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									Spinoreticulothalamic Pathway –
relays in the reticular formation of the brainstem

Substantia gelatinosa - contacted by sensory afferents & reticulospinal fibers,
especially raphe nucleus of medulla
It synapses on tract cells of the spinothalamic tract.

Spinothalamic fibers also synapse in
posterior thalamus – to insula & parietal cortex sensory association area
intralaminar – diffusely to frontal & parietal lobes, limbic areas & basal ganglia –
consciousness, autonomic responses, movement
mediodorsal – frontal lobe thought areas

Pain – Dorsal column/medial lemniscus central processes have collaterals that
synapse with substantia gelatinosa, making it inhibit the tract cells for pain
This inhibition can be overcome with a strong nociceptive input

Transection of the ventral lateral area of the spinal cord results in almost complete
loss of pain sensations on the opposite side of the body below the lesion, but
sensibility gradually returns, because of alternative pathways.
Section of the ventral white commissure also causes prolonged analgesia

Pain sensations after destruction of the postcentral gyrus is from spinothalamic &
reticulothalamic afferents to intralaminar & mediodorsal thalamic nuclei that
connect with the neocortex, as above.

Raphe nuclei release serotonin into the substantia gelatinosa.
The periaqueductal gray area stimulates the raphe nucleus

Opioid receptors are on the dorsal horn, raphe nucleus, periaqueductal gray nuclei

ALS - A-delta fast pain pathwy -
1st order - in dorsal root ganglion, central process in lateral bundle synapses
in lamina I, II, or V (nucleus proprius) of the dorsal horn of gray matter in the
spinal cord
2nd order dorsal horn axons cross the midline in the spinal cord in the
ventral white commissure, ascend in the ALS tract, and synapse at the VPL
nucleus of the thalamus like the dorsal column pathway
3rd order - VPL axons travel to the postcentral gyrus

From the face:
1st order - trigeminal ganglion
In the central process, V1 fibers are dorsal, V3 are ventral, V2 are inbetween;
they rotate as they enter so that in the spinal trigeminal tract, it’s the
The most dorsal part of the tract has fibers from VII, IX, and X.
2nd order - spinal trigeminal nucleus: three different parts:
pars caudalis - from pyramidal decussation to C3 - pain & temperature
pars interpolaris - to inferior olivary nucleus - pain from teeth
pars oralis - to chief sensory - mostly coarse touch; most superior part by
chief sensory nucleus has discriminitive touch
Included with all the pars is the adjacent reticular formation that functions
like the dorsal root.

processes from the 2nd order neuron cross the midline & travel through the
ventral & dorsal trigeminothalamic tracts to the ventral posterior medial
nucleus of the thalamus. VPM axons synapse in the post central gyrus

slow pain - divergent pathway -
sensitized C fibers
Axons from the dorsal root ganglion (1st order neuron) in the lateral bundle
of the dorsal root, a.k.a. dorsolateral fasciculus or Lissaur’s tract, synapses
on many neurons (see gate theory below) in the dorsal horn of gray matter
of the spinal cord, on the 2nd order neuron & interneurons:
Lamina I - many pain fibers terminate here, contribute to ALS tract –
Waldeyer cells
Lamina II-III - substantia gelatinosa - interneurons that are stimulated by A-
delta and C fibers and work in pain modulation
Laminae IV-VI - nucleus proprius - ALS tract nucleus for light touch & pain,
whose axon will cross the midline in the anterior white commissure,
ascending 1-2 levels as it crosses, ascend on the opposite (contralateral)
side in the anterolateral tract (aka spinal lemniscus) to synapse ......

in many places:
- VPL of the thalamus (historically the 3rd order) to go to the post central
gyrus of the cortex like the DCML pathway

- reticular formation (where pain modulating pathways are stimulated)

- interneurons in lamina I & II, transmitter is substance P, that synapse on
nucleus proprius whose axons joint the tract and exit at:
- midbrain - Spinomesencephalic tract - for eye, head & neck reflexes
involving pain, tract cell synapses in superior colliculus for head & eye
turning toward pain stimulus, and periaqueductal gray for pain modulation
- reticular formation - Spinoreticulothalamic tract - slow pain, primarily
from C fibers, tract cell collaterals synapse in the reticular formation of the
brainstem, can also be involved in pain modulation, and eventually will
synapse on the in the intralaminar nuclei of the thalamus to frontal & parietal
lobes & striatum, mediodorsal to frontal lobe thought areas – evoke emotion
and attention, sensory integration, affect personality, movement-
from the face - trigeminoreticulothalamic - to reticular formation and then
intralaminar nuclei
(temperature also goes to the reticular formation, thalamus, hypothalamus)

