Internal Medicine Journal 2003; 33: 436–442
CLINICAL PERSPECTIVES
Migraine: diagnosis and management
P. J. GOADSBY
Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, United Kingdom
Abstract
Migraine is the most common form of disabling primary
headache and affects approximately 12% of studied
Caucasian populations. Non-pharmacological manage-
ment of migraine largely consists of lifestyle advice to
help sufferers avoid situations in which attacks will be
triggered. Preventive treatments for migraine should
usually be considered on the basis of attack frequency,
particularly its trend to change with time, and tract-
ability to acute care. Acute care treatments for migraine
can be divided into non-specific treatments (general
analgesics, such as aspirin or non-steroidal anti-
inflammatory drugs) and treatments relatively specific to
INTRODUCTION
Headache is one of the most common human maladies
and books have been devoted to the subject.1–3 Migraine
is the commonest of the disabling primary headache
syndromes (Table 1). The World Health Organization
rates a day with severe migraine to be as disabling as a
day spent quadriplegic.4 The neurobiology of migraine is
as well understood now as any of the major neurological
illnesses, and interested readers are referred to a recent
review.5 The key to the clinical approach to migraine is
to understand its biology; this drives diagnosis and
management, while allowing the clinician to provide a
useful explanation to patients who seek information or
disease control, or both. I will first deal with traditional
migraine, by which I mean ‘episodic migraine’, as
defined by the International Headache Society (IHS)
Classification Committee (see Table 2).6 In the closing
section I will deal specifically with the recalcitrant
problem of frequent headache, and the migrainous
version of this, which will be called ‘chronic migraine’
when the IHS classification is revised to its second
edition.7 It deserves special mention, as clinicians will
realize, because frequent (daily) headache is a burden for
the sufferer,8 and a significant challenge for the treating
clinician.
Correspondence to: P. J. Goadsby, Institute of Neurology, Queen Square,
London, WC1N 3BG, United Kingdom. Email: peterg@ion.ucl.ac.uk
Received 5 September 2002; accepted 14 April 2003.
Funding: The work of P. J. Goadsby was supported by the Wellcome
Trust and the Migraine Trust.
Conflicts of interest: None
migraine (ergotamine and the triptans). The triptans –
sumatriptan, naratriptan, rizatriptan, zolmitriptan,
almotriptan, eletriptan and frovatriptan – are potent
serotonin, 5-HT1B/1D, receptor agonists which represent
a major advance in the treatment of acute migraine.
Chronic daily headache in association with analgesic
overuse is probably the major avoidable cause of head-
ache disability in the developed world. (Intern Med J
2003; 33: 436–442)
Key words: headache, treatment, serotonin agonist,
brainstem.
Migraine should be considered as an inherited,
episodic disorder of sensory modulation; a brain disorder
that results from dysfunction of brainstem9–11 or dien-
cephalic structures that normally regulate sensory traffic.
Migraine is not primarily a vascular headache, nor is it
simply a pain problem. Certainly, part of its patho-
physiology may involve nerve-driven vascular change;
neurovascular effects that are completely non-specific to
headache type.12 Migraine is probably, at its core, a
disorder of the central nervous system synchrony
mechanisms13 and is best understood and managed as a
neurological condition.
DIAGNOSIS
The production of the International Headache Society
IHS classification,6 and its widespread acceptance in the
headache community, must rank as one of the great
steps of the twentieth century in the field of headache. A
simplified version of the diagnostic criteria is listed in
Table 2. The IHS classification codifies what most clini-
cians had considered from first principles, that migraine
is a collection of symptoms, some more important than
others, but none really dominating. So while unilateral,
throbbing, severe pain with nausea is clearly migrainous,
it is also true that bilateral throbbing pain may be part of
the migrainous spectrum. The IHS classification simply
and very neatly accommodates this view.
Migraine manifesting as an episodic disorder
A fundamental principle of migraine is that it is episodic
in terms of its typical clinical presentation. I would
suggest that this is more or less universal, but that the
time constant of the disorder varies widely. The IHS
classification captures the great majority of migraine in

