Transcript Management of Pain Syndromes & Migraine

Management of Pain
Syndromes & Migraine
Mary Teeling
23rd February 2006
Topics
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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.
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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?