Diagnosis of headache in primary care
Every headache presentation is unique and challenging, requiring a flexible and individualised approach to headache
- Most headaches are benign primary headaches
- A few headaches are secondary to underlying pathology, which may be life threatening
Primary headaches can be difficult to diagnose and manage. People, who experience severe or recurrent primary headache,
can be subject to significant social, financial and disability burden.
We cannot cover all the issues associated with headache presentation in primary care; instead, our focus is on assisting
- Recognise presentations of secondary headaches
- Effectively diagnose primary headaches
- Manage primary headaches, in particular tension-type headache, migraine and cluster headache
- Avoid, recognise and manage medication overuse headache
Diagnosis of headache in primary care
The keys to headache diagnosis in primary care are:
- Ensuring occasional presentations of secondary headache do not escape notice
- Differentiating between the causes of primary headache
- Addressing patient concerns about serious pathology
Recognise serious secondary headaches by being alert for red flags and performing fundoscopy
Although primary care clinicians worry about missing serious secondary headaches, most people presenting with secondary
headache will have alerting clinical features. These clinical features, red flags, are not highly
specific but do alert clinicians to the need for particular care in the history, examination and investigation.
An exception to this may be slow growing intracranial tumours. For this reason fundoscopy, even though positive findings
are rare, is essential for every initial headache presentation and periodically thereafter. Slow growing frontal lobe
tumours are particularly liable to be silent. They may present with non-specific headache and subtle personality changes,
resulting in treatment for depression. In these situations, non-response to treatment may prompt further investigation.
Red Flags in headache presentation include:
- Over 50 years at onset of new headache
- Under 10 years at onset
- First, worst or different from usual headache
- Progressive headache (over weeks)
- Persistent headache precipitated by Valsalva manoeuvre (cough, sneeze, bending or exertion)
- Thunderclap headache (explosive onset)
- Atypical or prolonged aura (>1 hour)
- Aura occurring for the first time in woman on combined oral contraceptive
- New onset headache in a patient with a history of cancer or HIV
- Concurrent systemic illness
- Neurological signs
- Symptoms/signs of Giant Cell Arteritis (e.g. jaw claudication)
Causes of secondary headache
The presence of red flags prompts consideration of a wide range of diagnoses. Some of these
are listed below.
- Subdural hematoma
- Epidural hematoma
- Subarachnoid haemorrhage
- Venous sinus thrombosis
Toxins (e.g. carbon monoxide)
Giant cell arteritis
Minimal examination for headache presentation
For all initial presentations of headache, examination includes:
- Visual acuity
- Blood pressure measurement
- Examination of the head and neck for muscle tenderness, stiffness, range of movement and crepitation.
The presence of red flags or other features suggesting secondary headache indicate the need for more detailed examination.
The question of whether a neurological examination should be performed, and in how much detail, is more problematic when
there are no suspicious features and the history is characteristic of a primary headache.
Even when there are no red flags, a brief neurological examination, although unlikely to
be positive, is a strong source of reassurance to patients and will save time in future consultations with still-worried
Diagnosis of primary headache
Primary headache is usually caused by tension-type headache, migraine, with or without aura, or cluster headache. Mixed
headache types do occur, for example many people experience both migraine and tension-type headaches. Differentiation
between the primary headaches is important because there are effective interventions available for each of them.
Headache diaries are useful diagnostic tools, which help the diagnosis of headaches and identification of any predisposing
or precipitating factors.
Tension-type headache is the commonest form of primary headache
Most people will have at least one episode of tension-type headache during their lifetime. It is the commonest form
of primary headache. The headache is usually described as tightness or pressure, like a tight band, around the head and
often spreads to, or appears to arise from, the neck.
Tension-type headache is usually episodic, of low frequency and short duration but chronic tension-type headache can
occur on more days than it is absent. Photophobia or exacerbation by movement can occur but these are usually less prominent
features than in migraine.
Tension-type headaches are associated with stress and functional or musculoskeletal problems of the neck and often these
occur together. Muscles of the head or neck are often tight and tender.
It is often useful to explain to patients that the pain is related to tension in the muscles of the head and neck and
is often made worse by stress. This helps exploration of stressors without the patient feeling the clinician thinks ‘it
is all in my mind’.
