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Pain Management |
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Definition
Nociceptive pain is common and arises from damaged
tissues, the pain then mediated by an intact nervous
system.
Neuropathic pain, due to damage to the nervous system
itself, is less common, and much more difficult to
treat, partly because many of its causes are
irreversible and partly because its mechanisms are
different and less well understood.
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Neuropathic
pain
This term embraces all pain due to lesions of the
sensory pathways, both peripheral and central.
The many causes include:
1. damage to peripheral nerves
2. nerve root and spinal cord lesions
3. damage to the thalamic and critical areas in brainstem and cerebral
cortex and subcortex.
Conditions affecting the primary sensory neuron
(including the dorsal root ganglion and dorsal root) are
much more common than the central causes.
Deafferentation
The amount of sensory loss with neuropathic pain is
variable, even within a single diagnostic category and
shows no direct relationship to the severity of the
pain. However, the greater the deafferentation the more
likely it is that central nervous system mechanisms are
important in generating the pain. Secondly, methods of
counterstimulation, such as transcutaneous electrical
nerve stimulation (TENS), are less likely to be
effective if there is significant deafferentation, and
thirdly, any treatment that is likely to increase
already severe deafferentation may make the pain worse.
Clinical
features of neuropathic pain
A focus of damage in peripheral tissues often cannot be
demonstrated. The quality of the pain is outside the
patient's previous experience, making it difficult to
describe. There are often paroxysmal shooting or
shock-like pains in addition to continuous background.
Changes in emotional state and fatigue may cause
intensity to vary over short periods. The onset of
neuropathic pain is often delayed. For example, it is
characteristic for thalamic pain to develop at an
interval of 2 or 3 months following thalamic infarction,
and myelopathic pain may take many months to develop
following spinal cord trauma. Neuropathic pain and
associated hyperalgesia, allodynia (the perception of
pain from a normally non-painful stimulus), and
hyperpathia are not necessarily confined to the
territory of an affected nerve or root but may radiate
widely, indicating secondary central involvement; this
can cause diagnostic difficulty. However, there is often
a clear anatomical correlation of pain and sensory
abnormality, and the presence of sensory loss is
particularly helpful in distinguishing neuropathic from
nociceptive pain.
Associated abnormalities of local or regional
sympathetic activity are common, particularly with
peripheral nerve lesions, but may also occur with root,
cord, or thalamic lesions.
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Pain in peripheral neuropathy
Pain seems to be related to the acuteness of
degenerative change and preferential involvement of
small fibres by the underlying disease, particularly
when there is also marked regenerative activity in the
nerves. In some mononeuropathies there is tenderness at
the site of the nerve lesion which is due to local
inflammation and structural abnormality in the nerve.
This is pain signalled by the nervi nervorum and is thus
nociceptive rather than neuropathic in type.
Ischaemia can be shown to provoke pain and paraesthesiae
in certain situations, for example carpal tunnel
syndrome, and it is likely that ischaemia is a
contributory factor in some neuropathies, for example
diabetic mononeuropathy and the mononeuropathies
associated with connective tissue disease which have a
microangiopathic basis.
Abnormal sympathetic activity is important in
maintaining causalgia. Sympathetic block may relieve
pain and associated allodynia and hyperpathia in
patients with causalgia and other types of
post-traumatic neuralgia, whether or not there are signs
of abnormal sympathetic function in the affected limb.
Some symptoms and signs associated with peripheral nerve
injury implicate secondary changes in the central
nervous system, particularly in dorsal horn cells and
their funtions. These include the almost immediate onset
of pain and associated sensory abnormalities in some
patients (for example, causalgia following gunshot
wounds) which develop before the peripheral
abnormalities have had time to develop. Allodynia,
hyperpathia, and reflex sympathetic changes may all
extend beyond the territory of the affected nerve and
indicate central factors.
These secondary central changes may become irreversible
so that any therapeutic interventions, particularly
peripheral, are bound to have, at best, a limited
effect.