its limits of 4–72 h, and provides well-defined cases for
research purposes. However, this does not stop paedi-
atric migraine from often being shorter and less distinct,
nor does it preclude longer attacks. Indeed if one
considers patients with chronic migraine to have very
long time constants (in years) for the exacerbations of
their disease processes, then the principle of episodicity
is never violated.
Migraine and tension-type headache
The most challenging part of the diagnosis of primary
headache is the differentiation between migraine and
tension-type headache. Clinically, if one takes a history
that is vaguely suspicious of secondary headache, or if
there are any abnormal neurological signs, imaging is so
accessible that a brain scan will be done. Brain scans,
however, more often reveal findings that are unrelated to
the underlying primary headache.14 Suffice to say that
the clinical problem for most neurologists will be the
patient complaining of headache, with a normal neuro-
logical, and relevant general physical examination
(including blood pressure), and a normal brain scan.
Furthermore, given how common migraine and tension-
type headache are (Table 1), one of these is highly likely
to be the diagnosis.
As a rule – and I think it is reliable and will be shown
to be biologically sound – migraine is headache with
features of sensory sensitivity, sensitivity to light, sound,
smells and head movement, and with throbbing (effec-
tively movement of blood vessels), whereas tension-type
headache is headache without any of those features. It is
likely that migraine is a disorder of the brainstem,
probably the aminergic systems that normally regulate
sensory information and the pathways required for
attention; a disorder in effect of hypersynchrony.13 In
Table 1 Common causes of headache†
Primary headache
Type Lifetime prevalence (%)
Migraine 16.0
Tension-type 69.0
Cluster headache 0.4
Idiopathic stabbing 2.0
Exertional 1.0
†Table adapted from Rassmussen.47
Table 2 Modified† International Headache Society diagnostic criteria for migraine6
Migraine-episodic attacks of headache lasting 4-72 h
With two of the following
Unilateral
Throbbing
Aggravated by movement
Moderate/severe intensity of pain
†Table adapted from Goadsby et al.48
Diagnosis & treatment of migraine 437
contrast, tension-type headache, in the pure sense, is a
pain problem without other sensory-system involvement.
So for a simple, yet biologically plausible rule, ‘headache
plus’ is migraine, and ‘headache full-stop’ is tension-type
headache.
MANAGEMENT OF MIGRAINE
The management of migraine begins with an explanation
of certain things to the patient, notably:
• Migraine is an inherited tendency to cerebral
dysfunction, and cannot be cured
• Migraine can be modified and controlled by life-
style adjustment and the use of medicines
• Migraine is neither life threatening nor associated
with serious illness, with the exception of females
who smoke and are on the oestrogenic oral contra-
ceptives who are at increased risk for stroke, however
migraine can and often does make life a misery
• Migraine management takes time and co-operation
when information, such as that from a headache
diary, has to be collected.
Non-pharmacological management
Put very simply, non-pharmacological management of
migraine helps the patient identify things that make the
problem worse and encourages them to modify these. It
is important to explain to the patient that the tendency
to suffer an attack probably varies because of some
cycling changes in the brain that are not well under-
stood. This is why avoiding things on some days will
prevent attacks and, perversely, enjoying the same things
on other days produces no headache. The crucial piece
Secondary headache
Type Lifetime prevalence (%)
Systemic infection 63.0
Head injury 4.0
Sub-arachnoid haemorrhage <1.0
Vascular disorders 1.0
Brain tumour 0.1
With one of the following
Nausea/vomiting
Photophobia and phonophobia
Internal Medicine Journal 2003; 33: 436–442
438 Goadsby
of the puzzle is what the brain is doing and this is the
subject of intense study. Rather than make a long list of
things to avoid, patients should first be encouraged to
have regular habits and not to exceed their limits.
Regular sleep, exercise, meals, work habits, and some
time for relaxation will be very rewarding in terms of
reducing headache frequency. Avoiding what regularly
triggers attacks (and not being disturbed when the long
list of advice in the magazine is not useful) is good
general advice for migraineurs. Migraineurs are individ-
uals; encourage them to individualize their trigger
avoidance. Extensive and exclusive dietary advice is
rarely useful, and often seems to punish patients for their
poor choice of parents.
In the non-pharmacological arena it is remarkable that
certain disciplines – such as reflexology, osteopathy and
chiropractic – pursue the treatment of migraine without
controlled evidence. Consider the pathophysiology of
acute migraine with activation of trigeminocervical
afferents15 and the referral of pain to the occipital and
upper-cervical region that can be well demonstrated in
animal studies.16 It is logical, indeed expected, that
during migraine there may be neck discomfort and stiff-
