Chronic pain syndromes, CRPS, LS radiculopathy, Neuralgia, Cancer pain,Low back ache

1. CHRONIC PAIN SYNDROMES :
LBA,
SCIATICA,
CRPS,
Trigeminal neuralgia,
Cancer pain.
Dr Aftab Hussain

2. What is Pain?
 International Association for the Study of Pain (IASP)
defines pain as
An unpleasant sensory and emotional
experience associated with actual or
potential tissue damage, or described in
terms of such damage
 The Joint Commission on Accreditation of Healthcare
Organisation adopted pain as “the fifth vital sign”

3.  ACUTE v/s CHRONIC PAIN
Acute Pain Chronic Pain
Recent onset; usual
duration 0-7 days
Persisting > 3 months with less
sudden and defined onset
Cause usually known;
usually a definable event
More often leads to anxiety
and persuit of remedy
Pain usually subsides as
healing progresses
May or may not be the result of
tissue damage
More often leads to depression and
other behavioral changes
Pain persists, becoming a
disease unto itself

4. COMMON FORMS OF CHRONIC PAIN
 Musculoskeletal disorders
 Chronic visceral disorders
 Lesions of peripheral nerves, nerve roots, or dorsal
root ganglia (including diabetic neuropathy, causalgia,
phantom limb pain, and postherpetic neuralgia)
 Lesions of the central nervous system (stroke, spinal
cord injury, and multiple sclerosis), and cancer pain.

5. TYPES
 The pain of most musculoskeletal disorders (eg,
rheumatoid arthritis and osteoarthritis) is primarily
nociceptive.
 Pain associated with peripheral or central neural
disorders is primarily neuropathic.
 The pain associated with some disorders, eg, cancer
and chronic back pain (particularly after surgery), is
often mixed.

6. Dimensions of Chronic Pain
Loneliness Hostility
Social Factors
Anxiety Depression
Psychological Factors
Pathological
Process
Physical Factors
A.G. Lipman, Cancer Nursing, 2:39, 1980

7. LOW BACK PAIN
and
SCIATICA

8. Low Back Pain: Epidemiology
 60%–90% lifetime prevalence
 Second most common complaint to prompt a medical
evaluation
 Leading cause of long-term work disability
 Disability and costs are related to pain, not to the disease
process

9.  90 % of cases of LBP resolve without treatment within
6-12 weeks
 40-50 % LBP cases resolve without treatment in 1 week
 75 % of cases with nerve root involvement can resolve in 6
months
 LBP and lumbar surgery are:
 2nd and 3rd highest reasons for physician visits
 5th leading cause for hospitalization
 3rd leading cause for surgery

10. Causes of Low Back Pain
 Lumbar “strain” or “sprain” – 70%
 Degenerative changes – 10%
 Herniated disk – 4%
 Osteoporosis compression fractures – 4%
 Spinal stenosis – 3%
 Spondylolisthesis – 2%
 Myofascial pain- frequency not defined.

11.  Spondylolysis, diskogenic low back pain or other
instability – 2%
 Traumatic fracture - <1%
 Cancer – 0.7%
 Inflammatory arthritis – 0.3%
 Infections – 0.01%

12. Red Flags
 History of cancer
 Unexplained weight
loss
 Intravenous drug use
 Prolonged use of
corticosteroids
 Older age
• Major Trauma
• Osteoporosis
• Fever
• Back pain at rest or
at night
• Bowel or bladder
dysfunction

13. PATHOPHYSIOLOGY
3 compartment theory
 ANTERIOR- bounded by ALL & PLL.
 ALL stronger than PLL- broad and strong.
 PLL is intact throughout length of spinal column.
 From L1 it becomes progressively narrower until at
L5-S1.
 This inherent weakness is the point of greatest static &
kinetic strain.

14.  MIDDLE-
 Neuraxial compartment.
 Contains structures within bony & ligamentous
boundaries of spinal canal.
 Includes PLL, epidural space, meninges, spinal cord,
dorsal & ventral nerve roots, root sleeves and
ligamentum flavum.

15. Anatomy of Lumbar spine

16.  POSTERIOR-
 Contains facet joints, laminae, vertebral arches.
 Innervated by dorsal rami of the spinal nerves.
 LIGAMENTUM FLAVUM connecting the laminae can
contribute to spinal stenosis by folding inward during
UPRIGHT posture, EXTENSION of the back and
through HYPERTROPHY.

