How Pressure Points Work
Processing of Afferent Nociceptive Stimuli With Amplification of Subsequent Stimuli
Chris A. Johnston, Copyright May 25, 2000
As a martial artist I have taken up the study of anatomy in recent years, mainly in an attempt to describe various phenomena scientifically that clearly seem to work, but have never been adequately explained in Western terms. Specifically the study of pressure point striking (Kyusho) has prompted a great deal of questions. The older paradigms, which are not scientific by the conventional definition, leave much to be desired in terms of a logical relation to specific body structure and process. It works to strike a particular vulnerable point initially with great force, and logically less force produces a lesser trauma. What is less obvious is how striking another point initially allows the same point struck in the first example to be hit much more softly while the same reaction is caused. This type of striking sequence can cause a knock out using a light touch. Clearly the first strike somehow amplifies the effect of the second strike. The question is what physiological mechanisms are involved in this phenomenon? The following is an attempt to relate these phenomena to existing knowledge of the corticothalamocortical network.
1). PATH OF INITIAL NOCICEPTIVE STIMULUS
It is necessary to elucidate the sequence of events upon stimulation of
cutaneous and/or subcutaneous pain receptors. Initial stimulation initiates
a signal that projects through relay neurons to the spinal cord. The spinal
cord is divided into 10 vertical layers called spinal laminae, based on
discrete function and connectivity of the neuronal projections within each
lamina. Only some of these 10 laminae are involved in this explanation.
In the spinal lamina (layer) known as the Substantia Gelitinosa, which is
also called spinal lamina II, reflex actions involving gating (switching
on or off) of subsequent polymodal C fiber slow pain impulses may or may
not be initiated. Regardless the initial fast signal ascends through the
spinal column (in the neo-spino-thalamic tract, which transports fast pain
signals to the thalamus) to the medulla where the signals are split. One
branch targets the reticular activating system (RAS), which is an ascending
extension of the spinal cord involved in preparing various neurons for input,
specifically receptors, thalamic sensory relay neurons and the cortex. The
RAS serves to regulate visceral (internal) organs through various involuntary
processes (i.e. heart rate, breathing, secretions), as well as keeping a
person conscious by suppressing rhythmic burst firing processes associated
with sleep. The branch that targets the RAS is modulated (controlled; modified)
by input from the cerebrum that represents ongoing contextual events, then
a projection is sent to the centromedian thalamic nucleus. The centromedian
nucleus is phylogenetically the oldest part of the thalamus, and it sends
a diffuse projection to the cortex with a widespread pattern of innervation.
This portion of the ascending afferent projection is involved in ‘waking
up’ the cerebrum, creating a condition of greater vigilance with respect
to incoming sensory information. The other branch of the neo-spino-thalamic
tract merges with the medial lemniscus (the central ribbon shaped conglomeration
of ascending sensory nerve projections directed from the medulla to the
thalamus) and continues onward to the ventral lateral posterior thalamus.
Stimuli are targeted to different thalamic nuclei based on the nature and
origin of the stimulus. It is important to note that two separate but synergistic
ascending paths exist whereby pain is transmitted to the brain, the Neo-Spino-Thalamic
Tract and the Paleo-Spino-Reticulo-Diencephalic Tract. The nociceptive fast
receptors of cutaneous tissue project a pain stimulus to the area of thalamus
known as the ventral posterior nucleus via the Neo-Spino-Thalamic Tract.
The nociceptive thalamic nuclei are somatotopically organized (organized
in sequence equivalent or analogous to their relative positions of origin
in the body). These nuclei then project to the somatosensory cortex of the
post central gyrus (upward fold) of the parietal lobe, giving rise to a
complicated series of reciprocal projections back to the thalamus and also
to other areas. This reciprocal innervation is key in determining whether
subsequent ascending fast impulses are suppressed or amplified. During the
same response to stimulus, the secondary slow nociceptive (pain) impulses
are sent through unmylinated polymodal C fibers via the Paleo-Spino-Reticulo-Diencephalic
pathway of the spine, joining with the medial lemniscus at the medullar
level of the brain. These slower impulses then diverge from the medial lemniscus,
proceed through the reticular tissue and target the intralaminar thalamic
nuclei. These thalamic nuclei are so named due to the somatotopic representation
of the discrete spinal laminae in the intralaminar nuclei (i.e., these specific
sipnal areas are reflected in the intralaminar nuclei in an orderly representation).
