Peripheral Neuropathy

Peripheral neuropathy is the term for damage to nerves of the peripheral nervous system, which may be caused either by diseases of the nerve or from the side-effects of systemic illness. The four cardinal patterns of peripheral neuropathy are polyneuropathy, mononeuropathy, mononeuritis multiplex and autonomic neuropathy. The most common form is (symmetrical) peripheral polyneuropathy, which mainly affects the feet and legs. The form of neuropathy may be further broken down by cause, or the size of predominant fiber involvement, i.e., large fiber or small fiber peripheral neuropathy. Frequently the cause of a neuropathy cannot be identified and it is designated idiopathic.

Neuropathy may be associated with varying combinations of weakness, autonomic changes and sensory changes. Loss of muscle bulk or fasciculations, a particular fine twitching of muscle may be seen. Sensory symptoms encompass loss of sensation and "positive" phenomena including pain. Symptoms depend on the type of nerves affected; motor, sensory, autonomic, and where the nerves are located in the body. One or more types of nerves may be affected. Common symptoms associated with damage to the motor nerve are muscle weakness, cramps, and spasms. Loss of balance and coordination may also occur. Damage to the sensory nerve can produce tingling, numbness, and pain. Pain associated with this nerve is described in various ways such as the following: sensation of wearing an invisible "glove" or "sock", burning, freezing, or electric-like, extreme sensitivity to touch. The autonomic nerve damage causes problems with involuntary functions leading to symptoms such as abnormal blood pressure and heart rate, reduced ability to perspire, constipation, bladder dysfunction (e.g., incontinence), and sexual dysfunction.

Autonomic Neuropathy

Causes, Incidence, and Risk Factors:

Autonomic neuropathy affects approximately 8 out of 100,000 people. It is a form of peripheral neuropathy affecting the autonomic portion of the peripheral nervous system.

The peripheral nervous system includes the nerves used for communication to and from the brain and spinal cord (central nervous system) and all other parts of the body, including the internal organs, muscles, skin, blood vessels, and so on. Autonomic neuropathy includes damage to the nerves supplying the autonomic portion of the peripheral nervous system, which is the portion that supplies the internal organs, blood vessels, and other areas not under voluntary (purposeful) control.

Damage to the autonomic nerves causes abnormal or decreased function of the areas supplied by the affected nerve. For example, damage to the nerves of the gastrointestinal tract causes decreased ability to move food during digestion (decreased gastric motility), resulting in symptoms such as nausea, vomiting, diarrhea or constipation, and abdominal bloating. Damage to the nerves supplying blood vessels causes problems with regulation of blood pressure and body temperature (dilation of skin capillaries is used to dissipate heat from the body). Damage to other structures causes similar dysfunction.

Autonomic neuropathy is a group of symptoms, not a specific disease entity. The causes are multiple. Autonomic neuropathy is associated with alcoholic neuropathy, diabetic neuropathy, disorders involving sclerosis of tissues, surgical or traumatic injury to nerves (such as surgical vagotomy, used to control stomach ulcers and similar disorders), other forms of neuropathy, use of anticholinergic medications, and many other conditions.


Prevention or control of disorders that may be associated with autonomic neuropathy may reduce the risk. For example, diabetics should control blood sugar levels closely; alcoholics should stop drinking.


  • Abdomen, Swollen
  • Heat Intolerance, Induced by Exercise
  • Nausea After Eating
  • Vomiting of Undigested Food
  • Early Satiety (Feeling Full After Only a Few Bites)
  • Unintentional Weight Loss of More Than 5% of Body Weight
  • Male Impotence
  • Diarrhea
  • Constipation
  • Dizziness That Occurs When Standing Up
  • Urinary Incontinence (Overflow Incontinence)
  • Difficulty Beginning to Urinate
  • Feeling of Incomplete Bladder Emptying
Signs and tests:

Inspection of the abdomen may show distention, and listening to the abdomen with a stethoscope (auscultation) may show abnormal sounds indicating decreased gastric motility. An eye examination may show sluggish pupil reaction. Examination by touch or tapping (palpation and percussion) may indicate a distended bladder. Blood pressure examination may show a fall in blood pressure upon standing up (postural hypotension). Occasionally, other symptoms may indicate disturbed functioning of the autonomic nervous system, including high blood pressure, rapid or slow heart rate, irregular heart rhythms, excessive sweating (hyperhidrosis), difficulty swallowing, or other symptoms.