18. INTERVERTEBRAL DISC
 Inner 2/3- Nucleus pulposus (proteoglycan
matrix)
 Outer 1/3- Annulus fibrosus (fibrocartilaginous
ring)
 Aging : no. of viable cells decreased.
 Necrosis : 2% in infancy to 50% in young to
80% in elderly.
 Water content : Disc tends to dehydrate to 70%.
 When overstressed disc protrude along the path
of least resistance i.e. posterolaterally.

19. Other proposed theories
 Immune mediated theory
 Theory of oxidative stress
SMOKING
 Affects the vasculature of the disc.
 Causes reduction of solute exchange capacity, cellular
uptake and metabolism within the disc.

20. Herniated Disc
 Herniation of the nucleus pulposus through the annulus
fibrosis.
 Radicular symptoms due to compression and stretching of
the nerve roots exiting through the adjoining intervertebral
foramen.
 In more than 95% of cases, either L4-5or L5-S1 disc is
affected. The straight-leg raising test is highly suggestive of
disc herniation, although relatively nonspecific.

21. Disc Herniation vs Extrusion

23. Discogenic Pain
 Degenerative disc disease is a leading cause of LBP.
 Patients often present with deep, aching, axial midline
pain that may extend into the buttock, hip, groin or even in
the lower limb.
 Pain often gets exacerbated by prolonged sitting, standing
or bending forwards.
 Common in those with frequent motion of the spine i.e.
package handlers, truck drivers, jackhammer operators.

24. Spinal canal Stenosis
 “spinal Stenosis” refer to central canal narrowing, lateral
recess narrowing or foraminal narrowing.
 The typical presentation of spinal stenosis is an elderly
person with axial low back and leg pain (bilateral).
 The pain is more severe when walking downhill as such
activities cause extension of spine leading to further
narrowing of spinal canal.
 Patients are often seen bending forwards to obtain pain
relief.

25. Myofascial Pain
 Myofascial LBP often presents as deep aching pain
that is aggravated by activity and position changes.
 It may be localized to the low back or radiate into the
buttock, sacrum, thigh, abdominal wall or even calf
muscles, depending on the affected muscles.
 On physical examination, a tender, taut band of muscle
may be noted (trigger point) that when palpated results
in a characteristic local twitch response.

26.  Various physiotherapy techniques (spray and
stretch technique, massage) are used initially for
relieving myofascial pain.
 Injection of local anaesthetic with or without
steroids into the trigger points may be helpful.
 A recent trial has demonstrated that the injections
with botulinium toxin type-A is an effective
treatment in patients with chronic LBP.

27. What are the symptoms 0f
LBA?
 The main symptom is pain that shoots down one or
both legs.
 Numbness or tingling in the legs.
 Sometimes the muscles are weak.
 Rarely, there is a loss of bowel or bladder control.

28. Pathological Examination:
Straight-leg raise (SLR):
Elevation of lower extremity, seated or
standing, resulting in neural tension at
S1 nerve root with extremity pain.

29. Occupational Risk Factors:
 Low job satisfaction
 Monotonous or repetitious work
 Educational level
 Adverse employer-employee relations
 Recent employment
 Frequent lifting
 Especially exceeding 25 pounds
 Utilization of poor body mechanics in technique

30. DIAGNOSTIC TOOLS
 1. Laboratory:
• Performed primarily to screen for other disease etiologies
 Infection
 Cancer
 Spondyloarthropathies
• Specifics:
 WBC
 ESR or CRP
 HLA-B27
 Tumor markers: Kidney Breast Lung Thyroid Prostate

31.  2. Radiographs:
 Usually 3 views adequate with obliques only if
equivocal findings
 Indications:
 History of trauma with continued pain
 Less than 20 years or greater than 55 years with severe or
persistent pain
 Noted spinal deformity on exam
 Signs / symptoms suggestive of spondyloarthropathy
 Suspicion for infection or tumor

32.  3. EMG / NCV ( Electrodiagnostics):
 Can demonstrate radiculopathy or peripheral nerve
entrapment, but may not be positive in the extremities for the
first 3-6 weeks and paraspinals for the first 2 weeks
 Would not be appropriate in clinically obvious radiculopathy
 4. Bone scan:
 Very sensitive but nonspecific
 Useful for:
 Malignancy screening
 Detection for early infection
 Detection for early or occult fracture

