Somatosensory System



MINISTRY OF HEALTH OF UKRAINE

VINNYTSIA NATIONAL MEDICAL UNIVERSITY

NAMED AFTER M.I.PYROGOV

NEUROLOGY DEPARTMENT

MODULE - 1

Lessons # 2-3

Somatosensory System. Pathways.

Aids to the examination of the Somatosensory System.

1. Basic questions:

2.1. Peripheral Components of the Somatosensory System and Peripheral Regulatory Circuits:

2.1.1. Receptor Organs.

2.1.2. Receptor types.

2.1.3. Receptors in the Skin.

2.1.4. Receptors in Deeper Regions of the Body.

2.2. Peripheral Nerve, Dorsal Root Ganglion, Posterior Root:

2.2.1. Peripheral nerve: Anatomy of the spinal roots and nerves.

2.2.2. Nerve plexus and posterior root.

2.2.3. Dorsal root ganglion.

2.2.4. Somatosensory Innervation by Nerve Roots and Peripheral Nerves.

2.3. Posterior Columns.

2.4. Anterior Spinothalamic Tract.

2.5. Lateral Spinothalamic Tract.

2.6. Central Components of the Somatosensory System:

2.7.1. Sensorimotor integration.

2.7.2. Differentiation of somatosensory stimuli by their origin and quality.

2.7. Testing for somatosensory deficits.

2.8. Somatosensory Deficits due to Lesions at Specific Sites along the Somatosensory Pathways

Somatosensory System

Peripheral Components of the Somatosensory System

Receptors

Receptors are specialized sensory organs that register physical and chemical changes in the external and internal environment of the organism and convert (transduce) them into the electrical impulses that are processed by the nervous system.

They are found at the peripheral end of afferent nerve fibers. Some receptors inform the body about changes in the nearby external environment (exteroceptors) or in the distant external environment (teleceptors, such as the eye and ear). Proprioceptors, such as the labyrinth of the inner ear, convey information about the position and movement of the head in space, tension in muscles and tendons, the position of the joints, the force needed to carry out a particular movement, and so on. Finally, processes within the body are reported on by enteroceptors, also called visceroceptors (including osmoceptors, chemoceptors, and baroceptors, among others). Each type of receptor responds to a stimulus of the appropriate, specific kind, provided that the intensity of the stimulus is above threshold.

Most receptors in the skin are exteroceptors.

A second group of receptor organs lies deep to the skin, in the muscles, tendons, fasciae, and joints. In the muscles, for example, one finds muscle spindles, which respond to stretching of the musculature. Other types of receptors are found at the transition between muscles and tendons, in the fasciae, or in joint capsules (Fig 2.1)

Peripheral Nerve, Dorsal Root Ganglion, Posterior Root

The further “way stations” through which an afferent impulse must travel as it makes its way to the CNS are the peripheral nerve, the dorsal root ganglion, and the posterior nerve root, through which it enters the spinal cord.

Peripheral nerve. Action potentials arising in a receptor organ of one of the types described above are conducted centrally along an afferent fiber, which is the peripheral process of the first somatosensory neuron, whose cell body is located in a dorsal root ganglion.

Nerve plexus and posterior root. Once the peripheral nerve enters the spinal canal through the intervertebral foramen, the afferent and efferent fibers go their separate ways: the peripheral nerve divides into its two “sources,” the anterior and posterior spinal roots.

The anterior root contains the efferent nerve fibers exiting the spinal cord, while the posterior root contains the afferent fibers entering it.

A direct transition from the peripheral nerve to the spinal nerve roots is found, however, only in the thoracic region. At cervical and lumbosacral levels, nerve plexuses are interposed between the peripheral nerves and the spinal nerve roots (the cervical, brachial, lumbar, and sacral plexuses).

