Transcript Neuropathic pain

Neuropathic pain
1. Mechanism
2. Characteristic
3. Diagnosis
4. Treatment
Neuropathic pain
Mechanism of pain: caused by cancer
 nerve compression - nerve root
compression caused by a collapsed
vertebra
total tumor mass = neoplasm + surrounding
inflammation
 nerve infiltration by cancer
 nerve injury
Neuropathic pain
Mechanism of pain: caused by treatment
 postoperative (neurotomy)
 phantom limb pain, post-mastectomy pain
 radiotherapy (fibrosis) e.g. Brachial
plexopathy
 chemotherapy - peripheral neuropathy
(wincristine, cisplatine, taxol)
Neuropathic pain
Mechanism of pain:
 post-herpetic neuralgia
 diabetic neuropathy
 post-stroke pain
 uraemic neuropathy
Neuropathic pain
Pain characteristic:
 superficial burning pain
 spontaneous stabbing/shooting pain
 boring and radiating pain
 allodynia - pain caused by a stimulus
which does not normally provoke pain
 hyperalgesia - an increased response to a
stimulus which is normally painful
Neuropathic pain
Diagnosis:
 history
 clinical examination
 neurological examination
 MRI / CT
Neuropathic pain
Treatment:
I. Adiuvant analgesics
II. Corticosteroids
III. Analgesics (opioids)
IV. Neurolysis, spinal analgesia
Neuropathic pain
Corticosteroids (reduces total tumor mass)
e.g. Dexamethason 16-24mg at the
begining and then reduse dose
Antidepressants - tricyclic antidepressants
(amitriptyline, desipramine, doxepin,
imipramine, clomipramine)
SSRI (paroxetine, citalopram, fluoxetine)
Neuropathic pain
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Amitriptyline is effective in migraine and
other types of headache, chronic low back
pain, post-herpetic neuralgia, fibromialgia,
painful diabetic polyneuropathy, central
pain, cancer pain.
 Superficial burning pain, allodynia =
tricyclic antidepressants
 10-25mg nocte at the begining; max 75mg
 relief may not occur for 4-5 days, for
effect you have to wait even 1-2 weeks
Neuropathic pain
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Anticonvulsants - carbamazepine,
gabapentin, valproate, oxcarbazepine,
lamotrigine
spontaneous stabbing/shooting pain
carbamazepine 200-1600mg; effect after
10-14 days
adverse effects!
gabapentin - 300-3600mg; effect after one
week
Neuropathic pain
Other drugs:
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oral local anasthetics - mexiletine 450-600mg ;
lignocaine infusions
 NMDA receptor antagonists - dextromethorphan,
ketamine (in subanaesthetic doses), bupivacaine,
methadon
 muscle relaxants - Baclofen 10-15mg >>75-100mg
 topical agents - capsaicin, lignocaine patch,
EMLA
 benzodiazepines and neuroleptics
 spinal analgesia - epidural and intrathecal routes.
