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 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

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]

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

Classification of Pain

3. According to severity

MildModerateSevere

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 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

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 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

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 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

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 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

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:

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 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 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]

Methysergide

• Ergot derivative with predominantly serotoninergenic antagonist activity

*Hospital – use only as it causes fibrosis of heart valves, pleura and retroperitoneal fibrosis*

Any questions?