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Pain is an unpleasant sensation with no specific
stimulus and depends on individual's tolerance.
PHYSIOLOGY:
Transduction ( receptor activation )
It is the conversion of one form of energy, (thermal,
mechanical, or chemical), into a form that is accessible to the brain
(nerve impulse). The exact mechanism is not known, but a number of
mechanical and chemical interactions are known to influence activity
in primary afferent nociceptors at the free nerve endings of
the primary afferent fiber.
These nociceptors can be divided into 1. A-delta 2.
C-fiber
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A-Delta
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C-Fiber
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Myelinated,
Large
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Non-Myelinated,
small
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Respond to mechanical
stimuli and some to thermal also
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Responds to
any noxious stimuli.
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Receptive
fields consist of cluster of small spots
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Receptive
field is a single area rather than clusters
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May be
sensitized
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May be
sensitized.
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Resistant to
local anesthetics but susceptible to pressure
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Susceptible
to local anesthetics
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Inactivated
with higher temp
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Inactivated
at temp 55C
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Responsible
for I pain (early, sharp, brief pain)
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II pain
(dull, prolonged pain)
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These fibers are also responsible for deep pain (muscle
& joints) as well as visceral pain although not much is known
about them.
In addition to noxious stimuli, nociceptor can become
sensitive to variety of chemical factors present after a local
injury.
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Substance
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Source
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Potassium
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Damaged
Cells
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Serotonin
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Platelets
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Bradykinin
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Plasma
Kininogen
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Histamine
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Mast Cells
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Prosloglandins
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Arachidonic
acid ( from damaged cells)
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Substance -
P
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Primary
afferents.
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The size, site stimulated, the frequency with which
stimuli applied and the duration of the stimuli and the chemical
changes at the site will interact to produce the nerve impulse.
Transmission:
Neural impulses thus produced are carried along the
peripheral nerves, nerve roots, spinal cord, brainstem, thalamus and
the cortex that ultimately leads to an awareness of pain.
The majority of primary afferents- project to the spinal
cord through dorsal root. At the ventrolateral aspect of the
dorsal root A-delta and C fibers segregate and enter the spinal
cord. Some may project to the spinal cord through ventral root.
Recent studies suggest, they loop back and enter along
the dorsal root. In the spinal cord, the fibers become part of Lissaur's
tract which is located at the dorsolateral edge of the spinal
cord and divide into ascending and descending branches that extend
for one or two spinal segments.
Spinal cord grey matter is organized into ten laminae
(REX) C-fibers project mainly to I and II laminae and A-delta to
I to V. The neurons in the cord can be divided into projection
neurons (relay to higher centers), excitatory neurons (relay to
projection and other interneurons or to motor neuron that mediate
spinal reflexes) and inhibitory interneurons (contribute to the
control of nociceptive transmission). Laminae I, V, VII, VIII are the
major sources of rostarlly projecting nociceptor neuron. Laminae
II (substantia gelatinosa) make predominantly local connection
that result in important changes in the neuronal activity.
Among Nocicecptive Transmitters involved in the cord,
substance P is well known and found in dense concentration in laminae
I and II and in many dorsal root ganglion cells. Other substances are
somatostatin, vasoactive intestinal polypeptide, glutamate, aspartate
and adenosine triphosphate.
Gate Control Hypothesis suggests
interaction between myelinated and nonmyelinated neurons occurs at
inhibitory interneurons in substantia gelatinosa and at dorsal horn.
The myelinated afferents said to excite inhibitory interneurons and
inhibit pain. The nonmyelinated nociceptors inhibit the inhibitory
interneurons. The perceived intensity is the net effect. Although
current evidence suggest that it is incorrect, transcutaneous
electrical-neuron stimulator (TENS) is developed on this. The major
spinal pathways for pain travels in the anterolateral spinal quadrant
to the thalamus (spinothalamic tract) and crosses over to the
other side 2 or 3 segments above. Certain proportion of pain impulses
can be carried in ipsilateral pathway.
The Spino Thalamic Tract divides into
(a) lateral division which terminates in
posterior nuclear group and ventrobasal nuclei (VPM & VPC). The
major projection is from I & V laminae with receptive field
restricted to one side of the body usually part of a limb
(b) medial division is called paleo spinothalamic
tract and terminate in the central lateral nucleus. The major
projection is from entire body surface.
(c) Spino reticular projection appear to involve
V,VI VII & VIII laminae and have complex receptive fields from
both sides similar to paleo spino thalamic tract.