A 4-step analgesic ladder used either alone or
in conjunction with the WHO 3-step ladder
Spinal analgesia
Step 4
Class I antiarrhytmic
or cetamine
Step 3
Tricyclic antidepresant
and anticonvulsant
Step 2
Tricyclic antidepressant
or anticonvulsant
Step 1
Bone pain
1. Mechanism
2. Pain characteristic
3. Diagnosis
4. Treatment
Bone pain
Mechanism:
 metastases - breast, prostate, thyroid,
kidney, lung, colon
 cancer infiltration of the bone
 pathologic fracture
Bone pain
Pain characteristic:
- continuous, aching and localized pain
- is exacerbated by movements and sneezing
- may be unifocal
multifocal
generalized
Bone metastases
Symptoms:
 pain (75%)
 neurological symptoms
 pathologic fracture
 hypercalcaemia
 bone marrow failure
Bone pain
Diagnosis:
 history
 clinical examination
 rtg
 scintigram
 MRI / CT
Bone pain
Treatment:
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surgery - bone stabilisation, tumor excision
radiation therapy - is usually considered
when bone pain is focal and poorly controlled
with an opioid
chemotherapy (chemosensitive tumors)
hormonotherapy (hormonosensitive tumors breast, prostate)
Bone pain
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Radiopharmaceuticals that are absorbed at areas of
high bone turnover - strontium-89, rhenium-186,
samarium-153
strontium is only potentially effective in treatment
of pain due to osteoblastic bone lessions or lession
with an osteoblastic component e.g. prostate
cancer metastases
strontium
- initial clinical response occurs in 7-21 days
- the usual duration of benefit is 3-6 months
Bone pain
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Non-steroidal anti-inflammatory drugs
(NSAID)
opioids
corticosteroids
bisphosphonates (clodronate,
pamidronate)
calcitonin
neurolysis, spinal analgesia
Bone pain
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Bisphosphonates
- inhibit osteoclast activity and reduce bone resorption
-provide analgesia and decrease the use of analgesics
 clodronate:
- intravenous dose 600mg weekly
- oral dose - 1600mg daily
 pamidronate:
- intravenous dose 60-90mg every 3-4 weeks
- is safe in patients with impaired renal function
- adverse effect: occasional hypocalcaemia, nausea
Bone pain
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Calcitonin: mechanism of action is unclear
- increase endorphin levels in the central nervous
system
- interact with the serotonergic system
- anti-inflammatory action
- direct effect on osteoclasts
calcitonin
- subcutaneous - relatively low dose at the begining,
then gradually increased to 200 IU
- intranasal- 200 IU in one nostril; alternating nostril
everyday
Spinal cord compression
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Neurological emergency
3-5% of patients with advanced cancer
40% is associated with cancers of the
breast, lung, prostate
others are associated with: renal cell
cancer, lymphoma, myeloma, melanoma,
sarcoma, colorectal cancer
very rarely spinal cord syndromes are due
to epidural or cord metastases
Spinal cord compression
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Mechanism of compression:
- metastatic spread to vertebral body or
pedicle - 85%
- tumor extension through intervertebral
foramina - 10%
- intramedullary primary - 4%
- haematogenous dissemination - epidural
space - 1%
Spinal cord compression
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Clinical presentation: pain (>90%)
- pain of long duration which suddenly changes
-pain is aggravated by lying down
- pain may occur spontaneously
- radicular pains are often exacerbated by
neck flexion or straight leg raising, by
coughing, sneezing or straining
- funicular pain is less sharp, has a more
diffuse distribution and is sometimes
described as a cold unpleasant sensation
Spinal cord compression
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Clinical presentation:
- weakness > 75%
- paraesthesiae
- sensory loss (>50%) starting in the feet and
moving proximally
(is helpful in defining the level of the
compression)
- sphincter dysfunction >40%
loss of sphincter function is a bad prognostic
sign
Spinal cord compression
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Diagnosis:
- history
- clinical examination
- neurological examination
- rtg - shows vertebral metastasis / collapse
- MRI is the investigation of choice
- CT with myelography may be helpful if MRI
is not available
Spinal cord compression
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Treatment:
- high-dose steroids and radiation should
be offered to all patients.
Steroids can reduce pain and preserve
neurological function;
initial dosage - 100mg i.v.bolus (usually 2450mg) followed orally
halving of the dose every third day until the
end of radiation
Spinal cord compression
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Treatment:
- surgery is only occasionally indicated
- solitary vertebral metastasis
- neurological symptoms and signs
progress despite radiotherapy and high
dose dexamethason
- vertebral body resection with anterior
spinal stabilization is generally the
operation of choice
Corticosteroids in palliative care
Special indications (Dexamethason 2x8mg
10-14 days):
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superior vena cava syndrome
 lymphadenopathy
 lymphangitis carcinomatosa
 obstruction of a hollow viscus (e.g. Bowel, ureter)
 postradiation inflamatory
 pericarditis exudative
 hypercalcaemia
 hormonal therapy
Corticosteroids in palliative care
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Neuropathic pain
bone pain
neuropathic pain from infiltration or compression
of neural structures
increased intracranial pressure
arthralgia
neuromyopathy
Corticosteroids in palliative care
Other indications:
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anorexia
 cachexia
 difficulty with breathing
 nausea, vomiting
 fever