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Migraine: Mimics, borderlands and chameleons

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Diagnostically, headache is the easy part of migraine. It is the surrounds of migraine-the aura, prodrome and postdrome-that can be most challenging, and confused with other pathologies. This article examines the definition and variants of migraine; alternative diagnoses for which migraine may be mistaken (mimics); conditions that lie between migraine and other diagnoses (borderlands) and the possible presentations of migraine posing as other conditions (chameleons). The focus is on adults, with only passing reference to children. Migraine is more often a chameleon than a mimic; and it is the careful history that usually makes the distinction. Given migraine's prevalence of 10-15%, relatively uncommon features of migraine occur quite often, in comparison with frequent manifestations of less common diseases. Thus, even rare or under-recognised presentations of migraine come into the differential diagnosis of many presentations.
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Migraine: mimics, borderlands
and chameleons
Heather Angus-Leppan
Correspondence to
Dr Heather Angus-Leppan,
Department of Neurology,
Barnet and Royal Free
Hospitals, Pond Street,
London NW32QG, UK;
heather.angus-leppan@nhs.net
Published Online First
1 August 2013
To cite: Angus-Leppan H.
Pract Neurol 2013;13:
308318.
ABSTRACT
Diagnostically, headache is the easy part of
migraine. It is the surrounds of migrainethe
aura, prodrome and postdromethat can be
most challenging, and confused with other
pathologies. This article examines the definition
and variants of migraine; alternative diagnoses
for which migraine may be mistaken (mimics);
conditions that lie between migraine and other
diagnoses (borderlands) and the possible
presentations of migraine posing as other
conditions (chameleons). The focus is on adults,
with only passing reference to children. Migraine
is more often a chameleon than a mimic; and it
is the careful history that usually makes the
distinction. Given migraines prevalence of
1015%, relatively uncommon features of
migraine occur quite often, in comparison with
frequent manifestations of less common
diseases. Thus, even rare or under-recognised
presentations of migraine come into the
differential diagnosis of many presentations.
WHAT IS MIGRAINE? THE HEADACHE,
PREMONITORY SYMPTOMS, THE
AURA AND INTERICTAL
HYPERSENSITIVITY
Migraine headache is classified as one of
the primary headache disorders, defined as
recurrent attacks of moderate or severe
intensity lasting 472 h; typically with uni-
lateral location, pulsating quality, nausea
and/or photophobia and phonophobia,
worse with physical activity.
1
For the prac-
tical neurologist, only a minority of
patients with migraine fits entirely into this
International classification of headache dis-
orders (ICHD) definition
1
(figure 1).
Secondary migraine headaches (symptom-
atic migraine) are rare (figure 2), and asso-
ciated features usually make the underlying
cause obvious. Abnormal physical signs
should prompt investigation.
Despite the rarity of secondary
migraine, they create great anxiety: most
of our patients perceive severity of head-
ache as a marker of a sinister pathology.
It can be difficult to distinguish a mimic
from a primary migraine triggered by an
intercurrent conditionfor example, a
migraineur who develops a benign fever
and a primary migraine headache with
photophobia and phonophobia may lead
to investigation for meningitis.
Premonitory symptoms, defined as
non-headache symptoms up to 2 days
before a migraine episode, occur in 33
87% of patients
2
and include fatigue,
mood change, poor concentration,
change in bowel and bladder function
and neck stiffness. An electronic diary
study in which entries could not be
altered retrospectively showed that these
premonitory symptoms occurred before,
during and after migraine attacks, sug-
gesting that these are part of the migraine
phenotype.
3
Typical migraine aura is defined in the
ICHD as reversible positive and/or nega-
tive sensory, and/or visual and/or speech
focal neurological symptoms that usually
develop gradually, lasting between 5 and
60 min,
1
while hemipleg ic migraine is
defined separately and may be of longer
duration.
13
Their gradual onset helps to
differentiate these symptoms from sei-
zures and vascular events, and their
longer duration helps further to distin-
guish them from seizures.
Migraine auras are commonly atyp-
ical. A recent systematic review of the
usual duration of migraine aura found
that migraine aura lasted longer than 1 h
in a significant proportion of migraineurs
(up to 60% in aphasic aura).
4
The
authors suggested labelling of these
patients as having probable, rather than
definite, migraine is inappropriate.
Neurologists must untangle the myriad
of sensory, autonomic, motor, perceptual
and cognitive aura and symptoms with
which migraine may present (figure 3).
These are usually positive symptoms,
often with interictal hypersensitivity, and
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308 Angus-Leppan H. Pract Neurol 2013;13:308318. doi:10.1136/practneurol-2012-000502
particularly visual. Most migraineurs develop photo-
phobia, phonophobia and/or osmophobia.
