Management of Pain Syndromes & Migraine

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! • Pain is regarded as physiological in first instance – [Acts as warning to body so that it can remove itself from harmful stimulus] • 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 • 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 • 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

Classification of Pain • According to severityMildModerateSevereRemember 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 • 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

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 Postherpetic neuralgia [Phantom limb pain] MS Post stroke

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-convulsantsSuccess 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:

Normal physical examination • No other reasonable cause for the headache • At lease two of:- • Unilateral pain • Throbbing pain • Aggravation of pain by movement • Moderate or severe intensity of pain • 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 anti-emetic 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

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 Sumatriptan

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 / contra- indications 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?

Management of Pain Syndromes & Migraine