Peripheral neuropathy is defined as a condition in which there is alteration in function and structure of the motor, sensory, or autonomic components of a peripheral nerve. Although peripheral neuropathies are seldom a cause of concern in the acute care setting, there are a few exceptions which include acute processes such as Guillain-Barre syndrome (GBS), selected toxins, and some entrapment syndromes. With most neuropathies, the development of signs and symptoms follows a slower and chronic pattern. Patients with neuropathies are seen in primary care settings and in specialty clinics such as diabetes and HIV clinics. Between 2% and 10% of the general population have some form of peripheral neuropathy while in the HIV population the prevalence is 26% to 60%.1
Peripheral neuropathy is common in type 2 diabetic patients, reportedly 26.4% in patient3
and the predicted increase in number of people with diabetes mellitus (DM) is sure to increase the prevalence of peripheral neuropathy. People over the age of 55 years are most commonly affecting with a reported incidence of 8%.4
Nurses will see patients in acute care settings with chronic neuropathies related to existing comorbidity and also see patients in primary care or specialty clinic settings with new onset or existing neuropathies. The seemingly simple problem of neuropathies is much more complex than it may appear.
The peripheral nervous system (PNS) refers to the parts of the nervous system located outside the brain and spinal cord (Fig. 35-1
It includes the cranial nerves (CNs), spinal nerves and their roots and branches, ganglia, peripheral nerves, and neuromuscular junctions. The exceptions to the 12 CNs are the olfactory bulbs (a component of the olfactory nerves which are special extensions of the brain) and the optic nerves.6
Peripheral nerves are the major nerves in the extremities and are derived from associated plexuses (e.g., brachial, lumbosacral). Most peripheral nerves are classified as sensory, motor, or mixed indicating that they may contain sensory, motor, sensory and motor, as well as autonomic fibers (sympathetic or parasympathetic fibers). The anterior horn cells may be considered as part of the central nervous system (CNS) or classified with the PNS because they are part of the motor unit. The motor fibers that compose the peripheral nerves have their origin in the lower motor neurons. The main function of the PNS is to connect the CNS to the limbs and organs.
The cell bodies of several sensory neurons form structures called ganglia. Satellite cells
are the glial cells that surround each ganglion. Schwann cells
are the principle glial cells of the PNS; they wrap themselves around neurons in the PNS to form the myelin sheath (Fig. 35-2
). Nerves can be classified based on the myelination into three categories: large myelinated, small myelinated, and small unmyelinated. Motor axons are usually large myelinated fibers designed to conduct impulses rapidly. Sensory fibers may be any of the three types. Large-diameter sensory fibers conduct proprioception and vibratory sensation to the brain, while the smallerdiameter myelinated and unmyelinated fibers transmit pain and temperature sensation. Autonomic fibers are smaller in diameter. The myelin sheath is an excellent electrical insulator that significantly decreases ion flow through the membrane.
The internal composition of axons is a complex linear microtubular system designed to maintain the integrity of the membranes and the transport of substances (e.g., neurotransmitters) between dendrites and through cell body to the axon6
). As noted above, motor axons are usually large and myelinated. If one looks at a cross section of a myelinated motor fiber, the central core of the fiber is the axon. The axon is filled in its center with axoplasm, which is a viscid intracellular fluid. Surrounding the axon is the
myelin sheath that is often much thicker than the axon itself. The membrane of the axon is the membrane that actually conducts the action potential which is a change that spreads rapidly along the nerve fiber membrane.8
In order for both depolarization and repolarization of the nerve membrane to occur during the action potential, voltage-gated sodium channel play a role. A voltage-gated potassium channel also plays an important role in increasing the rapidity or repolarization of the membrane. These two voltage-gated channels are in addition to the Na+
Figure 35-1 ▪ Peripheral nervous system. (A) The cranial nerves. (B) The spinal nerves and peripheral nerve plexuses. (From: McConnell, T. H. (2007). The nature of disease pathology for the health professions, Philadelphia: Lippincott Williams & Wilkins.)