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Reflex sympathetic dystrophy and causalgia
Clinical
features
Reflex sympathetic dystrophy describes a group of
conditions, the common features of which include pain,
allodynia, hyperpathia, sudomotor and vasomotor changes,
and dystrophic changes which may affect both soft
tissues and bone, leading to major loss of function in
the affected limb. When dystrophic changes are marked,
it is sometimes called Sudeck's atrophy. This diagnosis
embraces a number of disorders such as algodystrophy,
post-traumatic osteoporosis, acute atrophy of bone, and
neurovascular dystrophy. The diagnosis is a clinical
one. The condition may be self-limiting and mild, but in
some cases it is relentlessly progressive, leading to a
painful, very sensitive, useless limb. Causalgia means
burning pain, a term commonly used to describe such pain
associated with partial lesions of major limb nerves,
when there is nearly always accompanying allodynia,
hyperpathia, and vasomotor and sudomotor abnormalities,
thus fulfilling the criteria for reflex sympathetic
dystrophy.
Pathogenesis
This is uncertain. The often widely radiating allodynia
and hyperpathia are mediated by large afferent
myelinated fibres and, in many patients, can be
temporarily relieved by sympathetic blockade. According
to the most popular explanation, the initiating painful
cause leads to noxious input to the spinal cord, which,
by an unknown mechanism, leads to reflex sympathetic
activation via sympathetic, preganglionic neurones in
the intermediolateral column of the spinal cord. This
increases sympathetic efferent postganglionic activity
which, again by some undetermined mechanism, is capable
of sensitizing the terminals of undamaged primary
afferent fibres in the periphery, lowering their
threshold to stimulation, leading to an increased
afferent barrage, in this way completing a vicious
circle. Sympathetic block would break the vicious circle
by removing the peripheral sensitization of primary
afferent terminals.
Treatment
Simple analgesia is rarely effective. Strong analgesics,
including opiates, often have only marginal effect.
Sympathetic block may sometimes dramatically relieve
symptoms. If so, a series of blocks combined with
physiotherapy may be sufficient gradually to reverse the
condition. In refractory cases, prolonged analgesia by
epidural local anaesthetic infusions together with
physiotherapy may be successful. There have been no
adequately controlled trials of any treatment of reflex
sympathetic dystrophy, but there are reports of
improvement with systemic corticosteroids, NSAIDs,
calcitonin, antiepileptic drugs, calcium-channel
blockers, and tricyclic antidepressants; in severe cases
none of these may be effective.
Requests for amputation by patients should be resisted
because of the high risk of the development of phantom
limb pain, although there is some evidence that the
incidence of stump and phantom pain may be reduced if
good analgesia can be produced prior to amputation for 2
or 3 days by spinal block and maintained preoperatively
and for a period postoperatively.
All patients suspected of having or developing reflex
sympathetic dystrophy should be urgently referred to a
pain clinic since there is evidence that early treatment
may prevent the development of severe consequences.
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Pain due to central nervous system lesions
The lesions that lead to central neuropathic pain
usually involve the spinothalamic tract or its rostral
thalamoparietal projection. Within the thalamus, lesions
involve the main sensory nuclei, which receive both the
medial lemniscal pathway and part of the spinothalamic
tract.
There is usually accompanying sensory impairment
although loss may be subtle and is often of dissociated
spinothalamic type. There is no clear correlation
between the severity of the pain and the degree of
sensory loss. Pain from spinal cord lesions may be
localized, unilateral, or bilateral, but is often
diffuse and widespread below the level of the lesion. It
is sometimes particularly severe in the perineum. The
pain is usually continuous and may have an aching,
stinging, burning, cramping, or vice-like quality.
Superimposed focal or diffuse paroxysmal pains are
common. Pain is usually unprovoked but may be
exacerbated by movement, fatigue, or emotion.
Vascular lesions in the pons and medulla are the
commonest brainstem lesions leading to pain. Multiple
sclerosis, tumours, syrinx, and tuberculoma are
occasional causes.
Thalamic pain is almost always caused by infarction;
haemorrhage and arteriovenous malformation are
occasional causes and, very rarely, tumours. Therapeutic
surgical lesions in the main thalamic sensory nuclei may
lead to thalamic pain and the naturally occurring
lesions causing pain always produce damage predominantly
in these nuclei, with sparing of the medial and
posterior nuclei.
Cortical and subcortical lesions leading to pain are
extremely rare but vascular lesions, trauma, and tumours
are recorded causes. Pain has also been observed after
hemispherectomy for severe epilepsy with infantile
hemiplegia, or for the treatment of tumour.