Features of Migraine
Adults with migraine usually have a family history of migraine and experience recurrent episodes of moderate or severe
headaches (which may be unilateral and/or pulsating) lasting for several hours or up to 3 days. These are typically associated
with gastrointestinal symptoms, limitation of activity and avoidance of light and noise. There is often a preceding aura.
People with migraine are free from symptoms between attacks.
When considering a differential diagnosis between migraine and tension headache, the following features are common in
migraine but not usually seen in tension headache.
- Unilateral headache
- Hypersensitivity, such as to light and noise
- Gastrointestinal symptoms, such as nausea or vomiting
The diagnostic criteria for migraine are reproduced in Table 1. These may be useful in the diagnosis of headache when
there is some doubt about the diagnosis, particularly when there is no aura. When migraine is accompanied by aura the
diagnosis is easier and only two episodes are required to make the diagnosis.
Table 1: Diagnostic criteria for migraine without aura
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||At least 5 attacks fulfilling criteria B-D
||Headache attacks lasting 4-72 hours* (untreated or unsuccessfully treated)
|| Headache has at least two of the following characteristics:
- Unilateral location*
- Pulsating quality (i.e. varying with the heartbeat)
- Moderate or severe pain intensity
- Aggravation by or causing avoidance of routine physical activity (e.g. walking or climbing stairs)
|| During headache at least one of the following:
- Nausea and/or vomiting*
- Photophobia and phonophobia
||Not attributed to another disorder
(history and examination do not suggest a secondary headache disorder or, if they do, it is ruled out
by appropriate investigations or headache attacks do not occur for the first time in close temporal relation to the
|*In children, attacks may be shorter-lasting, headache is more commonly bilateral, and
gastrointestinal disturbance is more prominent.
One third of people with migraine have preceding aura
Approximately one third of people who get migraine, experience preceding aura. Usually auras last for between 5 to 60
minutes before the onset of migraine headache and settle as headache commences. The most frequently reported auras are
visual disturbance, such as flickering or jagged lines or blind spots. Visual blurring or spots before the eyes are non-specific
symptoms and do not represent aura. Other transient focal neurological symptoms, such as unilateral paraesthesia of a
hand, arm or the face, and dysphasia, can also occur as aura in migraine.
Visual or other transient focal neurological signs presenting for the first time in older people always raise the possibility
of Transient Ischaemic Attacks (TIAs). Prolonged aura in all age groups, especially continuing after resolution of headache
and aura which involve muscular weakness, are indications for specialist investigation to exclude other causes.
Headache in migraine is not always unilateral
Although migraine headache is often unilateral it is not always so and the diagnosis of migraine should not be abandoned
when headache is bilateral. The headache of tension-type headache is usually bilateral, but may be unilateral.
Migraine is usually accompanied by hypersensitivity
Hypersensitivity to stimuli, which are not normally noxious, is a common feature of migraine. Photophobia and phonophobia
are the most frequently reported but hypersensitivity to touch (allodynia), smell (osmophobia), movement and pulsation
of the arteries are also often experienced.
Hypersensitivity in migraine appears to be related to the central sensitisation and resulting peripheral sensitisation
that occur in migraine.
Gastrointestinal upsets often prominent in migraine
Visual or other transient focal neurological signs presenting for the first time in older people
always raise the possibility of Transient Ischaemic Attacks (TIAs).
Nausea and vomiting in migraine may be related to vestibular hypersensitivity and can be a prominent disabling feature
of migraine episodes. Although anorexia and mild nausea may occur in tension-type headache, it is not usually a major
Features of Cluster Headache
Cluster headache, unlike migraine, affects mostly young men (male:female = 6:1). Typically, the headaches occur in bouts
for 6 to 12 weeks, once every year or two. The pain is severe, unilateral and disabling. During bouts, headache usually
occurs daily, at a similar time each day.
Associated autonomic features include ipsilateral conjunctival injection, lacrimation, rhinorrhea, nasal congestion
and ptosis. These do not always occur but the presence of one or two of these together with a typical cluster headache
pattern clinch the diagnosis.
