Chapter 3. The Nervous System

At the completion of this chapter, the reader will be able to:

1. Describe the various components of the central and peripheral nervous systems.

2. Describe the anatomic and functional organization of the nervous system.

3. Describe the various components and distributions of the cervical, brachial, and lumbosacral plexuses.

4. Describe the difference between balance and proprioception.

5. Define proprioception and the role it plays in function.

6. Describe and differentiate among the various joint mechanoreceptors.

7. Recognize the characteristics of a lesion to the central nervous system (CNS).

8. List the findings and the impairments associated with the more common peripheral nerve lesions.

9. Perform a comprehensive examination of the neurologic system.

10. Describe some of the common pathologies of the nervous system.

In order to perform a comprehensive neuromusculoskeletal examination, the clinician must have a clear understanding of the signs and the symptoms indicating a compromise of the nervous system. The human nervous system can be subdivided into two anatomic divisions: the CNS, comprising the brain and the spinal cord, and the peripheral nervous system (PNS), formed by the cranial and the spinal nerves. The PNS is further subdivided into somatic and autonomic divisions. The somatic division innervates the skin, the muscles, and the joints, while the autonomic system innervates the glands and the smooth muscle of the viscera and the blood vessels.1

The nerve cell, or neuron, which serves to store and process information, is the functional unit of the nervous system. The other cellular constituent is the neuroglial cell, or glia, which functions to provide structural and metabolic support for the neurons.2

Although neurons come in various sizes and shapes, there are four functional parts for each nerve fiber (Fig. 3-1):

• Dendrite. Dendrites serve a receptive function and receive information from other nerve cells or the environment.
• Axon. The axon cylinder, in which there is a bidirectional flow of axoplasm, conducts information and nutrition to other nerve cells and the tissues that the nerve innervates. Many axons are covered by myelin, a lipid-rich membrane. In myelinated fibers, there is a direct proportional relationship between fiber diameter and conduction velocity.3 This membrane is divided into segments, approximately 1-mm long, by small gaps, called nodes of Ranvier, in which the myelin is absent.4 Myelin has a high electrical resistance and low capacitance and serves to increase the nerve conduction velocity of neural transmissions through a process called salutatory conduction. The Schwann cell is responsible for laying down myelin around axons.
• Cell body. The cell body contains the nucleus of the cell and has important integrative functions.
• Axon terminal. The axon terminal is the transmission site for action potentials, the messengers of the nerve cell.

Peripheral nerves are enclosed in three layers of tissue of differing character. From the inside outward, these are the endoneurium, perineurium, and epineurium.2 The nerve fibers embedded in endoneurium form a funiculus surrounded by perineurium, a thin but strong sheath of connective tissue. A fluid exists in the endoneurial spaces, which following nerve injury can produce intraneural edema, which in turn can play a major role in acute and chronic nerve lesions.3 The nerve bundles are embedded in a loose areolar connective tissue framework, called the epineurium. The epineurium that extends between the fascicles is termed the inner or the interfascicular epineurium, whereas that surrounding the entire nerve trunk is called the epifascicular epineurium.5 The connective tissue outside the epineurium is referred to as the adventitia of the nerve or the epineural tissue.5 Although the epineurium is continuous with the surrounding connective tissue, its attachment is loose, so that nerve trunks are relatively mobile, except where tethered by entering vessels or exiting nerve branches (see Chap. 11).6 There are no connective tissue components in the spinal nerves comparable to the epineurium and the perineurium of the peripheral nerve; at least they are not developed to the same degree.7 As a result, the spinal nerve roots are more sensitive to both tension and compression. The spinal nerve roots also are devoid of lymphatics and, thus, are predisposed to prolonged inflammation.8

The communication of information from one nerve cell to another occurs at junctions called synapses, where a chemical is released in the form of a neurotransmitter. A difference in concentration exists across the cell membrane of potassium, sodium, and chloride ions. These ions can selectively permeate ion channels in the membrane so that an unequal distribution of net charge occurs. The resting membrane potential results from an internal negativity resulting from the active transport of sodium from inside to outside the cell, and potassium from outside to inside the cell.3

Central Nervous System

The CNS consists of the brain and an elongated spinal cord. The spinal cord participates directly in the control of body movements, the processing and transmission of sensory information from the trunk and the limbs, and the regulation of visceral functions.1 The spinal cord also provides a conduit for the two-way transmission of messages between the brain and the body. These messages travel along the pathways, or tracts, that are fiber bundles of similar groups of neurons. Tracts may descend or ascend.

The spinal cord is normally 42–45-cm long in adults and is continuous with the medulla and brain stem at its upper end (Fig. 3-2).4 The conus medullaris serves as the distal end of the cord, and, in adults, the conus ends at the L1 or L2 level of the vertebral column. A series of specializations, the filum terminales and the coccygeal ligament, anchor the spinal cord and the dural sac inferiorly and ensure that the tensile forces applied to the spinal cord are distributed throughout its entire length.9 The spinal cord has an external segmental organization. Each of the 31 pairs of spinal nerves that arise from the spinal cord has a anterior (ventral) root and a posterior (dorsal) root, with each root made up of one to eight rootlets and consisting of bundles of nerve fibers.4 In the posterior (dorsal) root of a typical spinal nerve lies a spinal (sensory) ganglion (posterior (dorsal) root ganglion), a swelling that contains nerve cell bodies (Fig. 3-2).4

Three membranes, or meninges, envelop the structures of the CNS: dura mater, arachnoid, and pia mater (Fig. 3-3). The meninges, and related spaces, are important to both the nutrition and the protection of the spinal cord. The cerebrospinal fluid that flows through the meningeal spaces, and within the ventricles of the brain, provides a cushion for the spinal cord. The meninges also form barriers that resist the entrance of various noxious organisms.

Dura Mater

The dura mater (Latin, tough mother) is the outermost and the strongest of the membranes and is composed of an inner meningeal layer and an outermost periosteal layer. The dura runs uninterrupted from the interior of the cranium through the foramen magnum and surrounds the spinal cord throughout its distribution from the cranium to the coccyx at the second sacral level (S2).9 The dura also is attached to the posterior surfaces of C2 and C3.10

The dura forms a vertical sac (dural sac) around the spinal cord, and its short lateral projections blend with the epineurium of the spinal nerves. The dura is separated from the bones and the ligaments that form the walls of the vertebral canal by an epidural space, which can become partly calcified or even ossified with age.4

Arachnoid

The arachnoid is a thin and delicate avascular layer, coextensive with the dura mater and the pia mater. Even though the arachnoid and the pia mater are interconnected by trabeculae, there is a space between them, called the subarachnoid space, which contains the cerebrospinal fluid. The supposedly rhythmic flow of this cerebrospinal fluid is the rationale used by craniosacral therapists to explain their techniques, although there is no evidence of this finding in the literature.

Pia Mater

The pia mater is the deepest of the layers. It is intimately related and firmly attached, via connective tissue investments, to the outer surface of the spinal cord and the nerve roots. The pia mater conveys the blood vessels that supply the spinal cord and has a series of lateral specializations, the denticulate (dentate) ligaments, which anchor the spinal cord to the dura mater.9 These ligaments, which derive their name from their tooth-like appearance, extend the whole length of the spinal cord.

Peripheral Nervous System: Somatic Nerves

The PNS consists of the cranial nerves (CNs) and the spinal nerves.

Cranial Nerves

The CNs, typically, are described as comprising 12 pairs, which are referred to by the roman numerals I through XII (Fig. 3-4). The CN roots enter and exit the brain stem to provide sensory and motor innervation to the head and the muscles of the face. CN I (olfactory) and CN II (optic) are not true nerves but rather fiber tracts of the brain. The examination of the CN system is described later in this chapter (see section “Orthopaedic Neurologic Testing”).

CN I (Olfactory)

The olfactory tract arises from the olfactory bulb on the inferior aspect of the frontal lobe, just above the cribriform plate. From here it continues posteriorly as the olfactory tract and terminates just lateral to the optic chiasm. The olfactory nerve is responsible for the sense of smell.

CN II (Optic)

The fibers of the optic nerve arise from the inner layer of the retina and proceed posteriorly to enter the cranial cavity via the optic foramen, to form the optic chiasm. The fibers from the nasal half of the retina decussate within the optic chiasm, whereas those from the lateral half do not. The optic nerve is responsible for vision.

CN III (Oculomotor)

The oculomotor nerve arises in the oculomotor nucleus and leaves the brain on the medial aspect of the cerebral peduncle. It then extends from the interpeduncular fossa and runs between the posterior cerebral artery and the superior cerebellar artery, before leaving the cranial cavity and entering the cavernous sinus by way of the superior orbital fissure. The somatic portion of the oculomotor nerve supplies the levator palpebrae superioris muscle; the superior, medial, and inferior rectus muscles; and the inferior oblique muscles. These muscles are responsible for some eye movements. The visceral efferent portion of this nerve innervates two smooth intraocular muscles: the ciliary and the constrictor pupillae. These muscles are responsible for papillary constriction.

CN IV (Trochlear)

The trochlear nerve arises from the trochlear nucleus, just caudal to the oculomotor nucleus at the anterior border of the periaqueductal gray (PAG) matter. The fibers cross within the midbrain and then emerge contralaterally on the posterior surface of the brain stem, before entering the orbit via the superior orbital fissure, to supply the superior oblique muscle.

Note: Because nerves III, IV, and VI are generally examined together, CN V is described after CN VI.

CN VI (Abducens)

The abducens nerve originates from the abducens nucleus within the inferior aspect of the pons. Its long intracranial course to the superior orbital fissure makes it vulnerable to pathology in the posterior and middle cranial fossa. The nerve innervates the lateral rectus muscle.

CN V (Trigeminal)

The trigeminal nerve is so named because of its tripartite division into the maxillary, ophthalmic, and mandibular branches. All three of these branches contain sensory cells, but the ophthalmic and the maxillary are exclusively sensory, the latter supplying the soft and hard palate, maxillary sinuses, upper teeth and upper lip, and mucous membrane of the pharynx. The mandibular branch carries sensory information but also represents the motor component of the nerve, supplying the muscles of mastication, both pterygoids, the anterior belly of digastric, tensor tympani, tensor veli palatini, and mylohyoid.

The spinal nucleus and the tract of the trigeminal nerve cannot be distinguished either histologically or on the basis of afferent reception from the cervical nerves. Consequently, the entire column can be viewed as a single nucleus and, legitimately, may be called the trigeminocervical nucleus.

CN VII (Facial)

The facial nerve is made up of a sensory (intermediate) root, which conveys taste, and a motor root, the facial nerve proper, which supplies the muscles of facial expression, the platysma muscle, and the stapedius muscle of the inner ear. The intermediate root, together with the motor nerve and CN VIII, travels through the internal acoustic meatus to enter the facial canal of the temporal bone. From here, the intermediate nerve swells to form the geniculate ganglion and gives off the greater superficial petrosal nerve, which eventually innervates the lacrimal and salivary glands via the pterygopalatine ganglion and the chorda tympani nerve, respectively. The facial nerve proper exits the skull through the stylomastoid foramen.

CN VIII (Vestibulocochlear)

The vestibulocochlear nerve subserves two different senses: balance and hearing. The cochlear portion of the nerve arises from spiral ganglia, and the vestibular portion arises from the vestibular ganglia in the labyrinth of the inner ear. The cochlear portion is concerned with the sense of hearing, whereas the vestibular portion is a part of the system of equilibrium, the vestibular system.

The vestibular system includes the vestibular apparatus of the inner ear, the vestibular nuclei and their neural projections, and the exteroreceptors throughout the body, especially in the upper cervical spine and the eyes.11

The apparatus of the inner ear consists of the static labyrinth, which comprises three semicircular canals (SCC) (Fig. 3-5), each orientated at right angles to the other. The labyrinth includes specialized sensory areas that are located in the utricle and the saccule (Fig. 3-5), within which otoliths are located (Fig. 3-5).

A series of filaments line the basement membrane of the SCC and project into endolymph, which deforms these filaments when head motion occurs. This deformation is registered by receptor cells, and when sudden perturbations occur, the frequency of nerve impulses along the afferent nerve supply of the cell body is altered.

Unlike the filaments of the SCC, the filaments of the utricle and saccule do not project into endolymph, but instead insert into a gelatinous mass, within which the otolith is embedded. Deformation of these filaments is produced by the weight of the otolith against the cilia, as the gelatinous mass is displaced during head movement.

The otoliths are responsible for providing information about gravitational forces, as well as vertical and horizontal motion. The filaments of the saccule also provide information about vertical motion. At rest, the endolymphatic fluid, or the gelatinous membrane, is stationary. When motion of the head occurs, the endolymphatic fluid, or the gelatinous membrane, initially remains stationary because of its inertia, while the canals move. This relative motion produces a dragging effect on the filaments and either increases or decreases the discharge rate, depending on the direction of shear. At the end of the head movement, the fluid and the membrane continue to move, and the cilia are now dragged in the opposite direction before coming to rest. In essence, the SCC receptors transmit a positive signal when movement begins, no signal when the motion has finished, and a normal level after the sensory cell has returned to its original position. As this occurs, other sensory cells orientated in the opposite direction react in the reverse fashion.

CN IX (Glossopharyngeal)

The glossopharyngeal nerve contains somatic motor, visceral efferent, visceral sensory, and somatic sensory fibers. The motor fibers originate in the nucleus ambiguous, leaving the lateral medulla to join the sensory nerve, which arises from cells in the superior and petrous ganglia. The glossopharyngeal nerve exits the skull through the jugular foramen and serves a number of functions, including supplying taste fibers for the posterior third of the tongue.

CN X (Vagus)

The functions of the vagus nerve are numerous and include the motor parasympathetic fibers to all the organs except the suprarenal (adrenal) glands, from its origin down to the second segment of the transverse colon. The vagus also controls some skeletal muscles, including:

• Cricothyroid muscle
• Levator veli palatini muscle
• Salpingopharyngeus muscle
• Palatoglossus muscle
• Palatopharyngeus muscle
• Superior, middle, and inferior pharyngeal constrictors
• Muscles of the larynx.

The vagus nerve is thus responsible for such varied tasks as heart rate, gastrointestinal peristalsis, sweating, speech, and breathing. It also has some afferent fibers that innervate the inner (canal) portion of the outer ear.

CN XI (Accessory)

The accessory nerve consists of a cranial component and a spinal component. The cranial root originates in the nucleus ambiguous and is often viewed as an aberrant portion of the vagus nerve. The spinal portion of the nerve arises from the lateral parts of the anterior horns of the first five or six cervical cord segments and ascends through the foramen magnum. The spinal portion of the accessory nerve supplies the sternocleidomastoid and the trapezius muscles.

CN XII (Hypoglossal)

The hypoglossal nerve is the motor nerve of the tongue, innervating the ipsilateral side of the tongue as well as forming the descendens hypoglossi, which anastomoses with other cervical branches to form the ansa hypoglossi. The latter, in turn, innervates the infrahyoid muscles.

Spinal Nerves

There are a total of 31 symmetrically arranged pairs of spinal nerves, each derived from the spinal cord.14 The spinal nerves are divided topographically into eight cervical pairs (C1–8), 12 thoracic pairs (T1–12), five lumbar pairs (L1–5), five sacral pairs (S1–5), and a coccygeal pair (Fig. 3-2).

The posterior (dorsal) and anterior (ventral) roots of the spinal nerves are located within the vertebral canal (Fig. 3-2). The portion of the spinal nerve that is not within the vertebral canal, and that usually occupies the intervertebral foramen, is referred to as a peripheral nerve. As the nerve roots begin to exit the vertebral canal, they must penetrate the dura mater before passing through dural sleeves within the intervertebral foramen. The dural sleeves are continuous with the epineurium of the nerves.

Essentially, there are four branches of spinal nerves4

• Primary posterior (dorsal). This type usually consists of a medial sensory branch and a lateral motor branch.
• Primary anterior (ventral). The primary anterior (ventral) division forms the cervical, brachial, and lumbosacral plexuses.
• Communicating ramus. The rami serve as a connection between the spinal nerves and the sympathetic trunk. Only the thoracic and upper lumbar nerves contain a white ramus communicans, but the gray ramus is present in all spinal nerves.
• Meningeal or recurrent meningeal (also known as sinuvertebral). These nerves carry sensory and vasomotor innervation to the meninges.

