Neuroscience 5b – Nociception
Anil Chopra
Nociception is the ability to detect overt or impending tissue damage. It is different
from pain in that pain is an experience that may arise from nociception or in the
absence of nociception. It is sensed by nociceptors. A nociceptive stimulus can be
measured.
Conduction Speed: as a general rule, larger axon diameters and myelination of axons
results in an increase in conduction velocity.
The nociceptors are all slow adapting nerve endings that are sensitive to mechanical
deformation, excessive heat and various chemicals that are released by damaged cells
such as transmitters, bradykinin, histamine, cytokines e.t.c. These all cause
depolarisation at nerve terminals on skin, muscles and visceral organs and result in the
sensation of pain. This generally has a high threshold.
Sensory Neurons
 Cell bodies are in the PNS (Doral root
ganglion or trigeminal ganglia)
 2 axon types:- 1) Aδ mechano or
thermoreceptor, faster, produces sharp pain,
leads to avoidance. 2) C fibres,
chemoreceptor, e.g. Bradykinin or histamine,
produces a dull aching pain, leads to guarding
to allow recovery
 Receptive fields are normally large
 Intensity is coded by the frequency of firing
 Receptors feed into the spinothalamic system
Pathway
Perception of pain and temperature also consists
of 3 neurones:
(1) From the limb/organ/dermatome it has its cell
body in the dorsal root ganglion. From the
dorsal root ganglion, it passes into the spinal
cord via the dorsal horn and synapses again in
the grey matter of the spinal cord. At the
pons, the spinothalamic tract becomes the
spinal leminiscus and attaches itself to the
medial leminiscus.
(2) From here it passes through the spinal cord
anterolaterally (opposite side) and travels
up to the thalamus along the Spinothalamic
tract up to synapse in the thalamus. Input
from the face also from trigeminal nerve (V) and trigeminal nerve ganglion.
(3) From the thalamus it then terminates in the appropriate section of the primary
somatosensory cortex.
NB: Organised somatotopically
Parts of the Brain which Process Nociceptive Information
 The spinothalamic tract carries information to several destinations in the brain:
o
To the VPL and VPM nuclei of the thalamus and then onto SI and SII in the
cortex, for analysis of localisation and intensity of the stimulus
o
To the reticular formation of the brainstem and the intralaminar nuclei of the
thalamus to signal the unpleasantness of the stimulus and give the emotional
component of pain – the affective pathway
o
To the periaqueductal grey of the midbrain – the central inhibition pathway
o
Both of these connections from the cortex are via collateral synapses
 The sensation of pain is emotionally neutral until it does down one of the
collateral branches, it is then perceived emotionally as pain
 The affective or secondary pain pathway is shown on the right
 The dotted line arrow shows it going on to SI and the thalamus, the collateral
branch to the cingulated cortex is part of the limbic system – giving emotion and
fitting in with the function of the limbic system
 As can be seen the collateral branches come of the spinothalamic tract before the
signal reaches the thalamus or cortex
Reticular Formation
If all the tracts and nuclei of the brainstem
are identified, anything left is known as the
reticular formation.
Central Inhibition
This is a process by which the feeling of pain can be
suppressed. Electrical stimulation from the periaqueductal grey matter travel down via the nuclei of
the reticular formation to the dorsal horn of the
spinal cord and cause inhibition of action
potential firing at nociceptors. The pathway
uses endogenous opioids and strong inputs
from hypothalamus and cerebral cortex.
Peripheral Inhibition
Peripheral inhibition is the
sensation of analgesia
when pain is rubbed.
Because
mechanoreceptors have a
low-threshold and pain
receptors have a high threshold, when the
mechanoreceptors fire action potential, they
inhibit the pain receptors around them by
lateral inhibition. This has an analgesic
effect. It takes place at the superficial levels
of the dorsal horn (substantis gelatinosa) and
is also known as the gate theory.
Secondary Pain Pathway:
• STT projects to cerebral cortex via
reticular formation and intralaminar
nuclei
• Triggers arousal
• Signals unpleasantness of the stimulus
• Registers awareness of pain at thalamic
level
Nociceptive Dysfunction
• Disruption of pathway – loss of pain
E.g. syringomyelia, Charcot joints
• Exacerbation of pain – hyperalgesia
E.g. thalamic syndrome, windup in dorsal horn