33.  5. Myelogram:
 Procedure of injecting contrast material into the spinal
canal with imaging via plain radiographs versus CT
 Gold standard for evaluation of the spinal canal and
neurological compression
 With potential complications, as well as advent of MRI and
CT, is less utilized.
 6. CT:
 Best for bony changes of spinal or foraminal stenosis
 Also best for bony detail to determine:
 Fracture
 Degenerative joint diseases
 Malignancy

34.  7. CT with myelogram:
 Can demonstrate much better anatomical detail than
myelogram alone
 Utilized for:
 Demonstrating anatomical detail in multi-
level disease in pre-operative state
 Determining nerve root compression etiology
of disc versus osteophyte
 Surgical screening tool if equivocal MRI or CT

35.  8. Discography (Diagnostic disc injection):
 Less utilized as initial diagnostic tool due to high incidence of
false positives as well as advent of MRI
 Utilizations:
 Diagnose internal disc derangement with normal
MRI / myelogram
 Determine symptomatic level in multi-level
disease
Criteria for response:
 Volume of contrast material accepted by the disc,
within normal of 0.5 to 1.5 cc
 Resistance of disc to injection
 Production of pain---MOST SIGNIFICANT

36.  9. MRI:
• Best diagnostic tool for:
 Soft tissue abnormalities:
• Infection
• Bone marrow changes
• Spinal canal and neural foraminal contents
 Benign vs. malignant compression fractures
 Osteomyelitis evaluation
 Evaluation with prior spinal surgery
 Done if pain > 6 weeks
 Has essentially replaced CT and myelograms for initial
evaluations.

37.  MRI with Gadolinium contrast:
 Gadolinium is contrast material allowing enhancement of
intrathecal nerve roots
 Utilization:
 Assessment of post-operative spine---most
frequent use
 Identifying tumors / infection within /
surrounding spinal cord

38.  10. Psychological tools:
 Includes:
• Pain Assessment Report, which combines:
 McGill Pain Questionnaire
 Mooney Pain Drawing Test
• Middlesex Hospital Questionnaire
• Cornell Medical Index
• Eysenck Personality Inventory

40. What is sciatica?
 Sciatica is a form of low back pain that runs down
one or both legs, causing pain, numbness or
tingling in the leg.

41. How does it occur?
 The sciatic nerve is formed from a group of nerves
that leave the spine and run down the leg.
 Anything that causes irritation along the course of
the nerve can cause sciatica.

42. COMMON CAUSES
 Overuse of back
 injury to back
 Overuse or injury can cause muscle tension or
spasm, back sprains, ligament or muscle tears
 Joint problems irritating the sciatic nerve.
 Infections, tumors, a ruptured disk, osteoporosis,
spondylosis
 Spinal stenosis

43. How is it treated?
 Most people with low back pain and sciatica get better
no matter what they do.
 Often, medicines for pain and inflammation, such as
ibuprofen and naproxen, can ease the pain.
 Ice massage or deep heat may help.
 Physical therapy sometimes helps back pain that doesn't
get better with the usual medicines.

44. Treatment
 Medications
 NSAIDS
 Membrane stabilizers
 TCA
 re-establish sleep patterns
 reduce radicular dysesthesias
 Muscle relaxants:
 re-establish sleep patterns
 more useful in myofascial/muscular pain
 Narcotics: rarely indicated
 Steroids: more useful for radiculitis
 Non-narcotic analgesics

45. ROLE OF STEROIDS
 Corticosteroids around nerve roots can reduce
inflammatory oedema, with improvement of
microcirculation.
 Ectopic discharges from an injured nerve root are
inhibited due to its membrane stabilizing effect.
 The pro inflammatory action of phospholipase-A2
(released from injured disc) is also inhibited by
epidural steroids.

46. Physical therapy
• electrical stimulation/TENS
• Postural education / body mechanics
• Massage / mobilization / myofascial
release
• Stretching / body work
• Exercise / strengthening
• Traction

47. COMMON INTERVENTIONS:
 Trigger point injection.
 Traditional epidural steroid injection.
 Transforaminal epidural injection.
 Facet joint intra-articular block.
 Steroids act against infammation and reduce
edema.
 Addition of hyaluronidase into epidural injectate
improves the spread of local anaesthetic and
steroid.

