PRIORITIES AND CLINICAL EFFECTIVENESS FORUM MANAGEMENT OF ADULT HEADACHE

Transcription

1 PRIORITIES AND CLINICAL EFFECTIVENESS FORUM MANAGEMENT OF ADULT HEADACHE o This is a new guideline produced jointly by GPs and Consultant Neurologists. o The aim is to reduce referrals to Consultants for the majority of headaches that can be safely managed in Primary Care. o This will facilitate faster assessment of those headache referrals that demonstrate red flag features, requiring specialist investigation. o Diagnostic guidance and treatment schedules are provided. Page 1 of 12

2 Patient Information Adult Headache Acknowledgements History & examination Diagnostic features (no red flags) Migraine: Without aura With aura Tension-type headache Cluster headache Medication overuse Trigeminal neuralgia Treatment schedules: Migraine Tension-type (TTH) Cluster headache Medication Overuse Headache (MOH) Trigeminal Neuralgia (Prodigy notes) Diagnostic uncertainty (no red flags) (Ix) Still consider the commonest causes: Tension-type Headache Migraine Analgesic Induced Headache Cervicogenic headache in the over 60 s ESR +/- CRP Red flag features Awoken by headache at night (not awakes with a headache). Worst in the morning Worsened by changes in posture, especially bending. Coughing, sneezing, straining, or vomiting exacerbates it. Associated with: o Vomiting & drowsiness. o Progressive neurological deficit. o Cognitive changes. Papilloedema. Meningeal irritation; look specifically for neck stiffness, back pain, and Kernig's sign. New neurological deficit Refer Therapeutic trials (At least 2 treatment options at adequate dosage, esp. migraine) Review diagnosis: Any more clues? (Diary, etc) Reviews & PILs Response No response Page 2 of 12

3 Notes: Acknowledgements: The following text is taken from the Prodigy Guidelines for Headache, Migraine and Trigeminal Neuralgia. The algorithm was designed by Richard Bull (REB) with the support of Consultant Neurologists: Markus Reuber & Marios Hadjivassiliou, and the valued input of GPs on the Clinical Guidelines Group, Chesterfield CG Group, NED PCT PEC and from Peter Burrill on behalf of PACEF. Headache: This algorithm is designed to be an aid: We would encourage you to familiarise yourself with the Prodigy Guidelines themselves ( ) rather than relying on what is necessarily a brief synopsis. In 1988 The International Headache Society published its classification and operational diagnostic criteria for all headache disorders. This has now been updated with the 2004 update: Headache Classification Sub-Committee of the International Headache Society. The international classification of headache disorders. Cephalalgia 2004;24(suppl 1): This update is now the gold standard and can be viewed and saved (but not printed) at It s also worth checking out but note these guidelines have not yet been updated in line with the new 2004 HIS guidelines History: The history is the most important diagnostic factor in the majority of people with headache. Although the examination, as guided by the history, must not be omitted, it rarely reveals any positive diagnostic features. Investigations are not helpful for most people with headache as there are no diagnostic tests for the most common causes. A headache diary is a particularly useful tool to aid diagnosis. Migraine is usually easily diagnosed from the history. Common and classic migraine account for 99% of cases. Migraine without aura This is an idiopathic, recurring disorder involving attacks that last 4-72 hours. Page 3 of 12

4 The headache is typically unilateral, pulsating, of moderate or severe intensity, and is aggravated by normal physical activity. It is associated with nausea, vomiting, photophobia, and phonophobia. Five or more attacks are required to make the diagnosis. Seventy-five per cent of sufferers have this form. Patients who consult with episodic headaches that significantly interfere with normal daily activities almost always have migraine (Dowson AJ et al. The prevalence and diagnosis of migraine in a primary care setting: Insights from the Landmark study. Headache Care2004; 1: In press). They can be given a default diagnosis of migraine (which is often confirmed at a later date). Migraine with aura This is an idiopathic, recurring disorder with attacks of neurological symptoms that arise in the cerebral cortex or the brain stem, creating the aura. The aura usually develops gradually over 5-20 minutes, lasts less than 60 minutes, and is completely reversible. Typical examples of an aura are: o Homonymous visual disturbance (the most common type), usually a fortification spectrum - a spreading, scintillating scotoma in the shape of a jagged crescent o Unilateral paraesthesia or numbness o Unilateral weakness o Dysphasia o A combination of the above The headache usually starts within 60 minutes of resolution of the aura, and lasts 4-72 hours. However, it may begin before the aura, or at the same time as the aura, or it may even be absent. The headache is typically unilateral, pulsating, of moderate or severe intensity, and is aggravated by normal physical activity. It is associated with nausea, vomiting, photophobia, and phonophobia. Two or more attacks are required to make the diagnosis. Twenty-five per cent of sufferers have this form. [Headache Classification Committee of the International Headache Society, 20004] What are the trigger factors? Trigger factors that precipitate attacks may be identified, but only in the minority of sufferers. Dietary triggers affect about 20% of people. Most attacks have no obvious trigger, and some triggers that are identified are unavoidable. Trigger factors include [BASH, 2000]: Stress (and relaxation after periods of stress) Certain foods (e.g. alcohol, cheese, citrus fruits, chocolate) Missing meals Too much or too little sleep Bright lights Loud noise Hormonal changes (menstruation and menopause) Page 4 of 12

