Comprehensive Review of Headache Medicine (Headache

Cooperative of New England)

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The Headache Cooperative of New England

Comprehensive
Review of
Headache Medicine

Edited by
MORRIS LEVIN, MD
Authors
Steven M. Baskin, PhD
Marcelo E. Bigal, MD, PhD
Richard B. Lipton, MD, FAAN
Herbert G. Markley, MD, FAAN, FAHS
Brian E. McGeeney, MD, MPH
Lawrence C. Newman, MD
Alan M. Rapoport, MD
Mark J. Rapoport, MD
Robert E. Shapiro, MD, PhD
Fred D. Sheftell, MD
Stewart J. Tepper,MD
Thomas N. Ward, MD
Randall E. Weeks, PhD

1
2008
1
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Library of Congress Cataloging-in-Publication Data

Comprehensive review of headache medicine / edited by Morris Levin.
p.; cm.
Includes bibliographical references and index.
ISBN 978-0-19-536673-0
1. Headache—Examinations, questions, etc. I. Levin, Morris, 1955-
[DNLM: 1. Headache Disorders—diagnosis—Problems and Exercises. 2. Headache Disorders—therapy—
Problems and Exercises. WL 18.2 C737 2008]
RB128.C67 2008
616.8’4910076—dc22
2007036891

987654321
Printed in the United States of America
on acid-free paper
 To my wife, Karen, for her support and love, and to
my patients, students, and colleagues in the field of
headache medicine
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Preface

Headache medicine has lately become a focus of interest for many neurologists,
pain medicine physicians, physiatrists, psychiatrists, primary care physicians
and other practitioners. For those of us who have been in the field for many
years this is not surprising. HM is not only intellectually challenging, with a
varied and intriguing population of patients, but is also extremely gratifying
most of the time. Clinical practice or research oriented around headache disor-
ders is rewarding on many levels, and this is of course evidenced by the increase
in training programs and trainees in HM.
The recent decision by the United Council for Neurologic Subspecialties
(UCNS) to accredit HM fellowship programs and to offer certification in HM
is a crucial step in the process of validating HM as a serious subspecialty. The
American Headache Society (AHS) has taken a number of steps to make HM
academic resources available to residents and fellows, as well as interested clini-
cians in practice. The American Academy of Neurology and American Pain
Society emphasize teaching of headache medicine in their conferences. A num-
ber of other headache related conferences and symposia are available around
the world, and headache research is growing dramatically.
There are several noted texts in the field of HM, including those by Silberstein
et al, Olesen et al and Lance and Goadsby. There are also several patient and
family oriented books about headache and its treatment. However, there is no
one concise synopsis of HM at the time of writing, hence the impetus for
this work.
The Headache Cooperative of New England first conceived this project as a
key resource for those planning on sitting for the HM certification examina-
tion. Soon however other purposes seemed appropriate. There seemed to be a
need for a concise but authoritative resource for clinicians who practice head-
ache medicine. In addition, with the increasing interest in HM, it seemed
important that there be a readable comprehensive text which could serve as an
introduction to the field.
This book is divided into sections similar to those outlined by the UCNS in
their excellent curriculum for HM training and follows the summary of topics
covered in the UCNS HM examinations. Part I deals with the anatomy, physiol-
ogy, pathophysiology and epidemiology of the headache disorders. Part II
covers classification and diagnosis in the primary headaches. Part III discusses

vii
viii Preface

diagnosis of non-primary headache. Part IV deals with treatment of primary

headache types, and Part V includes chapters concerning treatment of special
populations and treatments that are advanced or specialized.
This ordering of topics was not chosen only for its appropriateness in
preparing headache specialists for the certification examination. I and my fel-
low authors decided that it also mirrored the decision-making processes we all
go through in the practice of HM on a day-to-day basis. First, we think about
diagnosis. Is it a primary headache (Part II)? If so, which category does it fall
into? —migraine, tension type, trigeminal autonomic cephalalgia, indometha-
cin responsive headaches, etc. If primary headache diagnosis is not certain, what
are the possibilities for secondary causes (Part III)? Once we have firmed up a
diagnosis, treatment decision-making begins (Part IV). This will be based on
diagnosis again but the twin treatment decisions in headache management —
acute relief and prevention, are really different processes. When treatment fails
or when it is particularly challenging, decision making follows some different
paths (Part V).
We hope that this book fills a need for this type of information and presen-
tation. We think that reading it in order will be very helpful and we hope enjoy-
able. But the authors and editors have strive to make each chapter independent
and thus the reader can skip from one chapter or section to another. Please let
us know if you have any comments or suggestions. Thanks for reading!