Management of tension-type headache
Management of tension-type headache includes general exercise, stress reduction, treatment of any underlying musculoskeletal
problems and analgesia. Episodic use of aspirin or ibuprofen is usually sufficient. Paracetamol appears less effective.
Complementary therapies such as yoga, meditation and acupuncture may help some people.
Although treatment sounds easy, in practice, implementation may be complicated. Patients may be expecting high-tech
investigations to rule out serious pathology, physiotherapy and counselling may be unaffordable and often the stressors
associated with the headaches are not amenable to change. This can result in over-reliance on medication.
Chronic use of medication for pain relief carries high risk of medication overuse headache. Analgesia use, should therefore,
preferably be limited to no more than two days per week. Opiates, such as codeine, carry particularly high risk of medication
Chronic use of medication for pain relief carries high risk of medication overuse headache. Analgesia
use, should therefore, preferably be limited to no more than two days per week.
A three-week course of an NSAID, such as naproxen, may break the cycle of continuing pain and cover the early management
of predisposing and precipitating factors, such as musculoskeletal problems and stress.
If this fails, the prophylactic medication of choice is amitriptyline; starting very low (5-10 mg at night) and increasing
slowly every three weeks until symptoms are controlled, up to 75-150 mg at night. As in other chronic pain syndromes,
the effectiveness of amitriptyline does not depend on its antidepressant activity. If amitriptyline is not well tolerated,
nortriptyline has fewer side effects and may be an effective alternative.
A randomised controlled trial of botulinum toxin for chronic tension-type headache showed it to be ineffective.
Migraine management requires a systematic approach
Migraine management can be complicated and requires a systematic approach to:
- Management of predisposing factors
- Trigger identification and avoidance
- Acute pain relief
Managing predisposing factors in migraine
Several factors are known to predispose people to migraine. These include stress, depression, anxiety, head or neck
trauma and hormonal changes such as around menstruation or menopause. Management of these factors can have a significant
impact on migraine frequency and severity. Keeping a diary will help to identify any predisposing and triggering factors.
Identification and avoidance of trigger factors in migraine
Unfortunately, most migraine episodes have no obvious trigger, but if triggers can be identified, avoidance is often
very effective. Frequently reported triggers include:
- Relaxation after stress
- Change in habit, such as a missed meal, late night or travel
- Bright lights and loud noise
- Dietary triggers, such as certain alcoholic drinks, some cheeses
- Unaccustomed strenuous exercise
Management of acute migraine headache
A systematic, three-tiered approach to the management of acute migraine headache is useful. Additional measures for
emergency treatment at home and treatment of a relapse may be needed.
Using a systematic approach ensures each treatment modality is given a reasonable trial of effectiveness and highlights
which treatments are effective for particular patients. BASH suggests that failure of treatment on one tier on three occasions
should be the criterion for moving onto the next tier.
These tiers should all preferably be combined with rest and sleep; a stat dose of temazepam may be useful to achieve
- Tier one1: analgesic +/- antiemetic
- Tier two: specific anti-migraine drugs
- Tier three: combination therapies
- Emergency treatment: intramuscular NSAID and antiemetic
- Relapse: repeat symptomatic analgesics from step one and two and consider repeat of triptan
Tier one: analgesic +/- antiemetic
Step one consists of analgesia with aspirin or other NSAID, with the best evidence for ibuprofen and naproxen. These
are usually given orally with standard release preparations at higher doses, taken early
in the attack to avoid delayed absorption due to gastric stasis. Delayed release preparations are not
Recommended doses for adults are:
Aspirin: 600-900 mg, up to four doses in 24 hours
Ibuprofen: 400-600 mg, up to four doses in 24 hours
Naproxen2: 750-825 mg, with further 250-275 mg up to twice in 24 hours
Diclofenac-potassium3: 50-100 mg up to a total of 200 mg in 24 hours
General contraindications to NSAIDs must always be kept in mind but there is little evidence for paracetamol use on
its own in migraine. In practice, paracetamol does appear to be useful, especially when combined with metoclopramide.
Metoclopramide promotes gastric emptying. Even when nausea and vomiting are not present, this is likely to improve absorption
of analgesics and there is some evidence that metoclopramide on its own gives relief in migraine.
