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Ovid: Clinical Neuroanatomy

Authors: Snell, Richard S. Title: Clinical Neuroanatomy, 7th Edition Copyright ©2010 Lippincott Williams & Wilkins > Table of Contents > Chapter 3 – Nerve Fibers, Peripheral Nerves, Receptor and Effector Endings, Dermatomes, and Muscle Activity Chapter 3 Nerve Fibers, Peripheral Nerves, Receptor and Effector Endings, Dermatomes, and Muscle Activity A 45-year-old man was recovering from a mild upper respiratory tract infection when he suddenly noticed weakness in both legs while walking up stairs. He also developed a numb sensation over the lower part of both legs and the feet. Two days later, while shaving, he noticed a weakness of the muscles on the right side of his face. On physical examination, the patient did not appear to be ill. He had no pyrexia. Examination of his leg muscles showed obvious signs of muscle weakness involving both legs, especially below the knees. Both ankle reflexes were absent, and the right knee jerk was diminished. He had sensory deficits for touch and pain sensations in the distribution of the stocking area of both feet and lower legs and a mild form of facial nerve palsy involving the right side of the face. There was no neurologic evidence of loss of function of the brain or spinal cord. The patient was suspected of having Guillain-Barré syndrome and was admitted to the hospital for observation. The cause of this disease is unknown, although it is believed to be viral and involve the immune system. Histologically, the peripheral nerves show focal scattered areas of demyelination with an accumulation of lymphocytes and macrophages. As the myelin is lost, the axons are left naked and the Schwann cell bodies remain intact. In the majority of patients, recovery occurs in 2 to 4 weeks as remyelination occurs. Hospitalization is necessary in the early stages because the disease can spread rapidly to involve the intercostal and phrenic nerves, resulting in paralysis of the intercostal muscles and diaphragm. For the same reason, the coughing and swallowing reflexes should be watched carefully. A physician would find this disease impossible to understand without a knowledge of the structure of peripheral nerves. P.71 Chapter Objectives

  • To consider the basic structure and function of nerve fibers
  • To understand the process of nerve degeneration and regeneration
  • To review the special organs that lie at the ends of sensory and motor nerves
  • To examine the different sensory modalities
  • To learn the terms used in assessing skin sensory loss and abnormal muscle activity
  • To review the special organs that lie at the ends of sensory and motor nerves

In this chapter, the process of nerve degeneration and regeneration is described in detail because nerve lesions are very common in clinical practice and can be caused by a wide variety of diseases, including trauma, neoplasms, infection, metabolic dysfunction (diabetes), and chemical toxins such as lead. The process of nerve degeneration is fast and can take place in nerves in the central and peripheral nervous systems. The regeneration of nerves is slow and confined to the peripheral nervous system. Because so much research today is being devoted to investigating why regeneration in the central nervous system ceases within 2 weeks, the histologic changes that occur must be learned. The material in this chapter commonly forms the basis for examination questions. Nerve Fibers Nerve fiber is the name given to an axon (or a dendrite) of a nerve cell. The structure of axons and dendrites is described on page 47. Bundles of nerve fibers found in the central nervous system are often referred to as nerve tracts (Fig. 3-1); bundles of nerve fibers found in the peripheral nervous system are called peripheral nerves (Fig. 3-2). Two types of nerve fibers are present in the central and peripheral parts of the nervous system: myelinated and nonmyelinated. Myelinated Nerve Fibers A myelinated nerve fiber is one that is surrounded by a myelin sheath. The myelin sheath is not part of the neuron but is formed by a supporting cell (Figs. 3-2 and 3-3). In the central nervous system, the supporting cell is called the oligodendrocyte; in the peripheral nervous system, it is called the Schwann cell. The myelin sheath is a segmented, discontinuous layer interrupted at regular intervals by the nodes of Ranvier (Figs. 3-4 and 3-6). Each segment of the myelin sheath measures approximately 0.5 to 1.0 mm in length. In the central nervous system, each oligodendrocyte may form and maintain myelin sheaths for as many as 60 nerve fibers (axons). In the peripheral nervous system, there is only one Schwann cell for each segment of one nerve fiber. Formation of Myelin Myelin sheaths begin to form before birth and during the first year postnatally. The process has been studied with the electron microscope. In the peripheral nervous system, the nerve fiber or axon first indents the side of a Schwann cell (Fig. 3-4). Later, as the axon sinks farther into the Schwann cell, the external plasma membrane of the Schwann cell forms a mesaxon, which suspends the axon within the Schwann cell. Subsequently, it is thought, the Schwann cell rotates on the axon so that the plasma membrane becomes wrapped around the axon in a spiral. The direction of the spiral is clockwise in some segments and counterclockwise in others. To begin with, the wrappings are loose, but gradually the cytoplasm between the layers of the cell membrane disappears, leaving cytoplasm near the surface and in the region of the nucleus. The wrappings become tight with maturation of the nerve fiber. The thickness of the myelin depends on the number of spirals of Schwann cell membrane. Some nerve fibers are surrounded by only a few turns of the membrane, while others have as many as 50 turns. In electron micrographs of cross sections of mature myelinated nerve fibers, the myelin is seen to be laminated (Fig. 3-5). Each lamella measures 13 to 18 nm thick. The dark major dense line, about 2.5 nm thick, consists of two inner protein layers of the plasma membrane that are fused together. The lighter minor dense line, about 10 nm thick, is formed by the approximation of the outer surfaces of adjacent plasma membranes and is made up of lipid. The fused outer protein layers of the plasma membranes are very thin and form a thin intraperiod line situated in the center of the lighter lipid layer (Figs. 3-4 and 3-5). At the node of Ranvier, two adjacent Schwann cells terminate, and the myelin sheaths become thinner by the turning off of the lamellae (Fig. 3-6). At these regions, the plasma membrane of the axon, the axolemma, is exposed. The incisures of Schmidt-Lanterman are seen on longitudinal sections of myelinated nerve fibers. They represent areas where the dark major dense line is not formed as a result of the localized persistence of Schwann cell cytoplasm (Fig. 3-7). This persistence of cytoplasm involves all the layers of the myelin, and thus, there is a continuous spiral of cytoplasm from the outermost region of the Schwann cell to the region of the axon. This spiral of cytoplasm may provide a pathway for the conduction of metabolites from the surface region of the Schwann cell to the axon. P.72

Figure 3-1 Sections through the thoracic region of the spinal cord showing examples of nerve fibers entering or leaving the central nervous system; ascending and descending nerve fibers (tracts or pathways) are also shown.


Figure 3-2 Exploded view of a peripheral nerve showing the connective tissue sheaths and the structure of myelinated and nonmyelinated nerve fibers.


Figure 3-3 The relationship between an oligodendrocyte and myelinated nerve fibers in the central nervous system. Note the absence of a basement membrane.


Figure 3-4 A myelinated nerve fiber in the peripheral nervous system. A–D: Cross sections showing the stages in the formation of the myelin sheath. E: A longitudinal section of a mature myelinated nerve fiber showing a node of Ranvier. Note the presence of a basement membrane.


Figure 3-5 Electron micrograph of a transverse section of a peripheral nerve showing a myelinated axon with spiral myelin lamellae (center). Note the mesaxon (arrow). Parts of two other myelinated fibers are also shown. A number of nonmyelinated axons are enclosed in the peripheral cytoplasm of a Schwann cell (top). The mesaxons are indicated by arrows (÷28,000). (Courtesy Dr. H. de F. Webster.)


Figure 3-6 Electron micrograph of a longitudinal section of several myelinated axons showing the structure of a node of Ranvier (arrow). At the node, two adjacent Schwann cells terminate, and the myelin sheaths become thinner by the turning off of the lamellae. Note the many microtubules and microfilaments within the axons (÷12,220). (Courtesy Dr. H. de F. Webster.)


Figure 3-7 Schmidt-Lanterman incisures in the myelin sheath of a peripheral nerve. A: Transverse section of a myelinated nerve fiber. B: Schematic diagram of a myelinated nerve fiber in which the myelin sheath has been unrolled.

In the central nervous system, oligodendrocytes are responsible for the formation of the myelin sheaths. The plasma membrane of the oligodendrocyte becomes wrapped around the axon, and the number of layers will determine the thickness of the myelin sheath (Fig. 3-3). The nodes of Ranvier are situated in the intervals between adjacent oligodendrocytes. A single oligodendrocyte may be connected to the myelin sheaths of as many as 60 nerve fibers. For this reason, the process of myelination in the central nervous system cannot take place by rotation of the oligodendrocyte on the axon, as did the Schwann cell in the peripheral nervous system. It is possible that myelination in the central nervous system occurs by the growth in length of the process of the oligodendrocyte, the process wrapping itself around the axon. There are incisures of Schmidt-Lanterman in nerve fibers of the central nervous system. Table 3-1 provides a summary of facts concerning myelination in the central and peripheral nervous systems. Nonmyelinated Nerve Fibers The smaller axons of the central nervous system, the postganglionic axons of the autonomic part of the nervous P.79 system, and some fine sensory axons associated with the reception of pain are nonmyelinated.

Table 3-1 Myelination in the Peripheral and Central Nervous System
Location Cell Responsible Number of Nerve Fibers Served by Cell Nodes of Ranvier Schmidt-Lanterman Incisures Mesaxon
Peripheral nerve Schwann cell 1 Present Present Present
CNS tract Oligodendrocyte Up to 60 Present Present Absent
CNS, central nervous system.

In the peripheral nervous system, each axon, which is usually less than 1 µm in diameter, indents the surface of the Schwann cell so that it lies within a trough (Fig. 3-2). As many as 15 or more axons may share a single Schwann cell, each lying within its own trough or sometimes sharing a trough. In some situations, the troughs are deep and the axons are embedded deep in the Schwann cells, forming a mesaxon from the Schwann cell plasma membrane (Figs. 3-5 and 3-8). The Schwann cells lie close to one another along the length of the axons, and there are no nodes of Ranvier.

Figure 3-8 Electron micrograph of a transverse section of a myelinated nerve fiber and several nonmyelinated nerve fibers. (Courtesy Dr. J. M. Kerns.)

In areas where there are synapses or where motor transmission occurs, the axon emerges from the trough of the Schwann cell for a short distance, thus exposing the active region of the axon (Fig. 3-9). In the central nervous system, nonmyelinated nerve fibers run in small groups and are not particularly related to the oligodendrocytes. P.80

Figure 3-9 Autonomic neuromuscular junction between a nonmyelinated axon and a smooth muscle fiber.

Peripheral Nerves Peripheral nerves is a collective term for the cranial and spinal nerves. Each peripheral nerve consists of parallel bundles of nerve fibers, which may be efferent or afferent axons, may be myelinated or nonmyelinated, and are surrounded by connective tissue sheaths (Figs. 3-10 and 3-11). The nerve trunk is surrounded by a dense connective tissue sheath called the epineurium (Fig. 3-12). Within the sheath are bundles of nerve fibers, each of which is surrounded by a connective tissue sheath called the perineurium. Between the individual nerve fibers is a loose, delicate connective tissue referred to as the endoneurium. The connective tissue sheaths serve to support the nerve fibers and their associated blood vessels and lymph vessels. Peripheral nerve fibers can be classified according to their speed of conduction and size (Table 3-2).

Figure 3-10 Photomicrograph of a longitudinal section of a peripheral nerve stained with hematoxylin and eosin (÷400).
Figure 3-11 Photomicrograph of a transverse section of a peripheral nerve stained with hematoxylin and eosin (÷275).

Spinal Nerves and Spinal Nerve Roots There are 31 pairs of spinal nerves, which leave the spinal cord and pass through intervertebral foramina in the vertebral column. (For details, see p. 12.) Each spinal nerve is connected to the spinal cord by two roots: the anterior root and the posterior root (Fig. 3-13). The anterior root consists of bundles of nerve fibers carrying nerve impulses away from the central nervous system; these nerve fibers are called efferent fibers. The posterior root consists of bundles of nerve fibers carrying nerve impulses to the central nervous system; these nerve fibers are called afferent fibers. Because these fibers are concerned with conveying information to the central nervous system, they are called P.81 sensory fibers. The cell bodies of these nerve fibers are situated in a swelling on the posterior root called the posterior root ganglion.

Figure 3-12 Structure of a peripheral nerve.
Table 3-2 Classification of Nerve Fibers by Speed of Conduction and Size
Fiber Type Conduction Velocity (m/s) Fiber Diameter (µm) Functions Myelin Sensitivity to Local Anesthetics
A Fibers
   Alpha 70–120 12–20 Motor, skeletal muscle Yes Least
   Beta 40–70 5–12 Sensory, touch, pressure, vibration Yes  
   Gamma 10–50 3–6 Muscle spindle Yes  
   Delta 6–30 2–5 Pain (sharp, localized), temperature, touch Yes  
B Fibers 3–15 <3 Preganglionic autonomic Yes  
C Fibers 0.5–2.0 0.4–1.2 Pain (diffuse, deep), temperature, postganglionic autonomic No Most

Cranial Nerves There are 12 pairs of cranial nerves (Fig. 3-13), which leave the brain and pass through foramina in the skull. Some of these nerves are composed entirely of afferent nerve fibers bringing sensations to the brain (olfactory, optic, and vestibulocochlear), others are composed entirely of efferent fibers (oculomotor, trochlear, abducent, accessory, and hypoglossal), while the remainder possess both afferent and efferent fibers (trigeminal, facial, glossopharyngeal, and vagus). The cranial nerves are described in detail in Chapter 11. Sensory Ganglia The sensory ganglia of the posterior spinal nerve roots and of the trunks of the trigeminal, facial, glossopharyngeal, and vagal cranial nerves have the same structure. Each ganglion is surrounded by a layer of connective tissue that is continuous with the epineurium and perineurium of the peripheral nerve. The neurons are unipolar, possessing cell bodies that are rounded or oval in shape (Fig. 3-14). The cell bodies tend to be aggregated and separated by bundles of nerve fibers. A single nonmyelinated process leaves each cell body and, after a convoluted course, bifurcates at a T junction into peripheral and central branches. The former axon terminates in a series of dendrites in a peripheral sensory ending, and the latter axon enters the central nervous system. The nerve impulse, on reaching the T junction, passes directly from the peripheral axon to the central axon, thus bypassing the nerve cell body. Each nerve cell body is closely surrounded by a layer of flattened cells called capsular cells or satellite cells (Fig. 3-14). The capsular cells are similar in structure to Schwann P.82 P.83 cells and are continuous with these cells as they envelop the peripheral and central processes of each neuron.

