Temporal Mandibular Joint Syndrome – A Common Source of Jaw and Facial Pain

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.

Herpes Zoster (Shingles) – A Painful and Disabling Disorder

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.

Trigeminal Neuralgia — A Common Cause of Facial Pain

Trigeminal neuralgia (TN), tic douloreaux, is a common painful condition of the face that usually affects one side of the face producing brief, severe, sharp, and electric pain.

Trigeminal neuralgia is defined by the International Headache Society as "intermittent attacks of facial or frontal pain that last a few seconds to less than two minutes without neurological deficits or any other causes of facial pain." The pain has at least four of the following five characteristics: 1) distribution along the trigeminal nerve; 2) sharp, superficial, sudden, stabbing, or burning pain; 3) severe pain intensity; 4) precipitation from trigger areas or daily activities; and 5) no symptoms between attacks.

The prevalence of TN is 100 per 100,000 with an incidence of five per 100,000 per year. TN is twice as common in women. The average age on onset is 50 years of age. There is a family history of TN in five percent of patients who have subsequently have a greater likelihood of bilateral involvement.

Many cases of TN that were originally though to be idiopathic without any identifiable lesion are due to vascular compression. Fifty percent of these patients who undergo a decompression of the trigeminal nerve are pain free for an average period of 15 years. Additional types of lesions are found in up to 15% of TN patients.

TN must be differentiated from intracranial tumors, nasopharyngeal tumors, post herpetic neuralgia, dental disorders, cluster headaches, and migraine headaches.

Although the natural course of TN is not known, TN is considered to be a chronic condition that lasts a lifetime. Some patients can have long periods of remission lasting months to years.
Treatment for TN includes oral medications and surgical intervention. Tegretol is the drug of choice in treating TN. Other anticonvulsants have also been used to treat TN. The most frequent surgical treatments are gamma knife tractotomy, radiofrequency gangliolysis, retrogasserian glycerol injection and micro-vascular decompression.

Interstitial Cystitis — An Uncommon But Incapacitating Condition

Interstitial cystitis (IC), also referred to as painful bladder syndrome (PBS), is a chronic inflammatory condition of the bladder wall of unknown etiology. The prevailing opinion is that IC is a constellation of signs and symptoms arising from bladder inflammation that is aggravated by infectious, chemical, mechanical, allergic, autoimmune, neurogenic, and other factors. Some believe that a defect in the epithelial barrier, glycosaminoglycan (GAG) layer, of the bladder is a part of the pathogenesis of interstitial cystitis. IC is not psychosomatic and is not caused by stress.

Although IC can strike anyone of any age, race or gender, women are most commonly afflicted by IC. There are more than 700,000 cases of IC in the United States.

IC has been associated with other chronic conditions, such as vulvar vestibulitis, irritable bowel syndrome, and fibromyalgia.

IC produces symptoms like a urinary tract infection (UTI), but is not caused by a bacterial infection. A UTI, unlike IC, can be successfully treated with antibiotics and a UTI should be considered as a cause for an exacerbation of IC symptoms.

The most common symptoms of IC are urinary frequency, urgency and pain. Frequency can be the first symptom of IC in early or mild cases. The frequency of urination can be astonishing and disabling in severe cases up to 60 times in a 24-hour period. Urgency can be seen with pain, pressure and/or spasms. Pain is often located in the pelvis, bladder, urethral, or vaginal areas. Pain is commonly associated with sexual intercourse. Men can experience genital and/or perineal pain as well as painful ejaculation. Some patients can complain of muscle and joint pain. IC is not excluded in the absence of night time urination or lack of pain.

The first step in diagnosing IC is ruling out other disorders that can mimic IC. Urine cultures can detect the presence or absence of a UTI. Other disorders to exclude include bladder cancer, bladder TB, STDs, vaginal infections, endometriosis, radiation cystitis, spinal cord/CNS conditions, and rheumatological diseases.

IC is diagnosed with the use of cystoscopy and hydrodistention of the bladder to identify pinpoint hemorrhages (glomerulations) in the bladder wall. These findings are characteristic of IC and are found in 90% of IC patients. Ulcers on the bladder wall are present in 5 to 10% of IC patients.

