In Vivo studies
• Kuslich et al:OCNA April 1991. The tissue
of origin of low back pain and sciatica: A
report of pain response to tissue
stimulation during operations on the
lumbar spine using local anesthesia.
• Only the PLL, posterior and lateral
annulus, and compressed nerve root
produced pain consistently.
Sinu Vertebral Nerve
• Size: 0.5 – 1mm
• Formed bilaterally and segmentally
• Sensory spinal branch from the ventral ramus
and sympathetic branch from the grey ramus
communicans which is the major contribution.
• Enter spinal canal through inter vertebral
foramen passing just below the pedicle along
with the segmental vessels, lying anterior to the
nerve roots. Some time only multiple filaments
(upto 6) are seen
Sinuvertebral Nerve
• The nerve then sends transverse and
descending branches to the same level disc and
PLL and another branch which ascends along
the PLL to the next level. These branches
interdigitate with branches from the opposite
side.
• The sinuvertebral nerve supplies only structures
within the spinal canal. It innervates the anterior
surface of the dura, the vessels in the anterior
epidural space in addition to the PLL and
posterior disc.
Sinu Vertebral Nerve
The nerve fibres penetrate the outer 3
layers of the annulus, for a distance of
about 3 mm, and they are sparse.
Disc surface, peridiscal tissues and
PLL has a very rich network
Sinu Vertebral Nerve
• Sympathetic fibres are vasomotor
efferents and sensory fibres are
proprioceptive and nociceptive.
• A delta and C fibres.
Differential Innervation
• The lumbar vertebral endplate, particularly in its
central area adjacent to the nucleus pulposus, is
supplied with a neural pattern similar to the outer
annulus.
• The anterior annulus and ALL is supplied by
sympathetic fibres from the sympathetic trunk or
grey ramus.
• The lateral side of annulus has the richest
innervation, from the grey ramus and branches
of the ventral ramus.
The emerging concept is that disc,
unlike other joints, is provided with
a predominantly visceral type of
nerve supply.
Neural Sensitization
• ‘Peripheral sensitisation’ of the nerve endings take place
by the pro-inflammatory mediators of the granulation
tissue of the annular tears and also by the exposed
nuclear material which can irritate the spinal root and the
sinuvertebral nerve endings.
• The sympathetic afferents( mechanoreceptors and
nociceptive) are also sensitised peripherally by efferent
sympathetic fibres.
• The sympathetic afferents are also susceptible to ‘central
sensitisation’ as in other visceral pains by ‘stress’ which
will lower the pain threshold of the visceral afferents-in
chronic discogenic pain.
Neural Sensitization
• The pain response can be affected by
local reflex mechanisms and also by the
DRG satellite cells.
Innervation of Pathological Disc
• In the degenerate disc the nerve fibres
penetrate the outer half of the annulus and
in some painful degenerate discs upto the
inner third of the annulus.
• The fibres are seen in a perivascular
position in the granulation tissue growing
into the degenerate disc, neo-innervation.
Origin of discogenic low back pain
• Injury or overload in a normal or aging disc
• Annulus fibrosus disruption or tear.
• Repair by Inflammation(ingrowth of
macrophages and mast cells)
• Release of growth factors like bFGF and TGF b
and cytokines like TNF a
• Proliferation and differentiation of cells in disc
which produces fibrosis, neovascularisation and
neoinnervation
• Disc degeneration and discogenic back pain.
Discogenic low back pain
• The ingrowth of nerve endings to the deeper
layers of the annulus is the cause of the chronic
dull aching discogenic low back pain, which is
exacerbated by mechanical loading of the disc.
• The principle of discography is increasing the
intradiscal pressure stimulating these
mechanoreceptors in the annulus.
Disc deterioration and neuropathic
pain
• In addition to the local pain responses
described above leading to low back pain,
disc degeneration also produces
neuropathic pain by stimulating the cauda
equina, the DRG or the roots distal to
DRG with pain experience from the area of
distribution of the nerve.
• This can be due to mechanical
compression or inflammatory chemicals.
Effects of nucleus pulposus
• It contain pro-inflammatory mediators like
cytokines.
• Increases the discharge of nerve fibres, reduce
the conduction velocity of the spinal nerve root,
attract inflammatory cells , induce increased
intraneural capillary permeability, and influence
intraneural capillary blood flow, induce
degeneration of nerve fibres. This nerve damage
itself lead to macrophage stimulation.
Molecular factors and biomarkers.
• Neurotrophins, such as nerve growth factor,
brain derived neurotrophic factor and glial
derived neurotrophic factor act at the level of
DRG and nerve root and play role in chronic
pain mechasnisms.
• Levels of S-100 protein and neurofilament have
been found to be higher in the CSF of patients
with disc herniation and sciatica, indicating
axonal and Schwan cell damage.
Outcome of discogenic sciatica
& Pain generators
Convergence and Referred Pain
• Visceral autonomic nervous system
• Somatic autonomic nervous system
• Pattern recognition by CNS to the somatic
area
• Cardiac Pain referred to Lt shoulder
After all, what is pain?
• Pain is an unpleasant
sensory
and emotional experience
associated with actual or potential tissue
damage or described in terms of such
damage• International Association For The Study Of
Pain 1979
References
1.
