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Peripheral Nervous System: Somatic Nerves
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The PNS consists of the cranial nerves (CNs) and the spinal nerves.
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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”).
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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.
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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.
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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.
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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.
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Note: Because nerves III, IV, and VI are generally examined together, CN V is described after CN VI.
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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.
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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.
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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.
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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.
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CN VIII (Vestibulocochlear)
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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.
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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
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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).
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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.
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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.
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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.
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Clinical
Pearl
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The SCC detectors are so sensitive that they can detect angular accelerations as low as 0.2 degrees per second,12 a rate of acceleration that would turn the head through 90 degrees in 30 seconds and produce a terminal velocity of 6 degrees per second: about as fast as the movement of the second hand of a watch.13
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CN IX (Glossopharyngeal)
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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.
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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:
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- Cricothyroid muscle
- Levator veli palatini muscle
- Salpingopharyngeus muscle
- Palatoglossus muscle
- Palatopharyngeus muscle
- Superior, middle, and inferior pharyngeal constrictors
- Muscles of the larynx.
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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.
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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.
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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.
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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).
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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.
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Essentially, there are four branches of spinal nerves4
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- 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.
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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
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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
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Clinical
Pearl
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- A dermatome is the area of skin supplied by a single nerve root. Pain dermatomes have less overlap than light-touch dermatomes.15
- A myotome is a muscle or group of muscles supplied by a single nerve root.
- A sclerotome is an area of bone or fascia supplied by a single nerve root.
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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).
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- 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.
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Clinical
Pearl
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Most individuals have no C1 posterior (dorsal) root; therefore, there is no C1 dermatome. When present, the C1 dermatome covers a small area in the central part of the neck close to the occiput.4
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Collateral Branches of the Anterior Division
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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).
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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).
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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.
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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.
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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.
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Clinical
Pearl
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Compared with the tibial division, the common fibular (peroneal) division is relatively tethered at the sciatic notch, and the neck of the fibula and may, therefore, be less able to tolerate or distribute tension, such as that occurs in acute stretching or with changes in limb position or length.
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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:
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- 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
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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
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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).
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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.
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Terminal Branches of the Tibial Nerve
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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:
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- 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.
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Common Fibular (Peroneal) Nerve
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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).
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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.
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- 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.
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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
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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.
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Autonomic Nervous System
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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.
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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.
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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
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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.
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Neuromuscular Control
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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:
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- 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
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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
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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
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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
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Clinical
Pearl
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Motor programs are codes within the nervous system that when initiated produce coordinated movement sequences.143 These programs are usually under central control, the sensory input is used extensively in selecting the appropriate motor program, in monitoring whether or not movement is consistent with expectations and in reflexively modulating the movement so that it is specific to environmental variables.143,144
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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.
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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
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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
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- 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
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Clinical
Pearl
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The term musculotendinous kinesthesia refers to the capacity for musculotendinous structures to contribute proprioception information. Two types of muscle receptors are commonly described: muscle spindles and GTO (Box 3-1). It is most likely that the muscle and the joint receptors work complementary to one another in this complex afferent system, with each modifying the function of the other.151 The muscle spindle functions as a stretch receptor, whereas the GTO functions as a monitor for the degree of tension within a muscle and tendon. Based on extensive work of Voss,152 Peck et al.153 proposed that in the extremities, smaller muscles with high muscle spindle concentrations, arranged in parallel with larger, less spindle-dense muscles, function primarily as kinesthetic monitors.154
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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
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Clinical
Pearl
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Proprioception can play a protective role in an acute injury through reflex muscle splinting via stimulation of the muscle spindles.164
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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
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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
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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
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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.
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Proprioceptive deficits can also be found with aging,172 arthrosis,173 and joint instability.148,164,166,167,174–177
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The Neurophysiology of Pain
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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.
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Clinical
Pearl
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Patients' attitudes, beliefs, and personalities may strongly affect their immediate experience of acute pain.
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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.
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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:
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- 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
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Clinical
Pearl
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- Hyperalgesia is an increased response to noxious stimulus. Primary hyperalgesia occurs at the site of injury, whereas secondary hyperalgesia occurs outside the site of injury.
- Allodynia is defined as pain in response to a previously innocuous stimulus.
