OSTEOPOROSIS MEDICAL GROUP
Serving the communities of Southern California
Disclaimer: The content on this webpage has been prepared by Dr. Thang Le and is for educational purposes only. This site does not and cannot provide medical advice for any person who requires direct medical care. The information provided is only intended to aid in the communication between you and your physician. Furthermore, it is not intended for diagnosis and cannot provide a diagnosis for any particular individual and it should not be used as a substitute for medical care and the advise of your physician.
OA is the most common type of arthritis, generally affecting middle-age and older people. It is due to progressive damage of the joint cartilage , which acts as a “shock absorber”, and this may lead to fluid accumulation and bony overgrowth of the joint.
Most commonly affected are the weight-bearing joints—the knees, hips and spine – and the hands. Patients may develop bony knobs or “nodes” that enlarge finger joints, causing pain, stiffness or numbness and later restrict use of the fingers.
2. What causes OA?
While no one determinant appears to cause cartilage damage, excess weight, previous joint trauma or injury, and family history are all factors that may contribute to the deterioration of the joint cartilage.
3. How is OA diagnosed?
A physician will look for evidence of OA in the form of bony enlargement, fluid accumulation, limited range of motion, and a cracking sensation during movement. X-rays are very helpful in confirming the diagnosis.
4. How is OA treated?
The goal of treatment is to reduce pain and improve function of the affected joints. This can be achieved with a combination of drug therapy and physical measures. If severe, then surgery can be contemplated. Drug therapy is mainly in the form of pain relievers such as acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs). For more serious pain, stronger medications such as narcotics may be required. Joint injections with corticosteroids or a form of lubricant called hyaluronic acid may be beneficial.
5. What is the role of supplements in the treatment of OA?
Many nutritional supplements have claimed clinical efficacy in the treatment of OA, but most lack good research data. A recent study from the National Institute of Health showed that patients with moderate to severe pain from knee OA may benefit from chondroitin and glucosamine sulfate supplementation.
6. How is OA different from rheumatoid arthritis?
Both arthritic conditions may have similar symptoms and may affect the same joints. In their severe forms, the two can be quite disabling and result in joint destruction and deformities. The key distinguishing feature is that rheumatoid arthritis is an "inflammatory" arthritis. Patients with rheumatoid arthritis generally will have multiple visibly swollen, warm, and tender joints. They are particularly stiff in the morning and this stiffness can last for more than one hour. Osteoarthritis, on the other hand, is a "degenerative" arthritis and although patients can have joint swelling and morning stiffness, the severity of these symptoms are much less than that of individuals with rheumatoid arthritis.
RA is a chronic inflammatory disease that causes pain, stiffness, and swelling in multiple joints. It is the most common form of inflammatory arthritis and can affect patients of any age. The small joints of the hands and feet tend be involved more frequently than others. Inflammation can develop in other organs as well. Patients usually complain of joint stiffness in the morning, which can last for more than an hour or throughout the entire day.
8. How is RA diagnosed?
RA can be difficult to diagnose. Early on, the symptoms may be similar to many diseases including osteoarthritis, systemic lupus, and fibromyalgia. For this reason, patients suspected of having RA should be evaluated by a rheumatologist. Diagnosis is based on the patient’s complaints and findings on the physical examination. Tests such as a rheumatoid factor and an anti-CCP (cyclic citrullinated peptide) can be very helpful.
9. What causes RA?
The cause of RA is unknown. RA is an autoimmune disease, that develops because certain cells of the immune system begin attacking healthy joints.
10. How is RA diagnosed?
RA can be difficult to diagnose because it may begin with only subtle symptoms, such as achy joints or a little stiffness in the morning. Additionally, many diseases early on behave like RA. For this reason, patients suspected of having RA should be evaluated by a rheumatologist. X-rays can be very helpful in diagnosing RA, but may not show any abnormalities in the first 3–6 months of the arthritis. MRI and ultrasound are also being used more frequently to help detect the severity of RA.
It is important to remember that, for most patients with this disease, there is no single test that "confirms" a diagnosis of RA. Rather, diagnosis is established by evaluating the individual's symptoms, physical exam, laboratory tests, and X-rays.
