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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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 4–72 h; typically with unilateral location, pulsating quality, nausea and/or photophobia and phonophobia, worse with physical activity.1 For the practical neurologist, only a minority of patients with migraine fits entirely into this International classification of headache disorders (ICHD) definition1 (figure 1). Secondary migraine headaches (symptomatic migraine) are rare (figure 2), and associated 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 headache as a marker of a sinister pathology. It can be difficult to distinguish a ‘mimic’ from a primary migraine triggered by an intercurrent condition—for 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 patients2 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, suggesting that these are part of the migraine phenotype.3
Typical migraine aura is defined in the ICHD as reversible positive and/or negative sensory, and/or visual and/or speech focal neurological symptoms that usually develop gradually, lasting between 5 and 60 min,1 while hemiplegic migraine is defined separately and may be of longer duration.1 ,3 Their gradual onset helps to differentiate these symptoms from seizures and vascular events, and their longer duration helps further to distinguish them from seizures.
Migraine auras are commonly ‘atypical’. 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 particularly visual. Most migraineurs develop photophobia, 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 (upregulation).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 heightened sensitivity to certain visual stimuli. There may be significantly higher glucose metabolism bilaterally in the posterior subcortical cerebrum and in the cerebellum 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 necessarily contralateral to the headache. Apart from their importance as a problem to the patient, they tell us a lot about migraine—and argue against the idea that migraine is simply a vascular disturbance.
Several migraine variants are common in neurology clinics. Some authorities classify these as distinct primary headaches: the debate about their classification 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 population, and their link with migraine is less certain.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 headache—requires urgent investigation. Although nausea, neck stiffness, occipital location and impaired consciousness more frequently accompany subarachnoid headache,9 they are not invariable, and their absence cannot be relied upon10: 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 1–7 years shows no subarachnoid haemorrhage mortality,10–12 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 hospital 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 discussed below. The issue is unresolved, and hinges on whether angiography is showing pre-existent vasospasm, 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 episodic migraine, is a subtype of chronic daily headache, and may occur with or without analgesia overuse.14
This section comprises two distinct groups:
Primary headache conditions classified as separate entities, such as the trigeminal autonomic cephalgias1 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 autonomic features in conjunction with unilateral headache. 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 45–90 min, with 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 pathophysiology and treatment paradigms postulated for trigeminal 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 cardinal 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 presentations and responses to treatment of primary headache. 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 overlapping or changing phenotypes of primary headache in individual patients, and to modifications in our current classification.
It may be difficult to know whether headaches occurring 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.
Severe headache, with pain centred on one eye (sometimes 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 diagnosis, and look for ipsilateral neck pain, along with Horner's syndrome (40% of cases). Although Horner's 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 palsy—and papilloedema.
Acute and chronic meningitis
Acute meningitis is usually apparent from the accompanying fever, neck stiffness and other neurological features. Chronic meningeal infection, inflammation and malignant meningitis usually have other symptoms and signs.
Giant cell (temporal) arteritis
The characteristic headache of giant cell arteritis is throbbing, and the headache may be migrainous; but the associated features of scalp tenderness, jaw claudication, 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 headache—with or without additional neurological symptoms—associated 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 emphasised its link with migraine, with headache indistinguishable 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 symptomatic migraine and migrainous stroke.
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 channelopathies—most commonly voltage-gated calcium channel genes—is 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.
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 epileptic amnesia.30 In some patients, there is no specific aetiology; investigations are normal or non-contributory and prognosis is good.31 ,32 Transient epileptic amnesia is clearly distinguishable from transient global amnesia by having much shorter and recurrent episodes, together with characteristic progressive interictal memory problems, particularly autobiographical 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 migrainous 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 contradictory: diffusion-weighted imaging changes in patients with migraine do not imply generalised vascular 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
This section covers situations when migraine is the correct diagnosis—although 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 vertebro–basilar migraine, although lone transient bilateral blindness is an unusual migrainous phenomenon. It is more likely that this is a transient ischaemic event—generally posterior 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 4–13 years37; 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 onset, and negative symptom of visual loss would each be unusual for migraine aura.