There are three functional types of nerve fibers in the major nerve trunks, which vary in quantity depending on the particular nerve: afferent (sensory), autonomic (visceral efferent), and motor (somatic efferent) (Table 3-1). The faster nerve fibers such as A delta fibers are more concerned with speed and quality of human movement whereas the C fibers conduct far more slowly and are more involved with nociception and, by the compounds they release, the health of surrounding tissue.3

Sensory Nerves

The sensory nerves carry afferents (a nerve conveying impulses from the periphery to the CNS) from a portion of the skin. They also carry efferents (a nerve conveying impulses from the CNS to the periphery) to the skin structures. When a sensory nerve is compressed, symptoms occur in the area of the nerve distribution. This area of distribution, called a dermatome, is a well-defined portion of the skin (Fig. 3-6) and generally follows the segmental distribution of the underlying muscle innervation.4

Examples of sensory nerves in the body are the lateral (femoral) cutaneous nerve (LCN) of the thigh (Fig. 3-7), the saphenous nerve, and the interdigital nerves (see later).

• Motor nerves. The motor nerves carry efferents to muscles and return sensation from muscles and associated ligamentous structures. Any nerve that innervates a muscle also mediates the sensation from the joint upon which that muscle acts. Examples of a motor nerve include the suprascapular nerve and the posterior (dorsal) scapular nerve. A hierarchical recruitment pattern exists in the nervous system for muscle recruitment called the law of parsimony.16 The law of parsimony states that the nervous system tends to activate the fewest muscles or muscle fibers possible for the control of a given joint action. This hierarchical pattern of muscle recruitment makes practical sense from an energy perspective.16
• Mixed nerves. A mixed nerve is a combination of skin, sensory, and motor fibers to one trunk. Some examples of a mixed nerve are the median nerve, the ulnar nerve at the elbow as it enters the tunnel of Guyon, the fibular (peroneal) nerve at the knee, and the ilioinguinal nerve.

Cervical Nerves

The eight pairs of cervical nerves are derived from cord segments between the level of the foramen magnum and the middle of the seventh cervical vertebra.17 The spinal nerves from C3 to C7, exiting from the intervertebral foramen, divide into a larger anterior (ventral) ramus and a smaller posterior (dorsal) ramus. The anterior (ventral) ramus of the cervical spinal nerve travels on the transverse process in an anterior–lateral direction to form the cervical plexus and brachial plexus. The posterior (dorsal) ramus of the spinal nerve runs posteriorly around the superior articular process, supplying the facet (zygapophyseal) joint, ligaments, deep muscles, and skin of the posterior aspect of the neck.9

Each nerve joins with a gray communicating ramus from the sympathetic trunk and sends a small, recurrent meningeal branch back into the spinal canal to supply the dura with sensory and vasomotor innervation. It also branches into anterior and posterior primary divisions, which are mixed nerves that pass to their respective peripheral distributions. The motor branches carry a few sensory fibers that convey proprioceptive impulses from the neck muscles.

• Posterior primary divisions. The C1 (suboccipital) nerve is the only branch of the first posterior primary divisions. It is a motor nerve, serving the muscles of the suboccipital triangle, with very few, if any, sensory fibers.17
• Anterior primary divisions. The anterior primary divisions of the first four cervical nerves (C1–4) form the cervical plexus (Fig. 3-8).
  • Cervical plexus (C1–4)
  • Sensory branches (see Fig. 3-6)
• Small occipital nerve (C2,3). This nerve (Fig. 3-8) supplies the skin of the lateral occipital portion of the scalp, the upper median part of the auricle, and the area over the mastoid process.17
• Great auricular nerve (C2,3). This nerve (Fig. 3-8) supplies sensation to the ear and the face via the ascending ramus of the mandible. The nerve lies on or just below the deep layer of the investing fascia of the neck. It arises from the anterior rami of the second and third cervical nerves and emerges from behind the sternomastoid muscle, before ascending on it to cross over the parotid gland.
• Cervical cutaneous nerve (cutaneous coli) (C2,3). This nerve supplies the skin over the anterior portion of the neck.
• Supraclavicular branches (C3,4). These nerves supply the skin over the clavicle and the upper deltoid and pectoral regions, as low as the third rib.
• Communicating branches. The ansa cervicalis nerve (Fig. 3-8) is formed by the junction of two main nerve roots, derived entirely from anterior (ventral) cervical rami. A loop is formed at the point of their anastomosis, and sensory fibers are carried to the dura of the posterior fossa of the skull via the recurrent meningeal branch of the hypoglossal nerve. The communication with the vagus nerve from C1 is of undetermined function.
• Muscular branches. Communication with the hypoglossal nerve from C1 to C2 (Fig. 3-8) carries motor fibers to the geniohyoid and thyrohyoid muscles and to the sternohyoid and sternothyroid muscles by way of the superior root of the ansa cervicalis (Fig. 3-8). The nerve to the thyrohyoid branches from the hypoglossal nerve and runs obliquely across the hyoid bone to innervate the thyrohyoid. The nerve to the superior belly of the omohyoid branches from the superior root (Fig. 3-8) and enters the muscle at a level between the thyroid notch and a horizontal plane 2-cm inferior to the notch. The nerves to the sternohyoid and sternothyroid share a common trunk, which branches from the loop (Fig. 3-8). The nerve to the inferior belly of the omohyoid also branches from the loop (Fig. 3-8). The loop is most frequently located just deep to the site where the superior belly (or tendon) of the omohyoid muscle crosses the internal jugular vein. There is a branch to the sternocleidomastoid muscle from C2, and there are branches to the trapezius muscle (C3–4) via the subtrapezial plexus.

Smaller branches to the adjacent vertebral musculature supply the rectus capitis lateralis and rectus capitis anterior (C1), the longus capitis (C2,4) and longus colli (C1–4), the scalenus medius (C3,4) and scalenus anterior (C4), and the levator scapulae (C3–5).

The phrenic nerve (C3–5) (see Fig. 3-8) passes obliquely over the scalenus anterior muscle and between the subclavian artery and the vein to enter the thorax behind the sternoclavicular joint, where it descends vertically through the superior and middle mediastinum to the diaphragm.17 Motor branches supply the diaphragm. Sensory branches supply the pericardium, the diaphragm, and part of the costal and mediastinal pleurae.

Phrenic nerve involvement has been described in several neuropathies, including critical illness, polyneuropathy, Guillain–Barré syndrome, brachial neuritis, and hereditary motor and sensory neuropathy type 1.24,25 The symptoms depend largely on the degree of involvement, and whether one or both of the nerves are involved.17

• Unilateral paralysis of the diaphragm causes few or no symptoms except with heavy exertion.
• Bilateral paralysis of the diaphragm is characterized by dyspnea upon the slightest exertion and difficulty with coughing and sneezing.24,25
• Phrenic neuralgia, which can result from neck tumors, aortic aneurysm, and pericardial or other mediastinal infections, is characterized by pain near the free border of the ribs, beneath the clavicle, and deep in the neck.24,25

Brachial Plexus

The brachial plexus (Fig. 3-9) arises from the anterior primary divisions of the fifth cervical through the first thoracic nerve roots, with occasional contributions from the fourth cervical and the second thoracic roots. The roots of the plexus, which consist of C5 and C6, join to form the superior (upper) trunk; C7 becomes the middle trunk, and C8 and T1 join to form the inferior (lower) trunks. Each of the trunks divides into anterior and posterior divisions, which then form cords (Fig. 3-9). The anterior divisions of the upper and middle trunk form the lateral cord, the anterior division of the inferior (lower) trunk forms the medial cord, and all three posterior divisions unite to form the posterior cord. The three cords, named for their relationship to the axillary artery, split to form the main branches of the plexus. These branches give rise to the peripheral nerves: musculocutaneous (lateral cord), axillary and radial (posterior cord), ulnar (medial cord), and median (medial and lateral cords).26 Numerous smaller nerves arise from the roots, the trunks, and the cords of the plexus. Peripheral nerve injuries of the upper extremity and their respective clinical findings are listed in Table 3-2.

From the Roots

• The origin of the posterior (dorsal) scapular nerve (C5) frequently shares a common trunk with the long thoracic nerve (Fig. 3-9). The former passes through the scalenus medius anterior internally and posterior laterally, with the presence of some tendinous tissues. Leaving the long thoracic nerve, it often gives branches to the shoulder and the subaxillary region, before the branches join the long thoracic nerve again. The posterior (dorsal) scapular nerve supplies the rhomboids and the levator scapulae muscles. Posterior (dorsal) scapular nerve lesions can result from a forward posture of the head and the neck As this position increases tension in the anterior cervical spine, producing the potential for hypertonicity and hypertrophy of the medial scalene.27 The chief complaint is usually one of scapular pain radiating to the lateral shoulder and arm.
• The long thoracic nerve (C5–7) is purely a motor nerve that originates from the anterior (ventral) rami of the fifth, the sixth, and the seventh cervical roots (Fig. 3-9). It is the sole innervation to the serratus anterior muscle. The fifth and the sixth cervical roots, along with the posterior (dorsal) scapular nerve, pass through the scalenus medius muscle, whereas the seventh cervical root passes anterior to it.28 The nerve then travels beneath the brachial plexus and clavicle to pass over the first rib. From there, it descends along the lateral aspect of the chest wall, where it innervates the serratus anterior muscle. The long thoracic nerve extends as far inferior as the eighth or the ninth rib. Its long and relatively superficial course makes it susceptible to injury from any of the following causes:10,29–31
  • Entrapment of the fifth and the sixth cervical roots, as they pass through the scalenus medius muscle
  • Compression of the nerve during traction to the upper extremity by the undersurface of the scapula, as the nerve crosses over the second rib
  • Compression and traction to the nerve by the inferior angle of the scapula during general anesthesia or with vigorous passive abduction of the arm

Lesions of the long thoracic nerve are common and are the single most common peripheral nerve lesion at the shoulder. The most common cause of long thoracic nerve injury results from carrying a heavy object on the shoulder. Other causes include postinfection, postinjection, postpartum, and postoperative.32 Similar to other peripheral nerve injuries, trauma to the nerve can be caused by a direct blow or a traction force to the nerve. The traction injury can occur when concurrent head rotation away, side bending away, and neck flexion, are coupled with the arm positioned overhead.33–35 Other mechanisms that have been attributed to long thoracic nerve dysfunction include lifting weights overhead, driving a golf ball, and serving a tennis ball.36

The typical clinical presentation includes the following:

• Vague pain in the neck and the scapula region
• An inability to fully elevate the arm overhead
• Shoulder flexion and abduction are weak and limited in AROM due to the loss of the trapezius–serratus anterior force couple. The clinician should note winging of the scapula when testing the serratus anterior.

Conservative intervention includes protection of the serratus anterior with a brace or restraint,32,35,37 galvanic stimulation to the serratus anterior, muscle taping,38 strengthening exercises for the rhomboids, pectoralis, trapezius, and serratus anterior muscles.33,36,39 The average rate of return ranges from 3–7 months28,32 to 2 years.36

• A small branch from C5 passes to the phrenic nerve.
• Smaller branches from C6 to C8 extend to the scaleni and longus colli muscles.
• The first intercostal nerve extends from T1.

From the Trunks

A nerve extends to the subclavius muscle (C5–6) from the superior (upper) trunk, or fifth root. The subclavius muscle acts mainly on the stability of the sternoclavicular joint, with more or less intensity, according to the degree of the clavicular interaction with the movements of the peripheral parts of the superior limb, and seems to act as a substitute for the ligaments of the sternoclavicular joint.40

The suprascapular nerve originates from the superior (upper) trunk of the brachial plexus formed by the roots of C5 and C6 (see Fig. 3-9) at Erb's point.

From the Cords

• The medial and lateral pectoral nerves extend from the medial and lateral cords, respectively (see Fig. 3-9). They supply the pectoralis major and pectoralis minor muscles. The pectoralis major muscle has dual innervation.41 The lateral pectoral nerve (C5–7) is actually more medial in the muscle, travels with the thoracoacromial vessels, and innervates the clavicular and sternal heads. The medial pectoral nerve (C8–T1) shares a course with the lateral thoracic vessels and provides innervation to the sternal and costal heads.42 The main trunk of these nerves can be found near the origin of the vascular supply of the muscle.
• The three subscapular nerves from the posterior cord consist of:
  • The upper subscapular nerve (C5–6), which supplies the subscapularis muscle (see Fig. 3-9).
  • The thoracodorsal nerve, or middle subscapular nerve, which arises from the posterior cord of the brachial plexus with its motor fiber contributions from C6, C7, and C8 (see Fig. 3-9). This nerve courses along the posterior–lateral chest wall, along the surface of the serratus anterior, and deep to the subscapularis, giving rise to branches that supply the latissimus dorsi.
  • The lower subscapular nerve (C5–6) to the teres major and part of the subscapularis muscle (see Fig. 3-9).
• Sensory branches of the medial cord (C8–T143,44 or T1 alone44) comprise the medial cutaneous (antebrachial) nerve to the medial surface of the forearm and the medial cutaneous (brachial) nerve to the medial surface of the arm (see Fig. 3-9).

Obstetric Brachial Plexus Lesions

The pathomorphologic spectrum of traumatic brachial plexus impairments most often includes combinations of various types of injuries: compression of spinal nerves, traction injuries of spinal roots and nerves, and avulsions of spinal roots.45 If the rootlets are traumatically disconnected from the spinal cord, they normally exit the intradural space; in rare cases, however, they may also remain within the dural space.

Brachial plexus injuries are most commonly seen in children and usually are caused by birth injuries. Stretch (neurapraxia or axonotmesis) and incomplete rupture are more common in obstetric brachial plexus palsy than complete rupture or avulsion.

Obstetrical brachial plexus palsy is classified into upper (involving C5, C6, and usually C7 roots), lower (predominantly C8 and T1), and total (C5–C8 and T1) plexus palsies.46,47 Upper brachial plexus palsy, although described first by Duchenne,48 bears the name Erb's palsy.49 Most cases of obstetric brachial plexus palsy involve Erb's palsy, and the lesion is always supraclavicular. Lower brachial plexus palsy is extremely rare in birth injuries44 and is referred to as Klumpke's palsy.50

The infant with Erb's palsy typically shows the classic “waiter's tip” posture of the paralyzed limb.51,52 The arm lies internally rotated at the side of the chest, the elbow is extended (paralysis of C5,6) or slightly flexed (paralysis of C5–C7), the forearm is pronated, and the wrist and the fingers are flexed. This posture occurs because of paralysis and atrophy of the deltoid, biceps, brachialis, and brachioradialis muscles.53

Klumpke's paralysis is characterized by paralysis and atrophy of the small hand muscles and flexors of the wrist (the so-called claw hand). Prognosis of this type is more favorable. If the sympathetic rami of T1 are involved, Horner syndrome (ptosis, enophthalmos, facial reddening, and anhydrosis) may be present.

Peripheral Nerves of the Upper Quadrant

Spinal Accessory Nerve

The spinal accessory, or simply the accessory, nerve is formed by the union of CN XI (see Cranial Nerves) and the spinal nerve roots of C3 and C4, and innervates the trapezius and the sternocleidomastoid (SCM) muscles. Thus dysfunction of the nerve causes paralysis of the SCM and the trapezius muscles.

Isolated lesions to this nerve result from forces acting across the glenohumeral (G-H) joint. Combined lesions of the axillary nerve result from forces acting broadly across the scapulothoracic joint. These lesions are associated with fractures of the clavicle and/or scapula and subclavian vascular lesions.54

The superficial course of the nerve makes it susceptible to injury during operative procedures or blunt trauma.55 The accessory nerve is also vulnerable to stretch-type injuries,56,57 such as during a manipulation of the shoulder under anesthesia.58 However, stretch-type injuries do not always involve the SCM.59 Accessory nerve paresis can also result from serious pathology such as a tumor at the base of the skull, or from surgery.60

Clinical findings for this condition include:

• neck, shoulder, and medial scapular pain;
• decreased cervical lordosis;
• a downwardly rotated scapula;
• winging of the scapula;
• trapezius weakness, especially with active arm elevation.

A confirmatory test includes resisted adduction of the scapula while the clinician applies counterpressure at the medial border of the inferior scapular angle. This will highlight weakness on the affected side.