11. How is RA treated?
There is presently no cure for RA but treatment options have greatly improved over the past 2 decades. Successful management requires early diagnosis and, at times, aggressive treatment. Mainstay therapy is with disease-modifying anti-rheumatic drugs (DMARDs). DMARDs are often used in conjunction with NSAIDs and/or low-dose corticosteroids. DMARDs have greatly improved the symptoms and function as well as the quality of life for the vast majority of patients with RA and have been shown to slow down disease progression and reduce the risk for joint destruction. DMARDs include methotrexate, leflunomide (Arava), hydroxychloroquine (Plaquenil), sulfasalazine (Azulfidine), and azathioprine (Imuran).
For patients with more significant disease, medications referred to as “biologic DMARDs” can specifically target parts of the immune system that lead to inflammation, joint and tissue damage. They include adalimuma (Humira), anakinra (Kineret), etanercept (Enbrel), infliximab (Remicade), abatacept (Orencia), and rituximab (Rituxan). Typically these are used with methotrexate as the combination is more beneficial.
Regular visits with the rheumatologist are necessary to follow the course of the disease and monitor for any side effects related to medications. Regular blood tests and occasional X-rays or CT-scans are necessary as well to manage RA and medications effectively.
Systemic lupus erythematosus (also called SLE or lupus) is an autoimmue disease that can affect various parts of the body, including the joints, skin, kidneys, lungs, and nervous system.
13. What causes lupus?
SLE is an autoimmune disorder which develops when the body's own immune system, which normally protects against cancers and invading infections, begins to attack the patient's own tissues. This occurs first through the production of "auto-antibodies" (antibodies are products of the immune system cells that are designed to attack foreign microbes; auto-antibodies attack a person's own cells and obviously this is not a good thing). As the attack continues, other immune system cells join in the fight. This leads to inflammation, blood vessel damage (vasculitis) and deposition of immune system cells in organs which causes tissue damage.
It is not known why this inflammatory reaction begins, but it probably occurs because of some combination of genetic susceptibility and environmental factors (such as viruses and the ultraviolet rays in sunlight).
14. Who gets lupus?
SLE occurs 10 times more often in women than in men. The disorder typically develops in people in their 20s and 30s. SLE is more common in certain ethnic groups, particularly in blacks and Asians, who also tend to be more severely affected.
15. What does a positive ANA mean?
A positive antinuclear antibody (ANA) by itself does not necessarily indicate a disease. The result has to be properly interpreted by a rheumatologist, who takes into account the patient’s complaints, clinical history, and physical examination. Additional laboratory testing is generally required before lupus can be diagnosed.
16. How is lupus diagnosed?
Lupus is difficult to diagnosis and often patients are incorrectly diagnosed with the condition purely based on a positive antinuclear antibody (ANA) test. Although the ANA is present in virtually all patients with lupus, this test has a high rate of false-positivity and it is not highly specific for the disease. Up to 10% of individuals from a healthy population will test positive and it can be seen in other conditions including infections, thyroid diseases, drug reactions, liver diseases, and malignancies. The diagnosis of lupus cannot be based solely on a positive ANA. It is made through a combination of clinical symptoms, past medical history, physical exam findings, and further laboratory testing.
All patients suspected of lupus should be evaluated by a rheumatologist. Individuals with known disease should be monitored by a rheumatologist on a regular basis.
17. How is lupus treatment?
Treatment depends on symptoms and their severity. Conservative treatment is appropriate for patients with muscle or joint pain, fatigue, skin rash, and other features that are not life-threatening. Options include nonsteroidal anti-inflammatory drugs (NSAIDs) and anti-malarial medications such as hydroxychloroquine (Plaquenil).
More aggressive therapy is required for life-threatening and more serious manifestations such as kidney inflammation, lung or heart involvement, and central nervous system symptoms. Treatment in these circumstances might involve high-dose corticosteroids such as prednisone and other immunosuppressive drugs such as azathioprine (Imuran), mycophenolate mofetil (Cellcept), cyclosporine, cyclophosphamide (Cytoxan), and rituximab (Rituxan).
