Post-herpetic neuralgia is a lasting pain in the areas of your skin where you had shingles. Around one in five people with shingles will get post-herpetic neuralgia. People age 50 and over are particularly at risk. Many people with post-herpetic neuralgia make a full recovery within a year. But symptoms occasionally last for several years or may be permanent. The main symptom of post-herpetic neuralgia is intermittent or continuous nerve pain in an area of your skin previously affected by shingles.
The pain may come and go or be continuous. It can be described as burning, stabbing, shooting, aching, throbbing or like electric shocks. Treatment for postherpetic neuralgia aims to manage and reduce the pain until the condition goes away.
Pain therapy may include the following treatments. Pain relievers are also known as analgesics. Doctors often prescribe tricyclic antidepressants to treat depression, but these medications are also effective in treating pain caused by postherpetic neuralgia.
Tricyclic antidepressants can have side effects, like dry mouth and blurred vision. Anticonvulsants are usually prescribed to treat seizures, but doctors can prescribe them to treat postherpetic neuralgia pain as well. Commonly used anticonvulsants include:. Two doses of a herpes zoster vaccine called Shingrix reduce the risk of shingles by more than 90 percent. The vaccine also protects against postherpetic neuralgia.
Learn more about the Shingrix vaccine and its potential side effects. Postherpetic neuralgia is treatable and preventable. Most cases disappear in 1 to 2 months. In rare cases, it can last longer than a year. If you do develop postherpetic neuralgia, you have many treatment options to manage the pain.
Talk with your doctor to find the best treatment for you. Shingles without a rash is uncommon, but it can occur. Patient information: See related handout on shingles , written by the authors of this article. Whereas varicella is generally a disease of childhood, herpes zoster and post-herpetic neuralgia become more common with increasing age.
Factors that decrease immune function, such as human immunodeficiency virus infection, chemotherapy, malignancies and chronic corticosteroid use, may also increase the risk of developing herpes zoster.
Reactivation of latent varicella-zoster virus from dorsal root ganglia is responsible for the classic dermatomal rash and pain that occur with herpes zoster.
Burning pain typically precedes the rash by several days and can persist for several months after the rash resolves. With postherpetic neuralgia, a complication of herpes zoster, pain may persist well after resolution of the rash and can be highly debilitating.
Herpes zoster is usually treated with orally administered acyclovir. Other antiviral medications include famciclovir and valacyclovir. The antiviral medications are most effective when started within 72 hours after the onset of the rash. The addition of an orally administered corticosteroid can provide modest benefits in reducing the pain of herpes zoster and the incidence of postherpetic neuralgia. Ocular involvement in herpes zoster can lead to rare but serious complications and generally merits referral to an ophthalmologist.
Patients with postherpetic neuralgia may require narcotics for adequate pain control. Tricyclic antidepressants or anticonvulsants, often given in low dosages, may help to control neuropathic pain. Capsaicin, lidocaine patches and nerve blocks can also be used in selected patients. Herpes zoster results from reactivation of the varicella-zoster virus.
Unlike varicella chickenpox , herpes zoster is a sporadic disease with an estimated lifetime incidence of 10 to 20 percent. The incidence of herpes zoster increases sharply with advancing age, roughly doubling in each decade past the age of 50 years. Herpes zoster is uncommon in persons less than 15 years old. In a recent study, 1 patients more than 55 years of age accounted for more than 30 percent of herpes zoster cases despite representing only 8 percent of the study population.
In this same study, children less than 14 years old represented only 5 percent of herpes zoster cases. The normal age-related decrease in cell-mediated immunity is thought to account for the increased incidence of varicella-zoster virus reactivation. Patients with disease states that affect cell-mediated immunity, such as human immunodeficiency virus HIV infection and certain malignancies, are also at increased risk.
Chronic corticosteroid use, chemotherapy and radiation therapy may increase the risk of developing herpes zoster. The incidence of herpes zoster is up to 15 times higher in HIV-infected patients than in uninfected persons, and as many as 25 percent of patients with Hodgkin's lymphoma develop herpes zoster.
Race may influence susceptibility to herpes zoster. Blacks are one fourth as likely as whites to develop this condition. Household transmission rates have been noted to be approximately 15 percent. About 20 percent of patients with herpes zoster develop postherpetic neuralgia. The most established risk factor is age; this complication occurs nearly 15 times more often in patients more than 50 years of age.