Conservative intervention for this condition involves patient education to avoid traction to the nerve, specific upper, middle, and lower trapezius strengthening, neuromuscular electrical stimulation to the upper and lower trapezius, cervical proprioceptive neuromuscular facilitation (PNF) techniques, scapular PNF techniques, prone-on-elbows scapular stabilization exercises (see Chap. 25), and shoulder elevation strengthening. McConnell taping is also used to facilitate the middle and lower trapezius muscle.58

Suprascapular Nerve (C5–6)

The suprascapular nerve (Fig. 3-9) travels downward and laterally behind the brachial plexus and parallel to the omohyoid muscle beneath the trapezius to the superior edge of the scapula, through the suprascapular notch. The roof of the suprascapular notch is formed by the transverse scapular ligament. The suprascapular artery and vein initially run with the nerve and then run above the transverse suprascapular ligament over the notch. After passing through the notch, the nerve supplies the suprascapular muscle. It also provides articular branches to the G-H and acromioclavicular (A-C) joints and provides sensory and sympathetic fibers to two-thirds of the shoulder capsule and to the G-H and A-C joints. The nerve then turns around the lateral edge of the scapular spine to innervate the infraspinatus.

It is commonly taught that the suprascapular nerve provides the motor supply to the supraspinatus and infraspinatus muscles and sensory innervation to the shoulder joint but that it has no cutaneous representation. However, cutaneous branches are present in the proximal one-third of the arm,61–63 and their distribution overlaps with that of the supraclavicular and axillary nerves.

There are several ways the suprascapular nerve may be injured. These include compression traction and laceration.64 A direct blow at Erb's point can cause a compression-type injury.64 Compression neuropathy of the suprascapular nerve often occurs in the scapular notch under the transverse scapular ligament or at the spinoglenoid notch. This compression occurs through extraneural inflammation, lipoma or cyst development, scarring following distal clavicle resection, and ligament entrapment.27,33,65,66

Due to the location of this entrapment, entrapment of this nerve may be misdiagnosed as rotator cuff tendonitis, a tear of the rotator cuff, or cervical disk disease.67,68

The cause for this entrapment can be acute trauma resulting from a fall on an outstretched hand (FOOSH), scapular fracture, or overuse injuries involving repetitive overhead motions.65,68,69

As the suprascapular nerve is a mixed nerve, the patient presentation usually includes the following:

• A dull, deep ache at the posterior and lateral aspects of the shoulder, which may have a burning quality.
• Muscle atrophy and weakness of the supraspinatus and infraspinatus.
• Changes in G-H biomechanics with an increase of scapula elevation occurring during arm elevation. This may produce impingement-like findings and complicate the diagnosis.
• Full external rotation of the G-H joint and passive horizontal adduction are painful.266 Electromyography (EMG) is the definitive test for suprascapular neuropathy.70

Conservative intervention includes rest, ice, analgesics, and a series of perineural injections of corticosteroid to help reduce neural inflammation. A home exercise program of scapular pivoter strengthening (see Chap. 16), scapulohumeral coordination exercises (see Chap. 16), and activity-specific training may be indicated.33

Surgical intervention, involving neurolysis, cyst removal, or the excision of the transverse scapular ligament is indicated if symptoms persist.

Musculocutaneous Nerve (C5–6)

The musculocutaneous nerve (Fig. 3-10) is the terminal branch of the lateral cord, which in turn is derived from the anterior division of the upper and middle trunks of the fifth through seventh cervical nerve roots.71,72

The nerve arises from the lateral cord of the brachial plexus at the level of the insertion of the pectoralis minor72,73 and proceeds caudally and laterally, giving one or more branches to the coracobrachialis, before penetrating this muscle 3–8 cm below the coracoid process.72,74 The nerve then courses through, and supplies, the biceps brachii and brachialis muscles, before emerging between the biceps brachii and the brachioradialis muscles 2–5 cm above the elbow (see Fig. 3-11). At this level, now called the lateral cutaneous (antebrachial) nerve of the forearm, it divides into anterior and posterior divisions to innervate the anterior–lateral aspect of the forearm (Fig. 3-10).72

Atraumatic isolated musculocutaneous neuropathies are rare. Reported cases have been associated with positioning during general anesthesia,75 peripheral nerve tumors, and strenuous upper extremity exercise without apparent underlying disease.76–79 Mechanisms proposed for the exercise-related cases include entrapment within the coracobrachialis,76–78 as well as traction between a proximal fixation point at the coracobrachialis and a distal fixation point at the deep fascia at the elbow.72 Injury to this nerve can also result from demanding physical work involving shoulder flexion and repetitive elbow flexion with a pronated forearm.76,79,81 Although rare, an isolated lesion to the musculocutaneous nerve can result in weakness of the biceps, coracobrachialis, and brachialis (Table 3-3). These muscles help stabilize the elbow and the G-H joint50 and maintain the static position of the arm.80

The typical clinical presentation includes:

• reports or evidence of muscle wasting and sensory changes to the lateral side of the forearm;
• weakness of the biceps, brachialis, and coracobrachialis;
• diminished biceps reflex;
• decreased sensation at the lateral forearm; and
• positive EMG study.

Conservative intervention includes cessation of the strenuous activity and a gradual return to activity with resolution of symptoms.79

Axillary Nerve (C5–6)

The axillary nerve is the last nerve of the posterior cord of the brachial plexus before the latter becomes the radial nerve (see Fig. 3-11). The axillary nerve arises as one of the terminal branches of the posterior cord of the brachial plexus, with its neural origin in the fifth and sixth cervical nerve roots. The axillary nerve crosses the anterior–inferior aspect of the subscapularis muscle, where it then crosses posteriorly through the quadrilateral space and divides into two major trunks. Along its course across the subscapular muscle, the axillary nerve releases its first articular branch to the inferior–anterior G-H joint capsule. The posterior trunk of the axillary nerve gives a branch to the teres minor muscle and the posterior deltoid muscle, before terminating as the superior lateral cutaneous (brachial) nerve of the arm (see Fig. 3-11). The anterior trunk continues, giving branches to supply the middle and anterior deltoid muscle.

The axillary nerve is susceptible to injury at several sites, including the origin of the nerve from the posterior cord, the anterior–inferior aspect of the subscapularis muscle and G-H joint capsule, the quadrilateral space, and within the subfascial surface of the deltoid muscle (Table 3-3).

Axillary nerve lesions may result from acute G-H dislocation, surgery to the G-H complex, blunt trauma to the axilla, secondary hematoma and fibrous formation, entrapment, and tractioning.33,81–83

The typical clinical presentation includes:

• deep pain in the axilla, or in the anterior shoulder in the case of a G-H dislocation;
• tingling in the deltoid aspect of the shoulder;
• atrophy may be seen in the deltoid and teres minor;
• weakness when elevating the arm in flexion and abduction;33
• manual muscle testing will reveal weakness of the deltoid and teres minor; and
• sensory testing should highlight a loss of sensation at the lateral deltoid region.

The diagnostic test for this lesion is to ask the patient to abduct the arm to 90 degrees and to bring it back into horizontal extension. A patient with an axillary lesion will demonstrate extreme difficulty with this.84

Intervention for this lesion is initially conservative and consists of thermal modalities, protection, and strengthening exercises.33 Surgical exploration may be indicated in cases of complete denervation.

Radial Nerve (C6–8, T1)

The radial nerve (Fig. 3-12) is the largest branch of the brachial plexus. Originating at the lower border of the pectoralis minor as the direct continuation of the posterior cord, it derives fibers from the last three cervical and first thoracic segments of the spinal cord. During its descent in the arm, the radial nerve accompanies the profunda artery behind, and around, the humerus and in the musculospiral groove. It pierces the lateral intermuscular septum and reaches the lower anterior side of the forearm, where its terminal branches arise.

The radial nerve crosses the elbow immediately anterior to the radial head, just beneath the heads of the extensor origin of the extensor carpi radialis brevis (ECRB), and then divides, with the deep branch running through the body of the supinator muscle to the posterior aspect of the forearm.

The radial nerve in the arm supplies the triceps, the anconeus, and the upper portion of the extensor–supinator group of forearm muscles. In the forearm, the posterior interosseous nerve innervates all of the muscles of the six extensor compartments of the wrist, with the exception of the ECRB and extensor carpi radialis longus (ECRL).

The skin areas supplied by the radial nerve include the posterior cutaneous (brachial) nerve of the arm, to the posterior (dorsal) aspect of the arm; the posterior cutaneous (antebrachial) nerve of the forearm, to the posterior (dorsal) surface of the forearm; and the superficial radial nerve, to the posterior (dorsal) aspect of the radial half of the hand (see Fig. 3-12). The isolated area of supply is a small patch of skin over the posterior aspect of the first interosseous space (see Fig. 3-12).

Four radial nerve entrapments are commonly cited: high radial nerve palsy, posterior interosseous nerve palsy (PINS), radial tunnel syndrome, and superficial radial nerve palsy (see Chap. 17). The major disability associated with radial nerve injury is a weak grip, which is weakened because of poor stabilization of the wrist and the finger joints (Table 3-3). In addition, the patient demonstrates an inability to extend the thumb, the wrist, and the elbow, as well as the proximal phalanges. Pronation of the forearm and adduction of the thumb also are affected, and the wrist and the fingers adopt a position termed wrist drop. The triceps and other radial reflexes are absent, but the sensory loss is often slight, owing to overlapping innervation.

The site of the entrapment of the radial nerve can often be determined by the clinical findings, as follows:

• If the impairment occurs at a point below the triceps innervation, the strength of the triceps remains intact.
• If the impairment occurs at a point below the brachioradialis branch, some supination is retained.
• If the impairment occurs at a point in the forearm, the branches to the small muscle groups, extensors of the thumb, extensors of the index finger, extensors of the other fingers, and extensor carpi ulnaris may be affected.
• If the impairment occurs at a point on the posterior aspect of the wrist, only sensory loss on the hand is affected.

Conservative intervention for a radial nerve lesion depends on the location and the severity. As with all peripheral nerve injuries, every attempt must be made to maintain the appropriate range of the muscle or muscles innervated by the nerve, while helping to prevent contracture in those muscles antagonistic to the denervated muscle by using stretching techniques. In addition, muscle strengthening is prescribed for those uninvolved agonistic and synergistic muscles.

Median Nerve (C5–T1)

The trunk of the median nerve derives its fibers from the lower three (sometimes four) cervical and the first thoracic segment of the spinal cord. Although it has no branches in the upper arm, the nerve trunk descends along the course of the brachial artery and passes onto the anterior aspect of the forearm, where it gives off muscular branches, including the anterior interosseous nerve. It then enters the hand, where it terminates with both muscular and cutaneous branches (Fig. 3-13). The sensory branches of the median nerve supply the skin of the palmar aspect of the thumb and the lateral 2½ fingers as well as the distal ends of the same fingers (see Fig. 3-13).

The anterior interosseous nerve arises from the posterior aspect of the median nerve, approximately 5-cm distal to the medial humeral epicondyle, and passes with the main trunk of the median nerve between the two heads of the pronator teres.26 It continues along the palmar aspect of the flexor digitorum profundus and then passes between the flexor digitorum profundus and the flexor pollicis longus, running in close proximity to the interosseous membrane, to enter the pronator quadratus.26 It provides motor innervation to the flexor pollicis longus; the medial part of flexor digitorum profundus, involving the index and sometimes the middle finger; and to the pronator quadratus. It also sends sensory fibers to the distal radioulnar, radiocarpal, intercarpal, and carpometacarpal joints.85 Variations in the distribution of the nerve have been noted; it may supply all or none of the flexor digitorum profundus and part of the flexor digitorum superficialis.86

The clinical features of median nerve impairment (Table 3-3), depending on the level of injury, include the following17:

• Paralysis is noted in the flexor–pronator muscles of the forearm (resulting in weakness or loss of pronation), all of the superficial palmar muscles, except the flexor carpi ulnaris, and all of the deep palmar muscles, except the ulnar half of the flexor digitorum profundus and the thenar muscles that lie superficial to the tendon of the flexor pollicis longus.
• At the wrist, there is weak flexion and radial deviation, and the hand inclines to the ulnar side.
• In the hand, an ape-hand deformity can be present (see Fig. 3-13). This deformity is associated with
  • an inability to oppose or flex the thumb or abduct it in its own plane;
  • a weakened grip, especially in the thumb and index finger, with a tendency for these digits to become hyperextended, and the thumb adducted;
  • an inability to flex the distal phalanx of the thumb and index finger;
  • weakness of middle finger flexion; and
  • atrophy of the thenar muscles.
• There is a loss of sensation to a variable degree over the cutaneous distribution of the median nerve, most constantly over the distal phalanges of the first two fingers.
• Pain is present in many median nerve impairments anywhere along its distribution.
• Atrophy of the thenar eminence is seen early. Atrophy of the flexor–pronator groups of muscles in the forearm is seen after a few months.
• The skin of the palm is frequently dry, cold, discolored, chapped, and at times keratotic.

The most common condition associated with median nerve entrapment is carpal tunnel syndrome (see Chap. 18). The various interventions for median nerve entrapment are discussed in Chapters 17 and 18.

Ulnar Nerve (C8, T1)

The ulnar nerve is the largest branch of the medial cord of the brachial plexus. It arises from the medial cord of the brachial plexus and contains fibers from the C8 and T1 nerve roots, although C7 may contribute some fibers (Fig. 3-14). The ulnar nerve continues along the anterior compartment of the arm, and it passes through the medial intermuscular septum at the level of the coracobrachialis insertion. As the ulnar nerve passes into the posterior compartment of the arm, it courses through the arcade of Struthers, which is a potential site for its compression.

At the level of the elbow, the ulnar nerve passes posterior to the medial epicondyle, where it passes through the cubital tunnel. From there, the ulnar nerve passes between the two heads of the flexor carpi ulnaris origin and traverses the deep flexor–pronator aponeurosis. This aponeurosis is superficial to the flexor digitorum profundus, but deep to the flexor carpi ulnaris and flexor digitorum superficialis muscles.87,88

The ulnar nerve enters the forearm by coursing posterior to the medial humeral condyle and passing between the heads of the flexor carpi ulnaris, before resting on the flexor digitorum profundus91 (see Fig. 3-14). It then continues distally to the wrist passing between the flexor carpi ulnaris and the flexor digitorum profundus muscles, which it supplies. Proximal to the wrist, the palmar cutaneous branch of the ulnar nerve arises. This branch runs across the palmar aspect of the forearm and the wrist outside of the tunnel of Guyon to supply the proximal part of the ulnar side of the palm. A few centimeters more distally to the tunnel, a posterior (dorsal) cutaneous branch arises and supplies the ulnar side of the dorsum of the hand, the posterior (dorsal) aspect of the fifth finger, and the ulnar half of the forefinger. The ulnar nerve supplies the flexor carpi ulnaris, the ulnar head of the flexor digitorum profundus, and all of the small muscles deep and medial to the long flexor tendon of the thumb, except the first two lumbricales (see Fig. 3-14, indicated by terminal branches in hand). Its sensory distribution includes the skin of the little finger and the medial half of the hand and the ring finger (see Fig. 3-14).

The clinical features of ulnar nerve impairment (Table 3-3) include the following17:

• Claw hand (see Fig. 3-14), resulting from unopposed action of the extensor digitorum communis in the fourth and fifth digits.
• An inability to extend the second and distal phalanges of any of the fingers.
• An inability to adduct or abduct the fingers, or to oppose all the fingertips, as in making a cone with the fingers and the thumb.
• An inability to adduct the thumb.
• At the wrist, flexion is weak and ulnar deviation is lost. The ulnar reflex is absent.
• Atrophy of the interosseous spaces (especially the first) and of the hypothenar eminence.
• A loss of sensation on the ulnar side of the hand and ring finger and, most markedly, over the entire little finger.
• Partial lesions of the ulnar nerve may produce only motor weakness or paralysis of a few of the muscles supplied by the nerve. Lesions that occur in the distal forearm or at the wrist spare the deep flexors and the flexor carpi ulnaris.

The conservative interventions for the various ulnar nerve entrapments are discussed in Chapters 17 and 18.

