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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 4 – The Spinal Cord and the Ascending and Descending Tracts Chapter 4 The Spinal Cord and the Ascending and Descending Tracts A 35-year-old man was galloping his horse when he attempted to jump over a farm gate. The horse refused to jump, and he was thrown to the ground. His head struck a log, and his head and neck were excessively flexed. On initial evaluation in the emergency department after he had regained consciousness, he was found to have signs and symptoms of severe neurologic deficits in the upper and lower extremities. A lateral radiograph of the cervical region of the spine showed fragmentation of the body of the fourth cervical vertebra with backward displacement of a large bony fragment on the left side. After stabilization of the vertebral column by using skeletal traction to prevent further neurologic damage, a complete examination revealed that the patient had signs and symptoms indicating incomplete hemisection of the spinal cord on the left side. Any medical personnel involved in the evaluation and treatment of a patient with spinal cord injuries must know the structure of the spinal cord and the arrangement and functions of the various nerve tracts passing up and down this vital conduit in the central nervous system. Because of the devastating nature of spinal cord injuries and the prolonged disability that results, it is vital that all concerned with the care of such patients are trained to prevent any additional cord injury and provide the best chance for recovery. All medical personnel must have a clear picture of the extent of the cord lesion and the possible expectations for the return of function. P.133 Chapter Objectives

  • To learn how injuries to the spinal cord can occur
  • To understand the position of the main nervous pathways and nerve cell groups in the spinal cord as well as be able to correlate radiologic evidence of bone injury with segmental levels of the spinal cord and neurologic deficits
  • To review the basic structure of the delicate spinal cord and the positions and functions of the various ascending and descending tracts that lie within it
  • To make simple line drawings of each of the ascending and descending tracts, showing their cells of origin, their course through the central nervous system, and their destination

Spinal cord injuries are common and can occur as a result of automobile and motorcycle accidents, falls, sports injuries, and gunshot wounds. Spinal cord and spinal nerve damage may also be associated with vertebral fractures; vertebral infections; vertebral tumors, both primary and secondary; and herniated intervertebral discs. The student must learn the course and connections of the varuous tracts within the spinal cord in order to be able to diagnose and understand the treatment of cord injuries. Particular attention should be paid as to whether a specific tract crosses the midline to the opposite side of the central nervous system or remains on the same side. If the tract does cross the midline, the level of the crossover is important. The assessment of neurologic damage requires not only an understanding of the main nervous pathways within the spinal cord but an ability to correlate radiologic evidence of bone injury with segmental levels of the spinal cord. The close relationship of the spinal cord to the bony vertebral column necessitates a brief review of the vertebral column before the spinal cord is considered. A Brief Review of the Vertebral Column The vertebral column is the central bony pillar of the body. It supports the skull, pectoral girdle, upper limbs, and thoracic cage and, by way of the pelvic girdle, transmits body weight to the lower limbs. Within its cavity lie the spinal cord, the roots of the spinal nerves, and the covering meninges, to which the vertebral column gives great protection. Composition of the Vertebral Column The vertebral column (Figs. 4-1 and 4-2) is composed of 33 vertebrae—7 cervical, 12 thoracic, 5 lumbar, 5 sacral (fused to form the sacrum), and 4 coccygeal (the lower 3 are commonly fused). Because it is segmented and made up of vertebrae, joints, and pads of fibrocartilage called intervertebral discs, it is a flexible structure. The intervertebral discs form about one-fourth the length of the column. General Characteristics of a Vertebra Although vertebrae show regional differences, they all possess a common pattern (Fig. 4-2). A typical vertebra consists of a rounded body anteriorly and a vertebral arch posteriorly. These enclose a space called the vertebral foramen, through which run the spinal cord and its coverings. The vertebral arch consists of a pair of cylindrical pedicles, which form the sides of the arch, and a pair of flattened laminae, which complete the arch posteriorly. The vertebral arch gives rise to seven processes: one spinous, two transverse, and four articular (Fig. 4-2). The spinous process, or spine, is directed posteriorly from the junction of the two laminae. The transverse processes are directed laterally from the junction of the laminae and the pedicles. Both the spinous and transverse processes serve as levers and receive attachments of muscles and ligaments. The articular processes are vertically arranged and consist of two superior and two inferior processes. They arise from the junction of the laminae and the pedicles. The two superior articular processes of one vertebral arch articulate with the two inferior articular processes of the arch above, forming two synovial joints. The pedicles are notched on their upper and lower borders, forming the superior and inferior vertebral notches. On each side, the superior notch of one vertebra and the inferior notch of an adjacent vertebra together form an intervertebral foramen. These foramina, in an articulated skeleton, serve to transmit the spinal nerves and blood vessels. The anterior and posterior nerve roots of a spinal nerve unite within these foramina with their coverings of dura to form the segmental spinal nerves. Joints of the Vertebral Column Below the axis the vertebrae articulate with each other by means of cartilaginous joints between their bodies and by synovial joints between their articular processes. A brief review will be given here. Joints Between Two Vertebral Bodies Sandwiched between the vertebral bodies is an intervertebral disc of fibrocartilage (Fig. 4-3). Intervertebral Discs The intervertebral discs (Fig. 4-3) are thickest in the cervical and lumbar regions, where the movements of the vertebral column are greatest. They serve as shock absorbers when P.134 the load on the vertebral column is suddenly increased. Unfortunately, their resilience is gradually lost with advancing age.

Figure 4-1 Posterior view of the skeleton showing the vertebral column. The surface marking of the external occipital protuberance of the skull, the ligamentum nuchae (solid black line) and some important palpable spines (solid dots) are also shown.

Each disc consists of a peripheral part, the anulus fibrosus, and a central part, the nucleus pulposus (Fig. 4-3). The anulus fibrosus is composed of fibrocartilage, which is strongly attached to the vertebral bodies and the anterior and posterior longitudinal ligaments of the vertebral column. The nucleus pulposus in the young is an ovoid mass of gelatinous material. It is normally under pressure and situated slightly nearer to the posterior than to the anterior margin of the disc. The upper and lower surfaces of the bodies of adjacent vertebrae that abut onto the disc are covered with thin plates of hyaline cartilage. The semifluid nature of the nucleus pulposus allows it to change shape and permits one vertebra to rock forward or backward on another. A sudden increase in the compression load on the vertebral column causes the nucleus pulposus to become flattened, and this is accommodated by the resilience of the surrounding anulus fibrosus. Sometimes, the outward thrust is too great for the anulus fibrosus and it ruptures, allowing the nucleus pulposus to herniate and protrude into the vertebral canal, where it may press on the spinal nerve roots, the spinal nerve, or even the spinal cord. With advancing age, the nucleus pulposus becomes smaller and is replaced by fibrocartilage. The collagen fibers of the anulus degenerate, and as a result, the anulus cannot always contain the nucleus pulposus under stress. In old P.135 age, the discs are thin and less elastic, and it is no longer possible to distinguish the nucleus from the anulus.

Figure 4-2 A: Lateral view of the vertebral column. B: General features of different kinds of vertebrae.

Ligaments The anterior and posterior longitudinal ligaments run as continuous bands down the anterior and posterior surfaces of the vertebral column from the skull to the sacrum (Fig. 4-3). The anterior ligament is wide and is strongly attached to the front and sides of the vertebral bodies and to the intervertebral discs. The posterior ligament is weak and narrow and is attached to the posterior borders of the discs. P.136

Figure 4-3 A: Joints in the cervical, thoracic, and lumbar regions of the vertebral column. B: Third lumbar vertebra seen from above showing the relationship between intervertebral disc and cauda equina.

Joints Between Two Vertebral Arches The joints between two vertebral arches consist of synovial joints between the superior and inferior articular processes of adjacent vertebrae (Fig. 4-3). Ligaments

  • Supraspinous ligament (Fig. 4-3): This runs between the tips of adjacent spines.
  • Interspinous ligament (Fig. 4-3): This connects adjacent spines.
  • Intertransverse ligaments: These run between adjacent transverse processes.
  • Ligamentum flavum (Fig. 4-3): This connects the laminae of adjacent vertebrae.

In the cervical region, the supraspinous and interspinous ligaments are greatly thickened to form the strong ligamentum nuchae. P.137

Figure 4-4 The innervation of vertebral joints. At any particular vertebral level, the joints receive nerve fibers from two adjacent spinal nerves.

Nerve Supply of Vertebral Joints The joints between the vertebral bodies are innervated by the small meningeal branches of each spinal nerve (Fig. 4-4). The joints between the articular processes are innervated by branches from the posterior rami of the spinal nerves (Fig. 4-4); the joints of any particular level receive nerve fibers from two adjacent spinal nerves. The atlanto-occipital joints and the atlanto-axial joints should be reviewed in a textbook of gross anatomy. Gross Appearance of the Spinal Cord The spinal cord is roughly cylindrical in shape. It begins superiorly at the foramen magnum in the skull, where it is continuous with the medulla oblongata of the brain, and it terminates inferiorly in the adult at the level of the lower border of the first lumbar vertebra. In the young child, it is relatively longer and usually ends at the upper border of the third lumbar vertebra. Thus, it occupies the upper two-thirds of the vertebral canal of the vertebral column and is surrounded by the three meninges, the dura mater, the arachnoid mater, and the pia mater. Further protection is provided by the cerebrospinal fluid, which surrounds the spinal cord in the subarachnoid space. In the cervical region, where it gives origin to the brachial plexus, and in the lower thoracic and lumbar regions, where it gives origin to the lumbosacral plexus, the spinal cord is fusiformly enlarged; the enlargements are referred to as the cervical and lumbar enlargements (Fig. 4-5). Inferiorly, the spinal cord tapers off into the conus medullaris, from the apex of which a prolongation of the pia mater, the filum terminale, descends to be attached to the posterior surface of the coccyx. The cord possesses a deep longitudinal fissure called the anterior median fissure in the midline anteriorly and a shallow furrow called the posterior median sulcus on the posterior surface (Fig. 4-5). Along the entire length of the spinal cord are attached 31 pairs of spinal nerves by the anterior1 or motor roots and the posterior or sensory roots (Fig. 4-5). Each root is attached to the cord by a series of rootlets, which extend the whole length of the corresponding segment of the cord. Each posterior nerve root possesses a posterior root ganglion, the cells of which give rise to peripheral and central nerve fibers. P.138

Figure 4-5 Spinal cord. A: Posterior view, showing cervical and lumbar enlargements. B: Three segments of the spinal cord showing the coverings of dura mater, arachnoid mater, and pia mater.

Structure of the Spinal Cord The spinal cord is composed of an inner core of gray matter, which is surrounded by an outer covering of white matter (Figs. 4-6, 4-7, 4-8, 4-9 and 4-10); there is no indication that the cord is segmented. For a comparison of the structural details in different regions of the spinal cord, see Table 4-1. Gray Matter On cross section, the gray matter is seen as an H-shaped pillar with anterior and posterior gray columns, or horns, united by a thin gray commissure containing the small central canal (Fig. 4-6). A small lateral gray column or horn is present in the thoracic and upper lumbar segments of the cord. The amount of gray matter present at any given level of the spinal cord is related to the amount of muscle P.139innervated at that level. Thus, its size is greatest within the cervical and lumbosacral enlargements of the cord, which innervate the muscles of the upper and lower limbs, respectively (Figs. 4-6, 4-7, 4-8, 4-9 and 4-10).

Table 4-1 Comparison of Structural Details in Different Regions of the Spinal Corda
Region Shape White Matter Gray Matter
Anterior Gray Column Posterior Gray Column Lateral Gray Column
Cervical Oval Fasciculus cuneatus and fasciculus gracilis present Medial group of cells for neck muscles; central group of cells for accessory nucleus (C1-5) and phrenic nucleus (C3-5); lateral group of cells for upper limb muscles Substantia gelatinosa present, continuous with Sp.N. of cranial nerve V at level C2; nucleus proprius present; nucleus dorsalis (Clarke’s column) absent Absent
Thoracic Round Fasciculus cuneatus (T1-6) and fasciculus gracilis present Medial group of cells for trunk muscles Substantia gelatinosa, nucleus proprius, nucleus dorsalis (Clarke’s column), and visceral afferent nucleus present Present; gives rise to preganglionic sympathetic fibers
Lumbar Round to oval Fasciculus cuneatus absent; fasciculus gracilis present Medial group of cells for lower limb muscles; central group of cells for lumbosacral nerve Substantia gelatinosa, nucleus proprius, nucleus dorsalis (Clarke’s column) at L1-4, and visceral afferent nucleus present Present (L1-2 [3]); gives rise to preganglionic sympathetic fibers
Sacral Round Small amount; fasciculus cuneatus absent; fasciculus gracilis present Medial group of cells for lower limb and perineal muscles Substantia gelatinosa and nucleus proprius present Absent; group of cells present at S2-4, for parasympathetic outflow
aThe information in this table is useful for identifying the specific level of the spinal cord from which a section has been taken.

Structure As in other regions of the central nervous system, the gray matter of the spinal cord consists of a mixture of nerve cells and their processes, neuroglia, and blood vessels. The nerve cells are multipolar, and the neuroglia forms an intricate network around the nerve cell bodies and their neurites. Nerve Cell Groups in the Anterior Gray Columns Most nerve cells are large and multipolar, and their axons pass out in the anterior roots of the spinal nerves as alpha efferents, which innervate skeletal muscles. The smaller nerve cells are also multipolar, and the axons of many of these pass out in the anterior roots of the spinal nerves as gamma efferents, which innervate the intrafusal muscle fibers of neuromuscular spindles. For practical purposes, the nerve cells of the anterior gray column may be divided into three basic groups or columns: medial, central, and lateral (Fig. 4-6).2 The medial group is present in most segments of the spinal cord and is responsible for innervating the skeletal muscles of the neck and trunk, including the intercostal and abdominal musculature. The central group is the smallest and is present in some cervical and lumbosacral segments (Figs. 4-6 and 4-7). In the cervical part of the cord, some of these nerve cells (segments C3-5) specifically innervate the diaphragm and are collectively referred to as the phrenic nucleus (Fig. 4-7). In the upper five or six cervical segments, some of the nerve cells innervate the sternocleidomastoid and trapezius muscles and are referred to as the accessory nucleus (Figs. 4-6 and 4-7). The axons of these cells form the spinal part of the accessory nerve. The lumbosacral nucleus present in the second lumbar down to the first sacral segment of the cord is made up of nerve cells whose axons have an unknown distribution. The lateral group is present in the cervical and lumbosacral segments of the cord and is responsible for innervating the skeletal muscles of the limbs (Figs. 4-6, 4-7, 4-9, and 4-10). Nerve Cell Groups in the Posterior Gray Columns There are four nerve cell groups of the posterior gray column: two that extend throughout the length of the cord and two that are restricted to the thoracic and lumbar segments. The substantia gelatinosa group is situated at the apex of the posterior gray column throughout the length of the spinal cord (Figs. 4-6, 4-7, 4-8, 4-9 and 4-10). It is largely composed of Golgi type II neurons and receives afferent fibers concerned with P.140 pain, temperature, and touch from the posterior root. Furthermore, it receives input from descending fibers from supraspinal levels. It is believed that the inputs of the sensations of pain and temperature are modified by excitatory or inhibitory information from other sensory inputs and by information from the cerebral cortex.

Figure 4-6 Transverse sections of the spinal cord at different levels showing the arrangement of the gray matter and white matter.

The nucleus proprius is a group of large nerve cells situated anterior to the substantia gelatinosa throughout the spinal cord (Figs. 4-6, 4-7, 4-8, 4-9 and 4-10). This nucleus constitutes the main bulk of cells present in the posterior gray column and receives fibers from the posterior white column that are associated with the senses of position and movement (proprioception), two-point discrimination, and vibration. The nucleus dorsalis (Clarke’s column) is a group of nerve cells situated at the base of the posterior gray column and extending from the eighth cervical segment caudally to the third or fourth lumbar segment (Figs. 4-6, 4-7, 4-8 and 4-9). Most of the cells are comparatively large and are associated with proprioceptive endings (neuromuscular spindles and tendon spindles). P.141

Figure 4-7 Transverse section of the spinal cord at the level of the fifth cervical segment. (Weigert stain.)

The visceral afferent nucleus is a group of nerve cells of medium size situated lateral to the nucleus dorsalis; it extends from the first thoracic to the third lumbar segment of the spinal cord. It is believed to be associated with receiving visceral afferent information. Nerve Cell Groups in the Lateral Gray Columns The intermediolateral group of cells form the small lateral gray column, which extends from the first thoracic to the second or third lumbar segment of the spinal cord (Figs. 4-6 and 4-8). The cells are relatively small and give rise to preganglionic sympathetic fibers.

Figure 4-8 Transverse section of the spinal cord at the level of the second thoracic segment. (Weigert stain.)