Other possible risk factors for the development of post-herpetic neuralgia are ophthalmic zoster, a history of prodromal pain before the appearance of skin lesions and an immunocompromised state. Varicella-zoster virus is a highly contagious DNA virus. Varicella represents the primary infection in the nonimmune or incompletely immune person. During the primary infection, the virus gains entry into the sensory dorsal root ganglia. How the virus enters the sensory dorsal root ganglia and whether it resides in neurons or supporting cells are not completely understood.
The varicella-zoster virus genome has been identified in the trigeminal ganglia of nearly all seropositive patients. The virus remains latent for decades because of varicella-zoster virus—specific cell-mediated immunity acquired during the primary infection, as well as endogenous and exogenous boosting of the immune system periodically throughout life.
The reactivated virus travels down the sensory nerve and is the cause for the dermatomal distribution of pain and skin lesions.
The pathophysiology of postherpetic neuralgia remains unclear. However, pathologic studies have demonstrated damage to the sensory nerves, the sensory dorsal root ganglia and the dorsal horns of the spinal cord in patients with this condition. Herpes zoster typically presents with a prodrome consisting of hyperesthesia, paresthesias, burning dysesthesias or pruritus along the affected dermatome s.
The prodrome generally lasts one to two days but may precede the appearance of skin lesions by up to three weeks. During the prodromal phase, herpes zoster may be misdiagnosed as cardiac disease, pleurisy, a herniated nucleus pulposus or various gastrointestinal or gynecologic disorders.
Some patients may have prodromal symptoms without developing the characteristic rash. The prodromal phase is followed by development of the characteristic skin lesions of herpes zoster. The vesicles are generally painful, and their development is often associated with the occurrence of anxiety and flu-like symptoms. Typical dermatomal rash with hemorrhagic vesicles on the trunk of a patient with herpes zoster.
Pain is the most common complaint for which patients with herpes zoster seek medical care. Indeed, patients may have insomnia because of the pain. The most frequently involved cranial nerve dermatome is the ophthalmic division of the trigeminal nerve. Twenty or more lesions outside the affected dermatome reflect generalized viremia. Of these patients, approximately one half manifest other neurologic or visceral involvement, and as many as one in seven with viremia may die.
The vesicles eventually become hemorrhagic or turbid and crust over within seven to 10 days. As the crusts fall off, patients are generally left with scarring and pigmentary changes. Ocular complications occur in approximately one half of patients with involvement of the ophthalmic division of the trigeminal nerve.
These complications include mucopurulent conjunctivitis, episcleritis, keratitis and anterior uveitis. Cranial nerve palsies of the third, fourth and sixth cranial nerves may occur, affecting extraocular motility. The most common chronic complication of herpes zoster is postherpetic neuralgia. Pain that persists for longer than one to three months after resolution of the rash is generally accepted as the sign of postherpetic neuralgia.
Patients may also complain of pain in response to non-noxious stimuli. Even the slightest pressure from clothing, bedsheets or wind may elicit pain. Postherpetic neuralgia is generally a self-limited disease. Applied to the skin, it can relieve itching, burning, and pain from inflammation.
The patches can be cut to fit the affected area. Antidepressants : These affect key brain chemicals, such as serotonin and norepinephrine, which influence how the body interprets pain. Examples of drugs that inhibit the reuptake of serotonin or norepinephrine are tricyclic antidepressants , such as amitriptyline, desipramine Norpramin , nortriptyline Pamelor , and duloxetine Cymbalta. This treatment involves placing electrodes over the areas where pain occurs.
These emit small electrical impulses. The patient turns the TENS device on and off as required. Some people find that TENS relieves pain, while others do not. Its effectiveness has not been confirmed by research.
These devices offer a safe, efficient, and effective way to relieve many types of neuropathic pain conditions. Similar to TENS, they are implanted under the skin along the course of peripheral nerves.
Before implantation, doctors do a trial run using a thin wire electrode to determine patient response. The spinal cord stimulator is inserted through the skin into the epidural space over the spinal cord. The peripheral nerve stimulator is placed under the skin above a peripheral nerve.
As soon as the electrodes are in place, they are switched on to administer a weak electrical current to the nerve. Symptoms are usually limited to the area of skin where the shingles outbreak first occurred and may include:.
In rare cases, if the nerve also controls muscle movement, there may be muscle weakness or paralysis. Symptoms may make it hard to carry out some daily activities, such as bathing or dressing. PHN may also cause fatigue and sleeping difficulties. PHN is a persistent nerve pain that can occur as a result of shingles. Shingles is caused by the herpes varicella-zoster virus, the virus known to cause chickenpox.
After a person recovers from chickenpox, the virus remains inactive in the nervous system. Later in life, the herpes varicella-zoster virus may become reactivated, causing shingles.
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