- Referred pain is a site adjacent to or at a distance from the site of an injury's origin. Referred pain can occur from muscle, joint, and viscera. For example, the pain felt during a myocardial infarction is often felt in the neck, shoulders, and back rather than in the chest, the site of the injury.
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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:
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- The periosteum and joint capsule
- Subchondral bone, tendon, and ligament
- Muscle and cortical bone
- The synovium and articular cartilage
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Clinical
Pearl
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The aching type of pain, associated with degenerative arthritis and muscle disorders, is often accentuated by activity and lessened by rest. Pain that is not alleviated by rest, and that is not associated with acute trauma, may indicate the presence of a serious disorder such as a tumor or an aneurysm. This pain is often described as deep, constant, and boring and is apt to be more noticeable and more intense at night.207
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Chronic pain is typically more aggravating than worrying, lasts for more than 6 months, and has the following characteristics205:
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- 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
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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.
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Clinical
Pearl
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Referred pain, which can be either acute or chronic, is pain perceived to be in an area that seems to have little or no relation to the existing pathology.
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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:
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- 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
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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
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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.
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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.
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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:
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- 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.
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Clinical
Pearl
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Pain and nociceptive input can exert a strong influence on motor function and emotional state.178
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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.
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Clinical
Pearl
++
Several compounds, classified as biogenic amine transmitters or neuroactive peptides, exist that can facilitate or inhibit synaptic activity.
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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.
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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.
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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.
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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
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Clinical
Pearl
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It is important to assume that all reports of pain by the patient are serious in nature until proven otherwise with a thorough examination.219 In general, the greater the degree of pain radiation, the greater the chance that the problem is acute or that it is occurring from a proximal structure, or both.
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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
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Referred pain can be generated by:221
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- 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
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Macnab227 recommends the following classification for referred pain/symptoms:
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- Viscerogenic
- Vasculogenic
- Neurogenic
- Psychogenic
- Spondylogenic
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Viscerogenic Symptoms
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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.
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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:
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- 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.
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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.
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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.
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Clinical
Pearl
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A visceral source of the symptoms should always be suspected if the symptoms are not altered with movement or position changes.
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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).
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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.
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Vasculogenic Symptoms
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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
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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.
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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:
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- High thigh
- Above the knee
- Below the knee
- Ankle
- Forefoot
- Digit
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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.
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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.
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The neurologic tissues comprise those tissues that are involved in nerve conduction. Neurogenic causes of symptoms may include:
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- tumor compressing and irritating a neural structure of the spinal cord or the meninges;
- spinal nerve root irritation;
- peripheral nerve entrapment; and
- neuritis.
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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.
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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:
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- 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.
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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
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Clinical
Pearl
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It is important to remember that the Waddell and the SARS assessment tools are designed not to detect whether patients are malingering, but only to indicate whether they have symptoms of a nonorganic origin.
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Spondylogenic Symptoms
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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:
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- severe and unrelenting pain;
- the presence of a fever;
- bone tenderness; and
- unexplained weight loss.
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Pain Control Mechanisms
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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.
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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.
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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
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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.
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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.
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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.
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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.
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Nonpharmacological Control of Pain
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The pharmacological control of pain is discussed in Chapter 9. Clinicians can use several nonpharmacological therapeutic interventions to manage pain. These include:
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- 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.
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Orthopaedic Neurologic Testing
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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.
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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.
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Clinical
Pearl
++
A UMN lesion is characterized by spastic paralysis or paresis, little or no muscle atrophy, hyper-reflexive muscle stretch (deep tendon) reflexes in a nonsegmental distribution, and the presence of pathologic signs and reflexes.
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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.
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- 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
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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.
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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
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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
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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.
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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.
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Clinical
Pearl
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Medical etiologies for increased spasticity include a new or enlarged CNS lesion, genitourinary tract dysfunction (infection, obstruction, etc.), gastrointestinal disorders (bowel impaction, hemorrhoids, etc.), venous thrombosis, fracture, muscle strain, and pressure ulcers.
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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:
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- 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
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Wernicke's Encephalopathy
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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
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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
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Dysphonia presents as a hoarseness of the voice. Usually, no pain is reported. Painless dysphonia is a common symptom of Wallenberg syndrome.247
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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”).
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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.
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Miosis is defined as the inability to dilate the pupil (damage to sympathetic ganglia). It is one of the symptoms of Horner syndrome.