When nausea or vomiting render oral administration problematic, rectal preparations of analgesics and anti-emetics may
be more suitable. Diclofenac suppositories, 100 mg, used up to twice in 24 hours are recommended by BASH.
Anti-emetic suppositories are useful if nausea and vomiting is a problem. Prochlorperazine, 25 mg, is available as a
suppository in New Zealand.
There has been a recent resurgence of interest in the use of preparations containing fixed drug combinations. In a randomised
controlled trial, a fixed combination suppository of indomethacin, prochlorperazine and caffeine, was as effective as
Opiates and opioids should, in general, be avoided during acute migraine. They provide little additional benefit, have
potential for addiction and, as discussed here, can be associated with medication overuse headache. Any
history of alcohol or drug abuse or dependency is a strong warning that problems are likely.
Tier two: specific anti-migraine drugs
The triptans are serotonin agonists used in acute migraine management. Sumatriptan is the only funded
triptan in New Zealand.
Unlike symptomatic treatment, triptans should not be taken too early. They appear to be ineffective if given during
aura and most effective, whilst pain is still mild or at the onset of hypersensitivity. Unfortunately, triptans are associated
with return of symptoms within 48 hours in 20-50% of patients who initially respond.
Sumatriptan should not be repeated if the first dose has been ineffective but can be repeated if it was initially effective
but the headache has recurred (see below).
Sumatriptan, 50 mg orally, is usually tried in the first instance combined with metoclopramide. If this is not effective,
100 mg orally, can be tried in future attacks. Sumatriptan can, if necessary, be given subcutaneously at a dose of 6 mg.
Contraindications to triptans include:
- Ischaemic heart disease
- Prinzmetal's angina/coronary vasospasm
- Cerebrovascular disease (CVA) or transient ischaemic attack (TIA)
- Uncontrolled hypertension
- Severe hepatic impairment
- Concurrent use or use within two weeks after discontinuation of monoamine oxidase inhibitors
Ergotamine use, for migraine, is limited by a significant risk of toxicity and drug interactions. Major
side effects include: nausea, vomiting, paresthesia, and the convulsive and gangrenous effects of ergotism. Contraindications
are cardiovascular and cerebrovascular diseases, Raynaud's disease, arterial hypertension, renal failure, pregnancy and
Ergotamine is thought to have significantly lower relapse rates than sumatriptan and may be useful if relapse is a major
problem and cannot be managed with other medications. It should not be used for at least 12 hours after sumatriptan (see
Ergotamine is available in New Zealand combined with caffeine in Cafergot. One tablet contains 1 mg of ergotamine and
100 mg of caffeine. For first time users, two tablets are taken initially with a further tablet half hourly if needed.
Subsequently three tablets can be taken initially, if needed, with a further tablet half hourly. The maximum dose in
any 24 hour period is six tablets and a maximum of ten tablets in any week.
Tier three: combination therapies
There is some evidence that a combination of naproxen and sumatriptan is superior to either drug alone and it can be
worth trying this combination as Tier Three.
Emergency treatment: intramuscular NSAID and antiemetic
Emergency management of acute migraine is difficult, especially on house calls to patients not seen previously. Injections
of opiates, e.g. pethidine or morphine, are best avoided. Rebound headache, potential side effects and risk of dependency
generally outweigh the potential for additional pain relief.
BASH recommends for adults, when there are no contraindications, diclofenac, 75 mg, intramuscularly. However, diclofenac
injections can cause serious tissue damage and it is preferable to avoid them if possible. Medsafe recommends they be
given by deep intragluteal injection into the upper outer quadrant, if required.
NSAIDs by suppository are a safer alternative, and are often effective. Concurrent administration of prochlorperazine,
25 mg as a suppository is useful to control nausea and vomiting.
Chlorpromazine, 25-50 mg intramuscularly is useful as an anti-emetic and sedative in the emergency management of acute
Relapse: repeat analgesics and consider repeat of triptan
Relapse is recurrence of headache within the same episode of migraine despite initial efficacy. Management is difficult
because repeated doses, especially of triptans or opiates, if they have been used, can give rise to repeated rebound over
Repeat of previously used analgesics may be effective. A second dose of triptan is usually effective but does increase
the risk of further rebound. A minimum of two hours is required between doses. Ergotamine may be an alternative but must
be given at least 12 hours after sumatriptan.
