Somatosensory Pathways

by Annie Burke-Doe, PT, MPT, PhD

Practicing physical therapist and associate professor at the University of St. Augustine for Health
Sciences in San Diego, California

Slide 1: Somatosensory Pathways

Hello and welcome to neuroanatomy and physical therapy. I'm Dr. Annie Burke-Doe, a practicing
physical therapist and an associate professor at the University of St. Augustine for Health Sciences in
San Diego, California. This lecture series has been developed for physical therapists embarking on
the study of neurology. Neuroanatomy is the study of the anatomical organization of the brain, and
it is also considered a branch of neuroscience, which deals with the study of the gross structures of
the brain and the nervous system. The term somatosensory generally refers to body sensations of
touch, pain, temperature, vibration, and proprioception. In this series of slides, we will look at two
main pathways. We will also use anatomy of the three major long tracts to localize lesions in the
nervous system. We will discuss common disorders of the spinal cord and other locations that affect
these pathways.

Slide 2: Primary Sensory and Motor Areas

In the prior lecture, we discussed the corticospinal tract and other descending pathways related to
motor function. In this lecture, we will discuss the other two main long tracts of the nervous system:
the posterior column medial lemniscus pathway and the anterolateral pathways involved in
somatosensory function. Again, the primary sensory and motor areas that are shown here are
located on either side of the central sulcus, which divides the frontal lobe from the parietal lobe. The
primary motor cortex, in red, is in the pre-central gyrus, while the primary sensory cortex, in blue, is
in the post-central gyrus. The somatosensory association cortex in the parietal lobe, in pink, receives
inputs from the primary somatosensory cortex and is important in higher order sensory processing.
Higher order sensory processing involves the ability to take in, sort out, and give meaning to
information from the world around us. The somatic or sensory association area monitors activity in
the primary sensory cortex. It is the somatic sensory association area that allows you to recognize a
touch as light, as in the arrival of a mosquito on your arm, and gives you a chance before it bites.

Slide 3: Major Somatosensory Pathways

Here, on slide 3, I've provided a table with the main long tracts of the central nervous system (CNS),
their function, and the level at which they cross, or decussate, from one side of the CNS to the other.
When looking at sensation, the posterior or dorsal column medial lemniscal pathway carries
proprioception, vibration sense, and fine discriminative touch. The anterolateral pathways include
the spinothalamic tract and other associated tracts that convey pain, temperature sense, and crude
touch. You can see that some aspects of touch are carried by both pathways. Therefore, touch
sensation is typically not eliminated in lesions unique to either pathway.

Slide 4: Sensory Neuron Fiber Types

We can see here that nerve fibers transmit different types of signals, and they are classified
according to axon diameter, velocity, and the amount of myelination. Some signals need to be
transmitted to or from the central nervous system extremely rapidly, otherwise the information
would be ineffective. An example of this would be the sensory signals that tell the brain of
momentary positions of the legs at each fraction of a second during your morning run, allowing you
to stay upright. On the other end, some types of sensory information, such as that representing a
prolonged aching pain in the body, do not need to be transmitted rapidly, so slowly conducting
fibers are utilized. As shown in the table above, fibers come in all sizes between 0.5 to 20
micrometers in diameter, with larger diameters having a greater conduction velocity or speed. The
range of conduction velocities is between 0.5 and 120 meters per second. The table also describes
the general classification scheme that divides nerve fibers into types A and C, which can be further
subdivided into alpha, beta, gamma, and delta. Type A fibers are typically large and medium-size
myelinated fibers of spinal nerves. Type C fibers make up more than one-half of all sensory fibers in
most peripheral nerves, as well as all postganglionic autonomic fibers. Note that a few large
myelinated fibers can transmit at velocities as great as 120 meters per second, a distance in one
second that is longer than a baseball field. Conversely, the smallest fibers transmit impulses as
slowly as 0.5 meters per second, which may be described as a distance from the great toe to the
spinal cord in two seconds.