Thalamic Nuclei project to somoto
sensory of cortex (lateral spino thalamic tract). and limbic and
frontal lobes (medial and reticulo thalamic). SSC (
somato-sensory cortex )is involved in to localization and
identification. Limbic system and frontal lobe responsible for
emotional aspects suffering and anxiety.
Modulation:
The process by which the nervous system modifies the
nociceptor activity is called modulation. The modulatory network is
quite different from sensory system and involves a number of brainstem
regions (periaquenductal grey and immediately adjacent
midbrain, periventricular grey of hypothalamus, the lateral
and dorsolateral pontine tegmentum and rostro ventral
medulla). Stimulation of any of these sites reduce pains and
inhibit nociceptive neurones. Both nor adrenergic and serotonerigc
systems are involved. In addition these produce endogenous opiod
peptides which are at least partially responsible for analgesia. The
opiod peptides are
(1) Enkephalin (most extensively distributed)
(2) B-Endorphrin (most potent)
(3) Dynorphin similiar to enkeplin and less extensively distributed.
This modulatory system project to the spinal cord along
the dorsolateral funiculus. It doesn't work when there is no
pain.
In summary, pain involves a complex interaction.
Modification occurs at the spinal cord with interneurone and
descending modulatory network. Transmission to higher levels occur
through spino thalamic and reticulo thalamic tract to SSC and limbic
system and frontal lobe. The sense of pain is the net result of all
these.
MANAGEMENT:
Acute pain is an alerting or useful pain, signifying
tissue injury from a medically or operatively remediable somatic
cause, often accompanied by signs of autonomic hyperactivity.
Chronic Pain, however persists beyond the period of what
was believed to be curative treatment. The typical pattern involves
about six months of use of serial monotherapies, attempting a 'cure'
but yielding only partial and numerous exacerbations. Patients quickly
develop tranquilizer tolerance and dependence with increasing risk of
organ damage and accelerating chronic pain behavior. The chronic pain
may be cancerous and noncancerous.
Certainly, patients with Cancer Pain will have different
psycho social factors operating. However, approaches applied for the
pain can and should be the same for both types with obvious addition
of appropriate testing to rule out recurrent disease and of more
aggressive neuro surgical ablative techniques for patient with cancer
pain and a limited life expectancy.
1 ) Evaluation of chronic pain:
1. History will usually give a clue to the initial
triggering factor (injury, operation) and site of nociception.
Deafferentation components (, burning pain) can evolve from initial
neuritic dysfunction and present as 'new pain'. Numerical value to
pain or to mark the current severity of the pain on a 10cm line help
in reassessment.
2. Physical exam should include complete survey of
baseline sensory motor, circulatory and skeletal parameters. In
addition, a search for tender scars, region of vascular entrapment
and trigger points should be made.
3. Imaging and electrical studies will help in doubtful
cases.
4.Formal psychological evaluation is often sought in a
multi disciplinary pain management. Psychological tests (Minnesota
multi phasic personality inventory, beck depression scale) help
treatment planning.
2 ) Medications:
Analgesics should be prescribed as round the clock
medication to be effective and decrease the total drug required. Simpler
drugs (aspirin) should be maximized before switching to stronger
alternatives. Adjunctive drugs include those specific for the
etiology (eg., Phenytoin, carbamazepine of trigeminal neuralgia,
NSAID or muscle relaxants for chronic soft tissue and muscle
changes). Pain modulation may be stimulated by tricyclic
antidepressants (amitriptyline or doxepins 100-200mg at bed time).
Patients who require narcotics should be carefully followed up.
Withdrawal should be slow. The narcotics can be abruptly discontinued
and clonidine may help with drawl signs and symptoms if required.
3 ) Non pharmacological techniques:
a. Psychological techniques such as hypnotherapy,
meditation, stress management techniques, relaxation training or bio
feed back will help.
b. Rehabilitation should be included in all treatment
plans. Occupational therapy and vocational rehabilitation may also be
appropriate.
4 ) Neurosurgical intervention:
A survey revealed that only 3 to 10% of the patients
referred to general pain clinics for pain other than that of
malignant disease were treated by invasive neurosurgical intervention
and of this 50% obtained satisfactory relief.
Non specific procedures
are divided into two groups :
1. Stimulation procedures depend on blocking pain
pathways or reversible stimulation of inhibitory pathways and do not
ordinarily result in destruction and hence are reversible.