Reticular formation pain modulation sites:
Periaqueductal gray in midbrain - activates raphe nucleus
Raphe Magnus nucleus in medulla - neurotransmitter is serotonin - axons
go to spinal cord and synapse on the substantia gelatinosa that releases
Lateral tegmental nucleus in brainstem also is activated by PAG, which also
stimulates substantia gelatinosa to release enkephalins
Locus ceruleus in pons - also activated by PAG, releases norepinephrine to
suppress the release of substance P at the primary pain afferent endings,
collaterals inhibit raphe magnus

Enkephalins (opioids) produce analgesia - block pain transmission:
1. by hyperpolarizing both presynaptic ending & post-synaptic neuron
2. block transmission -bind to receptors on presynaptic primary afferent
fibers to block neurotransmitter release
3. receptors on PAG, raphe, dorsal horn nuclei

Pain Modulation: Gate theory - developed by Melzack & Wall - edits painful
(just the top diagram)

the 1st order neuron synapses on in the dorsal horn many places:
1. tract cell - laminas I & nucleus proprius - axon crosses the midline at the
ventral white commissure and continues on the opposite side of the spinal
cord to the brain
2. excites interneuron to inhibit the gate neuron in the substantia gelatinosa
(SG) (that inhibits pain - gate theory is below )
3. interneurons to the tract
4. interneurons to ventral horn motor area neurons (reflex withdrawl)
5. interneurons to lateral horn (autonomic) neurons
Collaterals from mechanoreceptors (i.e. dorsal column/medial lemniscus
pathway 1st order neuron) excite gate interneurons of the SG whose axons
release enkephalins (opioid) on the ALS tract cell &/or interneuron to the
tract cell that is directly stimulated by the 1st order ALS neuron.
(Substantia Gelatinosa also gets afferents from reticular formation)

- at least 1/2 of lamina I & nucleus proprius tract cells get input from SG
opioid interneurons -
- opioids reduce Ca+2 influx, hyperpolarize presynaptic endings to block pain
transmission & hyperpolarize postsynaptic terminals to make pain
transmission more difficult

Levels of pain inhibition:
1 - non-narcotic analgesics decrease synthesis of prostaglandins
2 - dorsal horn local inhibition from non-nociceptive afferents
3 - periaqueductal gray descending pathways
4 - stress hormones released thru the H-P-A pathway
5 - cortex
6 - Exogenous opioids bind to periaqueductal gray, raphe, and dorsal horn
neurons, inducing analgesia

chronic pain - burning, throbbing, chronic - pain that lasts beyond the period
of healing, relative absence of tissue destruction, excess nociceptor activity
that outlasts the healing period
- prostaglandins increase nociceptor excitability

pain produces autonomic and motor reflexes –
withdrawl reflex – crossed extensor reflex – a collateral of the central pain
fiber synapses on an interneuron that synapses on interneurons that cause
flexion (withdrawl) with inhibition of the antagonist on the ipsilateral side &
extension (excitation of antagonist, inhibition of the flexor) on the
contralateral side

visceral pain - transmitted with sympathetic nerve fibers, poorly localized
because of convergence, which can involve 2nd order anterolateral system
neurons; injury can cause sympathetic axons to sprout & activate dorsal root
ganglion cells
referred pain - perceived in one area but initiated in a different area - due to
convergence at the dermatome (diaphragm --> C3,4; heart -->left T1-4;
stomach --> left T6-9; gall bladder R T7-8; appendix --> right T10; kidney -->
Lumbar1-2); or brain interpretation
The cortex perceives the sensation, and projects that sensation to an area of
the body that may differ from the location of the stimulation, that has already
perceived pain from a different modality.
radicular pain - pain caused by activation of sensory fibers at the dorsal root
- herniated disks are a good example
phantom pain - pain from an amputated structure
other definitions:
hyperalgesia - increased sensitivity, lower threshold, of pain receptors,
primary (? increased # of Na+ channels), or secondary (surrounding tissues
become supersensitive), can be caused by lower pH
analgesia - absence of pain in response to pain stimulation
allodynia - pain from a stimulation that normally is not painful, also can be
caused by lower pH
neuralgia - pain in the distribution of a nerve
threshold - stimulus necessary to initiate pathway
tolerance - amount of pain one can tolerate
pain also incorporates visceral and emotional responses - ’emotional,
affective & arousal aspects of nociception (sensation of pain)’

1,2 – S = calcaneous tendon & Babinski

3,4 – L = quadriceps

5,6 – C = biceps

6,7 – C= triceps

7,8 – C = brachioradialis

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