Figure 3-13 A: Transverse section of the thoracic region of the spinal cord showing the formation of a spinal nerve from the union of an anterior and a posterior nerve root. B: Transverse section of the pons showing the sensory and motor roots of the trigeminal nerve.
Figure 3-14 Photomicrograph of a longitudinal section of a posterior root ganglion of a spinal nerve stained with hematoxylin and eosin (÷400).

Autonomic Ganglia The autonomic ganglia (sympathetic and parasympathetic ganglia) are situated at a distance from the brain and spinal cord. They are found in the sympathetic trunks, in prevertebral autonomic plexuses (e.g., in the cardiac, celiac, and mesenteric plexuses), and as ganglia in or close to viscera. Each ganglion is surrounded by a layer of connective tissue that is continuous with the epineurium and perineurium of the peripheral nerve. The neurons are multipolar and possess cell bodies that are irregular in shape (Fig. 3-15). The dendrites of the neurons make synaptic connections with the myelinated axons of preganglionic neurons. The axons of the neurons are of small diameter (C fibers) and unmyelinated, and they pass to viscera, blood vessels, and sweat glands. Each nerve cell body is closely surrounded by a layer of flattened cells called capsular cells or satellite cells. The capsular cells, like those of sensory ganglia, are similar in structure to Schwann cells and are continuous with them as they envelop the peripheral and central processes of each neuron. Peripheral Nerve Plexuses Peripheral nerves are composed of bundles of nerve fibers. In their course, peripheral nerves sometimes divide into branches that join neighboring peripheral nerves. If this occurs frequently, a network of nerves, called a nerve plexus, is formed. It should be emphasized that the formation of a nerve plexus allows individual nerve fibers to pass from one peripheral nerve to another, and in most instances, branching of nerve fibers does not take place. A plexus thus permits a redistribution of the nerve fibers within the different peripheral nerves.

Figure 3-15 Photomicrograph of a longitudinal section of a ganglion of the sympathetic trunk stained with hematoxylin and eosin (÷300).
Figure 3-16 Brachial plexus.

At the root of the limbs, the anterior rami of the spinal nerves form complicated plexuses. The cervical and brachial plexuses are at the root of the upper limbs (Fig. 3-16), and the lumbar and sacral plexuses are at the P.84 root of the lower limbs. This allows the nerve fibers derived from different segments of the spinal cord to be arranged and distributed efficiently in different nerve trunks to the various parts of the upper and lower limbs. Cutaneous nerves, as they approach their final destination, commonly form fine plexuses that again permit a rearrangement of nerve fibers before they reach their terminal sensory endings. The autonomic nervous system also possesses numerous nerve plexuses that consist of preganglionic and postganglionic nerve fibers and ganglia. Conduction in Peripheral Nerves In the resting unstimulated state, a nerve fiber is polarized so that the interior is negative to the exterior; the potential difference across the axolemma is about -80 mV and is called the resting membrane potential (Fig. 3-17). As has been explained previously (see p. 42), this so-called resting potential is produced by the diffusion of sodium and potassium ions through the channels of the plasma membrane and is maintained by the sodium-potassium pump. Three Na+ ions are pumped to the outside for each two K+ ions to the inside. The pump involves active transport across the membrane and requires adenosine triphosphate (ATP) to provide the energy.

Figure 3-17 Ionic and electrical changes that occur in a nerve fiber when it is conducting an impulse.

A nerve impulse (action potential) starts at the initial segment of the axon and is a self-propagating wave of electrical negativity that passes rapidly along the surface of the plasma membrane (axolemma). The wave of electrical negativity is initiated by an adequate stimulus being applied to the surface of the neuron (Fig. 3-18). Under normal circumstances, this occurs at the initial segment of the axon, which is the most sensitive part of the neuron. The stimulus alters the permeability of the membrane to Na+ ions at the point of stimulation. Now, Na+ ions rapidly enter the axon (Fig. 3-17). The positive ions outside the axolemma quickly decrease to zero. Therefore, the membrane potential is reduced to zero and is said to be depolarized. A typical resting potential is -80 mV, with the outside of the membrane positive to the inside; the action potential is about +40 mV, with the outside of the membrane negative to the inside. In small-diameter axons, the action potential may not rise to as much as 40 mV. P.85

Figure 3-18 Creation of the action potential by the arrival of a stimulus from a single presynaptic terminal. Note that the action potential generated at the initial segment will only occur if the threshold for excitation is reached at the initial segment. (From Snell, R. S. Clinical Neuroanatomy: A Review with Questions and Explanations [3rd ed., p. 7]. Baltimore: Lippincott Williams & Wilkins.)

The negatively charged point on the outside of the axolemma now acts as a stimulus to the adjacent positively charged axolemma, and in less than 1 msec, the polarity of the adjacent resting potential is reversed (Fig. 3-17). The action potential now has moved along the axolemma from the point originally stimulated to the adjacent point on the membrane. It is in this manner that the action potential travels along the full length of a nerve fiber to its end. As the action potential moves along the nerve fiber, the entry of the Na+ ions into the axon ceases, and the permeability of the axolemma to K+ ions increases. Now, K+ ions rapidly diffuse outside the axon (since the concentration is much higher within the axon than outside so that the original resting membrane potential is restored. The permeability of the axolemma now decreases, and the status quo is restored by the active transport of the Na+ ions out of the axon and the K+ ions into the axon. The outer surface of the axolemma is again electrically positive compared with that of the inner surface. This is a simplistic description of the movements of the Na+ and K+ ions. For further details on the voltage-gated Na+ and K+ channels, the Na+ and K+ pumps, and the Na+ and K+ leak channels, refer to a textbook of physiology. For a short time after the passage of a nerve impulse along a nerve fiber, while the axolemma is still depolarized, a second stimulus, however strong, is unable to excite the nerve. This period of time is called the absolute refractory period. The underlying reason for the refractory period is that the Na+ channels become inactivated, and no stimulation, however strong, will open the Na+ gates. This period is followed by a further short interval during which the excitability of the nerve gradually returns to normal. This latter period is called the relative refractory period. It is clear from this that the refractory period makes a continuous excitatory state of the nerve impossible and limits the frequency of the impulses. The conduction velocity of a nerve fiber is proportional to the cross-sectional area of the axon, with the thicker fibers conducting more rapidly than those of smaller diameter. In the large motor fibers (alpha fibers), the rate may be as high as 70 to 120 m/s; the smaller sensory fibers have slower conduction rates (see Table 3-2). In nonmyelinated fibers, the action potential passes continuously along the axolemma, progressively exciting neighboring areas of membrane (Fig. 3-19). In myelinated fibers, the presence of a myelin sheath serves as an insulator, and few ions can flow through the sheath. Consequently, a myelinated nerve fiber can be stimulated only at the nodes of Ranvier, where the axon is naked and the ions can pass freely through the plasma membrane between the extracellular fluid and the axoplasm. In these fibers, the action P.86 potential jumps from one node to the next (Fig. 3-19). The action potential at one node sets up a current in the surrounding tissue fluid, which quickly produces depolarization at the next node. This leaping of the action potential from one node to the next is referred to as saltatory conduction (Fig. 3-19). This is a more rapid mechanism than is found in nonmyelinated fibers (120.0 m/s in a large myelinated fiber compared with 0.5 m/s in a very small unmyelinated fiber).

Figure 3-19 Electrical changes that occur in stimulated myelinated axon (saltatory conduction) (A) and stimulated nonmyelinated axon (B).

Receptor Endings An individual receives impressions from the outside world and from within the body by special sensory nerve endings or receptors. Sensory receptors can be classified into five basic functional types:

  • Mechanoreceptors. These respond to mechanical deformation.
  • Thermoreceptors. These respond to changes in temperature; some receptors respond to cold and others to heat.
  • Nociceptors. These respond to any stimuli that bring about damage to the tissue.
  • Electromagnetic receptors. The rods and cones of the eyes are sensitive to changes in light intensity and wavelength.
  • Chemoreceptors. These respond to chemical changes associated with taste and smell and oxygen and carbon dioxide concentrations in the blood.

Anatomical Types of Receptors For convenience, the sensory endings can be classified, on a structural basis, into nonencapsulated and encapsulated receptors. Table 3-3 classifies and compares the receptor types. Nonencapsulated Receptors Free Nerve Endings Free nerve endings are widely distributed throughout the body (Fig. 3-20). They are found between the epithelial cells of the skin, the cornea, and the alimentary tract, and in connective tissues, including the dermis, fascia, ligaments, joint capsules, tendons, periosteum, perichondrium, haversian systems of bone, tympanic membrane, and dental pulp; they are also present in muscle. The afferent nerve fibers from the free nerve endings are either myelinated or nonmyelinated. The terminal endings are devoid of a myelin sheath, and there are no Schwann cells covering their tips. Most of these endings detect pain, while others detect crude touch, pressure, and tickle sensations, and possibly cold and heat. Merkel Discs Merkel discs are found in hairless skin, for example, the fingertips (Figs. 3-21 and 3-22), and in hair follicles. The nerve fiber passes into the epidermis and terminates as a disc-shaped expansion that is applied closely to a dark-staining epithelial cell in the deeper part of the epidermis, called the P.87 P.88 P.89 Merkel cell. In hairy skin, clusters of Merkel discs, known as tactile domes, are found in the epidermis between the hair follicles.

Table 3-3 Classification and Comparison of Receptor Types
Type of Receptor Location Stimulus Sensory Modality Adaptability Fibers
Nonencapsulated Receptors
Free nerve endings Epidermis, cornea, gut, dermis, ligaments, joint capsules, bone, dental pulp, etc. Mechanoreceptor Pain (fast), pain (slow), touch (crude), pressure, ? heat and cold Rapid A delta, C
Merkel discs Hairless skin Mechanoreceptor Touch Slow A beta
Hair follicle receptors Hairy skin Mechanoreceptor Touch Rapid A beta
Encapsulated Receptors
Meissner’s corpuscles Dermal papillae of skin of palm and sole of foot Mechanoreceptor Touch Rapid A beta
Pacinian corpuscles Dermis, ligaments, joint capsules, peritoneum, external genitalia, etc. Mechanoreceptor Vibration Rapid A beta
Ruffini corpuscles Dermis of hairy skin Mechanoreceptor Stretch Slow A beta
Neuromuscular spindles Skeletal muscle Mechanoreceptor Stretch— muscle length Fast A alpha, A beta
Neurotendinous spindles Tendons Mechanoreceptor Compression—muscle tension Fast A alpha
Figure 3-20 Free nerve endings in the skin. The nerve fibers in the epidermis are naked.
Figure 3-21 Merkel discs in the skin. A: Low magnification. B: Merkel disc showing the expanded ending of an axon with a stippled tactile cell.
Figure 3-22 Photomicrograph of digital skin showing fine nerve terminals ending in Merkel discs, stained by the silver method. (Courtesy Dr. N. Cauna.)

Merkel discs are slowly adapting touch receptors that transmit information about the degree of pressure exerted on the skin, such as when one is holding a pen. Hair Follicle Receptors Nerve fibers wind around the follicle in its outer connective tissue sheath below the sebaceous gland. Some branches surround the follicle, while others run parallel to its long axis (Figs. 3-23 and 3-24). Many naked axon filaments terminate among the cells of the outer root sheath. Bending of the hair stimulates the follicle receptor, which belongs to the rapidly adapting group of mechanoreceptors. While the hair remains bent, the receptor is silent, but when the hair is released, a further burst of nerve impulses is initiated. Encapsulated Receptors Encapsulated receptors show wide variations in size and shape, and the termination of the nerve is covered by a capsule. Meissner’s Corpuscles Meissner’s corpuscles are located in the dermal papillae of the skin (Figs. 3-25 and 3-26), especially that of the palm of the hand and the sole of the foot. Many also are present in the skin of the nipple and the external genitalia. Each corpuscle is ovoid in shape and consists of a stack of modified flattened Schwann cells arranged transversely across the long axis of the corpuscle. The corpuscle is enclosed by a capsule of connective tissue that is continuous with the endoneurium of the nerves that enter it. A few myelinated nerve fibers enter the deep end of the corpuscle; myelinated and unmyelinated branches decrease in size and ramify among the Schwann cells. There is a considerable reduction in the number of Meissner’s corpuscles between birth and old age.

Figure 3-23 Nerve endings around a hair follicle.

Meissner’s corpuscles are very sensitive to touch and are rapidly adapting mechanoreceptors. They enable an individual to distinguish between two pointed structures when they are placed close together on the skin (two-point tactile discrimination). Pacinian Corpuscles Pacinian corpuscles (Figs. 3-27 and 3-28) are widely distributed throughout the body and are abundant in the dermis, subcutaneous tissue, ligaments, joint capsules, pleura, peritoneum, nipples, and external genitalia. Each corpuscle is ovoid in shape, measuring about 2 mm long and about 100 to 500 µm across. It consists of a capsule and a central core containing the nerve ending. The capsule consists of numerous P.90 P.91concentric lamellae of flattened cells. A large myelinated nerve fiber enters the corpuscle and loses its myelin sheath and then its Schwann cell covering. The naked axon, surrounded by lamellae formed of flattened cells, passes through the center of the core and terminates in an expanded end.

