In this chapter, we will address the relevant anatomy, pathogenesis, epidemiology, clinical features, diagnostic testing, specific disorders, rehabilitative management, and prognosis related to radiculopathy and plexopathy.

Each nerve fiber is surrounded by an outer endoneurial sheath. Bundles of nerve fibers are collected into fasciculi, with each fasciculus surrounded by a perineural sheath that provides tensile strength and elasticity to the nerve. Fasciculi are set in areolar connective tissue packing called the epineurium, which protects the nerve from compression (see Fig. 72–1).¹

Roots

The dorsal roots carry afferent sensory neurons whose cell bodies reside in the dorsal root ganglion (DRG). The DRG is located in the intervertebral foramen. The ventral roots contain primarily alpha-, beta-, and gamma-type neurons carrying motor outflow from the spinal cord. As they exit the intervertebral foramen, the dorsal and ventral roots join to form the mixed spinal nerve. (Fig. 72–2)

The spinal nerves then divide into mixed dorsal and ventral rami. The dorsal rami innervate the paraspinal muscles and skin over the back of the neck and trunk. The ventral rami coalesce in the cervical, lumbar, and sacral regions to form their respective brachial, lumbar, and lumbosacral plexuses

Brachial Plexus

The brachial plexus is a complex network of intertwined nerves arising from the cervical spinal nerves, which innervates the shoulder and upper extremity. Just distal to their origin, the ventral spinal rami are joined by the gray ramus communicantes from corresponding cervical ganglia of the sympathetic chain to become the “roots” of the brachial plexus. The C5–C6 roots join to form the upper trunk, the C7 root becomes the middle trunk, and the C8–T1 roots combine as the lower trunk. The supraclavicular brachial plexus emerges between the anterior and middle scalenes and courses superficially along the posterior cervical triangle. As the plexus dives behind the clavicle and above the first rib, each of the three trunks splits into anterior and posterior divisions. The posterior divisions unite to form the posterior cord, which innervates the posterior aspect (sensory and motor) of the upper limb. The anterior divisions combine to form the medial and lateral cords, which innervate the anterior aspect (sensory and motor) in the upper limb. The cords are named according to their location relative to the axillary artery, but they also can be generally associated with the aspect of the limb that they innervate. The infraclavicular plexus runs through the axilla, where the cords ultimately split into their terminal branches as seen in Figure 72–3 and described in Table 72–1.^2,3

Cadaveric studies note that up to 53% of plexuses demonstrate some variant in brachial plexus innervation. A prefixed plexus, where C4 fibers provided a more prominent contribution, was present in 25.5% to 48% of cases, while 2% to 5% of cases exhibited a postfixed plexus with increased contribution of T2 fibers.^4–6

Lumbar Plexus

The ventral rami of the L1–L4 roots form the lumbar plexus, which lies in the retroperitoneum behind the psoas muscle. The most proximal nerves of the lumbar plexus are the iliohypogastric (L1), ilioinguinal (L1), and genitofemoral (L1–L2) nerves, which supply sensation to the inferior abdominal wall and medial groin. The lateral femoral cutaneous nerve (L2–L3) runs under the inguinal ligament near the superior iliac spine and supplies sensation to the anterolateral thigh. The two most prominent branches of the lumbar plexus are the obturator (L2–L4) and femoral (L2–L4) nerves. The obturator nerve passes medial to the psoas muscle and exits through the obturator foramen to supply innervation to the thigh adductors, as well as sensation to a small area on the medial thigh. The femoral nerve passes lateral to the psoas muscles and exits under the inguinal ligament to supply innervation to the hip flexors and knee extensors, as well as sensation to the medial calf (through the saphenous nerve) and anterior medial thigh (through the medial and intermediate cutaneous nerves of the thigh).

