, headache patients should be asked

about it, since proper diagnosis and timely treatment

would make it possible to improve patients’ quality of life.

Future research should be done to better clarify motion

sickness as a migraine trigger.

REFERENCES

1. Guía diagnóstica y terapéutica de la Sociedad Española de

Neurología 2015.

2. GBD 2015 Disease and injury incidence and prevalence

collaborators (2016)Global, regional, and national incidence,

prevalence, and years lived with disability for 310 diseases

and injuries, 1990–2015: a systematic analysis forthe Global

Burden of Disease Study 2015. Lancet 388:1545–1602

3. Bertolini G and Straumann D; Moving in a Moving world:

A Review on vestibular Motion Sickness; (2016), Front.

Neurol. 7:14.

4. Martínez F, Bots L; Motion sickness; Journal FASO, año

23,suplememento 2; 2016.

5. Sanchez Blanco C; Cinetosis. Rev. Soc. Otorrinolaringol.

Castilla Leon Cantab. La Rioja 2014 Nov. 5 (28): 233-251

6. Golding J.F; Predicting individual differences in motion

sickness susceptibility by questionnaire. Personality and

Individual Differences 41 (2006) 237–248.

7. Dawn M; Motion Sickness and Migraine; Headache 2007;

47: 607-610).

8. Joseph M.F; Rizatriptan reduces vestibular-induced motion

sickness in migraineurs; J Headache Pain (2011) 12:81–88.

9. Murdin L, Chamberlain F, Cheema S; Motion sickness in

migraine and vestibular disorders; J Neurol Neurosurg

Psychiatry 2015;86:585–587.

Graph 1. Headache patients with Motion Sickness.

Graph 2. MA: migraine with aura, MC: chronic migraine, ME:

episodic migraine; TA: trigemeno-autonomic cephalgias, Indet:

undetermined.

Graph 3. MA: migraine with aura, MC: chronic migraine, ME:

episodic migraine; TA: trigemeno-autonomic cephalgias, Indet:

undetermined, AC: cranial neuralgias.

10(2).indb 58 21/10/2019 18:25:26

Motion Sickness in Headache Patients

Olivier M, et al.

Headache Medicine, v.10, n.2, p.56-59, 2019

10. Schmäl F, Neuronal Mechanisms and the Treatment of

Motion Sickness; Pharmacology 2013; 91: 229–241.

11. Bisdorff A, Migraine and dizziness, Curr Opin Neurol 2014,

27:105–110.

12. De Marinis, M. Comment on Visual pattern repsonses in

migraine with and without motion sickness; Cephalalgia

2010, 30(12) 1537.

13. Carvalho, GF. Presence of vestibular symptoms and related

disability in migraine with and without aura and chronic

migraine; Cephalalgia 2019, 39(1) 29–37.

14. Golding J.F; Motion sickness susceptibility questionnaire

revised and its relationship to other forms of sickness. Brain

Research Bulletin, Vol. 47, No. 5, pp. 507–516, 1998.

15. Sanchez-Blanco C; Motion sickness; Rev. Soc.

Otorrinolaringol. Castilla Leon Cantab. La Rioja 2014 Nov. 5

(28): 233-251.

16. Cuomo-Granston A; Migraine and motion sickness: What is

the link?; Progress in Neurobiology 91 (2010) 300–312.

17. Lackner J.R; Motion sickness: more than nausea and

vomiting; Exp Brain Res (2014) 232:2493–2510.

18. Wesley W.O. Krueger, M.D.; Controlling Motion Sickness

and Spatial Disorientation and Enhancing Vestibular

Rehabilitation with a User-Worn SeeThrough Display;

Laryngoscope. 2011 January ; 121(0 2): S17–S35. doi:10.1002/

lary.21373.

19. Wang J, Lewis RF. Contribution of intravestibular sensory

conict to motion sickness and dizziness in migraine

disorders; J Neurophysiol 116: 1586 –1591, 2016.

20. Ashton Graybiel, DIAGNOSTIC CRITERIA FOR GRADING

ME SEVERITY OF ACUTE MOTION SICKNESS; Bureau of

Medicine and Surgery MR005.04-002 NASA Order R-93 1

.156 z; 1968.

21. Conforto A.B; Migraine and motion sickness independently

contribute to visual Discomfort; Cephalalgia 2010, Vol 30(2)

161–169.

22. Carvalho G.F; Presence of vestibular symptoms and related

disability in migraine with and without aura and chronic

migraine; Cephalalgia 2019, Vol. 39(1) 29–37.

23. Yates Bill J; Integration of Vestibular and Emetic

Gastrointestinal Signals that Produce Nausea and Vomiting:

Potential Contributions to Motion Sickness; Exp Brain Res.