Our patients (and colleagues) may find it hard to
believe that the aura can come before, during, after
the headache, or even without a headache; and an
important part of the management is reassurance and
education.
Research highlights potential pathophysiological
mechanisms for this, and imaging studies show
changes in the brainstem regions suggesting that
migraine involves sensory dysmodulation (upregula-
tion).
5
Electrophysiological studies show increased
amplitude of visual evoked responses in migraine, and
functional studies showing heightened ability of
migraine patients in low-level visual tasks, and heigh-
tened sensitivity to certain visual stimuli. There may
be significantly higher glucose metabolism bilaterally
in the posterior subcortical cerebrum and in the cere-
bellum in those with migraine, during headache-free
periods, compared with controls.
6
Migrainous auras
are usually visual and vestibular, but can be olfactory,
gustatory or auditory. They tend to be elementary or
unformed, variable in position and do not conform to
anatomical guidelines, in that they are not necess arily
Figure 1 What is migraine?
Figure 2 Migraine mimics and secondary causes.
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Angus-Leppan H. Pract Neurol 2013;13:308318. doi:10.1136/practneurol-2012-000502 309
contralateral to the headache. Apart from their
importance as a problem to the patient, they tell us a
lot about migraineand argue against the idea that
migraine is simply a vascular disturbance.
MIGRAINE VARIANTS
Several migraine variants are common in neurology
clinics. Some authorities classify these as distinct
primary headaches: the debate about their classifica-
tion highlights the difficulties when conditions do not
have clear biological markers, and their diagnosis is
based on a combination of clinical features.
Icepick headaches (primary stabbing headaches) are
isolated brief stabbing pains, usually in the orbital,
temporal or parietal area, which occur in 40% of
migraineurs.
7
They usually require no treatment
beyond reassurance, though will frequently respond to
migraine prophylaxis.
Icecream headaches occur in one-third of the popu-
lation, and their link with migraine is less cer tain.
8
Primary thunderclap headache is a diagnosis of
exclusion. Thunderclap headache of new onset
defined as headache reaching maximum intensity
within 10 s and including coital and other
exercise-induced headacherequires urgent investiga-
tion. Although nausea, neck stiffness, occipital loca-
tion and impaired consciousness more frequently
accompany subarachnoid headache,
9
they are not
invariable, and their absence cannot be relied upon
10
:
all patients need investigation. There is no consensus
on percentage of thunderclap headaches that are due
to subarachnoid haemorrhage: estimates range from
11% to 70%. Reassuringly, if investigations (at least
CT scan and lumbar puncture) exclude haemorrhage,
stroke or a sinister cause, follow-up for 17 years
shows no subarachnoid haemorrhage mortality,
1012
although thunderclap headaches recur in 24%.
9
This
supports the entity of benign thunderclap headache as
a migraine variant, and is in keeping with district hos-
pital clinical experience. Studies from tertiary centres,
which lack the long-term follow-up of studies on
primary thunderclap headache, suggest that primary
thunderclap headache is rare, and that most are due to
reversible cerebral vasospastic syndrome,
10 13
dis-
cussed below. The issue is unresolved, and hinges on
whether angiography is showing pre-existent vaso-
spasm, or whether it triggers vasospasm in patients
with acute migraine.
Chronic daily headache describes a phenotype
occurring 15 or more days per month for at least
3 months, with each attack averaging 4 h or more.
1
Chronic migraine, with or without a history of epi-
sodic migraine, is a subtype of chronic daily headache,
and may occur with or without analgesia overuse.
14
MIGRAINE MIMICS
This section comprises two distinct groups:
Primary headache conditions classified as separate
entities, such as the trigeminal autonomic cephalgias
1
which are distinguished by differences in their postulated
pathophysiology and treatment recommendations.
Secondary or symptomatic migraine, much less common
than primary migraine, but important to differentiate
because of their underlying causes.
Trigeminal autonomic cephalgias
The trigeminal autonomic cephalgias are a group of
primary headache disorders characterised by auto-
nomic features in conjunction with unilateral head-
ache. The group includes cluster headaches,
paroxysmal hemicranias, hemicrania continua and
short-lasting, unilateral, neuralgiform headache
attacks with conjunctival tearing (SUNCT). Cluster
headache is the most common of these, differing from
migraine in the boring quality of pain, often nocturnal
and usually orbital, lasting 4590 min, with
Figure 3 The migraine icecream.
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310 Angus-Leppan H. Pract Neurol 2013;13:308318. doi:10.1136/practneurol-2012-000502
prominent autonomic features, and a desire to walk
around rather than sit still. The clinical features and
treatments of trigeminal autonomic cephalgias are
described elsewhere.