5 Tension-type headache may be episodic or chronic. Each episode lasts between 30 minutes and 7 days, although the majority last less than 24 hours. The pain is of a pressing or tightening character, and is not pulsating. It is of mild to moderate intensity, which does not prohibit activity. It is usually bilateral. It is not aggravated by normal physical activity. There is no nausea or vomiting, although anorexia may occur. Photophobia or phonophobia are rare. Tension-type headache has no prodrome or aura. The pain can involve the frontal, temporal, occipital, or parietal regions; it may radiate to the neck or jaw; it can change location during an attack and tends to worsen across the day [Headache Classification Committee of the International Headache Society, 1988; Silberstein, 1993]. Cluster headache is unilateral and involves the eye and frontal region. Attacks may occur several times in 24 hours, and last from 15 minutes to 3 hours. Attacks occur in clusters, which usually last between 1 and 2 months; most sufferers experience one or two clusters a year. The pain is severe and associated with ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating, miosis, ptosis, and eyelid oedema. The character of the pain is burning, boring or piercing. It is six times more common in men than in women. The average age at onset is 30 years [Headache Classification Committee of the International Headache Society, 1988; Smetana, 2000]. Headache associated with raised cerebrospinal fluid pressure is often intermittent at first, but becomes constant and more severe as the cause of the raised pressure progresses. The pain is characteristically worse in the morning, and the person may be woken by it. It is worsened by changes in posture, particularly bending, and is improved by rest. Coughing, sneezing, straining, or vomiting exacerbates it. The headache is usually generalized. Headache is a feature in only a half of people with a cerebral tumour, and is the presenting symptom in less than 10% [Hilton-Jones, 2001]. Less than 1% of people with a non-migraine headache will have a brain tumour [DH, 2000]. Visual obscuration (episodes of blurred / cloudy vision) is associated with straining and is more likely to occur after periods of recumbancy. Medication overuse headache results from the chronic overuse of medication that is used to treat headache. It is estimated to affect 1 in 50 people. It was first recognized with ergotamine use. It is now associated with aspirin, paracetamol (especially when combined with codeine), NSAIDs, and 5HT 1 agonists (triptans). The headache varies in its quality, location, and intensity. Discontinuation of the drug worsens the headache before any improvement will occur; maximum improvement may take 6 months [Redillas and Solomon, 2000; BASH, 2000]. Trigeminal neuralgia is a painful affliction of the face. It is usually unilateral. It is characterized by brief lancinating pains limited to the distribution of one or more divisions of the trigeminal nerve. It is of unknown aetiology [Headache Classification Committee of the International Headache Society, 1988]. The diagnosis is made on the history alone. The features of the pain are characteristic. The pain occurs in paroxysms, which last from 2 seconds to 2 minutes. The frequency of the paroxysms can vary from several hundred a day to long periods of remission that can last for years [Headache Classification Committee of the International Headache Society, 1988; Zakrzewska, 2001]. Page 5 of 12