A similar group of cells found in the second, third, and fourth sacral segments of the spinal cord give rise to preganglionic parasympathetic fibers (Figs. 4-6 and 4-10). The Gray Commissure and Central Canal In transverse sections of the spinal cord, the anterior and posterior gray columns on each side are connected by a transverse gray commissure; the gray matter resembles the letter H (Figs. 4-6, 4-7, 4-8, 4-9 and 4-10). In the center of the gray commissure is situated the central canal. The part of the gray commissure that is situated posterior to the central canal is often referred to as the posterior gray commissure; similarly, P.142 the part that lies anterior to the canal is called the anterior gray commissure.

Figure 4-9 Transverse section of the spinal cord at the level of the fourth lumbar segment. (Weigert stain.)

The central canal is present throughout the spinal cord (Figs. 4-6, 4-7, 4-8, 4-9 and 4-10). Superiorly, it is continuous with the central canal of the caudal half of the medulla oblongata, and above this, it opens into the cavity of the fourth ventricle. Inferiorly in the conus medullaris, it expands into the fusiform terminal ventricle and terminates below within the root of the filum terminale. It is filled with cerebrospinal fluid and is lined with ciliated columnar epithelium, the ependyma. Thus, the central canal is closed inferiorly and opens superiorly into the fourth ventricle.

Figure 4-10 Transverse section of the spinal cord at the level of the second sacral segment. (Weigert stain.)

P.143

Figure 4-11 Transverse section of the spinal cord at the midcervical level showing the general arrangement of the ascending tracts on the right and the descending tracts on the left.

White Matter The white matter, for purposes of description, may be divided into anterior, lateral, and posterior white columns or funiculi (Figs. 4-5, 4-6, 4-7, 4-8, 4-9 and 4-10). The anterior column on each side lies between the midline and the point of emergence of the anterior nerve roots; the lateral column lies between the emergence of the anterior nerve roots and the entry of the posterior nerve roots; the posterior column lies between the entry of the posterior nerve roots and the midline. Structure As in other regions of the central nervous system, the white matter of the spinal cord consists of a mixture of nerve fibers, neuroglia, and blood vessels. It surrounds the gray matter, and its white color is due to the high proportion of myelinated nerve fibers. Arrangement of Nerve Fiber Tracts The arrangement of the nerve fiber tracts within the spinal cord has been deduced as the result of animal experimentation and study of the human spinal cord for degenerative nerve fibers resulting from injury or disease. Although some nerve tracts are concentrated in certain areas of the white matter, it is now generally accepted that considerable overlap is present. For purposes of description, the spinal tracts are divided into ascending, descending, and intersegmental tracts, and their relative positions in the white matter are described below. A simplified diagram, showing the general arrangement of the major tracts, is shown in Figure 4-11. The Ascending Tracts of the Spinal Cord On entering the spinal cord, the sensory nerve fibers of different sizes and functions are sorted out and segregated into nerve bundles or tracts in the white matter (Figs. 4-11 and 4-12). Some of the nerve fibers serve to link different segments of the spinal cord, while others ascend from the spinal cord to higher centers and thus connect the spinal cord with the brain. It is the bundles of the ascending fibers that are referred to as the ascending tracts. The ascending tracts conduct afferent information, which may or may not reach consciousness. The information may be divided into two main groups: (1) exteroceptive information, which originates from outside the body, such as pain, temperature, and touch, and (2) proprioceptive information, which originates from inside the body, for example, from muscles and joints. Anatomical Organization General information from the peripheral sensory endings is conducted through the nervous system by a series of neurons. In its simplest form, the ascending pathway to consciousness consists of three neurons (Fig. 4-12). The first neuron, the first-order neuron, has its cell body in the posterior root ganglion of the spinal nerve. A peripheral process connects with a sensory receptor ending, whereas a central process enters the spinal cord through the posterior root to synapse on the second-order neuron. P.144 The second-order neuron gives rise to an axon that decussates (crosses to the opposite side) and ascends to a higher level of the central nervous system, where it synapses with the third-order neuron (Fig. 4-12). The third-order neuron is usually in the thalamus and gives rise to a projection fiber that passes to a sensory region of the cerebral cortex (Fig. 4-12). This three-neuron chain is the most common arrangement, but some afferent pathways use more or fewer neurons. Many of the neurons in the ascending pathways branch and give a major input into the reticular formation, which, in turn, activates the cerebral cortex, maintaining wakefulness. Other branches pass to motor neurons and participate in reflex muscular activity.

Figure 4-12 Simplest form of the ascending sensory pathway from the sensory nerve ending to the cerebral cortex. Note the three neurons involved.

Functions of the Ascending Tracts Painful and thermal sensations ascend in the lateral spinothalamic tract; light (crude) touch and pressure ascend in the anterior spinothalamic tract (Fig. 4-13). Discriminative touch—that is, the ability to localize accurately the area of the body touched and also to be aware that two points are touched simultaneously, even though they are close together (two-point discrimination)— ascends in the posterior white columns (Fig. 4-13). Also ascending in the posterior white columns is information from muscles and joints pertaining to movement and position of different parts of the body. In addition, vibratory sensations ascend in the posterior white column. Unconscious information from muscles, joints, the skin, and subcutaneous tissue reaches the cerebellum by way of the anterior and posterior spinocerebellar tracts and by the cuneocerebellar tract (Fig. 4-13). Pain, thermal, and tactile information is passed to the superior colliculus of the midbrain through the spinotectal tract for the purpose of spinovisual reflexes (Fig. 4-13). The spinoreticular tract provides a pathway from the muscles, joints, and skin to the reticular formation, while the spino-olivary tract provides an indirect pathway for further afferent information to reach the cerebellum (Fig. 4-13). Pain and Temperature Pathways Lateral Spinothalamic Tract3 The pain and thermal receptors in the skin and other tissues are free nerve endings. The pain impulses are transmitted to the spinal cord in fast-conducting delta A-type fibers and slow-conducting C-type fibers. The fast-conducting fibers alert the individual to initial sharp pain, and the slow-conducting fibers are responsible for prolonged burning, aching pain. The sensations of heat and cold also travel by delta A and C fibers. The axons entering the spinal cord from the posterior root ganglion proceed to the tip of the posterior gray column and divide into ascending and descending branches (Fig. 4-14). These branches travel for a distance of one or two segments of the spinal cord and form the posterolateral tract of Lissauer (Fig. 4-14). These fibers of the first-order neuron terminate by synapsing with cells in the posterior gray column, including cells in the substantia gelatinosa. Substance P, a peptide, is thought to be the neurotransmitter at these synapses. The axons of the second-order neurons now cross obliquely to the opposite side in the anterior gray and white commissures within one spinal segment of the cord, ascending in the contralateral white column as the lateral spinothalamic tract (Fig. 4-14). The lateral spinothalamic tract lies medial to the anterior spinocerebellar tract. As P.145 the lateral spinothalamic tract ascends through the spinal cord, new fibers are added to the anteromedial aspect of the tract. Thus, in the upper cervical segments of the cord, the sacral fibers are lateral and the cervical segments are medial. The fibers carrying pain are situated slightly anterior to those conducting temperature.

Figure 4-13 Transverse section of the spinal cord showing the origin of the main ascending sensory tracts. Note that the sensations of pain and temperature ascend in the lateral spinothalamic tract, and light touch and pressure ascend in the anterior spinothalamic tract.

As the lateral spinothalamic tract ascends through the medulla oblongata, it lies near the lateral surface and between the inferior olivary nucleus and the nucleus of the spinal tract of the trigeminal nerve. It is now accompanied by the anterior spinothalamic tract and the spinotectal tract; together they form the spinal lemniscus (Fig. 4-14). The spinal lemniscus continues to ascend through the posterior part of the pons (Fig. 4-14). In the midbrain, it lies in the tegmentum lateral to the medial lemniscus. Many of the fibers of the lateral spinothalamic tract end by synapsing with the third-order neuron in the ventral posterolateral nucleus of the thalamus (Fig. 4-14). It is believed that here crude pain and temperature sensations are appreciated and emotional reactions are initiated. The axons of the third-order neurons in the ventral posterolateral nucleus of the thalamus now pass through the posterior limb of the internal capsule and the corona radiata to reach the somesthetic area in the postcentral gyrus of the cerebral cortex (Fig. 4-14). The contralateral half of the body is represented as inverted, with the hand and mouth situated inferiorly and the leg situated superiorly, and with the foot and anogenital region on the medial surface of the hemisphere. (For details, see p. 291.) From here, the information is transmitted to other regions of the cerebral cortex to be used by motor areas and the parietal association area. The role of the cerebral cortex is interpreting the quality of the sensory information at the level of consciousness. Pain Reception The perception of pain is a complex phenomenon that is influenced by the emotional state and past experiences of the individual. Pain is a sensation that warns of potential injury and alerts the person to avoid or treat it. Pain can be divided into two main types: fast pain and slow pain. Fast pain is experienced within about 0.1 second after the pain stimulus is applied; slow pain is felt 1.0 second or later after the stimulation. Fast pain is described by the patient as sharp pain, acute pain, or pricking pain and is the type of pain felt after pricking the finger with a needle. Fast pain is almost confined to the skin. Slow pain is described as burning pain, aching pain, and throbbing pain and is produced when there is tissue destruction, as for example, in the development of an abscess or in severe arthritis. Slow pain can occur in any tissue of the body. P.146

Figure 4-14 Pain and temperature pathways.

All types of pain reception take place in free nerve endings. Fast pain is experienced by mechanical or thermal types of stimuli, and slow pain may be elicited by mechanical, thermal, and chemical stimuli. Many chemical substances have been found in extracts from damaged tissue that will excite free nerve endings. These include serotonin; histamine; bradykinin; acids, such as lactic acid; and K ions. The threshold for pain endings can be lowered by prostaglandins and substance P, but they cannot stimulate the endings directly by themselves. The individual should be aware of the existence of stimuli that, if allowed to persist, will bring about tissue destruction; pain receptors have little or no adaptation. P.147 Conduction of Pain to the Central Nervous System Fast pain travels in peripheral nerves in large diameter A delta axons at velocities of between 6 and 30 msec. Slow pain travels in the small diameter C fibers at velocities between 0.5 and 2.0 msec. The fast pain impulses reach consciousness first to alert the individual to danger so that a suitable protective response may take place. Slow pain is appreciated later and lasts much longer. Conduction of Pain in the Central Nervous System The afferent pain fibers enter the spinal cord, for example, in the posterior roots of a spinal nerve and terminate predominantly in the superficial layers of the posterior gray horn. The main excitatory neurotransmitter released by the A delta fibers and the C fibers is the amino acid glutamate. Substance P, a neuropeptide, is also released from the C fibers. Whereas glutamate is a fast-acting localized neurotransmitter, substance P has a slow release and diffuses widely in the posterior horn and can influence many neurons. The initial sharp, pricking, fast-acting pain fibers stimulate the second-order neurons of the lateral spinothalamic tract. The axons immediately cross to the opposite side of the spinal cord and ascend to the thalamus where they are relayed to the sensory post central gyrus. The burning, aching, slow-acting pain fibers also stimulate the second-order neurons of the lateral spinal thalamic tract in the posterior gray horn and ascend with the axons of the fast-acting pain fibers. It is now believed, however, that most of the incoming slow fibers to the spinal cord take part in additional relays involving several neurons in the posterior horn before ascending in the spinal cord. The repeated arrival of noxious stimuli through the C fibers in the posterior gray horn during severe injury results in an increased response of the second-order neurons. This winding up phenomenon is attributed to the release of the neurotransmitter glutamate from the C fibers. The fast type of pain is precisely localized. For example, if one hits the thumb with a hammer, there is no doubt where the injury has occurred. The slow type of pain is only poorly localized. For example, in a patient with osteoarthritis of the hip joint, the individual can only vaguely localize the pain to the hip area and not to the specific site of the disease. This may be explained by the fact that fast pain fibers directly ascend the spinal cord in the lateral spinothalamic tract, whereas the slow pain fibers take part in multiple relays in the posterior gray horn before ascending to higher centers. Other Terminations of the Lateral Spinothalamic Tract It is now generally agreed that the fast pain impulses travel directly up to the ventral posterolateral nucleus of the thalamus and are then relayed to the cerebral cortex. The majority of the slow pain fibers in the lateral spinothalamic tract terminate in the reticular formation, which then activates the entire nervous system. It is in the lower areas of the brain that the individual becomes aware of the chronic, nauseous, suffering type of pain. As the result of research using the positron emission tomography scan, the postcentral gyrus, the cingulate gyrus of the limbic system, and the insular gyrus are sites concerned with the reception and interpretation of the nociceptor information. The postcentral gyrus is responsible for the interpretation of pain in relation to past experiences. The cingulate gyrus is involved with the interpretation of the emotional aspect of pain, whereas the insular gyrus is concerned with the interpretation of pain stimuli from the internal organs of the body and brings about an autonomic response. The reception of pain information by the central nervous system can be modulated first in the posterior gray horns of the spinal cord and at other sites at higher levels. Pain Control in the Central Nervous System The Gating Theory Massage and the application of liniments to painful areas in the body can relieve pain. The technique of acupuncture, which was discovered several thousand years ago in China, is also beneficial in relieving pain. Low-frequency electrical stimulation of the skin also relieves pain in certain cases. Although the precise mechanism for these phenomena is not understood, the gating theory was proposed some years ago. It was suggested that at the site where the pain fiber enters the central nervous system, inhibition could occur by means of connector neurons excited by large, myelinated afferent fibers carrying information of nonpainful touch and pressure. The excess tactile stimulation produced by massage, for example, “closed the gate” for pain. Once the nonpainful tactile stimulation ceased, however, “the gate was opened,” and information on the painful stimuli ascended the lateral spinothalamic tract. Although the gate theory may partially explain the phenomena, the analgesia system is probably involved with the liberation of enkephalins and endorphins in the posterior gray columns. The Analgesia System Stimulation of certain areas of the brainstem can reduce or block sensations of pain. These areas include the periventricular area of the diencephalon, the periaqueductal gray matter of the midbrain, and midline nuclei of the brainstem. It is believed that fibers of the reticulospinal tract pass down to the spinal cord and synapse on cells concerned with pain sensation in the posterior gray column. The analgesic system can suppress both sharp pricking pain and burning pain sensations. Recently, two compounds with morphinelike actions, called the enkephalins and the endorphins, have been isolated in the central nervous system. These compounds and serotonin serve as neurotransmitter substances in the analgesic system of the brain, and they may inhibit the release of substance P in the posterior gray column. Light (Crude) Touch and Pressure Pathways Anterior Spinothalamic Tract The axons enter the spinal cord from the posterior root ganglion and proceed to the tip of the posterior gray column, P.148 where they divide into ascending and descending branches (Fig. 4-15). These branches travel for a distance of one or two segments of the spinal cord, contributing to the posterolateral tract of Lissauer. It is believed that these fibers of the first-order neuron terminate by synapsing with cells in the substantia gelatinosa group in the posterior gray column (Fig. 4-15).

Figure 4-15 Light touch and pressure pathways.

