management of pain syndromes & migraine mary teeling 23 rd february 2006
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Management of Pain Syndromes & Migraine
Mary Teeling
23rd February 2006
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Topics
• Perception of pain
• Classification of pain
• Acute pain
• Chronic pain
• Neuropathic pain
• Migraine
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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
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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]
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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]
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Classification of Pain1. 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
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Classification of Pain2. According to durationAcute 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]
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Acute vs. chronic pain
Characteristic Acute Chronic
Duration Hours-days Months-years
Associated cause Present Commonly absent
Prognosis Predictable Unpredictable
Nerve conduction Rapid Slow
Associated illness Uncommon Depression, anxiety
Social sequelae Few/none Often profound
Treatment Primary analgesics Usually multimodal required
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Classification of Pain
3. According to severity
MildModerateSevere
Remember perception of degree of severity of pain may be affected by external influences
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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
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Management of Acute PainStep wise approach to pharmacological
managementA. 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
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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]
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Remember:
NSAIDs can be applied topically
Aspirin and paracetamol may be used together – to increase pain relief and reduce risk of ADRs
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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)
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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
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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***
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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
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Acute vs Chronic Pain
Characteristic Acute Chronic
Duration Hours-days Months-years
Associated cause Present Commonly absent
Prognosis Predictable Unpredictable
Nerve conduction Rapid Slow
Associated illness Uncommon Depression, anxiety
Social sequelae Few/none Often profound
Treatment Primary analgesics Usually multimodal required
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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”)
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Treatment Plan
Step 1
Look for cause /mechanism
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Step 2Pharmacological 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
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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
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Treatment PlanStep 3Relaxation therapyProgressive muscle relaxationPhysiotherapy – maximise functionOccupational therapy – retraining may be requiredNerve block therapy*Epidural pain relief therapies*Spinal cord stimulation* [modulates the transmission
of pain]* Involve specialist pain clinics
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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
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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
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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
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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
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MIGRAINE: definition
Migraine defined as repeated attacks of headache (4 – 72 hours) with the following features:
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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
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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
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Often clearly defined triggers such as:
-Weather change
-Bright lights
-Altered sleep or stress levels
-Menstruation
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MIGRAINE WITHOUT AURA = COMMON MIGRAINE
MIGRAINE WITH AURA =
CLASSIC MIGRAINE
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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
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Treatments for Migraine
Prevention Treatment
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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
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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
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Types of Triptans
Sumatriptan
First in class
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•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
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Other Therapies for treating migraine
Ergot Alkaloids
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•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)
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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
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Types of Prophylaxis
blockers But remember precautions / contra-
indications for usePizotifen (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]
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Methysergide
• Ergot derivative with predominantly serotoninergenic antagonist activity
*Hospital – use only as it causes fibrosis of heart valves, pleura and retroperitoneal fibrosis*
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Any questions?