Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

1. PAIN PATHWAY
DR PARTH/ SR NEUROSURGERY

2. IASP DEFINITION
 “Pain is an unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or
described in terms of such damage.”
 ASPECTS OF PAIN-
1. affective-motivational
2. sensory-discriminative aspects of pain
 Types of pain-
1. Nociceptive-response to injury
2. Inflammatory- upregulation of inflammatory
mediators
3. Neuropathic-caused by nerve injury

3.  PATHWAY

4.  NOCICEPTORS
 Nociceptive neurons are different from low-
threshold tactile afferents in terms of physiology,
morphology, and neurochemistry.
 PRO-NOCICEPTIVE substances/neuropeptides-
substance P, CGRP, and neuropeptide Y.
 ‘Plasticity in response’ to tissue conditions-
 alterations of neuronal phenotype.
 enhanced responsiveness during inflammation. or
in response to damage to the nerve itself.
‘This is an important contributor to Hyperalgesia and
abnormal pain states’

5.  1st order neurons-Small myelinated(A delta) and
unmyelinated primary afferents(c) that travel
through the dorsal root to synapse in the dorsal
horn.
 Superficially (in laminae I and II).
 Deeply (in laminae V, VI, and VII),
 Around the central canal

6.  Second-order neurons(lamina 2 and 5,6)-are usually
divided into two classes:
1. Wide dynamic range (wdr) neurons -receive
convergent input from both nociceptive and
nonnociceptive primary afferents
 Low thresholds-within the innocuous range.
 Code stimulus intensity through the noxious range(c/f
tactile aff.).
 Distributed Somatotopically within the dorsal horn.
 Large receptive fields-precludes localization.
 Common in the deeper dorsal horn
 Fn-allow normally nonpainful stimuli such as touch to
give rise to a sensation of pain under certain conditions

7. 2. Nociceptive-specific.
 Respond exclusively to noxious stimuli(a delta
mechanoreceptors or by both A delta and C
nociceptors.)
 Receptive fields are small, which indicates an
important role in stimulus localization.
 They are concentrated in the more superficial
layers-lamina 1& 2.

8. NOCICEPTIVE SPECIFIC PATHWAYS IN SPINAL
CORD.
 Spinothalamic pathway
1. Affective-motivational(MEDIAL THALAMUS)
2. Sensory-discriminative(LATERAL THALAMUS)
aspects of pain
 Spinoreticular pathway
 Spinomesencephalic
1. Conscious sensation
2. Arousal,
3. Autonomic and motor responses to noxious input.
4. Recruitment of descending control systems
 Spinoparabrachial

10.  Spinoparabrachial pathway consists of projections
of neurons primarily in lamina i and relays
information to the amygdala and hypothalamus, as
well as to the midbrain periaqueductal gray matter
(PAG) and caudal ventrolateral medulla.
 Spinohypothalamic - autonomic and reflex responses to
nociception.
 Spinotectal –initiating eye movement to painful
stimuli.

11.  3rd order neuron
Cell body in
thalamus, ascend
ipsilaterally to
project to
somatosensory
cortex, and other
higher centres.

12. SUPRASPINAL
RECEPTIVE
STATIONS-
“PAIN MATRIX”
 Brainstem
 Lateral thalamic nuclei
 Medial thalamic nuclei
 Primary somatosensory
Cortex
 Secondary somatosensory
Cortex
 Insula
 Anterior cingulate cortex
 Prefrontal cortex

13. THALAMUS
 LATERAL SYSTEM -include the
1. ventral posterior medial (VPM) nucleus
2. ventral posterior lateral (VPL) nucleus
3. ventral posterior inferior (VPI) nucleus.
4. Posterior Part of the Ventral Medial Nucleus
 MEDIAL SYSTEM
1. Intralaminar nuclei.
2. Ventral caudal part of the medial dorsal nucleus
VENTROCAUDAL
(VC) NUCLEUS.

