Peripheral Nerve Entrapments: Clinical Diagnosi...
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Peripheral nerve entrapments are a relatively rare and heterogeneous group of nerve disorders encompassing a wide variety of etiologies and clinical presentations. These conditions can present significant diagnostic challenges, owing to both the variety of symptoms these patients display, along with the anatomic variation that exists between individuals. Precise knowledge of the anatomic course, the common motor and sensory distributions of each of the peripheral nerves, and judicious use of imaging or electrodiagnostic testing can greatly assist in arriving at a correct diagnosis. In this article, we discuss in detail the anatomy, clinical presentation, diagnosis, and treatment options for peripheral nerve entrapments of the lower extremity involving the sural, saphenous and common, superficial, and deep peroneal nerves.
Symptoms due to nerve entrapment syndromes are a frequent reason for attendance at GP, rheumatology and orthopaedic clinics. This article outlines the presenting symptoms and signs of some of the more common syndromes and gives guidelines on the clinical diagnosis and subsequent management.
Peripheral nerves in the upper extremities are at risk of injury and entrapment because of their superficial nature and length. Injury can result from trauma, anatomic abnormalities, systemic disease, and entrapment. The extent of the injury can range from mild neurapraxia, in which the nerve experiences mild ischemia caused by compression, to severe neurotmesis, in which the nerve has full-thickness damage and full recovery may not occur. Most nerve injuries seen by family physicians will involve neurapraxia, resulting from entrapment along the anatomic course of the nerve. In the upper extremity, the brachial plexus branches into five peripheral nerves, three of which are commonly entrapped at the shoulder, elbow, and wrist. Patients with nerve injury typically present with pain, weakness, and paresthesia. A detailed history and physical examination alone are often enough to identify the injury or entrapment; advanced diagnostic testing with magnetic resonance imaging, ultrasonography, or electrodiagnostic studies can help confirm the clinical diagnosis and is indicated if conservative management is ineffective. Initial treatment is conservative, with surgical options available for refractory injuries or entrapment caused by anatomic abnormality.
Background: Entrapment of the middle cluneal nerve (MCN), a peripheral nerve in the buttock, can elicit low back pain (LBP). We examined the epidemiology, clinical course, and treatment of MCN entrapment (MCN-EN).
Peripheral nerve injury in the upper extremity is common, and certain peripheral nerves are at an increased risk of injury because of their anatomic location. Risk factors include a superficial position, a long course through an area at high risk of trauma, and a narrow path through a bony canal. The anatomy and function of upper extremity nerve roots, as well as specific risk factors of injury, are described in Online Table A. The most common nerve entrapment injury is carpal tunnel syndrome, which has an estimated prevalence of 3 percent in the general population and 5 to 15 percent in the industrial setting.1 Given the potential for longstanding impairment associated with nerve injuries, it is important for the primary care physician to be familiar with their presentation, diagnosis, and management.
The three categories of nerve injuries are neurapraxia, axonotmesis, and neurotmesis. Neurapraxia is least severe and involves focal damage of the myelin fibers around the axon, with the axon and the connective tissue sheath remaining intact. Neurapraxia typically has a limited course (i.e., days to weeks). Axonotmesis is more severe, and involves injury to the axon itself. Regeneration of the nerve is possible, but typically prolonged (i.e., months), and patients often do not have complete recovery. Neurotmesis involves complete disruption of the axon, with little likelihood of normal regrowth or clinical recovery.2,3
Ulnar Nerve at the Elbow: Cubital Tunnel Syndrome. The ulnar nerve at the elbow is very superficial and at risk of injury from acute contusion or chronic compression. Compression can be from an external or internal source. As the elbow flexes, the cubital tunnel volume decreases, causing internal compression. Cubital tunnel syndrome may cause paresthesias of the fourth and fifth digits. There may be elbow pain radiating to the hand, and symptoms may be worse with prolonged or repetitive elbow flexion. Paresthesias precede clinical examination findings of sensory loss. Weakness may occur, but is a late symptom. When present, motor findings are weak digit abduction, weak thumb abduction, and weak thumb-index finger pinch. Power grip is ultimately affected.