Thoracic Nerves

In the thoracic region, there is great variability in the topography of the nerves and the structures that they serve.92 Typically, the spinal root arises from the lateral end of the spinal nerve but, in 25% of cases, the spinal root is made up of two parts that arise from the superior border of the spinal nerve.93 The thoracic spinal nerves are segmented into posterior (dorsal) primary and anterior (ventral) primary divisions. As elsewhere, the dermatomes of this region are considered to represent the cutaneous region innervated by one spinal nerve through both of its rami.94

Anterior (Ventral) Rami

There are 12 pairs of thoracic anterior (ventral) rami. The anterior (ventral) rami (anterior branches) from T2 through T11 become intercostal nerves. The 12th anterior (ventral) ramus, the subcostal nerve, is located below the last rib. The intercostal nerve has a lateral branch, providing sensory distribution to the skin of the lateral aspect of the trunk, and an anterior branch, supplying the intercostal muscles, parietal pleura, and the skin over the anterior aspect of the thorax and the abdomen. All of the intercostal nerves mainly supply the thoracic and the abdominal walls, with the upper two also supplying the upper limb. The thoracic anterior (ventral) rami of T3–6 supply only the thoracic wall, whereas the lower five rami supply both the thoracic and the abdominal walls. The subcostal nerve supplies both the abdominal wall and the gluteal skin.

Each anterior (ventral) ramus is connected with an adjacent sympathetic ganglion by gray and white rami communicantes (Fig. 3-15). The communicating rami are branches of the spinal nerves that transmit sympathetic autonomic fibers to and from the sympathetic chain of ganglia. The fibers pass from spinal nerve to chain ganglia through the white ramus and in the reverse direction through the gray. In the cervical, lower lumbar, and sacral levels, only gray rami are present and function to convey fibers from the sympathetic chain to the spinal nerves, a mechanism that ensures that all spinal nerves contain sympathetic fibers.

From each intercostal nerve, a collateral and lateral cutaneous branch leave before the main nerve reaches the costal angle. The intercostobrachial nerve arises from the lateral–collateral branch of the second intercostal nerve, pierces the intercostal muscles in the midaxillary line, and then traverses the central portion of the axilla, where a posterior axillary branch gives sensation to the posterior axillary fold. From here, the nerve passes into the upper arm along the posterior–medial border to supply the skin of this region95 and to connect with the posterior cutaneous branch of the radial nerve.

Posterior (Dorsal) Rami

The distribution of all posterior (dorsal) rami is similar. The thoracic posterior (dorsal) rami travel posteriorly, close to the vertebral zygapophysial joints, before dividing into medial and lateral branches:

• The medial branches supply the short, medially placed back muscles (the iliocostalis thoracis, spinalis thoracis, semispinalis thoracis, thoracic multifidus rotatores thoracis, and intertransversarii muscles) and the skin of the back as far as the midscapular line. The medial branches of the upper six thoracic posterior (dorsal) rami pierce the rhomboids and trapezius, reaching the skin in close proximity to the vertebral spines, which they occasionally supply.
• The lateral branches supply smaller branches to the sacrospinalis muscles. The lateral branches increase in size the more inferior they are. They penetrate, or pass, the longissimus thoracis to the space between it and the iliocostalis cervicis, supplying both these muscles, as well as the levatores costarum. The 12th thoracic lateral branch sends a filament medially along the iliac crest, which then passes down to the anterior gluteal skin.

As mentioned previously, the recurrent meningeal or sinuvertebral nerve is functionally also a branch of the spinal nerve. This nerve passes back into the vertebral canal through the intervertebral foramen, supplying the anterior aspect of the dura mater, outer third of the annular fibers of the intervertebral disks, vertebral body, and the epidural blood vessel walls, as well as the posterior longitudinal ligament.96

The thoracic nerves may be involved in the same types of impairments that affect other peripheral nerves. A loss of function of one, or more, of the thoracic nerves may produce partial or complete paralysis of the abdominal muscles and a loss of the abdominal reflexes in the affected quadrants. With unilateral impairments of the nerve, the umbilicus usually is drawn toward the unaffected side when the abdomen is tensed (Beevor sign), indicating a paralysis of the lower abdominal muscles as a result of a lesion at the level of the 10th thoracic segment.

A specific syndrome, called the T4 syndrome,97–99 has been shown to cause vague pain, numbness, and paresthesia in the upper extremity and generalized posterior head and neck pain.

Lumbar Plexus

The lumbar plexus (Fig. 3-16) is formed from the anterior (ventral) nerve roots of the second, third, and fourth lumbar nerves (in approximately 50% of cases, the plexus also receives a contribution from the last thoracic nerve), as they lie between the quadratus lumborum muscle and the psoas muscle. It then travels anteriorly into the body of the psoas muscle to form the LCN, femoral, and obturator nerves.

L1, L2, and L4 divide into upper and lower branches (see Fig. 3-16). The upper branch of L1 forms the iliohypogastric and ilioinguinal nerves. The lower branch of L1 joins the upper branch of L2 to form the genitofemoral nerve (see Fig. 3-16). The lower branch of L4 joins L5 to form the lumbosacral trunk. Peripheral nerve entrapment syndromes of the lower extremity are listed in Table 3-4.

• Iliohypogastric nerve (T12, L1) (seeFig. 3-17). This nerve emerges from the upper lateral border of the psoas major and then passes laterally around the iliac crest between the transversus abdominis and internal oblique muscles, before dividing into lateral and anterior cutaneous branches. The lateral (iliac) branch supplies the skin of the upper lateral part of the thigh, while the anterior (hypogastric) branch descends anteriorly to supply the skin over the symphysis.
• Ilioinguinal nerve (L1) (seeFig. 3-17). This nerve is smaller than the iliohypogastric nerve. It emerges from the lateral border of the psoas major to follow a course slightly inferior to that of the iliohypogastric, with which it may anastomose. It pierces the internal oblique, which it supplies before emerging from the superficial inguinal ring to supply the skin of the upper medial part of the thigh and the root of the penis and scrotum or mons pubis and labium majores. An entrapment of this nerve results in pain in the groin region, usually with radiation down to the proximal inner surface of the thigh, sometimes aggravated by increasing tension on the abdominal wall through standing erect.
• Genitofemoral nerve (L1,2) (seeFig. 3-17). This nerve descends obliquely and anteriorly through the psoas major before emerging from the anterior surface of the psoas and dividing into genital and femoral branches. The genital branch supplies the cremasteric muscle and the skin of the scrotum or labia, whereas the femoral branch supplies the skin of the middle upper part of the thigh and the femoral artery.

Collateral muscular branches supply the quadratus lumborum and intertransversarii from L1 and L4, and the psoas muscle from L2 and L3 (Fig. 3-17). The lower branch of L2, all of L3, and the upper branch of L4 split into a small anterior and a large posterior division (see Fig. 3-16). The three anterior divisions unite to form the obturator nerve; the three posterior divisions unite to form the femoral nerve, and the LCN (see Fig. 3-16).

Femoral Nerve (L2–4)

The femoral nerve, the largest branch of the lumbar plexus, arises from the lateral border of the psoas just above the inguinal ligament. The nerve descends beneath this ligament to enter the femoral triangle on the lateral side of the femoral artery, where it divides into terminal branches. Above the inguinal ligament, the femoral nerve supplies the iliopsoas muscle, and, in the thigh, it supplies the sartorius, pectineus, and quadriceps femoris muscles.

The sensory distribution of the femoral nerve includes the anterior and medial surfaces of the thigh via the anterior femoral cutaneous nerve and the medial aspect of the knee, the proximal leg, and articular branches to the knee via the saphenous nerve (Fig. 3-18), the largest cutaneous branch of the femoral nerve. The saphenous nerve exits from the adductor (Hunter's, or subsartorial) canal, descends under the sartorius muscle, and then winds around the posterior edge of the sartorius muscle at its tendon portion.

• The infrapatellar branch pierces the sartorius muscle and courses anteriorly to the infrapatellar region.
• The descending branch passes down the medial aspect of the leg and, at the lower third of the leg, divides into two branches. One of the branches of the descending portion of the saphenous nerve courses along the medial border of the tibia and ends at the ankle, while the other branch passes anterior to the ankle and is distributed to the medial aspect of the foot, sometimes reaching as far as the metatarsophalangeal joint of the great toe.

Entrapment of the saphenous nerve often results in marked pain at the medial aspect of the knee.

Femoral nerve palsy has been reported after acetabular fracture, cardiac catheterization, total hip arthroplasty, or anterior lumbar spinal fusion, and spontaneously in hemophilia.100–102

Obturator Nerve (L2–4)

The obturator nerve (see Fig. 3-18) arises from the second, third, and fourth lumbar anterior divisions of the lumbar plexus and emerges from the medial border of the psoas, near the brim of the pelvis. It then passes behind the common iliac vessels on the lateral side of the hypogastric vessels and the ureter and descends through the obturator canal in the upper part of the obturator foramen to the medial side of the thigh. While in the foramen, the obturator nerve splits into anterior and posterior branches.

• The anterior division of the obturator nerve gives an articular branch to the hip joint near its origin. It descends anterior to the obturator externus and adductor brevis deep to the pectineus and adductor longus and supplies muscular branches to the adductors longus and brevis, the gracilis, and, rarely, to the pectineus.95 The anterior division divides into numerous named and unnamed branches, including the cutaneous branches to the subsartorial plexus and directly to a small area of skin on the middle internal part of the thigh, vascular branches to the femoral artery, and communicating branches to the femoral cutaneous and accessory obturator nerves.
• The posterior division of the obturator nerve pierces the anterior part of the obturator externus, which it supplies, and descends deep to the adductor brevis. It also supplies the adductors magnus and brevis (if it has not received supply from the anterior division) and gives an articular branch to the knee joint (see Fig. 3-18).

The obturator nerve may be involved by the same pathologic processes that affect the femoral nerve. Disability is usually minimal, although external rotation and adduction of the thigh are impaired, and crossing of the legs is difficult. The patient may also complain of severe pain, which radiates from the groin down the inner aspect of the thigh (see Fig. 3-18).104,105

LCN of the Thigh

The LCN of the thigh (Fig. 3-7) is purely sensory and is derived primarily from the second and third lumbar nerve roots, with occasional contributions from the first lumbar nerve root.106,107 Sympathetic afferent and efferent fibers are also contained within the nerve.108 The nerve leaves the lumbar plexus and normally appears at the lateral border of the psoas, just proximal to the crest of the ilium. From here, it courses laterally across the anterior surface of the iliacus (covered by iliac fascia) and approaches the lateral portion of the inguinal ligament posterior to the deep circumflex iliac artery. The nerve usually crosses beneath the inguinal ligament, just inferior–medial to the anterior superior iliac spine.109 The site at which the LCN exits the pelvis varies. Meralgia paresthetica (see Table 3-4), the term used to describe LCN entrapment, has been reported with each of the five known variants as follows110:

• The split lateral attachment of the inguinal ligament. As the nerve curves medially and inferiorly around the anterior superior iliac spine, it may be subjected to repetitive trauma in this osteofibrous tunnel.111
• The nerve may pass posterior to the inguinal ligament and anterior to a sharp ridge of iliacus fascia, which can lead to a bowstring deformity of the nerve when the patient is supine.112
• Occasionally, the LCN enters the thigh within or beneath the substance of the sartorius muscle.113
• Several cases have been reported in which the LCN crosses over the iliac crest lateral and posterior to the anterior superior iliac spine. The nerve typically lies in a groove in the ilium and is subject to pressure from tight garments or belts.112,113
• The nerve may exit the pelvis in multiple branches, with entrapment of a single branch.114
• Alternatively, the nerve may be absent, with a branch from the femoral nerve arising below the inguinal ligament, or it may be replaced by the ilioinguinal nerve.115

Sacral Plexus

The lumbosacral trunk (L4,5) descends into the pelvis, where it enters the formation of the sacral plexus. The sacral plexus (Fig. 3-16) is formed by the anterior (ventral) rami of the L4 and L5 and the S1 through S4 nerves and lies on the posterior wall of the pelvis, anterior to the piriformis and posterior to the sigmoid colon, ureter, and hypogastric vessels in front. The L4 and L5 nerves join medial to the sacral promontory, becoming the lumbosacral trunk. The S1 through S4 nerves converge with the lumbosacral trunk in front of the piriformis muscle, forming the broad triangular band of the sacral plexus. The superior (upper) three nerves of the plexus divide into two sets of branches: the medial branches, which are distributed to the multifidi muscles, and the lateral branches, which become the medial cluneal nerves. The medial cluneal nerves supply the skin over the medial part of the gluteus maximus. The lower two posterior primary divisions, with the posterior division of the coccygeal nerve, supply the skin over the coccyx.

Collateral Branches of the Posterior Division

Superior Gluteal Nerve

The roots of the superior gluteal nerve (L4,5; S1) arise within the pelvis from the sacral plexus (see Fig. 3-16) and enter the buttock through the greater sciatic foramen, above the piriformis. The nerve runs laterally between gluteus medius and gluteus minimus, which it innervates before terminating in the tensor fascia lata, which it also supplies. Because the nerve passes between the gluteal muscles, it is at risk during surgery on the hip.116

Inferior Gluteal Nerve

The inferior gluteal nerve (L5; S1,2) passes below the piriformis muscle and through the greater sciatic foramen and travels to the gluteus maximus muscle (see Fig. 3-16). Nerves to the piriformis consist of short smaller branches from S1 and S2.

Superior Cluneal Nerve

The medial branch of the superior cluneal nerve passes superficially over the iliac crest, where it is covered by two layers of dense fibrous fascia. When the medial branch of the superior cluneal nerve passes through the fascia against the posterior iliac crest and the osteofibrous tunnel consisting of the two layers of the fascia and the superior rim of the iliac crest, the possibility of irritation or trauma to the nerve is increased, making this a potential site of nerve compression or constriction.117

Posterior Cutaneous (Femoral) Nerve of the Thigh

The posterior cutaneous (femoral) nerve (PCN) of the thigh constitutes a collateral branch, with roots from both the anterior and the posterior divisions of S1 and S2 and the anterior divisions of S2 and S3 (Fig. 3-16). Perineal branches pass to the skin of the upper medial aspect of the thigh and the skin of the scrotum or labium majores. Despite its close proximity to the sciatic nerve, however, injury to the PCN of the thigh is quite rare.

Collateral Branches of the Anterior Division

Collateral branches from the anterior divisions extend to the quadratus femoris and gemellus inferior muscles (from L4, L5, and S1) and to the obturator internus and gemellus superior muscles (from L5, S1, and S2).

Sciatic Nerve

The sciatic nerve (Fig. 3-19) is the largest nerve in the body. It arises from the L4, L5, and S1 through S3 nerve roots as a continuation of the lumbosacral plexus. The nerve is composed of the independent tibial (medial) and common fibular (peroneal) (lateral) divisions, which are usually united as a single nerve down to the lower portion of the thigh. The tibial division is the larger of the two divisions. Although grossly united, the funicular patterns of the tibial and common fibular (peroneal) divisions are distinct, and there is no exchange of bundles between them. The common fibular (peroneal) nerve is formed by the upper four posterior divisions (L4,5; S1,2) of the sacral plexus, and the tibial nerve is formed from all five anterior divisions (L4,5; S1–3).

The sciatic nerve usually exits the pelvis through the anterior third of the greater sciatic foramen.118 Also running through the greater sciatic foramen is the superior gluteal artery, the largest branch of the internal iliac artery, and its accompanying vein.

Numerous variations have been described for the course of the sciatic nerve, including cases in which the sciatic nerve passes through the piriformis, and cases in which the tibial division passes below the piriformis while the common fibular (peroneal) division passes above or through the muscle. It seems that the tibial division always enters the gluteal region below the piriformis, and the variability is in the course of the common fibular (peroneal) division. Typically, the sciatic nerve descends along the posterior surface of the thigh to the popliteal space, where it usually terminates by dividing into the tibial and common fibular (peroneal) nerves (see Fig. 3-19). Innervation for the short head of the biceps femoris comes from the common fibular (peroneal) division, the only muscle innervated by this division above the knee. Rami from the tibial trunk pass to the semitendinosus and the semimembranosus muscles, the long head of the biceps femoris, and the adductor magnus muscle.

In most reports of sciatic nerve injury, regardless of the cause, the common fibular (peroneal) division is involved more frequently and often suffers a greater degree of damage than the tibial division; its susceptibility to injury being related to several anatomic features.