Lumbosacral Plexus

The ventral rami of L5–S4 roots form the lumbosacral plexus, which lies adjacent to the piriformis muscle. Branches of the L4 and L5 roots form the lumbosacral trunk, which joins the sacral plexus (S1–S3) to form the sciatic nerve. The sciatic nerve exits the pelvis through the greater sciatic foramen, passes under the piriformis muscle, and then innervates the knee flexors. It subsequently separates into the common peroneal and tibial nerves, which innervate the muscles of the leg, ankle, and foot and provide sensation to the entire lower leg and foot, with the exception of the medial calf (saphenous nerve). Distal to the takeoff of the lumbosacral plexus arises the superior gluteal nerve (L4–S1), which innervates the hip abductors and internal rotators, and the inferior gluteal nerve (L5–S2), which innervates the gluteus maximus muscle. Sensation to the lower buttock and posterior thigh is provided by the posterior cutaneous nerve of the thigh (S1–S3). The sacral plexus also contributes to the pudendal nerve (S2–S4), which innervates the external anal sphincter (Fig. 72–4).^7,8

The pathophysiology of nerve injury is related to the mechanism and the severity of insult. Two types of pathology can occur after insult to a nerve: axonal loss and demyelination. Axonal loss results in Wallerian degeneration distal to the lesion site. Insults to myelinated axons can cause demyelination and a related slowing of conduction or conduction block.⁹

Injury to a nerve can occur at the level of the root, plexus, or peripheral nerve. Processes that occur at the root level include spondylosis, disc herniation, tumor, infection, and nerve root avulsions. At the brachial plexus, traction is the most common cause of injury, followed by compression, lacerations, ischemia, neoplasms, radiation, thoracic outlet syndrome (TOS), and neuralgic amotrophy.¹⁰ Pure lumbosacral plexopathies are rare. Lumbosacral radiculoplexus neuropathies are more common, including inflammatory diabetic and nondiabetic lumbosacral radiculoplexus neuropathies.¹¹

Obtaining a thorough history and physical exam is the key to establishing an accurate diagnosis of nerve injury. Patients often present with a constellation of symptoms including pain, sensory loss, and weakness in the upper or lower extremities. It is important to determine the date of symptom onset, progression of symptoms, and any recent or antecedent history of malignancy, surgery, procedures, radiation, trauma, or infection. Knowledge of dermatomal, myotomal, and peripheral nerve innervation patterns is important to help clinically localize the lesion and hone the differential diagnosis (see Table 72–2 and Figs. 72–5 and 72–6).

Pain is a common symptom in both radiculopathies and plexopathies. In plexopathies, it may precede weakness and can be described as throbbing, aching, or burning. Brachial plexus lesion can result in pain following a sclerotomal pattern. Upper trunk lesions may refer to the shoulder or upper arm, middle trunk to the forearm, and lower trunk to the axilla, medial arm, or hand. Injury to the lumbar plexus can cause pain in the anterolateral and medial thigh, while lumbosacral plexus injury leads to pain in the posterior thigh, leg, and foot. Radicular pain is similarly neuropathic in nature but typically radiates along a more specific dermatomal pattern.⁷

Sensory loss or paresthesias are common findings in both radiculopathies and plexopathies. In radiculopathies, these sensory alterations present in a dermatomal pattern, while in plexopathy, sensory abnormalities present in a pattern along multiple peripheral nerves correlating with the affected areas of the plexus. Sensory symptoms are often vague or generalized, highlighting the importance of isolating true sensory loss with multimodal testing during the physical exam.

Weakness is also a common complaint with root and plexus lesions. Patchy or incomplete patterns of weakness may complicate the localization of a plexus injury. In radiculopathies, weakness follows a myotomal distribution. Patients may allude to new limitations in function (e.g., inability to comb hair or reach overhead in the setting of an upper trunk brachial plexopathy or C5–C6 radiculopathy).

A thorough neurologic examination includes muscle strength testing, multimodal sensory testing along dermatomal and peripheral nerve distributions, and assessment of muscle stretch reflexes. Atrophy of involved muscles may be evident with long-standing nerve injury. Reflexes are typically diminished, reflecting a lower motor neuron lesion. It is important to account for the pattern of findings and consider the overlap of dermatomes and myotomes when interpreting sensory and motor abnormalities upon examination.