Therapeutic considerations
How the many pathophysiological changes to central
nervous system damage interact is uncertain, but the
multiplicity of possible abnormalities may help explain
the great variations between patients in the development
of pain with either peripheral or central nervous system
lesions. Neuroablative treatments advocated in the past
have been unsuccessful and emphasis has now moved
towards stimulation procedures.
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Psychological aspects of pain
Psychological factors are often of great importance in
chronic pain. Individual responses to pain vary
enormously for many reasons, including importantly
personality, domestic and employment considerations,
cultural influences, and all too often the problem of
secondary gain from medical attention or medicolegal
considerations.
Psychiatric factors and chronic pain
Depression is common in patients with chronic pain and
may be an aggressive or even causative factor. Pain is a
common symptom too in patients who present with numerous
somatic symptoms associated with unshakeable conviction
that they have a serious disease (somatization
disorder). Others may be frankly hypochondriacal.
Psychogenic pain may be one manifestation of a number of
underlying problems. Clinicians in pain clinics see many
such patients whose management may need the help of a
psychiatrist.
Multidisciplinary pain clinics best comprise an
anaesthetist, physiotherapist, occupational therapist,
and psychologist, but the availability of others,
particularly a neurologist and a psychiatrist, is
important.
Local measures
Counterstimulation
Regardless of the type of pain, whether nociceptive or
neuropathic, counterstimulation techniques may be
helpful. These simple and effective methods are all too
often neglected in favour of systemic drug treatment.
Some musculoskeletal pains respond to heat, delivered by
a heat pad or radiant heat. Neuropathic pains tend to be
exacerbated by cold but an exception is post-herpetic
neuralgia in which regular application of cold packs for
20 minutes may reduce troublesome allodynia for up to
several hours.
Both nociceptive and neuropathic pains may respond to
vibration and ultrasound, of which vibration is the more
practical long term since it can be used regularly by
the patient at home.
Transcutaneous electrical stimulation (TENS), acting by
segmental inhibition, has been shown to be effective in
a wide range of different chronic pains, but is probably
more effective for neuropathic than nociceptive pains. A
trial period of 2–3 weeks, with the patient
experimenting with different electrode placements, is
essential before concluding that TENS is unhelpful.
Acupuncture probably works by segmental inhibition and
by diffuse noxious inhibitory control. Cerebrospinal
fluid endorphin levels are raised by acupuncture but not
by TENS, and TENS-induced analgesia is not reversed by
naloxone.
Simple lignocaine ointment, although poorly absorbed, is
sometimes helpful in areas of severe allodynia and
hyperpathia, particularly in patients with painful scar
syndromes, tender amputation stumps, and post-herpetic
neuralgia. Local capsaicin (0.075 per cent) may also be
effective in these situations.
Local anaesthetic blocks to peripheral tissues,
peripheral nerves, or roots may be useful in three ways.
First, the origin of a particular pain may be more
accurately defined. Secondly, injection into a
peripheral trigger point, for example in muscle, may
reduce widely radiating pain and offer effective
treatment with one or a series of injections; and
thirdly, in the case of neuropathic pain due to
peripheral nerve or root lesions, failure to relieve all
the pain with an adequate peripheral nerve or root block
indicates an element of secondary central pain, which
will be less amenable to peripheral measures. There is
some evidence that lesions including trigger points in
muscle, painful scars, and peripheral nerve lesions such
as neuromas may respond better to a combination of local
anaesthetic and corticosteroid.
Epidural injection of a local anaesthetic, with or
without an opiate, can produce analgesia over a wide
area. In relief of chronic pain, single or repeated
epidural injections may have a partial, lasting effect
in some patients. The use of highly lipid-soluble
opiates such as fentanyl ensures rapid local absorption
into neural tissue in the region, producing good
analgesia, with less risk of drug spread. Low back pain
with root pain not amenable to surgery, arachnoiditis,
and brachalgia with neck pain may respond well to such
treatment.
A further treatment of pain of non-malignant origin is
the epidural infusion of a local anaesthetic and an
opiate over periods of 2–3 weeks. In some patients this
may produce a degree of long-lasting or even permanent
pain relief.
A variable degree of motor block is produced by epidural
analgesia, together with loss of bladder and bowel
control, although it is usually possible to titrate the
amount of drug used to produce localized unilateral
sensory blockade which causes minimal motor deficit and
spares sphincter function. Epidural or intrathecal
infusion of opiate over long periods has proved useful
in the management of pelvic pain due to cancer.