48. Epidural injection
Midline Interlaminar L5-S1

49. USUAL PROTOCOL FOLLOWED
 STEP 1 : Epidurography
 STEP 2 : 80 mg methyl prednisolone + 1500 units of
hyalase in 5 ml saline
 STEP 3 : Adhesiolysis via percutaneous catheter
 STEP 4 : Foraminal block given

50. Parasagittal Interlaminar

51. Transforaminal Approach
L5-S1 Transforaminal

52. Facet Joint Interventions
 Intra-articular injections
 Medial branch block
 Radiofrequency ablation

53.  Facet Joint Interventions
Lumbar

54. Radiofrequency ablation
 Alternating electric field with oscillating frequency
5,00,000 Hz.
 Heat produced : Hottest part near the tip.
 0.5 mA : 0.25 V MINIMUM ---> Discharge.
 Cannula placed within 3 mm of nerve.
 RFG 3 C PLUS , RADIONICS USA.
 Adequate lesioning : 90 degrees C × 60 – 120 secs.
 Myelinated fibres more resistant.

55. Radiofrequency Vs Chemical Neurolysis
 Lesion size controlled.
 Good monitoring of lesion temperature.
 Good placement of electrode facilitated by electrical
stimulation.
 Performed ↓ LA with sedation.
 Rapid recovery & low morbidity.
 Ability to repeat radiofrequency if neural pathway
regenerates.
 Ability to utilize same cannula for different spinal
lesions.

56. PULSED RADIOFREQUENCY
 Better ---> No temp rise > 42 degrees C.
 Total voltage applied 25 – 35 V.
 Frequency 300 Hz × 30 ms out of a cycle.
 Action similar to TENS.

57. MINIMALLY INVASIVE INTERVENTIONS
 EPIDURAL NEUROPLASTY or EPIDURAL
ADHESIOLYSIS with steroid, LA, hypertonic
saline and hyaluronidase.
 EPIDUROSCOPY / SPINAL CANAL
ENDOSCOPY using a fiberoptic light source
and flexible fiberoptic catheter.

58.  PERCUTANEOUS RADIOFREQUENCY
DENERVATION of segmental spinal nerves by
applying heat to denature the nerves that innervate painful
facet joints.
 PERCUTANEOUS DISC DECOMPRESSION
USING NUCLEOPLASTY
Co ablation technique used with thermal treatment and
tissue removal.

59.  PERCUTANEOUS LASER DISC DECOMPRESSION
(PLDD)
Using Nd:YAG laser to “vaporise” a small portion of
the nucleus pulposus.
 INTRADISCAL ELECTROTHERMAL THERAPY
(IDET)
Catheter with an electrode passed into
nucleus pulposus
↓
Heat applied to shrink collagen at a target temp of 65 – 75
degrees C

60. SPINAL CORD STIMULATION
 Electrodes passed into the posterior epidural space for
electrical stimulation of the spinal cord.
 Approved by FDA .
 SCS has become a standard treatment for patients with
chronic pain in back or limbs who are not relieved from
other treatment.

61. INTRATHECAL PAIN PUMPS
INTRA THECAL DRUG DELIVERY
 Through a catheter and pump to treat intractable pain
both nociceptive and neuropathic.
 Indicated when opioid requirements are high enough to
cause side effects.
 A/K/A INTRA THECAL POLYANALGESIA.

62. Intrathecal Pain Pumps
 Size of a pacemaker .
 Has access- pump usually has
to be refilled as early as every 3
months- medication can be
reconstituted when refilled –
morphine, baclofen,
bupivicaine, clonidine.
 Pain pump is inserted under the
skin;usually in abdomen/
catheter is threaded into the
intrathecal space for continuous
delivery.

63. PERCUTANEOUS VERTEBROPLASTY
 t/t of osteoporotic body compression #.
 Utilizes bone cement ( PMMA ), tobramycin and
barium powder as non ionic contrast applied
through a special needle under fluoroscopy.
 It provides vertebral solidification.
PERCUTANEOUS KYPHOPLASTY
 Inflatable balloon applied inside collapsed
vertebral body.