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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.
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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.
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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.
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Clinical
Pearl
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The differing symptoms between a UMN lesion and an LMN lesion are the result of injuries to different parts of the nervous system. LMN impairment involves damage to a neurologic structure distal to the anterior horn cell, whereas UMN impairment involves damage to a neurologic structure proximal to the anterior horn cell, namely, the spinal cord or CNS.
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Complaints of Dizziness
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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
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- 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
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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:
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- 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.
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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.
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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
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Clinical
Pearl
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Although used extensively, the term deep tendon reflex is a misnomer because tendons have little to do with the response other than being responsible for mechanically transmitting the sudden stretch from the reflex hammer to the muscle spindle. In addition some muscle stretch reflexes have no tendons.272
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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:
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- 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.
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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.
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Clinical
Pearl
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Although several types of reflex hammers are popular today, no study has demonstrated any hammer to be superior to another.
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Reflex integrity is defined as the intactness of the neural path involved in a reflex and the assessment of reflexes is extremely important in the diagnosis and localization of neurologic lesions.2,273 The testing of the muscle stretch reflex provides the clinician with a direct way of assessing the peripheral nervous system and an indirect way of examining the CNS. Six of these are regularly tested (Table 3-17, Table 3-18): the biceps (C5), brachioradialis (C6), and triceps (C7) in the upper extremity, and the quadriceps (L4), extensor digitorum brevis (L5–S1) and Achilles (S1) in the lower extremities. It is worth noting that it is difficult to elicit a reflex response with the extensor digitorum brevis test, which is why it is not often performed.
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Clinical
Pearl
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The abdominal and cremaster reflexes (superficial skin reflexes) are decreased or absent on the side affected by a corticospinal tract lesion and, thus, serve as adjuncts to the muscle stretch and plantar reflexes.274
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Muscle Stretch Reflexes
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To perform a muscle stretch reflex, the chosen tendon is normally struck directly and smartly with the reflex hammer. An exception is the biceps reflex, which is best tested by tapping the thumb, which has been placed over the tendon. The limb to be tested should be relaxed and in a flexed or semiflexed position. The Jendrassik maneuver can be used during testing to enhance a muscle reflex that is difficult to elicit:275
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- For the upper extremity reflexes, the patient is asked to cross the ankles and then to isometrically attempt to abduct the legs.
- For the lower extremity reflexes, the patient is asked to interlock the fingers and then to isometrically attempt to pull the elbows apart (Fig. 3-28.)
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Clinical
Pearl
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In the elderly, up to 50% without neurologic disease lack an Achilles reflex bilaterally,276 and small percentages (3–5 percent) of normal individuals have generalized hypereflexia.277
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Two muscle stretch reflex scales can be used to grade a reflex: National Institute of Neurological Disorders and Stroke (NINDS) scale and the Mayo Clinic scale. The NINDS scale uses the following five-point grading system:
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- 0, absent (areflexia). The absence of a reflex signifies an interruption of the reflex arc.
- 1, slight and less than normal (hyporeflexia).
- 2, in the lower half of normal range.
- 3, in the upper half of normal range (brisk).
- 4, enhanced and more than normal (hyperreflexive). Includes clonus if present. A hyperreflexive reflex denotes a release from cortical inhibitory influences.
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One of the problems with the NINDS scale is that it does not have a separate category for normal, making it necessary to choose between a low normal or a high normal.
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The Mayo Clinic uses the following nine point scale:278
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- Absent: −4
- Just elicitable: −3
- Low: −2
- Moderately low: −1
- Normal: 0
- Brisk: +1
- Very brisk: +2
- Exhaustible clonus: +3
- Continuous clonus: +4
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An absent or exaggerated reflex is significant only when it is associated with one of the following:279
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- The reflex is unusually brisk compared with reflexes from a higher spinal level.
- The exaggerated reflexes are associated with other findings of the UMN disease.
- The absent reflexes are associated with other findings of LMN disease.