Figure 3-24 Photomicrograph of nerve endings around a hair follicle stained by the silver method. (Courtesy Dr. M. J. T. Fitzgerald.)
Figure 3-25 Detailed structure of a Meissner’s corpuscle in the skin.
Figure 3-26 Photomicrograph of a Meissner’s corpuscle of the skin. (Courtesy Dr. N. Cauna.)
Figure 3-27 Detailed structure of a pacinian corpuscle in the skin.
Figure 3-28 Photomicrograph of part of a pacinian corpuscle of the skin seen in transverse section showing concentric lamellae of flattened cells. (Courtesy Dr. N. Cauna.)

The pacinian corpuscle is a rapidly adapting mechanoreceptor that is particularly sensitive to vibration. It can respond to up to 600 stimuli per second. Ruffini Corpuscles Ruffini corpuscles are located in the dermis of hairy skin. Each corpuscle consists of several large unmyelinated nerve fibers ending within a bundle of collagen fibers and surrounded by a cellular capsule. These slowly adapting mechanoreceptors are stretch receptors, which respond when the skin is stretched. Function of Cutaneous Receptors In the past, it was believed that the different histologic types of receptors corresponded to specific types of sensation. It was soon pointed out that there are areas of the body that have only one or two histologic types of receptors and yet they are sensitive to a variety of different stimuli. Moreover, although the body has these different receptors, all nerves only transmit nerve impulses. It is now generally agreed that the type of sensation felt is determined by the specific area of the central nervous system to which the afferent nerve fiber passes. For example, if a pain nerve fiber is stimulated by heat, cold, touch, or pressure, the individual will experience only pain. Transduction of Sensory Stimuli Into Nerve Impulses Transduction is the process by which one form of energy (the stimulus) is changed into another form of energy P.92 (electrochemical energy of the nerve impulse). The stimulus, when applied to the receptor, brings about a change in potential of the plasma membrane of the nerve ending. Since this process takes place in the receptor, it is referred to as the receptor potential. The amplitude of the receptor potential is proportional to the intensity of the stimulus. By opening more ion channels for a longer time, a stronger mechanical pressure, for example, can produce a greater depolarization than does weak pressure. With chemoreceptors and photoreceptors, the receptor potential is produced by second messengers activated when the stimulus agent binds to the membrane receptors coupled to G proteins. If large enough, the receptor potential will generate an action potential that will travel along the afferent nerve fiber to the central nervous system.

Figure 3-29 Neuromuscular spindle showing two types of intrafusal fibers: the nuclear bag and nuclear chain fibers.

Joint Receptors Four types of sensory endings can be located in the capsule and ligaments of synovial joints. Three of these endings are encapsulated and resemble pacinian, Ruffini, and tendon stretch receptors. They provide the central nervous system with information regarding the position and movements of the joint. A fourth type of ending is nonencapsulated and is thought to be sensitive to excessive movements and to transmit pain sensations. Neuromuscular Spindles Neuromuscular spindles, or muscular spindles (Figs. 3-29 and 3-30), are found in skeletal muscle and are most numerous P.93 toward the tendinous attachment of the muscle. They provide the central nervous system with sensory information regarding the muscle length and the rate of change in the muscle length. This information is used by the central nervous system in the control of muscle activity.

Figure 3-30 Photomicrograph of a neuromuscular spindle.

Each spindle measures about 1 to 4 mm in length and is surrounded by a fusiform capsule of connective tissue. Within the capsule are 6 to 14 slender intrafusal muscle fibers; the ordinary muscle fibers situated outside the spindles are referred to as extrafusal fibers. The intrafusal fibers of the spindles are of two types: the nuclear bag and nuclear chain fibers. The nuclear bag fibers are recognized by the presence of numerous nuclei in the equatorial region, which consequently is expanded; also, cross striations are absent in this region. In the nuclear chain fibers, the nuclei form a single longitudinal row or chain in the center of each fiber at the equatorial region. The nuclear bag fibers are larger in diameter than the nuclear chain fibers, and they extend beyond the capsule at each end to be attached to the endomysium of the extrafusal fibers. There are two types of sensory innervation of muscle spindles: the annulospiral and the flower spray. The annulospiral endings are situated at the equator of the intrafusal fibers. As the large myelinated nerve fiber pierces the capsule, it loses its myelin sheath, and the naked axon winds spirally around the nuclear bag or chain portions of the intrafusal fibers. The flower-spray endings are situated mainly on the nuclear chain fibers some distance away from the equatorial region. A myelinated nerve fiber slightly smaller than that for the annulospiral ending pierces the capsule and loses its myelin sheath, and the naked axon branches terminally and ends as varicosities; it resembles a spray of flowers. Stretching (elongation) of the intrafusal fibers results in stimulation of the annulospiral and flower-spray endings, and nerve impulses pass to the spinal cord in the afferent neurons. Motor innervation of the intrafusal fibers is provided by fine gamma motor fibers. The nerves terminate in small motor end-plates situated at both ends of the intrafusal fibers. Stimulation of the motor nerves causes both ends of the intrafusal fibers to contract and activate the sensory endings. The equatorial region, which is without cross striations, is noncontractile. The extrafusal fibers of the remainder of the muscle receive their innervation in the usual way from large alpha-size axons. Function of the Neuromuscular Spindle Under resting conditions, the muscle spindles give rise to afferent nerve impulses all the time, and most of this information is not consciously perceived. When muscle activity occurs, either actively or passively, the intrafusal fibers are stretched, and there is an increase in the rate of passage of nerve impulses to the spinal cord or brain in the afferent neurons. Similarly, if the intrafusal fibers are now relaxed due to the cessation of muscle activity, the result is a decrease in the rate of passage of nerve impulses to the spinal cord or brain. The neuromuscular spindle thus plays a very important role in keeping the central nervous system informed about the length of a muscle and the rate of change of its length, thereby indirectly influencing the control of voluntary muscle. Stretch Reflex The neurons of the spinal cord involved in the simple stretch reflex are as follows. Stretching a muscle results in elongation of the intrafusal fibers of the muscle spindle and stimulation of the annulospiral and flower-spray endings. The nerve impulses reach the spinal cord in the afferent neurons and synapse with the large alpha motor neurons situated in the anterior gray horns of the spinal cord. Nerve impulses now pass via the efferent motor nerves and stimulate the extrafusal muscle fibers, and the muscle contracts. This simple stretch reflex depends on a two-neuron arc consisting of an afferent neuron and an efferent neuron. It is interesting to note that the muscle spindle afferent impulses P.94 inhibit the alpha motor neurons supplying the antagonist muscles. This effect is called reciprocal inhibition. Control of the Intrafusal Fibers of the Neuromuscular Spindle In the brain and spinal cord, there are centers that give rise to tracts that synapse with gamma motor neurons in the spinal cord. The reticular formation, the basal ganglia, and the cerebellum are examples of such centers. It is by these means that these centers can greatly influence voluntary muscle activity. The gamma efferent motor fibers cause shortening of the intrafusal fibers, stretching the equatorial regions and stimulating the annulospiral and flower-spray endings. This, in turn, initiates the reflex contraction of the extrafusal fibers described previously. It is estimated that about one-third of all the motor fibers passing to a muscle are gamma efferents; the remaining two-thirds are the large alpha motor fibers. It is believed that the nuclear bag fibers are concerned with dynamic responses and are associated more with position and velocity of contraction, whereas the nuclear chain fibers are associated with slow static contractions of voluntary muscle. Neurotendinous Spindles Neurotendinous spindles (Golgi tendon organs) are present in tendons and are located near the junctions of tendons with muscles (Fig. 3-31). They provide the central nervous system with sensory information regarding the tension of muscles.

Figure 3-31 A neurotendinous spindle.

Each spindle consists of a fibrous capsule that surrounds a small bundle of loosely arranged tendon (collagen) fibers (intrafusal fibers). The tendon cells are larger and more numerous than those found elsewhere in the tendon. One or more myelinated sensory nerve fibers pierce the capsule, lose their myelin sheath, branch, and terminate in club-shaped endings. The nerve endings are activated by being squeezed by the adjacent tendon fibers within the spindle when tension develops in the tendon. Unlike the neuromuscular spindle, which is sensitive to changes in muscle length, the neurotendinous organ detects changes in muscle tension. Function of the Neurotendinous Spindle Increased muscle tension stimulates the neurotendinous spindles, and an increased number of nerve impulses reach the spinal cord through the afferent nerve fibers. These fibers synapse with the large alpha motor neurons situated in the anterior gray horns of the spinal cord. Unlike the muscle spindle reflex, this reflex is inhibitory and inhibits muscle contraction. In this manner, the tendon reflex prevents the development of too much tension in the muscle. Although this function is probably important as a protective mechanism, its main function is to provide the central nervous system with information that can influence voluntary muscle activity. P.95 Effector Endings Innervation of Skeletal Muscle Skeletal muscle is innervated by one or more nerves. In the limbs and head and neck, the innervation is usually single, but in the large muscles of the abdominal wall, the innervation is multiple, the latter muscles having retained their embryonic segmental nerve supply. The nerve supply and blood supply to a muscle enter it at a more or less constant position called the neurovascular hilus. The nerve to a muscle contains motor and sensory fibers. The motor fibers are of three types: (1) large alpha myelinated fibers, (2) small gamma myelinated fibers, and (3) fine unmyelinated C fibers. The large myelinated axons of the alpha anterior horn cells supply the extrafusal fibers that form the main mass of the muscle. The small gamma myelinated fibers supply the intrafusal fibers of the neuromuscular spindles. The fine unmyelinated fibers are postganglionic autonomic efferents that supply the smooth muscle in the walls of blood vessels. The sensory fibers are of three main types: (1) the myelinated fibers, which originate in the annulospiral and flower-spray endings of the neuromuscular spindles; (2) the myelinated fibers, which originate in the neurotendinous spindles; and (3) the myelinated and nonmyelinated fibers, which originate from a variety of sensory endings in the connective tissue of the muscle.

Figure 3-32 Simple reflex arc consisting of an afferent neuron arising from neuromuscular spindles and neurotendinous spindles and an efferent lower motor neuron whose cell body is an alpha anterior horn cell within the spinal cord. Note that the efferent neuron terminates on muscle fibers at motor end-plates.

Motor Unit The motor unit may be defined as the single alpha motor neuron and the muscle fibers that it innervates (Fig. 3-32). The muscle fibers of a single motor unit are widely scattered throughout the muscle. Where fine, precise muscle control is required, such as in the extraocular muscles or the small muscles of the hand, the motor units possess only a few muscle fibers. Where precise control is not necessary, however, as in a large limb muscle such as the gluteus maximus, a single motor nerve may innervate many hundreds of muscle fibers. Neuromuscular Junctions in Skeletal Muscle Skeletal muscle fibers are innervated by large, alpha myelinated nerve fibers derived from large motor neurons in the anterior gray columns (horns) of the spinal cord or from the motor nuclei of cranial nerves. As each myelinated fiber enters a skeletal muscle, it branches many times. The number of branches depends on the size of the motor unit. A single branch then terminates on a muscle fiber at a site referred to as a neuromuscular junction or motor end-plate (Figs. 3-33 and 3-34). The great majority of muscle fibers are innervated by just one motor end-plate. On reaching the muscle fiber, the nerve loses its myelin sheath and breaks up into a number of fine P.96 P.97 branches. Each branch ends as a naked axon and forms the neural element of the motor end-plate (Fig. 3-35). The axon is expanded slightly and contains many mitochondria and vesicles (approximately 45 nm in diameter). At the site of the motor end-plate, the surface of the muscle fiber is elevated slightly to form the muscular element of the plate, often referred to as the sole plate (Fig. 3-33). The elevation is due to the local accumulation of granular sarcoplasm beneath the sarcolemma and the presence of numerous nuclei and mitochondria, the latter providing the ATP, which is the energy source for the synthesis of the transmitter acetylcholine (ACh).

Figure 3-33 A: A skeletal neuromuscular junction. B: Enlarged view of a muscle fiber showing the terminal naked axon lying in the surface groove of the muscle fiber.
Figure 3-34 Photomicrograph showing nerve fibers terminating on skeletal muscle fibers at motor end-plates, stained histochemically for acetylcholinesterase and counterstained with silver. (Courtesy Dr. M. J. T. Fitzgerald.)
Figure 3-35 A: Photomicrograph of a motor end-plate showing terminal branching of a nerve fiber. B: Electron micrograph of a terminal axon at a motor end-plate showing the axon lying in a groove on the surface of the muscle fiber. (Courtesy Dr. J. M. Kerns.)

The expanded naked axon lies in a groove on the surface of the muscle fiber outside the plasma membrane (sarcolemma). Each groove is formed by the infolding of the plasma membrane. The groove may branch many times, with each branch containing a division of the axon. It is important to realize that the axons are truly naked; the Schwann cells merely serve as a cap or roof to the groove and never project into it. The floor of the groove is formed of the plasma membrane, which is thrown into numerous small folds, called junctional folds; these serve to increase the surface area of the plasma membrane that lies close to the naked axon (Fig. 3-36). The plasma membrane of the axon (the axolemma or presynaptic membrane) is separated, by a space about 30 to 50 nm wide, from the plasma membrane of the muscle fiber (the sarcolemma or postsynaptic membrane). This space constitutes the synaptic cleft. The synaptic cleft is filled with the basement membranes of the axon and the muscle fiber (Fig. 3-33). The motor end-plate is strengthened by the connective tissue sheath of the nerve fiber (endoneurium), which becomes continuous with the connective tissue sheath of the muscle fiber (endomysium). P.98

Figure 3-36 Electron micrograph of a cross section of an axon at a motor end-plate showing the axon lying in a groove of folded sarcolemma. (Courtesy Dr. J. M. Kerns.)