Provocative physical tests may help support a diagnosis of radiculopathy. Spurling’s test (foraminal compression test) has a high specificity (but low sensitivity) for cervical radiculopathy.¹² In the evaluation of lumbosacral radiculopathy due to herniated disc, Lasegue’s sign (supine straight leg raise) has a high sensitivity, but variable specificity, while the crossed straight leg raise has a high specificity, but low sensitivity.^13–15 The femoral nerve stretch test is predictive of a lumbar level (L2–L4) root impingement.¹⁶ Additionally, the presence of upper motor neuron signs (e.g., hyperreflexia or the Hoffman or Babinski sign) are important findings that help discriminate cord from root or plexus injury.

Electrodiagnostic Testing

Electrodiagnostic testing includes sensory and motor nerve conduction studies (NCS) and needle electromyography (EMG). A well-planned electrodiagnostic evaluation will establish the location and type of injury, while ruling out competing differential diagnoses and minimizing the testing of unnecessary nerves and muscles.¹⁷

Sensory nerve conduction studies (NCSs) are important to differentiate plexopathy from radiculopathy. In general, an NCS will appear abnormal if a lesion occurs between the nerve cell body and the site tested. Because a plexopathy lesion occurs distal to the DRG, the observed NCS will be abnormal. The lesion in a radiculopathy occurs proximal to the DRG. Hence, the site of NCS testing is still in continuity with the DRG, and the related sensory NCS appears normal. Using sensory NCS to differentiate an L2, L3, or L4 radiculopathy from a plexopathy is difficult, given the relative lack of sensory NCS available at those levels.

Motor NCS are important in assessing the degree of motor demyelination, axonal loss, or both. The distal motor nerve response is an important prognostic factor after axonal injury.¹⁸

H waves can be used to demonstrate S1 radiculopathy. H waves are analogous to the monosynaptic stretch reflex at the S1 spinal cord level and are able to detect injury proximal to the dorsal sensory ganglion. The utility of F-wave responses in diagnosing radiculopathies is debated, as abnormalities of F waves can be seen in lesions of the nerve root, plexus, or peripheral nerve.¹⁹

Needle EMG helps localize the lesion. Abnormalities in needle EMG are generally seen in lower motor neuron lesions that are axonal in nature. The main goal of EMG is to identify the pattern of electrodiagnostic abnormality. In radiculopathy, muscles innervated by the same nerve root but coming from different peripheral nerves will be abnormal (e.g., L5 radiculopathy with abnormalities in the gluteus medius, peroneus longus, and anterior tibialis muscles). Spontaneous activity evident in a myotomal distribution is the most reliable indicator of radiculopathy. Other muscles in the same region and with the same peripheral nerve innervation, but with different root levels, must be investigated.²⁰ In a plexopathy, the abnormal muscles are localized to a specific portion of the plexus (e.g., lumbar plexus lesions may present with abnormalities in the vastus medialis and adductor longus muscles). See Table 72–3 for details on the electrodiagnostic workup for brachial pelxopathy.

EMG of the paraspinal muscles is important in differentiating between radiculopathy and plexopathy.¹⁸ The paraspinal muscles receive innervation from the dorsal mixed rami; a root lesion is proximal to this, so the paraspinal muscles are affected in radiculopathy. The plexus comes from the ventral rami, so a plexus lesion will have normal paraspinal muscles because their innervation arises proximal to the plexus. Paraspinals, however, may show spontaneous activity in asymptomatic patients, especially in older adults (over the age of 60).²¹ See Table 72–4 for details on differences between EMG and NCS for radiculopathy and plexopathy.

