Neurogenic Inflammation

in Chronic Pain Syndromes

Introduction
Conclusion
Discussion

Darwin Amir
 Neuroinflammation is a localized form of
inflammation occuring in both peripheral nervous
system (PNS) and central nervous system (CNS).
Introduction
Conclusion
Discussion

Neurogenic inflammation describes the mechanism

of the CNS or PNS that modulates or perhaps initiate
inflammatory and potentially autoimmune events.

Inflammatory mediators, produced during

inflammation, evokeds pain via direct activation
and sensitization of nociceptors.
 Introduction
Conclusion
Discussion

Inflammation is the body’s response to injury and infection

 Roles of Neurogenic Inflammation in Pain
Conclusion

Introduction
Discussion
 Roles of Neurogenic Inflammation in Pain
Conclusion

Introduction
Discussion
 Classification of Chronic Pain
The need for classification of Chronic Pain were rise after quite
ptotracted discussion and correspondence between IASP and WHO
for completed the ICD-10. It was agreed that there was a number
of pain syndromes that were best seen as general condition.
Conclusion

Introduction
Discussion

After thorough discussion, the original subcommittee on taxo

-nomy agreed that majority of syndromes would be described in
many fashion,

Each syndromes then was to be described in terms of the

following item definition, site, system involved, main features,
age of onset, duration, severity, and quality, associated
features, factors providing relief, sign characteristic and others.
 Classification of Chronic Pain
Chronic
Chronic primary Chronic cancer postsurgical and Chronic
pain pain posttraumatic neuropathic pain
pain
Is pain in 1 or more A frequent and Pain persist after Is caused by a lesion
anatomic regions that debilitating accom surgery and injuries, the or disease of the
Conclusion

Introduction
Discussion

persist for longer than 3 -paniment of Cancer entity postsurgical and somatosensory
months but not yet in ICD post traumatic pain Nervous Systems

Chronic Chronic
Chronic visceral musculoskeletal
headache and
pain pain
orofacial pain
The IHS differentiates Is persistent or recurrent Is defined as persistent or
between primary (idiophatic), pain that originates from the recurrent pain that arises as part
secondary (symptomatic) internal organs of the head, of a disease process directly
headache, and orofacial pain neck, thoracic, abdominal, affecting bone(s), joint(s),
including cranial neuralgias and pelvic cavities muscle(s), or related soft tissue(s)
 Mechanism of chronic pain syndromes caused by
neurogenic inflammation

Chronic primary
Details of major inflammatory and involved in pain.
mediator
Chronic There are:
neuropathic pain
Conclusion

Introduction
Discussion

 On pre-clinical trials showing that inflammatory

mediators play critical roles in NP pathogenesis.
 Hyper-regulated Inflammatory mediators by resident
cells and infiltrate leucocytes after peripheral nerve
injury, inducing peripheral sensitization. In CNS, in
spinal cord, inflammatory mediators broadly
contribute to glial cells activation after nervous
injury.
 Mechanism of chronic pain syndromes caused by
neurogenic inflammation

Chronic Postoperative or Post

Trauma Pain Syndrome
Conclusion

Introduction
Discussion

 Chronic
Inflamatory post surgical
response or postpost
develops truma painorseems
surgical traumato
andbeisconsequence of
characterized by
activation
the of residentprocess
inflammatory cells andtriggered
recruitmentbyofsurgical
peripheral leucocytes
or trauma and the
aggression,
release
but it isofalso
inflammaory mediators
manifestation of NP resulting from surgical injury of large
 Inflammatory response develops post surgical/trauma
peripheral nerve
 Recruitment of peripheral leucocyte and release mediator inflammatory such as:
 Different mechanism are responsible for different painful syndromes,
- Endogenous factors (RNA, DNA, heat shock protein
even in a single type of surgery.
- The
Damage Associated Molecular
neuroplasticity processPatterns
which is(DAMP)
complex and in constant change in
- membrane
Toll-like Receptors (TLR), Nuclear
excitability, Factor
reducing (NFkB) mechanism and increasing
inhibitory
- the excitatory synaptic
Pro-inflammatory fc (IL-1Befficacy
& IL-6, TLR (toll-like receptors)
- Several
Cytokinefactors contribute in chronic postoperative or traumatic pain.
an Chemokine
 Mechanism of chronic pain syndromes caused
by neurogenic inflammation

Chronic headache
 Characterized the release of potent vasoactive neuropeptidase,
Conclusion

Introduction
Discussion

likely;
- Calcitonin gene-related peptidase (CGRP),
- Substance P (SP) and
- Neurokinin A from activated peripheral nociceptive sensory
nerve terminals (usually C and A-delta fibers)
 The peptidase lead to a cascade of inflammatory tissue
responses including arteriolar vasodilation, plasma protein
extravasation, and degranulation of mast cell in their peripheral
target tissue.
 Involvement of neuropeptidase (SP, neurokinin A and CGRP) in
migraine headache.
 Mechanism of chronic pain syndromes caused
by neurogenic inflammation

Chronic orofacial pain

 In a tooth extraction site, the inflamed area is marked by
Conclusion

Introduction
Discussion

increased sensitivity to pressure that is mediated by sensitized

nociceptors.
 If the inflammatory process and activity is sufficient intensity
and has been neuronal damage, a central process is established
that increases sensitization, lowers the threshold of response,
and causes ectopic discharges (physiologic changes).
 A-b fibers begin signaling pain (dynamic allodynia), and
inhibitory effect is lost (anatomic changes and disinhibition).
 An increased central release of excitatory mediators, such as
glutamate and nitric oxide production
 Mechanism of chronic pain syndromes caused
by neurogenic inflammation
Chronic visceral pain
Neurogenic inflammation involves a change in function of sensory
neurons due to inflammatory mediators, inducing an enhanced
release of neuropeptides from the sensory nerve endings.
Conclusion

Introduction
Discussion

The effects produced by tachykinins and CGRP released from

peripheral endings.

There is histological evidence for the presence of cytokines (IL-6)

The release of proinflammatory cytokines

The postganglionic sympathetic neuron also play a role in

neurogenic inflammation. The potency of nociceptor afferents to
inhibit the sympathetically dependent bradykinin-induced
plasma extravasation was significantly increased
 Mechanism of chronic pain syndromes caused
by neurogenic inflammation
Chronic
musculoskeletal
pain (CMP)
Conclusion

Introduction
Discussion
 Conclusion
Every pain syndrome show different inflammatory
mediators and it’s difference indicated by the
inflammatory site.

Discussion
Conclusion

Introduction
At the inflammatory site, different of the kinin
proteins of the coagulation system, some prosta
-glandins, leukotrines and several other lipid
mediators act in a confined manner at the site of
infection and tissue damage and at more distant locale
to disperse and support the inflammation process.
 Conclusion
Inflammatory mediators, produced during
inflammation, evokeds pain via direct activation and
sensitization of nociceptors.

Discussion
Neurogenic inflammation play an important role in the
Conclusion

Introduction
pathogenesis of numerous diseases including in pain.
Chronic pain syndrome are pain were found in
different site and organ.
Neurogenic inflammation is initiated by sensory nerve,
which come from the distal root of spinal cord
 THANK YOU

Conclusion
Discussion
Introduction