Perspective

Peripheral nerve disorders can result in varied findings, including proximal or distal weakness, symmetric or asymmetric symptoms, and acute or chronic manifestations. Motor symptoms range from weakness to paralysis, whereas sensory symptoms range from numbness to pain.

Evaluation of peripheral nerve disorders requires an understanding of the anatomy of the spinal cord and the peripheral nervous system (Fig. 97.1). The peripheral nervous system is composed of 12 cranial nerves and 31 spinal nerves. Spinal nerves are formed from motor fibers whose cell bodies reside in the ventral horn of the spinal cord and from sensory fibers whose cell bodies are found in the dorsal root ganglion. The motor and sensory fibers join to form one nerve as it exits the spinal canal. Spinal nerves from several spinal levels merge at the cervical, brachial, lumbar, and sacral plexuses. Peripheral nerves originate either at these plexuses or, if they are formed from nerves of only one spinal level, as they exit the vertebral foramina.

Fig. 97.1 Cross section of the spine showing the relationship among the ventral and dorsal roots, dorsal root ganglion, spinal cord, vertebrae, and peripheral nerve.

Peripheral nerves consist of mixed fibers with variable amounts of motor, sensory, and autonomic fibers; small and large fibers; and myelinated and unmyelinated fibers. These fibers, which are surrounded by endoneurial fluid and covered in perineurium, form fascicles that are bundled together by the epineurial sheath. This sheath forms a protective barrier akin to the blood-brain barrier in the central nervous system.

In patients with symptoms concerning for a peripheral nerve disorder, the history and physical examination are important in localizing the lesion. Spinal nerve, or nerve root, lesions are called radiculopathies and result in myotomal weakness or dermatomal sensory loss. Plexus lesions can be variable, with symptoms that cross myotomes and dermatomes or involve multiple peripheral nerves. Symptoms depend on which trunk or cord is involved. Peripheral nerve lesions cause weakness and sensory loss that is limited to a specific peripheral nerve.

Systemic diseases affect the peripheral nervous system as well, and multiple peripheral nerves may be involved. Examples include disorders of the neuromuscular junction (NMJ), demyelinating disorders, diabetes, and toxic effects of drugs or chemicals (Box 97.1).

Pathophysiology

Spinal nerve compression results in radiculopathy, radicular pain, or both. Radiculopathy is due to blocked conduction along a spinal nerve and results in a neurologic deficit: dermatomal sensory loss or myotomal weakness. Radicular pain is due to irritation or inflammation of the spinal nerve, neurologic deficits are absent, and patients have purely painful symptoms that may not be isolated to a dermatome.

Causes of spinal nerve compression are varied; if a patient is younger than 50 years, the symptoms are more likely to be caused by disk herniation, and if older than 50 years, by degenerative changes.

Presenting Signs and Symptoms

As noted, sensory loss and weakness follow a dermatomal or myotomal distribution. Diminished reflexes may also assist in determining the nerve root that is involved (Table 97.1).

Table 97.1 Nerve Root and Associated Reflex

In the cervical region, C6 and C7 are the most commonly affected, with higher roots less frequently involved. This is true for the lumbosacral spinal nerves as well, with more patients having signs in the L5-S1 distribution. Sciatica is a particularly common syndrome of radicular pain and involves more than one of the L2-S1 spinal nerves.

Diagnostic Testing

A careful history and physical examination will help localize the symptoms of a radiculopathy. The straight leg raise should be used to test for lumbosacral involvement. While the patient is lying supine, the leg is raised with the knee in extension. The test is considered positive for spinal nerve involvement when symptoms are reproduced within 60 degrees of elevation.

If a patient has solely radicular pain, imaging may not be necessary because the symptoms resolve in 60% to 80% of patients within 6 to 12 weeks with conservative treatment. In patients whose symptoms fail to resolve, progress, or involve sensory loss or weakness, either computed tomography or magnetic resonance imaging (MRI) is indicated. Patients should also undergo imaging if they have a history of malignancy, long-term steroid use, intravenous drug abuse, human immunodeficiency virus (HIV) infection, diabetes, acute loss of neurologic function, or known trauma. In general, MRI is preferred because it has higher soft tissue resolution. For disk disease, it is important to note that the size of a disk herniation does not always correlate with clinical symptoms: patients without evidence of herniation may have significant symptoms, whereas patients with an incidental finding of disk herniation may have no symptoms.