- The reflex amplitude is asymmetric. Reflex asymmetry has more pathologic significance than the absolute activity of the reflex—a bilateral patella reflex of 3 is less significant than a 3 on the left and a 2 on the right. Additionally, in cases where the reflex findings are symmetrical, but either elevated or depressed, further investigation is required. For example, a patient presenting with symmetrically brisk patella tendon and Achilles stretch reflexes, while simultaneously having absent stretch reflexes in the upper extremity, requires further investigation (this is a typical finding with amyotrophic lateral sclerosis or Lou Gehrig disease, a mixed UMN and LMN pathology).280
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The findings from the muscle reflex testing can occur as a generalized, or local, phenomenon:
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- Generalized hyporeflexia. The causes of generalized hyporeflexia run the gamut from neurologic disease, chromosomal metabolic conditions, and hypothyroidism to schizophrenia and anxiety.206
- Nongeneralized hyporeflexia. Generally, an asymmetrically depressed or absent reflex is suggestive of pathology that is impacting the reflex arc directly, such as a LMN lesion or sensory paresis, which may be segmental (root), multisegmental (cauda equina), or nonsegmental (peripheral nerve). Nongeneralized hyporeflexia can result from peripheral neuropathy, spinal nerve root compression, and cauda equina syndrome. It is thus important to test more than one reflex and to evaluate the information gleaned from the examination, before reaching a conclusion as to the relevance of the findings.
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In those situations demonstrating an elevated or brisk reflex, the CNS's normal role of integrating reflexes may have been disrupted, indicating an UMN lesion, such as a brain stem or cerebral impairment, spinal cord compression, or a neurologic disease. However, the distinction has to be made between a brisk reflex and the one that is hyperreflexive. True neurological hyperreflexia contains a clonic component and is suggestive of CNS (UMN) impairment. The clinician also should note any additional recruitment that occurs during the reflex contraction of the target. A brisk reflex is a normal finding, provided that it is not masking a hyperreflexia caused by an incorrect testing technique. Unlike hyperreflexia, a brisk reflex does not have a clonic component. As with hyporeflexia, the clinician should assess more than one reflex before coming to a conclusion about a hyperreflexia. The presence of an UMN impairment can be confirmed by the presence of the pathologic reflexes (see next section).
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Clinical
Pearl
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Even though muscle stretch reflexes have long been assumed to be good objective signs, the interrater reliability of muscle stretch reflex grading for the same subject is quite variable and subjective due to both patient and clinician factors.278,281
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There are two basic pathologic reflexes: the Babinski and its variants (Chaddock, Oppenheim, Gordon, etc.) and the Hoffman and its variants (ankle and wrist clonus) (Table 3-19). A number of primitive reflexes are normally integrated by individuals as they develop. Pathologic reflexes occur when an injury or a disease process results in a loss of this normal suppression by the cerebrum on the segmental level of the brain stem or the spinal cord, resulting in a release of the primitive reflex.282 Thus, the presence of pathologic reflexes is suggestive of CNS (UMN) impairment and requires an appropriate referral.
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In this test, the clinician applies noxious stimuli to sole of the patient's foot by running a pointed object along the plantar aspect (Fig. 3-29).283 A positive test, demonstrated by extension of the great toe (extensor toe sign) and a splaying (abduction) of the other toes, is indicative of an injury to the corticospinal tract.284–286 A negative finding is slight toe flexion, smaller digits greater than the great toe. As Babinski observed,284 the pyramidal tracts are not well developed in infants, and these signs, which are abnormal past the age of 3 years, are usually present.
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The Gonda-Allen sign is a variant of the Babinski. The patient is positioned in supine. Grasping the patient's foot, the clinician provides a forceful downward stretch or snaps the distal phalanx of the second or fourth toe (Fig. 3-30). A positive response is the extensor toe sign.287 The Gonda-Allen method is considered more sensitive than the classic Babinski method.288
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The Allen-Cleckley sign (Fig. 3-31) is another variant of the Babinski. The patient is positioned in supine. Grasping the patient's foot, the clinician provides a sharp upward flick of the second toe or pressure over the distal aspect or ball of the toe. A positive response is the extensor toe sign.288
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The patient is positioned in supine. The clinician applies noxious stimuli along the shin of the patient's tibia by running a fingernail downward toward the foot (Fig. 3-32). A positive test, demonstrated by the extensor toe sign, is theoretically indicative of UMN impairment. However, the diagnostic value of this test is as yet unknown.289
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The patient is positioned in supine or sitting. The clinician strokes the lateral malleolus from proximal to distal with a solid, relatively sharp object (Fig. 3-33). A positive response is the extensor toe sign. The diagnostic value of this test is as yet unknown.289
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The patient is positioned in supine or sitting. The clinician provides a sharp, quick squeeze of the Achilles tendon (Fig. 3-34). A positive response is the extensor toe sign. This test remains unstudied for diagnostic value.