A nerve impulse (action potential), on reaching the presynaptic membrane of the motor end-plate, causes the opening of voltage-gated Ca2+ channels that allow Ca2+ ions to enter the axon. This stimulates the fusion of some of the synaptic vesicles with the presynaptic membrane and causes the release of acetylcholine into the synaptic cleft. The acetylcholine is thus discharged into the cleft by a process of exocytosis and diffuses rapidly across the cleft to reach the nicotinic type of ACh receptors on the postsynaptic membrane of the junctional folds. The postsynaptic membrane possesses large numbers of ACh-gated channels. Once the ACh-gated channels are opened, the postsynaptic membrane becomes more permeable to Na+ ions, which flow into the muscle cell, and a local potential called the end-plate potential is created. (The ACh-gated channels are also permeable to K+ ions, which flow out of the cell but to a lesser extent.) If the end-plate potential is large enough, the voltage-gated channels for Na+ ions are opened, and an action potential will be initiated and will spread along the surface of the plasma membrane (sarcolemma). The wave of depolarization is carried into the muscle fiber to the contractile myofibrils through the system of T tubules. This leads to the release of Ca2+ ions from the sarcoplasmic reticulum, which, in turn, causes the muscle to contract. The amount of acetylcholine released at the motor end-plate will depend on the number of nerve impulses arriving at the nerve terminal. Once the acetylcholine crosses the synaptic cleft and triggers the ionic channels on the postsynaptic membrane, it immediately undergoes hydrolysis due to the presence of the enzyme acetylcholinesterase (AChE) (Fig. 3-34). The enzyme is adherent to the fine collagen fibrils of the basement membranes in the cleft; some of the acetylcholine diffuses away from the cleft. The acetylcholine remains for about 1 msec in contact with the postsynaptic membrane, and it is rapidly destroyed to prevent reexcitation of the muscle fiber. After the fall in concentration of ACh in the cleft, the ionic channels close and remain closed until the arrival of more ACh. Skeletal muscle fiber contraction is thus controlled by the frequency of the nerve impulses that arrive at the motor nerve terminal. A resting muscle fiber shows small occasional depolarizations (end-plate potentials) at the motor end-plate, which are insufficient to cause an action potential and make the fiber contract. These are believed to be due to the sporadic release of acetylcholine into the synaptic cleft from a single presynaptic vesicle. The sequence of events that takes place at a motor end-plate on stimulation of a motor nerve can be briefly summarized as follows:

  • ACh → Nicotinic type of ACh receptor, ACh-gated channels opened → Na+ influx → End-plate potential created.
  • End-plate potential (if large enough) → Na+-gated channels opened → Na+ influx → Action potential created.
  • Action potential → Increased release of Ca2+ → Muscle fiber contraction.
  • P.99

  • Immediate hydrolysis of ACh by AChE → ACh-gated channels closed → Muscle fiber repolarization.

If drugs having a similar chemical structure to acetylcholine were to arrive at the receptor site of a motor end-plate, they might bring about the same changes as acetylcholine and mimic its action. Two examples of such drugs are nicotine and carbamylcholine. If, on the other hand, drugs having a similar chemical structure to acetylcholine were to arrive at the receptor site of a motor end-plate and were unable to bring about the sequence of changes normally induced by acetylcholine, they would occupy the receptor site and block access of acetylcholine. Such drugs would be competing with acetylcholine and are called competitive blocking agents. An example of such a drug is d-tubocurarine, which causes skeletal muscle to relax and not contract by preventing the action of locally produced acetylcholine (see p. 116). Neuromuscular Junctions in Smooth Muscle In smooth muscle, where the action is slow and widespread, such as within the wall of the intestine, the autonomic nerve fibers branch extensively; thus, a single neuron exerts control over a large number of muscle fibers. In some areas (e.g., the longitudinal layer of smooth muscle in the intestine), only a few muscle fibers are associated with autonomic endings, the wave of contraction passing from one muscle cell to another by means of gap junctions (Fig. 3-37).

Figure 3-37 Autonomic neuromuscular junction. The exposed axons are close to the smooth muscle fibers.

In smooth muscle, in which the action is fast and precision is required, such as in the iris, the branching of the nerve fibers is less extensive; thus, a single neuron exerts control over only a few muscle fibers. The autonomic nerve fibers, which are postganglionic, are nonmyelinated and terminate as a series of varicosed branches. An interval of 10 to 100 nm may exist between the axon and the muscle fiber. At the site where transmission is to occur, the Schwann cell is retracted so that the axon lies within a shallow groove on its surface (Fig. 3-37). Therefore, part of the axon is naked, permitting free diffusion of the transmitter substance from the axon to the muscle cell (Fig. 3-37). Here, the axoplasm contains numerous vesicles similar to those seen at the motor end-plate of skeletal muscle. Smooth muscle is innervated by sympathetic and parasympathetic parts of the autonomic system. Those nerves that are cholinergic liberate acetylcholine at their endings by a process of exocytosis, with the acetylcholine P.100 being present in the vesicles at the nerve ending. Those nerves that are noradrenergic liberate norepinephrine at their endings by a process of exocytosis, with the norepinephrine being present in dark-cored vesicles at the nerve endings. Both acetylcholine and norepinephrine bring about depolarization of the muscle fibers innervated, which thereupon contract. The fate of these neurotransmitter substances differs. The acetylcholine is hydrolyzed in the presence of acetylcholinesterase in the synaptic cleft of the muscle fiber, and the norepinephrine is taken up by the nerve endings. It is noteworthy that in some areas of the body (e.g., bronchial muscle), the norepinephrine liberated from postganglionic sympathetic fibers causes smooth muscle to relax and not contract. Neuromuscular Junctions in Cardiac Muscle Nonmyelinated postganglionic sympathetic and parasympathetic autonomic nerves extend into the connective tissue between the muscle fibers and terminate in close proximity to the individual cardiac muscle fibers. At the site where transmission takes place, the axon becomes naked because of the retraction of the Schwann cell. This permits free diffusion of the neurotransmitter substance from the axon to the muscle fiber. Because of the presence of intermittent desmosomes and gap junctions between abutting muscle fibers, excitation and contraction of one muscle fiber rapidly spread from fiber to fiber. Nerve Endings on Secretory Cells of Glands Nonmyelinated postganglionic autonomic nerves extend into the connective tissue of glands and branch close to the secretory cells (Fig. 3-38). In many glands, the nerve fibers have been found to innervate only the blood vessels.

Figure 3-38 Nerve fibers ending around glandular acini.

Segmental Innervation of Skin The area of skin supplied by a single spinal nerve and, therefore, a single segment of the spinal cord is called a dermatome. On the trunk, the dermatomes extend round the body from the posterior to the anterior median plane. Adjacent dermatomes overlap considerably, so to produce a region of complete anesthesia, at least three contiguous spinal nerves have to be sectioned. It should be noted that the area of tactile loss is always greater than the area of loss of painful and thermal sensations. The reason for this difference is that the degree of overlap of fibers carrying pain and thermal sensations is much more extensive than the overlap of fibers carrying tactile sensations. Dermatomal charts for the anterior and posterior surfaces of the body are shown in Figures 3-39 and 3-40. In the limbs, the arrangement of the dermatomes is more complicated because of the embryologic rotation of the limbs as they grow out from the trunk. (For details, see Figs. 3-39 and 3-40.) In the face, the divisions of the trigeminal nerve supply a precise area of skin, and there is little or no overlap to the cutaneous area of another division. Segmental Innervation of Muscles Skeletal muscle also receives a segmental innervation. Most of these muscles are innervated by more than one spinal nerve and, therefore, by the same number of segments of the spinal cord. Thus, to paralyze a muscle completely, it would be necessary to section several spinal nerves or destroy several segments of the spinal cord. To learn the segmental innervation of all the muscles of the body is an impossible task. Nevertheless, the segmental P.101 innervation of the following muscles should be known because it is possible to test them by eliciting simple muscle reflexes in the patient (Fig. 3-41):

Figure 3-39 Anterior aspect of the body showing the distribution of cutaneous nerves on the left side and dermatomes on the right side.
  • Biceps brachii tendon reflex C5-6 (flexion of the elbow joint by tapping the biceps tendon).
  • Triceps tendon reflex C6-7 and C8 (extension of the elbow joint by tapping the triceps tendon).
  • Brachioradialis tendon reflex C5-6 and C7 (supination of the radioulnar joints by tapping the insertion of the brachioradialis tendon).
  • Abdominal superficial reflexes (contraction of underlying abdominal muscles by stroking the skin). Upper abdominal skin T6-7; middle abdominal skin T8-9; lower abdominal skin T10-12.
  • Patellar tendon reflex (knee jerk) L2, L3, and L4 (extension of knee joint on tapping the patellar tendon).
  • Achilles tendon reflex (ankle jerk) S1 and 2 (plantar flexion of ankle joint on tapping the Achilles tendon—tendo calcaneus).

Muscle Tone and Muscle Action A motor unit consists of a motor neuron in the anterior gray column (horn) of the spinal cord and all the muscle fibers it supplies (Fig. 3-42). In a large buttock muscle, such as the gluteus maximus, where fine control is unnecessary, a given motor neuron may supply as many as 200 muscle fibers. In contrast, in the small muscles of the hand or the extrinsic muscles of the eyeball, where fine control is required, one nerve fiber supplies only a few muscle fibers. Every skeletal muscle, while resting, is in a partial state of contraction. This condition is referred to as muscle tone. Since there is no intermediate stage, muscle fibers are either fully contracted or relaxed; it follows that a few muscle fibers within a muscle are fully contracted all the time. To bring about this state and to avoid fatigue, different groups of motor units and, thus, different groups of muscle fibers are brought into action at different times. This is P.102 P.103accomplished by the asynchronous discharge of nervous impulses in the motor neurons in the anterior gray horn of the spinal cord.

Figure 3-40 Posterior aspect of the body showing the distribution of cutaneous nerves on the left side and dermatomes on the right side.
Figure 3-41 Biceps brachii tendon reflex. Note that the reflex arc passes through the fifth and sixth cervical segments of the spinal cord. This is usually monosynaptic, and the internuncial neuron (black) is absent (see p. 103).
Figure 3-42 Components of a motor unit.

Basically, muscle tone is dependent on the integrity of a simple monosynaptic reflex arc composed of two neurons in the nervous system (Fig. 3-43). The lengthening and shortening in a muscle are detected by sensitive sensory endings called muscle spindles (see p. 93), and the tension is detected by tendon spindles (see p. 94). The nervous impulses travel in the large afferent fibers to the spinal cord. There, they synapse with the motor neurons situated in the anterior gray column, which, in turn, send impulses down their axons to the muscle fibers (Fig. 3-43). The muscle spindles themselves are innervated by small gamma efferent fibers that regulate the response of the muscle spindles, acting synergically with external stretch. In this manner, muscle tone is maintained reflexly and adjusted to the needs of posture and movement.

Figure 3-43 Simple reflex arc consisting of an afferent neuron arising from neuromuscular spindles and neurotendinous spindles and an efferent neuron whose cell body lies in the anterior gray column (horn) of the spinal cord. Note that for simplicity, the afferent fibers from the neurotendinous spindle and the neuromuscular spindle are shown as one pathway; in fact, the neurotendinous receptor is inhibitory and reduces tone, whereas the neuromuscular spindle is excitatory and increases tone.

Should the afferent or efferent pathways of the reflex arc be cut, the muscle would lose its tone immediately and become flaccid. A flaccid muscle, on palpation, feels like a mass of dough that has completely lost its resilience. It quickly atrophies and becomes reduced in volume. It is important to realize that the degree of activity of the motor anterior column cells and, therefore, the degree of muscle tone depend on the summation of the nerve impulses received by these cells from other neurons of the nervous system. Muscle movement is accomplished by bringing into action increasing numbers of motor units and, at the same time, reducing the activity of the motor units of muscles that will oppose or antagonize the movement. When the maximum effort is required, all the motor units of a muscle are thrown into action. Summation of Motor Units When a muscle begins to contract, the smaller motor units are stimulated first. The reason for this is that the smaller motor units are innervated by smaller neurons in the spinal cord and brainstem, and they have a lower threshold of P.104excitability. As the contraction increases, progressively larger motor units are brought into action. This phenomenon causes a gradual increase in muscle strength as the muscle contracts. Muscle Fatigue The progressive loss of strength of a muscle with prolonged strong contraction is due to the reduction in the amounts of ATP within the muscle fibers. Nerve impulses continue to arrive at the neuromuscular junction, and normal depolarization of the plasma membrane of the muscle fiber occurs. Posture Posture may be defined as the position adopted by the individual within his or her environment. In the standing position, the line of gravity passes through the odontoid process of the axis, behind the centers of the hip joints, and in front of the knee and ankle joints (Fig. 3-44). In order to stabilize the body and prevent it from collapsing, it is not surprising to find that in humans, the antigravity muscles are well developed and exhibit the greatest degree of tone. Therefore, one can say that posture depends on the degree and distribution of muscle tone, which, in turn, depends on the normal integrity of simple reflex arcs centered in the spinal cord. An individual may assume a particular posture (sitting or standing) over long periods of time with little evidence of fatigue. The reason for this is that muscle tone is maintained through different groups of muscle fibers contracting in relays, with only a small number of muscle fibers within a muscle being in a state of contraction at any one time. The active muscle fiber groups are scattered throughout the muscle. In order to maintain posture, the simple muscle reflex, on which muscle tone is dependent, must receive adequate nervous input from higher levels of the nervous system (Fig. 3-45). For example, impulses arising from the labyrinths and neck muscles, information arising from the cerebellum, midbrain, and cerebral centers, and general information arising from other muscle groups, joints, and even skin receptors will result in nervous impulses impinging on the large anterior gray column cells (i.e., the final common pathway) controlling the muscle fibers. When an individual assumes a given posture, the tone of the muscles controlling that posture is constantly undergoing fine adjustments so that the posture is maintained. Normal posture thus depends not only on the integrity of the reflex arc but also on the summation of the nervous impulses received by the motor anterior gray column cells from other neurons of the nervous system (Fig. 3-46). The detail of the different nervous pathways involved in bringing the information to the anterior gray column cells is dealt with in Chapter 4.

Figure 3-44 Lateral view of the skeleton showing the line of gravity. Since the greater part of body weight lies anterior to the vertebral column, the deep muscles of the back are important in maintaining normal postural curves of the vertebral column in the standing position.