6 The pain is severe, and is described as intense, sharp, superficial, stabbing, burning, or like an electric shock. In each person the character of the pain is the same in different attacks [Headache Classification Committee of the International Headache Society, 1988; Zakrzewska, 2001]. The pain is felt in the distribution of one or more divisions of the trigeminal nerve. The most frequently affected divisions are the maxillary (35% of people) and mandibular (29%) alone; both the maxillary and mandibular divisions are affected in 19%. The ophthalmic division is the least frequently affected (4%of people). All three divisions are affected in only 1% of people. The pain occurs bilaterally in 3% of people [Katusic et al, 1990]. The pain is often triggered by trivial stimuli, e.g. touch, eating, washing, shaving, brushing the teeth, or talking [Headache Classification Committee of the International Headache Society, 1988; Zakrzewska, 2001]. Between paroxysms the person is asymptomatic. The person is usually free of pain at night. What else might it be? Dental disease (e.g. apical abscess) can cause paroxysmal as well as continuous pain. The overall features should, however, readily distinguish this from trigeminal neuralgia. Atypical facial pain causes a constant dull ache in the maxillary and cheek areas, which can extend to affect the whole side of the head and the neck. Cluster headache occurs in paroxysms, but the characteristic features readily distinguish this from trigeminal neuralgia. Cluster headache is unilateral and involves the eye and frontal region. Attacks may occur several times in 24 hours, and last from 15 minutes to 3 hours. Attacks occur in clusters, which usually last for between 1 and 2 months; most sufferers experience one or two clusters a year. The pain is severe and associated with ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating, miosis, ptosis, and eyelid oedema. The character of the pain is burning, boring, or piercing. Multiple sclerosis (MS) causes trigeminal neuralgia in 4% of affected people, although it is rarely a presenting feature. Trigeminal neuralgia tends to occur in younger people with MS, and may be bilateral. Postherpetic neuralgia is readily distinguished by the history of shingles in the distribution of the pain. Other cranial neuralgias (e.g. glossopharyngeal, nervus intermedius, superior laryngeal, occipital) can all cause pain that is of similar character to, but in a different site from, trigeminal neuralgia. Primary tumours of the trigeminal nerve, or compression of the nerve (e.g. by a tumour or aneurysm) can very rarely cause features of trigeminal neuralgia. They more commonly cause continuous pain or numbness, and usually there are abnormal clinical signs. Temporal Arteritis: Consider temporal arteritis in any patient over 50 presenting with new headache. Classic features include headaches with jaw claudication, enlarged, tender & non-pulsatile temporal arteries and possible visual catastrophe. ESR usually considerably raised, although if index of suspicion high and ESR low, check CRP. Page 6 of 12

7 Examination: A central nervous system (CNS) and general examination, as guided by the history, should be performed in all cases. It is likely to be normal in most people, but is essential in order to exclude serious causes of headache and to allay the person's anxiety. Of people referred to outpatients because of headache, less than 1% had an intracranial lesion; each person with an intracranial lesion had physical signs of it [BASH, 2000]. Fundoscopy and blood pressure must always be performed to exclude papilloedema and hypertension. It is often sensible to repeat fundoscopy at review appointments [BASH, 2000]. Look for meningeal irritation, specifically for neck stiffness, back pain, and Kernig's sign. Meningeal irritation may be due to infection, blood (e.g. subarachnoid haemorrhage), or neoplastic infiltration. Palpation of the face and neck, including the temporal arteries, is an important part of the examination. Investigations: Most people need no investigation. There are no diagnostic tests for the most common causes of headache. An erythrocyte sedimentation rate (ESR) measurement and possible temporal artery biopsy should be considered if the history suggests giant cell arteritis. Skull X-ray is useful following a severe head injury, but is otherwise obsolete. Neuroimaging (computed tomography, CT, or magnetic resonance imaging, MRI) is unlikely to reveal positive findings in people without a history suggestive of a serious cause of headache, or without abnormal clinical signs. A recent Cochrane review recommended that neuroimaging is not warranted in people with typical migraine; but that the role of neuroimaging in people with non-migraine headache is still unclear [Frishberg, 1994]. Red flags: Rule out serious causes of headache, particularly in the elderly (e.g. subarachnoid haemorrhage, meningitis, space-occupying lesion, giant-cell arteritis). Sinister features include headaches that are: Worst in the morning (it may wake the person from sleep). Worsened by changes in posture, especially bending. Coughing, sneezing, straining, or vomiting exacerbates it. Associated with: o Vomiting & drowsiness. o Progressive neurological deficit. o Cognitive changes. Page 7 of 12