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The Hoffmann sign, also referred to as the digital reflex, the snapping reflex, Tromner sign and Jakobson sign, is the upper limb equivalent of the Babinski. However, unlike the Babinski, some normal individuals can exhibit a Hoffmann sign.274 The clinician holds the patient's middle finger and briskly pinches the distal phalanx, thereby applying a noxious stimulus to the nail bed of the middle finger (Fig. 3-35).274 A positive test is adduction and opposition of the thumb and slight flexion of the fingers. There are no known studies assessing the interexaminer reliability of this test (Table 3-18), and its significance remains disputed in the literature. Denno and Meadows290 devised a dynamic version of this test to assist in the diagnosis of early spondylotic cervical myelopathy, which involved the patient performing repeated flexion and extension of the head before being tested for the Hoffmann sign.
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Cross Up Going Toe Sign
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This is another variation of the Babinski. The patient is positioned in supine. The clinician passively raises the opposite limb into hip flexion and then instructs the patient to hold the leg in flexion while the clinician applies a downward force against the leg (Fig. 3-36). A positive test is associated with great toe extension of the opposite leg during resistance the hip flexion. Of the few studies of this test, Willoughby and Eason found the test to have little value as a sensitive indicator of a pyramidal tract lesion in 125 normal subjects and 192 patients with neurological disorders due to the high frequency of false positive signs in normal subjects and patients with other neurological disorders.303
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The patient is positioned in supine or sitting. The technique can be applied to the wrist (sudden wrist extension) or to the ankle (sudden dorsiflexion) (Fig. 3-37). The stretch is then maintained. A positive response is more than three involuntary beats of the ankle or wrist (two to three twitches are considered normal). In some patients, there is a more sustained clonus; in others, there is only a very short-lived finding. During the testing, the patient should not flex the neck, as this can often increase the number of beats. A positive test is theoretically indicative of UMN impairment, but the diagnostic value of this test is as yet unknown.
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Other pathological reflexes include:
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Inverted Radial (Supinator) Reflex
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The inverted radial reflex sign, introduced by Babinski, is commonly used in clinical practice to assess cervical myelopathy. There are two components of this abnormal reflex: (1) an absence of contraction of the brachioradialis muscle when the styloid process of the radius is tapped (Fig. 3-38), and (2) a hyperactive response of the finger flexor muscles; a response that is subserved by a lower spinal cord segment (C8).291 To date, it is unknown whether the sign correlates with the presence or severity of myelopathy. Indeed, an isolated, inverted supinator reflex may be a variation of a normal clinical examination.292 Theoretically, a true response is likely related to increased alpha motor neuron excitability below the level of the lesion; however, a possible contribution of the dynamic muscle spindles cannot be excluded.
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The patient is positioned in sitting. The clinician asks the patient to hold all of his/her fingers in extension. A positive sign involves the involuntary flexion and abduction within 1 minute of extended and adducted fingers when held statically. To date there has only been one study293 that examined the sensitivity of the finger escape sign, which identified a sensitivity of 55% in a sample of 36 subjects with myelopathy.
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The patient is positioned in supine or sitting. A number of methods to elicit this reflex have been advocated. The clinician may stroke the thenar eminence of the hand in a proximal to distal direction with a reflex hammer (Fig. 3-39) or may stroke the hypothenar eminence in a similar fashion. The procedure can be repeated up to five times to detect a continuous response. If the response diminishes, the test is considered negative. A positive test is contraction of the mentalis and orbicular oris muscles causing wrinkling of the skin of the chin and slight retraction (and occasionally elevation of the mouth). A study by Owen and Mulley294 found that the reflex is often present in normal people and may be absent in disease states. The study concluded that testing merely for the presence or absence of the reflex lacks both specificity and sensitivity, but that a strong, sustained, and easily repeatable contraction of the mentalis muscle, which can be elicited by stimulation of areas other than the palm, is more likely to indicate cerebral damage. Another study295 found diagnostic value in using combinations of two or three pathologic reflexes to distinguish between neurologically damaged patients and normal age-matched controls.