Morris Levin, MD
Dartmouth Medical School
Hanover, New Hampshire
Acknowledgments

This book is a true team effort. The Headache Cooperative of New England is
a professional organization to which I have been privileged to belong for a
number of years. It is composed of many of the foremost headache clinicians,
researchers, teachers and writers in the United States and this book represents
their vast experience in the field of headache medicine. In order to compose a
coherent review of headache medicine, I coerced the authors to constrain
themselves to specific topics, many of which overlapped. I also tended to impose
my own vision for this project, and invariably my co-authors were kind enough
to go along. They will always have my gratitude for their generosity.
We have all been the recipients of mentoring by our teachers, many of whom
were true pioneers in the field. I would like to extend our esteem and thanks to
our role models in the field. And speaking of teaching, our best teachers have
actually been our patients. We benefit daily from their partnership in the quest
to understand and manage their headaches and are most appreciative of their
perseverance.
Finally, I would like to warmly thank our editor at Oxford University Press,
Craig Panner. First, for taking on this project and, more importantly, for main-
taining his unfailing patience and support throughout the process of produc-
ing this book.

Morris Levin, MD
Hanover, New Hampshire

ix
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Contents

Part I Headache Medicine Basic Science: Anatomy, Physiology,

and Epidemiology

1. Head Pain Anatomy and Physiology – Morris Levin 3

2. Pathophysiology and Genetics of Migraine and Cluster
Headache – Robert E. Shapiro 21
3. The Epidemiology and Burden of Headache – Marcelo E.
Bigal, and Richard B. Lipton 39

Part II Diagnosis of Primary Headache Disorders

4. The International Classification of Headache Disorders and

Classification and Diagnosis of Migraine – Morris Levin 59
5. Classification and Diagnosis of Chronic Daily Headache and
Tension-Type Headache – Herbert G. Markley 73
6. Classification and Diagnosis of Trigeminal Autonomic
Cephalalgias and Other Primary Headaches – Lawrence C.
Newman 91

Part III Diagnosis of Secondary Headache Disorders

7. Classification and Diagnosis of Secondary Headaches: Traumatic and

Vascular Causes – Alan M. Rapoport and Mark J. Rapoport 115
8. Classification and Diagnosis of Secondary Headaches: Altered
Intracranial Pressure, Neoplasm, and Infection – Brian E.
McGeeney 149
9. Classification and Diagnosis of Secondary Headaches: Substances,
Metabolic Disorders, EENT Causes, and Neuralgias – Lawrence C.
Newman 177
10. Psychiatric Comorbidity and Causes of Headache – Steven M.
Baskin 193

Part IV Headache Treatment

11. Pharmacologic Treatment of Acute Migraine – Alan M.

Rapoport 209

xi
xii Contents

12. Preventive Pharmacologic Treatment of Migraine and Tension-Type

Headache – Stewart J. Tepper 231
13. Pharmacologic Treatment of Trigeminal Autonomic
Cephalalgias and Other Primary Headaches – Brian E.
McGeeney 255
14. Treatment of Chronic Daily Headache – Fred D. Sheftell 265

Part V Treatment of Intractable Headache and Special Populations

15. Headache Treatment in Children, Pregnancy and Lactation,

the Elderly, and Renal Disease – Thomas N. Ward 277
16. Inpatient Headache Treatment – Thomas N. Ward 285
17. Non-Pharmacologic Headache Treatment – Randall E.
Weeks 293
18. Procedures for Headache – Thomas N. Ward 303

Index 311
Contributors

Steven M. Baskin, PhD Lawrence C. Newman, MD

Co-Director Associate Clinical Professor of Neurology
New England Institute for Behavioral Albert Einstein College of Medicine
Medicine Director, The Headache Institute
Stamford, CT St. Luke’s – Roosevelt Hospital Center
New York, NY
Marcelo E. Bigal, MD, PhD
Assistant Professor Alan M. Rapoport, MD
Department of Neurology Clinical Professor of Neurology
Albert Einstein College of Medicine David Geffen School of Medicine at UCLA
Director of Research Los Angeles, CA
The New England Center for Headache Founder and Director-Emeritus
Stamford, CT The New England Center for Headache, P.C.
Stamford, CT
Morris Levin, MD
Co-Director, Headache Clinic Mark J. Rapoport, MD
Associate Professor of Neurology Department of Radiology
Department of Neurology Northwestern University
Dartmouth-Hitchcock Medical Center Feinberg School of Medicine
Lebanon, NH Chicago, IL