  • An upper GI (gastrointestinal) with small bowel series may show decreased motility, delayed emptying of the stomach, or other abnormalities and may be used to rule out physical obstruction as a cause of vomiting or other GI symptoms.
  • An EGD (esophagogastroduodenoscopy) is used to rule out physical obstruction as a cause of GI symptoms.
  • An isotope study may indicate gastroparesis (decreased gastric motility).
  • A VCUG (voiding cystourethrogram) or other tests of bladder function may show a flaccid bladder (inability of the bladder to contract to cause emptying).

Other tests for autonomic neuropathy are guided by the suspected cause of the disorder, as suggested by the history, symptoms presented, and pattern of symptom development.


Treatment is supportive. Treatment may need to be chronic and prolonged, and the response to treatment varies. Several treatments may be attempted before a treatment that is successful in reducing symptoms is identified.

The use of elastic stockings and sleeping with the head elevated may reduce postural hypotension. Fludrocortisone or similar medications may be beneficial in reducing postural hypotension for some people.

Medications that increase gastric motility (such as Reglan), use of small frequent meals, sleeping with the head elevated, or other measures may be used to treat reduced gastric motility.

Manual expression of urine (a technique in which the hands are used to compress the bladder), intermittent catheterization, or medications such as bethanechol may be necessary to treat bladder dysfunction.

Impotence, diarrhea, constipation, or other symptoms are treated as appropriate. These symptoms may respond poorly to treatment.

Expectations (prognosis):

The outcome varies. If the cause can be identified and treated, there is a chance that the nerves associated with autonomic neuropathy may repair or regenerate. The symptoms may reduce with treatment, or they may persist or worsen despite treatment. Most symptoms of autonomic neuropathy are uncomfortable but are seldom life threatening.


  • Fluid or electrolyte imbalance such as hypokalemia (if excessive vomiting or diarrhea)
  • Malnutrition
  • Kidney failure (associated with reflux of urine)
  • Psychologic/social effects of impotence
  • Injuries from falls (associated with postural dizziness)

Diabetic Neuropathy


A late complication of diabetes mellitus that affects nerve tissue.

Causes, incidence, and risk factors:

People with diabetes may develop temporary or permanent damage to nerve tissue during their illnesses. Injury to the nerves is caused by decreased blood flow and high blood-sugar levels. Neuropathies are more likely to develop if blood-glucose levels are poorly supervised. Some diabetics will not develop neuropathy, while others may develop this condition relatively early. On average, the onset of symptoms occurs 10 to 20 years after diabetes has been diagnosed.

Peripheral neuropathies may affect cranial nerves or nerves from the spinal column and their branches. This type of neuropathy tends to develop in stages. Early on, intermittent pain and tingling is noted in the extremities, particularly the feet. In later stages, the pain is more intense and constant. Finally, a painless neuropathy develops when pain sensation is lost to an area, which greatly increases the risk of severe tissue injury without pain as an indicator of injury.

Autonomic neuropathies affect the nerves that regulate involuntary vital functions including the heart muscle, smooth muscles, and glands. Low blood pressure, diarrhea, constipation, sexual impotence, and other symptoms result from autonomic neuropathies. Cranial neuropathies may affect vision and cause eye pain. Mononeuropathies affect a single nerve and are often reversible spontaneously. The incidence of diabetic neuropathy is 6 out of 10,000 people.


Control of blood-glucose levels in people with diabetes may delay the onset or decrease the severity of neuropathies.


  • Numbness
  • Tingling
  • Decreased sensation to a body part
  • Loss of sensation to a body part or area
  • Diarrhea
  • Constipation
  • Loss of bladder control
  • Impotence
  • Facial drooping
  • Drooping eyelid
  • Drooping mouth
  • Vision changes
  • Dizziness
  • Weakness
  • Swallowing difficulty
  • Speech impairment
  • Muscle contractions

Note: Symptoms vary depending on the nerve(s) affected and may include symptoms other than those listed. Symptoms usually develop gradually over years.