15
There are distinct pathophysi-
ology and treatment paradigms postulated for trigem-
inal autonomic cephalgias. Although these entities are
presented as distinct syndromes, in clinical practice,
many patients with cluster headache have migrainous
features.
16 17
Some patients have attacks with the car-
dinal features of cluster headache, but also have a few
migrainous symptoms, especially a visual aura.
17
A
recent study found 24.5% of patients with cluster
headache had at least one migrainous feature.
18
The
term cluster migraine is used to denote syndromes
when there is significant overlap between cluster
headache and migraine.
19 20
Experienced neurologists
see changing patterns occurring in some patients, who
may have migraine with aura, migraine without aura,
cluster headache and cluster migraine at different
times in their lives.
17 21
Response to treatment is also
not exclusive: for example, migraine and other
primary headache may respond to high-flow oxygen
therapy as cluster headache does,
22 23
and cluster
headaches may respond to medications used for
migraine, such as pizotifen and propranolol.
21
While striving for diagnostic clarity and avoiding
unfocussed thinking, it is sensible to keep an open
mind to the rich permeations encountered in presen-
tations and responses to treatment of primary head-
ache. Some patients have headaches that move from
one phenotype to another (in the current headache
classification). In the future, other biological markers
may help with better understanding of the overlap-
ping or changing phenotypes of primary headache in
individual patients, and to mod ifications in our
current classification.
Arterial hypertension
It may be difficult to know whether headaches occur-
ring with newly recognised hypertension are solely
due to the hypertension, or represent a triggering of a
tendency to migraine. Either way, new migraine or
worsening migraine should always prompt checking
of blood pressure.
Acute glaucoma
Severe headache, with pain centred on one eye (some-
times with tenderness and hardness of the eye), with
blurred vision or visual loss, with haloes around
objects, or with redness of the eye, may each indicate
acute closed-angle glaucoma, and is an emergency.
Carotid artery dissection
The headache of carotid artery dissection is variable.
Most commonly it is distinguishable from migraine by
being dull and without throbbing; however, it may be
more migrainous, and even with a reported classical
visual aura. As headache may precede ischaemic
manifestations, it is important to consider the diagno-
sis, and look for ipsilateral neck pain, along with
Horners syndrome (40% of cases). Although
Horners syndrome is non-specific, it should prompt
investigation of possible carotid artery dissection at its
first presentation.
Structural intracranial lesions with or without raised
intracranial pressure
Raised intracranial pressure or mass lesions may
present with headache alone. This may be either
chronic daily or subacute daily headache, and may
have migrainous features; characteristically, however,
there is an early morning preponderance, vomiting
without nausea, visual obscurations, and later, clinical
signs of reduced alertness, cranial nerves palsies
including sixth nerve palsyand papilloedema.
Acute and chronic meningitis
Acute meningitis is usually apparent from the accom-
panying fever, neck stiffness and other neurological
features. Chronic meningeal infection, inflammation
and malignant meningitis usually have other symp-
toms and signs.
Giant cell (temporal) arteritis
The characteristic headache of giant cell arteritis is
throbbing, and the headache may be migrainou s; but
the associated features of scalp tenderness, jaw claudi-
cation, weight loss, fatigue and myalgia, in a person
over 60 years of age, are important indicators of the
diagnosis; any clinical suspicion should prompt urgent
investigation.
Reversible cerebral vasospastic syndrome
This entity is now defined as severe headachewith
or without additional neurological symptomsasso-
ciated with vasospasm on cerebral angiography. The
headaches are usually thunderclap.
24
There is an
underlying cause in about two-thirds of cases (post
partum, hypertension, drugs), with the remainder
having no known cause. Early descriptions empha-
sised its link with migraine, with headache indistin-
guishable from migraine and a good prognosis.
25
Vasospasm in migraine does occur,
26
and angiography
can trigger migrainous infarction. However, in one
series persistent focal cerebral events occurred at
similar rates in patients with migraine compared to
non-age-matched patients having angiography for
other reasons (2.6% compared to 2.8%), although
migraineurs had a 5% rate of transient deficits.
27
As
angiography is not usually carried out for acute
uncomplicated migraine, the incidence of vasospasm
is unknown.
THE BORDERLAND OF MIGRAINE
Some entities are difficult to categorise, such as symp-
tomatic migraine and migrainous stroke.
