1. BACK PAIN A Pain Specialist's Perspective

2. INTERVENTIONAL PAIN MANAGEMENT
DR J KURIAN MD MRCP FRCA FFPM
CONSULTANT
ANAESTHESIA AND PAIN MEDICINE

3. Background
Neurosurgical ablative treatments for pain since 19th century but now infrequently used
Ablation eclipsed by percutaneous injections or therapies that target central or peripheral pathways

4. Pain
An unpleasant sensory and emotional experience which we primarily associate with tissue damage or describe in terms of such damage, or both
Pain is “the perception of a noxious stimulus that begins in the dorsal horn and involves the entire spinal cord and brain.”
The International Association for the Study of Pain (IASP) defines pain as “an unpleasant sensory and emotional experience which we primarily associate with tissue damage or describe in terms of such damage, or both.”
Pain can be described in terms of sensory, emotional, and cognitive components. These 3 components of pain are reflected in the mechanisms of the transmission and modulation of painful stimuli. Such mechanisms are mediated through the nociceptor neurons, the spinal cord processes, and the cerebral or brain processes.
Many different taxonomies exist for the classification of pain. In the clinical setting, a physician must infer the pathophysiology of a pain syndrome from his or her patient’s clinical evaluation. The most common of these inferred pathophysiologies may be described as nociceptive, neuropathic, and mixed.
For more information, please see Pain Assessment.

5. Pain Pathophysiology Nociceptive pain Neuropathic pain
Pain is the human awareness of nociception and has been defined as “an unpleasant sensory and emotional experience associated with tissue damage or described in terms of such damage.” A much more complex phenomenon than simple nociception, pain may arise in 2 ways: (1) as a response to a pathophysiologic process occurring within the tissues, eg, inflammation, or (2) in response to a pathologic process occurring along and within the nervous system pain pathways.  
In the first instance, the pain signal generates from intact primary afferent nerves that signal noxious events, or nociceptors. This type of pain has been called nociceptive. Nociceptors can be sensitized by release of algogenic agents (eg, protons, prostaglandins, bradykinin, serotonin, adenosine, cytokines, etc). In the second instance, the pain signal is generated ectopically and often in the absence of ongoing noxious events by pathologic processes in the peripheral or central nervous system. This pain is termed neuropathic.
For more information, please see Pathophysiology of Pain.

6. Nociception
The detection of tissue damage by specialized transducers connected to A-delta and C-fibers
Nociception has been defined by Loeser (2000) as “the detection of tissue damage by specialized transducers connected to A-delta and C-fibers.”
Anatomically, this process occurs predominantly peripherally and involves the nociceptor neurons, which terminate in the dorsal horn of the spinal cord.
Nociceptors are the primary afferent neurons with specific nerve endings that can distinguish between noxious (thermal, chemical, and mechanical) and innocuous events, and can initially transmit this information centrally to the spinal cord.

7. Classification of Pain Nociception
Proportionate to the stimulation of the nociceptor
When acute
Physiologic pain
Serves a protective function
Normal pain
Pathologic when chronic
Pain is termed “nociceptive” when the clinical evaluation suggests that it is sustained primarily by the nociceptive system.
Nociceptive pain is pain that is proportionate to the degree of actual tissue damage. A more severe injury results in a pain that is perceived to be greater than that caused by a less severe injury.
Such pain serves a protective function. Sensing a noxious stimulus, a person behaves in certain ways to reduce the injury and promote healing (eg, pulling his finger away from a hot object). This “good” pain serves a positive function.
Some examples of nociceptive pain are acute burns, bone fracture, and other somatic and visceral pains.

8. Classification of Pain: Neuropathic Pain
Sustained by aberrant processes in PNS or CNS
Disproportionate to the stimulation of nociceptor
Serves no protective function
Pathologic pain
Neuropathic pain occurs through central nervous system (CNS) changes, such as the processes of “wind-up” phenomenon and central sensitization that can occur in patients with a prolonged exposure to noxious stimuli or nerve injury, or through peripheral nervous system (PNS) changes, such as neuroma formation. It is disproportionate to the degree of tissue damage; it can occur without nociception.
Also called neurogenic pain, neuropathic pain occurs when pathophysiologic changes become independent of the inciting event, thus serving no protective function.
Neuropathic pain does not serve a positive function for the overall health of the person.
Some examples of neuropathic pain are painful diabetic and other peripheral neuropathies, deafferentation and sympathetically-maintained pains, and nerve inflammation, compression, or laceration.
For more information, please see Pain Assessment and Neuropathic Pain.

9. Peripheral and Central Pathways for Pain
Ascending Tracts
Descending Tracts
Cortex
Thalamus
Midbrain
Pons
The physiology of normal pain transmission involves some basic concepts that are necessary to understand the pathophysiology of abnormal or nonphysiologic pain. These include the concept of transduction of the first- order afferent neuron nociceptors. The nociceptor neurons have specific receptors that respond to specific stimuli if a specific degree of amplitude of the stimulus is applied to the receptor in the periphery. If sufficient stimulation of the receptor occurs, then there is a depolarization of the nociceptor neuron.
The nociceptive axon carries this impulse from the periphery into the dorsal horn of the spinal cord to make connections directly, and indirectly, through spinal interneurons, with second-order afferent neurons in the spinal cord.
The second-order neurons can transmit these impulses from the spinal cord to the brain. Second-order neurons ascend mostly via the spinothalamic tract up the spinal cord and terminate in higher neural structures, including the thalamus of the brain.
Third-order neurons originate from the thalamus and transmit their signals to the cerebral cortex.
Evidence exists that numerous supraspinal control areas—including the reticular formation, midbrain, thalamus, hypothalamus, the limbic system of the amygdala and the cingulate cortex, basal ganglia, and cerebral cortex— modulate pain. Neurons originating from these cerebral areas synapse with the neuronal cells of the descending spinal pathways, which terminate in the dorsal horn of the spinal cord.
Medulla
Spinal Cord