ness, with perhaps over-activity of muscles such as
trapezius. This is part of the attack, not evidence of neck
disease requiring re-alignment of structures that are
bystanders to the pathophysiology of migraine. It is
worth reviewing the spinal manipulation literature here,
because I am sure many readers are confronted with
anecdote on this issue. A recent meta-analysis of spinal
manipulation in migraine17 listed three studies under
Chronic Migraine (which is an incorrect use of that
nomenclature but I will use it in this instance for discus-
sion). Of these three studies, two were old, low-quality
and did not use clear clinical definitions (i.e. non-IHS
classification).6 The one that is modern was given a
rather generous run by the peer-reviewers.18 First, there
was no control group. Second, there was no differenti-
ation of spinal manipulation from amitriptyline. If the
authors used amitriptyline as an active control, assuming
it works, then their study provides no evidence whatso-
ever for an effect of spinal manipulation. One might
observe that the evidence for amitriptyline is weak,19 but
that provides cold comfort. One study of high quality
used a clear case definition, migraine by the IHS classi-
fication, and a control group.20 However, it was single-
blinded, in the sense that the operators knew what they
were doing and thus knew who was in the active group
and who was in the placebo group. In short, there is no
single, well-conducted, placebo-controlled, double-blind
study demonstrating a positive effect for chiropractic
treatment of migraine.
Preventive treatments for migraine
The decision to start a patient on a preventive drug
requires input from both doctor and patient. The basis
for considering preventive treatment from a medical
viewpoint is a combination of acute attack frequency and
attack tractability. Attacks that are unresponsive to acute
attack medications are easily considered for prevention
at almost any frequency, whereas simply treated attacks
Internal Medicine Journal 2003; 33: 436–442
probably do not provide candidates for prevention. The
other part of the equation relates to the natural history.
If a patient diary shows a clear trend for increased
frequency it is probably better to get in early with
prevention than wait for the problem to become intrac-
table. A simple rule for frequency might be that: (i) for
one or two headaches per month there is usually no need
to start a preventive, (ii) for three or four headaches per
month it may be needed, but not necessarily and (iii) for
five or more headaches per month prevention should
definitely be on the agenda for discussion. Options avail-
able for preventive treatment are included in Table 3.
The most notable addition in recent times is topiramate,
with clear evidence of efficacy in large, placebo-
controlled, randomized clinical trials.21 These studies
are convincing from what I have seen, albeit only
abstracted as yet. Topiramate should be started at low
dose and slowly titrated to clinical response and side-
effects. The principles are common to neurological ther-
apeutics; start low, go slow and warn the patient of
potential side-effects.
Acute attack therapies for migraine
Acute attack treatments for migraine can be usefully
divided into: (i) disease non-specific treatments, such as
analgesics and non-steroidal anti-inflammatory drugs
(NSAIDs) and (ii) relatively disease-specific treatments,
such as ergot-related compounds and triptans
(Table 4). It must be emphasized that most acute attack
medications seem to have a propensity to aggravate
headache frequency and induce a state of refractory
daily or near-daily headache; ‘analgesic-associated
chronic daily headache (CDH)’. Codeine-containing
compound analgesics are a particular problem because
opioid receptor agonists produce troublesome with-
drawal symptoms and require careful monitoring. Not
all patients who stop taking regular analgesics will have
a miracle cure of their headache, but almost all feel in
some way better and will be easier to treat with standard
preventives (Table 3).
One simple approach to treatment is described as
‘stepped care’. In this model all patients are treated,
assuming no contraindications, with the simplest treat-
ment, such as aspirin with an antiemetic. This is an
effective strategy proven by double-blind controlled
clinical trials.22 The alternative strategy is known as
‘stratified care’, by which the physician determines, or
stratifies, treatment at the start based on likelihood of
response to levels of care. Lipton and Stewart have
proposed the Migraine Disability Assessment Scale
(MIDAS)23 and have demonstrated that patients with
greater disability (high MIDAS scores) may be better off
having earlier access to triptans.24 The MIDAS scale is
easy to use and freely available. Somewhere in between
these two treatment strategies is ‘stepped-care with
clinical modification’, which seems reasonably rational
to the author (Table 5).
Simple things, such as aspirin (900 mg) and para-
cetamol (1000 mg), are cheap, can be very effective
and are usefully employed in many patients. The
addition of domperidone (10 mg p.o.) or metaclopramide
 Diagnosis & treatment of migraine 439