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Angus-Leppan H. Pract Neurol 2013;13:308318. doi:10.1136/practneurol-2012-000502 311
Recent genetic advances have added a range of very
rare causes of secondary migraine, usually with other
specific features: such as mitochondrial cytopathies
and cerebral autosomal-dominant arteriopathy with
subcortical infarctions and leukoencephalopathy
(CADASIL). Familial hemiplegic migraine, and its
association with channelopathiesmost commonly
voltage-gated calcium channel genesis rare, but a
subject of much research.
28
These familial hemiplegic
migraines may be associated with epileptic seizures,
and sometimes with ataxia. Severe recurrent migraine
encephalopathy is usually secondary, for example, to a
mitochondrial encephalomyelopathy, but migraine
may be its only manifestation at onset. This may give
motor, visual and speech deficits, but can also result
in deafness, persistent vestibular, auditory or retinal
disturbance (chronic vertigo or tinnitus). It is essential
to investigate for other causes of stroke in patients
with migraine.
Migralepsy is defined as an epileptic seizure follow-
ing at a maximum of an hour after a migraine aura.
1
These have been covered in a previous article.
29
Rarely, migraine is less benign, with migrainous
infarction, leaving the patient with a fixed deficit.
The syndrome of transient global amnesia is
common, may be associated with migraine or vascular
disease, and must be distinguished from transient epi-
leptic amnesia.
30
In some patients, there is no specific
aetiology; investigations are normal or non-
contributory and prognosis is good.
31 32
Transient epi-
leptic amnesia is clearly distinguishable from transient
global amnesia by having much shorter and recurrent
episodes, together with characteristic progressive
interictal memory problems, particularly autobio-
graphical amnesia. Differentiating vascular from
migrainous causes of transient global amnesia is more
difficult, but table 1 outlines some helpful features,
for example, absence of vascular risk factors, low
recurrence rate and normal investigations, in migrain-
ous causes. The difference is important for prognosis
(excellent for migrainous transient global amnesia),
32
and for management, including advice on driving.
33
Clinical studies show a clear temporal link between
migrainous headache and transient global amnesia,
34
in some cases the amnesic episode being triggered
only by migraine.
35
Such a temporal link is similar to
that of other accepted migraine accompaniments, such
as visual aura, hemiplegia, or limb pain; all of which
are considered to be due to, or part of, a migraine
episode. Normal ictal and inter-ictal EEG, MRI and
Doppler studies support transient global amnesia
having a migrainous aetiology, but diffusion-weighted
MRI changes in transient global amnesia are contra-
dictory: diffusion-weighted imaging changes in
patients with migraine do not imply generalised vascu-
lar disease. Patients with migraine have a significantly
higher rates of non-specific diffusion-weighted
imaging abnormalities and other imaging changes
than controls, even when the MRI is normal.
36
MIGRAINE CHAMELEONS
This section covers situations when migraine is the
correct diagnosisalthough it looks like something
else. Migraine is most commonly confused with other
paroxysmal disorders, particularly epilepsy or stroke.
Table 2 summarises some common differentials, with
key distinguishing features.
Transient ischaemic attacks
Visual loss may present as part of vertebrobasilar
migraine, although lone transient bilateral blindness is
an unusual migrainous phenomenon. It is more likely
that this is a transient ischaemic eventgenerally pos-
terior circulation if bilateral, carotid if unilateral.
Transient lone visual loss in young people can be
benign, as documented in follow-up of 14 patients
over 413 years
37
; it is probably migrainous but can
present as part of a benign occipital epilepsy (see
below). In this series, investigations were normal, with
no deficits developing over the subsequent years. At
presentation, it is difficult to make this diagnosis: the
clinician must consider other causes and investigate
accordingly. Their brief duration (seconds), sudden
Table 1 Transient global amnesia: usual characteristics
Transient global amnesia
(migrainous)
Transient epileptic amnesia
(temporal lobe epilepsy)
Transient global amnesia
(vascular) Psychogenic amnesia
Middle-aged women Middle-aged men Vasculopaths Young
Anterograde amnesia Anterograde amnesia Anterograde amnesia Variable amnesia
224 h <1 h <24 h Variable duration
Recurrence uncommon Recurrence common Recurrence and new events Variable
Cannot learn new information Cannot learn new information Cannot learn new information May learn new information
Retained identity Retained identity Retained identity Personal identity lost
Any time of day Frequently from sleep Any time of day After acute stress/trigger
Headache/nausea/dizziness Variable headache Variable headache Variable headache
Normal investigations EEG temporal abnormalities EEG normal or non-specific EEG normal or non-specific
Memory normal Accelerated forgetting
Remote memory impairment
Related to vascular disease Variable
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onset, and negative symptom of visual loss would
each be unusual for migraine aura.
Stroke
The most frequent migraine auras are elementary
visual symptoms (40%).