[pic]

Anatomy of the spinal roots and nerves. In total, there are 31 pairs of spinal nerves; each spinal nerve is formed by the junction of an anterior and a posterior nerve root within the spinal canal. The numbering of the spinal nerves is based on that of the vertebral bodies. Even though there are only seven cervical vertebrae, there are eight pairs of cervical nerves, because the highest spinal nerve exits (or enters) the spinal canal just above the first cervical vertebra. Thus, this nerve, the first cervical nerve (C1), exits the spinal canal between the occipital bone and the first cervical vertebra (atlas); the remaining cervical nerves, down to C7, exit above the correspondingly numbered vertebra; and C8 exits between the seventh (lowest) cervical vertebra and the first thoracic vertebra. At thoracic, lumbar, and sacral levels, each spinal nerve exits (or enters) the spinal canal below the correspondingly numbered vertebra. There are, therefore, just as many pairs of nerves in each of these regions as there are vertebrae (12 thoracic, 5 lumbar, and 5 sacral). Lastly, there is a single pair of coccygeal nerves (or, occasionally, more than one pair).

Dorsal root ganglion. The dorsal root ganglion is macroscopically visible as a swelling of the dorsal root, immediately proximal to its junction with the ventral root (Fig. 2.4). The neurons of the dorsal root ganglion are pseudounipolar, i.e., they possess a single process that divides into two processes a short distance from the cell, in a T-shaped configuration. One of these two processes travels to the receptor organs of the periphery, giving off numerous collateral branches along the way, so that a single ganglion cell receives input from multiple receptor organs. The other process (the central process) travels byway of the posterior root into the spinal cord, where it either makes synaptic contact with the second sensory neuron immediately, or else ascends toward the brainstem. There are no synapses within the dorsal root ganglion itself.

The fibers of individual nerve roots are redistributed into multiple peripheral nerves by way of the plexuses, and each nerve contains fibers from multiple adjacent radicular segments. The fibers of each radicular segment regroup in the periphery, however (Fig. 2.6), to innervate a particular segmental area of the skin (dermatome). Each dermatome corresponds to a single radicular segment, which, in turn, corresponds to a single “spinal cord segment.”

[pic][pic]

When a peripheral nerve is injured, the fibers within it, derived from multiple nerve roots, can no longer rejoin in the periphery with fibers derived from the same nerve roots but belonging to other peripheral nerves—in other words, the fibers in the injured nerve can no longer reach their assigned dermatomes. The sensory deficit thus has a different distribution from that of the dermatomal deficit seen after a radicular injury (Fig. 2.8).

[pic]

Central Components of the Somatosensory System

Posterior Columns. We can feel the position of our limbs and sense the degree of muscle tension in them. We can feel the weight of the body resting on our soles (i.e., we “feel the ground under our feet”). We can also perceive motion in the joints. Thus, at least some proprioceptive impulses must reach consciousness. Such impulses are derived from receptors in muscles, tendons, fasciae, joint capsules, and connective tissue (Vater-Pacini and Golgi-Mazzoni corpuscles), as well as cutaneous receptors. The afferent fibers conveying them are the distal processes of pseudounipolar neurons in the spinal ganglia. The central processes of these cells, in turn, ascend the spinal cord and terminate in the posterior column nuclei of the lower medulla.

Central continuation of posterior column pathways. In the posterior funiculus of the spinal cord, the afferent fibers derived from the lower limbs occupy the most medial position. The afferent fibers from the upper limbs join the cord at cervical levels and lie more laterally, so that the posterior funiculus here consists of two columns (on either side): the medial fasciculus gracilis (column of Goll), and the lateral fasciculus cuneatus (column of Burdach). The fibers in these columns terminate in the correspondingly named nuclei in the lower medulla, i.e., the nucleus gracilis and the nucleus cuneatus, respectively. These posterior column nuclei contain the second neurons, which project their axons to the thalamus (bulbothalamic tract). All of the bulbothalamic fibers cross the midline to the other side as they ascend, forming the so-called medial lemniscus (Figs. 2.16b and 2.17). These fibers traverse the medulla, pons, and midbrain and terminate in the ventral posterolateral nucleus of the thalamus (VPL, Fig. 6.4). Here they make synaptic contact with the third neurons, which, in turn, give off the thalamocortical tract; this tract ascends by way of the internal capsule (posterior to the pyramidal tract) and through the corona radiata to the primary somatosensory cortex in the postcentral gyrus. The somatotopic organization of the posterior column pathway is preserved all the way up from the spinal cord to the cerebral cortex (Fig. 2.19). The somatotopic projection on the postcentral gyrus resembles a person standing on his head—an inverted “homunculus” (Fig. 9.19).