The axons of the second-order neuron now cross very obliquely to the opposite side in the anterior gray and white commissures within several spinal segments and ascend in the opposite anterolateral white column as the anterior spinothalamic tract (Fig. 4-15). As the anterior spinothalamic tract ascends through the spinal cord, new fibers are added to the medial aspect of the tract. Thus, in P.149 the upper cervical segments of the cord, the sacral fibers are mostly lateral and the cervical segments are mostly medial. As the anterior spinothalamic tract ascends through the medulla oblongata, it accompanies the lateral spinothalamic tract and the spinotectal tract, all of which form the spinal lemniscus (Fig. 4-15). The spinal lemniscus continues to ascend through the posterior part of the pons, and the tegmentum of the midbrain and the fibers of the anterior spinothalamic tract terminate by synapsing with the third-order neuron in the ventral posterolateral nucleus of the thalamus (Fig. 4-15). Crude awareness of touch and pressure is believed to be appreciated here. The axons of the third-order neurons in the ventral posterolateral nucleus of the thalamus pass through the posterior limb of the internal capsule (Fig. 4-15) and the corona radiata to reach the somesthetic area in the postcentral gyrus of the cerebral cortex. The contralateral half of the body is represented inverted, with the hand and mouth situated inferiorly, as described previously. (For details, see p. 291.) The conscious appreciation of touch and pressure depends on the activity of the cerebral cortex. The sensations can be only crudely localized, and very little discrimination of intensity is possible. Discriminative Touch, Vibratory Sense, and Conscious Muscle Joint Sense Posterior White Column: Fasciculus Gracilis and Fasciculus Cuneatus The axons enter the spinal cord from the posterior root ganglion and pass directly to the posterior white column of the same side (Fig. 4-16). Here, the fibers divide into long ascending and short descending branches. The descending branches pass down a variable number of segments, giving off collateral branches that synapse with cells in the posterior gray horn, with internuncial neurons, and with anterior horn cells (Fig. 4-16). It is clear that these short descending fibers are involved with intersegmental reflexes. The long ascending fibers may also end by synapsing with cells in the posterior gray horn, with internuncial neurons, and with anterior horn cells. This distribution may extend over numerous segments of the spinal cord (Fig. 4-16). As in the case of the short descending fibers, they are involved with intersegmental reflexes. Many of the long ascending fibers travel upward in the posterior white column as the fasciculus gracilis and fasciculus cuneatus (Fig. 4-16). The fasciculus gracilis is present throughout the length of the spinal cord and contains the long ascending fibers from the sacral, lumbar, and lower six thoracic spinal nerves. The fasciculus cuneatus is situated laterally in the upper thoracic and cervical segments of the spinal cord and is separated from the fasciculus gracilis by a septum. The fasciculus cuneatus contains the long ascending fibers from the upper six thoracic and all the cervical spinal nerves. The fibers of the fasciculus gracilis and fasciculus cuneatus ascend ipsilaterally and terminate by synapsing on the second-order neurons in the nuclei gracilis and cuneatus of the medulla oblongata (Fig. 4-16). The axons of the second-order neurons, called the internal arcuate fibers, sweep anteromedially around the central gray matter and cross the median plane, decussating with the corresponding fibers of the opposite side in the sensory decussation (Fig. 4-16). The fibers then ascend as a single compact bundle, the medial lemniscus, through the medulla oblongata, the pons, and the midbrain (Fig. 4-16). The fibers terminate by synapsing on the third-order neurons in the ventral posterolateral nucleus of the thalamus. The axons of the third-order neuron leave and pass through the posterior limb of the internal capsule and corona radiata to reach the somesthetic area in the postcentral gyrus of the cerebral cortex (Fig. 4-16). The contralateral half of the body is represented inverted, with the hand and mouth situated inferiorly, as described previously. (For details, see p. 291.) In this manner, the impressions of touch with fine gradations of intensity, exact localization, and two-point discrimination can be appreciated. Vibratory sense and the position of the different parts of the body can be consciously recognized. Many fibers in the fasciculus cuneatus from the cervical and upper thoracic segments, having terminated on the second-order neuron of the nucleus cuneatus, are relayed and travel as the axons of the second-order neurons to enter the cerebellum through the inferior cerebellar peduncle of the same side (Fig. 4-16). The pathway is referred to as the cuneocerebellar tract, and the fibers are known as the posterior external arcuate fibers. The function of these fibers is to convey information of muscle joint sense to the cerebellum. The main somatosensory pathways are summarized in Table 4-2. Muscle Joint Sense Pathways to the Cerebellum Posterior Spinocerebellar Tract The axons entering the spinal cord from the posterior root ganglion enter the posterior gray column and terminate by synapsing on the second-order neurons at the base of the posterior gray column (Fig. 4-17). These neurons are known collectively as the nucleus dorsalis (Clarke’s column). The axons of the second-order neurons enter the posterolateral part of the lateral white column on the same side and ascend as the posterior spinocerebellar tract to the medulla oblongata. Here, the tract joins the inferior cerebellar peduncle and terminates in the cerebellar cortex (Fig. 4-17). Note that it does not ascend to the cerebral cortex. Because the nucleus dorsalis (Clarke’s column) extends only from the eighth cervical segment caudally to the third or fourth lumbar segment, axons entering the spinal cord from the posterior roots of the lower lumbar and sacral segments ascend in the posterior white column until they reach the third or fourth lumbar segment, where they enter the nucleus dorsalis. The posterior spinocerebellar fibers receive muscle joint information from the muscle spindles, tendon organs, and joint receptors of the trunk and lower limbs. This information concerning tension of muscle tendons and the movements of muscles and joints is used by the cerebellum in the coordination of limb movements and the maintenance of posture. P.150

Figure 4-16 Discriminative touch, vibratory sense, and conscious muscle joint sense pathways.

Anterior Spinocerebellar Tract The axons entering the spinal cord from the posterior root ganglion terminate by synapsing with the second-order neurons in the nucleus dorsalis at the base of the posterior gray column (Fig. 4-17). The majority of the axons of the second-order neurons cross to the opposite side and ascend as the anterior spinocerebellar tract in the contralateral white column; the minority of the axons ascend as the anterior spinocerebellar tract in the lateral white column of the same side (Fig. 4-17). The fibers, having ascended through the medulla oblongata and pons, enter the cerebellum through the superior cerebellar peduncle and terminate in the cerebellar cortex. It is believed that those fibers that crossed over to the opposite side in the spinal cord cross back within the cerebellum (Fig. 4-17). The anterior spinocerebellar tract conveys muscle joint information from the P.151 P.152 muscle spindles, tendon organs, and joint receptors of the trunk and the upper and lower limbs. It is also believed that the cerebellum receives information from the skin and superficial fascia by this tract.

Table 4-2 The Main Somatosensory Pathways to Consciousnessa
Sensation Receptor First-Order Neuron Second-Order Neuron Third-Order Neuron Pathways Destination
Pain and temperature Free nerve endings Posterior root ganglion Substantia gelatinosa Ventral posterolateral nucleus of thalamus Lateral spinothalamic, spinal lemniscus Posterior central gyrus
Light touch and pressure Free nerve endings Posterior root ganglion Substantia gelatinosa Ventral posterolateral nucleus of thalamus Anterior spinothalamic, spinal lemniscus Posterior central gyrus
Discriminative touch, vibratory sense, conscious muscle joint sense Meissner’s corpuscles, pacinian corpuscles, muscle spindles, tendon organs Posterior root ganglion Nuclei gracilis and cuneatus Ventral posterolateral nucleus of thalamus Fasciculi gracilis and cuneatus, medial lemniscus Posterior central gyrus
aNote that all ascending pathways send branches to the reticular activating system.
Figure 4-17 Unconscious muscle joint sense pathways to the cerebellum.
Table 4-3 Muscle Joint Sense Pathways to the Cerebellum
Sensation Receptor First-Order Neuron Second-Order Neuron Pathways Destination
Unconscious
muscle
joint sense
Muscle
spindles,
tendon
organs,
joint
receptors
Posterior root
ganglion
Nucleus dorsalis Anterior and
posterior
spinocere-
bellar
Cerebellar
cortex

The muscle joint sense pathways to the cerebellum are summarized in Table 4-3. Cuneocerebellar Tract These fibers have already been described on page 149. They originate in the nucleus cuneatus and enter the cerebellum through the inferior cerebellar peduncle of the same side (Fig. 4-16). The fibers are known as the posterior external arcuate fibers, and their function is to convey information of muscle joint sense to the cerebellum. Other Ascending Pathways Spinotectal Tract The axons enter the spinal cord from the posterior root ganglion and travel to the gray matter where they synapse on unknown second-order neurons (Fig. 4-18). The axons of the second-order neurons cross the median plane and ascend as the spinotectal tract in the anterolateral white column lying close to the lateral spinothalamic tract. After passing through the medulla oblongata and pons, they terminate by synapsing with neurons in the superior colliculus of the midbrain (Fig. 4-18). This pathway provides afferent information for spinovisual reflexes and brings about movements of the eyes and head toward the source of the stimulation. Spinoreticular Tract The axons enter the spinal cord from the posterior root ganglion and terminate on unknown second-order neurons in the gray matter (Fig. 4-18). The axons from these second-order neurons ascend the spinal cord as the spinoreticular tract in the lateral white column mixed with the lateral spinothalamic tract. Most of the fibers are uncrossed and terminate by synapsing with neurons of the reticular formation in the medulla oblongata, pons, and midbrain (Fig. 4-18). The spinoreticular tract provides an afferent pathway for the reticular formation, which plays an important role in influencing levels of consciousness. (For details, see p. 297.) Spino-olivary Tract The axons enter the spinal cord from the posterior root ganglion and terminate on unknown second-order neurons in the posterior gray column (Fig. 4-18). The axons from the second-order neurons cross the midline and ascend as the spino-olivary tract in the white matter at the junction of the anterior and lateral columns. The axons end by synapsing on third-order neurons in the inferior olivary nuclei in the medulla oblongata (Fig. 4-18). The axons of the third-order neurons cross the midline and enter the cerebellum through the inferior cerebellar peduncle. The spino-olivary tract conveys information to the cerebellum from cutaneous and proprioceptive organs. Visceral Sensory Tracts Sensations that arise in viscera located in the thorax and abdomen enter the spinal cord through the posterior roots. The cell bodies of the first-order neuron are situated in the posterior root ganglia. The peripheral processes of these cells receive nerve impulses from pain4 and stretch receptor endings in the viscera. The central processes, having entered the spinal cord, synapse with second-order neurons in the gray matter, probably in the posterior or lateral gray columns. The axons of the second-order neurons are believed to join the spinothalamic tracts and ascend and terminate on the third-order neurons in the ventral posterolateral nucleus of the thalamus. The final destination of the axons of the third-order neurons is probably in the postcentral gyrus of the cerebral cortex. Many of the visceral afferent fibers that enter the spinal cord branch participate in reflex activity. P.153

Figure 4-18 Spinotectal, spinoreticular, and spino-olivary tracts.

The Descending Tracts of the Spinal Cord The motor neurons situated in the anterior gray columns of the spinal cord send axons to innervate skeletal muscle through the anterior roots of the spinal nerves. These motor neurons are sometimes referred to as the lower motor neurons and constitute the final common pathway to the muscles (Fig. 4-19). The lower motor neurons are constantly bombarded by nervous impulses that descend from the medulla, pons, midbrain, and cerebral cortex as well as those that enter along sensory fibers from the posterior roots. The nerve fibers that descend in the white matter from different supraspinal nerve centers are segregated into nerve bundles called the descending tracts. These supraspinal neurons and their tracts are sometimes referred to as the upper motor neurons, and they provide numerous separate pathways that can influence motor activity. Anatomical Organization Control of skeletal muscle activity from the cerebral cortex and other higher centers is conducted through the nervous system by a series of neurons (Fig. 4-19). The descending pathway from the cerebral cortex is often made up of three P.154 neurons. The first neuron, the first-order neuron, has its cell body in the cerebral cortex. Its axon descends to synapse on the second-order neuron, an internuncial neuron, situated in the anterior gray column of the spinal cord (Fig. 4-19). The axon of the second-order neuron is short and synapses with the third-order neuron, the lower motor neuron, in the anterior gray column (Fig. 4-19). The axon of the third-order neuron innervates the skeletal muscle through the anterior root and spinal nerve. In some instances, the axon of the first-order neuron terminates directly on the third-order neuron (as in reflex arcs).

Figure 4-19 Simple form of the descending motor pathway from the cerebral cortex to the skeletal muscle. Note the three neurons involved.

Functions of the Descending Tracts The corticospinal tracts (Fig. 4-20) are the pathways concerned with voluntary, discrete, skilled movements, especially those of the distal parts of the limbs. The reticulospinal tracts may facilitate or inhibit the activity of the alpha and gamma motor neurons in the anterior gray columns and may, therefore, facilitate or inhibit voluntary movement or reflex activity. The tectospinal tract (Fig. 4-20) is concerned with P.155 reflex postural movements in response to visual stimuli. Those fibers that are associated with the sympathetic neurons in the lateral gray column are concerned with the pupillodilation reflex in response to darkness. The rubrospinal tract (Fig. 4-20) acts on both the alpha and gamma motor neurons in the anterior gray columns and facilitates the activity of flexor muscles and inhibits the activity of extensor or antigravity muscles. The vestibulospinal tract (Fig. 4-20), by acting on the motor neurons in the anterior gray columns, facilitates the activity of the extensor muscles, inhibits the activity of the flexor muscles, and is concerned with the postural activity associated with balance. The olivospinal tract (Fig. 4-20) may play a role in muscular activity, but there is doubt that it exists. The descending autonomic fibers are concerned with the control of visceral activity.

Figure 4-20 Transverse section of the spinal cord showing the termination of the descending motor tracts. Note that there is now considerable doubt as to the existence of the olivospinal tract as a separate pathway.

Corticospinal Tracts Fibers of the corticospinal tract arise as axons of pyramidal cells situated in the fifth layer of the cerebral cortex (Fig. 4-21). About one-third of the fibers originate from the primary motor cortex (area 4), one-third originate from the secondary motor cortex (area 6), and one-third originate from the parietal lobe (areas 3, 1, and 2); thus, two-thirds of the fibers arise from the precentral gyrus, and one-third of the fibers arise from the postcentral gyrus.5 Because electrical stimulation of different parts of the precentral gyrus produces movements of different parts of the opposite side of the body, we can represent the parts of the body in this area of the cortex. Such a homunculus is shown in Figure 4-21. Note that the region controlling the face is situated inferiorly, and the region controlling the lower limb is situated superiorly and on the medial surface of the hemisphere. The homunculus is a distorted picture of the body, with the various parts having a size proportional to the area of the cerebral cortex devoted to their control. It is interesting to find that the majority of the corticospinal fibers are myelinated and are relatively slow-conducting, small fibers. The descending fibers converge in the corona radiata and then pass through the posterior limb of the internal capsule (Fig. 4-21). Here, the fibers are organized so that those closest to the genu are concerned with cervical portions of the body, while those situated more posteriorly are concerned with the lower extremity. The tract then continues through the middle three-fifths of the basis pedunculi of the midbrain (Fig. 4-21). Here, the fibers concerned with cervical portions of the body are situated medially, while those concerned with the leg are placed laterally. On entering the pons, the tract is broken into many bundles by the transverse pontocerebellar fibers (see Figs. 5-0, 5-0, and 5-0). In the medulla oblongata, the bundles become grouped together along the anterior border to form a swelling known as the pyramid (hence the alternative name, pyramidal tract) (see Fig. 5-0). At the junction of the medulla oblongata and the spinal cord, most of the fibers cross the midline at the decussation of the pyramids (Fig. 4-21) and enter the lateral white column P.156 of the spinal cord to form the lateral corticospinal tract (Fig. 4-20). The remaining fibers do not cross in the decussation but descend in the anterior white column of the spinal cord as the anterior corticospinal tract (Figs. 4-20 and 4-21). These fibers eventually cross the midline and terminate in the anterior gray column of the spinal cord segments in the cervical and upper thoracic regions.

Figure 4-21 Corticospinal tracts.

The lateral corticospinal tract descends the length of the spinal cord; its fibers terminate in the anterior gray column of all the spinal cord segments. Most corticospinal fibers synapse with internuncial neurons, which, in turn, synapse with alpha motor neurons and some gamma motor neurons. Only the largest corticospinal fibers synapse directly with the motor neurons. P.157 The corticospinal tracts are not the sole pathway for serving voluntary movement. Rather, they form the pathway that confers speed and agility to voluntary movements and is thus used in performing rapid skilled movements. Many of the simple, basic voluntary movements are mediated by other descending tracts. Branches

  • Branches are given off early in their descent and return to the cerebral cortex to inhibit activity in adjacent regions of the cortex.
  • Branches pass to the caudate and lentiform nuclei, the red nuclei, and the olivary nuclei and the reticular formation. These branches keep the subcortical regions informed about the cortical motor activity. Once alerted, the subcortical regions may react and send their own nervous impulses to the alpha and gamma motor neurons by other descending pathways.
Figure 4-22 Reticulospinal tracts.

Reticulospinal Tracts Throughout the midbrain, pons, and medulla oblongata, groups of scattered nerve cells and nerve fibers exist that are collectively known as the reticular formation. From the pons, these neurons send axons, which are mostly uncrossed, down into the spinal cord and form the pontine reticulospinal tract (Fig. 4-22). From the medulla, P.158 similar neurons send axons, which are crossed and uncrossed, to the spinal cord and form the medullary reticulospinal tract. The reticulospinal fibers from the pons descend through the anterior white column, while those from the medulla oblongata descend in the lateral white column (Fig. 4-22). Both sets of fibers enter the anterior gray columns of the spinal cord and may facilitate or inhibit the activity of the alpha and gamma motor neurons. By these means, the reticulospinal tracts influence voluntary movements and reflex activity. The reticulospinal fibers are also now thought to include the descending autonomic fibers. The reticulospinal tracts thus provide a pathway by which the hypothalamus can control the sympathetic outflow and the sacral parasympathetic outflow.

Figure 4-23 Tectospinal tract.