Subsequent projections go onward from the intralaminar nuclei to the fore
brain. These are thought to play a role in both emotional pain awareness
and are also one of the mechanisms that can initiate descending impulses
that are involved in the gating (switching on or off) of pain at the spinal
level. It is likely that the latency of the activities associated with the
paleo-spino-reticulo-diencephalic path are great enough that they do not
play a large part in pre-potentialing (chemically predisposing neurons to
more easily fire) dorsal thalamic nuclei for an amplification of any subsequent
signals directed through the thalamus. This type of effect is explained
in reference to fast pain signal response. The RAS (arising generally in
the upper tegmentum or roof of the medulla) also sends projections to the
thalamic intralaminar nuclei; these in turn modulate efferent (descending)
projections from the frontal cortex to the dorsal thalamic nuclei. This
circuit has been implicated in the modulation of behavioral states, specifically
arousal rom prolonged periods of neuronal bursting activity associated with
sleep. The thalamic intralaminar nuclei in turn exert an activating influence
on the brain stem reticular core(1). This particular aspect of the circuit
is not directly involved in the processing of ascending nociceptive stimuli;
rather it is involved in opening or closing the cortex to coherent information
from the body during the state of wakefullness.
The cerbral cortex is also organized in layers that are called cortical
laminae, based on structural and functional differences in the residing
neuron populations (these laminae are organized much like layers of an onion).
The importance of the particular lamina of termination of projections targeting
the cortex is due to the structural and functional properties of the reciprocal
corticothalamic projections (returning signals back to thalamus), and the
timing of the impulses that are returned through them. This determines the
sequence and structure of the reciprocal innervation. The segregation of
various kinds of afferents (projections to cortex) is maintained in the
thalamocortical projections to the somatosensory cortex (in Neocortex, postcentral
gyrus of Parietal lobe), with the nociceptive (pain) mechanoreceptive projections
most notably targeting area 3B of the somatosensory cortex (cortical areas
are functional boundaries organized much like states on a geographic map).
Terminations are largely in lamina (layer) IV of the somatosensory cortex,
but also deep in lamina III to a lesser extent. The border between lamina
IV and lamina III can be described as ill-defined in this respect (2). For
this reason some past studies have had difficulties in determining the role
of this projection. Recently some very extensive mapping of these associated
thalamocortical and corticothalamic projections has eliminated this confusion.
2). THE ROLE OF THE CORTICOTHALAMIC PROJECTION (from cortex to thalamus)
One major function of the descending projection from the cortex to the thalamus is to set the stage for reactions to be formulated in a manner relevant to ongoing activities. These reactions involve adjustments of cell membrane polarization in populations of neurons in various areas, effectively pre-potentialing cells to either fire easily or remain at a rest state. “The corticothalamic projection is involved in providing thalamic neuron populations receiving input from one part of a topographically organized system with information representing events occurring in other surrounding parts, defining the context upon which a stimulus driven event is superimposed” (3). Corticothalamic projections activate by facilitating or suppressing afferent (incoming) volleys traversing the relay nucleus of the thalamus (4). The amplification / suppression of subsequent ascending fast transmissions is most important in explaining how pressure points work together. This modulation is done through both direct synapse on relay neurons and also through synapse on local interneurons that are themselves suppressive (gabaergic). The thalamic reticular nucleus is also targeted, and this nucleus subsequently suppresses both relay neurons and also local thalamic interneurons, thus exerting a selective optimization or suppression dictated by cortical direction.
The structure of the corticothalamic reciprocal projection is complex in
that various elements of the
projection come from various laminae of cortex, each with different structural
wiring, function, and nerve cell type.
3). AFFERENT NOCICEPTIVE THALAMOCORTCAL STIMULUS PROCESSING (role of cortical laminae IV, V & VI)
As pain impulses exiting the thalamus are received initially by a population of neurons in lamina IV of the 3B area of the somatosensory cortex (5) these impulses penetrate to deeper cortical laminae. The first response back to the lower brain areas comes from Lamina V neurons of the somatosensory cortex. Two roles of this projection from lamina V are 1). Generally exciting ascending pathways and 2). Serving to activate descending projections that are involved in the initiation of suppressive gating in the Substantia Geletinosa of the spinal lamina II. Cortical lamina V neurons fire and exert an activating influence via fast signals. These neurons are heavily myelinated and large in axonal diameter and therefore propagate fast signals (6). The lamina V neurons innervate vast areas of the cortex via lamina V specific collateral branches, and have a high density of spine-like projections from their cell bodies. Usually a large dendrite (spine) invades supervening laminae, giving off oblique branches up to lamina I (7). These branches may be involved in filtering out marginal signals from the corticothalamic reciprocal projection. The axon projects to the thalamus giving off collateral (secondary) branches that continue on to various mid brain sites, the RAS, lower brain stem and spinal cord. It is important to note for the purpose of understanding the pressure points that the thalamic reticular nucleus is not innervated by this array from cortical lamina V. This differentiates this lamina V reciprocal projection from the subsequent lamina VI reciprocal projection, which has an entirely different structure and function. The lamina VI projection targets thalamic areas associated with the initial ascending thalamocortical projection, and also targets the thalamic reticular nucleus. The function of this architecture is to selectively facilitate (amplify) select thalamocortical channels associated with the initial relay projection, and also to suppress noise from unrelated channels.