[pic][pic]

[pic]

[pic]

[pic]

Lateral Spinothalamic Tract. The free nerve endings of the skin are the peripheral receptors for noxious and thermal stimuli.

These endings constitute the end organs that are, in turn, the peripheral processes of pseudounipolar neurons in the spinal ganglia. The central processes pass in the lateral portion of the posterior roots into the spinal cord and then divide longitudinally into short collaterals that terminate within one or two segments in the substantia gelatinosa, making synaptic contact with funicular neurons (second neurons) whose processes form the lateral spinothalamic tract (Fig. 2.16d). These processes cross the midline in the anterior spinal commissure before ascending in the contralateral lateral funiculus to the thalamus. Like the posterior columns, the lateral spinothalamic tract is somatotopically organized; here, however, the fibers from the lower limb lie laterally, while those from the trunk and upper limb lie more medially (Fig. 2.20).

[pic]

The fibers mediating pain and temperature sensation lie so close to each other that they cannot be anatomically separated. Lesions of the lateral spinothalamic tract thus impair both sensory modalities, though not always to the same degree.

Central continuation of the lateral spinothalamic tract. The fibers of the lateral spinothalamic tract travel up through the brainstem together with those of the medial lemniscus in the spinal lemniscus, which terminates in the ventral posterolateral nucleus of the thalamus (VPL). The third neurons in the VPL project via the thalamocortical tract to the postcentral gyrus in the parietal lobe (Fig. 2.19). Pain and temperature are perceived in a rough manner in the thalamus, but finer distinctions are not made until the impulses reach the cerebral cortex.

Anterior Spinothalamic Tract. The impulses arise in cutaneous receptors (peritrichial nerve endings, tactile corpuscles) and are conducted along a moderately thickly myelinated peripheral fiber to the pseudounipolar dorsal root ganglion cells, and thence by way of the posterior root into the spinal cord. Inside the cord, the central processes of the dorsal root ganglion cells travel in the posterior columns some segments upward, while collaterals travel 1 or 2 segments downward, making synaptic contact onto cells at various segmental levels in the gray matter of the posterior horn (Fig. 2.16c). These cells (the second neurons) then give rise to the anterior spinothalamic tract, whose fibers cross in the anterior spinal commissure, ascend in the contralateral anterolateral funiculus, and terminate in the ventral posterolateral nucleus of the thalamus, together with the fibers of the lateral spinothalamic tract and the medial lemniscus (Fig. 2.17). The third neurons in this thalamic nucleus then project their axons to the postcentral gyrus in the thalamocortical tract.

[pic]

Central Processing of Somatosensory Information. Fig. 2.17 traces all of the sensory pathways discussed above, in schematically simplified form and in spatial relation to one another, as they ascend from the posterior roots to their ultimate targets in the brain. The sensory third neurons in the thalamus send their axons through the posterior limb of the internal capsule (posterior to the pyramidal tract) to the primary somatosensory cortex, which is located in the postcentral gyrus (Brodmann cytoarchitectural areas 3a, 3b, 2, and 1). The third neurons that terminate here mediate superficial sensation, touch, pressure, pain, temperature, and (partly) proprioception (Fig. 2.19).

Sensorimotor integration. In fact, not all of the sensory afferent fibers from the thalamus terminate in the somatosensory cortex; some terminate in the primary motor cortex of the precentral gyrus. Thus, the sensory and motor cortical fields overlap to some extent, so that the precentral and postcentral gyri are sometimes together designated the sensorimotor area. The integration of function occurring here enables incoming sensory information to be immediately converted to outgoing motor impulses in sensorimotor regulatory circuits, about which we will have more to say later. The descending pyramidal fibers emerging from these circuits generally terminate directly—without any intervening interneurons—on motor neurons in the anterior horn. Finally, even though their functions overlap, it should be remembered that the precentral gyrus remains almost entirely a motor area, and the postcentral gyrus remains almost entirely a (somato)sensory area.