2014 August ; 232(8): 2455–2469.

24. III Edición de la Clasicación Internacional de las Cefaleas;

versión beta, ICHD-III 2013; Sociedad Internacional de

Cafeleas (IHS).

10(2).indb 59 21/10/2019 18:25:26

Headache Medicine, v.10, n.2, p.60-62, 2019

ABSTRACT

RESUMO

Descritores: Mastócito; Dura-máter; Humano; Artéria meningeal; Enxaqueca.

SHORT COMMUNICATION

Histomorphometric analysis of mast cells in different

regions of human intracranial dura mater

Análise histomorfométrica de mastócitos em diferentes

regiões da dura-máter intracraniana humana

Emanuela Paz Rosas

Silvania Tavares Paz

Ana Clara de Souza Neta

Raisa Ferreira Costa

Ana Paula Fernandes da Silva

Manuela Figueiroa Lyra de Freitas

Marcelo Moraes Valença

1,4

Programa de Pós-graduação em Biologia

Aplicada à Saúde-LIKA/UFPE;

Programa de Pós-graduação em Saúde

Translacional – CCS/UFPE;

Departamento de Nutrição – CCS/UFPE;

Programa de Pós-graduação em Ciências

Biológicas – CB/UFPE.

Departamento de Anatomia – CB/UFPE,

Recife, Pernambuco, Brazil.

*Correspondence

Emanuela Paz Rosas

E-mail: manu_pathy@hotmail.com

Received: April 2, 2019.

Accepted: May 4, 2019.

Creative Commons (CC BY) Attribution 4.0

International.

Objective: To analyze mast cell histomorphometry in three different regions

of the human intracranial dura mater. Method: Three specimens of dura

mater were collected after approval by the Ethics Committee (CAAE No.

57692216.5.0000.5208). Each dura mater was obtained from human cadavers

between 7 and 24 hours after death. After collection, the samples were xed,

cut into two fragments and longitudinally placed in the following way: external

(periosteum) and internal (meningeal) sides. The fragments (1.5 cm

) were taken

from three different regions: proximity of the right middle meningeal artery, the

proximity of the left middle meningeal artery and superior sagittal sinus. These

fragments were submitted to microtomy (10 µm), stained with 0.1% toluidine

blue and analyzed by optical microscopy. The histomorphometric parameters

adopted were: the distance from the mast cells to the vessels, the number and

if the mast cells were degranulated. Five elds from each case were analyzed.

For this analysis, the Image J 1.52a 2019 software was used. Results: A higher

number of mast cells was observed in the periosteal layer when compared with

the meningeal layer (p=0.026). When the distribution of the mast cells was

evaluated, we observed that the cells were localized in the proximity of the

middle meningeal artery (p<0.05). Conclusion: In human dura mater, the mast

cells are localized in the proximity of dural arteries.

Keywords: Mast cell; Dura mater; Human; Meningeal artery; Migraine.

Objetivo: Analisar a histomorfometria dos mastócitos em três regiões

diferentes da dura-máter intracraniana humana. Método: Três amostras de

dura-máter foram coletadas após aprovação pelo Comitê de Ética (CAAE nº

57692216.5.0000.5208). Cada dura-máter foi obtida de cadáveres humanos

entre 7 e 24 horas após a morte. Após a coleta, as amostras foram xadas,

cortadas em dois fragmentos e dispostas longitudinalmente da seguinte

maneira: face externa (periósteo) e interna (meníngeo). Os fragmentos

(1,5 cm

) foram retirados de três regiões diferentes: proximidade da artéria

meníngea média direita, proximidade da artéria meníngea média esquerda e

seio sagital superior. Esses fragmentos foram submetidos à microtomia (10 µm),

corados com azul de toluidina a 0,1% e analisados por microscopia óptica. Os

parâmetros histomorfométricos adotados foram: distância dos mastócitos aos

vasos, número e se os mastócitos estavam desgranulados. Foram analisados

cinco campos de cada espécime. Para esta análise, foi utilizado o software

Image J 1.52a 2019. Resultados: Observou-se maior número de mastócitos

na camada periosteal quando comparada à camada meníngea (p = 0,026).

Quando avaliada a distribuição dos mastócitos, observamos que as células

estavam localizadas nas proximidades da artéria meníngea média (p <0,05).

Conclusão: Na dura-máter humana, os mastócitos estão localizados nas

proximidades das artérias durais.

10(2).indb 60 21/10/2019 18:25:26

Histomorphometric analysis of mast cells in different regions

Rosas EP, et al.

Headache Medicine, v.10, n.2, p.60-62, 2019

INTRODUCTION

Recent evidence strongly suggests a vital role of

dura mater mast cell in the genesis of migraine.

1-5

Gupta and Harvima described the mast cells as

a “powerhouse” since they release “algogenic and

pruritogenic mediators, which initiate a reciprocal

communication with specic nociceptors on sensory

nerve bers.”

