Management of Pain Syndromes & Migraine Mary Teeling 23rd February 2006 Topics • • • • • • Perception of pain Classification of pain Acute pain Chronic pain Neuropathic pain Migraine Perception of Pain (1) • Pain is perceived in cerebral cortex • Passes from peripheral nervous system to spinal cord right up through brain to cerebral cortex • Opportunity for modifying factors along the way Perception of Pain (2) Painful stimulus Initial transfer via fast “A delta” sensory fibres [results in sensation of sharp localised pain lasting 3 – 5 minutes] Followed by transfer via slower “C” fibres. [Results in dull, aching pain of longer duration] Remember! 1. Pain is regarded as physiological in first instance – [Acts as warning to body so that it can remove itself from harmful stimulus] 2. Environment /past experiences / cultural factors may affect the body’s perception of pain [Remember the possibility of modifying factors along the pathway of sensation] Classification of Pain 1. According to aetiology: • Nociceptive [perception of pain due to tissue damage] Somatic Musculoskeletal Visceral • Neuropathic [pain initiated or caused by a primary lesion/dysfunction in nervous system] Phantom limb pain Post-herpetic neuralgia Classification of Pain 2. According to duration Acute pain defined as normal predicted physiological response to an adverse chemical, thermal or mechanical stimulus [usually identifiable cause] Chronic pain defined as continuous or intermittent pain or discomfort which has persisted for > 3 months and for which painkillers have been taken and treatment sought recently and frequently [may be due to sensitisation, demyelination of nerves involved, or due to influences from other areas of brain] Acute vs. chronic pain Characteristic Acute Chronic Duration Associated cause Prognosis Nerve conduction Associated illness Social sequelae Treatment Hours-days Present Predictable Rapid Uncommon Few/none Primary analgesics Months-years Commonly absent Unpredictable Slow Depression, anxiety Often profound Usually multimodal required Classification of Pain 3. According to severity Mild Moderate Severe Remember perception of degree of severity of pain may be affected by external influences Why Bother With Classification? •Pain is a complex and multidimensional symptom •It is important to be able to categorise pain in order to find the most appropriate pharmacological and/or other therapies Management of Acute Pain Step wise approach to pharmacological management A. • • • • • Paracetamol Acts at CNS level primarily (blocks PG activity) Very effective for mild – moderate acute pain Dose up to 4 gram/day in divided doses can be given Not gastro-toxic but mind liver toxicity Excellent for co-prescription with other treatments in more severe pain Acute Pain B. NSAIDs (including Aspirin) • Have analgesic and anti inflammatory effects • Effective for most types of acute pain • Exert their effect at peripheral level by binding COX enzymes and inhibiting PG synthesis • ADRs may be a problem especially in elderly [G1 toxicity, renal dysfunction, hypertension] Remember: NSAIDs can be applied topically Aspirin and paracetamol may be used together – to increase pain relief and reduce risk of ADRs Acute Pain C. Opioids • Mimic the effect of endorphins, the endogenous peptides released in response to many stimuli including pain, physical stress etc • Many different opiates and opioid-like agents available • Particularly suitable for moderate – severe pain • Problems with ADRs such as constipation, respiratory depression, sleepiness, dependence • Suitable for co-prescription with non-opioid agents e.g. paracetamol (improves safety) Other Treatment Modalities Appropriate physical therapeutic aids Such as: passive stretching in acute stage +/- ice packs for musculoskeletal pain Splinting / POP in bony fractures Debridement of dirty wound Summary •Acute pain starts out as a physiological response but •If not properly managed may lead to reduced / delayed healing (even in unconscious state) or may develop into a chronic pain syndrome ***Remember to look for cause of pain and treat that*** Chronic Pain Defined as continuous or intermittent pain or discomfort which has persisted for > 3 months and for which painkillers have been taken and treatment sought recently and frequently Acute vs Chronic Pain Characteristic Acute Chronic Duration Associated cause Prognosis Nerve conduction Associated illness Social sequelae Treatment Hours-days Present Predictable Rapid Uncommon Few/none Primary analgesics Months-years Commonly absent Unpredictable Slow Depression, anxiety Often profound Usually multimodal required Treatment Options for Chronic Pain Ideal is cure – not always possible Aims of treatment Decrease pain and suffering Improve physical and mental functioning Therefore interdisciplinary approach (“multimodal”) Treatment Plan Step 1 Look for cause /mechanism Step 2 Pharmacological treatments -Analgesics and/or anti-inflammatory agents as for acute pain [combinations particularly useful here] -Anti depressants (tricyclic anti depressants in particular) -Mechanism