38
Visual blurring is
common, but non-specific, and further questioning is
needed to distinguish an ill-defined difficulty in focus-
sing, unformed hallucinations (frosted glass),
reduced acuity, complex perceptual disturbances,
mental clouding or poor concentration.
Strokes rarely cause positive visual symptoms; but it
is important to remember the Charles Bonnet syn-
drome (visual hallucinations in the presence of severe
visual impairment) which may follow an occipital
stroke with visual field disturbance. This syndrome is
more common in older people, who may discuss
hallucinations reluctantly, fearing a psychiatric label.
Auras of gradual onset often include motor symp-
tomsa gradual onset of heaviness or numbness’—
easily distinguished from sudden onset ischaemic
events.
Dysphasia as an apparent migraine aura requires
investigation. It can often be distinguished clinically
from an ischaemic event by a stuttering onset, other
symptoms relating to more than one vascular territory,
past episodes and other features of migraine.
Misperceptions, such as prosopagnosia may occur
in migraine as an aura, sometimes with object agnosias
with hemianopia or memory disturbance.
39
These
usually recover if the diagnosis is migraine, but stroke
should obviously be the first consideration.
Epilepsy
Visual aura may be confused with the much rarer
occipital epilepsy, particularly in childhood.
40
Occipital epilepsy auras are well characterised through
migraine art;
41
their short duration (seconds) is the
most robust distinguishing feature (figure 4).
Autonomic symptoms of vomiting, pallor and sweat-
ing are very common, especially in children. It may be
difficult to differentiate migraine from childhood
occipital epilepsies, particularly as the pathognomonic
visual symptoms may be brief and overlooked, or may
not even occur.
40
Transient lone blindness can rarely
occur in occipital epilepsy; as well as in stroke and
migraine.
Olfactory and gustatory hallucinations are usually
attributed to temporal lobe seizures, and may be
under-recognised in migraine. The context and long
durationbetween 5 min and 24 hsuggest a
migrainous origin.
42
As with other sensory migrainous
phenomena, there may be altered olfaction between
attacks. In one study, atypically for migraine, there
was reduced (rather than heightened) olfaction in
18% of migraineurs versus 1% of controls.
43
In a
small series, seven patients reported olfactory and/or
gustatory hallucinations with most migraine attacks.
They reported distortions or body image as well as
abnormal perceptual experiences and mood change:
unsurprising, given that this is a temporallimbic
system disturbance.
44
Motor seizures are usually much briefer, lasting
only seconds or very few minutes, with a positive
elementsudden shaking, progressive shaking, dys-
tonia or hypermotorwhereas, this is exceedingly
rare in ischaemic or migrainous events.
It is crucial to distinguish migrainous dysphasia
from dysphasia due to a postictal (Todds) phenom-
enon, or intermittent dysphasia from a fixed lesion
such as tumour.
Neuropathy
Somatosensory auras, usually tingling or numbness,
comprise about one-third of all migraine auras, and
are the second most common after visual ones.
45
In
patients aged over 40 years, upper and lower limb
sensory symptoms occur in 24% of the 70% of
patients with somatosensory migrainous aura; they
have variable distribution, sometimes circumscribed
and peripheral.
26
A sensory migrainous aura may have
a pseudo-peripheral distribution.
46
Bilateral distal
upper and lower limb paraesthesia, entering the differ-
ential diagnosis of peripheral neuropathy
47
may occur
in migraineurs as an aura of varying duration, without
headache, including basilar migraine. I have seen
several patients with such recurrent migraine auras of
long duration
26
who have been investigated for per-
ipheral neuropathy, usually when headaches are absent
or inconspicuous, at initial presentation.
Radiculopathy, thoracic outlet syndrome and
musculoskeletal problems
Migraine limb pain syndrome is intermittent pain
occurring in upper or lower limbs, temporally related
Table 2 Migraine chameleons
Feature Onset Offset Duration Quality (usual modality) Loss of function
Acute migraine Gradual Gradual 5 min to several hours Positive (special sensory) Usually none, or temporary
Chronic migraine Gradual Ongoing Ongoing Positive (special sensory) Usually none, or temporary
Transient ischaemic attacks Sudden Sudden Minutes to 24 h Negative (loss of function) Temporary
Stroke Sudden Ongoing Long-term Negative Permanent, incomplete recovery
Epileptic seizures Sudden Sudden 1120 s Positive Nil, occasional temporary (Todds paresis)
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either to a migraine episode, cluster headache or
cluster migraine; it may be mistaken for cervical or
lumbar radiculopathy. Limb pain is usually ipsilateral
to the headache, but can alternate sides and may
spread with a migrainous march over 20 min or
more.