Figure 3-45 Nervous input from higher levels of the central nervous system, which can influence the activity of the anterior gray column (horn) cells of the spinal cord.


Figure 3-46 Normal postural tone of skeletal muscle is dependent not only on the integrity of the reflex arc but also on the summation of the nervous impulses received by the motor anterior gray column (horn) cells from other neurons of the nervous system.

P.107 P.108 P.109 P.110 P.111 P.112 P.113 P.114 P.115 P.116 P.117 P.118 P.119 Clinical Notes Response of Neurons to Injury The survival of the cytoplasm of a neuron depends on its being connected, however indirectly, with the nucleus. The nucleus plays a key role in the synthesis of proteins, which pass into the cell processes and replace proteins that have been metabolized by cell activity. Thus, the cytoplasm of axons and dendrites will undergo degeneration quickly if these processes are separated from the nerve cell body. Injury of the Nerve Cell Body Severe damage of the nerve cell body due to trauma, interference with the blood supply, or disease may result in degeneration of the entire neuron, including its dendrites and synaptic endings. In the brain and spinal cord, the neuronal debris and the fragments of myelin (if the processes are myelinated) are engulfed and phagocytosed by the microglial cells. Later, the neighboring astrocytes proliferate and replace the neuron with scar tissue.

Figure 3-47 A–D: Degeneration and regeneration in a divided nerve.

In the peripheral nervous system, the tissue macrophages remove the debris, and the local fibroblasts replace the neuron with scar tissue. Injury of the Nerve Cell Process If the axon of the nerve cell is divided, degenerative changes will take place in (1) the distal segment that is separated from the cell body, (2) a portion of the axon proximal to the injury, and (3) possibly the cell body from which the axon arises. Changes in the Distal Segment of the Axon The changes spread distally from the site of the lesion (Fig. 3-47) and include its terminations; the process is referred to as wallerian degeneration. In the peripheral nervous system, on the first day, the axon becomes swollen and irregular; by the third or fourth day, the axon is broken into fragments (Fig. 3-47), and the debris is digested by the surrounding Schwann cells and tissue macrophages. The entire axon is destroyed within a week. Meanwhile, the myelin sheath slowly breaks down, and lipid droplets appear within the Schwann cell cytoplasm (Fig. 3-47). Later, the droplets are extruded from the Schwann cell and subsequently are phagocytosed by tissue macrophages. The Schwann cells now begin to proliferate rapidly and become arranged in parallel cords within the persistent basement membrane. The endoneurial sheath and the contained cords of Schwann cells are sometimes referred to as a band fiber. If regeneration does not occur, the axon and the Schwann cells are replaced by fibrous tissue produced by local fibroblasts. In the central nervous system, degeneration of the axons and the myelin sheaths follows a similar course, and the debris is removed by the phagocytic activity of the microglial cells. Little is known about the role of oligodendrocytes in this process. The astrocytes now proliferate and replace the axons. Changes in the Proximal Segment of the Axon The changes in the proximal segment of the axon are similar to those that take place in the distal segment (Fig. 3-47) but extend only proximally above the lesion as far as the first node of Ranvier. The proliferating cords of Schwann cells in the peripheral nerves bulge from the cut surfaces of the endoneurial tubes. Changes in the Nerve Cell Body From Which the Axon Arises The changes that occur in the cell body following injury to its axon are referred to as retrograde degeneration; the changes that take place in the proximal segment of the axon commonly are included under this heading. The possible reason for these changes is that section of the axon cuts off the cell body from its supply of trophic factors derived from the target organs at the distal end of the axon. The most characteristic change occurs in the cell body within the first 2 days following injury and reaches its maximum within 2 weeks. The Nissl material becomes fine, granular (Figs. 3-48 and 3-49), and dispersed throughout the cytoplasm, a process known as chromatolysis. Chromatolysis begins near the axon hillock and spreads to all parts of the cell body. In addition, the nucleus moves from its central location toward the periphery of the cell, and the cell body swells and becomes rounded (Fig. 3-49). The degree of chromatolysis and the degree of swelling of the cell are greatest when the injury to the axon is close to the cell body. In some neurons, very severe damage to the axon close to the cell body may lead to death of the neuron. On the other hand, damage to the most distal process may lead to little or no detectable change in the cell body. The dispersal of the Nissl material—that is, the cytoplasmic RNA—and the swelling of the cell are caused by cellular edema. The apparent loss of staining affinity of the Nissl material is due to the wide dispersal of the cytoplasmic RNA. The movement of the nucleus away from the center of the cell may be due to the cellular edema. Synaptic terminals are seen to withdraw from the surface of the injured nerve cell body and its dendrites and are replaced by Schwann cells in the peripheral nervous system and microglial cells or astrocytes in the central nervous system. This process is called synaptic stripping. The possible causes of synaptic stripping are (1) loss of plasma membrane adhesiveness following injury and (2) stimulation of the supporting cells by chemicals released from the injured neuron. If the injury is sufficiently great, the cells of the immune system—namely, monocytes and macrophages—may migrate into the area. Recovery of Neurons Following Injury In contrast to the rapid onset of retrograde degeneration, the recovery of the nerve cell body and regeneration of its processes may take several months. Recovery of the Nerve Cell Body The nucleolus moves to the periphery of the nucleus, and polysome clusters reappear in the cytoplasm. This indicates that RNA and protein synthesis is being accelerated in preparation for the reformation of the axon. Thus, there is a reconstitution of the original Nissl structure, a decrease in the swelling of the cell body, and a return of the nucleus to its characteristic central position (Fig. 3-49). Regeneration of Axons in Peripheral Nerves Regrowth of the axons (motor, sensory, and autonomic) is possible in peripheral nerves and appears to depend on the presence of endoneurial tubes and the special qualities possessed by Schwann cells. Sprouts from the axons grow from the proximal stump and into the distal stump toward the nerve’s end-organs. The following mechanisms are thought to be involved: (1) the axons are attracted by chemotropic factors secreted by the Schwann cells in the distal stump, (2) growth-stimulating factors exist within the distal stump, and (3) inhibitory factors are present in the perineurium to inhibit the axons from leaving the nerve. The satisfactory regeneration of axons and the return of normal function depend on the following factors:

  • In crush nerve injuries, where the axon is divided or its blood supply has been interfered with but the endoneurial sheaths remain intact, the regenerative process may be very satisfactory.
  • In nerves that have been completely severed, there is much less chance of recovery because the regenerating fibers from the proximal stump may be directed to an incorrect destination in the distal stump—that is, cutaneous fibers entering incorrect nerve endings or motor nerves supplying incorrect muscles.
  • If the distance between the proximal and distal stumps of the completely severed nerve is greater than a few millimeters or the gap becomes filled with proliferating fibrous tissue or is simply filled by adjacent muscles that bulge into the gap, then the chances of recovery are very poor. The outgrowing axonal sprouts escape into the surrounding connective tissue and form a tangled mass or neuroma. In these cases, early close surgical approximation of the severed ends, if possible, greatly facilitates the chances of recovery.
  • When mixed nerves (those containing sensory, motor, and autonomic fibers) are completely severed, the chances of a good recovery are very much less than when the nerve is purely sensory or purely motor. The reason for this is that the regenerating fibers from the proximal stump may be guided to an incorrect destination in the distal stump; for example, cutaneous fibers may enter motor endoneurial tubes and vice versa.
    Figure 3-48 Photomicrographs of motor neurons of the anterior gray column of the spinal cord. A: Nissl substance in normal neurons. B: Following section of anterior roots of spinal nerve, showing chromatolysis.
  • Inadequate physiotherapy to the paralyzed muscles will result in their degeneration before the regenerating motor axons have reached them.
  • The presence of infection at the site of the wound will seriously interfere with the process of regeneration.

If one assumes that the proximal and distal stumps of the severed nerve are in close apposition, the following regenerative processes take place (Fig. 3-47). The Schwann cells, having undergone mitotic division, now fill the space within the basal lamina of the endoneurial tubes of the proximal stump as far proximally as the next node of Ranvier and in the distal stump as far distally as the end-organs. Where a small gap exists between the proximal and distal stumps, the multiplying Schwann cells form a number of cords to bridge the gap.

Figure 3-49 The changes that may take place in a nerve cell body following division of one of its processes.

Each proximal axon end now gives rise to multiple fine sprouts or filaments with bulbous tips. These filaments, as they grow, advance along the clefts between the Schwann cells and thus cross the interval between the proximal and distal nerve stumps. Many such filaments now enter the proximal end of each endoneurial tube and grow distally in contact with the Schwann cells (Fig. 3-50). It is clear that the filaments from many different axons may enter a single endoneurial tube. However, only one filament persists, the remainder degenerate, and that one filament grows distally to reinnervate a motor or sensory end-organ. While crossing the gap between the severed nerve ends, many filaments fail to enter an endoneurial tube and grow out into the surrounding connective tissue. It is interesting to note that the formation of multiple sprouts or filaments from a single proximal axon greatly increases the chances that a neuron will become connected to a sensory or motor ending. It is not known why one filament within a single endoneurial tube should be selected to persist while the remainder degenerate. Once the axon has reached the end-organ, the adjacent Schwann cells start to lay down a myelin sheath. This process begins at the site of the original lesion and extends in a distal direction. By this means, the nodes of Ranvier and the Schmidt-Lanterman incisures are formed.

Figure 3-50 Photomicrograph of a longitudinal section of the distal stump of the sciatic nerve showing evidence of degeneration and axon regeneration following injury. (Courtesy Dr. M. J. T. Fitzgerald.)

Many months may elapse before the axon reaches its appropriate end-organ, depending on the site of the nerve injury. The rate of growth has been estimated to be approximately 2 to 4 mm per day. If, however, one takes into consideration the almost certain delay incurred by the axons as they cross the site of the injury, an overall regeneration rate of 1.5 mm per day is a useful figure to remember for clinical use. Even if all the difficulties outlined above are overcome and a given neuron reaches the original end-organ, the enlarging axonal filament within the endoneurial tube reaches only about 80% of its original diameter. For this reason, the conduction velocity will not be as great as that of the original axon. Moreover, a given motor axon tends to innervate more muscle fibers than formerly; thus, the control of muscle is less precise. Regeneration of Axons in the Central Nervous System In the central nervous system, there is an attempt at regeneration of the axons, as evidenced by sprouting of the axons, but the process ceases after about 2 weeks. Long-distance regeneration is rare, and the injured axons make few new synapses. There is no evidence that restoration of function takes place. The regeneration process is aborted by the absence of endoneurial tubes (which are necessary to guide the regenerating axons), the failure of oligodendrocytes to serve in the same manner as Schwann cells, and the laying down of scar tissue by the active astrocytes. It has also been suggested that there is an absence of nerve growth factors in the central nervous system or that the neuroglial cells may produce nerve growth-inhibiting factors. Research has shown that the Schwann cell basal laminae contain laminin and cell adhesion molecules of the immunoglobulin family, both of which stimulate axon growth. The central nervous system contains only low concentrations of these molecules. In the embryo, when axon growth actively takes place in both the central and peripheral nervous systems, growth-promoting factors are present in both systems. Later in development, these factors disappear in the central nervous system. Myelin in the central nervous system inhibits axonal growth, and it is interesting to note that myelination in the central nervous system occurs late in the development process when growth of the main nervous pathways is complete. Central axons may not be as good at regeneration as peripheral axons. In tissue culture, peripheral axons are more successful at growth than central axons. Moreover, the ability of central axons to grow decreases with age. Neurobiologic Research Into Central Nervous System Regeneration Because traumatic injury to the central nervous system produces such devastating disabilities that are largely irreversible, neurobiologists are now enthusiastically pressing forward with research in this area. It is no longer doubted that differences exist between the environment in the central and peripheral systems. Moreover, the ability of central axons in lower vertebrates, such as frogs, to regenerate provides an enormous stimulus for future work. Research has taken the following directions:

  • Molecules present in the peripheral nervous system, such as laminins and neurotropins, have been introduced into the central nervous system at the site of injury to promote axon growth.
  • Schwann cells have been grafted into the central nervous system, and it has been found that central axons will grow into the graft.
  • Attempts have been made to reduce the inhibitory factors present in the central nervous system. Infusion of antibodies at the site of injury has been carried out with some success.
  • The introduction of anti-inflammatory agents to suppress the neuroglial and monocyte response has been used with success. Methylprednisolone is now commonly used as soon as possible after the incident in all patients with spinal cord injuries.