Injury to the sciatic nerve may result indirectly from a herniated intervertebral disk (protruded nucleus pulposus) or more directly from a hip dislocation, local aneurysm, or direct external trauma of the sciatic notch, the latter of which can be confused with a compressive radiculopathy of the lumbar or sacral nerve root.119 Following are some useful clues to help distinguish the two conditions:

• Pain from an irritated lumbar spinal nerve root (radiculopathy) should not significantly change with the introduction of hip rotation during the straight leg raise test (Chap. 11), whereas if there is a sciatic nerve entrapment by the piriformis muscle, pain is likely to be accentuated by introducing hip internal rotation, which stretches the muscle fibers, and relieved by moving the hip into external rotation.
• Sciatic neuropathy produces sensory changes on the sole of the foot, whereas lumbosacral radiculopathy generally does not, unless there is a predominant S1 involvement.
• Compressive radiculopathy below the L4 level causes palpable atrophy of the gluteal muscles, whereas a sciatic entrapment spares these muscles.
• The sciatic trunk is frequently tender from root compression at the foraminal level, whereas it is not normally tender in a sciatic nerve entrapment.120

Individual case reports of bone and soft-tissue tumors along the course of the sciatic nerve have been described as a rare cause of sciatica.121,122

Tibial Nerve

The tibial nerve (L4,5; S1–3) is formed by all five of the anterior divisions of the sacral plexus, thus receiving fibers from the lower two lumbar and the upper three sacral cord segments. Inferiorly, the nerve begins its own course in the upper part of the popliteal space, before descending vertically through this space, and passing between the heads of the gastrocnemius muscle, to the dorsum of the leg. The portion of the tibial trunk below the popliteal space is called the posterior tibial nerve; the portion within the space is called the internal popliteal nerve (Fig. 3-20). The tibial nerve supplies the gastrocnemius, plantaris, soleus, popliteus, tibialis posterior, flexor digitorum longus, and flexor halluces longus muscles (see Fig. 3-20).

Sural Nerve

The sural nerve (see Fig. 3-20) is a sensory branch of the tibial nerve. It is formed by the lateral sural cutaneous nerve from the common fibular (peroneal) nerve and the medial calcaneal nerve from the tibial nerve. The sural nerve supplies the skin on the posterior–lateral aspect of the lower one-third of the leg and the lateral side of the foot.

Terminal Branches of the Tibial Nerve

In the distal leg, the tibial nerve lies laterally to the posterior tibial vessels, and it supplies articular branches to the ankle joint and to the posterior–medial aspect of the ankle. From this point, its terminal branches include the following:

• Medial plantar nerve (comparable to the median nerve in the hand). This nerve supplies the flexor digitorum brevis, abductor halluces, flexor halluces brevis, and first lumbrical muscles and sensory branches to the medial side of the sole, the plantar surfaces of the medial 3½ toes, and the terminal ends of the same toes (see Fig. 3-20).
• Lateral plantar nerve (comparable to the ulnar nerve in the hand). This nerve supplies the small muscles of the foot, except those innervated by the medial plantar nerve, and sensory branches to the lateral portions of the sole, the plantar surface of the lateral 1½ toes, and the distal phalanges of these toes (see Fig. 3-20). The interdigital nerves are most commonly entrapped between the second and third and the third and fourth web spaces and the intermetatarsal ligaments as a result of a forced hyperextension of the toes, eventually resulting in an interdigital neuroma.
• Medial calcaneal nerve. As it passes beneath the flexor retinaculum, the tibial nerve gives off medial calcanean branches to the skin of the heel. An irritation of this nerve may result in heel pain.

Common Fibular (Peroneal) Nerve

The common fibular (peroneal) nerve (L4,5; S1–2) is formed by a fusion of the upper four posterior divisions of the sacral plexus, and thus derives its fibers from the lower two lumbar and the upper two sacral cord segments (see Fig. 3-21). In the thigh, it is a component of the sciatic nerve as far as the upper part of the popliteal space. The nerve gives off sensory branches in the popliteal space. These sensory branches include the superior and inferior articular branches to the knee joint and the lateral sural cutaneous nerve (see Fig. 3-20 and 3-21).

At the apex of the popliteal fossa, the common fibular (peroneal) nerve begins its independent descent along the posterior border of the biceps femoris and then crosses the dorsum of the knee joint to the upper external portion of the leg near the head of the fibula. The nerve curves around the lateral aspect of the fibula toward the anterior aspect of the bone, before passing deep to the two heads of the fibularis (peroneus) longus muscle, where it divides into three terminal rami: the recurrent articular, superficial, and deep fibular (peroneal) nerves.

• The recurrent articular nerve accompanies the anterior tibial recurrent artery, supplying the tibiofibular and knee joints, and a twig to the tibialis anterior muscle.
• The superficial fibular (peroneal) nerve arises deep to the fibularis (peroneus) longus (see Fig. 3-21). It then passes forward and downward between the peronei and the extensor digitorum longus muscles, to supply the fibularis (peroneus) longus and brevis muscles and provide sensory distribution to the lower front of the leg, the dorsum of the foot, part of the big toe, and adjacent sides of the second to fifth toes up to the second phalanges. When this nerve is entrapped, because it causes pain over the lateral distal aspect of the leg and the ankle, it is often confused with an intervertebral disk herniation involving the L5 nerve root.
• The deep fibular (peroneal) nerve passes anterior and lateral to the tibialis anterior muscle, between the fibularis (peroneus) longus and the extensor digitorum longus muscles, and to the front of the interosseous membrane and supplies the tibialis anterior, extensor digitorum longus, extensor halluces longus, and fibularis (peroneus) tertius muscles (see Fig. 3-21). At the level of the ankle joint, the deep fibular (peroneal) nerve passes behind the extensor halluces longus tendon and lies between it and the extensor digitorum longus tendon. The deep fibular (peroneal) nerve divides into a medial and lateral branch approximately 1.5 cm above the ankle joint. These terminal branches extend to the skin of the adjacent sides of the medial two toes (medial branch), to the extensor digitorum brevis muscle (lateral branch), and the adjacent joints (see Fig. 3-21). When the deep fibular (peroneal) nerve is entrapped, there is a complaint of pain in the great toe, which can be confused with a posttraumatic, sympathetic dystrophy.

An insidious entrapment of the common fibular (peroneal) nerve (and it is very vulnerable, especially at the fibula neck) can be confused with symptoms of a herniated intervertebral disk, tendonitis of the popliteus tendon, mononeuritis, idiopathic fibular (peroneal) palsy, intrinsic and extrinsic nerve tumors, and extraneural compression by a synovial cyst, ganglion cyst, soft-tissue tumor, osseous mass, or a large fabella.123 Traumatic injury of the nerve may occur secondary to a fracture, dislocation, surgical procedure, application of skeletal traction, or a tight cast.123

The pain from an entrapment of the common fibular (peroneal) nerve is typically on the lateral surface of the knee, the leg, and the foot. Lateral knee pain is a common problem among patients seeking medical attention, and entrapment of the common fibular (peroneal) nerve is frequently overlooked in the differential diagnostic considerations, especially in the absence of trauma or the presence of a palpable mass at the neck of the fibula.

Pudendal and Coccygeal Plexuses

The pudendal and coccygeal plexuses are the most caudal portions of the lumbosacral plexus and supply nerves to the perineal structures (Fig. 3-22).

• The pudendal plexus supplies the coccygeus, levator ani, and sphincter ani externus muscles. The pudendal nerve is a mixed nerve, and a lesion that affects it or its ascending pathways can result in voiding and erectile dysfunctions.124 A lesion in the afferent pathways of the pudendal nerve is often suspected clinically by suggestive patient histories, including organic neurologic disease or neurologic trauma. Lesions are also suspected when a neurologic physical examination to assess the function of signal segments S2, S3, and S4 is abnormal. The pudendal nerve divides into
  • the inferior hemorrhoidal nerves to the external anal sphincter and adjacent skin;
  • the perineal nerve; and
  • the posterior (dorsal) nerve of the penis.
• The nerves of the coccygeal plexus are the small sensory anococcygeal nerves derived from the last three segments (S4,5; C). They pierce the sacrotuberous ligament and supply the skin in the region of the coccyx.

Autonomic Nervous System

The autonomic system is the division of the peripheral nervous system that is responsible for the innervation of smooth muscle, cardiac muscle, and glands of the body. It functions primarily at a subconscious level.

The autonomic nervous system has two components, sympathetic (Fig. 3-23) and parasympathetic (Fig. 3-24), each of which is differentiated by its site of origin as well as the transmitters it releases.125 In general, these two systems have antagonist effects on their end organs.

The sympathetic system can be involved in the modulation of pain, although under normal conditions, the sympathetic system has little or no effect on the activity of the peripheral afferent receptors. According to Blumberg and Janig,126 the afferent neurons become hypersensitized as the result of direct trauma, producing allodynia, causalgia (complex regional pain syndrome type 1), and hyperalgesia.127 Sensitized posterior (dorsal) horn neurons increase their receptive fields and begin to respond to both low- and high-threshold peripheral stimuli.127,128

A lesion to the sympathetic system has also been associated with Horner syndrome (see later discussion) and with Raynaud disease, a disorder of the peripheral vascular system.

Neuromuscular Control

Neuromuscular control involves the integration of motor learning and motor control which is controlled by the descending motor systems. These systems include the corticospinal tracts, the rubrospinal tract, the vestibulospinal tracts, and the reticulospinal tracts:

• Corticospinal tract: critical for skilled voluntary movement throughout the body.129,130 There are two main divisions of the corticospinal tract, the lateral corticospinal tract and ventral (anterior) corticospinal tract. Most of the corticospinal fibers (approximately 80%) cross over to the contralateral side in the medulla oblongata (pyramidal decussation) and travel in the lateral corticospinal tract. 10% enter the lateral corticospinal tract on the same side. The remaining 10% cross over at the level that they exit the spinal cord, and these travel in the anterior corticospinal tract.
• Rubrospinal tract: important for rapid, coordinated movement of the entire limb, especially when the reach involves adapting the hand or foot to the shape of an object.131
• Vestibulospinal tracts: involved with integrating information from the vestibular system to control eye movements, head and neck movements, and postural reactions for balance.
• Reticulospinal tracts: activated in the early stages of movement, including movement planning, to help initiate the proper state in the postural control system and the proximal limb to support the distal movement that is to occur.132

Mobility and stability rely upon the combination of musculoskeletal properties and neural control. It is believed that there are certain programs for movement patterns that are inherent in the CNS and that these naturally develop during the maturation process of the CNS. For example, gait on a level surface is controlled by a set of neural circuits known as a central pattern generator (CPG). The locomotion-initiating systems in the brain stem rely upon the reticulospinal tracts as the principal route for initiation and regulation of locomotion.133 The parameters of gait (e.g., cadence) depend on the environmental demands. When walking must occur on unusual surfaces, the CPG continues to operate but with input from the lateral corticospinal and rubrospinal systems to translate the visual perception and allow accurate placement of the foot.134,135

In much the same way as there is a CPG for locomotion, the nervous system has a number of built-in corrections for postural stability—the ability to maintain a stable upright stance against internal and external perturbations—that can occur rapidly and automatically to counteract these perturbations (see Balance, later). Once a CPG is formed, the individual no longer has to concentrate on performing the activity, but can do so with very little cortical involvement. The motor program for each of these activities is saved in an engram (a hypothetical means by which a patterned response has been stabilized at the level of unconscious competence) within the cerebral cortex.136–138 Thousands of repetitions (practice) are required to begin the engram formation and millions are needed to perfect it.138 Skilled performance is developed in proportion to the number of repetitions of an engram practiced just below the maximal level of ability to perform.139,140

The remaining motor responses rely on processing and planning at different levels: spinal cord, the brainstem and cerebellum, and the cerebral cortex. The complexity of the necessary processing affects the speed of motor responses, with spinal reflexes representing the shortest neuronal pathway and consequently the most rapid response to afferent stimuli. Certain actions, such as signing one's name, do not require sensory information for modification. These movements are said to be under open-loop control. Other movements, such as reflexively withdrawing the foot from a painful stimuli, rely on feedback from the sensory system. This type of control is referred to as closed-loop control. In a feedback (reactionary) control system, parameters are monitored and compared to a reference set point. If monitored parameters fall outside the boundaries of the set point, the controller triggers a response that will correct the system (e.g., a thermostat system that regulate room temperature).141 In contrast, feedforward (anticipatory) actions differ in that they anticipate pending disturbances and act to prepare the system (e.g., an individual anticipates the need for new car and buys one before the existing car breaks down).141 Feedforward actions are based on knowledge or previous experience. Evidence suggests that both feedforward and feedback control mechanisms contribute to dynamic stability.142 Through feedforward and feedback controls, the sensorimotor system provides the direction that muscles require to achieve integrated multiplanar movements.141

A patient cannot succeed in functional and recreational activities if his or her neuromuscular system is not prepared to meet the demands of the specific activities.145 Two key components involved in neuromuscular control are proprioception and kinesthesia.

Proprioception

Proprioception is considered a specialized variation of the sensory modality of touch, which plays an important role in coordinating muscle activity and involves the integration of sensory input concerning static joint position (joint position sensibility), joint movement (kinesthetic sensibility), velocity of movement, and the force of muscular contraction from the skin, muscles, and joints.146,147 Proprioception can be both conscious, as occurs in the accurate placement of a limb, and unconscious, as occurs in the modulation of muscle function.147,148

All synovial joints of the body are provided with an array of receptor endings (nociceptors, thermoreceptors, and mechanoreceptors) imbedded in articular, muscular, and cutaneous structures with varying characteristic behaviors and distributions (Table 3-1). These receptors provide information for the somatosensory system which mediates signals related to multiple sensory modalities (pain, temperature, and proprioception). The nociceptors provide information with regard to pain, while the thermoreceptors provide feedback related to temperature. The mechanoreceptors, which are stimulated by mechanical forces (soft-tissue elongation, relaxation, compression, and fluid tension), are usually classified into three groups based on receptor type: joint, muscle, or cutaneous. There is no evidence as yet that cutaneous receptors contribute to dynamic joint stability. There are four primary types of joint receptors that include Pacinian corpuscles, Ruffini endings, Golgi tendon organ (GTO)-like endings, and bare nerve endings.17,149,150

• Ruffini endings. These slow-adapting, low-threshold stretch receptors are important postural mediators, signaling actual joint position or changes in joint positions.155 They are primarily located on the flexion side (detect the stretch with extension of the joint) of the joint capsule, but are also found in ligaments, primarily near the origin and the insertion.144,156 These slowly adapting receptors continue to discharge while the stimulus is present and contribute to reflex regulation of postural tone, to coordination of muscle activity, and to a perceptional awareness of joint position. An increase in joint capsule tension by active or passive motion, posture, mobilization, or manipulation causes these receptors to discharge at a higher frequency.150,157
• Pacinian corpuscles. These rapidly adapting, low-threshold receptors function primarily in sensing joint compression and increased hydrostatic pressure in the joint.158 They are primarily located in the subcapsular fibroadipose tissue, the cruciate ligaments, the anulus fibrosus, ligaments, and the fibrous capsule. These receptors are entirely inactive in immobile joints but become active for brief periods at the onset of movement and during rapid changes in tension. They also fire during active or passive motion of a joint, or with the application of traction. This behavior suggests their role as a control mechanism to regulate motor unit activity of the prime movers of the joint.
• GTO-like receptors. These receptors, also referred to as Golgi ligament organs, are found in the joint capsule, ligaments, and menisci.159 These slow-adapting and high-threshold receptors function to detect large amounts of tension. They only become active in the extremes of motion such as when strong manual techniques are applied to the joint. Their function is protective; to prevent further motion that would over displace the joint (a joint protective reflex), and their firing is inhibitory to those muscles that would contribute to excessive forces.
• Bare nerve endings. These high-threshold, nonadapting, free nerve ending receptors are inactive in normal circumstances but become active with marked mechanical deformation or tension.160,161 They may also become active in response to direct mechanical or chemical irritation, and their sensitivity usually increases when joints are inflamed or swollen.162

Thus, the CNS is organized in a hierarchical and parallel fashion with the cortical centers of the brain being the location of the most complex processing, and the spinal cord being the location of the most basic processing.144 At the upper end of the hierarchy, the motor cortex has a motor program, defined as an abstract plan of movement that, when initiated, results in the production of a coordinated movement sequence.141,143 At the lower end of the hierarchy, specific motor units must contract to accomplish the movement. Rapid motor responses to somatosensory feedback mediated in the spinal cord are referred to as spinal reflexes.144 These reflex actions include preparatory postural adjustments163 and reaction movements. The former are preprogrammed neural mechanisms. The latter occur too fast for the long loop feedback of the CNS so that they are automatic and occur subconsciously (see Supraspinal reflexes later). Although the hierarchy is well established, research suggests these components also work in parallel so that any of the components may predominate in controlling some aspects of movement; the system is built for efficiency and redundancy.141

Proprioceptive information is relayed to the cerebral cortex by one of the two major ascending systems, the dorsal column and the spinothalamic tract. Once processed and evaluated, the proprioceptive information is capable of influencing muscle tone, motor execution programs, and cognitive somatic perceptions or kinesthetic awareness.151,165 All of this information helps generate a somatosensory image within the CNS.151

The ability of a joint to remain stable depends in part on its resistance to motion when subjected to external loads, referred to as its degree of stiffness. A joint's stiffness is the result of three components: passive factors associated with the material properties of the musculotendinous tissues; active intrinsic properties associated with the cross bridge attachment and length tension properties of the muscles that cross the joint (see Chap. 1); and reflexes associated with length feedback and force feedback from muscle spindles, tendon organs, and the influence of other somatosensory feedback on the fusimotor system.144

Following an injury, alterations occur with the stiffness of a joint and in the normal recruitment pattern and timing of muscular contractions.166 These alterations are thought to result from an adjustment in the ratio of muscle spindles to GTO activity and a disruption of the proprioceptive pathway.142,167,168 Any delay in response time to an unexpected load placed on the dynamic restraints can expose the static restraint structures to excessive forces, increasing the potential for injury.169 Thus, the focus of neuromuscular rehabilitation must be directed toward creating an environment that promotes the restoration and development of motor responses and proprioception in the presence of altered sensory input.170

Fatigue may also play a part in injury, particularly if the fatigue produces a dominance of agonists or antagonists over the other.168 Fatigue also reduces the capability of a muscle to absorb or dissipate loads. It seems plausible that some forms of muscle spindle desensitization, or perhaps ligament relaxation and Golgi tendon desensitization, occur with excessive fatigue.171 This may then lead to a decreased efferent muscle response and reduced ability to maintain balance.