Mast cells are cells found in abundance in the

dura mater and by local mechanism regulates vascular

and neural functions, releasing substances such as

histamine. Scientic evidence suggests that mast cells

participate in the pathophysiology of triggering a

migraine attack by inducing local sterile inammation

near the dura mater nociceptors.

Curiously, the mast cells are located in the proximity

of the arteries in the dura mater, in close association

with neurons. These cells appear to be activated

through the trigeminal nerve. It is postulated that many

neuropeptides, namely calcitonin gene-related peptide

(CGRP), hemokinin A, neurotensin (NT), pituitary

adenylate cyclase-activating peptide (PACAP), and

substance P may activate mast cells, resulting in the

release of vasoactive and pro-inammatory mediators,

involved in the pathophysiology of migraine.

Mast cells

can also release substances with pro-inammatory

and vasoactive actions (e.g., interleukin-6 and vascular

endothelial growth factor (VEGF).

The objective of the present study was to analyze

mast cell histomorphometry in three different regions of

the human intracranial dura mater.

METHOD

Three specimens of dura mater were collected

after approval by the Ethics Committee (CAAE No.

57692216.5.0000.5208).

Each dura mater was obtained from human cadavers

between 7 and 24 hours after death.

After collection, the samples were xed, cut into two

fragments and longitudinally placed in the following way:

external (periosteum) and internal (meningeal) sides.

The fragments (1.5 cm

) were taken from three

different regions: proximity of the right middle meningeal

artery, the proximity of the left middle meningeal artery

and superior sagittal sinus.

These fragments were submitted to microtomy

(10 µm), stained with 0.1% toluidine blue and analyzed

by optical microscopy. The histomorphometric

parameters adopted were: the distance from the mast

cells to the vessels, the number and if the mast cells

were degranulated. Five elds from each case were

analyzed. For this analysis, the Image J 1.52a 2019

software was used.

RESULTS AND DISCUSSION

A higher number of mast cells was observed in the

periosteal layer when compared with the meningeal

layer (p=0.026).

When the distribution of the mast cells was evaluated,

we observed that the cells were localized in the proximity

of the middle meningeal artery (Figure 1), suggesting

that there is a signicant role played by the mast cells in

dura mater to regulate vascular function. Probably the

relationship between mast cells and meningeal arteries

is an essential component in the migraine pathogenesis.

Figure 1. Mast cell density per mm2 in relation to the

distance to the vessel. P versus 0-100 µm group, Kruskal-

Wallis test and Dunn´s multiple compatisons test.

The distance between the artery and the mast cell

was measured in 153 cells (57 65 m, min 0 - max 247;

median 33, 95%IC 46-67). No differences were observed

in the concentration of mast cells in convexity of the dura

mater versus the superior sagittal sinus.

In his study, with human dura mater postmortem,

60-70% of the mast cells were degranulated. Migraine is a

disorder with signicant autonomic dysfunction. Clinically,

long-lasting ushing suggests degranulation of mast cells.

In conclusion, in human dura mater, the mast cells

are localized in the proximity of dural arteries.

REFERENCES

1. Okragly AJ, Morin SM, DeRosa D, Martin AP, Johnson KW,

Johnson MP, Benschop RJ. Human mast cells release the

10(2).indb 61 21/10/2019 18:25:27

Histomorphometric analysis of mast cells in different regions

Rosas EP, et al.

Headache Medicine, v.10, n.2, p.60-62, 2019

migraine-inducing factor pituitary adenylate cyclase-activating

polypeptide (PACAP). Cephalalgia. 2018 Aug;38(9):1564-1574.

doi: 10.1177/0333102417740563. Epub 2017 Nov 5.

2. Kilinc E, Dagistan Y, Kukner A, Yilmaz B, Agus S, Soyler G,

Tore F. Salmon calcitonin ameliorates migraine pain through

modulation of CGRP release and dural mast cell degranulation

in rats. Clin Exp Pharmacol Physiol. 2018 Jun;45(6):536-546.

doi: 10.1111/1440-1681.12915. Epub 2018 Feb 13.

3. Baun M, Pedersen MH, Olesen J, Jansen-Olesen I. Dural mast

cell degranulation is a putative mechanism for headache

induced by PACAP-38. Cephalalgia. 2012 Mar;32(4):337-45.

doi: 10.1177/0333102412439354.

4. Theoharides TC, Donelan J, Kandere-Grzybowska K,

Konstantinidou A. The role of mast cells in migraine

pathophysiology. Brain Res Brain Res Rev. 2005

Jul;49(1):65-76.

5. Jansen-Olesen I, Hougaard Pedersen S. PACAP and its

receptors in cranial arteries and mast cells. J Headache

Pain. 2018 Feb 20;19(1):16. doi: 10.1186/s10194-017-0822-2.