Injection of very low concentrations of morphine into
the third ventricle may produce profound analgesia,
associated with a low risk of respiratory depression.
This procedure has been advocated for the relief of
bilateral pain due to cancer affecting the neck and
skull base.
Sympathetic blocks
Intravenous injection of phentolamine has some value in
indicating which patients have sympathetically
maintained pain and in predicting the response to other
types of sympathetic block, either local anaesthetic
block of cervical and lumbar sympathetic ganglia or
intravenous regional guanethidine block. For
sympathetically maintained pain associated with
peripheral nerve lesions, there is sometimes a
cumulative analgesic effect from a series of such
blocks. The results of permanent sympathectomy, produced
either surgically or chemically with phenol, are often
disappointing. For these reasons, repeated temporary
sympathetic blocks are preferable.
Systemic drugs
Analgesics are the mainstay of drug treatment. They
should be given regularly, if possible by mouth.
Paracetamol, aspirin, NSAIDs, weak opiates (e.g.
codeine, dihydrocodeine, dextropropoxyphene) partial
opiate agents (e.g. buprenophine) mixed
agonist/antagonist drugs (e.g. pentazocrine) and strong
opiates may be very efficacious in nociceptive pain, but
less so for those of neuropathic origin. In pain due to
cancer recourse to opiates is often necessary.
Psychotropic drugs: antidepressants,
minor tranquillizers, and neuroleptic drugs
In addition to true antidepressive effects which
may be useful, tricyclic agents enhance the bulbospinal
5-HT mediated analgesic pathway to the dorsal horn. An
analgesic effect of amitriptyline has been shown in some
neuropathic pains, notably post-herpetic neuralgia, but
zimoldine, which has greater serotoninergic effect than
amitriptyline, is less effective, and the newer,
serotonin re-uptake inhibitor drugs have not been shown
to be superior to amitriptyline in their analgesic
effect.
Benzodiazepines may be helpful for short-term relief of
anxiety and of muscle spasm, but sedation, dysphoria,
dependence, and severe withdrawal effects in some
patients limit their use.
Neuroleptic drugs have often been advocated for the
treatment of neuropathic pains but, in the absence of
clear evidence of useful effect in controlled studies,
these drugs are best avoided. An exception is
chlorprothixene, which is occasionally helpful in a
variety of neuropathic pains and which does not produce
extrapyramidal effects at the doses used (up to 45
mg/day).
Antiepileptic drugs have no effect in nociceptive pains.
With the exception of the specific effect of
carbamazepine in trigeminal neuralgia, antiepileptic
drugs are also disappointingly ineffective in
neuropathic pains. Although claims have been made for
carbamazepine, phenytoin, valproate, and clonazepam in a
variety of neuropathic pains, positive results have only
emerged from poorly controlled short-term trials.
Membrane-stabilizing drugs
Intravenous infusions of lignocaine at doses as small as
1 mg/kg have been shown to reduce neuropathic pain and
associated allodynia and hyperpathia, but this is not a
practical long-term treatment. Mexiletine, which can be
taken orally has been shown to have a short-term
analgesic effect in painful diabetic peripheral
neuropathy, but long-term treatment in this and other
neuropathies has no demonstrable analgesic effect.
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Role of surgery in the treatment of chronic pain
The indications for surgical treatment for chronic pain
are now few. A variety of approaches have limited
application. These include peripheral neurolysis,
rhizotomy, specific lesions to the dorsal root-entry
zone, antrolateral cordotomy, thalamotomy, or even
leucotomy.
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Rehabilitation
The importance of rehabilitation for patients with
chronic pain cannot be overemphasized. For many, their
pain has been the major focus of their lives for long
periods and the effects far reaching in terms of
limitation of work and other activities and impact on
personal relationships. Detailed discussion of
rehabilitation is beyond the scope of this chapter, but
one point is worth emphasizing. When any pain-relieving
procedure, however temporary, is successful, it is
essential that the use of the affected painful part
begins immediately. Thus, with sensory or sympathetic
blocks, the physiotherapist should be present to start
passive and active movements straight away. Analgesia
alone is insufficient to regain function and unless
strenuous immediate efforts are made, rehabilitation is
likely to fail.
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