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The patient is positioned supine, with the knees flexed and both feet flat on the bed. The patient is asked to raise the head against resistance, cough, or attempt to sit up with the hands resting behind the head.296 The clinician observes for motion at the umbilicus, which should remain in a straight line. Beevor sign, an upward deflection of the umbilicus on flexion of the neck, is the result of paralysis of the inferior portion of the rectus abdominis muscle, so that the upper fibers predominate, pulling the umbilicus upwards. The condition may be caused by spinal cord injury at or below the level of T10.253
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Clinical
Pearl
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Beevor sign is a common finding in patients with facioscapulohumeral dystrophy, even before functional weakness of abdominal wall muscles is apparent, but is absent in patients with other facioscapulohumeral disorders.297
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Lhermitte Symptom or “Phenomenon”
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This is not so much a pathologic reflex as it is a symptom, described as an electric shock-like sensation that radiates down the spinal column into the upper or the lower limbs with passive flexion of the neck with the patient in the long sit position (Fig. 3-40). It may also be precipitated by extending the head, coughing, sneezing, bending forward, or moving the limbs.298 Lhermitte sign is most prevalent in patients with multiple sclerosis,299 cervical spondylotic myelopathy, cervical radiation injury, and neck trauma.300 Smith and McDonald301 postulated that there is an increased mechanosensitivity to traction on the cervical cord of injured axons located within the posterior (dorsal) columns. Although a herniated disk is an anteriorly placed lesion and the spinothalamic tract is usually more affected than the posterior columns, flexion of the neck will produce stretching of the posterior aspects of the cord, but not the anterior part at the site of the impairment, and this may explain this particular symptom. To date, there are no reports investigating the interexaminer reliability of this test. One study302 reported a sensitivity of 27%, specificity of 90%, positive predictive value of 55%, and negative predictive value of 75% for the active flexion and extension test, which partly resembles this test.
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The patient is positioned in supine or sitting. The clinician taps on the dorsal aspect of the cuboid bone using the sharp end of a reflex hammer (Fig. 3-41). A positive response is flexion of the four lateral toes. This test remains unstudied for diagnostic value.
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The supraspinal reflexes produce movement patterns that can be modulated by descending pathways and the cortex. A number of processes, which are involved in locomotor function, are oriented around these reflexes and are referred to as righting reflexes. Righting reflexes can be subcategorized as the following: visual righting reflexes, labyrinthine righting reflexes, neck righting reflexes, body on head righting reflexes, and body on body righting reflexes. The primary purpose of the righting reflexes is to maintain a constant position of the head in relation to a dynamic external environment.
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The head and the neck are areas of intense reflex activity. Head movements, which occur almost constantly, must be regulated to maintain normal eye–head–neck–trunk relationships and to allow for visual fixation during head movements (Table 3-20). The visual field and pathway are important regulators of postural control. Visual input for postural control helps fixate the position of the head and the upper trunk in space, primarily so that the center of mass of the trunk maintains its position over the well-defined limits of foot support. Aside from the visual field itself providing an important source of postural control, the extraocular muscles may also provide proprioceptive information through two distinct pathways into the oculomotor nuclei, one serving to generate eye rotations, while the other providing sensory information regarding eye alignment and stabilization.304,305
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While the visual and vestibular systems are individually two of the most important providers of information, it is their constant interaction with each other and with cervical mechanoreceptors (particularly the short-range rotators, i.e., the obliquus capitis posterior inferior, rectus capitis posterior major, splenius capitis, and sternocleidomastoid) that makes the control of upright posture possible, especially when considering their combined role in the reflex modulation of muscular tone through various groups of postural muscles306:
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Vestibulo-Ocular Reflex (VOR)
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The VOR is stimulated by movement of the head in space and creates certain eye movements that compensate for head rotations or accelerations. The VOR may be subdivided into three major components:
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- The rotational VOR, which detects head rotation through the SCC.
- The translational VOR, which detects linear acceleration of the head via the utricle and saccule.
- The ocular counter-rolling response, or optokinetic reflex, which adapts eye position during head tilting and rotation.
