The peripheral nervous system (PNS) consists of spinal nerve roots, the brachial and lumbosacral plexi, peripheral nerves, autonomic ganglia, the neuromuscular junction, and muscles. This chapter focuses on the more proximal elements of the PNS, whereas Chapter 24 discusses the neuromuscular junction and muscle disorders. The symptoms and signs of PNS dysfunction often form recognizable patterns that can help localize deficits to one of these parts of the nervous system. Electrodiagnostic studies can also be particularly helpful in characterizing contributory lesions.

SPINAL NERVE ROOTS AND RADICULOPATHY

ANATOMY

The vertebral bodies form the bony building blocks of the spine. Intervertebral disks are located between the vertebral bodies. They provide some degree of cushioning and allow movement. Together with neighboring joints, the elements of the vertebral bodies above and below each intervertebral disk form a bony canal called an intervertebral foramen. Spinal nerve roots travel through the intervertebral foramina on their way to the limbs. Each spinal nerve root is formed by a combination of a ventral and dorsal nerve root leaving the spinal cord. Ventral nerve roots ultimately facilitate motor function; the muscles served by a ventral nerve root make up a myotome. Dorsal nerve roots transmit sensory information; the cutaneous region in the distribution of a dorsal root is referred to as a dermatome. It is important to note that there is overlap in the somatic territories from one myotome or dermatome to the next. As a result, strength and sensation may be relatively preserved on neurologic examination even if there is demonstrable injury to a given nerve root.

PATHOPHYSIOLOGY

Nerve root dysfunction is referred to as radiculopathy. Radiculopathy can result from structural or nonstructural causes. Structural causes are most common, and there are two main sources of nerve root compression: intervertebral disk herniation and degenerative changes in the spine. Acute disk herniation is common in younger individuals and is more likely to affect a single spinal nerve root. Degenerative changes include disk desiccation, arthritic bony growth (spondylosis and osteophyte formation), and changes in bony alignment (spondylolisthesis). Often these changes cause narrowing of the intervertebral foramina, with secondary impingement of nerve roots at multiple levels. Radiculopathies at the C7 and L5/S1 spinal levels are the most frequent ones in the cervical and lumbosacral regions respectively. Thoracic radiculopathies are relatively uncommon.

In the absence of a compressive cause, consideration must be given to infectious, inflammatory, infiltrative, and vascular etiologies. For instance, cytomegalovirus, herpes simplex, varicella zoster, and human immunodeficiency viruses and Lyme disease can cause radiculopathy. Sarcoidosis can be associated with an inflammatory radiculitis. Neoplastic processes can damage the nerve root through infiltration. Infarction (e.g., from vasculitis or diabetes) is an unusual cause of radiculopathies.

SYMPTOMS AND SIGNS

Pain, sensory changes, or both, radiating in the distribution of a spinal nerve root point to a radiculopathy. Accordingly, there can be some degree of sensory, strength, or reflex abnormality that helps specify the nerve root of interest (Table 23-1). When patients present with upper extremity symptoms, Spurling’s maneuver can be performed by putting gentle pressure on the head as it is turned toward the side of pain while the neck is extended; the test is considered positive if symptoms are reproduced. Of note, the assessment should be avoided in patients who could have spine instability, as in the setting of rheumatoid arthritis. The straight leg raise test can be helpful in corroborating a lumbosacral radiculopathy. The test is considered positive when the patient’s symptoms are reproduced when the leg is passively elevated, typically beyond 30 to 60 degrees, with the knee extended and the foot dorsiflexed.

DIAGNOSIS

A diagnosis of radiculopathy can usually be made on clinical grounds. Immediate imaging is warranted if infection or malignancy is a concern, if pain is accompanied by saddle anesthesia and urinary retention, or if symptoms are acute in onset and associated with progressive deficits. Magnetic resonance imaging (MRI) is best, when possible to obtain. Nerve conduction studies (NCSs) and electromyography (EMG) are most helpful in confirming the presence of a radiculopathy when performed at least 3 weeks after symptom onset and when there is clinical weakness. A lumbar puncture (LP) may be indicated when an infiltrative or infectious process is high on the differential. The results of investigative studies guide treatment approaches.

PLEXUS AND PLEXOPATHIES

ANATOMY

Multiple spinal nerve roots form an intricate network called a plexus, in the upper and lower limbs. In the arms, roots C5-T1 form the brachial plexus. The brachial plexus can be organized into trunks, divisions, cords, and branches before forming the individual nerves that serve the skin and muscles in the arms (Fig. 23-1). The brachial plexus lies behind the scalene and pectoralis muscles and clavicle. All of the major nerves in the legs arise from the lumbosacral plexus, a combination of the L1-S3 nerve roots. The upper portion of this plexus, the lumbar plexus, is depicted in Figure 23-2. The lumbosacral plexus lies behind the psoas muscles in the retroperitoneum before continuing below the pelvic outlet.

FIGURE 23-1. The brachial plexus. (Reprinted with permission from Williams A. Massage Mastery. 1st ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012. Figure 5.8.)