EMG abnormalities follow a specific pattern after acute injury. Spontaneous activity can be seen in the paraspinal muscles by day 7 after injury, in distal muscles by 5 to 6 weeks after injury, and most will disappear by 9 months.²⁰ Chronic radiculopathies demonstrate neurogenic motor unit action potential changes, with no evidence of spontaneous activity.

The EMG can also determine severity; a more severe lesion (or a complete lesion) will have more spontaneous activity and have fewer or no motor units presenting with activation. Determining axonal continuity is important for determining surgical need, as the presence of axonal continuity may postpone surgical exploration.²²

Dillingham and colleagues (2001) studied the number of muscles that need to be tested to provide a high sensitivity of detecting radiculopathy. For assessment of cervical radiculopathy, they concluded that testing six muscles with paraspinal sampling provided a 94% to 98% sensitivity. If paraspinal muscles were not tested, eight muscles were needed to achieve a similar sensitivity of 92% to 95%.¹⁹ When assessing for lumbosacral radiculopathy, including paraspinal muscles yielded 94% to 98% sensitivity when testing five limb muscles, and 98% to 100% when testing six limb muscles. Without screening paraspinals, eight muscles were needed to reach a diagnostic sensitivity of 90% for lumbosacral plexopathy.²³

Imaging

Imaging is an important diagnostic tool used to help identify the etiology of an injury. Obtaining a radiograph in a patient with neck pain will have low sensitivity in detecting tumors, infection and disc herniation. Magnetic resonance imaging (MRI) is the modality of choice for investigating cervical radiculopathy. While electrodiagnostic studies are highly specific for detecting radiculopathy, MRI is highly sensitive in detecting anatomical changes responsible for radiculopathy. MRI, however, also will discover anatomic changes in asymptomatic patients and is helpful in the diagnosis of radiculopathies caused by nerve root compression.²⁰ MRI is considered the optimal imaging technique for visualizing the extraforaminal plexus.⁹ Computerized tomography (CT) myelography has been found to be accurate in the diagnosis of central canal and foraminal stenosis.¹⁰ CT myelography is also useful in visualizing structures within the intraspinal canal, including the primary dorsal and ventral roots; it is especially useful in postlaminectomy patients with hardware in place.

Patients with a significant injury to the brachial plexus should have done a plain radiograph of the cervical spine, the shoulder girdle including the humerus and clavicle, and the chest to identify neoplasms and potential fractures and dislocations associated with traumatic injuries.

Laboratory testing is of limited use in the workup of root and plexus injuries. Identifying impaired glucose metabolism may be useful if an inflammatory process is suspected. In addition, erythrocyte sedimentation rate, antinuclear antibodies and other autoimmune markers should be included in the workup of inflammatory plexopathies (Table 72–5).⁷

Root Disorders

Radiculopathy is defined as pain, weakness, or numbness in a myotomal or dermatomal distribution.²⁴ It results from both compressive and noncompressive lesions to the nerve root.¹⁰

Compressive causes of radiculopathy include degenerative changes of the uncovertebral joints anteriorly and zygapophyseal joints posteriorly, also known as spondylosis.²⁵ These degenerative changes can cause impingement of exiting nerve roots. Disc bulges and prolapse of the nucleus pulposus can cause impingement of the DRG.¹⁰

A population-based survey estimated that the prevalence of cervical radiculopathy was approximately 3.5 cases per 1,000.²⁶ Peak incidence for cervical radiculopathy is during the sixth decade of life. The most common nerve roots involved in a cervical monoradiculopathy are C7, followed by C6.²⁷

Epidemiological data assessing risk factors and prevalence of lumbosacral radiculopathy demonstrated inconsistent trends. Prevalence of lumbosacral radiculopathy, or sciatica, was found to be 9.8 cases per 1,000.^28–30 Men present earlier (fifth decade) than women (sixth decade).^29,31 Risk factors cited for lumbosacral radiculopathy include prior history of low back pain and smoking duration, as well as occupations requiring manual labor, prolonged driving, or sustained lumbar flexion or rotation.^31,32