Tectospinal Tract Fibers of this tract arise from nerve cells in the superior colliculus of the midbrain (Fig. 4-23). Most of the fibers cross the midline soon after their origin and descend through the brainstem close to the medial longitudinal fasciculus. The tectospinal tract descends through the anterior white column of the spinal cord close to the anterior median fissure (Figs. 4-20 and 4-23). The majority of the fibers terminate in the anterior gray column in the upper cervical segments of the spinal cord by synapsing with internuncial neurons. These fibers are believed to be concerned with reflex postural movements in response to visual stimuli. P.159 Rubrospinal Tract The red nucleus is situated in the tegmentum of the midbrain at the level of the superior colliculus (Fig. 4-24). The axons of neurons in this nucleus cross the midline at the level of the nucleus and descend as the rubrospinal tract through the pons and medulla oblongata to enter the lateral white column of the spinal cord (Figs. 4-20 and 4-24). The fibers terminate by synapsing with internuncial neurons in the anterior gray column of the cord. The neurons of the red nucleus receive afferent impulses through connections with the cerebral cortex and the cerebellum. This is believed to be an important indirect pathway by which the cerebral cortex and the cerebellum can influence the activity of the alpha and gamma motor neurons of the spinal cord. The tract facilitates the activity of the flexor muscles and inhibits the activity of the extensor or antigravity muscles.

Figure 4-24 Rubrospinal tract.

Vestibulospinal Tract The vestibular nuclei are situated in the pons and medulla oblongata beneath the floor of the fourth ventricle (Fig. 4-25). The vestibular nuclei receive afferent fibers from the inner ear through the vestibular nerve and from the cerebellum. The neurons of the lateral vestibular nucleus give rise to the axons that form the vestibulospinal tract. The tract descends uncrossed through the medulla and through the length of the spinal cord in the anterior white column P.160 (Figs. 4-20 and 4-25). The fibers terminate by synapsing with internuncial neurons of the anterior gray column of the spinal cord.

Figure 4-25 Vestibulospinal tract.

The inner ear and the cerebellum, by means of this tract, facilitate the activity of the extensor muscles and inhibit the activity of the flexor muscles in association with the maintenance of balance. Olivospinal Tract The olivospinal tract was thought to arise from the inferior olivary nucleus and to descend in the lateral white column of the spinal cord (Fig. 4-26), to influence the activity of the motor neurons in the anterior gray column. There is now considerable doubt that it exists. Descending Autonomic Fibers The higher centers of the central nervous system associated with the control of autonomic activity are situated in the cerebral cortex, hypothalamus, amygdaloid complex, and reticular formation. Although distinct tracts P.161have not been recognized, investigation of spinal cord lesions has demonstrated that descending autonomic tracts do exist and probably form part of the reticulospinal tract.

Figure 4-26 Olivospinal tract. There is now considerable doubt as to the existence of this tract as a separate pathway.

The fibers arise from neurons in the higher centers and cross the midline in the brainstem. They are believed to descend in the lateral white column of the spinal cord and to terminate by synapsing on the autonomic motor cells in the lateral gray columns in the thoracic and upper lumbar (sympathetic outflow) and midsacral (parasympathetic) levels of the spinal cord. A summary of the main descending pathways in the spinal cord is shown in Table 4-4. Intersegmental Tracts Short ascending and descending tracts that originate and end within the spinal cord exist in the anterior, lateral, and posterior white columns. The function of these pathways is to interconnect the neurons of different segmental levels, and the pathways are particularly important in intersegmental spinal reflexes. P.162

Table 4-4 The Main Descending Pathways to the Spinal Corda
Pathway Function Origin Site of Crossover Destination Branches to
Corticospinal tracts Rapid, skilled, voluntary movements, especially distal ends of limbs Primary motor cortex (area 4), secondary motor cortex (area 6), parietal lobe (areas 3, 1, and 2) Most cross at decussation of pyramids and descend as lateral corticospinal tracts; some continue as anterior corticospinal tracts and cross over at level of destination Internuncial neurons or alpha motor neurons Cerebral cortex, basal nuclei, red nucleus, olivary nuclei, reticular formation
Reticulospinal tracts Inhibit or facilitate voluntary movement; hypothalamus controls sympathetic, para-sympathetic outflows Reticular formation Some cross at various levels Alpha and gamma motor neurons Multiple branches as they descend
Tectospinal tract Reflex postural movements concerning sight Superior colliculus Soon after origin Alpha and gamma motor neurons ?
Rubrospinal tract Facilitates activity of flexor muscles and inhibits activity of extensor muscles Red nucleus Immediately Alpha and gamma motor neurons ?
Vestibulospinal tract Facilitates activity of extensor inhibits flexor muscles Vestibular nuclei Uncrossed Alpha and gamma motor neurons ?
Olivospinal tract ?? Inferior olivary nuclei Cross in brainstem ? Alpha and gamma motor neurons
Descending autonomic fibers Control sympathetic and para-sympathetic systems Cerebral cortex, hypothalamus, amygdaloid complex, reticular formation   Sympathetic and parasympathetic outflows
aNote that the corticospinal tracts are believed to control the prime mover muscles (especially the highly skilled movements), whereas the other descending tracts are important in controlling the simple basic movements. For simplicity, the internuncial neurons are omitted from this table.

Reflex Arc A reflex may be defined as an involuntary response to a stimulus. It depends on the integrity of the reflex arc (Fig. 4-27). In its simplest form, a reflex arc consists of the following anatomical structures: (1) a receptor organ, (2) an afferent neuron, (3) an effector neuron, and (4) an effector organ. A reflex arc involving only one synapse is referred to as a monosynaptic reflex arc. Interruption of the reflex arc at any point along its course would abolish the response. In the spinal cord, reflex arcs play an important role in maintaining muscle tone, which is the basis for body posture. The receptor organ is situated in the skin, muscle, or tendon. The cell body of the afferent neuron is located in the posterior root ganglion, and the central axon of this first-order neuron terminates by synapsing on the effector neuron. Since the afferent fibers are of large diameter and are rapidly conducting and because of the presence of only one synapse, a very quick response is possible. P.163

Figure 4-27 A: A monosynaptic reflex arc. B: Multiple neurons synapsing with the lower motor neuron. Note the presence of the Renshaw feedback neuron.

Physiologic study of the electrical activity of the effector neuron shows that following the very quick monosynaptic discharge, there is a prolonged asynchronous discharge. The reason for this later discharge is that the afferent fibers entering the spinal cord frequently branch, and the branches synapse with many internuncial neurons, which ultimately synapse with the effector neuron (Fig. 4-28). These additional neuronal circuits prolong the bombardment of the effector neurons after the initial stimulation by the afferent neuron has ceased. The presence of internuncial neurons also results in the spread of the afferent stimulus to neurons at different segmental levels of the spinal cord. In considering reflex skeletal muscle activity, it is important to understand the law of reciprocal innervation (Fig. 4-28). Simply stated, it means that the flexor and extensor reflexes of the same limb cannot be made to contract simultaneously. For this law to work, the afferent nerve fibers responsible for flexor reflex muscle action must have branches that synapse with the extensor motor neurons of the same limb, causing them to be inhibited. Another interesting property of spinal reflexes should be pointed out. The evocation of a reflex on one side of the body causes opposite effects on the limb of the other side of the body. This crossed extensor reflex (Fig. 4-28) may be demonstrated as follows. Afferent stimulation of the reflex arc that causes the ipsilateral limb to flex results in the contralateral limb being extended. P.164

Figure 4-28 A: Multiple branching of afferent fibers entering the spinal cord and the presence of many internuncial neurons that synapse with the effector neuron. B: Law of reciprocal innervation and the crossed extensor reflex.

Influence of Higher Neuronal Centers on the Activities of Spinal Reflexes The spinal segmental reflex arc involving motor activity is greatly influenced by higher centers in the brain. These influences are mediated through the corticospinal, reticulospinal, tectospinal, rubrospinal, and vestibulospinal tracts. In the clinical condition known as spinal shock (see p. 169), which follows the sudden removal of these influences by severance of the spinal cord, the segmental spinal reflexes are depressed. When the so-called spinal shock disappears in a few weeks, the segmental spinal reflexes return, and the muscle tone is increased. This so-called decerebrate rigidity is due to the overactivity of the gamma efferent nerve fibers to the muscle spindles, which results from the release of these neurons from the higher centers (see pp. 103 and 104). The next stage may be paraplegia in extension with domination of the increased tone of the extensor muscles over the flexor muscles. Some neurologists believe that this condition is due to incomplete severance of all the descending tracts with persistence of the vestibulospinal tract. Should all the descending tracts be severed, the condition of paraplegia in flexion occurs. In this condition, the reflex responses are flexor in nature, and the tone of the extensor muscles is diminished. Renshaw Cells and Lower Motor Neuron Inhibition Lower motor neuron axons give off collateral branches as they pass through the white matter to reach the anterior roots of the spinal nerve. These collaterals synapse on neurons described by Renshaw, which, in turn, synapse on the lower motor neurons (Fig. 4-27). These internuncial neurons are believed to provide feedback on the lower motor neurons, inhibiting their activity. P.165 P.166 P.167 P.168 P.169 P.170 P.171 P.172 P.173 P.174 P.175 P.176 Clinical Notes General Anatomical Features of Clinical Importance The spinal cord may be described, for practical purposes, as consisting of columns of motor and sensory nerve cells, the gray matter, surrounded by ascending and descending tracts, the white matter. It lies within the vertebral canal and is protected by three surrounding fibrous membranes, the meninges. It is cushioned against trauma by the cerebrospinal fluid and is held in position by the denticulate ligaments on each side and the filum terminale inferiorly. The spinal cord is segmented, and paired posterior (sensory) and anterior (motor) roots corresponding to each segment of the cord leave the vertebral canal through the intervertebral foramina. The spinal cord is shorter than the vertebral column and terminates inferiorly in the adult at the level of the lower border of the first lumbar vertebra. The subarachnoid space extends inferiorly beyond the end of the cord and ends at the level of the lower border of the second sacral vertebra. Because of the shortness of the spinal cord relative to the length of the vertebral column, the nerve roots of the lumbar and sacral segments have to take an oblique course downward to reach their respective intervertebral foramina; the resulting leash of nerve roots forms the cauda equina. A spinal tap needle may be inserted into the subarachnoid space below the level of the second lumbar vertebra without damaging the spinal cord. (For details, see p. 19.) Lesions of the Anterior and Posterior Nerve Roots Each nerve root has a covering of pia, arachnoid, and dura mater. The anterior and posterior roots unite in the intervertebral foramina to form the spinal nerves. Here, the meninges fuse with the epineurium of the spinal nerves. Either or both spinal nerve roots may be involved in syphilitic spinal meningitis or pyogenic meningitis. The posterior roots may be involved in tabes dorsalis and herpes zoster. Their anatomical location, both in the vertebral canal and in the intervertebral foramina, exposes them to compression from tumors of the vertebral column and to irritation from abnormal constituents of the cerebrospinal fluid, such as blood following a subarachnoid hemorrhage. A herniated intervertebral disc, a primary or secondary vertebral tumor, vertebral destruction by tumor or infection, or a fracture dislocation can press on the spinal nerve roots in the intervertebral foramina. Even severe scoliosis may result in compression of the nerve roots. A lesion of one posterior spinal nerve root will produce pain in the area of skin innervated by that root and in the muscles that receive their sensory nerve supply from that root. Movements of the vertebral column in the region of the lesion will heighten the pain, and coughing and sneezing will also make it worse by raising the pressure within the vertebral canal. Before there is actual loss of sensation in the dermatome, there may be evidence of hyperalgesia and hyperesthesia. A lesion of an anterior root will result in paralysis of any muscle that is supplied exclusively by that root and a partial paralysis of any muscle that is supplied partially by that root. In both cases, fasciculation and muscle atrophy occur. Clinical Significance of Lamination of the Ascending Tracts Within the anterolateral white column of the spinal cord, the axons of the spinothalamic tracts from the sacral and lumbar segments of the body are deflected laterally by axons crossing the midline at successively higher levels. Within the posterior white column, the axons from the sacral and lumbar segments of the body are pushed medially by the axons from higher segments of the body. This deflection of the tracts produces lamination; thus, in the spinothalamic tracts (anterolateral system), the cervical to sacral segments are located from medial to lateral, whereas in the posterior white column (medial lemniscus system) the sacral to cervical segments are located from medial to lateral. This is shown diagrammatically in Figure 4-29. This detailed information is of practical value in patients in whom there is external pressure exerted on the spinal cord in the region of the spinothalamic tracts. It explains, for example, why patients will experience a loss of pain and temperature sensations first in the sacral dermatomes of the body and, if the pressure increases, in the other higher segmental dermatomes of the body. Injury to the Ascending Tracts Within the Spinal Cord Lateral Spinothalamic Tract Destruction of this tract produces contralateral loss of pain and thermal sensibilities below the level of the lesion. The patient will not, therefore, respond to pinprick or recognize hot and cold objects placed in contact with the skin. Anterior Spinothalamic Tract Destruction of this tract produces contralateral loss of light touch and pressure sensibilities below the level of the lesion. Remember that discriminative touch will still be present, because this information is conducted through the fasciculus gracilis and fasciculus cuneatus. The patient will not feel the light touch of a piece of cotton placed against the skin or feel pressure from a blunt object placed against the skin. Fasciculus Gracilis and Fasciculus Cuneatus Destruction of these tracts cuts off the supply of information from the muscles and joints to consciousness; thus, the individual does not know about the position and movements of the ipsilateral limbs below the level of the lesion. With the patient’s eyes closed, he or she is unable to tell where the limb or part of the limb is in space. For example, if you passively dorsiflex the patient’s big toe, he or she is unable to tell you whether the toe is pointing upward or downward. The patient has impaired muscular control, and the movements are jerky or ataxic. The patient also has loss of vibration sense below the level of the lesion on the same side. This is easily tested by applying a vibrating tuning fork to a bony prominence, such as the lateral malleolus of the fibula or the styloid process of the radius. There will also be a loss of tactile discrimination on the side of the lesion. This is tested most easily by gradually separating the two points of a compass until the patient can appreciate them as two separate points, not as one, when they are applied to the skin surface. Tactile discrimination varies from one part of the body to another. In a normal individual, the points have to be separated by about 3 to 4 mm before they are recognized as separate points on the tips of the fingers. On the back, however, the points have to be separated by 65 mm or more before they can be recognized as separate points.

Figure 4-29 Segmental organization of the tracts in the posterior, lateral, and anterior white columns of the spinal cord.

The sense of general light touch would be unaffected, as these impulses ascend in the anterior spinothalamic tracts. It should be pointed out that it is extremely rare for a lesion of the spinal cord to be so localized as to affect one sensory tract only. It is more usual to have several ascending and descending tracts involved. Somatic and Visceral Pain Somatic pain has been considered extensively in this chapter. The sense organs for somatic pain are the naked nerve endings. The initial sharp pain is transmitted by fast-conducting fibers, and the more prolonged burning pain travels in the slow-conducting nerve fibers (see p. 147). In the viscera, there are special receptors, chemoreceptors, baroreceptors, osmoreceptors, and stretch receptors that are sensitive to a variety of stimuli, including ischemia, stretching, and chemical damage. Afferent fibers from the visceral receptors reach the central nervous system via the sympathetic and parasympathetic parts of the autonomic nervous system. Once within the central nervous system, the pain impulses travel by the same ascending tracts as the somatic pain and ultimately reach the postcentral gyrus. Visceral pain is poorly localized and often associated with salivation, nausea, vomiting, tachycardia, and sweating. Visceral pain may be referred from the organ involved to a distant area of the body (referred pain). Treatment of Acute Pain Drugs such as salicylates can be used to reduce the synthesis of prostaglandin, a substance that sensitizes free nerve endings to painful stimuli. Local anesthetics, such as procaine, can be used to block nerve conduction in peripheral nerves. Narcotic analgesics, such as morphine and codeine, reduce the affective reaction to pain and act on the opiate receptor sites in the cells in the posterior gray column of the spinal cord, as well as other cells in the analgesic system in the brain. It is believed that opiates act by inhibiting the release of glutamate, substance P, and other transmitters from the sensory nerve endings. To minimize the side effects of morphine given by systemic injection, the narcotic can be given by local injection directly into the posterior gray horn of the spinal cord or by injection indirectly into the cerebrospinal fluid in the subarachnoid space. Long-term cancer pain has been treated successfully by the continuous infusion of morphine into the spinal cord. Treatment of Chronic Pain New techniques, such as acupuncture and electrical stimulation of the skin, are now being used with success. Relief of pain can be achieved by the use of placebos in a few patients. The anticipation of the relief of pain is thought to stimulate the release of endorphins, which inhibit the normal pain pathway. Relief of Pain by Rhizotomy or Cordotomy Surgical relief of pain has been used extensively in patients with terminal cancer. Posterior rhizotomy or division of the posterior root of a spinal nerve effectively severs the conduction of pain into the central nervous system. It is a relatively simple procedure, but, unfortunately, the operation deprives the patient of other sensations besides pain. Moreover, if the pain sensation is entering the spinal cord through more than one spinal nerve, it may be necessary to divide several posterior roots. Thoracic cordotomy has been performed with success in patients with severe pain originating from the lower abdomen or pelvis. Essentially, the operation consists of dividing the lateral spinothalamic tracts by inserting a knife into the anterolateral quadrant of the spinal cord. It is important to remember that the lateral spinothalamic fibers have originated in cells of the substantia gelatinosa in the opposite posterior gray column and that they cross the spinal cord obliquely and reach their tract in the white column three or four segments higher than their posterior root of entry. Cervical cordotomy has been performed successfully in patients with intractable pain in the neck or thorax. Tabes Dorsalis Tabes dorsalis is caused by syphilis. The organism causes a selective destruction of nerve fibers at the point of entrance of the posterior root into the spinal cord, especially in the lower thoracic and lumbosacral regions (Fig. 4-30). The following symptoms and signs may be present: (1) stabbing pains in the lower limbs, which may be very severe; (2) paresthesia, with numbness in the lower limbs; (3) hypersensitivity of skin to touch, heat, and cold; (4) loss of sensation in the skin of parts of the trunk and lower limbs and loss of awareness that the urinary bladder is full; (5) loss of appreciation of posture or passive movements of the limbs, especially the legs; (6) loss of deep pain sensation, such as when the muscles are forcibly compressed or when the tendo Achillis is compressed between the finger and thumb; (7) loss of pain sensation in the skin in certain areas of the body, such as the side of the nose or the medial border of the forearm, the thoracic wall between the nipples, or the lateral border of the leg; (8) ataxia of the lower limbs as the result of loss of proprioceptive sensibility (the unsteadiness in gait is compensated to some extent by vision; however, in the dark or if the eyes are closed, the ataxia becomes worse and the person may fall); (9) hypotonia as the result of loss of proprioceptive information that arises from the muscles and joints; and (10) loss of tendon reflexes, owing to degeneration of the afferent fiber component of the reflex arc (the knee and ankle tendon jerks are lost early in the disease). Muscle Activity Muscle Tone Muscle tone is a state of continuous partial contraction of a muscle and is dependent on the integrity of a monosynaptic reflex arc (see description on pp. 101 and 103). The receptor organs are the muscle spindles. The afferent neuron enters the spinal cord through the posterior root and synapses with the effector neuron or lower motor neuron in the anterior gray column. The lower motor neuron supplies the muscle fibers by traveling through the anterior roots, the spinal nerves, and peripheral nerves. Muscle tone is abolished if any part of that simple reflex arc is destroyed. An atonic muscle feels soft and flabby and atrophies rapidly.