Table 3 Preventative therapy for migraine†5

Drug Dose Selected side-effects

Proven or very well accepted treatments2

β-adrenergic receptor antagonists
Propranolol 40–120 mg b.i.d. Reduced energy, tiredness, postural symptoms
Metoprolol 100–200 mg/day Contraindicated in asthma.
Tricyclic antidepressants
Amitriptyline 25–75 mg nocte Drowsiness (Note: some patients are very sensitive and may
only need a total dose of 10 mg, although often 1 mg/kg
body weight is required for a response)
Pizotifen 0.5–3 mg/day Drowiness, weight gain
Valproate 400–600 mg bid Drowsiness, weight gain, tremor, hair loss, fetal
abnormalities, haematological and liver abnormalities
Topiramate21,49 25–200 mg/day Cognitive impairment, parasthesiae, weight loss
Flunarizine 5–15 mg/day Tiredness, weight gain, depression, Parkinsonism
Methysergide 1–6 mg/day Drowsiness, leg cramps, hair loss, retroperitoneal fibrosis
(a 1-month ‘drug holiday’ is required every 6 months)
Widely used with poor evidence§
Verapamil 160–320 mg/day Constipation, leg swelling and atrioventricular conduction
disturbances such as fluoxetine
SSRIs
Promising‡
Gabapentin50,51 900–2400 mg/day Tiredness, dizziness
SSRI, selective serotonin reuptake inhibitor. †Commonly used preventives are listed with reasonable doses and common side-effects. Local
prescribing information should be consulted before use. ‡Positive placebo-controlled studies but more data are required. §Compounds listed here
are widely used but the evidence for benefit is very poor.

Table 4 Oral acute migraine treatments required. Whereas ergotamine remains a useful anti-
migraine compound, its place as the first-choice has
Non-specific treatments† Specific treatments slipped in recent years and this trend is likely to
continue. There are particular situations in which ergot-
Aspirin (900 mg) Ergot derivatives amine is very useful, however its use must be strictly
Paracetamol (1000 mg) Ergotamine (1–2 mg) controlled because ergotamine overuse produces
NSAIDs Triptans dreadful headache in addition to a host of vascular prob-
Naproxen (500–1000 mg) Sumatriptan (50 or 100 mg) lems.26 The triptans have revolutionized the lives of
Ibuprofen (400–800 mg) Zolmitriptan (2.5 or 5 mg) many patients with migraine and are clearly the most
Tolfenamic acid (200 mg) Naratriptan (2.5 mg) powerful option available to stop a migraine attack. They
Rizatriptan (5 or 10 mg)‡ can be rationally applied by considering their pharmaco-
Almotriptan (12.5 mg)‡ logical, physicochemical and pharmacokinetic features,
Eletriptan (40 or 80 mg)‡ as well as the formulations that are available.27 Some
Frovatriptan (2.5 mg)‡,§ suggested situations in which particular triptans are
†Often used with antiemetic/prokinetics, such as domperidone (10 mg) helpful are detailed in Table 5, and a recent meta-
or metaclopramide (10 mg). ‡Not launched in Australia at the time of analysis compares the clinical trial data from 53
writing. §Not yet widely enough used in clinical practice, nor with controlled trials.28
enough published studies to make clear recommendations. NSAIDs,
non-steroidal anti-inflammatory drugs.
CHRONIC DAILY HEADACHE
(10 mg p.o.) can be very helpful. NSAIDs can be very Perhaps no clinical issue in headache provides as much
useful when tolerated. Their success is often limited by controversy nor as substantive a medical load as that of
inappropriate dosing: naproxen (500–1000 mg p.o. or daily headache. CDH is not one thing, but a collection
p.r. with an antiemetic), ibuprofen (400–800 mg p.o.) or of very different problems with different management
tolfenamic acid (200 mg p.o.) can be extremely effective. strategies. CDH is simply headache on ≥15 days per
Tolfenamic acid has been shown in a double-blind, month; certainly not all daily headache is tension-type
placebo-controlled study to have comparable efficacy to headache (Table 6). Population-based estimates of daily
sumatriptan 100 mg,25 a result that reinforces the headache are remarkable, demonstrating that nearly 5%
general clinical view that NSAIDs can be very useful of people in developed countries such as Spain,29
compounds in migraine. France30 and the USA31 are affected. Daily headache
When simple measures fail, or more aggressive treat- may again be primary or secondary, and it seems clini-
ment is required, the relatively specific treatments are cally useful to consider the possibilities in this way when

