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Transcript
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
1
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)
2
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).
3
4
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.”
5
6
7
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).
8
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).
9
10
11
12
13
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
14
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).
15
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.
16
17
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.
18
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
19
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.
20
- 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 painrelated 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
21
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.
22
23
- 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.
24