Figure 4-30 Site of a syphilitic lesion on the spinal cord.

Normal muscle tone exhibits a certain resilience or elasticity, and when a muscle is passively stretched by moving a joint, a certain degree of resistance is felt. Normal muscle tone depends on the integrity of the monosynaptic reflex arc described above and the control superimposed on it by impulses received through the descending tracts from supraspinal levels. Note that muscle spindles are excitatory to muscle tone, whereas neurotendinous receptors are inhibitory to muscle tone. Voluntary Movement Voluntary movement is initiated by the individual. A series of different muscles are made to contract for the purpose of reaching a goal. This would suggest that the descending tracts that influence the activity of the lower motor neurons are driven by information received by the sensory systems, the eyes, the ears, and the muscles themselves and are affected further by past afferent information that has been stored in the memory. Moreover, the whole process may be colored by past and present emotional input. The limbic structures appear to play a role in emotion, motivation, and memory and may influence the initiation process of voluntary movement by their projections to the cerebral cortex. The descending pathways from the cerebral cortex and the brainstem, that is, the upper motor neurons, influence the activity of the lower motor neurons either directly or through internuncial neurons. Most of the tracts originating in the brainstem that descend to the spinal cord also are receiving input from the cerebral cortex. The corticospinal tracts are believed to control the prime mover muscles, especially those responsible for the highly skilled movements of the distal parts of the limbs. The other supraspinal descending tracts play a major role in the simple basic voluntary movements and, in addition, bring about an adjustment of the muscle tone so that easy and rapid movements of the joints can take place. It is interesting to note that the basal ganglia and the cerebellum do not give rise directly to descending tracts that influence the activities of the lower motor neuron, and yet, these parts of the nervous system greatly influence voluntary movements. This influence is accomplished indirectly by fibers that project to the cerebral cortex and brainstem nuclei, which are the sites of origin of the descending tracts. Pyramidal and Extrapyramidal Tracts The term pyramidal tract is used commonly by clinicians and refers specifically to the corticospinal tracts. The term came into common usage when it was learned that the corticospinal fibers become concentrated on the anterior part of the medulla oblongata in an area referred to as the pyramids. The term extrapyramidal tracts refers to all the descending tracts other than the corticospinal tracts. Upper Motor Neuron Lesions Lesions of the Corticospinal Tracts (Pyramidal Tracts) Lesions restricted to the corticospinal tracts produce the following clinical signs:

  • The Babinski sign is present. The great toe becomes dorsally flexed, and the other toes fan outward in response to scratching the skin along the lateral aspect of the sole of the foot. The normal response is plantar flexion of all the toes. Remember that the Babinski sign is normally present during the first year of life because the corticospinal tract is not myelinated until the end of the first year of life. The explanation for the Babinski sign is thought to be the following. Normally, the corticospinal tracts produce plantar flexion of the toes in response to sensory stimulation of the skin of the sole. When the corticospinal tracts are nonfunctional, the influence of the other descending tracts on the toes becomes apparent, and a kind of withdrawal reflex takes place in response to stimulation of the sole, with the great toe being dorsally flexed and the other toes fanning out.
  • The superficial abdominal reflexes are absent. The abdominal muscles fail to contract when the skin of the abdomen is scratched. This reflex is dependent on the integrity of the corticospinal tracts, which exert a tonic excitatory influence on the internuncial neurons.
  • The cremasteric reflex is absent. The cremaster muscle fails to contract when the skin on the medial side of the thigh is stroked. This reflex arc passes through the first lumbar segment of the spinal cord. This reflex is dependent on the integrity of the corticospinal tracts, which exert a tonic excitatory influence on the internuncial neurons.
  • There is loss of performance of fine-skilled voluntary movements. This occurs especially at the distal end of the limbs.

Lesions of the Descending Tracts Other Than the Corticospinal Tracts (Extrapyramidal Tracts) The following clinical signs are present in lesions restricted to the other descending tracts:

  • Severe paralysis with little or no muscle atrophy (except secondary to disuse).
  • Spasticity or hypertonicity of the muscles. The lower limb is maintained in extension, and the upper limb is maintained in flexion.
  • Exaggerated deep muscle reflexes and clonus may be present in the flexors of the fingers, the quadriceps femoris, and the calf muscles.
  • Clasp-knife reaction. When passive movement of a joint is attempted, there is resistance owing to spasticity of the muscles. The muscles, on stretching, suddenly give way due to neurotendinous organ-mediated inhibition.

It should be pointed out that in clinical practice, it is rare to have an organic lesion that is restricted only to the pyramidal tracts or only to the extrapyramidal tracts. Usually, both sets of tracts are affected to a variable extent, producing both groups of clinical signs. As the pyramidal tracts normally tend to increase muscle tone and the extrapyramidal tracts inhibit muscle tone, the balance between these opposing effects will be altered, producing different degrees of muscle tone. Lower Motor Neuron Lesions Trauma, infection (poliomyelitis), vascular disorders, degenerative diseases, and neoplasms may all produce a lesion of the lower motor neuron by destroying the cell body in the anterior gray column or its axon in the anterior root or spinal nerve. The following clinical signs are present with lower motor neuron lesions:

  • Flaccid paralysis of muscles supplied.
  • Atrophy of muscles supplied.
  • Loss of reflexes of muscles supplied.
  • Muscular fasciculation. This is twitching of muscles seen only when there is slow destruction of the lower motor neuron cell.
  • Muscular contracture. This is a shortening of the paralyzed muscles. It occurs more often in the antagonist muscles whose action is no longer opposed by the paralyzed muscles.
  • Reaction of degeneration. Normally innervated muscles respond to stimulation by the application of faradic (interrupted) current, and the contraction continues as long as the current is passing. Galvanic or direct current causes contraction only when the current is turned on or turned off. When the lower motor neuron is cut, a muscle will no longer respond to interrupted electrical stimulation 7 days after nerve section, although it still will respond to direct current. After 10 days, the response to direct current also ceases. This change in muscle response to electrical stimulation is known as the reaction of degeneration.

Types of Paralysis

  • Hemiplegia is a paralysis of one side of the body and includes the upper limb, one side of the trunk, and the lower limb.
  • Monoplegia is a paralysis of one limb only.
  • Diplegia is a paralysis of two corresponding limbs (i.e., arms or legs).
  • Paraplegia is a paralysis of the two lower limbs.
  • Quadriplegia is a paralysis of all four limbs.

Relationship of Muscular Signs and Symptoms to Lesions of the Nervous System Abnormal Muscle Tone Hypotonia Hypotonia exists when the muscle tone is diminished or absent. It occurs when any part of the monosynaptic stretch reflex arc is interrupted. It also occurs in cerebellar disease as the result of diminished influence on the gamma motor neurons from the cerebellum. Hypertonia Hypertonia (spasticity, rigidity) exists when the muscle tone is increased. It occurs when lesions exist that involve supraspinal centers or their descending tracts but not the corticospinal tract. It also may occur at the local spinal segmental level and be produced by local excitation of the stretch reflex by sensory irritation (e.g., spasm of back muscles secondary to prolapsed intervertebral disc, spasm of abdominal muscles secondary to peritonitis). Tremors Tremors are rhythmic involuntary movements that result from the contraction of opposing muscle groups. These may be slow, as in parkinsonism, or fast, as in toxic tremors from thyrotoxicosis. They may occur at rest, as in parkinsonism, or with action, the so-called intention tremor, as seen in cerebellar disease. Spasms Spasms are sudden, involuntary contractions of large groups of muscles. Examples of spasms are seen in paraplegia and are due to lesions involving the descending tracts but not the corticospinal tract. Athetosis Athetosis means continuous, slow, involuntary, dysrhythmic movements that are always the same in the same patient and disappear during sleep. They impede voluntary movement. Athetosis occurs with lesions of the corpus striatum. Chorea Chorea consists of a series of continuous, rapid, involuntary, jerky, coarse, purposeless movements, which may occur during sleep. Chorea occurs with lesions of the corpus striatum. Dystonia Dystonia consists of frequent, maintained contractions of hypertonic muscles, leading to bizarre postures. It occurs with lesions of the lentiform nucleus. Myoclonus Myoclonus is a sudden contraction of an isolated muscle or part of a muscle. It occurs irregularly and commonly involves a muscle of a limb. It may be present with diseases that involve the reticular formation and the cerebellum. Normal myoclonic jerks sometimes occur in individuals as they are falling asleep and are believed to be due to a sudden temporary reactivation of the reticular formation. Hemiballismus Hemiballismus is a rare form of involuntary movement confined to one side of the body. It usually involves the proximal extremity musculature, and the limb involved is made to fly about in all directions. The lesion responsible occurs in the opposite subthalamic nucleus. Spinal Cord Injuries Acute Spinal Cord Injuries The incidence of acute spinal cord injuries in the United States is about 10,000 per year. The injury is catastrophic, since little or no regeneration of the severed nerve tracts takes place (see p. 110) and the individual is permanently disabled. Treatment has been restricted to anatomical realignment and stabilization of the vertebral column or decompression of the spinal cord. During the recovery process, the patient goes through intensive rehabilitation to optimize the remaining neurologic function. Apart from improved management of medical complications, very little new therapy has been successful despite an enormous amount of research into the problem of neuronal regeneration in the spinal cord. Recently, the use of certain drugs (GM1 ganglioside and methylprednisolone) administered to the patient soon after injury has resulted in some improvement in the neurologic deficit. Animal experiments appear to indicate that these drugs enhance the functional recovery of damaged neurons. Chronic Compression of the Spinal Cord If injuries to the spinal cord are excluded (see p. 17), the causes of compression may be divided into extradural and intradural. The intradural causes may be divided into those that arise outside the spinal cord (extramedullary) and those that arise within the cord (intramedullary). The extradural causes include herniation of an intervertebral disc, infection of the vertebrae with tuberculosis, and primary and secondary tumors of the vertebra; leukemic deposits and extradural abscesses may also compress the spinal cord. The two common extramedullary tumors are meningiomas and nerve fibromas. Intramedullary causes include primary tumors of the spinal cord, such as gliomas. The clinical signs and symptoms are produced by an interference with the normal anatomical and physiologic functions of the spinal cord. Pressure on the spinal arteries causes ischemia of the spinal cord with degeneration of nerve cells and their fibers. Pressure on the spinal veins causes edema of the spinal cord with interference in the function of the neurons. Finally, direct pressure on the white and gray matter of the spinal cord and the spinal nerve roots interferes with nerve conduction. At the same time, the circulation of the cerebrospinal fluid is obstructed, and the composition of the fluid changes below the level of obstruction. Clinical Signs One of the earliest signs is pain. This may be local pain in the vertebra involved or pain radiating along the distribution of one or more spinal nerve roots. The pain is made worse by coughing or sneezing and is usually worse at night, when the patient is recumbent. Interference with motor function occurs early. Involvement of the anterior gray column motor cells at the level of the lesion results in partial or complete paralysis of muscles, with loss of tone and muscle wasting. The early involvement of the corticospinal and other descending tracts produces muscular weakness, increased muscle tone (spasticity), increased tendon reflexes below the level of the lesion, and an extensor plantar response. The degree of sensory loss will depend on the nerve tracts involved. A lesion of the posterior white columns of the spinal cord will cause loss of muscle joint sense (proprioception), vibration sense, and tactile discrimination below the level of the lesion on the same side. Involvement of the lateral spinal thalamic tracts will cause loss of pain and heat and cold sensations on the opposite side of the body below the level of the lesion. A more detailed discussion of the symptoms and signs following injury to the ascending and descending tracts in the spinal cord is given on pages 165 and 167. Since many spinal tumors are benign and can be successfully removed (provided that irreversible damage to the spinal cord has not occurred as a result of compression of the blood supply), an early accurate diagnosis is essential. The following investigations should be performed: (1) radiography of the vertebral column, including computed tomography (CT) and magnetic resonance imaging (MRI); (2) spinal tap; and (3) myelography for those cases where determining the diagnosis is difficult. Clinical Syndromes Affecting the Spinal Cord Spinal Shock Syndrome Spinal shock syndrome is a clinical condition that follows acute severe damage to the spinal cord. All cord functions below the level of the lesion become depressed or lost, and sensory impairment and a flaccid paralysis occur. The segmental spinal reflexes are depressed due to the removal of influences from the higher centers that are mediated through the corticospinal, reticulospinal, tectospinal, rubrospinal, and vestibulospinal tracts. Spinal shock, especially when the lesion is at a high level of the cord, may also cause severe hypotension from loss of sympathetic vasomotor tone. In most patients, the shock persists for less than 24 hours, whereas in others, it may persist for as long as 1 to 4 weeks. As the shock diminishes, the neurons regain their excitability, and the effects of the upper motor neuron loss on the segments of the cord below the lesion, for example, spasticity and exaggerated reflexes, will make their appearance. The presence of spinal shock can be determined by testing for the activity of the anal sphincter reflex. The reflex can be initiated by placing a gloved finger in the anal canal and stimulating the anal sphincter to contract by squeezing the glans penis or clitoris or gently tugging on an inserted Foley catheter. An absent anal reflex would indicate the existence of spinal shock. A cord lesion involving the sacral segments of the cord would nullify this test, since the neurons giving rise to the inferior hemorrhoidal nerve to the anal sphincter (S2-4) would be nonfunctioning. Destructive Spinal Cord Syndromes When neurologic impairment is identified following the disappearance of spinal shock, it can often be categorized into one of the following syndromes: (1) complete cord transection syndrome, (2) anterior cord syndrome, (3) central cord syndrome, or (4) Brown-Séquard syndrome or hemisection of the cord. The clinical findings often indicate a combination of lower motor neuron injury (at the level of destruction of the cord) and upper motor neuron injury (for those segments below the level of destruction). Complete Cord Transection Syndrome Complete cord transection syndrome (Fig. 4-31) results in complete loss of all sensibility and voluntary movement below the level of the lesion. It can be caused by fracture dislocation of the vertebral column, by a bullet or stab wound, or by an expanding tumor. The following characteristic clinical features will be seen after the period of spinal shock has ended:

  • Bilateral lower motor neuron paralysis and muscular atrophy in the segment of the lesion. This results from damage to the neurons in the anterior gray columns (i.e., lower motor neuron) and possibly from damage to the nerve roots of the same segment.
  • Bilateral spastic paralysis below the level of the lesion. A bilateral Babinski sign is present, and depending on the level of the segment of the spinal cord damaged, bilateral loss of the superficial abdominal and cremaster reflexes occurs. All these signs are caused by an interruption of the corticospinal tracts on both sides of the cord. The bilateral spastic paralysis is produced by the cutting of the descending tracts other than the corticospinal tracts.
  • Bilateral loss of all sensations below the level of the lesion. The loss of tactile discrimination and vibratory and proprioceptive sensations is due to bilateral destruction of the ascending tracts in the posterior white columns. The loss of pain, temperature, and light touch sensations is caused by section of the lateral and anterior spinothalamic tracts on both sides. Because these tracts cross obliquely, the loss of thermal and light touch sensations occurs two or three segments below the lesion distally.
  • Bladder and bowel functions are no longer under voluntary control, since all the descending autonomic fibers have been destroyed.