8 Papilloedema. Hypertension, especially onset with headache. Meningeal irritation; look specifically for neck stiffness, back pain, and Kernig's sign. Urgent referral is indicated for people with the following symptoms or signs: Presentation with 'first and worst' headache, especially acute onset with associated neurological signs A new headache with subacute onset that is progressively worsening (over days or weeks) Headache with unexplained fever, nausea, or vomiting Associated focal neurological signs, papilloedema, changes in consciousness or cognition, or stiff neck The Department of Health Referral Guidelines for Suspected Brain Tumours recommend urgent referral, under the 2 week standard, for people with headache, vomiting, and papilloedema. They also recommend that urgent referral, under the 2 week standard, is considered for 'people with non-migrainous headaches of recent onset, present for at least one month, when accompanied by features suggestive of raised intracranial pressure e.g. woken by headache, vomiting, drowsiness'. However GPs should use 'their discretion to decline urgent referral if there are other known features e.g. depression, somatisation disorder, making a diagnosis of brain tumour extremely unlikely.' The Department of Health Referral Guidelines for Suspected Children's Tumours recommend urgent referral, under the 2 week standard, for children (under 15 years) with headache of recent onset with one or more of the following features: Increasing in severity and frequency Worse in the mornings or causing early morning wakening Associated with vomiting Associated with neurological signs (e.g. squint, ataxia) Associated with behavioural change or deterioration in school performance Treatment: Migraine: It is important to note that the NNT (Number Needed to Treat) for even the best migraine prophylactic therapies is 3: In other words, to get a response in one person (> 50% reduction in pain/severity or frequency vs. placebo), 3 patients have to receive the drug. Corollary: You will be less successful with two out of every three patients treated. Therefore, the basis of migraine treatment is try and try again with increasing doses of migraine prophylactic treatment until one of three end-points is achieved: Success Page 8 of 12

9 Side-effects: Reduce to previous dose (if partially effective) or move on to next prophylactic. Maximum dose: Move on to next prophylactic. The Consultant neurologists would approach migraine treatment in exactly the same fashion: This can be more appropriately conducted in primary care. Acute Treatment options (1 st line): Analgesia +/- antiemetic. Aspirin 900mg + metoclopramide 10mg or domperidone 10mg (stat.) at earliest point following onset of indication of headache (pain or aura). If aspirin not tolerated (or C/I): Substitute with paracetamol 1g or ibuprofen 400mg 600mg. Alternatives include: Diclofenac, naproxen or tolfenamic acid. The first two are not specifically licensed for migraine, but are often used and are specifically mentioned in Prodigy. Note: Soluble forms are generally recommended to speed absorption. If vomiting problematic: Try domperidone 30mg + diclofenac Na 25mg suppositories tds, reverting to oral therapy when vomiting settled. Acute Treatment options (2 nd line): Triptans. Replace analgesic with triptan, used at earliest point following onset/indication of headache (pain or aura). The North Derbyshire Formulary includes two based on efficacy and cost: - Almotriptan Rizatriptan If there is no initial response: A further dose should not be taken for the same attack (except Zolmitriptan). Revert to first line Rx. If headache recurs: Another dose can be taken provided it is >2hrs (4hrs for Naratriptan) after the initial dose was taken. Note: Use should be strictly limited to no more than 12 doses per month, as it is now recognised that triptans can cause MOH (Medication Overuse Headache). Prophylactic treatment options: Consider with: 2* attacks/month (Prodigy) * It has been suggested that >2 attacks per week should be the threshold for prophylaxis (Lancet 2004; 363:381-91), although other reviews suggest 2 attacks/month (NEJM 2002; 346: & Ann Intern Med 2002; 137:840-49) if Page 9 of 12