Slide 5: Posterior Column: Medial Lemniscal Pathway

Let's follow the sensations of vibration, proprioception, and light touch on their pathways to the
somatosensory cortex. Remember that almost all sensory information from the somatic segments of
the body enter the spinal cord through the dorsal roots. Sensory neuron cell bodies are located in
the dorsal root ganglion (DRG), and each dorsal root ganglion has a stem axon that bifurcates,
resulting in one long process that conveys information into the spinal cord through the roots. There
is also a peripheral region innervated by sensory fibers from a single nerve root level that is called a
dermatome. These dermatomes will form a map on the surface of the body that can be useful in
localizing lesions. The dorsal column medial lemniscal (DCML) pathway, as its name implies, carries
signals upward to the medulla of the brain. Then after the signals synapse, they cross to the opposite
side of the brain in the medulla and continue upward through the brain stem to the thalamus by way
of the medial lemniscus. The DCML is composed of large-diameter myelinated axons that transmit
signals to the brain at velocities of 30 to 110 meters per second. Sensations of fine touch,
proprioception, and vibration enter the spinal cord via the dorsal root on the same side of the
posterior columns to ascend all the way to the posterior column nuclei, in blue, in the medulla. It is
helpful if you picture fibers adding on the lateral side from higher levels as the posterior column
ascends. The medial portion of the dorsal column of the spinal cord is called gracilis fasciculus. It
carries information from the legs and lower trunk. The more lateral aspect is called cuneatus
fasciculus, which carries information from the upper trunk above T6 from the arms and the neck.
The first-order neurons that have axons in the gracilis and cuneatus fascicului synapse onto second-
order neurons in the nucleus gracilis and nucleus cuneatus, respectively, both located in the
medulla. Axons of the second-order neurons decussate as the internal arcuate fibers and then form
the medial lemniscus on the other side of the medulla. The next major synapse occurs when the
medial lemniscal axons terminate in the ventral posterolateral nucleus (VPL) of the thalamus. The
neurons of the VPL then project through the posterior limb of the internal capsule in the thalamic
somatosensory radiations to reach the primary sensory cortex.
Slide 6: Anterolateral Pathways

Now, let's look at the anterolateral pathways, which have smaller diameter and unmyelinated axons
carrying information about pain and temperature sense. This pathway, as you can see, also enters
the spinal cord via the dorsal root; however, these axons make their first synapse immediately in the
gray matter of the spinal cord, mainly in the dorsal horn. Some axon collaterals will ascend or
descend for a few segments in Lissauer's tract before entering the central gray matter. Axons from
the second-order sensory neurons in the central gray matter cross over the spinal cord into the
anterior commissure to ascend in the anterolateral white matter. It should be noted that it takes
two or three spinal segments for the decussating fibers to reach the opposite side, so a lateral cord
lesion will affect contralateral pain and temperature sensation beginning a few segments below the
level of a lesion. The anterolateral pathways of the spinal cords have a somatotopic organization, in
which the feet are mostly laterally represented. To help us remember this organization, picture the
fibers from the anterior commissure adding medially, as the anterolateral pathway ascends in the
spinal cord. When the anterolateral pathways reach the medulla, they are located laterally, running
in the groove between the olives and into the inferior cerebellar peduncles. They enter the pontine
tegmentum to lie just lateral to the medial lemniscus in the pons and midbrain. The next major
synaptic relay is again in the thalamus, which projects via the thalamic somatosensory radiation to
the primary somatosensory cortex. The anterolateral pathway consists of three tracts: the spinal
thalamic tract, best known for and mediates discriminative aspects of pain and temperature, such as
location and intensity; the spinoreticular tract, which is thought to participate in the emotional and
arousal aspects of pain; and the spinomesencephalic tract in the periaqueductal gray participates in
the central modulation of pain. The spinothalamic and spinomesencephalic tracts arise mainly from
the spinal cord laminae 1 through 5, while the spinoreticular arises diffusely from the intermediate
zone to the ventral horn laminae 6 through 8. In addition to pain and temperature, some crude
touch sensations can be conveyed by the anterolateral pathways when the posterior column is
damaged. To summarize, if you step on a thumbtack with your left foot, your spinothalamic tract
enables you to realize "something sharp is puncturing the sole of my foot." Your spinothalamic
intralaminar projections and spinoreticular tract cause you to feel "ouch, that hurts," and your
spinomesencephalic tract leads to pain modulation allowing you to eventually think "aah, that feels
better."