2. Destructive lesions or ablative procedures
deprive the patient of pain and possibly of other sensations and not
reversible. Decision making involves assessment of the risk to
benefit ratio. Many ablative procedures do not work in the long run
and do not have a place in non malignant chronic pain. Generally, the
higher the lesions, the less likelihood for permanent relief, so that
the most peripheral procedures are considered first. Although
stimulation procedures do not necessarily result in permanent
dysfunction, greater risk is associated with some than with others.
Stimulation procedures:
1. Transcutaneous Stimulation in which a
controlled electrical stimulus to the skin is a popular one with
about 50% success rate regardless of cause of pain and various
battery operated kits are freely available. According to gate theory
when large myelinated fiber activity is increased by non painful
stimulus, the pathway for non-myelinated small fibers transmitting
pain is closed. Rubbing an injured part similarly reduces pain.
2. Peripheral Nerve Stimulation is similar to
above with electrode around the individual peripheral nerve in
neuropathic pains confined to a single nerve.
3. Dorsal Column Stimulation applies a train of
electrical stimuli to the dorsal aspect of the cord by means of an
apparatus that can be controlled by the patient. This attempts to
stimulate the collaterals of the large fibers as they ascend in the
dorsal column, resulting in increasing the rate and inhibits
perception of pain. Percutaneous insertion allows a trial. If there
is satisfactory result, a laminectomy is done and electrodes are
placed in sub dural / sub arachnoid space and connected
subcutaneously to a receiver placed subcutaneously at a convenient
location. Patients control the stimulus by adjusting battery operated
radio transmitter that they carry.
4. Deep Brain Stimulation is an outgrowth of the
above and still an investigational procedure, despite the development
of steretactic procedures. The internal capsule, ventral posterior
nuclear complex are the usual targets. This helps in pain secondary
to cord lesions, thalamic syndrome, or phantom limb pains.
Periventricular or periaqueductal grey is a recent target and related
to endogenous opiate analgesia.
Ablative procedures:
Peripheral Nerve Blockade:
It is of limited value, but easily available, also serve
to test the possible result of permanent denervation.
Posterior Spinal Root Blockade:
Judicious amount of phenol or ethyl alcohol into the
spinal subarachnoid space would damage the adjacent sensory rootlets
sufficiently to block afferent impulses for several months. Subarachnoid
injections are most effective from the low thoracic level. At higher
levels, some prefer extradural injections. Depending on the
concentration and duration of exposure, phenols could cause
reversible or irreversible block. Immediate effect is that of a local
anesthetic. The permanent effects are due to degeneration. Long
acting steroid (Depomedrol) is often used these days along with local
anesthetics especially in chronic pain of radicular origin.
Posterior Rhizotomy:
If the course of pain can be accurately delineated by
segmented boundaries and is limited to few divisions, rhizotomy
should provide permanent relief. Such conditions include traumatic
lesions of peripheral nerves, operations scars, intercostal or
occipital neuralgias. Unfortunately the results are unpredictable
because of wandering root filaments, and segmental overlaps. It is
recommended that at least, 3-5 adjacent roots and dorsal root ganglia
are excised.
Anterolateral cordotomy:
Extremely useful in cancer pain.
Open cordotomy: Usually performed at one
of the two levels, the T3 for pain below midthoracic level and C1-2
for pain above the mid thoracic. Surgical observation show that to
obtain the maximum benefit, it may be necessary to extend the
cordotomy virtually to the midline anteriorly and to include all the
distal segments it is necessary to extend it a millimeter or so
posterior to the attachment of ligamentum denticulatum. Division of
and the traction on the ligamentum denticulatum will usually provide
sufficient access. Division of adjacent posterior root will afford
greater mobility.
Complications:
1. Respiratory Failure: Most likely in those with low
pulmonary efficiency, for variety of reasons. Bilateral procedures at
the same session is likely to prove dangerous. Persistence of
pharmacological respiratory depression due to prolonged pre op
narcotics may be possible cause. It is recommended to stop such drugs
two days before the procedure.
2. Hypotension: Sudden drop in BP is often recorded
immediately after incision in the spinal cord, most severe and
protracted in bilateral procedures. Sympathetic disturbances is
blamed.
3. Disturbed sphincter control and paresis as in any
spinal procedure, especially in bilateral procedure.
4. Dysaesthesiae:
a) Soreness at about these segmental levels of the
cordotomy with girdle distribution. It tends to be temporary.
b) Below the level is often more serious. It is usually
delayed. It emerges on simultaneously with return of sensation and
may take the form of tingling, pins and needles or other sensations.