Richard B. Lipton, MD, FAAN Robert E. Shapiro, MD, PhD

Professor of Neurology, Epidemiology Associate Professor of Neurology
and Social Medicine Medical Director, UVM Office of Clinical
The Saul R. Korey Department of Neurology Trials Research
Albert Einstein College of Medicine Department of Neurology
Bronx, NY University of Vermont
College of Medicine
Herbert G. Markley, MD, FAAN Burlington, VT
Director
New England Regional Headache Center Fred D. Sheftell, MD
Worcester, MA Assistant Clinical Professor of Neurology
and Psychiatry
Brian E. McGeeney, MD, MPH Albert Einstien College of Medicine
Assistant Professor of Neurology Bronx, NY
Boston University School of Medicine Founding Director
Department of Neurology New England Center for Headache
Boston University School of Medicine Stamford, CT
Boston, MA

xiii
xiv Contributors

Stewart J. Tepper, MD Randall E. Weeks, PhD

Center for Headache and Pain Co-Director
Cleveland Clinic New England Institute for Behavioral
Cleveland, OH Medicine
Stamford, CT
Thomas N. Ward, MD
Co-Director, Headache Clinic
Professor of Neurology
Department of Neurology
Dartmouth-Hitchcock Medical Center
Lebanon, NH
I
Headache Medicine Basic Science:
Anatomy, Physiology, and
Epidemiology
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1
Head Pain Anatomy and Physiology

Morris Levin, MD

Virtually all tissues of the head, face, and neck are pain-sensitive, with only
a few exceptions (Table 1–1). Pain sensation from the front of the head and face,
as well as the anterior skull contents, is mostly carried by the trigeminal nerve.
Pain from the posterior scalp and more posterior and inferior intracranial
structures is carried by the upper cervical roots C2 and C3 (see Table 1–2 for
innervation of specific regions and Fig. 1–1 for dermatomes of the head). In
this chapter, pain-sensitive structures and their innervation will be described,
followed by a discussion of pain physiology as it relates to headache pain.

SOURCES OF HEAD PAIN AND THEIR NOCICEPTIVE INNERVATION

Scalp and skull inflammation can produce head pain, generally of obvious
cause. Bone is relatively insensate, but periostea are quite painful. Scalp mus-
cles, vessels, and skin are highly sensitive as well. Muscular causes of pain are
often considered in patients with head pain but are generally not significant.
Scalp muscles are basically all connected by aponeurosis, with the frontalis and
occipitalis forming the anterior and posterior portions (Fig. 1–2). A number of
upper cervical region muscles can be pain sources as well. Suboccipital muscles
connect the atlas and the posterior base of the skull. The long capitis muscles
(longissimus and longus) run along the spine and connect to the skull base, and
the splenius muscles also connect the spine to the skull (mastoid). The sterno-
cleidomastoid and scalene muscles connect clavicle and rib cage elements to
the skull and upper spine. The muscles attached to the hyoid bone include the
stylohyoid, mylohyoid, and geniohyoid and can also be sources of facial pain,
generally around the jaw and pharynx. The temporalis muscle, interestingly a
very common site of perceived pain in headache, is one of the most prominent
of the scalp region muscles. The temporalis as well as the other muscles of mas-
tication (masseter and lateral and medial pterygoids) can also be painful. Facial
expression muscles are complex, but all are innervated by the facial nerve,
which serves both motor and sensory functions of these muscles (see Fig. 1–2).
Dural pain is particularly intense and is probably the cause of most pain
related to increased intracranial pressure and intracranial mass effect. The
arachnoid is also very pain-sensitive, which explains the intense headache of
meningitis and subarachnoid hemorrhage. Above the tentorium, meningeal

3
4 Headache Medicine Basic Science

Table 1–1 Pain-Sensitive Structures of the Head

Dura
Dural veins and arteries
Intracranial arteries
Cranial nerves V, VII, IX, X
Cervical root C1–3
Periosteum of the skull
Scalp
Scalp muscles
Scalp vessels
Sinuses
Eyes
Ears
Teeth and gums
Carotid and vertebral arteries
Cervical spine
Cervical muscles and tendons
Pain-Insensitive Structures:
Parenchyma
Pia, ventricles
Skull, cervical spine

sensation is subserved by the first division of the trigeminal nerve, but below
the tentorium there is more complex innervation, with contributions from the
facial, glossopharyngeal, and vagal nerves as well as C2 and C3.
The cerebral arteries are particularly sensitive, which explains the presence
of significant headache in virtually all cases of cerebral vasculitis (either
primary or secondary). Arteries of the circle of Willis are innervated by the
first division of the trigeminal nerve. Dural veins and cortical arteries are
served by meningeal nerves (either ophthalmic nerve or C2–3-derived).