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 focussing, 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 syndrome (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 symptoms—a 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.
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 sweating 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 duration—between 5 min and 24 h—suggest 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 temporal–limbic system disturbance.44
Motor seizures are usually much briefer, lasting only seconds or very few minutes, with a positive element—sudden shaking, progressive shaking, dystonia or hypermotor—whereas, this is exceedingly rare in ischaemic or migrainous events.
It is crucial to distinguish migrainous dysphasia from dysphasia due to a postictal (Todd's) phenomenon, or intermittent dysphasia from a fixed lesion such as tumour.
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 differential diagnosis of peripheral neuropathy47 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 duration26 who have been investigated for peripheral 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 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 presentation; other initially suspected diagnoses may include cervical radiculopathy, thoracic outlet syndrome, arthritis or nerve entrapment. The diagnosis may become apparent only later, when both limb pain and headache are reported or discovered on direct questioning. Sporadic reports go back to 1873,48 with the first series suggesting an incidence of 1–2%;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 psychological disturbance. Limb pain may vary in position, excluding local joint pathology. Limb pain accompanies migraine in children with an incidence of 2.6%.50 One family had limb pain in childhood followed by migraine in adulthood.51
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 vertigo—between 5 min and 72 h,—and a negative Hallpike's manoeuvre, are important distinguishing features. The International Headache Society will acknowledge 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 bilateral 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 structural 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 hemiparesis due to migrainous infarction. This diagnosis can only be made with a clear history of migraine with episodic tinnitus, and exclusion of other causes.
Cyclical vomiting is a curious entity, which is sometimes a form of migraine. The International Headache Society includes it as a childhood syndrome that commonly 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 pleasant 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.
In adults, jaw, neck, shoulder and chest pain—sometimes 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 (Prinzmetal's angina) and with Raynaud's disease, hypothesised to form part of a generalised vasospastic disorder. This issue has not been resolved.57
Syncope in vertebro–basilar 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 involvement of territories within vertebro–basilar distribution, and sometimes long duration of the syncope should help to distinguish it.
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 conspicuous 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.
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 syndrome. Vague or fluctuant sensory symptoms, disequilibrium and fatigue, without neurological signs, may be described as ‘functional’ disorders, or ascribed to chronic fatigue syndrome, especially if other migrainous 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 characterised by withdrawal from, and disinterest in, usual activities.
Psychiatric illness, organic psychoses and confusional states
Hallucinations accompany many neurodegenerative conditions—classically, in Parkinson's disease, with preserved insight—and 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 Carroll's description of Alice's adventures in Wonderland, reputedly inspired by Carroll's own migraine experiences.59
Complex visual hallucinations are described in children as well as adults with recurrent attacks of impairment of time sense, body image and visual analysis of the environment.60 The same differential diagnosis applies as for elementary visual hallucinations, including psychiatric illness, neurodegeneration, encephalitis, and in withdrawal states, such as delirium tremens. The patient may be fearful and reluctant to discuss them, owing to concerns about having a psychiatric 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 concentrating and in performing tasks (executive dysfunction) 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 migraineurs.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 perception—detachment from the environment or other people, fears, disturbances of speech or thought, or somatic symptoms.61 Out-of-body experiences, including autoscopy and duplicate or parasomatic experiences62 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 al63 describe a 69-year-old man with longstanding migraine with aura who had four psychotic episodes lasting 7–28 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 migraine64 occurs in children, adolescents, as well as adults. Between 0.45% and 7.8% of children with migraine present with acute confusional migraine, but the disorder is probably underdiagnosed. 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.
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 made, a large part of our role is to educate and to reassure, as well as to treat.
Migraine is differentiated from autonomic cephalgias, but overlap syndromes, such as cluster migraine, may also occur. Other important mimics must not be missed—such as headache from hypertension, carotid artery disease, acute glaucoma, intracranial mass lesions, raised intracranial pressure, meningitis, giant cell arteritis and reversible cerebral vasospastic syndrome. Borderland conditions include mitochondrial cytopathies, migralepsy, and migrainous 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.
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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