64. Kyphoplasty/Vertebroplasty

65. Kyphoplasty/Vertebroplasty
 How it works – helps with
axial load, cement is very hot
and theory is that
intraosseous nerve endings
are burned and that helps
with pain relief – usually
immediate

66.  SURGERIES as laminectomy, micro discectomy,
foramenotomy and spinal fusion considered:
1) Failure to respond to conservative mgt >3months
2) Profound / progressive neurological deficit
2) Recurring episodes of intactable sciatica involving same
segment – to avoid cumulative disability of repeated
events.

67. How can we help prevent sciatica?
 Avoid lifting heavy weight.
 Avoid frequent bending or other activities that make the pain
worse.
 Lose weight .
 Do regular aerobic exercise to keep your back and
abdominal muscles in shape
(this can be as simple as walking),
 Learn to lift properly.
Bend your knees and hips and keep your back straight when
you lift a heavy object.

68. Complex Regional Pain Syndrome

69. Complex Regional Pain Sydrome I (RSD)
 History of initiating injury or immobilization
 Continuing pain, allodynia, or hyperalgesia out of
proportion to the initiating event
 Evidence at some time of edema, changes in skin blood
flow or abnormal pseudomotor activity in the painful area
 No other cause of the pain exists

70. Complex Regional Pain Syndrome II
(causalgia)
 Differs from CRPS I by the presence of a known nerve
injury
 Devastating injury has occurred, which by definition has
caused a major nerve injury .
 The burning pain is often of extreme severity
 Often, there is also significant vascular compromise.

71. Causes
• Injuries to peripheral tissues (e.g., fractures, dislocations, and
postoperative
State)
• Inflammatory conditions (e.g., fasciitis, tendonitis, bursitis, and
arthritis)
• Immobilization as a result of injury or cast application
• Peripheral nerve injury resulting from direct compression or
ischemia (e.g.,
brachial plexopathy, postherpetic neuralgia, and nerve root injury)
• Central nervous system insults (e.g., head injury, ischemia, and
brain tumor)
• Spinal cord lesions
• Idiopathic

72. DEVELOPMENT OF CRPS
• Abnormal discharges in sympathetic and nociceptive
afferents produced by trauma
• Sensitization of peripheral sensory receptors produced
by sympathetic
hyperactivity
• Formation of ephapses (artificial synapses) after
peripheral nerve injury
• Spontaneous neuronal ectopy at the site of
demyelination or axonal injury
• Central reorganization of pain processing

73. Pathophysiologic Mechanisms of
CPRS
• Sensory abnormalities
• Autonomic dysfunction
• Neurogenic inflammation
• Motor abnormalities

74. Sensory Abnormalities in
CRPS
 Dysesthesia / hyperalgesia throughout the affected
half of the body.
 Increased thresholds to mechanical and thermal
stimuli on the affected side.
 Due to changes in the thalamus and cortex.
 PET studies have demonstrated adaptive changes in
the thalamus.

75. Autonomic Dysfunction
 About 85% of CRPS report pain relief after
sympathetic interruption; however, the pain relief is
temporary in the majority of patients
 Catecholamines can activate peripheral nociceptors
after thermal or chemical sensitization in the absence
of nerve injury
 After nerve injury, surviving cutaneous afferents
develop noradrenergic sensitivity.
 Hyperhydrosis

76. Early phase
Skin temperature and perfusion high
Norepinephrine levels low
Intermediate phase
Temperature and perfusion either warmer or
colder, depending on the level of sympathetic
activity
Late phase
Skin temperature and perfusion low
Norepinephrine levels low
Skin lactate increased

77. Neurogenic Inflammation
• Extensive plasma extravasation in patients with
acute CRPS
• Increased joint effusions, protein and synovial
hypervascularity
• Increased systemic CGRP in the acute phase
• Increased tissue levels of TNFα and IL-6
• Increased production of nitric oxide from
peripheral monocytes .

78. Motor Abnormalities
• About 50% of CRPS patients develop
– Decreased range of motion
– Physiological tremor
– Reduction in active motor force
• About 10% of CRPS patients develop
dystonia in the affected extremity.