Treatment depends upon an individual assessment of risks and benefits. Most immunosuppressive medications, for instance, may cause significant side effects such as increased risk of infections, nausea, vomiting, hair loss, diarrhea, high blood pressure, and osteoporosis. Rheumatologists may also reduce or discontinue a medication after the disease goes into remission for a period of time.
Clinical trials to evaluate new treatments are always being undertaken, with the hope that more promising drugs will be identified and made more widely available.
Fibromyalgia is a clinical syndrome defined by chronic widespread muscular pain, fatigue and tenderness. Often times, individuals with fibromyalgia will also have chronic fatigue, chronic headaches, irritable bowel syndrome, irritable bladder, cognitive and memory problems (often called "fibro fog"), temporomandibular joint disorder, pelvic pain, restless leg syndrome, sensitivity to noise and temperature, and anxiety and depression.
19. Is fibromyalgia a “real” diagnosis?
This is a question is that commonly asked by physicians, patients, and patients’ families. In the past decade, much progress has been made in the understanding of the disorder. It is not a "psychiatric" diagnosis. Research, including neuroimaging studies, has shown that the "volume control" in these individuals may be turned up too high in the brain’s processing areas. Patients with fibromyalgia can also have abnormal levels of substance P in their spinal fluid. This chemical is known to aid in the transmission and amplification of pain signals to and from the brain.
And so, yes, fibromyalgia is a real diagnosis.
20. What causes fibromyalgia?
No one knows what causes fibromyalgia. Genetics appear to play a role leading to a familial tendency to develop fibromyalgia. It is not an autoimmune or inflammatory disease and although the symptoms can be quite disabling it is not a degenerative process.
21. Who gets fibromyalgia?
While men and adolescents can develop fibromyalgia, this condition is more common in women. The disorder tends to develop during early and middle adulthood or during a woman's childbearing years. It is very common for patients with lupus and rheumatoid arthritis to eventually have fibromyalgia as well.
22. How is fibromyalgia diagnosed?
The diagnosis is based solely on the patient’s symptoms. There are no diagnostic tests such as x-rays, blood test, or muscle biopsy that will confirm the diagnosis.
A rheumatologist will usually send off tests to exclude other diagnoses such as hypothyroidism, polymyalgia rheumatica, rheumatoid arthritis, and lupus.
23. How is fibromyalgia treated?
Drug therapy primarily treats the symptoms. Commonly used agents include cyclobenzaprine, amitriptyline, and antidepressants. Recently, two medications – Cymbalta and Lyrica – have gained FDA approval for the treatment of fibromyalgia and the clinical results have been promising.
Long-acting opioid agents are typically not recommended for the management of fibromyalgia. These drugs are not generally of great benefit in terms of pain relief.
Complementary and alternative therapies can be useful in pain management for people with fibromyalgia, although these treatments have generally not been well tested. Therapeutic massage to manipulate the muscles and soft tissues of the body may alleviate pain, discomfort, muscle spasms and stress.
Osteoporosis is a silent disease of the bones that makes them weaken and prone to fracture. The disease is "silent" because there are no symptoms when you have osteoporosis, and the condition may come to attention only after you break a bone. When you have osteoporosis, this can occur even after a minor injury, such as a fall. The most common fractures occur at the spine, wrist and hip. The goal of treating osteoporosis is to prevent such fractures in the first place.
25. What causes osteoporosis?
Many factors will increase your risk of developing osteoporosis and suffering a fracture. Recognizing your own risk factors is important so you can take steps to prevent this condition from developing or treat it before it becomes worse. Major risk factors include:
- Older age (starting in the mid-30s but accelerating after 50 years of age)
- Non-Hispanic white and Asian ethnic background
- Small bone structure
- Family history of osteoporosis or osteoporosis-related fracture in a parent or sibling
- Previous fracture following a low-level trauma, especially after age 50
- Sex hormone deficiency, particularly estrogen deficiency, both in women (e.g. menopause) and men
- Anorexia nervosa
- Cigarette smoking
- Alcohol abuse
- Low dietary intake or absorption of calcium and vitamin D
- Sedentary lifestyle or immobility
- Medications: glucocorticoid medications such as prednisone, excess thyroid hormone replacement; certain anti-convulsant medications such as phenytoin.