Internal Medicine Journal 2003; 33: 436–442

440 Goadsby

making management decisions. It should be said that
results from population-based studies support evidence
from clinical practice and a large group of refractory
daily headache patients overuse various over-the-counter
preparations.
Chronic daily headache and migraine
Whereas it is widely accepted that some of the primary
headaches – tension-type headache, cluster headache
and paroxysmal hemicrania – have chronic varieties,6 the
question of frequent migraine is only now being system-
atically addressed. Few headache authorities would
argue that migraine can never, ever be chronic in terms of
frequency. However, the question of whether patients
with frequent headache, which fulfils some of standard
criteria for migraine, and some standard criteria tension-
type headache, have a single migrainous problem in
biological terms is vexed.

Table 5 Clinical stratification of acute specific migraine treatments

Clinical situation Treatment options

Failed analgesics/NSAIDs Rapid effects

– Sumatriptan 50 mg or 100 mg po
– Rizatriptan 10 mg p.o.
– Zolmitriptan 2.5 mg p.o.
– Almotriptan 12.5 mg p.o.
– Eletriptan 40 mg p.o.
Slower effect/better tolerability
– Naratriptan 2.5 mg
– Frovatriptan 2.5 mg
Infrequent headache
– Ergotamine 1–2 mg p.o.†
Early nausea or problem taking tablets Nasal route
– Sumatriptan 20 mg nasal spray
– Zolmitriptan 5 mg nasal spray
Oral: rapidly dissolving
– Rizatriptan 10 mg MLT wafer
– Zolmitriptan (RapiMelt) 2.5 mg
Headache recurrence Ergotamine (perhaps most effective p.r.)
Eletriptan 80 mg p.o.
Naratriptan 2.5 mg p.o.
Tolerating acute treatments poorly Naratriptan 2.5 mg
Almotriptan 12.5 mg
Frovatriptan 2.5 mg
Early vomiting Sumatriptan 25 mg p.r. (available in Europe)
Sumatriptan 6 mg s.c.
Menstrually related headache Prevention
– Consider tri-cycling oral contraceptive to reduce menstrual attacks
– Ergotamine p.o. nocte
– Oestrogen patches
Treatment
– Triptans
Very rapidly developing symptoms Sumatriptan 6 mg s.c.
Dihydroergotamine 1 mg i.m.i.
†Expert consensus suggests there are now very few first-line uses for ergotamine in migraineurs.26 NSAIDs, non-steroidal anti-inflammatory drugs.