There are a variety of treatment options for the IC patient including diet, nutritional supplements, oral medications, physical therapy, bladder instillation techniques and surgery. Surgical options include laser treatment of bladder ulcers; sacral nerve root stimulation for treatment of bladder urgency and frequency; and only as a last resort internal pouch construction, urinary diversion or bladder augmentation. Urethral dilatation and urethrotomy are not surgical treatment options for IC.

Spinal Cord Stimulation – Treating Radiculopathy and Spine Pain

Spinal cord stimulation (SCS) has been used for controlling intractable back and leg pain for more than 30 years. The SCS system stimulates the dorsal column of the spinal cord by tiny electrical impulses from small electrical wires placed on the spinal cord.

Spinal cord stimulation typically consists of one or two wires with a number of electrodes and a pulse generator or battery. The wire carries the electrical stimulation from the pulse generator or battery to the posterior column of the spinal cord.

Some believe that the stimulation blocks pain transmission through the spinal cord, while others believe there is activation of supraspinal pain inhibition, and still others think there is activation of neurotransmitters or neuromodulators that provide pain relief.

Pain relief from SCS varies therefore all patients considered for SCS must undergo a trial. The trial involves percutaneous placement of the wires with an external power source for five to seven days. The trial is considered successful if the patient reports good pain coverage, stimulation tolerance, pain relief, increased function, and improved sleep. The trial will determine whether or not the patient is a candidate for surgical implantation of a SCS system.

The advent of newer techniques such as retrograde wire placement have improved the efficacy of SCS in the treatment of limb and axial pain. Other applications have been successful in treating pelvic pain, bladder dysfunction, chronic angina pain and headaches.

Radiofrequency Surgery in Pain Management

The advantages of radiofrequency surgery include controlled lesion size, accurate temperature monitoring, limited need for anesthesia, precise probe placement under fluoroscopic imaging, low incidence of morbidity or mortality, and rapid post-procedure recovery. High frequency alternating current causes vibration of the electrons in the tissues in the vicinity of the radiofrequency (RF) probe, resulting in an increase in temperature. Radiofrequency surgery is performed at temperatures between 60 and 90°C depending on the structure that is causing the pain.

This pain management surgical procedure is used to treat a variety of painful conditions, such as chronic neck and back pain, headaches, trigeminal neuralgia, reflex sympathetic dystrophy (RSD), sciatica, facet syndrome, sacroiliac joint dysfunction, TMJ and cancer pain.

The procedure is performed under fluoroscopic guidance to ensure proper positioning of the RF probe. The surgery lasts approximately 30 to 60 minutes depending on the application. Some patients will experience a burning sensation at the surgery site after the procedure that is controlled with medication until it resolves in about three weeks. Nerves can regenerate over a period of one to two years that might require another RF surgery depending on whether or not the pain returns with nerve regeneration and to what degree.

Lumbar Spine Disc Degeneration – Disease or Aging Process

There is confusion as to what constitutes degenerative disc changes from what normally occurs with aging. This often times leads to misinterpretation of normal intervertebral disc and spine aging as findings with degeneration. Fibrous tissue normally replaces the mucoid matrix of the nucleus pulposus over time with aging without leading to a loss of disc height. This is considered to be a non-pathologic aspect of aging that manifests as a small to moderate decrease in the signal intensity of the nucleus pulposus on T-2 weighted MRI images and should be uniformly present throughout the spine.

Intervertebral disc margins do not become irregular as a result of aging alone. Annular pathology, such as isolated radial fissures, are rarely present in those over the age of 40 as a part of normal aging. The presence of small amounts of intradiscal gas on imaging studies is not unusual for older individuals. Osteophytes involving the anterior and lateral margins of the vertebral body are considered a natural part of the aging process whereas the existence of posterior osteophytes and endplate erosions are considered to be degenerative.

Degenerative disc changes begin in response to repetitive micro trauma from eccentric or torsional loading producing early signs of mechanical failure. Tears involving the outer annulus within the region of disc innervation can produce back pain. Circumferential tears eventually coalesce and the nucleus pulposus loses its hydrophilic properties both of which lead to further disc degeneration.

Discogenic Low Back Pain – Underappreciated and Misunderstood

Discogenic low back pain (DLBP) is a common cause for chronic axial back pain that is often unrecognized and misdiagnosed. This occurs because of the lack of objective findings, a low index of suspicion and limitations of imaging studies.