Signs and tests:

Physical examination including neurological and sensory tests may reveal many neuropathies.


The goals of treating diabetic neuropathy are to prevent progression and reduce the symptoms of the disease. Tight control of glucose is important to prevent progression. To reduce the symptoms, topical treatment with Capsaicin or oral medication like amitriptyline, gabapentin, and carbamazepine have been used successfully. Analgesics (pain medications) are rarely of much benefit in the treatment of painful neuropathy.

Expectations (prognosis):

The mechanisms of diabetic neuropathy are poorly understood. At present, treatment alleviates pain and can control some associated symptoms, but the process is generally progressive.


There is an increased risk of injury because of loss of sensation and/or motor functioning.

Femoral Neuropathy


Femoral neuropathies can occur secondary to direct trauma, compression, fracture, stretch injury, or ischemia. Femoral neuropathy causes weakness of the quadriceps, which results in difficulty with ambulation.


Knowledge of femoral nerve anatomy is essential to understanding the mechanism of its injury and to localizing the lesion.

The femoral nerve is part of the lumbar plexus. It is formed by L2-4 roots and reaches the front of the leg by penetrating the psoas muscle before it exits the pelvis by passing beneath the medial inguinal ligament to enter the femoral triangle just lateral to the femoral artery and vein. Approximately 4 cm proximal to passing beneath the inguinal ligament, the femoral nerve is covered by a tight fascia at the iliopsoas groove. The nerve can be compressed anywhere along its course, but it is particularly susceptible within the body of the psoas muscle, at the iliopsoas groove, and at the inguinal ligament.

The main motor component innervates the iliopsoas (a hip flexor) and the quadriceps (a knee extensor). The motor branch to the iliopsoas originates in the pelvis proximal to the inguinal ligament. The sensory branch of the femoral nerve, the saphenous nerve, innervates skin of the medial thigh and the anterior and medial aspects of the calf.


  • Weakness of the quadriceps muscle and decreased patellar reflex are the most striking examination findings.
  • If the neuropathy is advanced and chronic, wasting of the quadriceps may be noted.
  • In some patients, the iliopsoas muscle is involved. In such cases, the lesion must be above the inguinal ligament, as the motor branch to this muscle comes off before the inguinal ligament.
  • In isolated femoral neuropathies, the thigh adductors are normal. Although the thigh adductors share common lumbar roots with the muscles innervated by the femoral nerve, they are innervated by the obturator nerve and, along with the sciatic nerve, are spared. Sensory deficits consist of numbness of the medial thigh and the anteromedial calf.
  • If a retroperitoneal hematoma is present, hip extension may cause pain.

  • The femoral nerve is predisposed to compression within the psoas muscle. This commonly is associated with hemorrhage into this muscle due to hemophilia, anticoagulation therapy, or trauma.
  • Direct trauma to the femoral nerve can occur as a result of penetrating wounds or fractures of the hip or pelvis.
  • Lithotomy positioning during delivery or gynecological/urological procedures also has been associated with compressive femoral neuropathies. In this position, the sharp flexion of the hip can compress the nerve at the inguinal ligament. Excessive hip abduction and external rotation cause additional stretch on the nerve.
  • Compression of the femoral nerve also can be due to aortic or iliac aneurysms or tumors.
  • Diabetic patients have an unusual predilection for femoral and proximal mononeuropathies. The etiology is suspected to be a vasculitic.
  • Iatrogenic causes of femoral mononeuropathy include direct pressure or trauma to the nerve during pelvic or abdominal surgery or focal damage at the femoral triangle due to a difficult femoral line placement

  • Evaluation for femoral nerve dysfunction includes nerve conduction studies (NCS) and needle electromyography (EMG).
  • NCS should include sensory studies of the saphenous nerve and motor studies of the femoral nerve.
  • When evaluating femoral NCS, results on the symptomatic side should be compared to those on the asymptomatic side.
  • On EMG, the quadriceps should show neuropathic changes.