Table 6 Daily or near-daily headache†

Primary daily headache Secondary daily headache

Chronic migraine Chronic headache with intracranial pathology, such as subdural, brain tumour
Chronic tension-type headache Inflammatory disease, such as giant cell arteritis
Chronic cluster headache Chronic headache after dural irritation, such as postinfectious or postbleed
Chronic paroxysmal hemicrania Chronic headache after trauma, such as blunt head trauma or neurosurgical procedures
Primary new daily persistent headache52 Chronic headache with cerebrospinal fluid pressure abnormalities, such as low or raised
pressure
†Daily as used in this terminology implies headache on ≥15 days per month.45

Internal Medicine Journal 2003; 33: 436–442


Considering the population-based surveys quoted
above and current thinking on the classification of head-
ache, approximately half of daily headache patients have
chronic tension-type headache and the other half have
‘chronic migraine’ (previously called ‘transformed
migrane’).32 The philosophy behind chronic migraine is
that some patients who inherit a migrainous biology end
up with frequent headache because they are susceptible
to headache by virtue of that inheritance. The typical
patient will have daily headache of a dull, non-specific
type, punctuated by more severe attacks that would
often, in isolation, fulfil standard criteria for migraine. In
headache speciality clinics this group is dominant, with
approximately 90% of patients in referral headache
clinics having chronic migraine, often with analgesic
overuse.33 It could be suggested that they have a biolog-
ically more difficult problem and this is the basis for their
over-representation in referral centres. If it is accepted
that all other forms of primary headache have chronic
counterparts – particularly the quintessentially episodic
primary headache, cluster headache – having frequent
migraine is not so difficult a concept.
Treatment of frequent headache with migrainous
features requires control of analgesic, ergotamine or
triptan overuse,34,35 and instigation of preventive treat-
ments. The crucial component of the management of
frequent headache is to get the prevention right. It is
exceptional for a patient with medication misuse to be
successfully treated with preventives unless the use of
acute medications is controlled. The most useful preven-
tives are tricylics, or anticonvulsants such as valproate,36
gabapentin37 or topiramate.38 Comorbidity with depres-
sion is common in migraine,39,40 so appropriate
management of comorbid depression or anxiety is
important. Admission41 and treatment with a course of
i.v. dihydroergotamine42 can be a very effective way to
break the cycle of persistent headache. Some centres use
a course of i.v. lidocaine in this setting,41,43,44 and some
advocate a short course of methylprednisolone.3 Inter-
ested readers are referred to recent, more detailed,
considerations of CDH45 and its management.46
REFERENCES
1 Lance JW, Goadsby PJ. Mechanism and Management of
Headache, 6th edn. London: Butterworth-Heinemann; 1998.
2 Olesen J, Tfelt-Hansen P, Welch KMA. The Headaches, 2nd
edn. Philadelphia: Lippincott Williams & Wilkins; 2000.
3 Silberstein SD, Lipton RB, Goadsby PJ. Headache in Clinical
Practice, 2nd edn. London: Martin Dunitz; 2002.
4 Menken M, Munsat TL, Toole JF. The global burden of disease
study – implications for neurology. Arch Neurol 2000; 57:
418–20.
5 Goadsby PJ, Lipton RB, Ferrari MD. Migraine – current
understanding and treatment. N Engl J Med 2002; 346: 257–70.
6 Headache Classification Committee of The International
Headache Society. Classification and diagnostic criteria for
headache disorders, cranial neuralgias and facial pain.