These abnormal sensations are more likely related to disturbances of
the pattern of ascending impulses.
c) Referred sensation to the opposite side which is
poorly localized, may be due to the disease process and this pain was
not appreciated by the patient because of the intensity of pain in
the area of complaint. This referred pain may warrant bilateral
section.
5. Recurrence: It may be due to insufficient
spinothalamic fibers have been divided but repeat procedure does not
help. Other possibility is the regeneration of fibers. The other
& more likely possibility is the development of alternate
pathways.
Percutaneous cordotomy requires
a cooperative patient and specialized equipments and is recommended
for unilateral pain. It involves physiological localization in an
awake patient and graded radio frequency electrical destruction of
the tract. Complications are less often
Dorsal root entry zone (DREZ) cordotomy:
A destructive lesion is created in the postero lateral
sulcus of the spinal cord at the point of entry of the dorsal roots.
Ideally R. F. lesioning is made under radiographic control. Some
advocate laser lesions. DREZ lesions are designed to destroy regions
of neuronal dysfunction in deafferentation states involving particularly
Lissauer's tract and I,II & V Rex layers. These areas show
increased neuronal activity in experimental deafferentation models.
DREZ lesions help in deafferentation pain such as causalgia, root
avulsions, herpetic neuralgia etc.
Commisural myelotomy:
The spinothalamic fibers can be interrupted as they
cross the ant. commissure by a vertical incision in the median plane.
The result is bilaterally symmetrical area of analgesia. This
procedure is not widely accepted.
Spinothalamic tractomy in the brainstem:
Medullary, pontine, mesencephalic tractomies have been
described. Due to high mortality and morbidity, they never became
popular. Stereo tactic techniques have also been tried. It may have a
role in cancer pain involving the head and neck.
Sympathectomy:
Repeated temporary anesthetic blockade should proceed
symphathectomy - causalgia, sympathetic dystrophy and painful
ischemic states are the main indications. It is also helpful in
visceral Ca. Open sympathtectomy has been replaced with per cutaneous
method using R.F . lesioning, phenol injections and endoscopic
techniques.
A localized type of sympathetic block with
I.V.guanethidine which displaces norepinephrine the neurotransmitter
at the sympathetic nerve endings and occupies the storage sites. When
it is given I.V.. with proximal tourniquet, the storage applied for
about 20 minutes, Guanethidine is fixed to the tissues and it
abolishes sympathetic activity locally.
Phenoxy - Benzamine (adrenergic receptor blocker) is
given orally at frequent intervals for about six weeks and then
tapered off. This reportedly gives equal results.
Stereotaxic
thalamic lesioning:
This involves lesioning thalamic nuclei and hence
disturbs nociception. There is a shift of stereotaxic lesions away
from ventral lateral (specific) nuclei to the ventral posterior
medial and interlaminar (nonspecific) nuclei. Since the introduction
percutaneous cordotomy, the thalamotomies have became rare.
Pituitary destruction:
For pain associated with advanced Ca breast and
prostate, pituitary destruction was once a routine treatment. Open
Hypophysectomy, transphenoidal percutaneous radio frequency
coagulation and other techniques have been reported with about 75%
pain relief. But the relief lasts for only few months. The mechanism
of pain relief is not understood, it may be related to hormones.
Operations on the cortex and subcortex:
The aim is to create lesions deep to secondary sensory
are which severs its links with thalamus. Leucotomy was once
practiced. Stereotactic cingulomotomy and infero medial quadrant
frontal section have proved helpful. All aim to disturb pain
perception.
Conclusion:
Pain may be classified into 'normal' pain and abnormal
pain.
'Normal pain' is due to nociceptive stimuli such as
scar, arachnoiditis, malignant infiltration or any such demonstrable
lesion. When such lesion cannot be treated effectively and
conservative measures have failed, surgical intervention such as
nerve blockade, intrathecal injection, peripheral neurectomy, dorsal
rhizotomy and cordotomy. Unlike others. cordotomy abolishes only pain
sensations and preserve other neural functions.
'Abnormal Pain' include
Hyperalgesia (normal painful stimulus produce abnormally
severe pain),
Allodynia (gentle touch cause intensive pain),
Hyperpathia (pain threshold is increased but once
reached it causes intense pain),
Causalgia (above with features of sympathetic dystrophy
such as shiny skin and tropic changes) are due to abnormal
transmission '(deafferentaion) and DREZ is a popular procedure.
Long standing normal pain may become associated with
abnormal pain, compounding your problem and resulting in failure.
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