79. STAGING OF CRPS

80. Stage I
• Severe pain limited to the site of injury
• Hyperesthesia
• Localized swelling
• Muscle cramps
• Stiffness and limited mobility
At onset, skin is usually warm, red, and dry; then may
change to blue (cyanotic).
• Increased sweating (hyperhydrosis).

81. Stage II
• Severe and more diffuse pain.
• Swelling tends to spread and it may change from a
soft to hard (brawny) type.
• Hair may become coarse then scant, nails may
grow faster and become brittle, cracked, and heavily
grooved.
• Osteoporosis
• Muscle wasting

82. Stage III
• Marked wasting of tissue (atrophic) eventually
becomes irreversible.
• For many patients, the pain becomes intractable
and may involve the entire limb.
•A small percentage of patients have developed
generalized reflex sympathetic
dystrophy (RSD), affecting the entire body.

83. Complex Regional Pain Syndrome and the Sympathetic
Nervous System
 Interactions between sympathetic fibers and sensory
fibers in the dorsal root ganglion
 Sensitization of dorsal horn cells secondary to
activation of afferent fibers by sympathetic efferent
actions.

84. Role of psychological factors?
 Sufferers may become seriously affected psychologically,
and sometimes show features of major depression.
(as expected in anyone who is in constant pain, who may
have lost their job and had their family and social life
shattered).

85. Pharmacologic Management
 WHO Ladder
 Non-opioid therapy / Co-analgesics
 Opioids

87. Modified WHO Analgesic Ladder
Proposed
4th Step
Pain
Step 1
Nonopioid
 Adjuvant
Pain persisting or increasing
Step 2
Opioid for mild to moderate pain
Nonopioid  Adjuvant
Pain persisting or increasing
Pain persisting or increasing
Step 3
Opioid for moderate to severe pain
Nonopioid Adjuvant
Invasive treatments
Opioid Delivery
Quality of Life

88. Adjuvants
Antidepressants
 TCAs for neuropathic
pain
Anticonvulsants
Corticosteroids
Neuroleptics
Alpha2 – agonists
 Benzodiazepines
 Antispasmodics
 Muscle relaxants
 NMDA-blockers
 Systemic local
anesthetics

89. Non-Pharmacologic Management
 Exercise programs
 Hypnosis
 Counseling
 Music
 Acupuncture
 Yoga
 Cold/heat
 Massage
 Vibration
 TENS units

90. Stellate ganglion block
 The preganglionic sympathetic outflow to the
upper extrimity is derived from T2-T9.
 These fibres synapse with the postganglionic
neurons in the stellate ganglion.
 Therefore stellate ganglion block interrupts the
sympathetic outflow to the upper extremity.

91. Dye spread
around stellate
ganglion
Stellate ganglion block

92. Signs of successful stellate ganglion block
 Eye: - ptosis, narrowing of palpebral fissure,
miosis,lacrimation.
 Face and neck:- anhidrosis, elevated local temp and nasal
stuffiness
 Plethysmographic evidence of improved cutaneous blood
flow.

93. Intravenous regional
blockade.
 Intracath is inserted into a
peripheral vein.
 The limb is then isolated from
the circulation for 20 min using
a sphygmomanometer cuff
inflated to supra-systolic level.
 Guanethidine or another
sympatholytic drug is then
injected through the needle.
 The procedure is often painful,
and the drug is therefore usually
combined with local
anaesthetic.

94. TRIGEMINAL NEURALGIA

95. TRIGEMINAL NEURALGIA
 Trigeminal neuralgia (TN), tic douloureux[
(also known as prosopalgia, the Suicide Disease
or Fothergill's disease is a neuropathic disorder
characterized by episodes of intense pain in the
face, originating from the trigeminal nerve.
 It has been described as among the most painful
conditions known.
 1 in 15,000 people suffer from TN

96.  TN symptoms usually appears after the age of 40,. It is
more common in females than males.
 The trigeminal nerve is a paired cranial nerve that has
three major branches: the ophthalmic nerve (V1), the
maxillary nerve (V2), and the mandibular nerve (V3).
One, two, or all three branches of the nerve may be
affected. 10-12% of cases are bilateral.