21
Limb pain and headache may alternate in
severity in different attacks. It is often unrecognised,
as limb pain may not coincide with headache at pres-
entation; other initially suspected diagnoses may
include cervical radiculopathy, thoracic outlet syn-
drome, arthritis or nerve entrapment. The diagnosis
may become apparent only later, when both limb pai n
and headache are reported or discovered on direct
questioning. Sporadic reports go back to 1873,
48
with
the first series suggesting an incidence of 12%;
21
a
subsequent prospective series suggested that 4.4% of
245 migraineurs had limb pain.
49
Limb pain, by either day or night, may be the only
or the first manifestation of migraine in childhood;
once again, a careful elucidation of other features may
give the clue. The child may be pale and photophobic.
Migraine limb pain in children may be mistaken for
joint or bone pathology, growing pains or psycho-
logical disturbance. Limb pain may vary in posi tion,
excluding local joint pathology. Limb pain accompan-
ies migraine in children with an incidence of 2.6%.
50
One family had limb pain in childhood followed by
migraine in adulthood.
51
The physiological basis for migraine limb pain syn-
drome may be the convergence of nociceptive input
from meningeal vessels in the cervical spinal cord,
brainstem, thalamus and cortex.
52 53
Vestibular and auditory disorders
Migrainous vertigo is extremely common, usually giving
a sense of disequilibrium rather than true rotation. It is
often missed, it may be labelled as an acute vestibular
neuritis. It may be triggered by a change in position, and
may be difficult to distinguish from benign paroxysmal
positional vertigo. The longer duration of migrainous
vertigobetween 5 min and 72 h,and a negative
Hallpikes manoeuvre, are important distinguishing fea-
tures. The International Headache Society will acknow-
ledge migrainous vertigo in the next classification,
hopefully increasing its recognition.
54
The incidence of auditory hallucinations in migraine
is uncertain, but they do occur in both children and
adults.
55
Simple auditory hallucinations, such as bilat-
eral or unilateral tinnitus, are probably frequent and
may be misdiagnosed as idiopathic. It is always worth
enquiring about migraine in patients with tinnitus, given
its potential for treatment. The context, associations,
hearing and examination help to distinguish migrainous
vertigo from the effects of vestibular toxins, and struc-
tural or inflammatory causes, particularly if unilateral.
In some patients with migraine, intermittent tinnitus
may become a chronic fixed deficit, just as a few patients
with motor migraine are left with a persistent hemipar-
esis due to migrainous infarction. This diagnosis can
only be made with a clear history of migraine with epi-
sodic tinnitus, and exclusion of other causes.
Gastrointestinal disease
Cyclical vomiting is a curious entity, which is some-
times a form of migraine. The International Headache
Figure 4 Elementary visual aurasdifferentiation.
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314 Angus-Leppan H. Pract Neurol 2013;13:308318. doi:10.1136/practneurol-2012-000502
Society includes it as a childhood syndrome that com-
monly precedes migraine,
1
but do not recognise it as
adult syndrome. However, it can be migrainous in
adults; sometimes ascribed to idiopathic gastroparesis.
It must be distinguished from gastric stasis due to
autonomic neuropathy, particularly from diabetes
mellitus.
Abdominal migraine in children may be mistaken
for local pathologies, particularly appendicitis and
gastroenteritis; or with psychological disturbance or
school refusal. Children with abdominal migraine are
often pale and quiet, and withdraw briefly from pleas-
ant activities. They may have associated headache,
photophobia and dizziness, and it is important to ask
specifically about this. The symptoms are often much
briefer than in adults, so that some diagnostic features
could be overlooked.
Cardiac disease
In adults, jaw, neck, shoulder and chest painsome-
times with limb pain (see above)may occur with or
without headache, and be confused with ischaemic
heart disease: the painful areas are often allodynic.
56
There is a significant association between migraine
with atypical chest pain (Prinzmetals angina) and
with Raynauds disease, hypothesised to form part of
a generalised vasospastic disorder. This issue has not
been resolved.
57
Syncope
Syncope in vertebrobasilar migraine occurs, but with
an unknown incidence. It may be mistaken for
syncope due to other causes, or with epileptic drop
attacks, but the initial symptoms indicating involve-
ment of territories within vertebrobasilar distribu-
tion, and sometimes long duration of the syncope
should help to distinguish it.
Multiple sclerosis
Intermittent tingling without objective sensory
change is the most common somatosensory symptom
in migraine. Paraesthesia may involve the limbs, face
or tongue. Particularly in young women, in whom
migraine and demyelination are each common, the
symptoms may be mistaken for multiple sclerosis
(table 3). In young people worried about multiple
sclerosis, other migraine symptoms may be less con-
spicuous and their identification requires direct
questioning.