SIGNS, SYMPTOMS, AND CLINICAL PRESENTATIONS
Disorders of one or more peripheral nerves cause various signs and symptoms that correspond to the anatomic distribution and normal function of the nerve. Some peripheral nerves are purely motor, some are purely sensory, and others are mixed. Diagnostic accuracy depends on a thorough knowledge of specific sensory dermatomes, muscle innervation, reflexes, and autonomic function related to a particular peripheral nerve. The general signs and symptoms of a peripheral nerve disorder include pain, paresthesia, dysesthesias, sensory loss, weakness, fasciculations, cramping, spasms, unstable balance, and autonomic or trophic changes.11
They may occur in any combination depending on the peripheral nerve or nerves involved.
When sensory nerves or components are affected, there is decrease or loss of light touch and pinprick sensation along the involved dermatome. Clinically, tingling, numbness, paresthesias, and dysesthesias are common. Paresthesias are sensations such as “pins and needles” whereas dysesthesias are unpleasant sensations such as burning. Neuropathic pain is a feature of some neuropathies, especially if small fibers within the nerves are affected. The sensation of pain can take on many forms including burning, jabbing, hypersensitivity to non-noxious stimuli (called allodynia), or tight band-like pressure pain. Pain may be hyperalgesic, which is an increased pain response to noxious stimuli. Examples of polyneuropathies associated with pain include those related to diabetes, alcoholism, porphyria, rheumatoid arthritis, and acquired immune deficiency syndrome (AIDS). Pain is also a common finding with many entrapment neuropathies such as carpal tunnel syndrome. Finally, sensory loss may be described as a “dead” feeling in an extremity.
TABLE 35-2 CLASSIFICATION OF PERIPHERAL NEUROPATHIES BASED ON PROXIMAL TO DISTAL
DESCRIPTION OF ABNORMALITY
Involves the cell bodies of a neuron; produces sensory, motor, or autonomic dysfunction individually; also further classified into sensory and motor neuronopathy
Forms of peroneal muscular atrophy
Involves a single nerve root
Most often seen with compression due to a herniated disc or an osteophyte
Involves damage to multiple nerve roots; main feature that distinguishes radiculopathy from other neurologic disorders is that the symptoms and signs of radiculopathy follow sensory and motor nerve root distributions
Most common cause of acute polyradiculopathy is acute inflammatory demyelinating polyradiculopathy (also known as Guillain-Barre syndrome)
Involves a network of nerves; two main types of plexopathy, brachial or lumbosacral; usually caused by localized trauma such as dislocated shoulder
Brachial plexopathy and lumbosacral plexopathy
An inflammatory disorder that affects the peripheral nerves at multiple spinal root levels Involves both the nerve roots and peripheral nerve trunks
Involves multiple peripheral nerves simultaneously resulting in a symmetric, bilateral pattern of functional loss, usually occurring distally before proximally; seen with many systemic processes;
Presentation may be mainly sensory (e.g., amyloidosis, leprosy) or mainly motor (e.g., porphyria).
Involves pathological changes to axons
Acute: Guillain-Barre syndrome
Chronic: Nonsystemic vasculitis neuropathy
Involves pathological changes to the myelin sheath
Mononeuropathy simplex or mononeuropathy
Involves a single peripheral nerve most often due to an entrapment or local trauma
Median nerve compression resulting in carpal tunnel syndrome
Involves multiple individual nerves in a random fashion; most often due to inflammation of the vasa nervorum (i.e., small arteries that provide blood supply to peripheral nerves)
Seen with disseminated vasculitis as in diabetes mellitus or polyarteritis
From: Kincaid, J. C. (2009). Neuropathy. In J. Biller (Ed.), Practical neurology (3rd ed., pp. 633-642). Philadelphia: Lippincott Williams & Wilkins.
Involvement of the motor fibers of purely a motor nerve or a mixed nerve results in lower motor neuron weakness or paralysis of the muscles innervated by the involved peripheral nerve. Atrophy of the specific muscle groups and related deformities follow. Fasciculations may also be noted. Deep tendon reflexes of the involved muscles are decreased or absent. The weakness may be described as unilateral or symmetric; a proximal or distal distinction may also be made. Autonomic and trophic changes are noted in the affected area. Skin may become dry, thin, scaly, inelastic, and cold and cease to sweat. The nails may become curved and brittle; nail and hair growth is stunted.