Slide 7: Somatotopic Organization

Here, on slide 7, we have demonstrated a cord-level look at the somatotopic organization of the
dorsal column medial lemniscal (DCML) and anterolateral pathway. Remember that the somatotopic
organization preserves the spatial orientation of the central nervous system. Here you can visualize,
attempt to draw, or trace the pathway of the DCML, which will transmit sensations of fine touch,
proprioception, and vibration entering the spinal cord via the dorsal root on the same side of the
sensation into the posterior columns. It is helpful if you picture fibers, again adding on the lateral
aspects as you ascend higher into the posterior column. So if we begin in the lower extremity and
ascend in the cord, we see upper trunk to arm to neck is added as we rise. The anterolateral
pathways, which carry pain, temperature, and crude touch, also have somatotopic organization in
which the feet are mostly laterally represented. If we use the left side of the body as the location for
the sensory stimulation, you can picture fibers coming into the DRG and decussating at the cord
level in the anterior commissure and adding on medially, as the anterolateral pathway ascends in
the spinal cord. Slide 8: Spinal Cord Sensory and Motor Pathways

Here on slide 8, we can see both ascending pathways in blue and descending pathways in red. Let's
use this slide to review some of the concepts in the lecture series. Stop and take time to answer the
following questions: - At what level does the decussation occur for the dorsal column medial
lemniscal pathway? - At what level does the decussation occur for the anterolateral spinothalamic
pathway? - If your patient had a lesion on the left half of the spinal cord, which side of the body
would have loss of pain and temperature? - Which side of the body would have loss of
proprioception and vibration? - Which side of the body would have loss of motor function? - What
side will these deficits be on if the lesion was in the left cerebral cortex? Answers to these questions
will be related in the case at the end of the lecture series.

Slide 9: Somatosensory Cortex

Somatosensory information that arrives at the thalamus is brought to the primary somatosensory
cortex. The information is somatotopically organized with the face most lateral and the legs most
medial. This information is also carried to the association areas, specifically Brodmann areas 5 and 7.
Remember that association areas assist with higher level sensory function and store information
related to past experiences. Both the primary and association areas have extensive connections with
the motor cortex. Lesions in a somatosensory cortex produce deficits referred to as cortical sensory
loss.
Slide 10: Central Pain Modulation
One of the most important findings in pain research was the discovery that the brain has modulatory
circuits whose main function is to regulate the perception of pain. Because pain is highly dependent
on experience and therefore varies from person to person, it is difficult to treat clinically. Advances
in pain research have led to some important pain therapies. The initial side of modulation is the
spinal cord, which is pictured here, where inner connections between nociceptive and non-
nociceptive pathways can control the transmission of pain to higher centers in the brain. This
interaction was discovered in the 1960s and is called the Gate Control Theory, which is the basis for
the use of transcutaneous electrical nerve stimulation (TENS). In TENS, electrodes are used to
stimulate large-diameter afferent fibers that overlap the area of injury. Stimulation of the dorsal
columns via surface electrodes presumably relieves pain because it activates large numbers of type
A-beta fibers synchronously. This would be analogous to rubbing your shin after hitting it against a
hard object, thus modulating your pain. The periaqueductal gray receives inputs from the
hypothalamus, amygdala, and cortex, and it inhibits pain transmission. In research animals, it was
found that direct stimulation of the periaqueductal gray produces a profound and selective
analgesia. This stimulation was very specific in that the animal can still respond to touch, pressure,
and temperature within the body area that was in analgesic, but simply had less pain. Since the
discovery that opiates applied directly to the spinal cord produce a potent analgesic effect, this has
led to the administration of opiates in certain conditions by means of intrathecal or epidural roots.
Injection of opiates, such as morphine, into specific regions of the brain also produces powerful
analgesic by inhibiting the firing of nociceptive neurons in the dorsal horn. The periaqueductal gray
region is among the most sensitive sites for eliciting such analgesics.
Slide 11: Thalamus
The thalamus, which is located in the diencephalon, processes most of the information reaching the
cerebral cortex from the rest of the CNS including sensation, motor inputs from the cerebellum and
the basal ganglia, limbic inputs, and widespread modulation inputs involved with behavioral arousal
and sleep/wake cycles. It is an essential link in the transfer of sensory information, other than
olfaction, from receptors in the periphery to sensory processing regions in the cerebral hemispheres.
It was previously thought to be only a relay station, but it is now clear that it plays a gating and
modulatory role in relaying sensation. The thalamus is divided into a medial nuclear group, a lateral
nuclear group, and a ventral anterior nuclear group, which is separated by a Y-shaped white matter
structure called the internal medullary lamina. Nuclei located within the internal medullary lamina
itself are called intralaminar nuclei. The midline thalamic nuclei are an additional thin collection of
nuclei lying adjacent to the third ventricle, several of which are continuous and functionally very
similar to the intralaminar nuclei. Finally, the thalamic reticular nucleus forms an extensive but thin
sheet enveloping the lateral aspect of the thalamus.
Slide 12: Three Categories of Thalamic Nuclei
The thalamic nuclei that make up the relaying nuclei are the anterior group, thought to play a role in
memory and emotion; the medial group, which is implicated in memory; the ventral group, which
conveys somatosensory information; and the posterior group, which conveys auditory and visual
information. The intralaminar nuclei project to limbic structures in the basal ganglia and receive
inputs from the spinal cord, brain stem, and cerebellum and are thought to mediate cortical arousal
and integration of sensory submodalities. The reticular nucleus is not interconnected with the
cortex, but their axons terminate on the other nuclei of the thalamus. The reticular nucleus
modulates activity in other thalamic nuclei.