Differentiation of somatosensory stimuli by their origin and quality. It has already been mentioned that somatosensory representation in the cerebral cortex is spatially segregated in somatotopic fashion: the inverted sensory homunculus has been encountered in Fig 2.19 and will be seen again in Fig 9.19. But somatosensory representation in the cortex is also spatially segregated by modality: pain, temperature, and the other modalities are represented by distinct areas of the cortex.

Stereognosis. The recognition by touch of an object laid in the hand (stereognosis) is mediated not just by the primary sensory cortex, but also by association areas in the parietal lobe, in which the individual sensory features of the object, such as its size, shape, consistency, temperature, sharpness/dullness, softness/hardness, etc., can be integrated and compared with memories of earlier tactile experiences.

TESTING FOR SOMATOSENSORY DEFICITS

Testing for Pain

Have the patient discriminate between the point (“sharp”) and head (“dull”) of a pin. You have to be careful to avoid simply tapping into the sense of touch. One should avoid using the same pin with different patients, as there is evidence that certain viruses can be transmitted in this fashion.

Testing for Proprioception

Have the patient attempt to localize his or her limb in space following passive movement by the examiner (with patients eyes closed) or indicate the state of flexion or extension of one’s limb. However, perhaps the easiest and certainly one of the most sensitive and specific tests of proprioception is to passively extend or flex a digit (e.g., the great toe or a finger) while asking the patient to indicate the direction in which it is being moved. One also may check the integrity of the posterior columns by asking the patient to stand erect with the feet together. If the patient shows considerably more difficulty maintaining balance with the eyes closed than opened, this suggests posterior column compromise (Romberg’s sign). If comparable difficulties are noted regardless of whether the eyes are open or closed, cerebellar disease should be suspected.

Testing for Stereognosis

Here we might ask the patient to differentiate shapes, textures, or similarly configured small objects (e.g., a paper clip versus a safety pin) by touch. The patient also may be asked to identify numbers written on the fingertip or palm of the hand (graphesthesia), to make two-point discriminations, or to localize stimuli applied to various parts of the face, limbs, or torso.

Testing for Vibration

This procedure basically calls for the application of a tuning fork (256 cps) to bony prominences of the distal upper and lower extremities. The examiner must perform trials with and without the tuning fork vibrating to assure reliability and comprehension of the test. The patient is instructed to indicate whether the tuning fork is vibrating when touching the limbs, and if it is when the vibration appears to stop. A vibratory sensory level can be determined by starting distally and working one’s way proximately up the limb. The latter procedure would be important if a neurologist expects a peripheral neuropathy.

Testing for Temperature

The patient is asked to discriminate between objects of different temperatures. The examiner should ensure that the temperatures are readily discriminable, but neither is extreme. Test tubes filled with warm and cool water make reasonable testing devices. In all cases, the examiner always should compare performances on the right versus the left side of the body. One should be alert to the possibility of cortical neglect as well as old central or peripheral injuries or disease processes that might have an effect on peripheral processes, such as peripheral neuropathy secondary to diabetes or chronic alcohol abuse.

LESIONS AFFECTING THE ASCENDING AND DESCENDING TRACTS

Posterior column lesions. The posterior columns mainly transmit impulses arising in the proprioceptors and cutaneous receptors. If they are dysfunctional, the individual can no longer feel the position of his or her limbs; nor can he or she recognize an object laid in the hand by the sense of touch alone or identify a number or letter drawn by the examiner’s finger in the palm of the hand. Spatial discrimination between two stimuli delivered simultaneously at different sites on the body is no longer possible. As the sense of pressure is also disturbed, the floor is no longer securely felt under the feet; as a result, both stance and gait are impaired (gait ataxia), particularly in the dark or with the eyes closed. These signs of posterior column disease are most pronounced when the posterior columns themselves are affected, but they can also be seen in lesions of the posterior column nuclei, the medial lemniscus, the thalamus, and the postcentral gyrus.

The clinical signs of a posterior column lesion are, therefore, the following:

- Loss of the sense of position and movement (kinesthetic sense): the patient cannot state the position of his or her limbs without looking.

- Astereognosis: the patient cannot recognize and name objects by their shape and weight using the sense of touch alone.

- Agraphesthesia: the patient cannot recognize by touch a number or letter drawn in the palm of the hand by the examiner’s finger.