4). CORTICOTHALAMIC RECIPROCAL INNERVATION SEQUENCE
Upon receiving a nociceptive projection from the thalamus, the somatosensory
cortex activates a sequence of reciprocal projections that serve to activate
ascending pathways in general and also to specifically target the area of
thalamus from which the initial thalamocortical stimulus was projected.
Information is used from the oral pulvinar regarding salience (relevance)
of nociceptive signals. The first reciprocation is the fast lamina V signal,
with both corticothalamic projections and also less direct collateral innervation.
The lamina V collateral intrainnervation is pervasive in its innervation
of the dorsal thalamus. However the idea of lamina V projections implementing
cortical determinations at this level about what areas of thalamus are relevant
and will therefore be targeted for excitation is equivocal. Rather it is
certain that the excitation is a distributed array, as with various other
activating systems. This implies a lamina V stimulation of relay paths in
a general excitatory role. As the lamina V axons project downward out of
the cortex, they bifurcate, forming 2 reticula (diffuse arrays). One targets
the thalamus in general, the other innervates various mid brain sites, the
RAS, lower brain stem and spinal cord (8). This projection acts on ascending
relay projections to pre-potential them to facilitate tonic firing sequences
in the dorsal thalamus. This in effect sensitizes ascending relay pathways,
and also in some respects operates very similarly to the action of the reticular
activating system during arousal from sleep. This mechanism explains one
way that a strike to a first point can amplify the effect of a strike to
a second point. The portion of the lamina V corticothalamic projection that
targets the RAS is sometimes capable of effecting an excessive de-polarization
(excitation) of the targeted neurons. This can particularly occur during
rapid sequential lamina V impulses in combination with incoming ascending
sensory information from the spine. This overwhelms these neurons, preventing
a normal recovery from firing; thus the reticular activating system shuts
down temporarily. This causes sudden unconsciousness due to a loss of activating
influence that normally halts the synchronized firing associated with sleep
and other unconscious states (i.e. seisures). Due to the convergence of
many projections from many different sensory modalities on individual cells
in the RAS, the specificity of input often cannot be maintained. Since the
RAS also has descending projections that control breathing, heart rate,
and secretions in various visceral organs, such trauma can effect the function
of various internal organs.
The other bifurcation of the Lamina V reciprocal innervation is thought
to play a role in the initiation of descending inhibitory impulses that
modulate gating activities in the spine via contact with the reticular magnocellular
core(9). The portion that targets the thalamus innervates the intralaminar
nuclei and effects a general stimulating effect via glutamatergic transmission
and subsequently acts to pre-potential relay neurons. After the thalamocortical
impulses trigger the fast reciprocation from lamina V, the lamina VI neurons
are triggered. These are a population of small axonal diameter, medium speed
neurons. The primary purpose of this population is to initiate a reciprocal
innervation of the dorsal thalamic nuclei, but also collateral branches
are given off that innervate the thalamic reticular nucleus. While the lamina
VI projection is excitatory in the chemical sense, inhibitory effects also
occur due to a synapse on local interneurons of thalamic relay nuclei, and
these interneurons are GABAergic and therefore suppressive themselves. The
lamina VI projection uses an excitatory synergistic action involving Calcium
Glutamate and Acetylcholine. The portion of this projection that directly
targets the dorsal thalamus is largely excitatory in effect, synapsing directly
on relay axons or proximally on their dendritic trees (those branches emanating
from the cell bodies of the nerves). This manner of connection suggests
a strong excitatory influence on these relay neurons. This excitatory projection
returns to the thalamus from the cortex following the same general path
as the initial nociceptive signal. However it terminates in a diffuse array
that covers not only the exact thalamic origin but also surrounding areas
(10). These innervated thalamic areas, being somatotopically organized,
represent spatially associated body areas (11). Subsequent stimulation of
these associated body areas would effectively be amplified due to this mechanism,
as the ascending pain signals would encounter relay neurons that were pre-potentialed
to readily fire.