Treatment

In the acute phase of injury, painful symptoms are typically treated conservatively with nonsteroidal antiinflammatory drugs (NSAIDs) and physical therapy. Low-quality evidence suggests that there is no difference between bed rest and activity for patients with sciatica.¹ However, a randomized controlled trial showed that the addition of physical therapy is more effective than counseling and pain medications alone, although it may not be as cost-effective.² Persistent or severe symptoms may require more invasive measures, from local corticosteroid injections to neurosurgical intervention.³ For the cervical spinal nerves, some evidence has shown that conservative therapy consisting of pain control has favorable short-term outcomes when compared with surgical intervention, although long-term outcomes appear to be similar.⁴ Surgical outcomes can be dependent on the mechanism of injury; for example, with spinal stenosis, 70% of patients will still have persistent loss of function. Chronic pain symptoms may be treated with medications used for neuropathic pain, such as antidepressants or anticonvulsants.

Epidemiology

As with radiculopathy, compression of peripheral nerves is the most common cause of peripheral mononeuropathy, the most frequent being median mononeuropathy (Fig. 97.2). Women older than 55 years are most commonly affected, with a 4.6% prevalence in women and 2.8% in men.⁵ The second most frequent cause is ulnar mononeuropathy; specifically, cubital tunnel syndrome. Other common peripheral mononeuropathies include involvement of the radial nerve in the upper extremity and the peroneal and lateral cutaneous femoral nerves in the lower extremity.

Fig. 97.2 Anatomy of the carpal tunnel.

Pathophysiology, Presenting Signs and Symptoms, and Diagnostic Testing

For mononeuropathies, the history and physical examination largely lead to the appropriate diagnosis. Findings in patients with common mononeuropathies and diagnostic maneuvers are presented in Table 97.2.^6–12 In patients with a history of trauma or acute symptoms, plain films may be necessary to rule out fracture or dislocation. Patients with subacute or chronic symptoms should be asked about chronic conditions. Mononeuropathies can occur with several systemic diseases, including diabetes mellitus, amyloidosis, HIV, and states that cause edema, such as pregnancy.¹³ Outpatient testing may be more appropriate for individuals with chronic symptoms. MRI or electrodiagnostic testing such as electromyography or nerve conduction studies may be necessary, and the patient should be referred to a neurologist. MRI may demonstrate chronic nerve injury, whereas electrodiagnostic testing may show slowing of nerve conduction. These studies may aid in deciding whether surgical repair or decompression is necessary for certain syndromes.

Treatment

Primary treatment should be aimed at the precipitating event for both acute and chronic mononeuropathy.

With acute mononeuropathy, the primary cause of injury is generally trauma. Fractures and dislocations should be reduced appropriately and immobilized with the guidance of surgical consultation.

Initial treatment of chronic mononeuropathy is typically conservative and supportive. Modification of behavior is a key component of treatment and prevention of further injury. For carpal tunnel syndrome, behavior modification includes weight loss and avoidance of caffeine, nicotine, and alcohol. Patients should be instructed to decrease any possible trauma related to repetitive use by making changes in workplace ergonomics, reducing repetitive use, and changing posture. Some neuropathies may require supportive devices; for example, the carpal tunnel may benefit from wearing a wrist splint, the ulnar nerve from wearing a sling or a long arm posterior splint, the radial nerve from wearing a volar splint, and the peroneal nerve from wearing a posterior splint.^8,9 NSAIDs are typically prescribed for relief of symptoms, although they may be ineffective without appropriate behavioral modification. In patients with a systemic disease, the primary process should be treated. Diuretics may be given if edema is believed to be contributing significantly to the patient’s symptoms. More invasive procedures, such as local nerve block for meralgia paresthetica or surgical decompression for carpal tunnel syndrome, are reserved for severe cases.

Epidemiology

Guillain-Barré syndrome (GBS) is also known as acute inflammatory demyelinating polyradiculopathy or Landry-Guillain-Barré syndrome. Its worldwide incidence is 0.6 to 4 per 100,000 individuals annually.¹⁴

Pathophysiology

GBS is characterized by immune-mediated destruction of the myelin sheath of peripheral nerves. Biopsy frequently reveals a mononuclear inflammatory infiltrate. Although its exact etiology remains unknown, two thirds of cases are preceded by an infection. Associations have been made with viral or febrile illness, Campylobacter jejuni infection, vaccinations, and even surgery or trauma.

GBS is a monophasic illness with progressive symptoms that reach a nadir in 2 to 4 weeks. Recovery can vary from weeks to a year. Mortality has been reported in 4% to 15% of patients, whereas another 10% to 20% have significant residual motor dysfunction.

Presenting Signs and Symptoms