Table 1–2 Nociceptive Innervation of Specific Head Regions

Face and frontal head regions V1-3

Eyes V1
Sinuses
Frontal and anterior ethmoid V1
Maxillary, sphenoid, post-ethmoid V2
Muscles of facial expression VII
Throat IX, X
Arteries of circle of Wills V1
Cortical and meningeal arteries V1, C2-3
Dura above tentorium V1
Dura in posterior fossa C2-3, VII, IX, X
Anatomy and Physiology 5

Ophthalmic
nerve
Great occipital nerve
(dorsal rami C2 and 3)

Maxillary
nerve
Lesser occipital nerve
(ventral ramus C2)

Great auricular nerve

(ventral rami C2 and 3)

Dorsal rami
Mandibular C3, 4 and 5
nerve
Transverse
cutaneous nerve of neck
(ventral rami C2 and 3)

Supraclavicular nerves
(ventral rami C3 and 4)

Figure 1–1 Dermatomes of the head and neck. (Used with permission from
Standring, S. Gray’s anatomy: The anatomical basis of clinical practice. Elsevier, 2004)

Meningeal arteries can be branches of the internal carotid, external carotid, or

vertebral artery and can be pain sources; they are also innervated by the first
division of the trigeminal nerve and upper cervical roots. Referral patterns of
these intracranial arteries can be complex (Fig. 1–3). Blood vessels of the scalp
include the occipital artery, the auriculotemporal artery, and the temporal artery.
All are derived from the external carotid artery and are pain-sensitive. (There are
some anterior branches derived from the ophthalmic artery, an internal carotid
artery branch.) The most important of the scalp arteries is the temporal artery,
which, when inflamed, can be intensely painful (Fig. 1–4). Typical of other
cervical and cranial arteries, the cervical portion of the carotid artery is pain-
sensitive (innervated by C2, C3, and C4), but interestingly, as shown by Raskin
in 1978, processes affecting it can produce surprising pain referral patterns,
including areas of the scalp, teeth, gums, eye, nose, cheek, and jaw.
Involvement of any of several cranial nerves can lead to significant head-
ache. The trigeminal nerve is most important. Its dermatomal distribution cov-
ers most of the face and frontal scalp (see Fig. 1–1). The ophthalmic nerve
carries sensation from the frontal scalp, forehead, upper eyelid, the conjunctiva
and cornea of the eye, the nose, nasal mucosa, the frontal sinuses, and parts of
the meninges as above. The maxillary nerve carries sensation from the lower
eyelid; nares; nasal mucosa; the maxillary, ethmoid, and sphenoid sinuses; cheek;
 6
Frontal belly of occipitofrontalis

Orbital part of orbicularis oculi

Temporalis
Palpebral part of orbicularis oculi
Levator labii superioris alaeque nasi
Levator labii superioris
Occipital belly of occipitofrontalis
Nasalis
Zygomaticus major
Zygomaticus minor
Masseter Levator anguli oris
Orbicularis oris
Modiolus
Stemocleidomastoid
Depressor labii inferioris
Depressor anguli oris
Trapezius Buccinator
Platysma (cut)
Omohyoid (superior belly)
Omohyoid (inferior belly)
Thyrohyoid

Sternohyoid

Figure 1–2 Muscles of the head and face. (Used with permission from Standring, S. Gray’s anatomy: The anatomical basis of clinical practice.
Elsevier, 2004)
Anatomy and Physiology 7

Figure 1–3 Cortical and meningeal arteries and their pain referral patterns. (Used
with permission from Lance, J.W., & Goadsby, P.J. Mechanisms and management of
headache. Elsevier, 2004)

Anterior (frontal) branch

Lacrimal artery of superficial temporal artery
Posterior (parietal) branch
of superficial temporal
Supraorbital artery artery
Facial artery
in levator labii superioris
alaequae nasi
Lateral nasal
branch

Septal branch
Levator anguli
oris Transverse facial artery
Superior labial
artery Superficial temporal
Buccinator artery
Maxillary artery
Inferior labial
artery Posterior auricular artery
Submental artery
Occipital artery
Facial artery
Lingual artery