The maximum dose of sumatriptan in any 24 hour period is:
- Oral dosage in 24 hours, 300 mg
- Sub-cutaneous dosage in 24 hours, 12 mg
Limit use of acute migraine therapy to two days per week
Regular use of acute migraine therapies for more than two days per week carries significant risk of initiating or escalating
medication overuse headache and should be avoided. Regular requirement of acute migraine therapy for more than one day
per week is an indication to evaluate how the medication is being used and review the diagnosis.
- Tier one incorporates stages one and two of the BASH recommendations, which split oral and rectal analgesia
+/- antiemetic into separate stages.
- This is naproxen 250 mg plus naproxen 500 mg, or naproxen sodium 275 mg plus naproxen sodium 550 mg.
- Cataflam or voltaren rapid. These appear to be more rapidly absorbed than diclofenac sodium.
- EBM Reviews - Cochrane Central Register of Controlled Trials Di Monda V, Nicolodi M, Aloisio A, et al Efficacy
of a fixed combination of indomethacin, prochlorperazine, and caffeine versus sumatriptan in acute treatment of multiple
migraine attacks: a multicenter, randomized, crossover trial. Headache. 2003; 43(8):835–44
Migraine prophylaxis is indicated when symptoms cannot be adequately controlled with acute therapy. As migraine is cyclical,
permanent use of prophylaxis is not usually required; it can be tapered off, after 4-6 months, to test the need for continued
The choice of medication for prophylactic therapy for individual patients is guided by:
- Evidence of effectiveness
- Potential benefits
- Potential risks
- Ease of use
The medications most useful in primary care are shown in Table 2. In general, prophylactic therapies are started at
low doses and gradually increased to avoid side effects. Once a full dose is achieved, a reasonable trial of therapy is
approximately 6-8 weeks.
Table 2: Medications for migraine prophylaxis in primary care
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||Comorbidities to consider
|Beta blockers Good evidence base
||RCTs for metoprolol, propanolol, nadolol and atenolol
||Cold extremities, reduced exercise tolerance, dizziness
50–100 mg BD
Propanolol LA 80 mg daily to 160 mg BD
|Asthma, heart failure, peripheral vascular disease, depression
|Tricyclics Adequate evidence base
||Evidence for effectiveness from small RCTs of amitriptyline
||Helps with coexistent tension headache, other pain conditions, disturbed sleep and depression. Some
evidence of synergy with beta blockers
||Sedation, dry mouth, dizziness, nausea Less side effects with nortriptyline
|Concurrent use of other anti-cholinergic medications
|Sodium valproate Good evidence base
||Nausea, weight gain, alopecia, spontaneous bruising, liver dysfunction
||300-1000 mg BD
||Contra-indicated in pregnancy
|RCT = Randomised Controlled Trial
Pizotifen and clonidine have little evidence of effectiveness and are now superseded for the prophylaxis of migraine
in adults. There is some evidence for the effectiveness of verapamil and the evidence for the use of fluoxetine is inconclusive.
Acupuncture is often used for migraine and trials have shown reduction in the severity and frequency of episodes. However,
the quality of these trials has been questioned. There are the usual problems associated with testing complementary therapies.
Medications are subject to trials before introduction, whereas complementary therapies are not usually subject to trial
until they have been used for many years and positions have become entrenched. Decisions will depend on the enthusiasm
of individual clinicians and patients for this modality of treatment.
Migraine in children
In children, migraine attacks may be shorter-lasting, headache is more commonly bilateral and gastrointestinal disturbance
is more prominent.
Generally, children with migraine, which cannot be controlled with simple analgesics, are best referred for specialist
care. Anti-emetics are not recommended.