- Certain diseases can affect bone, such as endocrine disorders (hyperthyroidism, hyperparathyroidism, Cushing's disease, etc.) and inflammatory arthritis (rheumatoid arthritis, ankylosing spondylitis, etc.)
26. Who gets osteoporosis?
Osteoporosis is more common in older individuals and non-Hispanic white women, but can occur at any age, in men as well as in women, and in all ethnic groups.
Those over the age of 50 are at greatest risk of developing osteoporosis and suffering related fractures. In this age group, one in two women and one in six men will suffer an osteoporosis-related fracture at some point in their life. Non-Hispanic white and Asian people are most likely to experience osteoporosis and osteoporosis-related fractures. Hispanic and non-Hispanic black people also can develop osteoporosis and related fractures, but have a lower risk when compared to non-Hispanic whites and Asians.
27. How is osteoporosis diagnosed?
A simple test that measures bone mineral density (BMD) at different parts of your body, such as your spine and your hip, can help determine if you have osteoporosis. Dual energy x-ray absorptiometry (DEXA) is the best current test to measure BMD. The test is similar to having an x-ray taken, but uses much less radiation.
28. How is osteoporosis treated?
To maintain bone health:
- Make sure there is enough calcium in your diet (1000 mg per day of calcium for women before menopause and 1500 mg per day for women who are postmenopausal).
- Get adequate vitamin D intake, which is important for calcium absorption and to maintain muscle strength (400IU per day until age 60, 600-800 IU per day after age 60). Doses can be adjusted according to blood levels of vitamin D.
- Get regular exercise, especially weight bearing exercise.
A number of medications are also used for the prevention and treatment of osteoporosis. Bisphosphonates, which include alendronate (Fosamax), risedronate (Actonel), ibandronate (Boniva), and zoledronate (Reclast) have been FDA-approved for the treatment of osteoporosis in postmenopausal women. These medications help slow down bone loss and have been shown to decrease the risk of fractures. With the exception of intravenous Boniva and Reclast, all are pills that must be taken on an empty stomach with water. Because they have the potential for irritating the esophagus, remaining upright for at least an hour after taking these medications is recommended. Intravenous Boniva and Reclast are given every 3 and 12 months, respectively. Other therapeutic options include Forteo, estrogen replacement therapy, Evista, and calcitonin.
29. What is the relationship between bisphosphonate therapy and osteonecrosis of the jaw?
There have been reports of jaw osteonecrosis (permanent bone damage of the bones of the jaw) resulting from high dose IV bisphosphonates used primarily in the management of people with underlying cancers. The risk for this problem in those taking these medications at doses recommended for osteoporosis management is not clearly established, but appears to be low.
30. What is Reclast?
Reclast is an intravenous bisphosphonate that has recently received FDA approval for the treatment of osteoporosis. It is a once-a-year infusion that takes about 15 minutes to administer. Unlike the oral bisphosphonates such as Fosamax, Actonel, and Boniva, it does not generally cause heartburn or stomach upset, and so it may be a good choice for patients who have trouble tolerating these pills. In order to receive Relast, patients need to have good kidney function.
31. What is Forteo?
Forteo is a form of parathyroid hormone that helps stimulate bone formation. It is a potent bone medication and is approved for use in postmenopausal women and men at high risk for osteoporotic fracture. It is given as a daily injection under the skin and can be used for up to 2 years.
32. What good preventive measures are there for osteoporosis?
Lifestyle changes may be the best way of preventing osteoporosis:
- Make sure you are getting enough calcium in your diet (roughly 1000-1500 mg/day, but will depend on your age)
- Make sure you are getting enough vitamin D (between 400-800 IU/day)
- Stop smoking
- Avoid excess alcohol intake
- Engage in weight-bearing exercises
- Treat underlying medical conditions that can cause osteoporosis
- Minimize or change medications that can cause osteoporosis; never stop taking any medication without speaking with your doctor first
- If you are at high risk for falls, consider using hip protectors, which will help prevent a hip fracture if you fall.