J Randy Jinkin: the anatomic and physiologic basis of local, referred and
radiating lumbosacral pain syndromes related to diseases of the spine. J
Neuroradiol 31:163-80 (2004)
2.
3.
M A Edgar . The nerve supply of the lumbar intervertebral disc. JBJS (2006)
Peng B et al. possible pathogenesis of painful intervertebral disc degeneration.
Spine 31(5) 560-566 (2006)
4.
Wiltse LL. The anatomy of the extradural compartments of the lumbar spinal
canal- Peridural membrane and circumneural sheath. Radiologic Clinics of North
America 38(6). 1177-1205 (2000)
5.
Mulleman D et al: pathophysiology of disc related low back pain and sciatica.IIEvidence supporting treatment with TNF-ά antagonists. Joint Bone Spine 73:270277 (2006)
6.
Brisby H. pathology and possible mechanisms of nervous system response to disc
degeneration. JBJS 88:68-71 (2006)
.Bogduk N. The innervation of the lumbar spine. Spine 8(3) 286-93 (1983)
7.
It is now clear that if we can effectively treat the pain despite the underlying
cause, it will be possible for patients to regain normal functioning. The key to
more successful pain treatment is to understand the mechanisms that
generate and maintain chronic pain.
Nociception is essential for survival whereas pathological pain is
maladaptive and often unresponsive to pharmacotherapy. Voltage-gated
sodium channels, Nav1.1–Nav1.9, are essential for generation and
conduction of electrical impulses in excitable cells. Human and animal
studies have identified several channels as pivotal for signal
transmission along the pain axis, including Nav1.3, Nav1.7, Nav1.8, and
Nav1.9, with the latter three preferentially expressed in peripheral
sensory neurons and Nav1.3 being upregulated along pain-signaling
pathways after nervous system injuries. Nav1.7 is of special interest
because it has been linked to a spectrum of inherited human pain
disorders.
Only when we have the tools to identify the
mechanism
responsible for the pain in a particular
individual, and
t h e n the capacity to reverse the
mechanisms, will the
management of neuropathic pain really
advance. The onus
on the clinician will then be to use the
history, examination,
investigation, and diagnostic tools as a way
to
identify the mechanisms that operate in
their patients and
use this information to select appropriate
treatment.
We highlight current theories about
peripheral neuropathic pain and show
that progress in management is
contingent
on targeting treatment not at the
aetiological factors or the symptoms
but at the mechanisms that operate to
produce
the symptoms. This approach will
require substantial progress in our
understanding of the pathophysiology
of
neuropathic pain, the development of
accurate diagnostic tools to discover
what mechanisms contribute to the pain
syndrome in an individual, and effective
treatments aimed specifically at the
mechanisms.
Neuropathic pain is a pathological pain
The capacity to experience pain has a protective role: it
warns us of imminent or actual tissue damage and elicits
coordinated reflex and behavioural responses to keep such
damage to a minimum. If tissue damage is unavoidable,
a set of excitability changes in the peripheral and central
nervous system establish a profound but reversible pain
hypersensitivity in the inflamed and surrounding tissue.
This process assists wound repair because any contact
w i t h the damaged part is avoided until healing has
occurred. By contrast, persistent pain syndromes offer no
biological advantage and cause suffering and distress. Such
maladaptive pain typically results from damage to the
nervous system—the peripheral nerve, the dorsal root
ganglion or dorsal root, or the central nervous system—and
is known as neuropathic pain. Such syndromes comprise a
complex combination of negative symptoms or sensory
deficits, such as partial or complete loss of sensation, and
positive symptoms that include dysaethesia, paraesthesia,
and pain.
● The pathways of low back pain and radicular
pain were clinically studied using a randomized
control trial for L2 spinal nerve infiltration.
● The low back pain pathway was likely interrupted
by L2 block in the treatment groups studied.
● The radicular pain pathway was interrupted for a
short duration by L2 block in the clinical cases studied.
● The main afferent fibers of the low back pain
pathway and part of those of the radicular pain
pathway were thought to involve the L2 spinal
nerve root, presumably via sympathetic afferents.
● An L2 block is useful in reducing LBP due to the
disorders of L2 spinal nerve-innervated structures,
such as the disc, facet joint, and sacroiliac joint.
However, the therapeutic value of an L2 block may
be occasionally insufficient to alleviate pain completely
because of the short duration of its effect.
It appears that only a small amount of investigation has
been performed into the diagnostic accuracy of clinical
tests to identify the tissue source of low back pain. There
are tests for the disc and SIJ that have some diagnostic
value but no test for the facet joint that appears informative.
The usefulness of these tests in clinical practice,
particularly for guiding treatment selection, remains unclear.
There are inherent limitations in the
accuracy of all diagnostic tests. The tests
used to diagnose the source of a patient’s
chronic low back pain require accurate
determination of the abolition or
reproduction of
the patient’s painful symptoms.
Examination of the back
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1 gait
2 spine contours
3 range of motion and rhythm
4 reflexes
5 strength
6 root irritation signs
7 root tension
8 hip
9 pulses 10 non organic signs