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Key Points:: Questions For Students
Key Points:: Questions For Students
Key Points:: Questions For Students
MODULE 1
Lessons # 1-2
Elements of the Nervous System. Anatomy, physiology, morphology of the Nervous System.
Somatosensory System. Pathways. Aids to the examination of the Somatosensory System. Somatosensory
Deficits due to Lesions at Specific Sites along the Somatosensory Pathways.
Key points:
1. Elements of the Nervous System.
2. Peripheral Components of the Somatosensory System
3. Posterior Columns.
4. Spinothalamic Tracts.
5. Central Components of the Somatosensory System
7. Testing for somatosensory deficits.
8. Somatosensory Deficits due to Lesions at Specific Sites along the Somatosensory Pathways
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Elements of the Nervous System.
NEURONS are classified by the number of processes (Figure 1-1).
A. PSEUDOUNIPOLAR NEURONS are located in the spinal (dorsal root) ganglia and sensory ganglia
of cranial nerves (CN) V, VII, IX, and X.
B. BIPOLAR NEURONS are found in the cochlear and vestibular ganglia of CN VIII, in the olfactory
nerve (CN I), and in the retina.
C. MULTIPOLAR NEURONS are the largest population of nerve cells in the nervous system. This group
includes motor neurons, neurons of the autonomic nervous system, interneurons, pyramidal cells of the cerebral
cortex, and Purkinje cells of the cerebellar cortex.
D. There are approximately 1011 neurons in the brain and approximately 1010 neurons in the neocortex.
NISSL SUBSTANCE is characteristic of neurons. It consists of rosettes of polysomes and rough endoplasmic
reticulum; therefore, it has a role in protein synthesis. Nissl substance is found in the nerve cell body
(perikaryon) and dendrites, not in the axon hillock or axon.
AXONAL TRANSPORT mediates the intracellular distribution of secretory proteins, organelles, and
cytoskeletal elements. It is inhibited by colchicine, which depolymerizes microtubules.
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C. FAST RETROGRADE TRANSPORT returns used materials from the axon terminal to the cell body
for degradation and recycling at a rate of 100 to 200 mm/day. It transports nerve growth factor, neurotropic
viruses, and toxins, such as herpes simplex, rabies, poliovirus, and tetanus toxin. It is mediated by
neurotubules and dynein.
CHROMATOLYSIS is the result of retrograde degeneration in the neurons of the CNS and PNS. There is a loss
of Nissl substance after axotomy.
THE BLOOD - BRAIN BARRIER consists of the tight junctions of nonfenestrated endothelial cells; some
authorities include the astrocytic foot processes. Infarction of brain tissue destroys the tight junctions of
endothelial cells and results in vasogenic edema, which is an infiltrate of plasma into the extracellular space.
THE BLOOD - CSF BARRIER consists of the tight junctions between the cuboidal epithelial cells of the choroid
plexus. The barrier is permeable to some circulating peptides (e.g., insulin) and plasma proteins (e.g.,
prealbumin).
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PIGMENTS AND INCLUSIONS
A. LIPOFUSCIN GRANULES are pigmented cytoplasmic inclusions that commonly accumulate with
aging. They are considered residual bodies that are derived from lysosomes.
B. MELANIN (NEUROMELANIN) is blackish intracytoplasmic pigment found in the substantia nigra
and locus coeruleus. It disappears from nigral neurons in patients who have Parkinson’s disease.
C. LEWY BODIES are neuronal inclusions that are characteristic of Parkinson’s disease.
D. NEGRI BODIES are intracytoplasmic inclusions that are pathognomonic of rabies. They are found in
the pyramidal cells of the hippocampus and the Purkinje cells of the cerebellum.
E. HIRANO BODIES are intraneuronal, eosinophilic, rodlike inclusions that are found in the
hippocampus of patients with Alzheimer’s disease.
F. NEUROFIBRILLARY TANGLES consist of intracytoplasmic degenerated neurofilaments. They are
seen in patients with Alzheimer's disease.
G. COWDRY TYPE A INCLUSION BODIES are intranuclear inclusions that are found in neurons and
glia in herpes simplex encephalitis.
Somatosensory System
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.
Receptors 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.
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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.
CUTANEOUS RECEPTORS (Figure 1-5) are divided into two large groups: free nerve endings and
encapsulated endings.
A. Free nerve endings are nociceptors (pain) and thermoreceptors (cold and heat).
B. Encapsulated endings are touch receptors (Meissner’s corpuscles) and pressure and vibration receptors
(Pacinian corpuscles).
C. Merkel disks are unencapsulated light touch receptors.
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.
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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. There are 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. 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.”
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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).
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POSTERIOR (DORSAL) COLUMN–MEDIAL LEMNISCUS PATHWAY (Figures 2.15, 2.16, 2.17)
A. FUNCTION. The lateral spinothalamic tract mediates pain and temperature sensation.
B. RECEPTORS are free nerve endings. The lateral spinothalamic tract receives input from fast- and
slow-conducting pain fibers (i.e., A-8 and C, respectively).
C. FIRST-ORDER NEURONS are found in the spinal (dorsal root) ganglia at all levels. They project
axons to the spinal cord through the dorsolateral tract of Lissauer (lateral root entry zone) to second-order
neurons.
D. SECOND-ORDER NEURONS are found in the dorsal horn. They give rise to axons that decussate in
the ventral white commissure and ascend in the contralateral lateral funiculus. Their axons terminate in the VPL
nucleus of the thalamus.
E. THIRD-ORDER NEURONS are found in the VPL nucleus of the thalamus. They project through the
posterior limb of the internal capsule to the primary somatosensory cortex (Brodmann’s areas 3, 1, and 2).
F. TRANSECTION OF THE LATERAL SPINOTHALAMIC TRACT results in contralateral loss of
pain and temperature below the lesion.
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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).
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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.
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TESTING FOR SOMATOSENSORY DEFICITS
Testing for pain
The best screening test for sensory loss uses a safety pin to lightly prick the face, torso, and 4 limbs; the
patient is asked whether the pinprick feels the same on both sides and whether the sensation is dull or sharp.
The pin is discarded after use to avoid potential transmission of bloodborne disorders (e.g., HIV infection,
hepatitis).
Testing for light touch
A cotton wisp can be used to test light touch.
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Romberg test
Inability to stand with feet together and eyes closed (Romberg test) indicates impaired position sense in
the lower extremities. When cerebellar disease is present, the patient stands with the feet apart but as close
together as possible without falling and only then closes the eyes.
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: the patient cannot distinguish between 1 and 2 simultaneous, closely
placed pinpricks on the fingertips.
- 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. 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).
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.
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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.
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- 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.
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