Slide 13: Specific Thalamic Relay Nuclei

Here is a table of the most well-known and clinically relevant thalamic nuclei with main inputs, main
outputs, and functions. Cover the right side and name the major nuclei that are responsible for
visual inputs, limbic inputs, and inputs to the basal ganglia.
Slide 14: Clinical Sensory Dysfunction
Sensory dysfunction can be caused by lesions anywhere in the somatosensory pathways. We are
now going to take a look at some of the clinical manifestations that may occur as part of your clinical
practice. We will explore sensory loss, paresthesia, spinal cord lesions, and bowel, bladder, and
sexual dysfunction.
Slide 15: Sensory Loss: Patterns and Locations
Again, sensory loss can be caused by lesions anywhere in the somatosensory pathways, and if we
review that pathway, it can include peripheral nerves, nerve roots, the posterior column medial
lemniscal and anterolateral pathways, the thalamus, thalamocortical white matter, and the primary
somatosensory cortex. Over the next few slides, we will look in detail at lesions in each of these
locations listed here on slide 15.
Slide 16: Lesion of Primary Sensory Cortex or Thalamic
In the following illustrations, lesions are shown in red, and sensory loss is shown in green. Here we
see a lesion of the primary sensory cortex and/or the thalamus. With the pathways drawn, we can
see that the deficit is contralateral to the lesion, and the clinical manifestations can vary depending
on the lesion size and exact location. This left-sided cortical lesion can potentially affect the sensory
modalities related to the posterior column medial lemniscal system including touch, joint position,
and vibration, as well as the anterolateral and trigeminothalamic systems for pain, temperature, and
touch on the right side of the body. Large lesions may affect adjacent cortical areas that involve
higher order abilities such as recognition of objects by touch, motor deficits such as hemiparesis, or
corticobulbar function.
Slide 17: Lateral Pontine or Medullary Lesions
Here on slide 17 the lesion is in the lateral pons or medulla, and we can see that it involves the
anterolateral pathways and the spinal trigeminal nucleus on the ipsilateral side, causing loss of pain
and temperature sensation in the body opposite the lesion and loss of pain and temperature
sensation in the face on the same side as the lesion.
Slide 18: Medial Medullary
On this slide, we haHere on slide 18 we are looking at sensory loss in a lesion of the medial medulla.
The lesion will therefore involve the medial lemniscus and will cause contralateral loss of vibration
and proprioception. Slide 19: Nerve Roots or Peripheral Nerves
Lesions in nerve roots or peripheral nerves can cause sensory disturbances. Distal symmetrical
polyneuropathies can cause bilateral sensory loss in a stocking and glove pattern in all modalities.
Associated deficits of lesions in the peripheral nerves often include lower motor neuron weakness
and other reflex changes.