If there is a complete fracture dislocation at the L2-3 vertebral level (i.e., a level below the lower end of the cord in the adult), no cord injury occurs and neural damage is confined to the cauda equina, and lower motor neuron, autonomic, and sensory fibers are involved. Anterior Cord Syndrome Anterior cord syndrome (Fig. 4-31) can be caused by cord contusion during vertebral fracture or dislocation, from injury to the anterior spinal artery or its feeder arteries with resultant ischemia of the cord, or by a herniated intervertebral disc. The following characteristic clinical features are seen after the period of spinal shock has ended:

  • Bilateral lower motor neuron paralysis in the segment of the lesion and muscular atrophy. This is caused by damage to the neurons in the anterior gray columns (i.e., lower motor neuron) and possibly by damage to the anterior nerve roots of the same segment.
  • Bilateral spastic paralysis below the level of the lesion, the extent of which depends on the size of the injured area of the cord. The bilateral paralysis is caused by the interruption of the anterior corticospinal tracts on both sides of the cord. The bilateral muscular spasticity is produced by the interruption of tracts other than the corticospinal tracts.
  • Bilateral loss of pain, temperature, and light touch sensations below the level of the lesion. These signs are caused by interruption of the anterior and lateral spinothalamic tracts on both sides.
  • Tactile discrimination and vibratory and proprioceptive sensations are preserved because the posterior white columns on both sides are undamaged.

Central Cord Syndrome Central cord syndrome is most often caused by hyperextension of the cervical region of the spine (Fig. 4-31). The cord is pressed on anteriorly by the vertebral bodies and posteriorly by the bulging of the ligamentum flavum, causing damage to the central region of the spinal cord. Radiographs of these injuries often appear normal because no fracture or dislocation has occurred. The following characteristic clinical features are seen after the period of spinal shock has ended:

  • Bilateral lower motor neuron paralysis in the segment of the lesion and muscular atrophy. This is caused by damage to the neurons in the anterior gray columns (i.e., lower motor neuron) and possibly by damage to the nerve roots of the same segment.
  • Bilateral spastic paralysis below the level of the lesion with characteristic sacral “sparing.” The lower limb fibers are affected less than the upper limb fibers because the descending fibers in the lateral corticospinal tracts are laminated, with the upper limb fibers located medially and the lower limb fibers located laterally (Fig. 4-29).
  • Bilateral loss of pain, temperature, light touch, and pressure sensations below the level of the lesion with characteristic sacral “sparing.” Because the ascending fibers in the lateral and anterior spinothalamic tracts are also laminated, with the upper limb fibers located medially and the lower limb fibers located laterally, the upper limb fibers are more susceptible to damage than the lower limb fibers (Fig. 4-29).

It follows from this discussion that the clinical picture of a patient with a history of a hyperextension injury of the neck, presenting with motor and sensory tract injuries involving principally the upper limb, would strongly suggest central cord syndrome. The sparing of the lower part of the body may be evidenced by (1) the presence of perianal sensation, (2) good anal sphincter tone, and (3) the ability to move the toes slightly. In patients whose damage is caused by edema of the spinal cord alone, the prognosis is often very good. A mild central cord syndrome that consists only of paresthesias of the upper part of the arm and some mild arm and hand weakness can occur.

Figure 4-31 Spinal cord syndromes.

Brown-Séquard Syndrome or Hemisection of the Cord Hemisection of the spinal cord can be caused by fracture dislocation of the vertebral column, by a bullet or stab wound, or by an expanding tumor (Fig. 4-31). Incomplete hemisection is common; complete hemisection is rare. The following characteristic clinical features are seen in patients with a complete hemisection of the cord (Fig. 4-32) after the period of spinal shock has ended:

  • Ipsilateral lower motor neuron paralysis in the segment of the lesion and muscular atrophy. These signs are caused by damage to the neurons on the anterior gray column and possibly by damage to the nerve roots of the same segment.
  • Ipsilateral spastic paralysis below the level of the lesion. An ipsilateral Babinski sign is present, and depending on the segment of the cord damaged, an ipsilateral loss of the superficial abdominal reflexes and cremasteric reflex occurs. All these signs are due to loss of the corticospinal tracts on the side of the lesion. Spastic paralysis is produced by interruption of the descending tracts other than the corticospinal tracts.
  • Ipsilateral band of cutaneous anesthesia in the segment of the lesion. This results from the destruction of the posterior root and its entrance into the spinal cord at the level of the lesion.
  • Ipsilateral loss of tactile discrimination and of vibratory and proprioceptive sensations below the level of the lesion. These signs are caused by destruction of the ascending tracts in the posterior white column on the same side of the lesion.
  • Contralateral loss of pain and temperature sensations below the level of the lesion. This is due to destruction of the crossed lateral spinothalamic tracts on the same side of the lesion. Because the tracts cross obliquely, the sensory loss occurs two or three segments below the lesion distally.
  • Contralateral but not complete loss of tactile sensation below the level of the lesion. This condition is brought about by destruction of the crossed anterior spinothalamic tracts on the side of the lesion. Here, again, because the tracts cross obliquely, the sensory impairment occurs two or three segments below the level of the lesion distally. The contralateral loss of tactile sense is incomplete because discriminative touch traveling in the ascending tracts in the contralateral posterior white column remains intact.
Figure 4-33 Skin area in which the sensations of pain and temperature are lost in syringomyelia.

Syringomyelia Syringomyelia, which is due to a developmental abnormality in the formation of the central canal, most often affects the brainstem and cervical region of the spinal cord. At the site of the lesion, there is cavitation and gliosis in the central region of the neuroaxis (Fig. 4-33). The following characteristic signs and symptoms are found:

  • Loss of pain and temperature sensations in dermatomes on both sides of the body related to the affected segments of the cord. This loss commonly has a shawllike distribution caused by the interruption of the lateral spinothalamic tracts as they cross the midline in the anterior gray and white commissures. The patient commonly complains of accidental burning injuries to the fingers.
  • Tactile discrimination, vibratory sense, and proprioceptive sense are normal. The reason is that the ascending tracts in the posterior white column are unaffected.
  • Lower motor neuron weakness is present in the small muscles of the hand. It may be bilateral, or one hand may suffer before the other. As the lesion expands in the lower cervical and upper thoracic region, it destroys the anterior horn cells of these segments. Later, the other muscles of the arm and shoulder girdles undergo atrophy.
  • Bilateral spastic paralysis of both legs may occur, with exaggerated deep tendon reflexes and the presence of a positive Babinski response. These signs are produced by the further expansion of the lesion laterally into the white column to involve the descending tracts.
    Figure 4-32 Brown-Séquard syndrome with a spinal cord lesion at the right 10th thoracic level.
  • Horner syndrome may be present. This is caused by the interruption of the descending autonomic fibers in the reticulospinal tracts in the lateral white column by the expanding lesion.

Poliomyelitis Poliomyelitis is an acute viral infection of the neurons of the anterior gray columns of the spinal cord (Fig. 4-31) and the motor nuclei of the cranial nerves. Immunization has greatly reduced the incidence of poliomyelitis, which was once a feared disease. Following death of the motor nerve cells, there is paralysis and wasting of the muscles. The muscles of the lower limb are more often affected than the muscles of the upper limb. In severe poliomyelitis, respiration may be threatened due to the paralysis spreading to the intercostal muscles and diaphragm. The muscles of the face, pharynx, larynx, and tongue may also be paralyzed. Improvement usually begins at the end of the first week as the edema in the affected area subsides and function returns to the neurons that have not been destroyed. Multiple Sclerosis Multiple sclerosis is a common disease confined to the central nervous system, causing demyelination of the ascending and descending tracts. It is a disease of young adults, and the cause is unknown. Autoimmunity, infection, and heredity, alone or in combination, may play a role in its etiology. It has been suggested that a breach in the integrity of the blood-brain barrier in an individual who is genetically predisposed to the disease may be responsible. This could result in the invasion of the brain and spinal cord by some infection allowing leukocytes to enter the normally immunologically protected central nervous system. The inflammation and demyelination with loss of the myelin sheath results in the breakdown of the insulation around the axons, and the velocity of the action potentials is reduced and ultimately becomes blocked. Although myelin is relatively rich in lipid (70% to 80%), it also contains proteins that play a role in myelin compaction. It has been found that many of the proteins in the myelin of the central nervous system differ from those in the peripheral nervous system. Experimentally, it has been shown that basic myelin proteins injected into animals can produce a strong immune response and demyelination in the central nervous system occurs. It is possible that mutations in the structure of myelin protein can occur and be responsible for some inherited forms of demyelination. It is also possible that autoantigens develop in multiple sclerosis. The course of multiple sclerosis is chronic with exacerbations and remissions. Because of the widespread involvement of different tracts at different levels of the neuroaxis, the signs and symptoms are multiple, but remissions do occur. Weakness of the limbs is the most common sign of the disease. Ataxia due to involvement of the tracts of the cerebellum may occur, but spastic paralysis may also be present. Recent research has suggested that the remissions in multiple sclerosis may in part be explained by the remodeling of the demyelinated axonal plasma membrane so that it acquires a higher than normal number of sodium channels, which permit conduction of action potentials despite the loss of myelin. In patients who have the progressive form of the disease without remissions, it is has been shown that they have a substantial damage to the axons as well as the myelin. This would suggest that multiple sclerosis is not just a demyelinating disease but one in which there is axonal pathology. Amyotrophic Lateral Sclerosis Amyotrophic lateral sclerosis (Lou Gehrig disease) is a disease confined to the corticospinal tracts and the motor neurons of the anterior gray columns of the spinal cord (Fig. 4-31). It is rarely familial and is inherited in about 10% of patients. Amyotrophic lateral sclerosis is a chronic progressive disease of unknown etiology. Typically, it occurs in late middle age and is inevitably fatal in 2 to 6 years. The lower motor neuron signs of progressive muscular atrophy, paresis, and fasciculations are superimposed on the signs and symptoms of upper motor neuron disease with paresis, spasticity, and Babinski response. The motor nuclei of some cranial nerves may also be involved. Parkinson Disease Parkinson disease is associated with neuronal degeneration in the substantia nigra and, to a lesser extent, in the globus pallidus, putamen, and caudate nucleus. The degeneration of the inhibitory nigrostriate fibers results in a reduction in the release of the neurotransmitter dopamine within the corpus striatum. This leads to hypersensitivity of the dopamine receptors in the postsynaptic neurons in the corpus striatum, which become overactive. The characteristic signs of the disease include tremor and cogwheel rigidity (hyperkinetic activity) and difficulty initiating voluntary movements, which are slow (hypokinetic activity). (For further details, see p. 322.) Pernicious Anemia Pernicious anemia, a form of megaloblastic anemia, is caused by vitamin B12 deficiency. The disease may produce extensive damage to the tracts in the posterior and lateral white columns of the spinal cord as well as peripheral nerve degeneration. Widespread sensory and motor losses may be present due to involvement of the ascending and descending tracts of the spinal cord. Radiographic Appearances of the Vertebral Column The views commonly used in radiography are anteroposterior, lateral, and oblique. Vertebral destruction due to tuberculosis or primary or secondary tumors of the vertebrae or fractures due to trauma usually can be revealed by radiographic examination. Erosion of the pedicles by a tumor within the intervertebral foramina may be seen. Narrowing of the space between the vertebral bodies with bony spurs because of osteoarthritic changes in adjacent vertebral bodies can also be seen. Computed Tomography and Magnetic Resonance Imaging of the Vertebral Column and Spinal Cord CT scans of the vertebrae and joints can be obtained (Fig. 4-34). A protrusion of an intervertebral disc can be identified and the presence of narrowing of the vertebral canal (spinal stenosis) can be diagnosed. Sagittal MRI is increasingly being used to replace CT and myelography. The parts of a vertebra, the intervertebral disc, the posterior longitudinal ligament, and meningeal sac (thecal sac) can easily be identified (Fig. 4-35).

Figure 4-34 Horizontal (axial) CT scan of the fourth lumbar vertebra.

Myelography The subarachnoid space can be studied radiographically by the injection of a contrast medium into the subarachnoid space by spinal tap. Iodized oil has been used with success. This technique is referred to as myelography (Figs. 4-36 and 4-37). If the patient is sitting in the upright position, the oil sinks to the lower limit of the subarachnoid space at the level of the lower border of the second sacral vertebra. By placing the patient on a tilting table, the oil can be made to gravitate gradually to higher levels of the vertebral column. A normal myelogram will show pointed lateral projections at regular intervals at the intervertebral space levels. The reason for this is that the opaque medium fills the lateral extensions of the subarachnoid space around each spinal nerve. The presence of a tumor or a prolapsed intervertebral disc may obstruct the movement of the oil from one region to another when the patient is tilted. With the recent technologic advances in CT scans and MRIs, it is now unusual to require an intrusive procedure, such as myelography, to make a diagnosis.

Figure 4-36 Posteroanterior myelogram of the cervical region of a 22-year-old woman.
Figure 4-35 Sagittal MRI of the lumbosacral part of the vertebral column showing several prolapsed intervertebral discs. (Courtesy Dr. Pait.)
Figure 4-37 Diagrammatic explanation of the myelogram shown in Figure 4-36.