Although a vast amount of research still needs to be done, a combination of treatments may provide the return of some function to these patients with central nervous system injuries. Transneuronal Degeneration The responses of a single neuron to injury were considered in the previous section. In the central nervous system, if one group of neurons is injured, then a second group farther along the pathway, serving the same function, may also show degenerative changes. This phenomenon is referred to as anterograde transneuronal degeneration. For example, if the axons of the ganglion cells of the retina are severed, not only do the distal ends of the axons that go to the lateral geniculate bodies undergo degeneration but also the neurons in the lateral geniculate bodies with which these axons form synapses undergo degeneration. In fact, a further set of neurons may be involved in the degenerative process in the visual cortex. In situations in the central nervous system in which multiple neurons synapse with a single distal neuron, injury to one of the proximal neurons is not followed by degeneration of the distal neuron. Experimentation on animals with artificial lesions of the central nervous system has shown that retrograde transneuronal degeneration may occur in certain situations. Neuronal Degeneration Associated With Senescence Many neurons degenerate and disappear during fetal development. This process is believed to be due to their failure to establish adequate functional connections. During postnatal life, further gradual neuronal degeneration continues to occur. It has been estimated that in old age, an individual may have lost up to 20% of the original number of neurons. This may account to some extent for the loss of efficiency of the nervous system that is associated with senescence. Atrophy of Voluntary Muscle and Other End-Organs Following Peripheral Nerve Degeneration Voluntary muscle undergoes degenerative changes following motor nerve section. First, there is an altered response to acetylcholine, followed by gradual wasting of the sarcoplasm, and finally loss of the fibrils and striations. Eventually, the muscle completely atrophies and is replaced by fibrous tissue. Reinnervation of the muscle halts its degeneration, and if the muscle atrophy is not too advanced, normal structure and function return. Furthermore, if the motor nerve that supplies fast white voluntary muscle fibers is exchanged for a motor nerve that supplies slow red voluntary muscle fibers, the muscle fibers change their structural and functional properties to comply with the new type of innervation. This experimental result strongly suggests not only that voluntary muscle cells are dependent on the presence of intact motor nerves but also that the nerve has some trophic influence on the muscle and even determines the type of muscle that it innervates. Another end-organ, the taste bud, also depends on the integrity of the sensory nerve. If the nerve is sectioned, the taste bud quickly atrophies. Once the sensory nerve regenerates into the mucous membrane, new taste buds develop. Traumatic Lesions of Peripheral Nerves Seddon (1944) described three clinical types of nerve injury:

  • Neuropraxia is the term applied to a transient block. The paralysis is incomplete, recovery is rapid and complete, and there is no microscopic evidence of nerve degeneration. Pressure is the most common cause. It is essentially a temporary interference in function.
  • Axonotemesis is the term applied to a nerve lesion in which the axons are damaged but the surrounding connective tissue sheaths remain more or less intact. Wallerian degeneration occurs peripherally. Functional recovery is more rapid and more complete than after complete section of the nerve trunk. The explanation of the more rapid and more complete recovery is that the nerve fibers, although severely damaged, for the most part retain their normal anatomical relationships to one another, owing to the preservation of the connective tissue sheaths. Crush injuries, traction, and compression are the most common causes.
  • Neurotmesis is the term applied to complete section of the nerve trunk.

Symptoms and Signs of Neurotmesis Motor Changes The muscles that are innervated show flaccid paralysis and rapidly waste. The reflexes in which the muscles participate are lost. The paralyzed muscle ceases to respond to faradic stimulation after 4 to 7 days. After 10 days, the muscle responds only sluggishly to galvanic stimulation, and the strength of the current must be greater than that required for a normal innervated muscle. This altered response of muscle to electrical stimulation is known as the reaction of degeneration. Sensory Changes There is a total loss of cutaneous sensibility over the area exclusively supplied by the nerve. This area is surrounded by a zone of partial sensory loss where adjacent sensory nerves overlap. The skin area in which the sensation of light touch is lost is much greater than the area lost to pinprick. Vasomotor, Sudomotor, and Trophic Changes Section of a peripheral nerve results in the interruption of postganglionic sympathetic fibers traveling in the nerve. As a result of the loss of vascular control, the skin area at first becomes red and hot. Later, the affected area becomes blue and colder than normal, especially in cold weather. Because of the loss of sudomotor control, the sweat glands cease to produce sweat, and the skin becomes dry and scaly. Nail growth becomes retarded as the direct result of poor peripheral circulation. If a large area of the body is denervated, as in cases in which the sciatic nerve is sectioned, the bones undergo decalcification as a result of disuse and loss of circulatory control. Symptoms and Signs of Recovery Following Neurotmesis Assuming that the divided peripheral nerve has been carefully sutured together, a physician must be aware of the symptoms and signs of recovery and their sequence. Motor Recovery Regenerating motor axons grow at an average rate of about 1.5 mm per day. The proximal muscles will recover first, and the distal muscles will recover later. The muscles may respond to faradic stimulation before voluntary control returns. Sensory Recovery Sensory recovery occurs before there is a return of voluntary movement. The part of the nerve distal to the section becomes very sensitive to mechanical stimulation once the regenerating sensory axons have entered the distal segment. Simple tapping of the distal nerve trunk gives rise to a tingling sensation in the area of cutaneous distribution of the nerve. This sign is referred to as the Tinel sign. Recovery of deep cutaneous sensibility—that is, pain caused by deep pressure—is the first sign of recovery. This is followed by the return of poorly localized, superficial cutaneous pain. Vasomotor control also returns at about this time. Later, the sensations of heat and cold are recovered. Light touch and tactile discrimination are the last sensations to return; these sensations return many months later and are often incomplete. Specific Spinal Nerve Injuries While a detailed description of the neurologic deficits following the many spinal nerve injuries seen in clinical practice is beyond the scope of this book, it seems appropriate to include a table that summarizes the important features found in cervical and lumbosacral root syndromes (Table 3-4). Tables that summarize the branches of the brachial (Table 3-5) and lumbar and sacral (Table 3-6) plexuses and their distribution are also included. These tables can assist the reader in determining the specific nerve lesion associated with a particular motor or sensory deficit in the upper or lower limbs. Cranial nerve injuries are considered in Chapter 11. Some Basic Clinical Principles Underlying Peripheral Nerve Injuries

  • In open, dirty wounds, where there is a high risk of infection, the sectioned nerve should be ignored, and the wound infection should be treated. Later, when the wound has healed satisfactorily, the nerve should be explored, and the cut ends of the nerve should be sutured together.
    Table 3-4 Important Features Found in Cervical and Lumbosacral Root Syndromes
    Root Injury Dermatome Pain Muscles Supplied Movement Weakness Reflex Involved
    C5 Lateral side of upper part of arm Deltoid and biceps brachii Shoulder abduction, elbow flexion Biceps
    C6 Lateral side of forearm Extensor carpi radialis longus and brevis Wrist extensors Brachioradialis
    C7 Middle finger Triceps and flexor carpi radialis Extension of elbow and flexion of wrist Triceps
    C8 Medial side of forearm Flexor digitorum superficialis and profundus Finger flexion None
    L1 Groin Iliopsoas Hip flexion Cremaster
    L2 Anterior part of thigh Iliopsoas, sartorius, hip adductors Hip flexion, hip adduction Cremaster
    L3 Medial side of knee Iliopsoas, sartorius, quadriceps, hip adductors Hip flexion, knee extension, hip adduction Patellar
    L4 Medial side of calf Tibialis anterior, quadriceps Foot inversion, knee extension Patellar
    L5 Lateral side of lower leg and dorsum of foot Extensor hallucis longus, extensor digitorum longus Toe extension, ankle dorsiflexion None
    S1 Lateral edge of foot Gastrocnemius, soleus Ankle plantar flexion Ankle jerk
    S2 Posterior part of thigh Flexor digitorum longus, flexor hallucis longus Ankle plantar flexion, toe flexion None
  • For a patient with a healed wound and no evidence of nerve recovery, the treatment should be conservative. Sufficient time should be allowed to elapse to enable the regenerating nerve fibers to reach the proximal muscles. If recovery fails to occur, the nerve should be explored surgically.
  • In those cases in which connective tissue, bone fragments, or muscles come to lie between the cut ends of a severed nerve, the nerve should be explored; if possible, the cut ends of the nerve should be brought together and sutured.
  • The nutrition of the paralyzed muscles must be maintained with adequate physiotherapy. Warm baths, massage, and warm clothing help to maintain adequate circulation.
  • The paralyzed muscles must not be allowed to be stretched by antagonist muscles or by gravity. Moreover, excessive shortening of the paralyzed muscles leads to contracture of these muscles.
  • Mobility must be preserved by daily passive movements of all joints in the affected area. Failure to do this results in the formation of adhesions and consequent limitation of movement.

Once voluntary movement returns in the most proximal muscles, the physiotherapist can assist the patient in performing active exercises. This not only aids in the return of a normal circulation to the affected part but also helps the patient to learn once again the complicated muscular performance of skilled movements.

Table 3-5 Branches of the Brachial Plexus and Their Distribution
Branches Distribution
   Dorsal scapular nerve (C5) Rhomboid minor, rhomboid major, levator scapulae muscles
   Long thoracic nerve (C5-7) Serratus anterior muscle
Upper trunk
   Suprascapular nerve (C5-6) Supraspinatus and infraspinatus muscles
   Nerve to subclavius (C5-6) Subclavius
Lateral cord
   Lateral pectoral nerve (C5-7) Pectoralis major muscle
   Musculocutaneous nerve (C5-7) Coracobranchialis, biceps brachii, brachialis muscles; supplies skin along lateral border of forearm when it becomes the lateral cutaneous nerve of forearm
   Lateral root of median nerve (C5-7) See medial root of median nerve
Posterior cord
   Upper subscapular nerve (C5-6) Subscapularis muscle
   Thoracodorsal nerve (C6-8) Latissimus dorsi muscle
   Lower subscapular nerve (C5-6) Subscapularis and teres major muscles
   Axillary nerve (C5-6) Deltoid and teres minor muscles; upper lateral cutaneous nerve of arm supplies skin over lower half of deltoid muscle
   Radial nerve (C5-8, T1) Triceps, anconeus, part of brachialis, brachioradialis, extensor carpi radialis longus; via deep radial nerve branch supplies extensor muscles of forearm: supinator, extensor carpi radialis brevis, extensor carpi ulnaris, extensor digitorum, extensor digiti minimi, extensor indicis, abductor pollicis longus, extensor pollicis longus, extensor pollicis brevis; skin, lower lateral cutaneous nerve of arm, posterior cutaneous nerve of arm, and posterior cutaneous nerve of forearm; skin on lateral side of dorsum of hand and dorsal surface of lateral 3½ fingers; articular branches to elbow, wrist, and hand
Medial cord
   Medial pectoral nerve (C8, T1) Pectoralis major and minor muscles
   Medial cutaneous nerve of arm joined by intercostal brachial nerve from second intercostals nerve (C8, T1-2) Skin of medial side of arm
   Medial cutaneous nerve of forearm (C8, T1) Skin of medial side of forearm
Ulnar nerve (C8, T1) Flexor carpi ulnaris and medial half of flexor digitorum profundus, flexor digiti minimi, opponens digiti minimi, abductor digiti minimi, adductor pollicis, third and fourth lumbricals, interossei, palmaris brevis, skin of medial half of dorsum of hand and palm, skin of palmar and dorsal surfaces of medial 1½ fingers
Medial root of median nerve (with lateral root) forms median nerve (C5-8, T1) Pronator teres, flexor carpi radialis, palmaris longus, flexor digitorum superficialis, abductor pollicis brevis, flexor pollicis brevis, opponens pollicis, first two lumbricals (by way of anterior interosseous branch), flexor pollicis longus, flexor digitorum profundus (lateral half), pronator quadratus, palmar cutaneous branch to lateral half of palm and digital branches to palmar surface of lateral 3½ fingers; articular branches to elbow, wrist, and carpal joints

Nerve Transplantation Nerve grafts have been used with some success to restore muscle tone in facial nerve palsy. In mixed nerve injuries, nerve grafts have succeeded only in restoring some sensory function and slight muscle activity. The presence of two suture lines and the increased possibility of mixing the nerve fibers is probably the reason for the lack of success with nerve grafts. In most nerve injuries, even when the gap between the proximal and distal ends is as great as 10 cm, it is usually possible to mobilize the nerve or alter its position in relation to joints so that the proximal and distal ends may be brought together without undue tension; the ends are then sutured together. Tumors of Peripheral Nerves A peripheral nerve consists essentially of nerve fibers (axons), each of which is associated with Schwann cells; the fibers are either myelinated or nonmyelinated. The nerve fibers are arranged in parallel bundles and are surrounded by connective tissue sheaths.

Table 3-6 Branches of the Lumbar and Sacral Plexuses and Their Distribution
Branches Distribution
Femoral nerve (L2-4) Iliacus, pectineus, sartorius, quadriceps femoris muscles; skin, medial cutaneous and intermediate cutaneous nerves of thigh, saphenous nerve to medial side of leg, medial side of foot as far as ball of big toe; articular branches to hip and knee joints
Obturator nerve (L2-4) Pectineus, adductor longus, adductor brevis, adductor magnus (adductor portion), gracilis muscles; skin, medial side of thigh; articular branches to hip and knee joints
Sciatic nerve (L4-5, S1-3)
   Common peroneal nerve Biceps femoris muscle (short head); skin, lateral cutaneous nerve of calf, sural communicating branch to lateral side of leg, lateral side of foot, and little toe
   Superficial peroneal nerve Peroneus longus and brevis muscles; skin, lower leg, and dorsum of foot
   Deep peroneal nerve Tibialis anterior, extensor hallucis longus, extensor digitorum longus, peroneus tertius, extensor digitorum brevis muscles; skin, cleft between the first and second toes; articular branches to tibiofibular, ankle, and foot joints
   Tibial nerve Semitendinosus, biceps femoris (long head), semimembranosus, adductor magnus (hamstring part), gastrocnemius, soleus, plantaris, popliteus, tibialis posterior, flexor digitorum longus, flexor hallucis longus muscles; skin, medial side of ankle; articular branches to hip, knee, and ankle joints
   Medial plantar nerve Abductor hallucis, flexor digitorum brevis, flexor hallucis brevis, first lumbrical muscles; skin, medial side of sole of foot; articular branches to foot joints
   Lateral plantar nerve Flexor accessorius, abductor digiti minimi, flexor digiti minimi brevis, second, third, and fourth lumbricals, adductor hallucis, all interossei muscles; skin of lateral side of sole of foot

A benign fibroma or a malignant sarcoma may arise in the connective tissue of the nerve and does not differ from similar tumors elsewhere. Neurilemmomas are believed to arise from Schwann cells. They arise from any nerve trunk, cranial or spinal, and in any part of its course. Primary tumors of the axons are very rare. Blood Vessels, Lymphatics, and Endoneurial Spaces Within Peripheral Nerves Peripheral nerves receive branches from arteries in the regions through which they pass. The anastomotic network that exists within a nerve is considerable, and local ischemia does not occur if a single artery is obstructed. A plexus of lymph vessels lies within the epineurial connective tissues, and this drains to regional lymph nodes. As demonstrated by the results of experiments in which dyes have been injected into peripheral nerves, spaces exist between individual nerve fibers. There seems to be little doubt that these endoneurial spaces provide a potential route for the ascent of tetanus toxin to the spinal cord. Action of Local Anesthetics on Nerve Conduction Local anesthetics are drugs that block nerve conduction when applied locally to a nerve fiber in suitable concentrations. Their site of action is the axolemma (plasma membrane), and they interfere with the transient increase in permeability of the axolemma to Na+, K+, and other ions. The sensitivity of nerve fibers to local anesthetics is related to the size of the nerve fibers (Table 3-2). Small nerve fibers are more susceptible than large fibers; small fibers are also slower to recover. Cocaine has been used clinically to block nerve conduction. Unfortunately, it is a strong stimulant of the cerebral cortex and readily causes addiction. Procaine is a synthetic compound that is widely used as a local anesthetic agent. Apparent Recovery of Function of the Central Nervous System Following Injury Axon regeneration in the brain and spinal cord is minimal following a lesion, yet considerable functional recovery often occurs. Several explanations exist, and more than one mechanism may be involved.