Gout is a painful and potentially disabling form of arthritis. Initial symptoms usually consist of intense episodes of painful swelling in single joints, most often in the feet (especially the big toe).
34. What causes gout?
Gout occurs when excess uric acid (a normal waste product of protein metabolism) accumulates in the body, and crystals deposit in the joints. This may happen because either uric acid production increases or, more often, the kidneys are unable to remove uric acid from the body adequately. Certain foods, such as shellfish and alcohol, may increase uric acid levels and lead to gout attacks.
Some medications also can increase uric acid levels. Examples of such medications include moderate-dose aspirin (81 mg used for prevention of heart attack and stroke has minimal effect and can generally be continued), diuretics such as hydrochlorothiazide, and immunosuppressants used in organ transplantation such as cyclosporine and tacrolimus. With time, increased uric acid levels in the blood may lead to deposits of monosodium urate crystals in and around the joints. These crystals can attract white blood cells, leading to severe gout attacks. Uric acid also can deposit in the urinary tract, causing kidney stones.
35. How is gout diagnosed?
Several other kinds of arthritis can mimic gout, so proper diagnosis is essential. Gout is suspected when a patient experiences joint swelling and intense pain followed, at least at first, by pain-free periods between attacks. Initial gout attacks often occur at night.
A correct diagnosis may depend on finding the characteristic crystals. The physician will use a needle to extract fluid from an affected joint and examine that fluid under a microscope to determine whether monosodium urate crystals are present. Crystals also can be found in deposits under the skin (called tophi) that occur in advanced gout. Uric acid levels in the blood can be misleading, as these may be temporarily normal or even low during attacks. Uric acid levels also are often elevated in people who do not have gout.
36. How is gout treated?
Acute attacks of gout are generally treated with colchicine and NSAIDs. Colchicine is most effective when used within 48 hours of an attack. Indomethacin and naproxen are NSAIDs commonly given. For patients who are unable to take NSAIDs (stomach ulcer, kidney disease, taking blood thinners), corticosteroids are an option. Resting the affected joint and applying cold compresses to the area also may help alleviate pain.
Efforts to normalize blood uric acid levels should be considered for patients who have repeated gout attacks, unusually high levels of serum uric acid, or tophi or kidney stones. Probenecid helps the kidneys eliminate uric acid. Allopurinol blocks production of uric acid and is most often the agent selected to normalize blood levels.
Drinking alcohol should be reduced or stopped. Diets that restrict foods rich in purines (substances found in meat and certain types of seafood or high fructose beverages) may help in difficult cases.
PMR occurs only in older adults, and rarely in people younger than 50. The average age of onset of symptoms is 70. The typical symptoms of PMR are severe aching and stiffness around the upper arms, neck, lower back and thighs. Symptoms tend to develop quickly, over a period of several days or weeks, and occasionally even overnight.
Aching and stiffness are worse in the morning, and tend to improve gradually as the day goes by, but periods of inactivity, such as a long car ride or sitting too long in one position, will cause stiffness to return. Stiffness may be so severe that there is pain at night, difficulty getting dressed in the morning (for example, putting on a jacket or bending over to pull on socks and shoes), or difficulty getting up from a low chair. Occasionally, aching occurs in distal joints such as those of the hands and wrists.
38. What causes PMR?
The cause of PMR is unknown. The tendency for symptoms to begin abruptly suggests the possibility of an infection but, so far, no specific infection has been found.
39. How is PMR diagnosed?
In PMR, results of blood tests – sedimentation rate, CRP – that detect inflammation are usually abnormally increased. In a small proportion of patients, these tests may be normal or only slightly increased.
40. How is PMR treated?
If PMR is suspected, a trial of low-dose corticosteroids is given. If PMR is present, these medications will control the pain quickly. The response to corticosteroids can be dramatic – sometimes patients are better after only one dose – but improvement can be slower. However, if symptoms have not been completely relieved after 2 to 3 weeks of treatment, the diagnosis of PMR must be called into question.