of action appears to be independent of the anti-depressant effect (used at a lower dose than that required for treating depression) -Related to effect on neurotransmitter(s) -Also helps with associated disorders such as insomnia Step 2 contd. - Anticonvulsants such as Carbamazepine ) affect sodium Phenytoin ) channels Gabapentin /pregabalin [alpha2 - delta ligands affecting calcium channels] Side-effects such as somnolence, dizziness, ataxia may occur Treatment Plan Step 3 Relaxation therapy Progressive muscle relaxation Physiotherapy – maximise function Occupational therapy – retraining may be required Nerve block therapy* Epidural pain relief therapies* Spinal cord stimulation* [modulates the transmission of pain] * Involve specialist pain clinics Neuropathic Pain Pain caused by lesion in / dysfunction of the nerves in either the peripheral or contral nervous system Results in either: stimulus – independent pain or Pain hypersensitivity Neuropathic Pain Chronic pain manifested as: Shooting, burning, sharp (or aching) painful sensations, hyperalgesia, allodynia Examples of Neuropathic Pain Diabetic Neuropathy MS Postherpetic neuralgia Post stroke [Phantom limb pain] Management of Neuropathic Pain (1) • Analgesics are effective in minority (NSAIDs not beneficial) Opioids (in short-medium term studies) may provide relief in 50% • Antidepressants / anti-convulsants Success varies between studies • Topical anaesthetics may be useful for localised allodynia, hyperalgesia Management of Neuropathic Pain (2) • Combinations of different modalities may be useful • Behavioral therapy important • Nerve block – may not be effective depending on nature of damage • Acupuncture – not formally evaluated MIGRAINE: definition Migraine defined as repeated attacks of headache (4 – 72 hours) with the following features: A. Normal physical examination B. No other reasonable cause for the headache C. At lease two of:• Unilateral pain • Throbbing pain • Aggravation of pain by movement • Moderate or severe intensity of pain D. At least one of:• Nausea or vomiting • Photophobia and phonophobia Migraine : Some Facts • Approx 15% people in USA and Europe suffer from migraine • May be described as “head pain with associated features” – this is important for differential diagnosis Often clearly defined triggers such as: -Weather change -Bright lights -Altered sleep or stress levels -Menstruation MIGRAINE WITHOUT AURA = COMMON MIGRAINE MIGRAINE WITH AURA = CLASSIC MIGRAINE MIGRAINE: Causes Genetic component: often a positive family history • Original theory: based on hypothesis that migraine was due to vascular phenomena i.e. vasoconstriction followed by reactive vasodilatation (and headache) – Cannot explain all of effects • Current imaging research suggests functional changes in brain Treatments for Migraine Prevention Treatment Treatment of Migraine • Simple analgesics (paracetamol, aspirin, NSAIDs, opioids) with/without an antiemetic agent (e.g. metoclopramide) May be sufficient if attack not severe / based on patient’s previous response • 5-HT1 agonists (triptans) These agents act on the 5-HT 1B and 1D receptors • They are effective in relieving an established migraine headache Conditions with use of Triptans • Contra-indicated in established ischaemic heart disease, previous stroke, coronary vasospasm, severe hypertension • Side effects include flushing, dizziness, tightness in chest/ throat • Should not be used with other acute therapies for migraine • Should not be used in the prophylaxis of migraine Types of Triptans Sumatriptan First in class Sumatriptan •Active Orally (50-100 mg) Intranasally (10-20 mg) Subcutaneously (6mg) [rectal] •Max dose is twice the initial dose in 24 hours (at least 2 hours between each dose) (Specific warnings about cardiovascular toxicity have been issued for this triptan) Several other triptans authorised for use Other Therapies for treating migraine Ergot Alkaloids •Derived from fungus - known for centuries •Act as partial agonists at several neurotransmitter receptors, therefore precise mechanism of action here is unknown Ergotamine: •Subject to extensive first pass metabolism therefore given orally or rectally •Use has been surpassed by triptans [Has similar toxicity profile but of worse severity] use is limited to twice per month (intervals of not < 4 days apart) Prevention of Migraine Attacks For regular / debilitating attacks* • Search for triggers (lifestyle, stress, other medications) • If can’t be found / patient is intolerant of treatments than give prophylaxis as follows: * Rarely migraine may predispose to migranous infarction Types of Prophylaxis blockers But remember precautions / contraindications for use Pizotifen (0.5 – 2mg daily) Anti-histamine with serotoninergic antagonist properties [Other drugs such as tricyclic antidepressants and sodium valproate have been used but this use may be outside the term of the licence] Methysergide • Ergot derivative with predominantly serotoninergenic antagonist activity *Hospital – use only as it causes fibrosis of heart valves, pleura and retroperitoneal fibrosis* Any questions?