PATHOPHYSIOLOGY

Trauma, compression, inflammation, metabolic disturbance, malignancy, and radiation can cause plexus lesions. Trauma is the most common etiology of brachial plexopathies in adults. Specifically, motorcycle and other motor vehicle accidents can result in damage from abrupt traction when the head is pulled away from the shoulder. Inflammatory brachial plexopathies, also referred to as brachial neuritis or Parsonage-Turner syndrome, are also often acute in onset. Triggers can include antecedent illness, vaccination, surgical procedures, or exercise; some triggers are difficult to identify. An apical lung (Pancoast) tumor can lead to a more insidious development of a brachial plexopathy from local infiltration or direct compression. Similarly, radiation therapy may be associated with a slowly developing brachial plexopathy, even a year following the conclusion of treatment to the shoulder or chest region. In neonates, brachial plexopathies may result from traction injuries at birth, particularly in the setting of shoulder dystocia.

Type 2 diabetes, in the form of diabetic amyotrophy, is the most common cause of lumbosacral plexopathy. As with brachial plexopathies, neoplasias can be associated with lumbosacral plexopathies. Compression (e.g., from a neonate’s skull) in the peripartum period or from a retroperitoneal hematoma, is also a cause of lumbosacral plexopathies.

FIGURE 23-2. The lumbosacral plexus (left), and upper (lumbar) plexus alone (right). Reprinted with permission from Anderson MK. Foundations of Athletic Training. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012. Figure 12.4.

SYMPTOMS AND SIGNS

Plexus lesions cause patchy pain and sensory symptoms and signs. It can be helpful to think about brachial plexus lesions in two main etiologic categories: (1) structural (e.g., a brachial plexopathy from a tumor, traction injury during trauma or surgery, or laceration due to line placement) and (2) inflammatory (e.g., as in brachial neuritis or Parsonage-Turner syndrome). In a classic Parsonage-Turner syndrome, patients awaken from sleep in the early hours of the morning with pain in the periscapular and shoulder girdle regions. Typically, pain is severe and can last up to 4 weeks before abating spontaneously. The pain is ultimately associated with weakness (sometimes resulting in scapular winging) and muscle atrophy. If brachial neuritis is on the differential, it is important to assess for scapular winging but also to look for a Horner’s syndrome; the latter can be caused by an apical lung tumor.

Typically, patients with lumbosacral plexopathies present with leg pain, sensory change, atrophy, and asymmetric weakness. Weakness of knee extension, adduction hip flexion, or combinations of these, points to a lumbar plexus problem. Foot drop is more consistent with a lumbosacral plexopathy. In diabetic amyotrophy, there is associated weight loss and autonomic dysfunction.

DIAGNOSIS

EMGs can be very helpful in characterizing plexus lesions. In certain situations, imaging is important to evaluate for structural compression of the plexus. An analysis of serology for infectious, autoinflammatory, and metabolic disturbances and, less commonly, cerebrospinal fluid analysis, may help determine a cause and guide management. Ultimately, plexopathies due to inflammation often recover spontaneously over months, whereas compressive lesions may require intervention.

PERIPHERAL NERVES AND MONO- AND POLYNEUROPATHIES

Peripheral nerve deficits can be classified according to whether they affect motor, sensory, autonomic, or combinations of fibers. Further, neuropathies may preferentially affect large-diameter fibers responsible for proprioception, or small-diameter fibers that relay pain and temperature information. The pattern of nerve involvement can give hints to underlying pathophysiology (Box 23-1).

PATHOPHYSIOLOGY

A myriad of acquired and genetic processes can underlie peripheral nerve lesions. Infectious, inflammatory, toxic, and metabolic conditions may play roles in acquired conditions; diabetes is a particularly common cause of neuropathies (Table 23-2). Genetic variations, such as those associated with Charcot–Marie–Tooth (CMT) disease, can be seen in hereditary disorders. Injured nerves can react only in a limited number of ways. Accordingly, key information gleaned from the history, exam, and investigative studies help characterize the type of peripheral nerve lesion.

SYMPTOMS AND SIGNS

Patients may describe positive or negative sensory, motor, and autonomic symptoms. For example, tingling and “pins and needles” sensations, together with reduced joint position sense and reflexes suggest large fiber dysfunction. Burning, shooting, and jabbing pain, combined with deficits in pain and temperature sensation, often indicate a small fiber neuropathy. Weakness can accompany sensory changes, or, less often, be the primary symptom. Autonomic symptoms include blood pressure (BP) dysregulation (particularly orthostatic hypotension), abnormal sweating, urinary retention, and impotence. The temporal course (e.g., acute, subacute, or insidious) and the pattern of progression (e.g., gradually progressive, stepwise, or relapsing-remitting) can point to specific etiologies. It is equally important to gather data about the patient’s medical history (e.g., the presence of diabetes, thyroid dysfunction, malignancy, or autoimmune disease), medication use (e.g., chemotherapy), habits (e.g., alcohol intake), and occupational history (e.g., work that requires lots of typing) that may inform the search for a cause.

BOX 23-1. Approach to the Classification of Peripheral Neuropathy

Related posts:

The Sensory System The Approach to Coma and Altered Consciousness Head Trauma Neuro-Ophthalmology Demyelinating Diseases of the Central Nervous System Disorders of the Spinal Cord

Stay updated, free articles. Join our Telegram channel

Join