15. SOMATOSENSORY CORTEX

16. SOMATOSENSORY CORTEX
 PRIMARY(S1)
 Nociception of discriminating location and intensity.
 Si activation has been linked specifically to pain
intensity
 Sustained noxious stimulation -produce a
decreased cortical signal in this region

17.  SECONDARY(S2)
 Unambiguous role in cortically mediated
nociception.
 Recognition of
1. Painful and thermal stimuli,
2. Pain-related learning, and integration of tactile and
nociceptive information.
Thalamic input to the sii comes largely from the vpi
Have large receptive fields, with contralateral or
bilateral activation.

19. INSULA
 Central structure in pain matrix.
 Anterior insula- nociceptive
information.
 Posterior insula-tactile processing.
 Insula codes for intensity of the
stimulus.
 Lesions of insula-
1. Increased pain tolerance
2. Loss of affective quality of pain
while able to detect intensity
thresholds.

20. ANTERIOR CINGULATE CORTEX
 Affective and motivational aspects of pain.
 ‘Emotional distress of pain and in selection of
responses to painful stimuli’
 Gets stimulated in response to noxious stimulus almost
in parallel to s2.
 Input to the acc comes from medial thalamic nuclei, the
mediodorsal nuclei, and the parafascicular nuclei.
 Lesioning-therapeutic cingulotomy !
Pain ratings were improved only modestly, but the pain
was considered less bothersome or distressing

21. PREFRONTAL CORTEX
 higher cognitive function and endogenous
modulation of pain.
 medial prefrontal cortex & dorsolateral prefrontal
cortex
 FUNCTION-
 Executive function, attention, and execution of high-
order tasks.
 The dorsolateral prefrontal cortex is specifically
involved in the placebo response, in which pain
sensations are modulated by expectation.

22. ROLE OF DORSAL COLUMN PATHWAY IN
VISCERAL PAIN
 Observation-midline myelotomy relieved pain in
patients with cancer involving pelvic visceral
structures !!
 significant projection ascending ipsilaterally through
the dorsal columns and transmitting information to
the ventroposterolateral nucleus of the thalamus
 may not contribute to pain sensation under normal
conditions, but it could become sensitized by
visceral inflammation.

23. DESCENDING MODULATORY SYSTEMS
1. PAG/RVM system
 Employs endogenous opioids as neurotransmitters-
in the PAG and RVM --contribute to the pain-
modulating function of this system.
 Supports opioid analgesia-these regions are
required for the analgesic actions of systemically
administered opioid.
 Opioids act directly on inhibitory neurons that
normally inhibit the pain-inhibiting output neurons.
Opioids thus activate descending inhibition through
disinhibition
 Bidirectional control.

24. 2. Dorsal reticular nucleus in the caudal medulla
(which mediates effects of counterirritation)
3. Noradrenergic systems in the dorsolateral pontine
tegmentum

25. NEURAL BASIS FOR BIDIRECTIONAL CONTROL
Two populations of
rostral ventromedial
medulla (RVM) neurons,
ON-cells and OFF-cells,
provide the neural basis
for bidirectional control
of spinal processing by
the RVM

26. CRANIOFACIAL PAIN PATHWAY

28. CRANIOFACIAL PAIN SYNDROMES
 CEPHALIC NEURALGIAS
1. Trigeminal neuralgia
 vascular compression
 MS
2. Glossopharyngeal neuralgia : pain usually in base of
tongue and adjacent pharynx.- PICA
3. Geniculate neuralgia : otalgia – nervus inermedius-
somatosensory branch of facial n.
4. Tic convulsif : geniculate neuralgia with hemifacial
spasm-AICA-
5. Occipital neuralgia

29. 6. Herpes zoster: characteristic vesicles and crusting
usually follow pain, most often in distribution of V1
7. Post herpetic neuralgia (Ramsay-hunt syndrome)
8. Supraorbital neuralgia (s.o.n)
9. Trigeminal neuropathic pain (AKA trigeminal
deafferentation pain): injuries from sinus or dental
surgery, head trauma.
 OPTHALMOPLEGIAS
 OTALGIAS
 VASCULAR PAIN SYNDROMES.

30. CLINICAL IMPLICATIONS OF PATHWAYS

32. THANK YOU