Allodynia (pain from non-noxious stimuli) in the
face occurs in up to 70% of people with migraine.
58
Allodynia in the limbs may be ipsilateral, bilateral or
contralateral to the headache, and is thus not simply a
cortical ischaemic phenomenon.
5
When the allodynia
varies in position and intensity, and occurs with other
migrainous features, the diagnosis is straightforward.
Functional disorders
Occipito-temporal white matter involvement in
migraine fits the clinical preponderance of visual
symptoms. The hypersensitivity may be confused with
psychiatric or functional illness or chronic fatigue syn-
drome. Vague or fluctuant sensory symptoms, disequi-
librium and fatigue, without neurological signs, may
be described as functional disorders, or ascribed to
chronic fatigue syndrome, especially if other migrain-
ous symptoms are not carefully sought. The absence
of sensory signs with central problems (including
migraine) may falsely reinforce a functional diagnosis.
Children with migraine, especially abdominal
migraine, may be mislabelled as having school refusal
or a psychological disturbance, as it may be charac-
terised by withdrawal from, and disinterest in, usual
activities.
Psychiatric illness, organic psychoses and confusional
states
Hallucinations accompany many neurodegenerative
conditionsclassically, in Parkinsons disease, with
preserved insightand acute organic psychoses,
including drug-induced and drug-withdrawal states.
Complex visual hallucinations rarely occur in
migraine; the clinician must consider other causes
first. They have been the subject of considerable
speculation. Macropsia is most famously represented
by Lewis Carrolls description of Alice s adventures in
Wonderland, reputedly inspired by Carrollsown
migraine experiences.
59
Table 3 Sensory symptoms
Diagnosis* Prevalence Usual symptom duration Key features Comments
Migraine 150/1000 >5 min to hours Variable intensity and topography No signs, ±headache
Neuropathy 60/1000 Fixed Distal sensory loss and arreflexia May be painful
Stroke 15/1000 Ongoing Focal deficits Fixed deficits (50%)?
Transient ischaemic attack 3/1000 Minutes24 hours Numbness May have deficits
Sensory seizures 1/1000 Seconds Positive (eg, tingling) Structural cause common
Multiple sclerosis 1/1000 Variable Upper motor neuron signs Interpret MRI with care
Chronic fatigue syndrome 0.3/1000? Frequent, intermittent Hypersensitivity May have migraine plus
Functional ? Frequent, intermittent Variable, diffuse, no signs May have migraine plus
*Variable percentages of these patients will have sensory symptoms.
REVIEW
Angus-Leppan H. Pract Neurol 2013;13:308318. doi:10.1136/practneurol-2012-000502 315
Complex visual hallucinations are described in chil-
dren as well as adults with recurrent attacks of impair-
ment of time sense, body image and visual analysis of
the environment.
60
The same differential diagnosis
applies as for elementary visual hallucinations, includ-
ing psychiatric illness, neurodegeneration, encephal-
itis, and in withdrawal states, such as delirium
tremens. The patient may be fearful and reluctant to
discuss them, owing to concerns about having a psy-
chiatric illness.
Minor degrees of transient or intermittent cognitive
clouding commonly accompany migraine; in the
setting of other symptoms, they are usually readily
recognised. Patients often report difficulty in concen-
trating and in performing tasks (executive dysfunc-
tion) during times of frequent migraine headaches.
These changes are important to the patient and little
researched. One small series suggested that abnormal
perceptual experiences occur in 15% of migrai-
neurs.
44
Blau gave an account of the free interval’—
the gap between the end of the visual aura and
headache onset in migraine with aura. In 22/25
migraineurs with migraine with visual aura, the free
interval of about 1 h was marked by altered mood
and perceptiondetachment from the environment
or other people, fears, disturbances of speech or
thought, or somatic symptoms.
61
Out-of-body experi-
ences, including autoscopy and duplicate or paraso-
matic experiences
62
may be ascribed to acute
psychosis or to intoxication. Recurrent psychosis after
migraine may occur and leads to consideration of an
organic psychosis or mitochondrial cytopathy. Fuller
et al
63
describe a 69-year-old man with longstanding
migraine with aura who had four psychotic episodes
lasting 728 days during a 17-year period. During
attacks, he developed formed visual hallucination and
delusions.
Fully blown forms of migrainous encephalopathy or
coma are rare, but mild forms are common. Acute
confusional migraine
64
occurs in children, adoles-
cents, as well as adults. Between 0.45% and 7.8% of
children with migraine present with acute confusional
migraine, but the disorder is probably underdiag-
nosed. In adults, the incidence is harder to estimate,
and the diagnosis requires exclusion of some life-
threatening causes of confusion, such as non-
convulsive status epilepticus, ischaemia, haemorrhage,
neoplasm, intoxication and encephalitis.
