2. Objectives
• Review the anatomy and physiology of pain
• Gain knowledge of the pathophysiology of pain in
Multiple Sclerosis (MS)
• Understand the types of pain commonly experienced by
people with MS
• Consider the impact of pain on people living with Multiple
Sclerosis
• Neuropathic Pain medications
• Identify the need for specialist assessment
3. What is pain?
Williams, Amanda C. de C.; Craig, Kenneth D. PAIN: November 2016 - Volume 157 - Issue 11 - p 2420–2423
5. Pain in Multiple Sclerosis
• Prevalence 57% to 65%
• At disease onset, pain ranges from 11-23% with
approximately half of patients having pain at any given
point in their disease.
• People with MS are more likely to complain of moderate
to severe pain that has an impact on daily living.
(O’Connor 2008)
6. Common Causes of Pain in MS
• Acute pain due to inflammation
• Chronic or intermittent pain as a result of CNS lesion
• Secondary to spasticity
• Spasm and muscle cramps from higher motor neuron
lesions
• MSK- Maladaptive body positions and general
deconditioning
7. Co-morbidity - Neuropathic pain
18
27
33
36
39
55
60
0 10 20 30 40 50 60 70
Poor appetite
Anxiety
Depression
Concentration difficulties
Drowsiness
Lack of energy
Difficulty sleeping
% patients with moderate to very severe discomfort due to symptoms (n=126)
Meyer-Rosberg K et al. Eur J Pain 2001; 5: 379–389.
9. Nociception
• Transduction-
• noxious stimuli converted to electrical signal
in the nerve cell
• Transmission-
• information relayed along A-delta and C
fibres to dorsal horn, spinothalamic tract,
brain stem & thalamus
• Perception-
• conscious awareness of pain
• Modulation-
• Inhibition of ascending pathways-
endogenous opioids, descending pathways
Melzack and Wall 2008
13. The continuum of pain
<1 month
Time to resolution
≥3–6 months
Acute
pain
Chronic
pain
• Usually obvious tissue damage
• Increased nervous system activity
• Pain resolves upon healing
• Serves a protective function
• Pain for 3–6 months or more
• Pain beyond expected period
of healing
• Usually has no protective
function
Degrades health and function
Insult
15. Defining Neuropathic Pain
IASP (NeuPSIG) 2008 as
"pain arising as direct
consequence of a lesion or
disease affecting the
somatosensory system,"
–and a grading system of "definite,"
"probable," and "possible"
neuropathic pain
R. -D. Treede, MD, T. S. Jensen, MD, PhD, J. N. Campbell, MD, G. Cruccu, MD, J. O. Dostrovsky, PhD, J. W. Griffin, MD, P.
Hansson, MD, DMSc, DDS, R. Hughes, MD, T. Nurmikko, MD, PhD and J. Serra, MD -Neurology 2008
16. Neuropathic Pain
• Disease of the pain signalling system
• Central or peripheral malfunctioning in the pain
signalling pathway – Neuroplastic changes
• Perception of pain in the absence of
tissue damage
• Serves no useful biological purpose
18. Symptoms of Neuropathic Pain
• Spontaneous or Evoked
• Shooting, burning,
electric shock
• Allodynia
• Hyperalgesia
• Dysesthesia
Dickenson AH. Brit J Anaesthesia 1995;75:193-200
Dworkin RH et al. Arch Neurol 2003; 60: 1524–1534.
19. Diagnosing neuropathic pain
• Diagnosis is based on:1
–Medical history
–Patient’s description of the pain
–Physical and neurological examination
–Appropriate laboratory tests and investigations
• The LANSS (Leeds Assessment of Neuropathic
Symptoms and Signs)
. 1. Dworkin RH et al. Arch Neurol 2003; 60: 1524–1534. 2. Bennett M. Pain 2001; 92: 147–157.
22. Lhermitte’s Sign- Barbers chair syndrome
• Neuropathic Pain
• Shooting pain from the neck down the spine
–16 in every 100 people with MS
–Sudden, brief
–Buzzing
–Can travel into arms and legs, fingers and toes
• Triggers include heat, stress & fatigue
• Manage triggers as well as symptoms and impact!
23. Central Neuropathic Dysaesthesia
extremity pain
• Caused by lesions in the CNS nociceptive pathway.
• Continuous, burning, pricking or stabbing pain, worse at
night.
• Most commonly presents in lower limbs & feet.
• Can be exacerbated by movement, exercise or
temperature.
• ‘Dante-esque’ – ‘Hells hottest knives’
Osterberg et al 2005
24. The MS Hug
• Neuropathic Pain
• Spasm of the intercostal muscles- MS Girdling
–Squeezing
–Crushing
–Crawling
–Hot/ Cold
–Pins and needles
• Triggers include heat, stress & fatigue
• Manage triggers as well as symptoms and impact!
25. Trigeminal Neuralgia
• Neuralgia refers to nerve pain that’s
brief, electric shock like, lancinating
and stabbing.
• Affects the movement of the jaw
muscles – V3 distribution
• Confused with dental pain.
• Triggered by innocuous stimulation
such as taking, touching the face,
eating and brushing teeth.
• Spontaneous with no trigger.
26. • Can be the first symptom of MS, its 20 times more common than in general
population.
• High suspicion in people under the age of 40yrs.