Cephalalgia 1988; 8: 1–96.
7 Headache Classification Committee of The International
Headache Society. Classification and diagnostic criteria for
headache disorders, cranial neuralgias and facial pain.
Cephalalgia 2004; 24: in press.
Diagnosis & treatment of migraine 441
8 von Korff M, Stewart WF, Simon DJ, Lipton RB. Migraine and
reduced work performance: a population-based diary study.
Neurology 1998; 50: 1741–5.
9 Weiller C, May A, Limmroth V, Juptner M, Kaube H, Schayck RV
et al. Brain stem activation in spontaneous human migraine
attacks. Nat Med 1995; 1: 658–60.
10 Bahra A, Matharu MS, Buchel C, Frackowiak RSJ, Goadsby PJ.
Brainstem activation specific to migraine headache. Lancet 2001;
357: 1016–7.
11 Matharu MS, Bartsch T, Ward N, Frackowiak RSJ, Weiner RL,
Goadsby PJ. Central modulation in chronic migraine with
implanted suboccipital stimulators. Neurology 2003; 60:
A404–A405.
12 May A, Buchel C, Turner R, Goadsby PJ. MR-angiography in
facial and other pain: neurovascular mechanisms of trigeminal
sensation. J Cereb Blood Flow Metabol 2001; 21: 1171–6.
13 Niebur E, Hsiao SS, Johnson KO. Synchrony: a neural
mechanism for attentional selection? Curr Opin Neurobiol 2002;
12: 190–4.
14 Quality Standards Subcommittee of the American Academy of
Neurology. The utility of neuroimaging in the evaluation of
headache patients with normal neurologic examinations.
Neurology 1994; 44: 1353–4.
15 Goadsby PJ, Hoskin KL. The distribution of trigeminovascular
afferents in the non-human primate brain Macaca nemestrina:
a c-fos immunocytochemical study. J Anat 1997; 190: 367–75.
16 Bartsch T, Goadsby PJ. Stimulation of the greater occipital nerve
induces increased central excitability of dural afferent input. Brain
2002; 125: 1496–509.
17 Bronfort G, Assendelft WJJ, Evans R, Haas M, Bouter L. Efficacy
of spinal manipulation for chronic headache: a systematic review.
J Manipulative Physiol Therapeutics 2001; 24: 457–66.
18 Nelson CF, Bronfort G, Evans R, Boline P, Goldsmith C,
Anderson AV. The efficacy of spinal manipulation, amitriptyline
and the combination of both therapies for the prophylaxis of
migraine headaches. J Manipulative Physiol Therapeutics 1998;
21: 511–9.
19 Silberstein SD, Rosenberg J. Multispecialty consensus on
diagnosis and treatment of headache. Neurology 2000; 54: 1553.
20 Tuchin PJ, Pollard H, Bonello R. A randomized controlled trial of
chiropractic spinal manipulative therapy for migraine.
J Manipulative Physiol Ther 2000; 23: 91–5.
21 Mathew NT, Schmitt J, Jacobs D, Neto W. Topiramate in the
migraine prevention (MIGR-001): effect on migraine frequency.
Neurology 2003; 60: A336.
22 Tfelt-Hansen P, Henry P, Mulder LJ, Scheldewaert RG,
Schoenen J, Chazot G. The effectiveness of combined oral lysine
acetylsalicylate and metoclopramide compared to oral sumatriptan
for migraine. Lancet 1995; 346: 923–6.
23 Lipton RB, Stewart WF, Sawyer J, Edmeads JG. Clinical utility of
an instrument assessing migraine disability: the migraine disability
assessment (MIDAS) questionnaire. Headache 2001; 41:
854–61.
24 Lipton RB, Stewart WF, Stone AM, Lainez MJA, Sawyer JPC.
Stratified care vs step care strategies for migraine. The Disability
in Strategies of Care (DISC) Study: a randomized trial. J Am
Med Assoc 2000; 284: 2599–605.
25 Myllyla VV, Havanka H, Herrala L, Kangasniemi P, Rautakorpi I,
Turkka J et al. Tolfenamic acid rapid release versus sumatriptan in
the acute treatment of migraine: comparable effect in a double-
blind, randomized, controlled, parallel-group study. Headache
1998; 38: 201–7.
26 Tfelt-Hansen P, Saxena PR, Dahlof C, Pascual J, Lainez M,
Henry P et al. Ergotamine in the acute treatment of migraine –