Electrodiagnostic testing consists of nerve conduction studies and electromyography (EMG). Nerve conduction studies assess the integrity of sensory and motor nerves. Areas of nerve injury or demyelination appear as slowing of conduction velocity along the nerve segment in question. EMG records the electrical activity of a muscle from a needle placed into the muscle, looking for signs of denervation.21,22 The combination of nerve conduction studies and EMG can help distinguish peripheral from central nerve injuries. Electrodiagnostic testing is commonly used to evaluate for carpal tunnel syndrome and cubital tunnel syndrome. Nerve conduction studies have been shown to confirm carpal tunnel syndrome with a sensitivity of 85 percent and a specificity of 95 percent.23 Nerve conduction studies also may help confirm the diagnosis in patients who have a history or physical examination findings that are atypical of carpal tunnel syndrome. For most patients who have a typical presentation, nerve conduction studies do not change the diagnosis or management.24,25
Symptoms can range from mild to disabling, but are rarely life-threatening. The symptoms depend on the type of nerve fibers affected and the type and severity of damage. Symptoms may develop over days, weeks, or years. In some cases, symptoms improve on their own and may not require advanced care. Unlike nerve cells in the CNS, peripheral nerve cells continue to grow throughout life.
Smoking constricts the blood vessels that supply nutrients to the peripheral nerves and can worsen neuropathic symptoms. Exercise can deliver more blood, oxygen, and nutrients to far-off nerve endings, improve muscle strength, and limit muscle atrophy. Self-care skills in people with diabetes and others who have an impaired ability to feel pain can alleviate symptoms and often create conditions that encourage nerve regeneration. Strict control of blood glucose levels can reduce neuropathic symptoms and help people with diabetic neuropathy avoid further nerve damage.
Local anesthetics and related drugs that block nerve conduction may help when other medications are ineffective or poorly tolerated. Medications put on the skin (topically administered) are generally appealing because they stay near the skin and have fewer unwanted side effects. Lidocaine patches or creams applied to the skin can be helpful for small painful areas, such as localized chronic pain from mononeuropathies such as shingles. Another topical cream is capsaicin, a substance found in hot peppers that can desensitize peripheral pain nerve endings. Doctor-applied patches that contain higher concentrations of capsaicin offer longer term relief from neuropathic pain and itching, but they worsen small-fiber nerve damage. Weak over-the-counter formulations also are available. Lidocaine or longer acting bupivacaine are sometimes given using implanted pumps that deliver tiny quantities to the fluid that bathes the spinal cord, where they can quiet excess firing of pain cells without affecting the rest of the body. Other drugs treat chronic painful neuropathies by calming excess signaling.
Transcutaneous electrical nerve stimulation (TENS) is a noninvasive intervention used for pain relief in a range of conditions. TENS involves attaching electrodes to the skin at the site of pain or near associated nerves and then administering a gentle electrical current. Although data from controlled clinical trials are not available to broadly establish its efficacy for peripheral neuropathies, in some studies TENS has been shown to improve neuropathic symptoms associated with diabetes.
NINDS-funded research ranges from clinical studies of the genetics and the natural history of hereditary neuropathies to discoveries of new cause and treatments for neuropathy, to basic science investigations of the biological mechanisms responsible for chronic neuropathic pain. Together, these diverse research areas will advance the development of new therapeutic and preventive strategies for peripheral neuropathies. Understanding the causes of neuropathy provides the foundation for finding effective prevention and treatment strategies.
Rapid communication between the peripheral nervous system and the central nervous system often depends on myelination, a process through which special cells called Schwann cells create an insulating coating around axons. Several NINDS-funded studies focus on understanding how myelin protein and membrane production and maintenance in Schwann cells is regulated and how mutations in genes involved in these processes cause peripheral neuropathies. Schwann cells play a critical role in the regeneration of nerve cell axons in the peripheral nervous system. By better understanding myelination and Schwann cell function, researchers hope to find targets for new therapies to treat or prevent nerve damage associated with neuropathy.
In inflammatory peripheral neuropathies such as Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP), the body's immune system mistakenly attacks peripheral nerves, damaging myelin and weakening signaling along affected nerves. NINDS-supported researchers hope to better understand how antibodies to cell membrane components cause peripheral nerve damage and how the effects of these antibodies can be blocked. Researchers are also studying how mutations in the Autoimmune Regulator (AIRE) gene in a mouse model of CIDP cause the immune system to attack peripheral nerves. NINDS research has helped discover that some types of small-fiber polyneuropathy appear to be immune-caused, particularly in women and children. 59ce067264