Proprioceptive deficits can also be found with aging,172 arthrosis,173 and joint instability.148,164,166,167,174–177

Kinesthesia

Kinesthesia, a sub-modality of proprioception, refers to the sense of movement of the body or one of the segments. Although the articular receptors quite clearly play a very active role, the stretch reflex controlled by two other sensors, the muscle spindle and the GTO, is also important. Information about movement sense travels up the spinocerebellar tract (Box 3-2).

Motor Learning and Skill Acquisition

Motor learning is a complex set of internal processes that involve the relatively permanent acquisition and retention of a skill or task through practice.180–182

• Performance: involves the acquisition of a skill. A change in performance is dependent upon practice or experience.
• Learning: involves both acquisition and retention of a skill. Two main types of learning are recognized:183
  • Declarative—the learning of facts.
  • Procedural—learning that is dependent on practice, association (associating a particular stimulus with another stimulus, or certain stimulus with a certain response, or certain response with a certain result), and adaptation (making adjustments based on previous results), habituation (filtering out irrelevant stimuli), and sensitization (integration of relevant stimuli).

For learning to occur there must be a goal. Inherent in the idea of the goal is motivation.183

• Motor task. There are three basic types of motor tasks or skills:143,184
  • Discrete: involves a movement with a recognizable beginning and end. For example, throwing a ball, or opening a door.
  • Serial: involves a series of discrete movements that are combined in a particular sequence. For example, the sequence of tasks that are involved in getting out of a chair when using crutches.
  • Continuous: involves repetitive, uninterrupted movements that have no distinct beginning and ending. Examples include walking and cycling.

Stages of Motor Learning

There are three stages of motor learning:185

• Cognitive. This stage begins when the patient is first introduced to the motor task. This stage requires great concentration and variable performances filled with errors because the patient must determine the objective of the skill as well as the relational and environmental cues to control and regulate the movement. The patient is more concerned with what to do and how to do it. During this phase, the clinician should provide frequent and explicit positive feedback using various forms of feedback (verbal, tactile, visual), and allow trial and error to occur within safe limits.
• Associative. The patient is less concerned about every detail and more with performing and refining the skills. The important stimuli have been identified and their meaning is known. Conscious decisions about what to do become more automatic and the patient concentrates more on the task and appears less rushed. During this phase, the clinician should begin to increase the complexity of the task, emphasize problem solving, avoid manual guidance, and vary the sequence of tasks.
• Autonomous. This stage is characterized by an efficient and nearly automatic kind of performance. For example, when walking occurs automatically without conscious thought. During this phase, the clinician should set up a series of progressively more difficult activities the patient can do independently, such as increasing the speed, the distance, and the complexity of the task.

Practice

Practice, repeatedly performing a movement or series of movements in a task, is probably the single most important variable in learning a motor skill.184,185 The various types of practice for motor learning are as follows:184

• Part versus whole.
  • Part. A task is broken down into separate components and the individual components (usually the more difficult ones) are practiced. After mastery of the individual components, the components are combined in a sequence so that the whole task can be practiced.
  • Whole. The entire task is performed from beginning to end and is not practiced in separate components.
• Blocked, random, and random blocked.
  • Blocked. The same task or series of tasks is performed repeatedly under the same conditions and in a predictable order. For example, consistently practicing walking in a straight line on a flat surface.
  • Random. Slight variations of the same task are carried out in an unpredictable order. For example, a patient could practice walking on various walking surfaces and in different directions.
  • Random blocked. Variations of the same task are performed in random order, but each variation of the task is performed more than once. For example, the patient walks on a particular surface and then repeats the same task a second time before moving on to a different surface.
• Massed versus distributed.
  • Massed. Involves participation in a long bout of practice, where substantially less time is spent in rest compared to practice during the practice period. The disadvantages of this type of practice are that the patient is not able to reflect on his or her performance between practices, there is more potential for fatigue and an increased likelihood of a slight detriment for learning.143
  • Distributed. This type of practice involves participation in a series of practices throughout the day. The advantage of this type of practice is that the patient is able to reflect on his or her performance between practices.
• Physical versus mental.
  • Physical. The movements of a task are actually performed.
  • Mental. A cognitive rehearsal of how a motor task is to be performed occurs prior to actually doing the task.
• Constant versus varied.
  • Constant. Occurs when the skill is practiced repeatedly without changing anything. For example, shooting hoops from only the foul line.
  • Varied. Occurs when a parameter is changed throughout the practice session. For example, shooting hoops from various areas of the court.

Feedback

Second only to practice, feedback is considered the next most important variable that influences learning. The various types of feedback associated with motor learning are as follows:184

• Intrinsic versus extrinsic (augmented).
  • Intrinsic. Intrinsic feedback is a natural part of task.143 It can take the form of a sensory cue (proprioceptive, kinesthetic, tactile, visual, or auditory), or set of cues, inherent in the execution of the motor task. The feedback can arise from within the learner and be derived from performance of the task. This type of feedback may immediately follow completion of a task or may occur even before the task has been completed.
  • Extrinsic. Extrinsic feedback is supplemental feedback that is not normally an inherent part of the task. This type of feedback can include sensory cues from an external source (verbal, visual, or auditory). Unlike intrinsic feedback, the clinician can control the type, the timing, and the frequency of extrinsic feedback.
• Knowledge of results (KR) versus knowledge of performance (KP).
  • KR: immediate, posttask, extrinsic feedback about the outcome of a motor task. This type of feedback is primarily reserved for instances when individuals are unable to generate this type of information for themselves, or when the information may serve as a motivational tool.143
  • KP: feedback given about the nature or quality of the performance of the motor task. This type of feedback better facilitates motor skill learning than KR.

Feedback about performance can be provided at various times:

• Continuous versus Intermittent versus.
  • Continuous: is ongoing. This type of feedback improves skill acquisition more quickly during the initial stage of learning than intermittent feedback.
  • Intermittent: occurs irregularly, randomly. Intermittent feedback has been shown to promote learning more effectively than continuous feedback.
• Immediate, delayed, and summary.
  • Immediate: is given directly after a task is completed. This type of feedback is used most frequently during the cognitive (initial) stage of learning.
  • Delayed: is given after an interval of time elapses, allowing the learner to reflect on how well or poorly a task was done. This type of feedback promotes retention and generalizability of the learned skills.
  • Summary: is given about the average performance of several repetitions of the movement or task. This type of feedback is used most frequently during the associative stage of learning.

Skill Acquisition

A number of theories of skill acquisition have been proposed with respect to the predictability of the environment:

• Open (temporal and spatial factors in an unpredictable environment) versus closed skills (spatial factors only in a predictable environment), involving a single dimensional continuum. Using sports as an example, a closed skill could include shooting a foul shot in basketball. An everyday example of a closed skill is drinking from a cup. An example of an open skill in everyday life would be stepping onto a moving walkway, whereas in sport an open skill would involve throwing a touchdown pass. While closed skills allow an individual to evaluate the environment and perform the movement without much modification, open skills require more cognitive processing and decision making in choosing and adjusting the movement.170 Open and closed skills can be viewed as a continuum, where the perceptual and habitual nature of a task determines whether the task is open or closed.
• Gentile taxonomy of motor tasks.186 This is a two-dimensional classification system for teaching motor skills. Using the concept that motor skills range from simple to complex, Gentile expanded the popular one-dimensional classification system of open and closed skills to combine the environmental context together with the function of the action:184,185
  • The environmental (closed or open) context in which the task is performed. Regulatory conditions (other people, objects) in the environment may be either stationary (closed skills) or in motion (open skills).
  • The intertrial variability (absent or present) of the environment that is imposed on the task. When the environment in which a task is set is unchanging from one performance of a task to the next, intertrial variability is absent—the environmental conditions are predictable. For example, walking on a flat surface. Intertrial variability is present when the demands change from one attempt or repetition of the task to the next. For example, walking over varying terrain.
  • The need for a person's body to remain stationary (stable) or to move (transport) during the task. Skills that require body transport are more complex than skills that require no body transport as there are more variables to consider. For example, a body transport task could include walking in a crowded shopping mall.
  • The presence or absence of manipulation of objects during the task. When a person must manipulate an object, the skill increases in complexity because the person must do two things at once—manipulate the object correctly and adjust the body posture to fit the efficient movement of the object.

Balance

Balance, or postural control, is a complex motor control task involving the detection and integration of sensory information to assess the position and motion of the body in space and the execution of appropriate musculoskeletal responses to control body position within its stability limits, and within the context of the environment and task, whether stationary or moving.187 Posture is the relative position of the various parts of the body with respect to one another, to the environment, and to gravity (see Chap. 6).188

Balance results from an integration of three components:188

• The nervous system, which provides sensory processing for perception of body orientation in space provided mainly by the visual, vestibular, and somatosensory systems. The sensory motor integration provides motor strategies for the planning, the programming, and the execution of balance responses.189
• Musculoskeletal contributions including postural alignment, flexibility, joint integrity, muscle performance, and mechanoreceptor sensation.
• Contextual effects that interact with the nervous and the musculoskeletal systems. These effects include whether the environment is closed (predictable) or open (unpredictable), the support surface, the amount of lighting, the effects of gravity and inertial forces on the body, and the characteristics of the task (new versus well learned, predictable versus unpredictable, single versus multiple).

Impaired balance can be caused by injury or disease to any of the structures involved in the stages of information processing.

An individual's balance is greatest when the body's center of gravity (COG) is maintained over its base of support (BOS). Functional tasks require different types of balance control, including:187

• Static balance: involves maintaining a stable antigravity position while at rest, such as when standing and sitting.
• Dynamic balance: the ability to stabilize the body when the support surface is moving or when the body is moving on a stable surface, such as during sit to stand transfers or walking.
• Automatic postural reactions: the ability to maintain balance in response to unexpected external perturbations, such as standing on a bus that suddenly decelerates.

The maintenance of balance requires the integration of sensory information from a number of different systems: vision, vestibular, and somatosensory.151 The vestibular system, with contributions from the inner ear (see Cranial Nerves), provides information about movement and spatial orientation. The visual system, which involves CN II, III, IV, and VI, assists in balance control by providing input about the position of the head or the body in space (see Supraspinal reflexes later). Through the vestibulo-ocular input, signals from the muscle spindles in the extraocular muscles, the position of the eyeball is controlled so that a visual image is maintained on the fovea. The coordination of eye movements during gaze is a complex affair and is controlled by efferent signals from the trochlear, the abducens, and the oculomotor nuclei via the fourth, the sixth, and the third CNs, respectively (refer to the discussion of cervico-ocular and vestibular reflexes later in this chapter).12 Coordination of these nuclei is achieved by gaze centers in the reticular formation, the midbrain, and the cortex, and by the cerebellum, which have fibers that project into the three eye muscle nuclei and control the orbital movements concerned with slow and rapid eye movements.12

Automatic Postural Responses

To maintain balance, the body must continually adjust its position in space. A certain amount of anteroposterior and lateral sway normally occur while maintaining balance. For example, normal anteroposterior sway in adults is 12 degree from the most posterior to the most anterior position.190 If the sway exceeds the limits of stability, some strategy must be employed to regain balance. Horak and Nashner191 describes several different strategies used to maintain balance, including the ankle, the hip, and the stepping strategies, which are designed to adjust the body's COG so that the body is maintained within the BOS to prevent the loss of balance or falling:

• The ankle strategy, in which muscles around the ankles are used to provide postural stability in the anteroposterior plane, is employed with small perturbations.
• Weight-shift strategy is a movement strategy utilized to control medial–lateral perturbations involving shifting the bodyweight laterally from one leg to the other.
• Suspension strategy, which involves lowering the body's COG by flexing the knees, causing associated flexion of the ankles and the hips or a slight squatting motion.
• The hip strategy, in which muscles around the thigh, the hip, and the trunk are recruited, is employed with larger perturbations.
• The stepping strategy, in which a step is taken to maintain postural control, is employed if the two previous strategies are insufficient.

Most healthy individuals use combinations of the above strategies to maintain balance depending on the control demands.188

Anticipatory and Compensatory Postural Adjustments

Anticipatory postural adjustments occur in response to internal perturbations such as voluntary movements of the body by activating muscle synergies in advance of the actual perturbation. Research has shown that anticipatory postural adjustments are highly adaptable and vary according to the task demands.192–194 For example, postural muscles in standing humans are activated prior to (and during) voluntary movement of an upper limb and are specific to this movement. Anticipatory postural adjustments have also been studied during leg movements,195,196 trunk movements,197,198 arm movements in standing subjects,192,199 and during load release from extended arms.200–202

While anticipatory reactions are initiated by the subject, compensatory reactions, which occur later, are initiated by sensory feedback triggering signals. With anticipatory reactions, the CNS tries to predict postural perturbations associated with a planned movement and minimize them with anticipatory corrections in a feedforward manner, while compensatory reactions deal with actual perturbations of balance that occur because of the suboptimal efficacy of the anticipatory components.

The Neurophysiology of Pain

Pain, at some point or other, is felt by everyone and is considered an emotional experience that is highly individualized and extremely difficult to evaluate. Our knowledge of the pain system has greatly improved over the past few years with discoveries that have increased our understanding of the role of nociceptors and the processing of nociceptive information. Furthermore, new findings have illuminated our knowledge about the descending pathways that modulate nociceptive activity.

Types of Pain

Pain is the most common determinant for a patient to seek intervention. Pain is a broad and significant symptom that can be described using many descriptors. In addition, the pain perception and the response to the painful experience can be influenced by various cognitive processes, including anxiety, tension, depression, past pain experiences, and cultural influences.203 Perhaps, the simplest descriptors for pain are acute and chronic.

Acute pain can be defined as “the normal, predicted physiological response to an adverse chemical, thermal, or mechanical stimulus … associated with surgery, trauma, and acute illness.”204 This type of pain usually precipitates a visit to a physician, because it has one or more of the following characteristics205:

• It is new and has not been experienced before.
• It is severe and disabling.
• It is continuous, lasting for more than several minutes, or recurs very frequently.
• The site of the pain may cause alarm (e.g., chest and eye).
• In addition to the sensory and affective components, acute pain is typically characterized by anxiety. This may produce a fight-or-flight autonomic response, which is normally used for survival needs. This autonomic reaction is also associated with an increase in systolic and diastolic blood pressure, a decrease in gut motility and salivatory flow, increased muscle tension, and papillary distention.17,206

Acute pain following trauma, or the insidious onset of a musculoskeletal condition, is typically chemical in nature. Although motions aggravate the pain, they cannot be used to alleviate the symptoms. In contrast, cessation of movement (absolute rest) tends to alleviate the pain, although not necessarily immediately. The structures most sensitive to chemical irritation in order of sensitivity are:

• The periosteum and joint capsule
• Subchondral bone, tendon, and ligament
• Muscle and cortical bone
• The synovium and articular cartilage

Chronic pain is typically more aggravating than worrying, lasts for more than 6 months, and has the following characteristics205:

• It has been experienced before and has remitted spontaneously, or after simple measures.
• It is usually mild to moderate in intensity.
• It is usually of limited duration, although it can persist for long periods (persistent pain).
• The pain site does not cause alarm (e.g., knee and ankle).
• There are no alarming associated symptoms. However, patients with chronic pain may be more prone to depression and disrupted interpersonal relationships.208–211

The symptoms of chronic pain typically behave in a mechanical fashion, in that they are provoked by activity or repeated movements and reduced with rest or a movement in the opposite direction.