a review and European consensus. Brain 2000; 123: 9–18.
27 Goadsby PJ. The pharmacology of headache. Prog Neurobiol
2000; 62: 509–25.
Internal Medicine Journal 2003; 33: 436–442
442 Goadsby
28 Ferrari MD, Roon KI, Lipton RB, Goadsby PJ. Triptans
(serotonin, 5-HT1B/1D agonists) in acute migraine treatment –
a meta-analysis of 53 trials. Lancet 2001; 358: 1668–75.
29 Castillo J, Muqoz P, Guitera V, Pascual J. Epidemiology of
chronic daily headache in the general population. Headache
1999; 39: 190–6.
30 Lanteri-Minet M, Auray JP, El Hasnaoui A, Dartigues JF, Duru G,
Henry P et al. Prevalence and description of chronic daily
headache in the general population in France. Pain 2003; 102:
143–9.
31 Scher A, Stewart WF, Liberman J, Lipton RB. Prevalence of
frequent headache in a population sample. Headache 1998; 38:
497–506.
32 Silberstein SD, Lipton RB, Sliwinski M. Classification of daily and
near-daily headaches: a field study of revised IHS criteria.
Neurology 1996; 47: 871–5.
33 Silberstein SD, Lipton RB, Goadsby PJ. Headache in Clinical
Practice. Oxford: ISIS Medical Media; 1998.
34 Limmroth V, Katsarava Z, Fritsche G, Przywara S, Diener H-C.
Features of medication overuse headache following overuse of
different acute headache drugs. Neurology 2002; 59: 1011–4.
35 Katsarava Z, Fritsche G, Muessig M, Diener HC, Limmroth V.
Clinical features of withdrawal headache following overuse of
triptans and other headache drugs. Neurology 2001; 57: 1694–8.
36 Mathew NT, Ali S. Valproate in the treatment of persistent
chronic daily headache. An open label study. Headache 1991; 31:
71–4.
37 Beran RG, Spira PJ. Gabapentin in chronic daily headache.
Neurology 2001; 56: A220–A221.
38 Shuaib A. Efficacy of topiramate in prophylaxis of frequent severe
migraines or chronic daily headaches: experience with 68 patients
over 18 months. Cephalalgia 2000; 20: 423.
39 Breslau N, Davis GC, Andreski P. Migraine, psychiatric disorders,
and suicide attempts: an epidemiologic study of young adults.
Psychiatry Res 1991; 37: 11–23.
Internal Medicine Journal 2003; 33: 436–442
40 Breslau N, Davis GC. Migraine, physical health and psychiatric
disorder: a prospective epidemiological study in young adults.
J Psychiatric Res 1993; 27: 211–21.
41 Jauslin P, Goadsby PJ, Lance JW. The hospital management of
severe migrainous headache. Headache 1991; 31: 658–60.
42 Raskin NH. Repetitive intravenous dihydroergotamine as therapy
for intractable migraine. Neurology 1986; 36: 995–7.
43 Burke M. Intravenous lignocaine for migraine headache.
Australian Family Physician 1989; 18: 1559.
44 Hand PJ, Stark RJ. Intravenous lignocaine infusions for severe
chronic daily headache. Med J Aust 2000; 172: 157–9.
45 Welch KMA, Goadsby PJ. Chronic daily headache: nosology and
pathophysiology. Curr Opin Neurol 2002; 15: 287–95.
46 Goadsby PJ, Boes C. Chronic daily headache. J Neurol
Neurosurg Psychiatry 2002; 72: ii2-ii5.
47 Rasmussen BK. Epidemology of headache. Cephalalgia 1995; 15:
45–68.
48 Goadsby PJ, Olesen J. Diagnosis and management of migraine. Br
Med J 1996; 312: 1279–82.
49 Silberstein S, Karim R, Kamin M, Jordan D, Hulihan J.
Topiramate prophylaxis in patients suffering from migraine
without aura: results from a randomized, double-blind, placebo-
controlled trial. European J Neurol 2002; 9: 44.
50 Mathew NT, Rapoport A, Saper J, Magnus L, Klapper J,
Ramadan N et al. Efficacy of gabapentin in migraine prophylaxis.
Headache 2001; 41: 119–28.
51 Di Trapani G, Mei D, Marra C, Mazza S, Capuano A.
Gabapentin in the prophylaxis of migraine: a double-blind,
randomized, placebo-controlled study. Cephalalgia 2000; 20:
345.
52 Goadsby PJ, Boes CJ. New daily persistent headache. J Neurol
Neurosurg Psychiatry 2002; 72: ii6-ii9.