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The VOR can be tested in a number of ways:
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Dynamic Visual Acuity269
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After establishing baseline visual acuity with a Snellen chart, this test measures visual acuity with concurrent head movement. The patient's head is moved from side to side at a frequency of 1 Hz while the patient reads the Snellen chart. A decrease by two lines is suspicious and by three or more is indicative of an abnormal VOR.
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The clinician faces the patient, who fixes gaze on the clinician's nose. The clinician then oscillates the patient's head 30 degrees side to side at 0.5–1 Hz. Eye movements that are not smooth but interrupted by saccades toward the fixation target indicate bilateral vestibular lesions.
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Head-Shaking Nystagmus Test269
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The clinician holds the patient's head firmly, with the palms of the hands against the patient's cheeks, and produces a series of rapid but small horizontal head turns for approximately 30 seconds, with the patient's eyes closed. Upon opening the eyes, the nystagmus will beat away from the side of a unilateral peripheral vestibular lesion, or toward the lesioned side in patients with Ménière disease.
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The patient fixates gaze on the clinician's nose. The clinician then moves the patient's head in a horizontal plane in a rapid, passive manner with unpredictable timing and direction. If the reflexive movement of the eyes is inappropriate (too big or too small), a corrective (saccadic) movement will occur. A patient with vestibular loss will have difficulty in maintaining gaze fixation, requiring a corrective saccade (fast eye movement) to maintain gaze fixation on the nose. Presence of this corrective action may indicate a lesion of the vestibular nerve.307
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The Cervico-Ocular Reflex
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The cervico-ocular reflex serves to orient eye movement to changes in neck and trunk position. Visual fixation at high speeds requires the contraction of the extraocular muscles to allow eye movements to counteract the effect of the head movements, even if the head is turning in the opposite direction. The ability to track and focus on a moving target that is moving across a visual field is termed smooth pursuit and requires a greater degree of voluntary control than the cervico-ocular and VORs can provide. The area in the brain stem where this integration of horizontal eye movements takes place is the paramedian pontine reticular formation. The ability to read a book or to scan a page requires saccadic eye movements. Unlike smooth pursuit, saccades can occur with a visual stimulus, by sound, verbal command, or tactile stimuli. However, like smooth pursuit, saccades are generated in the paramedian pontine reticular formation. The cervico-ocular reflex can be tested using three methods:
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- Visual fixation. The patient is seated and is asked to look straight ahead and focus on the tip of a pencil, which is held by the clinician at an arm's length from the patient. The test is repeated, with the patient's eyes turned to the extremes of horizontal and vertical gaze and the pencil tip positioned accordingly.
- Smooth pursuit can be tested by having the patient fix his or her gaze on an object placed directly in front. The object is then moved to the right, while the patient follows it with the eyes. The clinician looks to see if the patient has any difficulty tracking the object. An abnormal response is observed if the patient's fixation on the target moving synchronously with the head is interrupted by rapid eye movements or saccades, which indicates that the pursuit is not holding the eye on the moving target. The object is moved back to the start position before being moved to the left, while the patient again follows it with the eyes. The object can then be moved in various directions, combining horizontal, vertical, and diagonal movements, to test if the patient can follow the object with the eyes without saccadic movements.
- Saccade test. The patient is asked to rapidly move the eyes back and forth between two widely spaced targets while keeping the head still. An abnormal finding is if the patient takes multiple eye movements, rather than a single jump, to exactly fix on a target.
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Difficulty with these tests may indicate a lesion of the cerebellum, reticular formation, cerebral cortex, or a CN lesion (oculomotor, trochlear, or abducens).307
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The Cervicocollic Reflex (CCR)
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The CCR serves to orient the position of the head and the neck in relation to disturbed trunk posture. Acting similarly to a stretch reflex, this reflex involves reflexive correction of cervical spine position through cocontraction of specific cervical muscles.
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The Vestibulocollic Reflex (VCR)
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The VCR maintains postural stability by actively stabilizing the head relative to space, through reflexive contraction of those cervical muscles opposite to the direction of cervical spine perturbation. It should be noted that this reflex is distinct and largely dissociated from the vestibulospinal reflex, which orients the extremities to the position of the head and the neck.306
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The CCR and VCR reflexes appear perfectly suited through their dynamic and somatotopic characteristics to compensate for positional disturbances of the head and the neck with respect to the trunk.308–310