Slide 20: Isolated Nerve Root Lesions

In isolated nerve root lesions, the sensory loss is in specific territories related to the nerves'
innervation. Again, associated deficits of lesions in peripheral nerves often include lower motor
neuron weakness and reflex changes.
Slide 21: Paresthesias
Paresthesias are considered an abnormal sensation in the absence of nociceptor stimulation. They
arise due to dysfunction of neurons and are often reported clinically as tingling, prickling sensations.
Lesions can be anywhere along the nociceptive pathways from peripheral nerves to the
somatosensory cortex. In addition to paresthesia, other common terms for sensory abnormalities
include dysesthesia, an unpleasant abnormal sensation; allodynia, a painful sensation provoked by a
normally nonpainful stimuli such as light touch; and hyperalgesia, an enhanced pain to normally
painful stimuli.

Slide 22: Spinal Cord Lesions

Spinal cord lesions can occur at any level and can be due to trauma, vascular dysfunction, infections
neoplasms, as well as other causes. Spinal cord lesions can have a significant impact on motor,
sensory, and autonomic pathways. Signs and symptoms of spinal cord dysfunction may correspond
to the level of the lesion. In the following slides, we will look at the signs and symptoms and spinal
cord syndromes.

Slide 23: Acute Spinal Cord Lesions

In acute spinal cord lesions, such as those that occur with trauma on a football field, there is often an
initial phase of spinal shock that is characterized by flaccid paralysis below the lesion, loss of tendon
reflexes, impaired sympathetic outflow to vascular smooth muscles causing decreased blood
pressure, and absent sphincter reflex and tone. Over weeks to months, spasticity and upper motor
neuron signs develop, and some sphincter and erectile reflexes may return. Other causes of cord
dysfunction may include degenerative disorders of the spine, tumors, infarction, malformations,
myelitis, and abscesses.

Slide 24: Transverse Cord Lesion

In the slides that follow, we will discuss important spinal cord syndromes that have sensory and
motor findings that can be helpful in localizing lesions. In a transverse cord lesion, pictured here, all
motor and sensory pathways are either partially or completely interrupted. There is often a sensory
level, meaning a diminished sensation in all dermatomes below the level of the lesion. The pattern
of motor loss or weakness and reflex loss can also help determine the lesion's spinal cord level.
Common causes of transverse lesions are trauma, tumors, multiple sclerosis, and transverse myelitis.

Slide 25: Central Cord Lesions

In small central cord lesions, damage to spinothalamic fibers crossing the ventral commissures
causes bilateral regions of suspended sensory loss to pain and temperature. Lesions of the cervical
cord produce a classic cape distribution, pictured above; however, suspended dermatomes of pain
and temperature can occur with lesions at other levels as well.
Slide 26: Central Cord Lesions
With larger central cord lesions, the anterior horn cells are damaged, producing lower motor neuron
deficits at the level of the lesion. In addition, the corticospinal tracts are affected, causing upper
motor neuron signs, and the posterior columns may be involved. Because the anterolateral
pathways are compressed from their medial surface by large lesions, there may be a complete loss
of pain and temperature below the level of the lesion except for in a region of sacral sparing.
Common causes of central cord syndrome include spinal cord contusion, non-traumatic or
posttraumatic syringomyeliam, and intrinsic spinal cord tumors. Slide 27: Hemicord Lesion
In hemicord lesions, also known as Brown-Squard syndrome, damage to the lateral corticospinal
tract causes ipsilateral upper motor neuron-type weakness. Interruption of the posterior columns
causes ipsilateral loss of vibration and proprioception sense. Interruption of the anterolateral
systems, however, causes contralateral loss of pain and temperature sensation. This often begins
slightly below the lesions because the anterolateral fibers ascend two or three segments as they
cross in the ventral commissure. Common causes of Brown-Squard syndrome include penetrating
injuries, multiple sclerosis, and lateral compression from tumors.

Slide 28: Posterior Cord

Lesions of the posterior column cause loss of vibration and position sense below the level of the
lesion. With larger lesions, there may also be encroachment on the lateral corticospinal tracts
causing upper motor neuron-type weakness. Common causes include trauma, extrinsic compression
from posteriorly located tumors, and multiple sclerosis.