Management of migraine during pregnancy and breast-feeding
There are no clinical trials specifically evaluating the drug treatment of migraine during pregnancy. Fortunately, migraine
frequency is usually reduced during this time. (Ever et al, 2006)
Table 3: Management of migraine during pregnancy
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||Can be used throughout pregnancy and breast-feeding
||Avoid in the third trimester to avoid fetal renal damage and patent ductus. In the first and second
trimester short acting NSAIDs, such as ibuprofen, are preferred
||Unlikely to cause harm through pregnancy and breast-feeding
|Triptans and ergotamine
However, women who have taken sumatriptan inadvertently in pregnancy can be reassured current evidence
suggests they are at no greater risk of birth defects than the general population
||Beta blocker with best evidence of safety during pregnancy
||Lowest effective dose may be used
Avoidance, recognition and management of medication overuse headache
Medication overuse headache occurs most frequently from chronic overuse of analgesics, such as aspirin, NSAIDs, paracetamol
and codeine, to treat headache. Frequent lower doses appear to carry greater risk than higher weekly doses. It also occurs
because of rebound headache following triptan use.
Medication overuse headache may take a long time to resolve after the medication is withdrawn. Re-introduction of headache
medication may resolve the headache in the short term but escalates the long-term problem.
There is no specific type of headache associated with medication overuse but patients often describe them as oppressive,
often worse on wakening and aggravated by physical exercise. They are not usually accompanied by nausea or vomiting.
Headaches evolve over weeks or longer, with increased frequency of the headache, often accompanied by increased analgesia
use, until eventually, medication is taken in anticipation of headaches. Prophylactic medication is ineffective. Often
the pattern of headaches and medication use can only be understood with the help of an accurate headache and medication
Other forms of primary and secondary headache should be carefully excluded.
There are four objectives in the management of medication overuse headache:
- Withdrawal from the overused medication
- Recovery from the headache
- Re-assessment of any underlying primary headache
- Prevention of relapse
Withdrawal of overused medication
Motivation: For people who experience medication overuse headache, the outcome of withdrawal is usually
good. The alternative is ever-worsening headache.
Warning: Headaches may worsen for three to seven days following withdrawal of medication. Patients need
encouragement and support over this time and absence from work may be required.
Diary: Recording symptoms and medication use during medication withdrawal, allows a more objective assessment
of the results of withdrawal.
Good hydration: This is thought to help.
Abrupt withdrawal: This is more successful than gradual withdrawal. When withdrawal cannot be achieved,
it may be effective to offer regular naproxen 250 mg tds or 500 mg bd for three weeks to cover the withdrawal period.
The aim is to prevent people responding to headache by taking medication.
Recovery from headache
The time to recovery from the headache depends on the medication type.
Triptan: 7-10 days
Simple analgesics: 2-3 weeks
Opiates: 2-4 weeks
When recovery does not follow a reported withdrawal, the headache may have other causes, or medication overuse may be
Re-assessment of underlying primary headache
An underlying primary headache, usually tension-type or migraine, often becomes apparent within two months. This should
be managed systematically. The analgesics, which were implicated in the overuse headache, can be re-introduced after two
months, if required, but care has to be taken that these are used appropriately.
Prevention of relapse
There is a high risk of relapse and good support will be required.
Brief update on the pathophysiology of migraine and anti-migraine drugs
Migraine is a group of familial disorders; individual susceptibility is conferred by genetics and exposure to triggering
Migraine aura is strongly associated with a slowly spreading wave of decreased electrical activity that travels across
the cortex at approximately 2-3 mm per minute. This is termed Cortical Spreading Depression (CSD). CSD is thought to also
occur in migraine without aura, but is clinically silent.
An episode of CSD is followed by long-lasting suppression of neuronal activity and activation of the trigeminovascular
system. Consequent release of neuropeptides produces vascular dilation and neurogenic inflammation. Headache results because
of meningeal irritation and the sensitisation of nerve fibres to previously innocuous stimuli, such as the pulsing of
Beta blockers, valproate and amitriptyline, the first choice drugs for migraine prophylaxis in primary care, have all
been demonstrated to reduce the number of CSDs in animal experiments. The mechanism by which this occurs has not yet been
demonstrated, but the discovery of CSD does provide an avenue for the development of new prophylactic anti-migraine drugs.
Triptans and ergotamine, used in acute migraine, reduce headache by blocking release of the neuropeptides responsible
for meningeal irritation and sensitisation of central nerve fibres.