CONCLUSIONS
Migraine headaches are generally easy to diagnose,
but the aura may be misleading. Migraine aura is
usually a positive phenomenon. Most hallucinations
are elementary rather than complex, with unformed
visual aura being the most common, and usually very
characteristic. Migraine is a functional disorder, in
the broadest sense of the term. Investigations in
patients migraine are usually normal: even when
abnormalities are found, they are often incidental. It
is helpful to be aware of the uncommon aura, as well
as migraine variants, such as icepick headache. Once
the diagnosis is ma de, a large part of our role is to
educate and to reassure, as well as to treat.
Migraine is differentiated from autonomic cephal-
gias, but overlap syndromes, such as cluster migraine,
may also occur. Other important mimics must not be
missedsuch as headache from hypertension, carotid
artery disease, acute glaucoma, intracranial mass
lesions, raised intracranial pressure, meningitis, giant
cell arteritis and reversible cerebral vasospastic syn-
drome. Borderland conditions include mitochondrial
cytopathies, migralepsy, and migrain ous stroke.
Importantly, migraine is often diagnosed as something
else (a chameleon), being particularly mistaken for
other paroxysmal events, such as cerebrovascular
disease and epilepsy; but also peripheral nervous
system disorders, vestibular disorders, gastrointestinal
and cardiac disease, syncope, multiple sclerosis, and
functional and psychiatric illness.
Acknowledgements Thanks to Professor Jim Lance and
Dr Geoff Lambert who inspired my interest in clinical and
physiological aspects of migraine; and to Professor Roberto
Guiloff for helpful comments on the manuscript. I thank all the
patients who have shared their stories.
Competing interests None.
Provenance and peer review Commissioned; externally peer
reviewed. This paper was reviewed by Peter Goadsby,
San Francisco, USA; and by Richard Stark, Melbourne,
Australia.
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Background According to the International Classification of Headache Disorders diagnostic criteria, the differences between migraine and cluster headache (CH) are clear. In addition to headache attack duration and pain characteristics, the symptoms accompanying headache represent the key features in a differential diagnosis of these 2 primary headache disorders. Just a few studies of patients with CH exist examining the presence of nausea, vomiting, photophobia, phonophobia, and aura, the features commonly accompanying migraine headache. The aim of this study was to determine the presence of migraine-like features (MF) in patients with CH and establish the significance of these phenomena related to other clinical features and response to treatment. Methods One hundred and fifty-five patients with CH were studied, and 24.5% of them experienced at least one of MF during every CH attack. Nausea and vomiting were the most frequently reported MF. The clinical presentation between CH patients with and without MF was not significantly different with the exception of aggravation of pain by effort (20.6% vs 4.1%) and facial sweating (13.2% vs 0.85%), both more frequent in CH patients with MF. Conclusion Inferred from the results of our study, the presence of MF in CH patients had no important influence on the diagnosis and treatment of CH patients. The major differences of these 2 primary headache disorders, attack duration, lateralization, and the nature of associated symptoms, as delineated in the International Classification of Headache Disorders, are still useful tools for effective diagnosis.
Article
Background According to ICHD-II, and as proposed for ICHD-III, non-hemiplegic migraine aura (NHMA) symptoms last between five and 60 minutes whereas hemiplegic migraine aura can be longer. In ICHD-III it is proposed to label aura longer than an hour and less than a week as probable migraine with aura. We tested whether this was appropriate based on the available literature.Methods We performed a systematic literature search identifying articles pertaining to a typical or prolonged duration of NHMA. We also performed a comprehensive literature search in order to identify all population-based studies or case series in which clinical features of NHMA, including but not restricted to aura duration, were reported, in order to gain a complete coverage of the available scientific data on aura duration.ResultsWe did not find any article exclusively focusing on the prevalence of a prolonged aura or more generally on typical NHMA duration. We found 10 articles that investigated NHMA features, including the aura duration. Five articles recorded the proportion of patients in whom whole NHMA lasted for more than one hour, which was the case in 12%-37% of patients. Six articles reported some information on the duration of single NHMA symptoms: visual aura disturbances lasting for more than one hour occurred in 6%-10% of patients, sensory aura in 14%-27% of patients and aphasic aura in 17%-60% of patients.Conclusions The data indicate the duration of NHMA may be longer than one hour in a significant proportion of migraineurs. This seems to be especially true for non-visual aura symptoms. The term probable seems inappropriate in ICHD-III so we propose reinstating the category of prolonged aura for patients with symptoms longer than an hour and less than one week.