10 attacks are disabling. GPs should use their professional judgement to define with their patients when prophylactic treatment is justified. Less frequent but severe or prolonged attacks Frequent use of acute treatments (to reduce incidence of MOH) Note on acute Rx: May still be required as severity and frequency are usually only reduced by prophylaxis. Note on prophylactic Rx: Prophylactic drugs need to be tried for 1-3 months before the full effect is seen. It is possible that patients may need a monthly review at each dose level. Prophylactic Rx may then be continued at the most appropriate dose for 6 months before a trial off Rx (gradual withdrawal) to see whether they are still required. If required, subsequent trials can be conducted when deemed appropriate by GP and Patient. 1 st option: Betablockers (E.g. propranolol but also metoprolol or atenolol (unlicensed)) Assuming no C/I, try propranolol at 40mg bd, increasing to 120mg bd, or maximum tolerated dose, by increases of %, at no sooner than monthly intervals. 2 nd option: Amitriptylline (unlicensed): Try starting with 10mg nocte, increasing to 100mg, or maximum tolerated dose, by increases of %, at no sooner than monthly intervals. (A slow and cautious start to treatment with amitriptylline often helps avoid abandoning Rx due to S/E). 3 rd options: Valproate, Nifedipine, NSAIDs (e.g. naproxen), pizotifen & clonidine (although RCTs suggest ineffective and not recommended by BNF), verapamil, SSRIs (e.g. fluoxetine), topiramate, etc: Multiple options, but see prodigy for further details ( ) 4 th option: Acupuncture may be worth suggesting: (See BMJ 2004; 328:744-7 & 747-9) Tension-type headache (TTH): 1 st /2 nd option: Betablockers (E.g. propranolol but also metoprolol or atenolol (unlicensed)) Assuming no C/I, try propranolol at 40mg bd, increasing to 320mg, or maximum tolerated dose, by increases of %, at no sooner than monthly intervals. 1 st /2 nd option: Amitriptylline (unlicensed): Try starting with 10mg nocte, increasing to 100mg, or maximum tolerated dose, by increases of %, at no sooner than monthly intervals. (A slow and cautious start to treatment with amitriptylline often helps avoid abandoning Rx due to S/E). 3 rd option: Counselling: Those with obvious psychosocial stresses may benefit more through counselling, particularly if lifelong coping strategies are learnt. Page 10 of 12

11 4 th option: Valproate: (BMJ 2002; 325:881-6) Cluster headache: Acute attacks: Notes: Analgesics have no place in acute treatment Avoid alcohol or nitrates (if considered triggers). Try triptan injection or nasal spray. Oxygen (See BNF & BMJ 2002; 325:881-6) Prophylaxis: 1 st option: Verapamil 240 (-960)mg/day 2 nd option: Topiramate or Valproate A short course of oral steroids is often helpful whilst introducing prophylactic Rx; e.g. prednisolone 20mg/day x6 days. 3 rd options: Lithium (or Methylsergide: Only prescribed by specialist.) Medication Overuse Headache (MOH): Withdrawal of offending analgesic but beware temporary exacerbation of MOH. A six day course of prednisolone 20mg/day may be helpful in this situation. Reassess any residual headache for diagnosis and appropriate Rx if needed. Trigeminal Neuralgia: 1 st option: Carbamazepine: mg bd increasing slowly to 1.2g/day. Sometimes doses as high as 1.6-2g/day might be necessary. 2 nd option: Phenytoin: 100mg od increasing slowly to 300-(350mg) od (but beware S/E and non-linear pharmacodynamics) 3 rd option: Gabapentin: Try 300mg once daily, increasing to 300mg bd on day 2, then 300mg tds on day 3: Thereafter, dose can be increased by increments of 300mg per day, up to 1800mg/day, but is better tolerated at slower increases, e.g. bi-weekly. 4 th option: Sodium Valproate: Try 200mg bd, increasing to 2400mg, or maximum tolerated dose, by increases of 200mg, at no sooner than weekly intervals. Page 11 of 12

12 Note 1: Lamotrigine and baclofen may also be tried, and amitriptylline might prove helpful. Note 2: Tricyclic antidepressants have been shown to be effective in the treatment of neurogenic pain generally. However there are no studies of their efficacy specifically in trigeminal neuralgia, although anecdotally, they may prove helpful in some patients. Prodigy: Also see the Prodigy guidelines (hyperlinked): Migraine: Acute Rx 1 st line Acute Rx failure Prophylaxis Non-migrainous headache Trigeminal neuralgia Referrals: Temporal arteritis: Same day admission under Physician on-call. (Treatment with steroids should normally be commenced on suspicion of the diagnosis: Initial dose 40mg/day; consider 60mg/day if visual symptoms). Red flag referrals: Neurologists: 2w Urgent Undiagnosed headache or Unresponsive headaches: Neurologists (or GPSI headache clinic): Routine. Referrals must show evidence of: At least two treatment approaches at adequate dosage for diagnosed headaches, or At least two therapeutic trials at adequate dosage for undiagnosed headaches. Patient Information: Non-migraine headache: Headaches: A summary Tension-type headache Medication overuse headache Migraine: Migraine Migraine - Drugs to Prevent Attacks Migraine Action Association Migraine Trust Trigeminal neuralgia: Trigeminal neuralgia Trigeminal Neuralgia Association UK REB:19/05/2004 Page 12 of 12