• Onset commonly 11yrs post onset of MS.
• 18% more likely to be bilateral in MS.
• TGN caused by pressure on the nerve by a blood vessel, causing wearing
of myelin sheath, causing the nerve to become more excitable.
• Usually atypical.
Trigeminal Neuralgia & MS
30. Tramadol
• Synthetic analogue of Codeine
• Agonist properties at all opioid receptors but particularly at Mu receptor
• Inhibits reuptake of serotonin and noradrenaline
• Absorbed gut, oral bioavailability 70 -90%
• Metabolized liver, excreted in urine
• Max Dose 400mgs daily, IR & MR
31. Tapentadol
• Synthetic analgesic – moderate – severe pain
• Dual mechanism of action, binds to mu opioid receptor &
inhibits the reuptake of norepinephrine. Weak effects on the
reuptake of serotonin.
• Available as Palexia IR & MR 50, 75 & 100mgs
• Dose 50mgs 4- 6 hourly, max 600mgs daily. Onset analgesia
30 mins
• Half life 4 hours
32.
33. Long term effects of opioids
• Nausea
• Sedation
• Cognitive impact
• Chronic constipation
• Immune system compromise
• Sex Hormones
• Opioid induced hyperalgesia
• Long term osteoporosis
36. NICE Recommendations
• Consider contraindications and side effects
• Co-morbid conditions
• Patient preference
• Titrate according to response
• Use one drug at a time
• For localised pain consider 0.075% Axsain
cream
37. Antidepressants
• Originally developed for the treatment of
depression.
• Mode of action:
– Block the re-uptake of serotonin and
noradrenalin, leading to activation of the
body's own descending inhibitory system
• Side effects: drowsiness, dry mouth,
constipation, low blood pressure, fast
heart rate, urinary retention and weight
gain
• Drugs: TCA- amitriptyline / nortriptyline
• SNRI – Duloxetine 60mg OD
38. Anticonvulsants
• Treatment of cerebral seizures
• Mode of action binds to the voltage-
gated calcium channels to blocks
neuronal sodium and calcium channels
Side effects: headache, dizziness,
drowsiness, tiredness, depression,
gastrointestinal symptoms
• Drugs: *gabapentin, pregabalin,
carbamazepine (TGN)
41. Small Localised areas of Neuropathic pain
• Capsaicin cream 0.025% or 0.075%
• Small amount applied 4 times a day
• 6 weeks to gain optimum benefit
• Reduces the release of substance P
45. Important Factors to Consider
for your patient with Neuropathic pain
• Listen to the patient’s concerns
• Explain the Pain does not equal harm
• REASSURANCE! REASSURANCE!
• Diagnose Neuropathic pain
• Realistic expectations – medication
-30-50% pain relief, may take 4-6
weeks effective.
46. Referral to Specialist Pain Service
• Where pain management needs are complex and cannot
be met by primary care or secondary specialist MS/
Neurology services.
• Where patients have failed to respond to first line
treatment (NICE 2016)
• Where pain is the predominating feature
• Difficult to manage Neuropathic pain
Note: Neuropathic pain is a clinical description (and not a diagnosis) which requires a demonstrable lesion or a disease that satisfies established neurological diagnostic criteria. The term lesion is commonly used when diagnostic investigations (e.g. imaging, neurophysiology, biopsies, lab tests) reveal an abnormality or when there was obvious trauma. The term disease is commonly used when the underlying cause of the lesion is known (e.g. stroke, vasculitis, diabetes mellitus, genetic abnormality). Somatosensory refers to information about the body per se including visceral organs, rather than information about the external world (e.g., vision, hearing, or olfaction). The presence of symptoms or signs (e.g., touch-evoked pain) alone does not justify the use of the term neuropathic. Some disease entities, such as trigeminal neuralgia, are currently defined by their clinical presentation rather than by objective diagnostic testing. Other diagnoses such as post herpetic neuralgia are normally based upon the history. It is common when investigating neuropathic pain that diagnostic testing may yield inconclusive or even inconsistent data. In such instances, clinical judgment is required to reduce the totality of findings in a patient into one putative diagnosis or concise group of diagnoses. Neuropathic pain results from damage to the warning system of the body that normally signals impending injury to organs or tissues. Patients with neuropathic pain typically exhibit a mixture of sensory loss—reduced responsiveness to external stimuli—with ongoing spontaneous pain and sometimes enhanced sensitivity to externally applied painful stimuli (hyperalgesia).
Peripheral sensitization – tissue damage releases chemicals – prostaglandins, serotonin, histamine, substance p, cause chemical excitation and activate nociceptors, this prolonged noxious stimuli causes changes along the neuron & DRG resulting in the nerves responding to a lower threshold. Sunburn.
Limbic centre – stores memory of pain- this is replayed continuously
Key message
Diagnosing neuropathic pain can be difficult. The LANSS Pain Scale can help differentiate neuropathic pain from nociceptive pain
Other information
The LANSS Pain Scale1
Helps to distinguish patients with neuropathic pain from those with nociceptive pain, based on symptoms and signs
The scale is based on analysis of sensory description through interview, using a questionnaire and an assessment of sensory dysfunction by examination
Reference:
Bennett M. The LANSS Pain Scale: the Leeds Assessment of Neuropathic Signs and Symptoms. Pain 2001; 92: 147–157.