- Loss of two-point discrimination.

- Loss of vibration sense: the patient cannot perceive the vibration of a tuning fork placed on a bone.

- Positive Romberg sign: The patient cannot stand for any length of time with feet together and eyes closed without wobbling and perhaps falling over. The loss of proprioceptive sense can be compensated for, to a considerable extent, by opening the eyes (which is not the case, for example, in a patient with a cerebellar lesion).

Lesions of the lateral spinothalamic tract. The lateral spinothalamic tract is the main pathway for pain and temperature sensation. It can be neurosurgically transected to relieve pain (cordotomy); this operation is much less commonly performed today than in the past, because it has been supplanted by less invasive methods and also because the relief it provides is often only temporary. The latter phenomenon, long recognized in clinical experience, suggests that pain-related impulses might also ascend the spinal cord along other routes, e. g., in spinospinal neurons belonging to the fasciculus proprius. If the lateral spinothalamic tract is transected in the ventral portion of the spinal cord, pain and temperature sensation are deficient on the opposite side one or two segments below the level of the lesion, while the sense of touch is preserved (dissociated sensory deficit).

Lesions of the anterior spinothalamic tract. As explained above, the central fibers of the first neurons of this tract ascend a variable distance in the ipsilateral posterior columns, giving off collaterals along the way to the second neurons, whose fibers then cross the midline and ascend further in the contralateral anterior spinothalamic tract. It follows that a lesion of this tract at a lumbar or thoracic level generally causes minimal or no impairment of touch, because many ascending impulses can circumvent the lesion by way of the ipsilateral portion of the pathway. A lesion of the anterior spinothalamic tract at a cervical level, however, will produce mild hypesthesia of the contralateral lower limb.

A unilateral lesion of the somatosensory cortex produces a subtotal impairment of the perception of noxious, thermal, and tactile stimuli on the opposite side of the body; contralateral discrimination and position sense, however, are totally lost, as they depend on an intact cortex. Astereognosis. Injury to an area in the inferior portion of the parietal lobe impairs the ability to recognize objects by touch with the contralateral hand. This is called astereognosis.

Somatosensory Deficits due to Lesions at Specific Sites along the Somatosensory Pathways

Figure 2.21 shows some typical sites of lesions along the somatosensory pathways; the corresponding sensory deficits are discussed below.

- A cortical or subcortical lesion in the sensorimotor area corresponding to the arm or leg (a and b, respectively, in Fig. 2.21) causes paresthesia (tingling, etc.) and numbness in the contralateral limb, which are more pronounced distally than proximally. An irritative lesion at this site can produce a sensory focal seizure; because the motor cortex lies directly adjacent, there are often motor discharges as well (jacksonian seizure).

- A lesion of all sensory pathways below the thalamus (c) eliminates all qualities of sensation on the opposite side of the body.

- If all somatosensory pathways are affected except the pathway for pain and temperature (d), there is hypesthesia on the opposite side of the body and face, but pain and temperature sensation are unimpaired.

- Conversely, a lesion of the trigeminal lemniscus and of the lateral spinothalamic tract (e) in the brainstem impairs pain and temperature sensation on the opposite side of the body and face, but does not impair other somatosensory modalities.

- If the medial lemniscus and anterior spinothalamic tract (f) are affected, all somatosensory modalities of the contralateral half of the body are impaired, except pain and temperature.

[pic]

- Lesions of the spinal nucleus and tract of the trigeminal nerve and of the lateral spinothalamic tract (g) impair pain and temperature sensation on the ipsilateral half of the face and the contralateral half of the body.

- Posterior column lesions (h) cause loss of position and vibration sense, discrimination, etc., combined with ipsilateral ataxia.

- If the posterior horn of the spinal cord is affected by a lesion (i), ipsilateral pain and temperature sensation are lost, but other modalities remain intact (dissociated sensory deficit).

- A lesion affecting multiple adjacent posterior roots (j) causes radicular pain and paresthesiae, as well as impairment or loss of all sensory modalities in the affected area of the body, in addition to hypotonia or atonia, areflexia, and ataxia if the roots supply the upper or lower limb.

................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download