SELECTED PERIPHERAL NEUROPATHIES
The number of neuropathies is long and beyond the scope of this chapter. The following section addresses the selected common neuropathies related to chronic illnesses, entrapment syndromes, and GBS.
Neuropathies Related to Chronic Conditions
Neuropathies related to DM, vasculitis, HIV, vitamin deficiency, toxic exposures, alcohol abuse, and metastatic lesions, are commonly encountered in clinical practice, and are briefly discussed. In addition, chronic inflammatory demyelinating polyneuropathy (CIDP) is discussed.
Diabetic sensorimotor polyneuropathy is the most frequent form of diabetic neuropathy seen in general clinical practice, and is a consequence of poor long-term glucose control in patients with DM, especially in insulin-dependent diabetics. It causes decreased sensation (e.g., numbness, insensitivity to pain or temperature), paresthesias, extreme sensitivity to touch, decreased position and vibration sense, sharp pain or cramps, decreased reflexes (e.g., especially of ankle reflex), and decreased muscle strength in the
lower extremities resulting in balance dysfunction.20
Diabetic peripheral neuropathy is caused by microvascular abnormalities resulting in nerve damage.
Ropper and Samuels6
outline several distinct neuropathic clinical syndromes related to DM.6
Distal, symmetric, mostly sensory polyneuropathy affecting feet and legs greater than hands that progresses slowly (most common)
Acute diabetic ophthalmoplegia (affects third and sometimes CN VI) unilaterally
Acute mononeuropathy of limbs or trunk including a painful thoracolumbar radiculopathy
Acute/subacute evolving, painful asymmetric, mostly motor neuropathy that affects the upper lumbar roots and proximal leg muscles
Symmetric proximal motor weakness and wasting often without pain and with variable sensory loss pursuing a subacute or chronic course
Autonomic neuropathy with bowel, bladder, and circulatory reflexes
These syndromes may be seen individually or in any combination. Neuropathies often occur in combination with vascular complications, such as retinopathy and nephropathy.
Treatment of diabetic peripheral neuropathies fall into two categories; prevention/disease modification and symptom control.17
Prevention and disease modification of DM through intensified glucose control is the best approach to patients with diabetes, especially type 1 diabetics.6
Daily glucose levels by self-monitoring and periodic glycosylated hemoglobin (A1c) are useful indicators of short- and long-term glucose control. No therapeutic modality aside from tight glucose control by whatever means necessary is recommended. Other strategies include: foot care to reduce infections, ulceration, and amputation; physiotherapy gait and balance training to strengthen muscle and improve balance as a means to improve mobility and prevent falls; and other forms of exercise such as tai chi to assist with balance and mobility.23
These patients are at high risk for falls because of impaired sensitivity of the feet as well as imbalance and muscle weakness. Therefore, patient and family education addressing safety is important.
Current symptom management of diabetic neuropathy is focused on treatment of pain. The drug of choice for treatment of neuropathic pain associated with DM is Pregabalin.17
However, patients with severe diabetic peripheral neuropathy often have significant peripheral edema, but a side effect of Pregabalin is peripheral edema, and is, therefore, not a good choice. Other drug options include venlafaxine, duloxetine, amitriptyline, gabapentin, valproate, dextromethorphan, morphine sulphate, tramadol, and oxycodone.17
Amitriptyline is particularly effective for the treatment of painful diabetic neuropathy and postherpetic neuralgia, and is helpful for a patient who is depressed.25
Nonopioid drugs are also used for neuropathic pain. Patients who fail nonopioid therapy may be offered methadone.26
Some patients have comorbid conditions that prohibit use of any of the oral drugs. For those patients, topical therapy such as Capsaicin cream applied to the affected area three times daily may provide temporary relief for some patients. Another option is transcutaneous electrical nerve stimulation.27
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