Slide 29: Anterior Cord

The last of our cord syndromes is anterior cord syndrome, which results in damage to the
anterolateral pathways causing loss of pain and temperature sensation below the level of the lesion,
as well as damage to the anterior horn cells producing lower motor neuron-type weakness at the
level of the lesion. With larger lesions, the corticospinal tract may also be involved, causing upper
motor neuron signs. Incontinence is also common because descending pathways controlling
sphincter function tend to be more ventrally located. Common causes include trauma, multiple
sclerosis, and anterior spinal artery infarct.

Slide 30: Bowel, Bladder and Sexual Dysfunction

Let's now go forward to bowel, bladder, and sexual dysfunction. Normal function requires the
complex interplay of sensory and both voluntary and involuntary motor pathways at numerous
levels in the nervous system. Sensory information from the rectum, bladder, urethra, and genitalia is
carried to the spinal cord by sacral roots S2 through S4. Reflexive bladder function requires afferents
from T11 through L2 and S2 through S4, involving somatic, sympathetic, and parasympathetic
efferents. This information ascends to higher levels of the nervous system through both posterior
and anterolateral columns. Bladder emptying in normal adults is completely under voluntary control.
In general, for lesions that affect bowel, bladder, or sexual dysfunction, bilateral pathways must be
involved.

Slide 31: Bowel, Bladder and Sexual Dysfunction

Voluntary control of voiding involves information sent from the reflex center for urination to the
brain. The brain initiates voiding by corticospinal inhibition of lower motor neurons that innervate
the external sphincter and the brain stem pathways to autonomic efferents. Bowel control signal to
empty is stretch of the wall of the rectum. Afferent signals are conveyed to the brain, and efferent
signal will be sent to relax.

Slide 32: Bowel, Bladder and Sexual Dysfunction

In bowel and bladder dysfunction, there are several types of resulting incontinence, depending on
the lesion location, including acute central lesions, chronic central lesions, and peripheral lesions. In
acute central lesions, the bladder is flaccid and acontractile with continued reflex contraction of the
urethral sphincter. It results in urinary retention, bladder distention, and overflow incontinence. The
bladder does not completely empty. In chronic central lesions, the bladder becomes hyperreflexic.
The voluntary reflex bladder contractions occur. There may be a sense of urinary urgency or urge
incontinence caused by the detrusor sphincter dyssynergia. The bladder spasms at low urine volume.
Common spinal cord lesions causing acontractile or hyperreflexic bladder include trauma, tumors,
transverse myelitis, and multiple sclerosis. In lesions of peripheral nerves or of the spinal cord at
S2/S4, usually cause a flaccid areflexic bladder or significantly impaired bladder contractility
resembling an acontractile bladder. This can be due to a loss of parasympathetic outflow to the
detrusor and/or a loss of afferent sensory information from the bladder and urethra. Overflow
incontinence is often present. Common causes include diabetic neuropathy and compression of the
conus medullaris or cauda equina syndrome by trauma, tumor, or disc herniation.

Slide 33: Bowel, Bladder and Sexual Dysfunction

The lower spinal cord is important for sexual function. Erection of the penis or clitoris is controlled
by parasympathetic fibers from S2 to S4. Ejaculation is controlled by sympathetic nerves L1 to L4
levels and the pudendal nerve S2 to S4. Lesions at multiple levels can affect these functions since
they are controlled by local networks of the sacral spinal cord, descending inputs from the brain and
forebrain including the medial frontal lobes. In spinal cord lesions, reflex erection and reflex
ejaculation may still occur, but this is highly variable. Peripheral nerve lesions, higher order cortical
lesions, medications, and psychological factors can also cause sexual dysfunction.

Slide 34: Clinical Case 2

The following clinical cases have been developed for your review. They contain subject matter that is
clinically related and will reinforce lecture slide content. The questions for the case follow the
introduction of the case slide, and the discussion for the case is in the slide notes. I recommend not
looking for the answers in the discussion notes until you have attempted to answer the questions on
your own using the slide content. Good luck, and I will see you in the next topic.

Slide 35: Questions

Slide 36: References