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May/June 2006
Volume 2, Issue 3
In this Issue:
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Herpes Zoster (Shingles): A Painful and Disabling Disorder
An Original Contribution by Frank J. E. Falco, M.D.
Herpes Zoster (shingles) has a 10% to 20% lifetime incidence that increases with age. The incidence doubles with each decade after the age of 50 years. Shingles occurs from the reactivation of the varicella-zoster virus. The normal decrease in cell mediated immunity with age and diseases that affect cell mediated immunity (such as malignancy, HIV, and chronic corticosteroid use) are thought to be reasons for developing herpes zoster.
The varicella-zoster virus is a highly contagious DNA virus that enters the sensory dorsal root ganglion during the primary infection and remains dormant for decades. Virus reactivation occurs when there is a decrease in the virus specific cell mediated immunity. The reactivated virus travels down the sensory nerve leading to a rash and pain within the dermatomal distribution of the nerve.
A maculopapular rash evolves into vesicles with an erythmatous base. The vesicles eventually crust over in 7 to 10 days. Scars and pigment changes occur when the crusts fall off. Shingles pain is described as burning, stinging, and unrelenting. The T5 and T6 spinal nerves are the most commonly affected vertebral dermatomes and the ophthalmic division of the trigeminal nerve is the most commonly affected cranial nerve dermatome.
Post herpetic neuralgia (PHN) occurs in 20% of those with herpes zoster. Age is the most established risk factor for PHN with an incidence 15 times more often in those over age 50. Other risk factors include ophthalmic zoster, prodromal pain, and an immunocompromised state. Prodromal pain presents as hyperesthesias, paresthesias, burning dysethesias, or pruritis along the affected dermatome lasting one to two days and up to three weeks before the rash. PHN tends to be self-limited over time with 25% having pain at six months and five percent having pain at one year.
Shingles treatment is aimed at the acute viral infection, pain, and preventing post herpetic neuralgia. Oral antiviral agents (acyclovir, famciclovir, valacyclovir) decrease the duration and pain of the rash if used within the first 72 hours and can reduce the incidence of PHN. Oral prednisone has variable results for the acute viral infection, but reduces the acute pain when combined with acyclovir. Prednisone can diminish the onset of PHN and is often recommended in those over the age of 50 who are at a greater risk for PHN.
Treatment of the acute pain associated with Shingles includes the use of OTC medications, calamine lotion on vesicles, capsaicin cream for crusted lesions, opioids, prednisone, steroid injections of vesicles, epidurals and nerve root blocks. The same medications used for acute Shingles pain are used to treat PHN along with anticonvulsants and tricyclic antidepressants. Peripheral nerve stimulation is an effective last resort if other measures for pain control fail.
Temporal Mandibular Joint Syndrome:
A Common Source of Jaw and Facial Pain
An Original Contribution by Frank J. E. Falco, M.D.
Temporal Mandibular Joint (TMJ) Syndrome presently affects 10 million Americans and afflicts women four times more often than men between 20 and 40 years of age. TMJ syndrome is divided into three categories involving the mastication muscles and the joint.
Treatment outcome is improved with early diagnosis. Some cases of TMJ syndrome are self-limiting but most progress to a chronic state especially those with coexisting ear symptoms.
Myofascial pain dysfunction (MPD) involves the mastication muscles and is considered the most common TMJ disorder. MPD is a stress related disorder with a centrally induced increase in mandibular muscle tension that results in muscle spasm, pain and dysfunction.
Internal Derangement (ID) refers to a mechanical dysfunction between the TMJ articular disc and the mandibular condyle, fossa and articular eminence. There is an organic problem with the joint. The mandibular muscle spasm is secondary to the mechanical joint dysfunction and is not the primary problem as seen in MPD.
Degenerative Joint Disease (DJD) describes the degeneration of the articular surfaces within the TMJ.
The primary symptoms of TMJ are dull jaw pain, increased pain with chewing, limited mouth opening, and jaw clicking or popping. Secondary symptoms include earache, headache, and neck pain. Examination findings demonstrate restricted mouth opening, facial muscle spasms, TMJ tenderness, TMJ clicking or popping, TMJ crepitus, and mandibular lateral deviation. Diagnostic evaluation includes x-rays, CT and/or MRI.
Conservative care consists of analgesics, muscle relaxants, moist heat, massage, and physical therapy. Interventional treatment includes intra-articular TMJ steroid injections, Botox injections of the temporalis muscle, and radiofrequency. TMJ joint arthroplasty is considered as a last result in appropriate candidates with refractory pain. |