  • The function of nerve fibers may be interfered with as the result of compression by edema fluid. Once the edema subsides, a substantial recovery may take place.
  • The damaged nerve fiber proximal to the lesion may form new synapses with neighboring normal neurons.
  • Following a lesion to branches of a nerve, all the neurotransmitters may pass down the remaining branches, producing a greater effect.
  • Following a lesion of an afferent neuron, an increased number of receptor sites may develop on a postsynaptic membrane. This may result in the second neuron responding to neurotransmitter substances from neighboring neurons.
  • Nonfunctioning neurons may take over the function of damaged neurons.
  • The damaged nerve fiber proximal to the lesion may form new synapses with neighboring normal neurons.
  • The normal neighboring nerve fibers may give off branches distal to the lesion, which then follow the pathway previously occupied by the damaged fibers.
  • If a particular function, such as the contraction of voluntary muscle, is served by two neural pathways in the central nervous system and one pathway is damaged, the remaining undamaged pathway may take over the entire function. Thus, it is conceivable that if the corticospinal tract is injured, the corticoreticulospinal tract may take over the major role of controlling the muscle movement.
  • It is possible with intensive physiotherapy for patients to be trained to use other muscles to compensate for the loss of paralyzed muscles.

Herpes Zoster Herpes zoster, or shingles, is a relatively common condition caused by the reactivation of the latent varicella-zoster virus in a patient who has previously had chickenpox. The infection is found in the first sensory neuron in a cranial or spinal nerve. The lesion is seen as an inflammation and degeneration of the sensory neuron with the formation of vesicles with inflammation of the skin. The first symptom is pain in the distribution of the sensory neuron, followed in a few days by a skin eruption. The condition occurs most frequently in patients over the age of 50 years. Polyneuropathy Polyneuropathy is an impairment of function of many peripheral nerves simultaneously. There are many causes, including infection (endotoxin of diphtheria, Guillain-Barré syndrome [see Clinical Example at beginning of chapter]), metabolic disorders (vitamins B1 and B12 deficiency, poisoning by heavy metals, drugs), and endocrine disorders (diabetes). Axon degeneration and/or segmental demyelination may take place, and the neuron cell body may be involved. In mild cases, the condition is reversible, but in severe cases, it may be permanent. Both sensory and motor symptoms and signs may be evident. Receptors Sensory endings are found throughout the body in both somatic and visceral areas. It is fortunate that they are so widely distributed, because they enable the human subject to react to changes in the external and internal environment. To make a diagnosis or study the effect of treatment on a disease process, a physician relies almost entirely on the patient’s ability to describe changes in subjective sensations or to respond to specific stimuli during a physical examination. Such descriptions, such as “knifelike pain,” “dull and aching pain,” “colicky pain,” “pins and needles,” and “cannot feel anything” are very familiar to the practicing physician. Each main type of sensation that can be experienced, such as pain, temperature, and touch and pressure, is called a modality of sensation. The type of modality felt by a patient from a particular part of the body is determined by the specific area of the central nervous system to which the afferent nerve fiber passes. However, it is clinically useful to remember that axons carrying specific modalities are associated with one or more anatomically distinct receptors (Table 3-7).

Table 3-7 Receptors and Associated Functions
Receptor Associated Function
Free nerve endings Pain, touch, pressure, tickle sensations, ?cold and heat
Merkel discs Touch and pressure
Hair follicle receptor Touch
Meissner’s corpuscles Touch (two-point tactle discrimination)
Pacinian corpuscles Pressure and vibration
Ruffini corpuscles Stretch
Neuromuscular spindles Elongation of muscle (stretch)
Neurotendinous spindles Tension

Sensory Receptors and Age With life expectancy increasing, many patients now reach the age when sensory receptor degeneration can cause disequilibrium. This critical age varies in different individuals, but once it starts, there is a progressive deterioration in the sensory systems, involving not only visual and auditory systems but also proprioception and the ability to integrate the afferent information entering the central nervous system. Examination of Individual Sensory Modalities An accurate physical examination may enable the neurologist to make a precise diagnosis. He or she may be able to determine whether a particular sensation can or cannot be appreciated or whether it is less than normal. The physician will be able to determine the precise area over the surface of the body where impairment of sensation is found. The following sensations are usually tested:

  • Light touch. This is tested by gently touching the skin with a wisp of cotton; the patient has the eyes closed and responds “yes” whenever the stimulus is felt. It is important to realize that different areas of the skin normally exhibit different thresholds for touch. The back and buttocks are less sensitive than the face or fingertips. On hairy surfaces, the slightest movement of a hair usually can be felt.
  • Localization of touch. After detecting the light touch with the eyes closed, the patient is asked to place a finger on the exact site touched. Failure to accomplish this may be due to damage to the cerebral cortex.
  • Two-point tactile discrimination. Two blunt points are applied to the skin surface while the patient’s eyes are closed. Gradually, the points are brought closer together until the patient is unable to distinguish two definite points. A normal person is able to distinguish two separate points on the tip of the index finger when they are separated by a distance greater than about 3 mm. On the back, however, they have to be separated by as much as 3 to 4 cm.
  • Pain. The skin may be touched with the sharp end of a pin. First, the pain threshold is established and then the areas of diminished or lost pain sensation are mapped out. It is advisable to apply the stimulus in an irregular manner, first using the sharp end of the pin and then the dull head, with the patient responding “sharp” or “dull.” In certain diseases, such as tabes dorsalis or polyneuropathy (polyneuritis), there is a delay of up to 3 seconds before the patient recognizes the sharp pain.
  • Pressure pain. This poorly localized pain is perceived by deep pressure on a muscle or by squeezing a tendon.
  • Temperature testing. Test tubes filled with hot or cold water may be used. When the test tubes are applied to the skin, the patient responds with either “warm” or “cold.” First, the temperature threshold is established and then the areas of diminished or lost temperature sensation are mapped out.
  • Vibration. When the handle of a vibrating tuning fork is applied to the skin over bone (e.g., the medial malleolus of the tibia or the olecranon process of the ulna), a tingling sensation is felt. This is due to the stimulation of superficial and deep pressure receptors. The patient is asked to respond when the first vibration is felt as well as when the vibration can no longer be detected. The perception of vibration in the legs is usually diminished after the age of 60 years.
  • Appreciation of form (stereognosis). With the patient’s eyes closed, the examiner places common objects, such as coins or keys, in the patient’s hands. The patient normally should be able to identify objects by moving them around in the hand and feeling them with the fingers.
    Table 3-8 Drugs and Diseases Affecting the Motor End-Plates in Skeletal Muscle
    Drug or Disease Increasing ACh Release Decreasing ACh Release Acting on ACh Receptors AChE Inhibition
    Depolarizing Blockade ACh Receptor Blockade
    4-Aminopyridines Yes        
    Guanidine hydrochloride Yes        
    Succinylcholine     Yes    
    d-Tubocurarine,       Yes  
    dimethyltubocurarine,       Yes  
    gallamine,       Yes  
    benzoquinonium       Yes  
    Physostigmine,         Yes
    neostigmine         Yes
    Botulinum toxin   Yes      
    Myasthenia gravis     Destruction of receptors    
    ACh, acetylcholine; AChE, acetylcholinesterase.
  • Passive movements of joints. This test may be carried out on the fingers or toes. With the patient completely relaxed and in the supine position with eyes closed, the digit is flexed or extended irregularly. After each movement, the patient is asked, “Is the digit ‘up’ or ‘down’?” A normal individual not only can determine that passive movement is taking place but also is aware of the direction of the movement.
  • Postural sensibility. This is the ability to describe the position of a limb when it is placed in that position while the patient’s eyes are closed. Another way to perform the test is to ask the patient, with eyes closed, to place the limb on the opposite side in the same position as the other limb. The application and interpretation of the results of these tests will be understood more fully when the afferent or sensory pathways have been discussed (see p. 143).

