It is a disease or dysfunction of one or more peripheral nerves, typically causing numbness or weakness.
It has two types
Polyneuropathy is a specific term that refers to a generalized, relatively homogeneous process affecting many peripheral nerves, with the distal nerves usually involved most prominently.
Mononeuropathy refers to a single nerve's focal involvement, usually due to a local cause such as trauma, compression, or entrapment. Carpal tunnel syndrome is a typical example of mononeuropathy.
Diabetic — Diabetic polyneuropathy is generally considered predominantly axonal; however, variable degrees of demyelination are often present, at least electrophysiologically. The mechanism underlying the development of diabetic neuropathy is extraordinarily complex and likely relates to inflammatory, metabolic, and ischemic effects.
Other systemic — Other systemic diseases generally cause predominantly axonal polyneuropathies. Examples of these include the polyneuropathies associated with the following conditions:
Autoimmune — Most acute autoimmune neuropathies, namely Guillain-Barré syndrome, are predominantly demyelinating. Various clinical and experimental data have implicated both humoral and cell-mediated immune phenomena, which damage myelin and/or the myelin-producing Schwann cells. However, axonal forms of this disease also exist. One unusual but well-described variant of Guillain-Barré syndrome is acute motor axonal polyneuropathy (AMAN). In this disorder, the primary invasion of axons by inflammatory cells has been described. Toxic — Many toxic neuropathies, such as those due to alcohol, chemotherapy exposure, and most heavy metals, produce a predominantly axonal disorder that can be acute, subacute, or chronic, depending on the level and severity of the exposure. Nonetheless, it is incorrect to classify all toxic neuropathies as axonal since many exceptions exist. As an example, n-hexane exposure leads to neuropathy that has a substantial demyelinating component.
Aside from chemotherapeutic drugs, a variety of commonly used medications have been implicated in toxic neuropathies. Examples include antimicrobials (e.g., dapsone, fluoroquinolones, isoniazid, metronidazole, nitrofurantoin), antiretrovirals (e.g., didanosine, stavudine), amiodarone, colchicine, disulfiram, phenytoin, pyridoxine, and tumor necrosis factor inhibitors (e.g., infliximab). In many cases, the magnitude of risk is relatively low, and recognition of the adverse effect may require a high index of suspicion, especially for commonly used drugs such as fluoroquinolones.
Hereditary — The most common forms of hereditary neuropathy, namely CMT types 1A, 1B, and X-linked, are predominantly demyelinating in nature, although the substantial coexistent axonal loss is usually also identified. Other rare hereditary diseases that cause demyelinating polyneuropathies primarily include those secondary to metabolic diseases of childhood, such as Krabbe disease, metachromatic leukodystrophy, adrenoleukodystrophy, and mitochondrial disorders.
Peripheral neuropathies associated with mitochondrial disorders most often exhibit an axonal pattern, as occurs with CMT type 2A and the syndrome of neuropathy, ataxia, and retinitis pigmentosa (NARP) . Other mitochondrial disorders are associated with a demyelinating neuropathy, as occurs with mitochondrial neurogastrointestinal encephalomyopathy (MNGIE).
Porphyric neuropathy is primarily an axonal motor neuropathy that usually presents in the context of acute neurovisceral attacks, with variable manifestations of neuropathy, abdominal pain, confusion, and other neurologic and systemic symptoms. Acute hepatic porphyrias are inherited disorders caused by partial enzyme deficiencies affecting heme biosynthesis. Neurovisceral attacks are manifestations of four types of hepatic porphyria. The most common of these is acute intermittent porphyria; the others are hereditary coproporphyria, variegate porphyria, and delta-aminolevulinic acid dehydratase porphyria.
Environmental — Environmental factors can also impact nerve health in powerful ways. Neuropathies associated with vibration-induced nerve damage, prolonged cold exposure, or hypoxemia have been well described. These disorders are mainly axonal.
Idiopathic — Although population-based data are lacking, no specific cause is identified in up to 46 percent of patients with polyneuropathy at referral centers despite extensive investigations. Various terms have been employed to describe this disorder, including chronic idiopathic axonal polyneuropathy (CIAP), chronic sensory polyneuropathy, chronic polyneuropathy of undetermined cause, unclassified peripheral neuropathy, and idiopathic neuropathy. Most such cases present in adults ≥50 years of age and progress slowly over months to years. The symptoms are typically sensory, involving paresthesia, numbness, or pain. Electrodiagnostic studies show primarily axonal polyneuropathy. Proposed but unproven causes include impaired glucose tolerance, hypertension, dyslipidemia, and increased oxidative stress.
Treatment of symptoms and prevention of complications — Gabapentin may reduce pain associated with polyneuropathy and is generally well tolerated. Tricyclic antidepressants have been utilized for many years for this condition and are generally considered adequate.
The management of pain associated with diabetic neuropathy and vasculitic neuropathy is discussed in separate topic reviews.
Many other medications have also been tried to treat painful polyneuropathy with varying success, including duloxetine, pregabalin, carbamazepine, phenytoin, topiramate, baclofen, mexiletine, and dextromethorphan. Unfortunately, no well-executed studies are comparing the effectiveness of these drugs for this condition, thereby limiting practitioners' ability to make evidence-based decisions.
Simultaneous treatment with drugs such as tramadol, nonsteroidal anti-inflammatory drugs (NSAIDs), or low-dose narcotics may be necessary for some patients for occasional "breakthrough pain."
Physical therapy evaluation is essential in patients with significant weakness. Appropriate use of ankle-foot orthoses, splints, and walking assistance devices can significantly improve lifestyle in the face of substantial disability.
Patients with distal polyneuropathy are at increased risk for developing foot ulcers; proper foot and nail care is significant in this population. Regular visits to a podiatrist can also help prevent problems.
EXERCISES TO IMPROVE SYMPTOMS
Side leg raise
Using a chair or counter, steady your balance with one hand.
Stand straight with feet slightly apart.
Slowly lift one leg to the side and hold for 5–10 seconds.
Lower your leg at the same pace.
Repeat with the other leg.
As you improve balance, try this exercise without holding onto the counter.
Using a chair or counter, steady your balance.
Lift the heels of both feet off the ground so you’re standing on your toes.
Slowly lower yourself down.
Repeat for 10–15 reps.
Some examples of aerobic exercises are: