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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-Séquard 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-Séquard 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