10. “Healthy” nociceptors
Nociceptive Pain
Neuropathic Pain
PNS
peripheral nervous
system
PNS
Peripheral
sensitization
“Healthy” nociceptors
Abnormal
nociceptors
CNS
central
nervous system
CNS
Central sensitization
Normal
transmission
The interplay of PNS and CNS pain mechanisms is complex. This slide highlights the interaction of physiologic and pathologic processes: 1) the activation of “healthy” nociceptors associated with central sensitization in response to a noxious stimulus, trauma, or inflammatory disease (nociceptive pain), and 2) because of still poorly-known mechanisms, the development of ectopic nociceptor activity and the occurrence of dorsal horn/CNS reorganization.
Central
reorganization
Physiologic state
Pathologic
state
Pappagallo M

11. Overview

12. Chronic Pain Syndrome
End result of a variety of pathological and psychological mechanisms that may have included, at some stage tissue or nerve damage.

13. Pain Interventions
Nerve blocks and injections should be seen as part of a process of education and rehabilitation, allowing an opportunity for mobilization and return to normal activity.

14. Nerve Blocks (1)
Diagnostic: local anaesthetic only, to clarify mechanism or simulate effects of therapy
Therapeutic: anaesthetise a site or pathway temporarily(local anaesthetic) or “permanently”(lytic agent, cryo, radiofrequency) or reduce inflammation (corticosteroids)
A block may be diagnostic and therapeutic eg. Symapthetic block or trigger point injection

15. Nerve Blocks (1)
Diagnostic: local anaesthetic only, to clarify mechanism or simulate effects of therapy
Therapeutic: anaesthetise a site or pathway temporarily(local anaesthetic) or “permanently”(lytic agent, cryo, radiofrequency) or reduce inflammation (corticosteroids)
A block may be diagnostic and therapeutic eg. Symapthetic block or trigger point injection

16. Nerve Blocks (II) Common blocks for chronic pain include
-Trigger-point injection
-Bier block
-Peripheral nerve injection (eg. Ilioinguinal,lateral femoral cutaenous, greater occipital)
-Epidural injection
-Intra-articular(eg.facet, SI joint)
Sympathetic block(cervical, lumbar)
Plexus block (coeliac, hypogastric)

17. Nerve Blocks (III)
Case reports, preclinical data support long lasting effects of local anaesthetic blockade - RCTs support lytic coeliac block
However, unclear how much clinical improvement reflects placebo effects, irrevelant cues, systematic absorption of local anaesthetic, expectations
Side effects possible
Rarely successful as a stand alone strategy for chronic pain

18. Trigger Point Injection
Myofascial pain syndrome
Taut band palpable (if muscle is accessible)
Exquisite spot tenderness of a nodule in a taut band
Pressure on tender nodule reproduces pain
Range of motion with stretch limited by pain
Techniques
Dry needling
Local anaesthetic only
Local anaesthetic and steroid
Botulinum toxin

19. Epidural Injection (I)
Employed for decades using various techniques materials and patients
Limited RCT evidence of efficacy
Cervical, Thoracic, Lumbar , Caudal
Trans laminar
Transforaminal

20. Epidural Injection(II)
Applied for symptomatic relief in
Disc protrusion with radiculopathy
Spinal stenosis(circumferential or transforaminal)
Acute pain, local inflammation of vertebral fracture
Acute herpes Zoster
May facilitate rehabilitation, avert surgery when applied within multidisciplinary frame work

22. Steroid Injections
Interlaminar Epidural

25. Nerve Root Injection Diagnostic Establish or confirm mechanism of pain
Therapeutic Local anaesthetic plus corticosteroid
Technique Fluroscopy or CT essential for needle placement with contrast confirmation

31. INTRA ARTICULAR INJECTIONS
Facet and Sacroiliac joints most common
Diagnostic facet syndrome or SI joint pain
Simulate results of potential spinal fusion or denervation of medial branch of dorsal ramus
Therapeutic (local anaesthetic + corticosteroid)
Reduce inflammation, pain
Increase mobility, facilitate rehabilitation

32. Specific anatomic syndromes
Facet syndrome
Continuous pain worsened by rotation and extension
Radiation into the leg or gluteal area, in a non-dermatomal
distribution
Tenderness over the joints and paravertebral muscle spasm

36. Sacroiliac joint injection

37. Symapthetic Blocks Diagnostic Therapeutic Technique Stellate ganglion
Lumbar
Therapeutic
CRPS of upper and lower extremity
Vascular insufficiency
Refractory angina
Technique
Local anaesthetic, Neurolytic

38. MISCELLANEOUS Trigeminal ganglion Glossopharyngeal nerve
Sphenopalatine ganglion

41. NEWER DEVELOPMENTS PULSED RADIOFREQUENCY VERTEBROPLASTY
IDET, DISCTRODE
DORSAL COLUMN STIMULATORS
PERIPHERAL NERVE STIMULATORS
DEEP BRAIN STIMULATORS
IMPLANTABLE PUMPS

45. Managing Pain

46. CONCLUSION
Interventional approaches are often reserved for patients with well established problems, failure of other treatments and pronounced disability.
Do we miss an opportunity for early cost effective preventive treatment by reserving interventions for those least likely to benefit?
“Doctors think a lot of patients are cured who have simply quit in disgust”
DON HEROLD 1889