Transmission of Pain

A nociceptive neuron is the one that transmits pain signals. The nociceptive system is normally a quiescent system requiring strong, intense, potentially damaging stimulation before it becomes activated.178 Any tissue that contains free nerve endings involved with nociception is capable of being a source of pain. Pain receptors (nociceptors), unlike other receptors, are nonadapting in nature; that is, they will continue to fire for as long as the stimulus is present. It is apparent that many peripheral nociceptors are polymodal. Nociceptor stimulation can only occur in one of the three ways179:

• Mechanical deformation resulting in the application of sufficient mechanical forces to stress, deform, or damage a structure.
• Excessive heat or cold.
• The presence of chemical irritants in sufficient quantities or concentrations. Key mediators that have been identified include bradykinin, serotonin, histamine, potassium ions, adenosine triphosphate, protons, prostaglandins, nitric oxide, leukotrienes, cytokines, and growth factors.204 The effects of these mediators involve binding to specific receptors, activation of ion channels for depolarization, activation of intracellular second messenger systems, and release of a range of neuropeptides to promote neurogenic inflammation, and alteration of neuronal properties by modifying gene transcription.178,204

One of the most fundamental influences on nociceptor sensitivity is the pH of the surrounding tissue.178 High local proton concentrations are known to occur in many inflammatory states and the consequent reduction in pH can contribute to sensitization and activation of polymodal nociceptors.178,212

The transmission of pain to the CNS occurs via two distinct pathways, which correspond to the two different types of pain: fast-conducting A delta and slow-conducting C fibers (Table 3-1), although not all the fibers are necessarily nociceptors. Each of these types of fibers has different pain characteristics: A delta fibers evoke a rapid, sharp, lancinating pain reaction; C fibers cause a slow, dull, crawling pain.

Rapid Pain

The fast, or dermatomal, pain signals are transmitted in the peripheral nerves by small, myelinated A fibers at velocities between 6 and 30 m (20 and 98 ft) per second. The fast pain impulse is a signal telling the subject that a threat is present and provoking an almost instantaneous and often reflexive response. This signal often is followed a second or more later by a duller pain that tells of either tissue damage or continuing stimulation.

Slow Pain

Slow, or sclerotomal, pain is transmitted in even smaller and unmyelinated C nerve fibers at much slower velocities, between 0.5 and 2 m (1.6 and 6.6 ft) per second. On entering the posterior (dorsal) horn of the spinal cord, the pain signals from both visceral and somatic tissues do one of the following three things:

• Synapse with interneurons that synapse directly with motor nerves and produce reflex movements.
• Synapse with autonomic fibers from the sympathetic and parasympathetic systems and produce autonomic reflexes.
• Synapse with interneurons that travel to the higher centers in the brain.
  • The fast signals of the C fibers terminate in laminae I and V of the posterior (dorsal) horn (Fig. 3-25). Here they excite neurons (internuncial neurons, segmental motor neurons, and flexor reflex afferents) that send long fibers to the opposite side of the cord and then upward to the brain in the lateral division of the anterior–lateral sensory pathway (lateral spinothalamic tract (Box 3-3).
  • The slow signals of the C fibers terminate in laminae II and III of the posterior (dorsal) horn (Fig. 3-25). Most of the signal then passes through another short fiber neuron to terminate in lamina V. Here, the neuron gives off a long axon, most of which joins with the fast signal axons to cross the spinal cord and continue upward in the brain in the same spinal tract. Approximately 75–90% of all pain fibers terminate in the reticular formation of the medulla, pons, and mesencephalon. From here, other neurons transmit the signal to the thalamus, hypothalamus (pituitary), limbic system, and the cerebral cortex.

The central pathways for processing nociceptive information begin at the level of the spinal cord (and medullary) posterior (dorsal) horn. As with the periphery, the posterior (dorsal) horn of the spinal cord contains many transmitters and receptors, both identified and accepted, including several neuroactive peptides (substance P, calcitonin gene-related peptide, somatostatin, neuropeptide Y, and galanin), excitatory amino acids (aspartate and glutamate), inhibitory amino acids (γ-aminobutyric acid and glycine), nitric oxide, the arachidonic acid metabolites, the endogenous opioids, adenosine, and the monoamines (serotonin and noradrenaline).213 This list indicates that there are diverse therapeutic possibilities for the control of the transmission of nociceptive information to the brain.

Interneuronal networks in the posterior (dorsal) horn are responsible not only for the transmission of nociceptive information to neurons that project to the brain, but also for the modulation of that information. The information is passed to other spinal cord neurons, including the flexor motoneurons and the nociceptive projection neurons (e.g., certain patterns of stimulation can lead to enhanced reflex actions and the sensitization of projection neurons and increased nociceptive transmission). Other inputs result in the inhibition of projection neurons.

A small number of fast fibers are passed directly to the thalamus, and then to the cerebral cortex, bypassing the brain stem. It is believed that these signals are important for recognizing and localizing pain, but not for analyzing it. Of the slow signals, none, or at least very few, avoid the reticular system. Because most of the fast, and all of the slow, pain signals go through the reticular formation, they can have wide-ranging effects on almost the entire nervous system.

Lamina V (Fig. 3-25) is the area for convergence, summation, and projection. The response of the cells in lamina V depends largely on the intensity of the stimulus. High-intensity stimulation leads to facilitation of the cell, and relatively easy transmission across the cord to the other side and, from here, upward. More gentle stimulation inhibits this transmission. This inhibition is, according to theory, the result of pre- and postsynaptic effects produced by the cells of laminae II and III. Thus, the net effect at lamina V will determine whether the pain signal is relayed upward. If mild mechanoreceptor input dominates, the pain signal is stopped at this point. If, however, pain input dominates, or if the mechanoreceptor input is too strong, transmission of the pain signal occurs.

Over the last decade, researchers have begun to investigate the influence of pain on patterns of neuromuscular activation and control.178 It has been suggested that the presence of pain leads to inhibition or delayed activation of muscles or muscle groups that perform key synergistic functions to limit unwanted motion.214 This inhibition usually occurs in deep muscles, local to the involved joint, that perform a synergistic function in order to control joint stability.215–217 It is now also becoming apparent that in addition to being influenced by pain, motor activity and emotional state can, in turn, influence pain perception.178,218

Although the pain intensity and the functional response to symptoms are subjective, patterns of pain response to stimulation of the pain generator are quite objective (e.g., antalgic gait).220

Referred pain can be generated by:221

• convergence of sensory input from separate parts of the body to the same posterior (dorsal) horn neuron via primary sensory fibers (convergence-projection theory)208,222–224;
• secondary pain resulting from a myofascial trigger point (MTrP)225;
• sympathetic activity elicited by a spinal reflex226; and
• pain-generating substances.208

Macnab227 recommends the following classification for referred pain/symptoms:

• Viscerogenic
• Vasculogenic
• Neurogenic
• Psychogenic
• Spondylogenic

Viscerogenic Symptoms

The pain/symptoms in this category can be referred from any viscera in the trunk or abdomen. Visceral pain can be produced by chemical damage, ischemia, or spasm of the smooth muscles.

Viscerogenic pain may be produced when the nociceptive fibers from the viscera synapse in the spinal cord with some of the same neurons that receive pain from the skin. When the visceral nociceptors are stimulated, some are transmitted by the same neurons that conduct skin nociception and take on the same characteristics. Visceral pain has five important clinical characteristics:

• It is not evoked from all viscera.
• It is not always linked to visceral injury.
• It is diffuse and poorly localized.
• It is referred to other locations.
• It is often accompanied by autonomic reflexes, such as nausea and vomiting.

Viscerogenic pain tends to be diffuse because of the organization of visceral nociceptive pathways in the CNS. This organization demonstrates an absence of a separate pathway for visceral sensory information and a low proportion of visceral afferent nerve fibers compared with those of somatic origin.

Pain arising from problems in the peritoneum, pleura, or pericardium differs from that of other visceral impairments because of the innervation of these structures. The parietal walls of these structures are supplied extensively with both fast and slow pain fibers and, thus, can produce the sharp pain of superficial impairments.

In general, symptoms from a musculoskeletal condition are provoked by certain postures, movements, or activities and relieved by others. However, this generalization must be viewed as such. It is also important to remember that musculoskeletal structures can refer symptoms (Table 3-5). Determining the mechanism often will clarify the cause of the symptoms. In addition, what appears to be a musculoskeletal injury can actually be a systemic problem. For example, acute low back pain (LBP) can result in symptoms of varying intensity and distribution that can be caused by neuromuscular structures as well as underlying or coexisting systemic pathology (Table 3-6), such as a gastrointestinal pathology (Table 3-7).

Signs and symptoms that could increase suspicion for a gastrointestinal pathology include a report of pain that has no specific mechanism of injury, is unrelated to activity, and that occurs following eating. In addition, reports of night pain unrelated to movement, fever, unexpected weight loss, nausea/vomiting, bowel dysfunction, and food intolerance should also highlight the possibility of a gastrointestinal source. An abdominal palpation examination can be used to identify gross masses, pulsating masses, and/or pain.228 Palpatory findings of tenderness, gross abnormal masses, or abnormal pulsations are indicative of a broad range of abdominal pathologies, including tumor, obstruction, and infection.

Vasculogenic Symptoms

Vasculogenic symptoms tend to result from venous congestion or arterial deprivation to the musculoskeletal areas. Vasculogenic pain may mimic a wide variety of musculoskeletal, neurologic, and arthritic disorders, because this type of pain is often worsened by activity. An example of a vasculogenic cause of symptoms occurs with an abdominal aortic aneurysm (Table 3-8).228,229

To help exclude a vasculogenic cause, it is important to review the cardiopulmonary, hematologic, and neurologic systems during the examination. Clinical evidence of arterial insufficiency includes lower extremity asymmetry, skin condition changes, skin temperature and color changes, and diminishing pulses.

Doppler examination, which is not within the scope of physical therapy practice, is the cornerstone of the vascular examination. This test examines blood flow in the major arteries and veins in the arms and the legs with the use of ultrasound. The ultrasound transducer produces high-frequency sound waves that echo off the blood vessels, resulting in a “swishing” noise during blood flow. A faster flow produces a higher pitch and a steeper waveform. In the lower extremity, segmental pressures are usually taken from six sites:

• High thigh
• Above the knee
• Below the knee
• Ankle
• Forefoot
• Digit

A pressure gradient of less than 20-mm Hg is normal, 20–30 mm Hg is borderline, and greater than 30 mm Hg is considered abnormal. Pressure differences of less than 20 mm Hg between limbs are considered normal.

After the segmental pressures of the lower extremity are measured, brachial pressure on both sides is measured. Comparisons are made between ankle–arm, forefoot–arm, and digit–arm ratios. Normal values are >1 for the ankle–arm index, >0.75 for the forefoot–arm, and >0.65 for each digit–arm index.

Neurogenic Symptoms

The neurologic tissues comprise those tissues that are involved in nerve conduction. Neurogenic causes of symptoms may include:

• tumor compressing and irritating a neural structure of the spinal cord or the meninges;
• spinal nerve root irritation;
• peripheral nerve entrapment; and
• neuritis.

Psychogenic Symptoms

It is common to find emotional overtones in the presence of pain, particularly with lowback and neck pain. These overtones are thought to result from an inhibition of the pain control mechanisms of the CNS from such causes as grief, the side effects of medications, or fear of reinjury. Somatosensory amplification refers to the tendency to experience somatic sensation as intense, noxious, and disturbing. Barsky and colleagues230 introduced the concept of somatosensory amplification as an important feature of hypochondriasis. Somatosensory amplification is observed in patients whose extreme anxiety leads to an increase in their perception of pain.

The term nonorganic was proposed by Waddell et al.231 to define the abnormal illness behaviors exhibited by patients who have depression, emotional disturbance, or anxiety states. The presence of three of the following five Waddell signs has been correlated significantly with disability232:

• Superficial or nonanatomic tenderness to light touch that is widespread and refers pain to other areas.
• Simulation tests. These are a series of tests that should be comfortable to perform. Examples include axial loading of the spine through the patient's head with light pressure to the skull and passive hip and shoulder rotation with the patient positioned standing. Neither of these tests should produce LBP. If pain is reported with these tests, a nonorganic origin should be suspected.
• Distraction test.233 This test involves checking a positive finding elicited during the examination on the distracted patient. For example, if a patient is unable to perform a seated trunk flexion maneuver, the same patient can be observed when asked to remove his or her shoes. A difference of 40–45 degrees is significant for inconsistency.
• Regional disturbances. These signs include sensory or motor disturbances that have no neurologic basis.
• Overreaction. This includes disproportionate verbalization, muscle tension, tremors, and grimacing during the examination.

The Somatosensory Amplification Rating Scale (SARS; Table 3-9) is a version of the Waddell's nonorganic physical signs, which has been modified to allow for a more accurate appraisal of the patient with exaggerated illness behavior.230

Spondylogenic Symptoms

A number of conditions can affect the musculoskeletal system, frequently producing pain. These include infections (e.g., osteomyelitis), inflammatory disorders, neoplasms, and metabolic disorders. Several findings are helpful in diagnosing such pathologic processes. These findings may include:

• severe and unrelenting pain;
• the presence of a fever;
• bone tenderness; and
• unexplained weight loss.

Pain Control Mechanisms

One of the earliest pain control mechanisms was proposed by Melzack and Wall234 who postulated that interneurons in the substantia gelatinosa functioned like a gate to modulate sensory input. They proposed that the substantia gelatinosa interneuron projected to the second-order neuron of the pain–temperature pathway located in lamina V, which they called the transmission cell. It was reasoned that if the substantia gelatinosa interneuron were depolarized, it would inhibit the transmission of cell firing and, thus, decrease further transmission of input ascending in the spinothalamic tract. The degree of modulation appeared to depend on the proportion of input from the large A fibers and the small C fibers, so that the gate could be closed by either decreasing C fiber input or increasing A fiber or mechanoreceptive input. The gate theory was, and is, supported by practical evidence (e.g., rubbing a sore area appears to decrease the pain), although the experimental evidence for the theory is lacking. Researchers have identified many clinical pain states that cannot be fully explained by the gate control theory.235 A problem with this theory is that there is an evidence to suggest that the A-beta fibers from the mechanoreceptor do not synapse in the substantia gelatinosa. In this case, the modulation at the spinal cord level must occur in lamina V, where there is a simple summation of signals from the pain fibers and the mechanoreceptor fibers. However, severe or prolonged pain tends to have the segment identifying all input as painful, and summation modulation has little, if any, effect.

Melzack and Wall expanded upon the gate theory and argued that the gate could be modified by a descending inhibitory pathway from the brain, or brain stem,236 suggesting that the CNS apparently plays a part in this modulation in a mechanism called central biasing.

Numerous investigations have since been made of what is known as the descending analgesia systems. The thalamus represents the final link in the transmission of impulses to the cerebral cortex, processing almost all sensory and motor information prior to its transfer to cortical areas. The key brain sites involved in pain perception include the anterior cingulate cortex, anterior insular cortex, primary somatosensory cortex, secondary somatosensory cortex, a number of regions in the thalamus and cerebellum, and, interestingly, areas such as the premotor cortex that are normally linked to motor function.178,237 Indeed, it is clear that both the basal ganglia (associated with planned action), the periaqueductal gray (PAG) of the midbrain region, and the raphe nucleus in the pons and the medulla receive nociceptive input as well as coordinating important aspects of movement and motor control.178,238,239

The PAG area of the upper pons sends signals to the raphe magnus nucleus in the lower pons and the upper medulla. This nucleus relays the signal down the cord to a pain-inhibitory complex located in the posterior (dorsal) horn of the cord. The nerve fibers derived from the PAG area secrete enkephalin and serotonin, whereas the raphe magnus releases enkephalin only. The PAG is also believed to be involved in complex behavioral responses to stressful or life-threatening situations or to promote recuperative behavior after a defense reaction.