Figure 1–4 Temporal artery and other arteries of the scalp. (Used with permission
from Standring, S. Gray’s anatomy: The anatomical basis of clinical practice.
Elsevier, 2004)
 8
Sensory root Lesser Petrosal nerve
Trigeminal nerve
Motor root Greater petrosal nerve
Trigeminal ganglion Geniculate ganglion
Ophthalmic nerve
Nerve of pterygoid canal Tympanic branch of glossopharyngeal nerve
(from tympanic plexus)
Maxillary nerve Tympanic membrane
Ganglionic branches Nervus spionosus
Chorda tympani
Nerve to tensor tympani
Pterygopalatine ganglion Otic ganglion
Anterior division of mandibular nerve Auriculotemporal nerve
Nerve to tensor veli palatini Sympathetic plexus
Lingual nerve
Medial pterygoid nerve Facial nerve

Middle meningeal artery

Inferior alveolar nerve

Buccinator
Inferior alverolar artery

External carotid artery

Lingual nerve
Superior constrictor of pharynx
(retracted downwards)
Medial pterygoid
Mylohyoid artery
Mylohyoid nerve
Mylohyoid (cut)

Figure 1–5 Trigeminal (Gasserian) ganglion, sphenopalatine (pterygopalatine) ganglion, and associated structures. (Used with permission from
Standring, S. Gray’s anatomy: The anatomical basis of clinical practice. Elsevier, 2004)
Anatomy and Physiology 9

upper lip; upper teeth and gums; the palate; and parts of the meninges. The
mandibular nerve carries sensory information from the lower lip, the lower
teeth and gums, the floor of the mouth, the anterior two thirds of the tongue,
the chin and jaw (except the angle of the jaw, which is innervated by C2 and
C3), anterior parts of the external ear, and parts of the meninges. Innervation
of the tympanic membrane has been controversial but is probably almost
entirely trigeminal.
The ophthalmic branch passes through the superior orbital fissure and the
cavernous sinus. The maxillary branch passes through the foramen rotundum
and also the cavernous sinus. The mandibular division passes through the
foramen ovale, bypassing the cavernous sinus. The three branches of the
trigeminal nerve converge within Meckel’s cave (located at the tip of the petrous
part of the temporal bone) to form the trigeminal ganglion (also known as the
Gasserian or semilunar ganglion) (Fig. 1–5). The proximal processes of the
nociceptive neurons of the trigeminal nerve enter the brain stem at the level of
the pons. They descend in the spinal trigeminal tract to synapse in the spinal
trigeminal nucleus (STN), located in the upper cervical spinal cord and
lower medulla. Processes affecting any of the branches of the trigeminal nerve
anywhere along their course can result in pain in the distribution of that branch
as well as referred pain to other parts of the head. These include disease
processes of the facial bones, eye, cavernous sinus, meninges, skull base, and
brain stem.
Some nociceptive sensation from the anterior head is carried by cranial
nerves VII, IX, and X, which synapse in the STN as well. Lesions or dysfunction
of the sensory portions of these nerves can thus also lead to head pain. Sensory
branches of VII innervate facial muscles of expression and parts of the external
auditory canal and pharynx. Their bodies are located in the geniculate ganglion
in the facial canal. Glossopharyngeal and vagal afferents carry some pharyngeal
and palatal sensation and posterior tongue sensation is carried by IX. The glos-
sopharyngeal nerve also innervates the middle ear. Cranial nerves IX and X also
innervate the dura of the posterior fossa. Both pass through the jugular foramen
on their way to the brain stem.
Upper cervical roots, primarily C2 and C3, carry pain sensation from poste-
rior portions of the head as well as the dura in the posterior fossa (see Fig. 1–1).
C2 passes between the atlas and axis, and C3 in the foramen between C2 and C3
bodies, on their way to the spinal cord. C1 emerges between the base of the
skull and the atlas and is essentially a motor nerve innervating several suboc-
cipital muscles.
Certain branches of the trigeminal nerve and cervical roots in the scalp are
prone to trauma and other dysfunction. Particularly vulnerable are the occipi-
tal nerve (derived from C2) and the supratrochlear and supraorbital nerves
(derived from V1) since their path is minimally protected (Fig. 1–6).
Paranasal sinuses are liberally innervated with nociceptive afferents, gener-
ally derived from the first two divisions of the trigeminal nerve (frontal and