Phantom Limb Wherever a particular sensory pathway is stimulated along its course from the receptor to the sensory cortex of the brain, the sensation experienced by the individual is referred to the site of the receptor. For example, if the pain fibers from the receptors in the little finger are stimulated in the ulnar nerve at the elbow, the individual will experience pain in the little finger and not at the elbow. Following the amputation of a limb, the patient may experience severe pain in the absent limb due to pressure on the nerve fibers at the end of the stump. This phenomenon is referred to clinically as phantom limb. Action of Drugs and Other Agents on Skeletal Neuromuscular Junctions Table 3-8 gives some examples of drugs and diseases affecting the motor end-plates in skeletal muscle. Neuromuscular Blocking Agents d-Tubocurarine produces flaccid paralysis of skeletal muscle, first affecting the extrinsic muscles of the eyes and then those of the face, the extremities, and finally the diaphragm. Dimethyltubocurarine, gallamine, and benzoquinonium have similar effects. These drugs combine with the receptor sites at the postsynaptic membrane normally used by acetylcholine and thus block the neurotransmitter action of acetylcholine. Therefore, they are referred to as competitive blocking agents, since they are competing for the same receptor site as acetylcholine. As these drugs are slowly metabolized, the paralysis passes off. Decamethonium and succinylcholine also paralyze skeletal muscle, but their action differs from that of competitive blocking agents because they produce their effect by causing depolarization of the motor end-plate. Acting like acetylcholine, they produce depolarization of the postsynaptic membrane, and the muscle contracts once. This is followed by a flaccid paralysis and a blockage of neuromuscular activity. Although the blocking action endures for some time, the drugs are metabolized, and the paralysis passes off. The actual paralysis is produced by the continued depolarization of the postsynaptic membrane. It must be remembered that continuous depolarization does not produce continuous skeletal muscle contraction. Repolarization has to take place before further depolarization can occur. Neuromuscular blocking agents are commonly used with general anesthetics to produce the desired degree of muscle relaxation without using larger doses of general anesthetics. Because the respiratory muscles are paralyzed, facilities for artificial respiration are essential. Anticholinesterases Physostigmine and neostigmine have the capacity to combine with acetylcholinesterase and prevent the esterase from inactivating acetylcholine. In addition, neostigmine has a direct stimulating action on skeletal muscle. The actions of both drugs are reversible, and they have been used with success in the treatment of myasthenia gravis. Bacterial Toxins Clostridium botulinum, the causative organism in certain cases of food poisoning, produces a toxin that inhibits the release of acetylcholine at the neuromuscular junction. Death results from paralysis of the respiratory muscles. The course of the disease can be improved by the administration of calcium gluconate or guanidine, which promote the release of ACh from the nerve terminals. Motor Nerve and Skeletal Muscle Not only does the motor nerve control the activity of the muscle it supplies but also its integrity is essential for the muscle’s normal maintenance. Following section of a motor nerve, the muscle fibers rapidly atrophy and are replaced by connective tissue. The total bulk of the muscle may be reduced by three-fourths in as little as 3 months. This degree of atrophy does not occur if the muscle simply is immobilized; that is, it is not just disuse atrophy. It is apparent that the maintenance of normal muscle is dependent on the continued reception of acetylcholine at the postsynaptic membrane at the neuromuscular junction. Denervation Supersensitivity of Skeletal Muscle After approximately 2 weeks of denervation, skeletal muscle fibers respond to externally applied acetylcholine at sites other than the neuromuscular junctions. This supersensitivity could be explained on the basis that many new acetylcholine receptors have developed along the length of the muscle fibers following denervation. Myasthenia Gravis Myasthenia gravis is a common disease characterized by drooping of the upper eyelids (ptosis), double vision (diplopia), difficulty in swallowing (dysphagia), difficulty in talking (dysarthria), and general muscle weakness and fatigue. Initially, the disease most often involves the muscles of the eye and the pharynx, and the symptoms can be relieved with rest. In the progressive form of the disease, the weakness becomes steadily worse, and ultimately death occurs. The condition is an autoimmune disorder in which antibodies are produced against the nicotinic acetylcholine receptors on the postsynaptic membrane. The cause of the autoimmune disorder is unknown. The antibodies interfere with the synaptic transmission by reducing the number of receptors or by blocking the interaction of ACh with its receptors. The size of the junctional folds is also reduced, and the width of the synaptic cleft is increased. Together, these changes result in a reduced amplitude in end-plate potentials. The condition can be temporarily relieved by anticholinesterase drugs such as neostigmine, which potentiates the action of acetylcholine. In adults with myasthenia gravis, about 70% show evidence of hyperplasia of their thymus glands. It is in the thymus that T cells, which mediate immune protection, undergo maturation. Excessive synthesis of thymic hormones that stimulate the development of T cells may contribute to the autoimmune response. A rare congenital form of myasthenia gravis may exist from birth, and in this form, there is no abnormal antibody present. The causes of the congenital disease include a deficiency of acetylcholinesterase at the motor end-plates, impaired release of ACh, impaired capacity of the receptors to interact with ACh, and a reduced number of ACh receptors. Hypokalemic Periodic Paralysis and Hyperkalemic Paralysis Hypokalemic periodic paralysis and hyperkalemic paralysis are diseases due to decreased or increased blood potassium levels. It is known that the ability of acetylcholine to initiate electrical changes in the postsynaptic membrane of the neuromuscular junction can be greatly influenced by the level of blood potassium, and it is this blood change that is responsible for the paralysis in these patients. Action of Drugs on Neuromuscular Junctions in Smooth Muscle, Cardiac Muscle, and Nerve Endings on Secretory Cells It has been stated that in normal body physiology, acetylcholine released from postganglionic parasympathetic fibers can bring about depolarization and resulting contraction of smooth muscle fibers. Acetylcholine, however, is a useless drug to be administered by the physician, because it is rapidly destroyed by the cholinesterases. As well, its actions are so widespread that it cannot be used selectively. By slightly changing the structure, as in the case of methacholine chloride or carbachol, the drugs are less susceptible to destruction by the cholinesterases but still possess the ability to react with the receptors. Atropine and scopolamine are drugs that compete with acetylcholine for the same receptors. These drugs are competitive antagonists of acetylcholine at receptor sites of smooth muscle, cardiac muscle, and various secretory cells. Norepinephrine is released from postganglionic sympathetic fibers and can bring about depolarization of smooth muscle in the walls of arteries, for example, resulting in their contraction. At other sites, such as the bronchi, it causes smooth muscle relaxation. Sympathetic receptors have been classified as alpha and beta. The functions associated with alpha receptors are vasoconstriction, mydriasis (dilatation of the pupil), and relaxation of the smooth muscle of the intestine. Beta receptors are associated with vasodilatation, cardioacceleration, bronchial relaxation, and intestinal relaxation. Phenoxybenzamine has been found to block alpha receptors, while propranolol blocks beta receptors. The structure of these receptors is not known. Abnormalities in Sensory Perception Abnormalities in sensory perception should be looked for on the face, trunk, and limbs. Areas of diminished pain sensation (hypalgesia) or touch sensation (hypesthesia) or heightened sensation (hyperesthesia) should be identified. Abnormal sensations (paresthesia), such as pins and needles, may be experienced by a patient who has a lesion located anywhere along the sensory pathway from the peripheral nerve to the cerebral cortex. The areas of sensory abnormality should be precisely defined and recorded, with each modality being recorded separately. Testing sensory function requires practice and experience. Many patients have difficulty in responding to a physician’s examination of the sensory system. Some individuals try to assist the examiner by wrongfully anticipating the correct response. This problem can largely be overcome by testing for cutaneous sensibility with the patient’s eyes closed. In this way, the patient cannot see which areas of skin are being tested. Other patients find it difficult to understand exactly what information is required of them. Some intelligent patients respond more to differences in intensity of stimulation rather than giving a simple “yes” or “no” answer to the question “Can you feel anything?” The physician must always be aware of the possibility of hysteria, which is when a patient complains of sensory loss that has no neuroanatomical explanation. For example, a total loss of skin sensation on one side of the face, including the angle of the jaw, would infer that the patient has a lesion involving the fifth cranial nerve in the pons and the greater auricular nerve (C2-3), which is anatomically very unlikely. Patience and objectivity are required, and if doubt exists as to the accuracy of the assessment, the patient should be reexamined on another occasion. Segmental Innervation of the Skin Because large nerve plexuses are present at the roots of the upper and lower limbs, it follows that a single spinal nerve may send both motor and sensory fibers to several peripheral nerves, and conversely, a single peripheral nerve may receive nerve fibers from many spinal nerves. Moreover, it follows that a lesion of a segment of the spinal cord, or posterior root, or spinal nerve will result in a sensory loss that is different from that occurring after a lesion of a peripheral nerve. The area of skin supplied by a single spinal nerve and, therefore, a single segment of the spinal cord is called a dermatome. A physician should remember that dermatomes overlap and that in the trunk, at least three contiguous spinal nerves have to be sectioned to produce a region of complete anesthesia. A physician should remember also that the degree of overlap for painful and thermal sensations is much greater than that for tactile sensation. A physician should have a working knowledge of the segmental (dermatomal) innervation of skin, since with the help of a pin or a piece of cotton, he or she can determine whether the sensory function of a particular spinal nerve or segment of the spinal cord is normal. When examining the dermatomal charts, one should note that because of the development of the upper limbs, the anterior rami of the lower cervical and first thoracic spinal nerves have lost their cutaneous innervation of the trunk anteriorly, and at the level of the second costal cartilage, the fourth cervical dermatome is contiguous with the second thoracic dermatome. In the sensory innervation of the head, the trigeminal (fifth cranial) nerve supplies a large area of the face and scalp, and its cutaneous area is contiguous with that of the second cervical segment. Since the dermatomes run longitudinally along the long axis of the upper limbs, sensation should be tested by dragging a wisp of cotton or a pin along the long axis of the medial and lateral borders of the limbs. On the trunk, the dermatomes run almost horizontally, so the stimulus should be applied by moving in a vertical direction. Segmental Innervation of the Muscles It is important to remember that most skeletal muscles are innervated by more than one spinal nerve and, therefore, by the same number of segments of the spinal cord. Complete destruction of one segment of the spinal cord as the result of trauma or pressure from a tumor will cause weakness of all the muscles that are innervated from that segment. To paralyze a muscle completely, several adjacent segments of the spinal cord have to be destroyed. Because of the presence of the cervical, brachial, and lumbosacral plexuses, the axons of motor anterior gray column cells are redistributed into a number of peripheral nerves. A physician, knowing this, is able to distinguish between a lesion of a segment of the spinal cord, an anterior root, or a spinal nerve on the one hand and a lesion of a peripheral nerve on the other hand. For example, the musculocutaneous nerve of the arm, which receives nerve fibers from the fifth, sixth, and seventh cervical segments of the spinal cord, supplies a finite number of muscles—namely, the biceps brachii, the brachialis, and the coracobrachialis muscles— and section of that nerve would result in total paralysis of these muscles; a lesion of the fifth, sixth, and seventh cervical spinal segments, or their anterior roots or their spinal nerves, would result in paralysis of these muscles; a lesion of the fifth, sixth, and seventh cervical spinal segments, or their anterior roots or their spinal nerves, would result in paralysis of these muscles and also partial paralysis of many other muscles, including the deltoid, supraspinatus, teres minor, and infraspinatus. The segmental innervation of the biceps brachii, triceps, brachioradialis, muscles of the anterior abdominal wall, quadriceps femoris, gastrocnemius, and soleus should be memorized, as it is possible to test them easily by eliciting their reflex contraction (see p. 100). Muscle Tone Skeletal muscle tone is due to the presence of a few muscle fibers within a muscle being in a state of full contraction all the time. Muscle tone is controlled reflexly from afferent nerve endings situated in the muscle itself. It follows, therefore, that any disease process that interferes with any part of the reflex arc will abolish the muscle tone. Some examples are syphilitic infection of the posterior root (tabes dorsalis); destruction of the motor anterior gray column cells, as in poliomyelitis or syringomyelia; destruction of a segment of the spinal cord by trauma or pressure from a tumor; section of an anterior root; pressure on a spinal nerve by a prolapsed intervertebral disc; and section of a peripheral nerve, as in a stab wound. All these clinical conditions will result in loss of muscle tone. Although it has been emphasized that the basic mechanism underlying muscle tone is the integrity of the spinal segmental reflex, it must not be forgotten that this reflex activity is influenced by nervous impulses received by the anterior horn cells from all levels of the brain and spinal cord. Spinal shock, which follows injury to the spinal cord and is caused by loss of functional activity of neurons, will result in diminished muscle tone. Cerebellar disease also results in diminished muscle tone because the cerebellum facilitates the stretch reflex. The reticular formation normally tends to increase muscle tone, but its activity is inhibited by higher cerebral centers. Therefore, it follows that if the higher cerebral control is interfered with by trauma or disease, the inhibition is lost and the muscle tone is exaggerated (decerebrate rigidity). It must not be forgotten that primary degeneration of the muscles themselves (myopathies) can cause loss of muscle tone. Posture The posture of an individual depends on the degree and distribution of muscle tone and, therefore, on the activity of the motor neurons that supply the muscles. The motor neurons in the anterior gray columns of the spinal cord are the points on which converge the nervous impulses from many posterior nerve roots and the descending fibers from many different levels of the brain and spinal cord. The successful coordination of all these nervous influences results in a normal posture. When one is in the standing posture, there is remarkably little muscular activity taking place in the muscles of the limbs and trunk. The reason for this is that the center of gravity of any part of the body is mainly above the joints on which its weight is directed. Moreover, in many joints, such as the hip and the knee, the ligaments are very strong and support the body in the erect posture. However, it must be stressed that a person cannot remain standing if all muscles are paralyzed. Once a person starts to fall, either forward, backward, or laterally, the muscle spindles and other stretch receptors immediately increase their activity, and the reflex arcs come into play; thus, reflex compensatory muscle contractions take place to restore the state of balance. The eyes and the receptors in the membranous labyrinth also play a vital part in the maintenance of balance. The importance of the eyes in maintaining the erect position can easily be tested in a normal person. Once the eyes are closed, the person shows a tendency to sway slightly because he or she now must rely exclusively on muscle and labyrinthine receptors to preserve his or her balance. It follows that a pathologic alteration in muscle tone will affect posture. For example, in hemiplegia or in Parkinson disease, in which there is hypertonicity, posture will be changed. As with cerebellar disease, hypotonicity will cause drooping of the shoulder on the affected side. Lesions involving peripheral nerves that innervate antigravity muscles will produce wristdrop (radial nerve) and footdrop (common peroneal nerve). Clinical Observation of Muscular Activity Muscular Power Ask the patient to perform movements for which the muscle under examination is primarily responsible. Next, ask the patient to perform each movement against resistance and compare the strengths of the muscles on the two sides of the body. Section of the peripheral nerve that supplies the muscle or disease affecting the anterior gray column cells (e.g., poliomyelitis) will clearly reduce the power of or paralyze the muscles involved. Muscle Wasting Muscle wasting occurs within 2 to 3 weeks after section of the motor nerve. In the limbs, it is easily tested by measuring the diameter of the limbs at a given point over the involved muscle and comparing the measurement obtained with that at the same site on the opposite limb. Muscular Fasciculation Twitching of groups of muscle fibers is seen most often in patients with chronic disease that affects the anterior horn cells (e.g., progressive muscular atrophy). Muscular Contracture Muscular contracture occurs most commonly in the muscles that normally oppose paralyzed muscles. The muscles contract and undergo permanent shortening. Muscle Tone A muscle without tone—that is, one in which the simple spinal reflex arcs are not functioning—is noncontractile and doughlike on palpation. Degrees of loss of tone may be tested by passively moving the joints and comparing the resistance to the movements by the muscles on the two sides of the body. Increase in muscle tone can occur following the removal of the cerebral inhibition on the reticular formation (see p. 168). Muscular Coordination To determine muscular coordination, ask the patient to touch, with the eyes open, the tip of the nose with the tip of the forefinger and then ask to repeat the process with the eyes closed. A similar test of the lower limbs may be carried out with the patient lying down. Ask the patient to place one heel on the opposite knee, with the eyes open and then ask to repeat the process with the eyes closed. Another test is to ask the patient to quickly supinate and pronate both forearms simultaneously. Disease of the cerebellum, for example, which coordinates muscular activity, would result in impaired ability to perform these rapid repetitive movements. Involuntary Movement of Muscles

  • Tic. This is a coordinated, repetitive movement involving one or more muscles.
  • Choreiform movements. These are quick, jerky, irregular movements that are nonrepetitive. Swift grimaces and sudden movements of the head or limbs are examples of this condition.
  • Athetosis. This consists of slow, sinuous, writhing movements that most commonly involve the distal segments of the limbs.
  • Tremor. This is the alternating contraction of the agonists and antagonists of a joint.
  • Myoclonus. This consists of shocklike muscular contractions of a portion of a muscle, an entire muscle, or a group of muscles.
  • Tonic spasm. This term refers to a sustained contraction of a muscle or group of muscles, as in the tonic phase of an epileptic seizure.

Neurologic Sensory and Motor Symptoms—Are They Always of Primary Neurologic Origin? A neurologic diagnosis depends on determining the site of the lesion and the nature of the pathology causing the disease. The physician cannot consider the nervous system in isolation, because the neurologic symptoms and signs may depend on disorders mainly involving another system. For example, a cerebral embolism may follow the formation of a blood clot on the ventricular wall of a patient with coronary thrombosis. A cerebral abscess may follow the formation of a lung abscess. It follows that a neurologic examination in many patients should be accompanied by a more general physical examination involving other systems. P.120 P.121 P.122 P.123 P.124 P.125 Clinical Problem Solving 1. A 20-year-old man was seen in the emergency department following an automobile accident. A diagnosis of fracture dislocation of the fourth thoracic vertebra was made, with injury to the spinal cord as a complication. A laminectomy was performed to decompress the spinal cord in order to avoid permanent injury to the tracts of the cord. What is a nerve tract in the spinal cord? How does this differ in structure from a peripheral nerve? View Answer1. Nervous tracts are bundles of nerve fibers found in the brain and spinal cord, most of which are myelinated. Some of the main structural differences between a myelinated nerve tract and a myelinated peripheral nerve fiber are as follows: Nerve Tract

  • Oligodendrocyte
  • Mesaxon absent
  • Schmidt-Lanterman incisures present
  • Nerve fibers supported by neuroglia

Peripheral Nerve Fiber

  • Schwann cell
  • Mesaxon present
  • Schmidt-Lanterman incisures present
  • Nerve fibers supported by connective tissue sheaths,
  • endoneurium, perineurium, and epineurium

2. Multiple sclerosis is an example of a demyelinating disease of the nervous system. Many other diseases of the nervous system also have the common pathologic feature of destruction of the myelin sheaths of nerve fibers. How does myelination normally take place in peripheral nerves and central nervous system tracts? When does myelination of nerves normally take place? View Answer2. Myelination is fully described on page 71. Myelin sheaths begin to form during fetal development and during the first year postnatally. 3. The myelin sheath is said to be formed in the peripheral nervous system by the rotation of Schwann cells on the axon so that the plasma membrane becomes wrapped around the axon in a spiral. In the central nervous system, do the oligodendrocytes

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