6. Kalpna Gupta, Ilkka T. Harvima. Mast cell-neural

interactions contribute to pain and itch Immunol Rev.

Author manuscript; available in PMC 2019 Mar 1. Published

in nal edited form as: Immunol Rev. 2018 Mar; 282(1): 168–

187. doi: 10.1111/imr.12622

10(2).indb 62 21/10/2019 18:25:27

Headache Medicine, v.10, n.2, p.63-64, 2019

IMAGENS

Migraine with aura: MRI with perfusion aspects in the ictal

and interictal phases

Enxaqueca com aura: aspectos da ressonância magnética

com perfusão nas fases ictal e interictal

Paulo Sergio Faro Santos

Bruno Augusto Telles

Instituto de Neurologia de Curitiba,

Departamento de Neurologia -

Curitiba - PR - Brasil

Instituto de Neurologia de Curitiba,

CETAC - Diagnóstico por Imagens -

Curitiba - PR - Brasil

*Correspondence

Paulo Sergio Faro Santos

E-mail: dr.paulo.faro@gmail.com

Received: October 4, 2019.

Accepted: October 4, 2019.

Creative Commons (CC BY) Attribution 4.0

International.

We describe the case of a 16-year-old adolescent with diagnostic

previous of migraine without and with aura (only sensory), who presented

with aphasia of speech, associated with severe retroorbital pain and frontal

headache on the left, associated with nausea, photo and phonophobia.

He was admitted to the emergency room with suspected stroke and was

submitted to magnetic resonance perfusion imaging of the brain (Figure 1).

After ruling out suspected cerebral ischemia, treatment with symptomatic

medications was performed, progressing to improvement of symptoms

after about 2 hours.

Figure 1. A-D demonstrated fast protocol to exclude recent ischemia or bleeding,

with patency of large intracranial vessels and without signicant changes in structural

images (Diffusion, Gradient-Echo and FLAIR). E-H with the reconstructions of the

perfusion study and highlighting the important increase in time to the plateau (TTP

- gure G) and mean transit time (MTT - gure F), with no changes of the other

parameters. I-M with the perfusion control study and characterizing the regression of

the previously evidenced changes.

Approximately 1 month later, a new perfusion MRI was performed for

comparison, which revealed complete disappearance of the alterations

of the rst exam. In this interval, the patient presented only episodes of

migraine without aura.

Migraine with aura (MwA) accounts for about 30% of all cases of

migraine and predominates in females

(1)

. Its diagnosis was recently updated

by the third edition of the International Classication of Headache Disorders

(2)

. Visual aura accounts for 99% of auras, followed by sensory (54%) and

speech / language (32%)

(1)

10(2).indb 63 21/10/2019 18:25:28

Migraine with aura

Santos PSF, et al.

Headache Medicine, v.10, n.2, p.63-64, 2019

Usually at the rst manifestation or at the change in

the aura pattern, neuroimaging is necessary, considering

secondary headache, because one of the main

differential diagnoses is the stroke. The gradual onset of

neurological decits, the association with headache that

is typically migrainous, and the absence of ischemia on

neuroimaging exams are suggestive of MwA

(2,3)

. Perfusion

MRI in the ictal phase reveals decreased cerebral blood

ow, with no abnormalities in the DWI sequence, that is,

at sub-ischemic levels. Vascular alteration that is reversed

in the interictal period

(3)

REFERENCES

1. DeLange JM, Cutrer FM. Our evolving understanding

of migraine with aura. Curr Pain Headache Rep.

2014;18(10):453.

2. Headache Classication Committee of the International

Headache Society. The International Classication of

Headache Disorders. Cephalalgia. 2018; 38 (3rd edition):

1-211.

3. Russo A, Silvestro M, Tessitore A, Tedeschi G. Recent insights

in migraine with aura: a narrative review of advanced

neuroimaging. Headache. 2019 Apr;59(4):637-649.

10(2).indb 64 21/10/2019 18:25:28

Headache Medicine Volume 10 Número 1 - 2019

Editorial

► Tenth year of Headache Medicine Journal, 25 years

Original Article

► ID-Migraine is a sensitive tool for screening

migraine among patients with multiple sclerosis

► Aerobic exercise training for migraine prevention:

A trigger-based analysis

► Melatonin reverts CGRP expression induced by

capsaicin

Views and Reviews

►

thrombin and vitamin K inhibitors on migraine

treatment

► Cerebral energetic metabolism of individuals with

migraine through 31P-MRS: A systematic review

► Of the available triptans, which should be chosen

and how should they be used?

Case Report

► Cardiac cephalalgia: A deadly case report

► Coexistence of Sunct Syndrome and pituitary

tumor: A possible association to be recognized

Capav10n1.indd 1 22/10/19 18:13