97. SIGNS AND SYMPTOMPS
 The disorder is characterized by episodes of intense
facial pain that last from a few seconds to several
minutes or hours. The episodes of intense pain may
occur paroxysmally.
 A trigger area on the face so sensitive that touching
or even air currents can trigger an episode.
 It affects lifestyle as it can be triggered by common
activities such as eating, talking, shaving and
brushing teeth

98.  Wind, high pitched sounds, loud noises such as
concerts or crowds, chewing, and talking can
aggravate the condition in many patients.
The attacks are said by those affected to feel like
stabbing electric shocks, burning, pressing,
crushing, exploding or shooting pain that becomes
intractable.

99. ETIOLOGY
Nerve compression at the opening from the inside to the
outside of the skull;
An enlarged blood vessel - possibly the superior
cerebellar artery - compressing or throbbing against the
microvasculature of the trigeminal nerve near its
connection with the pons. Such a compression can injure
the nerve's protective myelin sheath and cause erratic
and hyperactive functioning of the nerve

100. MANAGEMENT
Pharmacological
 The anticonvulsants carbamazepine is the first line
treatment; second line medications include baclofen,
lamotrigine, oxcarbazepine, phenytoin, gabapentin, and
sodium valproate.
 Low doses of some antidepressants such as amitriptyline
are thought to be effective in treating neuropathic pain.
Surgical
 Microvascular decompression appears to result in the
longest pain relief.

101. Percutaneous procedure
 Percutaneous radiofrequency trigeminal gangliolysis.
(PRTG)
 Percutaneous retrogasserian glycerol/phenol
rhizotomy.
 Percutaneous baloon microcompression.
Percutaneous radiofrequency thermorhizotomy may also be
effective as may gamma knife radio surgery .

102. CANCER PAIN
 30% patients with cancer have pain at the time of
diagnosis.
 85% of patients with cancer have pain in advanced
stages.
 36% patients of people have pain sufficient enough to
cause functional disability.

103. COMPONENTS OF CANCER PAIN
 SENSORY
 AFFECTIVE
 PSYCHOLOGICAL

104. ETIOLOGY
 Presence and progression of the tumor itself.
 Indirect effect of the tumor i.e. metabolic ,
infective, venous or lymphatic obstruction.
 Consequence of cancer treatment i.e.
chemotherapy, radiotherapy and surgery.
 Unrelated mechanisms like migraine or myofascial
pain.

105. PAIN ASSESSMENT IN CANCER
 Step wise approach
 History, examination and data collection ending with
clinical diagnosis.
 Assessment involves features of pain like location,
intensity, quality, timings, exacerbating and relieving
factors and response to previous analgesia.
 Psychological status of the patient.
 Associated co-morbidities.

106. Management
 Removing source of pain by surgery , chemotherapy,
radiotherapy or other form of treatments.
 Over the counter prescriptions (NSAIDs, Aspirin) or
strong opioid medications. (Oral, I.V., patches)
Patient controlled analgesia
 Intravenous PCA is very advantageous for patient with
chronic cancer pain .
 It allows to self administer medication and find their own
comfort zone between the side effects and pain control
within limits set by the physician.

107. The PCA device is a computerised
programmable lightweight battery operated
portable pump with the capability of storage
and retrieval of data by a microprocessor.

108.  3 modes of delivery
1. Continous per hour rate infusion.
2. Continous with boluses for breakthrough pain
3. Boluses with lock out time in mins set by the
physician.
 PCA can also be provided by the subcutaneous,
epidural or intrathecal route.
 Apart from various medical complication, another
aspect limiting the widespread use of PCA is its
cost.

109. Nerve blocks and interventions in cancer pain
 Coeliac plexus block using Phenol/alcohol is especially
helpful in Pancreatic cancer and and upper GI tumor pain.
 Stellate ganglion block in head and arm cancers.
 Lumbar sympathectomy in lower limb cancers.
 Intercostal nerve blocks in pathological fracture of ribs.
 Ganglion Impar block for Vulval cancer.
 Procedure is carried under C-arm guidance.
 In bony metastasis strengthening of bone is done by
kyphoplasty and vertebroplasty.
 TENS have also being utilized for pain relief albeit
temporarily.
 Intrathecal pumps for drug delivery.
 Percutaneous cordotomy has been succesfully used for
unilateral pain arising out of cancer pain in mesothelioma

110. Coeliac Plexus Block
Crescent shaped dye spread
around coeliac plexus

111. Pain insists upon being attended to
--- C S Lewis
THANKS