Enkephalin is believed to produce presynaptic inhibition of the incoming pain signals to lamina I–V, thereby blocking pain signals at their entry point into the cord.240 It is further believed that the chemical releases in the upper end of the pathway can inhibit pain signal transmission in the reticular formation and the thalamus. The inhibition from this system is effective on both fast and slow pains.

In the cortex, a negative-feedback loop, called the corticofugal system, originates at the termination point of the various sensory pathways.241 Excessive stimulation of this feedback loop results in a signal being transmitted down from the sensory cortex to the posterior horn of the level from which the input arose. This response produces lateral or recurrent inhibition of the cells adjacent to the stimulated cell, thereby preventing the spread of the signal. This is an automatic gain control system to prevent overloading of the sensory system.

Finally, two other neuroactive peptides, beta endorphin and dynorphin, have recently been discovered, both of which are theorized to be used as analgesics in the body to numb or dull pain in addition to promoting feelings of well-being and increasing relaxation.

Nonpharmacological Control of Pain

The pharmacological control of pain is discussed in Chapter 9. Clinicians can use several nonpharmacological therapeutic interventions to manage pain. These include:

• Transcutaneous electrical nerve stimulation (TENS). TENS is frequently used to treat a number of pain conditions including back pain, osteoarthritis, in fibromyalgia to name a few (see Chap. 8).
• Interferential current (see Chap. 8). Clinically, interferential current therapy is beneficial for treating painful conditions such as osteoarthritic pain. The potential mechanisms behind this pain control include an increase in blood flow, and the same mechanisms as TENS—segmental inhibition and activation of descending inhibitory pathways
• Thermal modalities (see Chap. 8).
• Cryotherapy (see Chap. 8).
• Manual therapy (see Chap. 10).
• Exercise (see Chaps. 12, 13, 14 and 15).
• Patient education. Patients can be educated on pain management techniques (relaxation, cognitive behavioral approaches, and biofeedback), positions and activities to avoid, and positions and activities to adopt.

Orthopaedic Neurologic Testing

An examination of the transmission capability of the nervous system can be performed as part of the orthopaedic examination to detect the presence of either an upper motor neuron (UMN/CNS) lesion or a lower motor neuron (LMN/PNS) lesion. In essence, neurological tissue is tested during active, passive, and resisted isometric movement, as well as those tests specific to the nervous system (e.g., reflex testing, sensory testing). Neurodynamic mobility testing is covered in Chapter 11.

UMNs are located in the white columns of the spinal cord and the cerebral hemispheres. A UMN lesion, also known as a central palsy, is a lesion of the neural pathway above the anterior horn cell or motor nuclei of the CNS. Signs and symptoms associated with a UMN lesion follow.

Nystagmus

Nystagmus is characterized by an involuntary loss of control of the conjugate movement of the eyes (approximately one or more axes) involved with smooth pursuit or saccadic movement. When the eyes oscillate like a sine wave, it is called pendular nystagmus. If the nystagmus consists of drifts in one direction with corrective fast phases, it is called jerk nystagmus. The more benign types of nystagmus include the proprioceptive causes of spontaneous nystagmus, postural nystagmus, and nystagmus that is elicited with head positioning or induced by movement (vestibular nystagmus). A unidirectional nystagmus is related to the geometric relationship of the semicircular canal, with a change in head position often exacerbating the nystagmus. On the other hand, a central vestibular nystagmus, which is caused by disease of the brain stem or the cerebellum, exhibits bidirectionality to the nystagmus (i.e., left beating on left gaze and right beating on right gaze).242 The more serious causes of nystagmus include, but are not limited to, vertebrobasilar ischemia, tumors of the posterior cranial fossa, intracranial bleeding, craniocervical malformations, and autonomic dysfunction. Differentiation between the benign and serious causes of nystagmus is very important.

• Proprioceptive nystagmus occurs immediately upon turning the head (i.e., there is no latent period).
• The ischemic type of nystagmus has a latent period and is usually only evident when the patient's neck is turned to a position and maintained there for a period of a few seconds up to 3 minutes.243,244

Dysphasia

Dysphasia is defined as a problem with vocabulary and results from a cerebral lesion in the speech areas of the frontal or temporal lobes. The temporal lobe receives most of its blood from the temporal branch of the cortical artery of the vertebrobasilar system and may become ischemic periodically, producing an inappropriate use of words.

Wallenberg Syndrome

This is the result of a lateral medullary infarction.245 Classically, sensory dysfunction in lateral medullary infarction is characterized by selective involvement of the spinothalamic sensory modalities with dissociated distribution (ipsilateral trigeminal and contralateral hemibody/limbs).246 However, various patterns of sensory disturbance have been observed in lateral medullary infarction that includes contralateral or bilateral trigeminal sensory impairment, restricted sensory involvement, and a concomitant deficit of lemniscal sensations.247,248

Ataxia

Ataxia is often most marked in the extremities. In the lower extremities, it is characterized by the so-called drunken-sailor gait pattern, with the patient veering from one side to the other and having a tendency to fall toward the side of the lesion. Ataxia of the upper extremities is characterized by a loss of accuracy in reaching for, or placing, objects. Although ataxia can have a number of causes, it generally suggests CNS disturbance, specifically a cerebellar disorder, or a lesion of the posterior columns.249–251

Spasticity252–254

Spasticity is defined as a motor disorder characterized by a velocity-dependent increase (resistance increases with velocity) in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. The spinal cord experiences spinal shock immediately following any trauma causing tetraplegia or paraplegia, resulting in the loss of reflexes innervated by the portion of the cord below the site of the lesion. The direct result of this spinal shock is that the muscles innervated by the traumatized portion of the cord, the portion below the lesion, as well as the bladder, become flaccid. Spinal shock, which wears off between 24 hours and 3 months after injury, can be replaced by spasticity in some, or all of these muscles.

Spasticity occurs because the reflex arc to the muscle remains anatomically intact, despite the loss of cerebral innervation and control via the long tracts. During spinal shock, the arc does not function, but as the spine recovers from the shock, the reflex arc begins to function without the inhibitory or regulatory impulses from the brain, creating local spasticity and clonus.

Drop Attack

A drop attack is described as a loss of balance resulting in a fall, but with no loss of consciousness. Because it is the consequence of a loss of lower extremity control, it is never a good or benign sign. The patient, usually elderly, falls forward, with the precipitating factor being extension of the head. Recovery is usually immediate. Causes include:

• a vestibular system impairment255;
• neoplastic and other impairments of the cerebellum256;
• vertebrobasilar compromise257 (see Chap. 24);
• sudden spinal cord compression;
• third ventricle cysts;
• epilepsy; and
• type 1 Chiari malformation.258

Wernicke's Encephalopathy

This is an impairment, typically localized to the posterior (dorsal) part of the midbrain,259 that produces the classic triad of abnormal mental state, ophthalmoplegia, and gait ataxia.260

Vertical Diplopia

A history of “double vision” should alert the clinician to this condition. Patients with vertical diplopia complain of seeing two images, one atop or diagonally displaced from the other.261

Dysphonia

Dysphonia presents as a hoarseness of the voice. Usually, no pain is reported. Painless dysphonia is a common symptom of Wallenberg syndrome.247

Hemianopia

This finding, defined as a loss in half of the visual field, is always bilateral. A visual field defect describes sensory loss restricted to the visual field and arises from damage to the primary visual pathways linking the optic tract and striate cortex (see section “Supraspinal Reflexes”).

Ptosis

Ptosis is defined as a pathologic depression of the superior eyelid such that it covers part of the pupil. It results from a palsy of the levator palpebrae and Müller's muscle.

Miosis

Miosis is defined as the inability to dilate the pupil (damage to sympathetic ganglia). It is one of the symptoms of Horner syndrome.

Horner Syndrome

This syndrome is caused by interference to the cervicothoracic sympathetic outflow resulting from a lesion of (1) the reticular formation, (2) the descending sympathetic system, and (3) the oculomotor nerve caused by a sympathetic paralysis.262 The other clinical signs of Horner syndrome are ptosis, enophthalmos, facial reddening, and anhydrosis. If Horner syndrome is suspected, the patient should immediately be returned or referred to a physician for further examination.

Dysarthria

Dysarthria is defined as an undiagnosed change in articulation. Dominant or nondominant hemispheric ischemia, as well as brain stem and cerebellar impairments, may result in altered articulation.

The LMN begins at the α motor neuron and includes the posterior (dorsal) and anterior (ventral) roots, spinal nerve, peripheral nerve, neuromuscular junction, and muscle–fiber complex.263 The LMN consists of a cell body located in the anterior gray column and its axon, which travels to a muscle by way of the cranial or peripheral nerve. Lesions to the LMN can occur in the cell body or anywhere along the axon. An LMN lesion is also known as a peripheral palsy. These lesions can be the result of direct trauma, toxins, infections, ischemia, or compression. The characteristics of an LMN lesion include muscle atrophy and hypotonus, diminished or absent muscle stretch (deep tendon) reflex of the areas served by a spinal nerve root or a peripheral nerve, and absence of pathologic signs or reflexes.

Complaints of Dizziness

Although most causes of dizziness can be relatively benign, dizziness may signal a more serious problem, especially if it is associated with trauma to the neck or the head or with motions of cervical rotation and extension (e.g., vertebral artery compromise). The clinician must ascertain whether the symptoms result from vertigo, nausea, giddiness, unsteadiness, or fainting, among others. Nausea is an uneasiness of the stomach that often accompanies the urge to vomit but does not always lead to the forcible voluntary or involuntary emptying of stomach contents through the mouth (vomiting). If vertigo is suspected, the patient's physician should be informed, for further investigation. However, in and of itself, vertigo is not usually a contraindication to the continuation of the examination. Differential diagnosis includes primary CNS diseases, vestibular and ocular involvement, and, more rarely, metabolic disorders.264 Patients complaining of dizziness can be classified into four subtypes (Table 3-10). Careful questioning can help in the differentiation of the cause. This differentiation is important, as certain types of dizziness are amenable to physical therapy interventions (Table 3-11); others produce contraindications to certain interventions, while still other causes of dizziness require medical referral.265 The presence of presyncope would suggest compromise of the function of the cerebral hemispheres or the brainstem.265 Different conditions can cause either a pancerebral hypoperfusion (Table 3-12) or a selective hypoperfusion of the brainstem, the latter of which includes vertebrobasilar insufficiency, vertebrobasilar infarction, and subclavian steal syndrome.265 The presence of vertigo, nystagmus, hearing loss or tinnitus, and brainstem signs can help the clinician differentiate between a central or a peripheral vestibular lesion (Table 3-13).265 Peripheral vertigo is manifested with general complaints such as unsteadiness and lightheadedness. Central vertigo is usually caused by a cerebellar disorder, an ischemic process, or a disturbance of the vestibular system (Table 3-14). Cervical vertigo, on the other hand, may be produced by localized muscle changes and receptor irritation.244

• Dizziness provoked by head movements or head positions could indicate an inner ear dysfunction. Dizziness provoked by certain cervical motions, particularly extension or rotation, also may indicate vertebral artery compromise. Dizziness resulting from vertebral artery compromise should be associated with other signs and symptoms, which could include neck pain and nausea. The pain associated with vertebral artery compromise develops on one side of the neck in one-fourth of patients and usually is confined to the upper anterolateral cervical region.266 Persistent, isolated neck pain may mimic idiopathic carotidynia, especially if it is associated with local tenderness. Pain is also usually the initial manifestation of a carotid artery dissection, and the median time to the appearance of other symptoms is 4 days.266
• Dizziness associated with tinnitus or a hearing loss could indicate a tumor of CN VIII.
• Dizziness can occur if the calcareous deposits that lie on the vestibular receptors are displaced to new and sensitive regions of the ampulla of the posterior canal, evoking a hypersensitive response to stimulation with certain head positions or movements.267,268 The Dix–Hallpike test can be used to help determine if the cause of the patient's dizziness is a vestibular impairment (benign paroxysmal positional vertigo, or BPPV), resulting from an accumulation of utricle debris (otoconia), which can move within the posterior SCC and stimulate the vestibular sense organ (cupula). This test usually is performed only if the vertebral artery test and instability tests do not provoke symptoms. The test involves having the clinician move the patient rapidly from a sitting to a supine position with the head turned so that the affected ear (provocative position) is 30–45 degree below the horizontal to stimulate the posterior SCC.8 The endpoint of the test is when the patient's head overhangs the end of the table, so that the cervical spine is extended (Fig. 3-26). A positive test reproduces the patient's symptoms of vertigo and/or nystagmus.
• Dizziness associated with a recent change in medication is suggestive of an adverse drug reaction.269

Strength Testing

A myotome is defined as a muscle or group of muscles served by a single nerve root. Key muscle is perhaps a more accurate term. Manual muscle testing is traditionally used by the clinician to assess the strength of a muscle or muscle group that is representative of the supply from a particular nerve root. Valuable information can be gleaned from these tests, including:

• The amount of force the muscle is capable of producing and whether the amount of force produced varies with the joint angle.
• Whether any pain or weakness is produced with the contraction.
• The endurance of the muscle and how much substitution occurs during the test.

From the neurologic perspective, strength testing assesses the nerve supplying the muscle (Table 3-15, Table 3-16). Muscle weakness, if elicited, may be caused by a UMN lesion (along with spasticity, hyperactive reflexes, etc.), injury to a peripheral nerve, pathology at the neuromuscular junction, a nerve root lesion, or a lesion or disease (myopathy) of the muscle, its tendons, or the bony insertions themselves.270 Pain, fatigue, and disuse atrophy can also cause weakness. For suspected nerve root lesions, key muscle testing is the method of choice, and the clinician attempts to determine if there are any specific patterns of muscle weakness (weakness in muscles served by the same nerve root). However, as manual muscle test was originally developed to examine motor function in patients with polio, an LMN syndrome, their use may be inappropriate for patients with a UMN syndrome. More information about strength testing is provided in Chapter 4.

Reflex Testing

As previously discussed, a reflex is a subconscious, programmed unit of behavior in which a certain type of stimulus from a receptor automatically leads to the response of an effector. The response can be a simple behavior, movement, or activity. Indeed, many somatic and visceral activities are essentially reflexive. The circuitry that generates these patterns varies greatly in complexity, depending on the nature of the reflex, with each influenced by a hierarchy of control mechanisms. The muscle stretch reflex (myotatic or deep tendon) is one of the simplest known reflexes, depending on just two neurons and one synapse,271 which is influenced by cortical and subcortical input, and from the stimulation of two types of receptors: the GTO and the muscle spindle. Thus, tendon reflex activity depends on the status of the large motor neurons of the anterior horn (alpha motor neurons), the muscle spindles with the afferents fibers, and the small anterior horn cells (gamma neurons) whose axons terminate on the small intrafusal muscle fibers within the spindles.272

Muscle stretch reflexes are elicited by a short, sharp tap with the tendon hammer delivered to the tendon of a gently extended muscle. The physiology behind a muscle stretch reflex is described using the quadriceps reflex as an example. The tap of a reflex hammer on the tendon of the quadriceps femoris muscle, as it crosses the knee joint (Fig. 3-27), causes a brief stretch of the tendon and the muscle belly where the GTO and the muscle spindle are stimulated. Impulses are conducted along the axons of these motor neurons to the neuromuscular junctions, exciting the effectors (quadriceps femoris muscle), and producing a brief, weak contraction, which results in a momentary straightening of the leg (knee jerk).271 The stretch reflex can be divided into the following two:

• Dynamic stretch reflex, in which the primary endings and type Ia fibers are excited by a rapid change in length. The speed of conduction along the type Ia fibers and the monosynaptic connection in the cord ensure that a very rapid contraction of the muscle occurs to control the sudden and potentially dangerous stretch of the muscle. The dynamic stretch reflex is over within a fraction of a second, but a secondary static reflex continues from the secondary afferent nerve fibers.
• Static stretch reflex. As long as a stretch is applied to the muscle, both the primary and the secondary endings in the nuclear chain continue to be stimulated, causing prolonged muscle contraction for as long as the excessive length of the muscle is maintained, thereby affording a mechanism for prolonged opposition to prolonged stretch.

The most important observation during reflex examination is the reflex's amplitude.272 When a load is suddenly removed from a contracting muscle, shortening of the intrafusal fibers reverses both the dynamic and the static stretch reflexes, causing both sudden and prolonged inhibition of the muscle such that rebound does not occur.