DLBP results from a fissure or tear of the outer annulus that surrounds the disc nucleus.

The fissures or tears can result from trauma such as a slip and fall, MVA, or a lifting, twisting or bending event. The injury leads to intense back pain that can radiate into the buttocks, posterior thigh or sometimes into the groin. The pain is typically higher with sitting, driving, standing, bending or lifting and lower in a recumbent position.

There are few findings on exam such as muscle spasms, painful range of motion and pain with palpation. The neurological exam is normal. Imaging studies are often unremarkable. A "high intensity" finding in the annulus can be present on MRI that has a 90% positive predictive value for DLBP but this finding is present in less than 20% of patients with DLBP.

Discography is the only reliable means of diagnosing DLBP. Contrast is injected into the disc in an attempt to recreate the pain and to detect any annular tears. The contrast injections are followed by a CT scan for a more detailed evaluation.

Primary treatment for DLBP is aggressive PT supplemented with pain medications. Discography is considered in those who fail six months of conservative treatment. Depending on the results, interventional treatment options include an IDET procedure or spine surgery.

Cancer Pain – Indication and Efficacy

Despite our best efforts, advances in treatment and new technology, pain and suffering continues to afflict those with cancer. Even in those who are cured of their cancer, many will experience devastating physical, psychological and financial devastation.

Although the use of opioids to treat cancer pain is more accepted today, there still are many physicians, patients and family members that are fearful of using opioids because of concerns for addiction, side effects, and religious implications

Pharmacological therapy continues to be the primary method for controlling cancer pain. In fact, the use of non-opioid and opioid analgesics along with adjuvant medications can adequately control the pain in 85% of cancer patients. The World Health Organization (WHO) developed a three-step approach in treating malignant and chronic benign pain. This approach, along with medications to treat the side effects from opioids (namely nausea, constipation, pruritis and sedation), has been effective in controlling cancer pain.

In cancer pain refractory to pharmacological management (15% of cancer patients have unrelieved pain or drug side effects), invasive methods of pain control, such as intrathecal pump drug delivery (IPDD), have been successful in reducing pain and drug toxicity.

Smith et al (Curr Oncol Rep 6:291-296,2004) evaluated 202 patients with a VAS =7.5 and taking = 200 mg morphine or opiod equivalent in a prospective, randomized study. The patients were divided into IPDD and medical management groups. The IPDD patients had better clinical success with lower pain (52% vs. 39%), lower drug toxicity (50% vs. 17%) and lived longer when compared to the medical group. IPDD also lower pain by 27% and lower drug toxicity by 50% in the most refractory of cancer patients who first failed to experience any improvement in the medical group.

Low Back Pain – Do's, Don'ts and Red Flags

Low back pain (LBP) is the second most common reason, other than having a cold, that we seek medical care. Approximately 90% of us will suffer a significant episode of LBP in our lifetime. LBP is the leading cause for disability under the age of 45 and second for those over 45.

The good news is that nine out of ten patients will recover from their back pain within four weeks with or without treatment. Tips (DO'S) to prevent back pain include:

* Lift with the legs not the back
* Do not lift heavy objects
* Wear low heeled shoes
* Get consistent sleep
* Shift heavy purses/briefcases
* Stop activity that hurts
* Do not stoop, and
* Exercise regularly.

Low back pain typically is due to injuries of the soft tissue structures, spinal joints, or discs. Risk factors (DON'TS) for developing low back pain include: poor posture, repetitive motion, prolonged sitting/standing, smoking, poor nutrition, and incorrect bending, lifting, and twisting.

Seek medical attention if your pain does not improve or if it increases over a period of two to three weeks. In addition, you should seek immediate medical care for any of the following RED FLAGS:

* Sudden pain onset if > age 50 O LBP related to a fall or trauma
* Sciatica (leg pain)
* Loss of bowel or bladder control
* Loss of groin or rectal sensation
* Leg weakness
* Falling when walking
* Fever or weight loss, and
* LBP worse at night.

Osteoporosis – Diagnosing and Treating

The most common method of diagnosing osteoporosis is via a DEXA (Dual Energy X-ray Absorptiometry) scan. Osteopenia, osteoporosis and severe osteoporosis are respectively defined as DEXA scan T scores of -1 to -2.5, less than -2.5 and less than -2.5 with a fragility fracture.