It is interesting to note that the corticothalamic reciprocal projection
in general has about 10 times as many fibers as the thalamocortical projection
(12). Of that corticothalamic projection, most of the fibers are devoted
to the reciprocal innervation arising in cortical lamina VI. This implicates
the lamina VI aspect of the corticothalamic reciprocal projection as a major
player in the modulation (control) of thalamic relay activity. Thus amplification
of a second nociceptive stimulus is controlled by the Lamina VI projection.
The portion of the lamina VI reciprocal projection that targets the thalamic
reticular nucleus stimulates a population of GABAergic neurons that act
in an inhibitory
manner, causing hyperpolarization of the neurons they synapse on thereby
decreasing the tendency to fire. This is a similar function to the intrinsic
interneurons found in the thalamic tissue, but the interneurons project
only locally whereas the reticular neurons act as a suppressive array on
remote areas. This suppressive action is steered by the lamina VI projection.
Two basic actions are carried out through the thalamic reticular nucleus.
First, the reticular fibers synapse on relay neurons that have been cortically
identified as irrelevant to the current stimulus. This effectively blocks
the irrelevant paths, and increases the signal to noise ratio (13). Second,
some fibers synapse on local inhibitory interneurons, thus strengthening
signals traversing paths controlled by these particular relay neurons subsequently.
In this way the lamina VI reciprocal projection acts both directly on the
thalamic signal source in an excitatory manner, pre-potentialling nearby
projections to fire easily, and also indirectly through the thalamic reticular
nucleus to suppress unrelated noise. Also Gabaergic interneurons are suppressed
in the specific area of activity which causes further amplification. A study
of mice revealed that upon stimulation of one whisker, a signal is sent
through a barrel of fibers to the thalamus and subsequently to the somatosensory
cortex. Next, the mechanisms outlined above sensitize areas of thalamic
tissue that represent the other whiskers (14). After such a preparatory
stimulation the level of stimulation required to promote a response was
much lower. This suggests optimization of signals from spatially related
body areas. Convergence of cortical input on individual thalamic interneurons
suggests that vastly different cortical areas modulate amplification/inhibition
in different situations. Cortical structures that formulate such decisions
have yet to be elucidated.
SUMMARY
There is a time after an initial nociceptive (pain) stimulus during which
a subsequent nociceptive stimulus is likely to be amplified, by virtue of
both initial stimulation of the reticular activating system and also cortical
projections originating in lamina V of area 3B of the somatosensory cortex.
These lamina V projections, among other functions, initiate a pre-potentialing
activation of thalamic, mid-brain, medulla, reticular activating system
and spinal neuron populations. Beyond this effect there are also possible
augmentations which can give rise to further amplification of a secondary,
already partially optimized signal. This can happen when 1). The secondary
nociceptive signal originates in a topographically related area of the body
or 2). The second nociceptive signal traverses an area of thalamus that
has for any reason been targeted for dis-inhibition, or amplification. Cortical
mechanisms that are involved in the selective targeting of thalamic relay
projections should be the subject of further research. Also, the exact pattern
of synapsing of interneurons on other interneurons, and of lamina VI and
reticular neurons on interneurons, is not known to a point necessary to
define exactly how much inhibition is a general result, and how much may
be a specific cortically programmed result. The possibility of unconsciousness
is dependant on both the complexity and intensity of the neurological impact
on the reticular activating system (RAS), which must remain active to support
the conscious state. Since the RAS also controls the continual periodic
adjustments to the internal organs that allow for normal function in varying
circumstances, strikes that change the operation of the RAS may also change
the operation of these organs. Precise mapping of the inputs to the RAS
and subsequent control projections to visceral organs should reveal this
mechanism further. Finally, the exact role of the thalamic pulvinar nucleus
in discriminating somatosensory salience (relevance) is not known. The pulvinar
thalamic nucleus receives nociceptive somatosensory (pain) signals in a
portion called the oral pulvinar. The greater part of the pulvinar is devoted
to discriminating visual signals. In general, the pulvinar acts to discriminate
between irrelevant and salient visual inputs, and decisions about salience
are sent to the cortex and factored into its decisions about what to send
back to the thalamus. Presumably this applies to the small portion of pulvinar
dealing with somatosensory information as well, but the exact role of the
resulting decisions has yet to be elucidated. Certainly the reticular activating
system combines internally originating information from the forebrain with
spinal sensory information to arrive at an integrated contextual background
upon which to base decisions about what distant areas of the brain need
to be activated.
Bibliographical Information:
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the Corticothalamic Projection
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