P.177 P.178 P.179 P.180 Clinical Problem Solving 1. A 53-year-old widower was admitted to the hospital complaining of a burning pain over his right shoulder region and the upper part of his right arm. The pain had started 3 weeks previously and, since that time, had progressively worsened. The pain was accentuated when the patient moved his neck or coughed. Two years previously, he had been treated for osteoarthritis of his vertebral column. The patient stated that he had been a football player at college, and since that time, he continued to take an active part in the game until he was 42 years old. Physical examination revealed weakness, wasting, and fasciculation of the right deltoid and biceps brachii muscles. The right biceps tendon reflex was absent. Radiologic examination revealed extensive spur formation on the bodies of the fourth, fifth, and sixth cervical vertebrae. The patient demonstrated hyperesthesia and partial analgesia in the skin over the lower part of the right deltoid and down the lateral side of the arm. Using your knowledge of neuroanatomy, make the diagnosis. How is the pain produced? Why is the pain made worse by coughing? View Answer1. This patient was suffering from spondylosis, which is a general term used for degenerative changes in the vertebral column caused by osteoarthritis. In the cervical region, the growth of osteophytes was exerting pressure on the anterior and posterior roots of the fifth and sixth spinal nerves. As the result of repeated trauma and of aging, degenerative changes occurred at the articulating surfaces of the fourth, fifth, and sixth cervical vertebrae. Extensive spur formation resulted in narrowing of the intervertebral foramina with pressure on the nerve roots. The burning pain, hyperesthesia, and partial analgesia were due to pressure on the posterior roots, and weakness, wasting, and fasciculation of the deltoid and biceps brachii muscles were due to pressure on the anterior roots. Movements of the neck presumably intensified the symptoms by exerting further traction or pressure on the nerve roots. Coughing or sneezing raised the pressure within the vertebral canal and resulted in further pressure on the nerve roots. 2. A 66-year-old woman was admitted to the hospital because of her increasing difficulty with walking. Two weeks before admission, she had been able to walk with the help of a stick. Since that time, walking had become increasingly difficult, and for the past 2 days, she could not walk at all. She had complete control of micturition and defecation. On examination, the handgrip was weak on both sides, but power was normal in the proximal segments of the upper extremities. The tendon reflexes of the upper limbs and the sensory function were normal. Both lower limbs showed muscular weakness with increased muscle tone, especially on the left side. The knee jerks and ankle jerks (tendon reflexes) in both lower limbs were grossly exaggerated, and there were bilateral extensor plantar responses. The patient had a loss of sensation of pain below the fifth thoracic dermatome on both sides of the body. Postural sense was impaired in both great toes, and vibration sense was absent below the fifth thoracic segmental level. Radiologic examination, including an MRI, of the vertebral column showed nothing abnormal. A myelogram in the lumbar region revealed a complete block at the lower border of the fourth thoracic vertebra. Using your knowledge of neuroanatomy, suggest a possible diagnosis. How would you treat this patient? Name the tracts in the spinal cord that are responsible for conduction of the sensation of pain. What is the position of these tracts in the spinal cord? Name the tracts responsible for the conduction of postural sense and vibration sense from the spinal cord to the brain. Why did the patient have increasing difficulty in walking? Why were the tendon reflexes in the lower limbs exaggerated, and why did the patient exhibit bilateral extensor plantar responses? View Answer2. The patient was operated on and a laminectomy of the third, fourth, and fifth thoracic vertebrae was carried out. At the level of the fourth thoracic vertebra, a small swelling was seen on the posterior surface of the spinal cord; it was attached to the dura mater. Histologic examination showed that it was a meningioma. The tumor was easily removed, and the patient successfully recovered from the operation. There was a progressive recovery in the power of the lower limbs, with the patient walking without a stick. This patient emphasizes the importance of making an early, accurate diagnosis because benign extramedullary spinal tumors are readily treatable. The lateral spinal thalamic tracts are responsible for the conduction of pain impulses up the spinal cord. These tracts are situated in the lateral white columns of the spinal cord (see p. 144). Postural sense and vibration sense are conducted up the spinal cord in the posterior white column through the fasciculus cuneatus from the upper limbs and the upper part of the thorax and in the fasciculus gracilis from the lower part of the trunk and the leg. The difficulty in walking was due to pressure on the corticospinal tracts in the lateral white column. The exaggeration in the tendon reflexes of the lower limbs and the bilateral extensor plantar responses were due to the pressure on the descending tracts in the spinal cord at the level of the tumor. This also resulted in spastic paralysis of the muscles of the lower limbs. 3. A 20-year-old male student celebrated the passing of an examination by drinking several beers at a party. On the way home, he drove his car head-on into a bridge abutment. On examination in the emergency department, he was found to have a fracture dislocation of the ninth thoracic vertebra with signs and symptoms of severe damage to the spinal cord. On physical examination, he had an upper motor neuron paralysis of the left leg. He also had loss of muscle joint sense of the left leg. On testing of cutaneous sensibility, he had a band of cutaneous hyperesthesia extending around the abdominal wall on the left side at the level of the umbilicus. Just below this, he had a narrow band of anesthesia and analgesia. On the right side, there was total analgesia, thermoanesthesia, and partial loss of tactile sense of the skin of the abdominal wall below the level of the umbilicus and involving the whole of the right leg. Using your knowledge of neuroanatomy, state the level at which the spinal cord was damaged. Was the spinal cord completely sectioned? If not, on which side did the hemisection occur? Explain the sensory losses found on examination in this patient. View Answer3. A fracture dislocation of the ninth thoracic vertebra would result in severe damage to the 10th thoracic segment of the spinal cord. The unequal sensory and motor losses on the two sides indicate a left hemisection of the cord. The narrow band of hyperesthesia on the left side was due to the irritation of the cord immediately above the site of the lesion. The band of anesthesia and analgesia was due to the destruction of the cord on the left side at the level of the 10th thoracic segment; that is, all afferent fibers entering the cord at that point were interrupted. The loss of pain and thermal sensibilities and the loss of light touch below the level of the umbilicus on the right side were caused by the interruption of the lateral and anterior spinothalamic tracts on the left side of the cord. 4. A 35-year-old woman was admitted to the hospital for investigation. She had symptoms of analgesia and thermoanesthesia on the medial side of the left hand that persisted for 6 months. Three weeks prior to her admittance, she had severely burned the little finger of her left hand on a hot stove and was unaware that the burn had occurred until she smelled the burning skin. On physical examination, she was found to have considerably reduced pain and temperature sense involving the eighth cervical and first thoracic dermatomes of the left hand. However, her sense of tactile discrimination was perfectly normal in these areas. Examination of the right arm showed a similar but much less severe dissociated sensory loss involving the same areas. No further abnormal signs were discovered. Using your knowledge of neuroanatomy, state which tract or tracts were involved in this pathologic process. Name this disease. View Answer4. This patient has the early signs and symptoms of syringomyelia. The gliosis and cavitation had resulted in interruption of the lateral and anterior spinothalamic tracts as they decussated in the anterior gray and white commissures of the spinal cord at the level of the eighth cervical and first thoracic segments of the spinal cord. Because of uneven growth of the cavitation, the condition was worse on the left side than on the right side. Since tactile discrimination was normal in both upper limbs, the fasciculus cuneatus in both posterior white columns was unaffected. This dissociated sensory loss is characteristic of this disease. 5. A 60-year-old man walked into the neurology clinic, and the physician paid particular attention to his gait. The patient raised his feet unnecessarily high and brought them to the ground in a stamping manner. While he was waiting for the physician, it was noticed that he stood with his feet wide apart. On questioning, the patient said that he was finding it increasingly difficult to walk and was starting to use a stick, especially when he went out for walks in the dark. The physician asked the patient to stand with his toes and heels together and to close his eyes. The patient immediately started to sway, and the nurse had to steady him to prevent him from falling. On further examination, the patient was found to have loss of muscle joint sense of both legs and was unable to detect any feeling of vibration when a vibrating tuning fork was placed on the medial malleolus of either leg. No other sensory losses were noted. Using your knowledge of neuroanatomy, name the ascending pathways that are involved, by disease, in this patient. Name a disease that could be responsible for these findings. View Answer5. The peculiar stamping gait and the swaying posture on closing the eyes are the characteristic signs of loss of appreciation of proprioceptive sensation from the lower limbs. These, together with the inability to detect the vibrations of a tuning fork placed on the medial malleoli of both legs, indicated that the patient had a lesion involving the fasciculus gracilis in both posterior white columns. Further questioning of this patient indicated that he had been treated for syphilis. The diagnosis was tabes dorsalis. 6. A 68-year-old man had an advanced inoperable carcinoma of the prostate with multiple metastases in the lumbar vertebrae and hip bones. Apart from the severe intractable pain, the patient was still able to enjoy life among his family. After a full discussion of the prognosis with the patient and his wife, the wife turned to the physician and said, “Can’t you do something to stop this terrible pain so that my husband can die happy?” What can a physician do to help a patient under these circumstances? View Answer6. The treatment of intractable pain in terminal cancer is a difficult problem. The narcotic drugs with their strong analgesic action are generally used. The likelihood that these drugs will be habit-forming is accepted in a dying patient. Alternative treatments include the continuous infusion of morphine directly into the spinal cord (see p. 166) or the surgical section of the nerve fibers carrying the sensations of pain into the nervous system. The techniques of posterior rhizotomy and cordotomy are described on page 166. 7. A third-year medical student attended a lecture on the effects of trauma on the vertebral column. The orthopedic surgeon described very superficially the different neurologic deficits that may follow injury to the spinal cord. At the end of the lecture, the student said he did not understand what was meant by the term spinal shock. He could not understand what the underlying mechanism for this condition was. He also asked the surgeon to explain what was meant by paraplegia in extension and paraplegia in flexion. Could the surgeon explain why one condition sometimes passes into the other? These are good questions. Can you answer them? View Answer7. Spinal shock is a temporary interruption of the physiologic function of the spinal cord following injury. It may in part be a vascular phenomenon involving the gray matter of the spinal cord; on the other hand, some authorities believe it is due to the sudden interruption of the influence of the higher centers on the local segmental reflexes. Whatever the cause, it usually disappears after 1 to 4 weeks. The condition is characterized by a flaccid paralysis and loss of sensation and reflex activity below the level of the lesion; this includes paralysis of the bladder and rectum. Paraplegia in extension and paraplegia in flexion follow severe injury to the spinal cord. Paraplegia in extension indicates an increase in the extensor muscle tone owing to the overactivity of the gamma efferent nerve fibers to the muscle spindles as the result of the release of these neurons from the higher centers. However, some neurologists believe that the vestibulospinal tracts are intact in these cases. Should all the descending tracts be severed, the condition of paraplegia in flexion occurs where the reflex responses are flexor in nature when a noxious stimulus is applied. It should be emphasized that paraplegia in extension and paraplegia in flexion occur only after spinal shock has ceased. Paraplegia in extension may change to paraplegia in flexion if the damage to the spinal cord becomes more extensive and the vestibulospinal tracts are destroyed. 8. While examining a patient with a right-sided hemiplegia caused by a cerebrovascular accident, the neurologist asked the student which clinical signs could be attributed to an interruption of the corticospinal tracts and which signs could be attributed to damage to other descending tracts. Using your knowledge of neuroanatomy, answer this question. View Answer8. If it is assumed that this patient had a lesion in the left internal capsule following a cerebral hemorrhage, the corticospinal fibers would have been interrupted as they descended through the posterior limb of the internal capsule. Since most of these fibers crossed to the right side at the decussation of the pyramids or lower down at the segmental level of the spinal cord, the muscles of the opposite side would have been affected. Interruption of these corticospinal fibers would have produced the following clinical signs: (a) a positive Babinski sign; (b) loss of superficial abdominal and cremasteric reflexes; and (c) loss of performance of fine, skilled voluntary movements, especially at the distal ends of the limbs. In patients with severe hemorrhage into the internal capsule, subcortical connections between the cerebral cortex and the caudate nucleus and the globus pallidus and other subcortical nuclei may be damaged. Moreover, some of the nuclei themselves may be destroyed. The interruption of other descending tracts from these subcortical centers would produce the following clinical signs: (a) severe paralysis on the opposite side of the body; (b) spasticity of the paralyzed muscles; (c) exaggerated deep muscle reflexes on the opposite side of the body to the lesion (clonus may be demonstrated); and (d) clasp-knife reaction, which may be felt in the paralyzed muscles. 9. A large civilian aircraft was forced to abort its takeoff because three tires had burst as the plane sped along the runway. The pilot miraculously managed to halt the plane as it veered off the runway and came to an abrupt halt in a ditch. All the passengers escaped injury, but one of the stewardesses was admitted to the emergency department with suspected spinal cord injury. On questioning, the 25-year-old patient said that although she had her seat belt fastened, she was thrown violently forward on impact. She said she could not feel anything in either leg and could not move her legs. On examination, there was complete motor and sensory loss of both legs below the inguinal ligament and absence of all deep tendon reflexes of both legs. Twelve hours later, it was noted that she could move the toes and ankle of her left lower limb, and she had a return of sensations to her right leg except for loss of tactile discrimination, vibratory sense, and proprioceptive sense. She had a band of complete anesthesia over her right inguinal ligament. Her left leg showed a total analgesia, thermoanesthesia, and partial loss of tactile sense. Her right leg was totally paralyzed, and the muscles were spastic. There was a right-sided Babinski response, and it was possible to demonstrate right-sided ankle clonus. The right knee jerk was exaggerated. Using your knowledge of neuroanatomy, explain the symptoms and signs found in this patient. Which vertebra was damaged? View Answer9. A lateral radiograph of the thoracic part of the vertebral column showed a fracture dislocation involving the tenth 10th vertebra. The first lumbar segment of the spinal cord is related to this vertebra. The first lumbar dermatome overlies the inguinal ligament, and the total anesthesia over the right ligament would suggest a partial lesion of the spinal cord involving the total sensory input at that level. The loss of tactile discrimination and vibratory and proprioceptive senses in the right leg was caused by the interruption of the ascending tracts in the posterior white column on the right side of the spinal cord. The loss of pain and temperature senses in the skin of the left leg was due to destruction of the crossed lateral spinothalamic tracts on the right side at the level of the lesion. The loss of tactile sense in the skin of the left leg was caused by the destruction of the crossed anterior spinothalamic tracts on the right side. The spastic paralysis of the right leg and the right-sided ankle clonus were due to the interruption of the right-sided descending tracts other than the corticospinal tracts. The right-sided Babinski response was brought about by the interruption of the corticospinal fibers on the right side. The complete motor and sensory loss of both legs and the absence of all deep tendon reflexes of both legs during the first 12 hours were due to spinal shock. 10. Why is it dangerous to move a patient who is suspected of having a fracture or dislocation of the vertebral column? View Answer10. The spinal cord occupies the vertebral canal of the vertebral column, and therefore, under normal circumstances, it is well protected. Unfortunately, once the integrity of the bony protection is destroyed by a fracture dislocation, especially in the thoracic region, where the canal is of small diameter, the bone can damage the cord and sever it just as a knife cuts through butter. It is essential that all patients suspected of having an injury to the spine be handled with great care to prevent the bones undergoing further dislocation and causing further injury to the cord. The patient should be carefully lifted by multiple supports under the feet, knees, pelvis, back, shoulders, and head and placed on a rigid stretcher or board for transportation to the nearest medical center. 11. An 18-year-old man was admitted to the hospital following a severe automobile accident. After a complete neurologic investigation, his family was told that he would be paralyzed from the waist downward for the rest of his life. The neurologist outlined to the medical personnel the importance of preventing complications in these cases. The common complications are the following: (a) urinary infection, (b) bedsores, (c) nutritional deficiency, (d) muscular spasms, and (e) pain. Using your knowledge of neuroanatomy, explain the underlying reasons for these complications. How long after the accident do you think it would be possible to give an accurate prognosis in this patient? View Answer11. Urinary infection secondary to bladder dysfunction is extremely common in paraplegic patients. The patient has not only lost control of the bladder but also does not know when it is full. An indwelling Foley catheter is placed in the bladder immediately for continuous drainage, and antibiotic therapy is instituted. Bedsores are very common in patients who have lost all sensory perception over their bony points, such as the ischial tuberosities and the sacrum. Bedsores are best prevented by (a) keeping the skin scrupulously clean, (b) frequently changing the position of the patient, and (c) keeping soft padding beneath the bony points. Nutritional deficiency is common in active individuals who are suddenly confined to their beds and who are paralyzed. Loss of appetite must be combated by giving the patients a high-calorie diet that has all the required ingredients, especially vitamins. Muscle spasms occur in paraplegia in extension or paraplegia in flexion and may follow only minor stimuli. The cause is unknown, but neuronal irritation at the site of injury may be responsible. Warm baths are helpful, but occasionally, in extreme cases, nerve section may be necessary. Pain occurs in the anesthetic areas in about one-fourth of patients who have a complete section of the spinal cord. The pain may be burning or shooting and superficial, or deep visceral. Here again, neuronal irritation at the site of injury may be responsible. Analgesics should be tried, but in some individuals, rhizotomy or even chordotomy may be necessary. An accurate prognosis is not possible until the stage of spinal shock has ended, and this may last as long as 4 weeks. 12. A 67-year-old man was brought to the neurology clinic by his daughter because she had noticed that his right arm had a tremor. Apparently, this had started about 6 months previously and was becoming steadily worse. When questioned, the patient said he noticed that the muscles of his limbs sometimes felt stiff, but he had attributed this to old age. It was noticed that while talking, the patient rarely smiled and then only with difficulty. It was also noted that he infrequently blinked his eyes. The patient tended to speak in a low, faint voice. When asked to walk, the patient was seen to have normal posture and gait, although he tended to hold his right arm flexed at the elbow joint. When he was sitting, it was noted that the fingers of the right hand were alternately contracting and relaxing, and there was a fine tremor involving the wrist and elbow on the right side. It was particularly noticed that the tremor was worse when the arm was at rest. When he was asked to hold a book in his right hand, the tremor stopped momentarily, but it started again immediately after the book was placed on the table. The daughter said that when her father falls asleep, the tremor stops immediately. On examination, it was found that the passive movements of the right elbow and wrist showed an increase in tone, and there was some cogwheel rigidity. There was no sensory loss, either cutaneous or deep sensibility, and the reflexes were normal. Using your knowledge of neuroanatomy, make a diagnosis. Which regions of the brain are diseased? View Answer12. The characteristic coarse tremor of the right hand (pill rolling) and right arm, the unsmiling masklike face with unblinking eyes, and the cogwheel rigidity of the involved muscles make the diagnosis of early Parkinson disease (paralysis agitans) certain. Degenerative lesions occur in the substantia nigra and other subcortical nuclei, including the lentiform nucleus. The loss of normal function of these subcortical areas and the absence of their influence on the lower motor neurons are responsible for the increased tone and tremor. 13. Name a center in the central nervous system that may be responsible for the following clinical signs: (a) intention tremor, (b) athetosis, (c) chorea, (d) dystonia, and (e) hemiballismus. View Answer13. (a) Intention tremor occurs in cerebellar disease. (b) Athetosis occurs in lesions of the corpus striatum. (c) Chorea occurs in lesions of the corpus striatum. (d) Dystonia occurs in disease of the lentiform nucleus. (e) Hemiballismus occurs in disease of the opposite subthalamic nucleus. P.181 P.182 P.183 P.184 Review Questions Directions: Each of the numbered items in this section is followed by answers. Select the ONE lettered answer that is CORRECT. 1. The following statements concern the spinal cord: (a) The anterior and posterior gray columns on the two sides are united by a white commissure. (b) The terminal ventricle is the expanded lower end of the fourth ventricle. (c) The larger nerve cell bodies in the anterior gray horns give rise to the alpha efferent nerve fibers in the anterior roots. (d) The substantia gelatinosa groups of cells are located at the base of each posterior gray column. (e) The nucleus dorsalis (Clarke’s column) is a group of nerve cells found in the posterior gray column and restricted to the lumbar segments of the cord. View Answer1. C is correct. The larger nerve cell bodies in the anterior gray horns give rise to the alpha efferent nerve fibers in the anterior roots (see p. 139). A. The anterior and posterior gray columns on the two sides of the spinal cord are united by a gray commissure formed of gray matter. B. The terminal ventricle is the expanded lower end of the central canal. D. The substantia gelatinosa group of cells is located at the apex of each posterior gray column throughout the length of the spinal cord. E. The nucleus dorsalis (Clarke’s column) is a group of nerve cells found in the posterior gray column and extending from the eighth cervical segment of the cord to the third or fourth lumbar segment. 2. The following statements concern the white columns of the spinal cord: (a) The posterior spinocerebellar tract is situated in the posterior white column. (b) The anterior spinothalamic tract is found in the anterior white column. (c) The lateral spinothalamic tract is found in the anterior white column. (d) The fasciculus gracilis is found in the lateral white column. (e) The rubrospinal tract is found in the anterior white column. View Answer2. B is correct. In the spinal cord, the anterior spinothalamic tract is found in the anterior white column (see p. 149). A. The posterior spinocerebellar tract is situated in the lateral white column (see p. 000). C. The lateral spinothalamic tract is found in the lateral white column. D. The fasciculus gracilis is found in the posterior white column. E. The rubrospinal tract is found in the lateral white column. 3. The following statements concern the spinal cord: (a) The spinal cord has a cervical enlargement for the brachial plexus. (b) The spinal cord possesses spinal nerves that are attached to the cord by anterior and posterior rami. (c) In the adult, the spinal cord usually ends inferiorly at the lower border of the fourth lumbar vertebra. (d) The ligamentum denticulatum anchors the spinal cord to the pedicles of the vertebra along each side. (e) The central canal does not communicate with the fourth ventricle of the brain. View Answer3. A is correct. The spinal cord has a cervical enlargement for the brachial plexus (see Fig. 4-5). B. The spinal cord possesses spinal nerves that are attached to the cord by anterior and posterior nerve roots (see p. 137). C. In the adult, the spinal cord usually ends inferiorly at the lower border of the first lumbar vertebra. D. The ligamentum denticulatum anchors the spinal cord to the dura mater along each side. E. The central canal, which contains cerebrospinal fluid, communicates with the fourth ventricle of the brain. Directions: Matching Questions. Questions 4 through 9 apply to the following figure. Match the numbers listed on the left with the appropriate lettered structure listed on the right. Each lettered option may be selected once, more than once, or not at all.