Vertebral compression fractures are the most common complication of osteoporosis at a cost of 10 to 15 billion dollars every year. There are approximately 700,000 vertebral compression fractures per year in the United States that result in spinal deformity (kyphosis/lordosis), acute/chronic pain, disability and reduced vital respiratory capacity. An osteoporotic vertebral compression fracture should be considered in anyone over the age of fifty with a complaint of acute or chronic back pain. The most common location for vertebral compression fractures are at the T7-8 and T12-L1 levels which correspond to the most mechanically compromised spine regions. The diagnostic work up for someone suspected of having a spinal compression fracture includes spine x-rays looking for wedged shaped vertebral fractures as well as MRI imaging with T2 and STIR sequences to evaluate the acuity of the fracture. Nuclear bone scans and CT can also be helpful in evaluating vertebral compression fractures.

Vertebral compression fractures lead to decreased physical function, restricted activities of daily living, sleep disturbances, early satiety, psychological disturbances and reduced pulmonary function. The subsequent risk of additional vertebral fractures increased after the first fracture. Women with a vertebral fracture had a >20% higher mortality rate adjusted for age. Patients with vertebral fractures are 2-3 times more likely to die of pulmonary causes typically due to COPD and pneumonia complications.

Kyphoplasty is a minimally invasive percutaneous procedure that restores vertebral body height, provides fracture stability and reduces pain associated with vertebral compression fractures. The procedure involves the placement of a balloon catheter through a needle introducer into the vertebral fracture, inflation of the balloon (which creates a cavity and restores vertebral body height) and injection of cement into the cavity. The indications for kyphoplasty include an osteoporotic or malignant spinal compression fracture, persistent back pain, progressive vertebral collapse, spinal deformity and a correct diagnosis from imaging studies. Contraindications consist of bone retropulsion with neurological complications, infection and greater than 80% loss of vertebral body height. Clinical studies have demonstrated that kyphoplasty is a highly effective treatment for compression fractures and provides correction of spinal deformities with significant pain relief, improved quality of life and increased physical function.

Osteoporosis and Vertebral Compression Fractures

Osteoporosis is the most common metabolic bone disease in the United States and is a chronic progressive disease that can affect almost the entire skeleton. It is characterized by low bone mass and bone weakening that increases the risk for bone fractures. Osteoporosis often does not become clinically evident until a complication occurs such as a bone fracture that can lead to severe pain, disability and a poor quality of life.

There are about 10 million people in the United States that have osteoporosis and 14 to 18 million that have osteopenia – low bone mass. Osteoporosis affects one in every three women and one in every eight men worldwide.

Osteoblasts are specialized cells that make bone and osteoclasts are unique cells that resorb bone. These cells are constantly remodeling the skeletal system with bone resorption followed by bone formation known as coupling. Osteoporosis occurs when there is a disruption in the coupling process that leads to a reduction in skeletal mass.

During the post menopausal state bone loss is due to excessive osteoclast activity whereas the loss of osteoblasts leads to skeletal mass loss in the elderly.

Osteoporosis can be divided into primary and secondary disorders. Primary osteoporosis can be categorized as juvenile, postmenopausal, and age related or senile. Juvenile osteoporosis occurs in children or young adults with an onset of 8 to 14 years of age. The characteristic finding in juvenile osteoporosis is the abrupt commencement of bone pain or a trauma related fracture. Post menopausal (type I) osteoporosis occurs in women from the age of 50 to 65 years old. This form of osteoporosis is exemplified by accelerated bone loss. The skeletal loss occurs primarily from trabecular bone leading to distal forearm and vertebral body fractures. Senile osteoporosis (type II) occurs in both men and women over the age of 70 years and is due to the loss of cortical as well as trabecular bone. Fractures of the wrist, spine and hip are often seen with type II osteoporosis.

Secondary causes of osteoporosis are due to disorders classified as genetic (congenital), endocrine, hypogonadal states, deficiency states, drug-induced, inflammatory states, hematologic, neoplastic and miscellaneous.

Risk factors for the development of osteoporosis include advanced age, alcohol use, androgen or estrogen deficiency, amenorrhea, body weight less than 127 pounds, Caucasian or Asian ethnicity, calcium deficiency, early menopause, family history of osteoporosis, female gender, fragility fracture, late menarche, physical inactivity and tobacco use.