image

4. Number 1 (a) Nucleus proprius (b) Preganglionic sympathetic outflow (c) Nucleus dorsalis (d) Substantia gelatinosa (e) None of the above View Answer4. D is correct. 5. Number 2 (a) Nucleus proprius (b) Preganglionic sympathetic outflow (c) Nucleus dorsalis (d) Substantia gelatinosa (e) None of the above View Answer5. A is correct. 6. Number 3 (a) Nucleus proprius (b) Preganglionic sympathetic outflow (c) Nucleus dorsalis (d) Substantia gelatinosa (e) None of the above View Answer6. C is correct. 7. Number 4 (a) Nucleus proprius (b) Preganglionic sympathetic outflow (c) Nucleus dorsalis (d) Substantia gelatinosa (e) None of the above View Answer7. B is correct. 8. Number 5 (a) Nucleus proprius (b) Preganglionic sympathetic outflow (c) Nucleus dorsalis (d) Substantia gelatinosa (e) None of the above View Answer8. E is correct. The structure is the anterior gray horn. 9. Number 6 (a) Nucleus proprius (b) Preganglionic sympathetic outflow (c) Nucleus dorsalis (d) Substantia gelatinosa (e) None of the above View Answer9. E is correct. The structure is the gray commissure. Directions: Each of the numbered items in this section is followed by answers. Select the ONE lettered answer that is CORRECT. 10. The following statements concern the cell of origin of the tracts listed below: (a) The fasciculus cuneatus arises from the cells in the substantia gelatinosa. (b) The anterior spinal thalamic arises from the cells in posterior root ganglion. (c) The fasciculus gracilis arises from the cells in the nucleus dorsalis (Clarke’s column). (d) The anterior spinocerebellar arises from the cells in the posterior root ganglion. (e) The lateral spinothalamic arises from the cells in the substantia gelatinosa. View Answer10. E is correct. In the spinal cord, the lateral spinothalamic tract arises from the cells in the substantia gelatinosa (see p. 139). A. The fasciculus cuneatus arises from the cells in the posterior root ganglion. B. The anterior spinal thalamic arises from the cells in the substantia gelatinosa. C. The fasciculus gracilis arises from the cells in the posterior root ganglion. D. The anterior spinocerebellar arises from the cells in Clarke’s column. 11. The following statements concern the courses taken by the tracts listed below: (a) The fasciculus gracilis does not cross to the opposite side of the neural axis. (b) The spinotectal tract does not cross to the opposite side of the spinal cord. (c) The lateral spinothalamic tract does not cross to the opposite side of the spinal cord. (d) The posterior spinocerebellar tract does cross to the opposite side of the neural axis. (e) The anterior spinothalamic tract immediately crosses to the opposite side of the spinal cord. View Answer11. A is correct. The fasciculus gracilis does not cross to the opposite side of the neural axis (see p. 149). B. The spinotectal tract crosses to the opposite side of the spinal cord. C. The lateral spinothalamic tract does cross to the opposite side of the spinal cord. D. The posterior spinocerebellar tract does not cross to the opposite side of the spinal cord. E. The anterior spinothalamic tract crosses very obliquely to the opposite side of the spinal cord. 12. The following statements concern the nucleus of termination of the tracts listed below: (a) The posterior white column tracts terminate in the inferior colliculus. (b) The spinoreticular tract terminates on the neurons of the hippocampus. (c) The spinotectal tract terminates in the inferior colliculus. (d) The anterior spinothalamic tract terminates in the ventral posterolateral nucleus of the thalamus. (e) The anterior spinocerebellar tract terminates in the dentate nucleus of the cerebellum. View Answer12. D is correct. The anterior spinothalamic tract terminates in the ventral posterolateral nucleus of the thalamus (see p. 149). A. The posterior white column tracts terminate in the nucleus gracilis and cuneatus (see p. 149). B. The spinoreticular tract terminates on the neurons of the reticular formation in the medulla, pons, and midbrain. C. The spinotectal tract terminates in the superior colliculus. E. The anterior spinocerebellar tract terminates in the cerebellar cortex (see p. 150). 13. The following statements relate sensations with the appropriate nervous pathways: (a) Two-point tactile discrimination travels in the lateral spinothalamic tract. (b) Pain travels in the anterior spinothalamic tract. (c) Unconscious muscle joint sense travels in the anterior spinocerebellar tract. (d) Pressure travels in the posterior spinothalamic tract. (e) Vibration travels in the posterior spinocerebellar tract. View Answer13. C is correct. Unconscious muscle joint sense travels in the anterior spinocerebellar tract (see p. 144). A. Two-point tactile discrimination travels in the fasciculus cuneatus. B. Pain travels in the lateral spinothalamic tract. D. Pressure travels in the anterior spinothalamic tract. E. Vibration travels in the fasciculus gracilis (see p. 149). 14. The following statements concern the gating theory of pain: (a) Stimulation of small non-pain-conducting fibers in a peripheral nerve may reduce pain sensitivity. (b) Massage applied to the skin over a painful joint may reduce pain sensitivity. (c) Stimulation of delta A- and C-type fibers in a posterior root of a spinal nerve may decrease pain sensitivity. (d) Degeneration of large non-pain-conducting fibers in a peripheral nerve decreases pain sensitivity. (e) Inhibition of pain conduction in the spinal cord does not involve connector neurons. View Answer14. B is correct concerning the gating theory of pain. Massage applied to the skin over a painful joint may reduce pain sensitivity (see p. 147). A. Stimulation of large nonpain-conducting fibers in a peripheral nerve may reduce pain sensitivity. C. Stimulation of delta A- and C-type fibers in a posterior root of a spinal nerve may increase pain sensitivity (see p. 147). D. Degeneration of large nonpain-conducting fibers in a peripheral nerve increases pain sensitivity. E. Inhibition of pain conduction in the spinal cord could be brought about by means of connector neurons. 15. The following statements concern the reception of pain: (a) Serotonin is not a transmitter substance in the analgesic system. (b) Substance P, a protein, is thought to be the neurotransmitter at the synapses where the first-order neuron terminates on the cells in the posterior gray column of the spinal cord. (c) The enkephalins and endorphins may serve to stimulate the release of substance P in the posterior gray column of the spinal cord. (d) Many of the tracts conducting the initial, sharp, pricking pain terminate in the dorsal anterolateral nucleus of the thalamus. (e) The slow-conducting C-type fibers are responsible for prolonged, burning pain. View Answer15. E is correct. The slow-conducting C-type fibers are responsible for prolonged, burning pain (see p. 147). A. Serotonin is a transmitter substance in the analgesic system (see p. 147). B. Substance P is a peptide and is thought to be the neurotransmitter at the synapses where the first-order neuron terminates on the cells in the posterior gray column of the spinal cord. C. The enkephalins and endorphins may serve to inhibit the release of substance P in the posterior gray column of the spinal cord. D. Many of the tracts conducting the initial, sharp, pricking pain terminate in the ventral posterolateral nucleus of the thalamus. 16. The following statements concern the corticospinal tracts: (a) They occupy the posterior limb of the internal capsule. (b) They are mainly responsible for controlling the voluntary movements in the proximal muscles of the limbs. (c) They arise as axons of the pyramidal cells in the fourth layer of the cerebral cortex. (d) Those that control the movements of the upper limb originate in the precentral gyrus on the medial side of the cerebral hemisphere. (e) Those that are concerned with the movements of the lower limb are located in the medial area of the middle three-fifths of the basis pedunculi. View Answer16. A is correct. The corticospinal tracts occupy the posterior limb of the internal capsule (see Fig. 4-11). B. The corticospinal tracts are mainly responsible for controlling the voluntary movements in the distal muscles of the limbs (see p. 154). C. They arise as axons of the pyramidal cells in the fifth layer of the cerebral cortex (see p. 155). D. Those that control the movements of the upper limb originate in the precentral gyrus on the lateral side of the cerebral hemisphere. E. Those that are concerned with the movements of the lower limb are located in the lateral area of the middle three-fifths of the basis pedunculi. 17. The following statements concern the course taken by the tracts listed below: (a) The rubrospinal tract crosses the midline of the neuroaxis in the medulla oblongata. (b) The tectospinal tract (most of the nerve fibers) crosses the midline in the posterior commissure. (c) The vestibulospinal tract crosses the midline in the midbrain. (d) The lateral corticospinal tract has crossed the midline in the medulla oblongata. (e) The anterior corticospinal tract crosses the midline in the midbrain. View Answer17. D is correct. The lateral corticospinal tract crosses the midline in the medulla oblongata (see Fig. 4-21). A. The rubrospinal tract crosses the midline of the neuroaxis in the midbrain. B. The tectospinal tract (most of the nerve fibers) crosses the midline in the midbrain. C. The vestibulospinal tract does not cross the midline and descends through the medulla oblongata and spinal cord in the anterior white column (see Figs. 4-20 and 4-25). E. The anterior corticospinal tract crosses the midline in the spinal cord. 18. The following statements concern the nerve cells of origin for the tracts listed below: (a) The vestibulospinal tract originates from cells of the medial vestibular nucleus situated in the pons. (b) The tectospinal tract originates from cells in the inferior colliculus. (c) The lateral corticospinal tract originates from cells in area 4 of the cerebral cortex. (d) The rubrospinal tract originates from cells in the reticular nucleus. (e) The reticulospinal tract originates from cells in the reticular formation that is confined to the midbrain. View Answer18. C is correct. The lateral corticospinal tract originates from cells in area 4 of the cerebral cortex. (see p. 155). A. The vestibulospinal tract originates from cells of the lateral vestibular nucleus situated in the pons. B. The tectospinal tract originates from cells in the superior colliculus. D. The rubrospinal tract originates from cells in the red nucleus. E. The reticulospinal tract originates from cells in the reticular formation in the midbrain, pons, and medulla oblongata (see p. 157). 19. The following statements concern muscle movement: (a) Muscular fasciculation is seen only when there is rapid destruction of the lower motor neurons. (b) Muscle spindle afferent nerve fibers send information only to the spinal cord. (c) In Parkinson disease, there is a degeneration of dopamine-secreting neurons that originate in the vestibular nucleus. (d) Brain neuronal activity preceding a voluntary movement is limited to the precentral gyrus (area 4). (e) Hyperactive ankle-jerk reflexes and ankle clonus indicate a release of the lower motor neurons from supraspinal inhibition. View Answer19. E is correct. Hyperactive ankle-jerk reflexes and ankle clonus indicate a release of the lower motor neurons from supraspinal inhibition (see p. 168). A. Muscular fasciculation is seen only when there is slow destruction of the lower motor neurons. B. Muscle spindle afferent nerve fibers send information to the brain as well as to the spinal cord. C. In Parkinson disease, there is a degeneration of dopamine-secreting neurons in the substantia nigra. D. Brain neuronal activity preceding a voluntary movement is not limited to the precentral gyrus (area 4) (see p. 167). 20. After a hemorrhage into the left internal capsule in a right-handed person, the following sign or symptom might be present: (a) Left homonymous hemianopia (b) Right astereognosis (c) Left hemiplegia (d) Normal speech. (e) Left-sided positive Babinski response View Answer20. B is correct. Right astereognosis (see p. 297). A. There is right homonymous hemianopia (see p. 358). C. Right hemiplegia is present. D. There is aphasia. E. There is a right-sided positive Babinski response. 21. A patient with a traumatic lesion of the left half of the spinal cord at the level of the eighth cervical segment might present the following sign(s) and symptom(s): (a) Loss of pain and temperature sensations on the left side below the level of the lesion (b) Loss of position sense of the right leg (c) Right hemiplegia (d) Left positive Babinski sign (e) Right-sided lower motor paralysis in the segment of the lesion and muscular atrophy View Answer21. D is correct. Left positive Babinski sign is present (see p. 171). A. There is loss of pain and temperature sensations on the right side below the level of the lesion. B. There is a loss of position sense of the left leg. C. There is a left hemiplegia. E. There is a left-sided lower motor paralysis in the segment of the lesion and muscular atrophy. Directions: Each of the numbered items in this section is followed by answers. Select the ONE lettered answer that is BEST in each case. 22. Which of the signs and symptoms listed below is indicative of a cerebellar lesion? (a) Cogwheel rigidity (b) Hemiballismus (c) Chorea (d) Intention tremor (e) Athetosis View Answer22. D is correct. Intention tremor is present (see p. 244). A. Cogwheel rigidity occurs in Parkinson disease when the muscle resistance is overcome as a series of jerks (see p. 322). B. Hemiballismus is a rare form of involuntary movement confined to one side of the body; it occurs in disease of the subthalamic nuclei (see p. 253). C. Chorea consists of a series of continuous, rapid, involuntary, jerky, coarse, purposeless movements, which may take place during sleep; it occurs with lesions of the corpus striatum. E. Athetosis consists of continuous, slow, involuntary, dysrhythmic movements that are always the same in the same individual, and they disappear during sleep; it occurs with lesions of the corpus striatum. 23. Which of the following regions of white matter would not contain corticospinal fibers? (a) Pyramid of medulla oblongata (b) Lateral white column of the spinal cord (c) Cerebral peduncle of the midbrain (d) Anterior limb of the internal capsule (e) Corona radiata View Answer23. D is correct. The anterior limb of the internal capsule does not contain corticospinal fibers (see p. 268). Directions: Each case history is followed by questions. Read the case history, then select the ONE BEST lettered answer. A 59-year-old woman was experiencing pain in the back and showed evidence of loss of pain and temperature sensations down the back of her left leg. Three years previously, she underwent a radical mastectomy followed by radiation and chemotherapy for advanced carcinoma of her right breast. On examination, it was found that she was experiencing pain over the lower part of the back, with loss of the skin sensations of pain and temperature down the back of her left leg in the area of the S1-3 dermatomes. No other neurologic deficits were identified. Radiographic examination of the vertebral column showed evidence of metastases in the bodies of the 9th and 10th thoracic vertebrae. An MRI revealed an extension of one of the metastases into the vertebral canal, with slight indentation of the spinal cord on the right side. 24. The pain in the back could be explained in this patient by the following facts except: (a) Osteoarthritis of the joints of the vertebral column. (b) The presence of metastases in the bodies of the 9th and 10th thoracic vertebrae. (c) The pressure of the tumor on the posterior roots of the spinal nerves. (d) A prolapsed intervertebral disc pressing on the spinal nerves. (e) Spasm of the postvertebral muscles following pressure of the tumor on the posterior white columns of the spinal cord. View Answer24. E is correct. Spasm of the postvertebral muscles would not be produced by pressure on the posterior white columns of the spinal cord.

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