When symptoms have been controlled, the dose of corticosteroid medication is decreased gradually. The goal is to find the lowest dose that keeps the individual comfortable. Some people can stop corticosteroids within a year, but most will need a small amount of this medication for 2 to 3 years, sometimes longer, to keep aching and stiffness under control.
Psoriatic arthritis is a form of arthritis associated with psoriasis, a chronic disease in which scaly red and white patches develop on the skin. Like rheumatoid arthritis, it results when the body's immune system goes into overdrive and attacks the joints, causing excessive inflammation.
Psoriatic arthritis can affect any joint within the body and cause symptoms that periodically show up, or flare, and then subside.
42. What causes psoriatic arthritis?
The exact cause of psoriatic arthritis is unknown, but researchers suspect that the disorder develops because of a combination of genetic (hereditary) and environmental (external) factors. As many as 40 percent of people with psoriatic arthritis have a family history of psoriasis or arthritis, indicating that they are prone to develop arthritis because of their genetic makeup, especially when their immune system is stimulated by an environmental trigger such as an infection.
43. How is psoriatic arthritis treated?
If the symptoms are constant and significant, psoriatic arthritis is treated with disease modifying anti-rheumatic drugs (DMARD) in a manner similar to rheumatoid arthritis. These include sulfasalazine (Azulfidine), methotrexate, cyclosporine, and anti-TNF agents such as etanercept (Enbrel), infliximab (Remicade), and adalimumab (Humira).
Carpal tunnel syndrome is possibly the most common nerve disorder experienced today. The carpal tunnel is located at the wrist on the palm side of the hand just beneath the skin surface. Eight small wrist bones form three sides of the tunnel, giving rise to the name carpal tunnel. The remaining side of the tunnel is composed of soft tissues, consisting mainly of a ligament called the transverse carpal ligament. This ligament stretches over the top of the tunnel.
The median nerve and nine flexor tendons to the fingers pass through the carpal tunnel. Flexor tendons help flex or bend the fingers. When this median nerve in the wrist is compressed, it slows or blocks nerve impulses from travelling through the nerve. Because the median nerve provides muscle function and feeling in the hand, disabling the nerve results in symptoms ranging from mild occasional numbness to hand weakness, loss of feeling and loss of hand function.
Usually carpal tunnel syndrome affects only one hand, but can affect both at the same time, causing symptoms in all or some of the fingers including thumb, index, middle and adjacent half of the ring finger but rarely the little finger (pinkie). In addition to numbness, those with the syndrome may experience tingling, pins and needle sensation or burning of the hand occasionally extending up to the forearm.
Frequently, symptoms surface in the morning upon awakening, or may cause waking during the night. Symptoms can occur with certain activities such as driving, holding a book or other repetitive activity with the hands, especially those requiring prolonged grasping or flexing (bending) of the wrist. Hand functional activities, such as buttoning, may become difficult, and sufferers may drop things more easily.
Individuals often shake their hands trying to obtain relief and may experience the sensation of swelling when, in fact, no swelling is actually present.
44. What causes carpal tunnel syndrome?
Carpal tunnel syndrome may be found in patients who are pregnant, overweight or have various medical conditions, including thyroid disease, diabetes or arthritis, or injuries such as wrist fractures. Whether repetitive work activities cause carpal tunnel syndrome is still controversial, but it is thought that some repetitive hand activities, especially those involving vibratory motion, can worsen the symptoms. Just as frequently, the syndrome occurs on its own.
45. How is carpal tunnel syndrome diagnosed?
The diagnosis of carpal tunnel syndrome is often made by the physician based on an accurate description of the symptoms. During physical examination, testing may identify weakness of the muscles supplied by the median nerve in the hand including some thumb muscles affected by the syndrome. There may be decreased sensation in the hand to pin prick or light touch. Bending the wrist to 90 degrees for one minute may cause symptoms to appear in the hand (Phalen test) or tapping on the wrist with a reflex hammer may cause an electric shock-like sensation (Tinel Sign). Late in the disease, there may be thinning of the muscles or muscle atrophy at the base of the thumb.
The diagnosis of carpal tunnel syndrome can be confirmed with a nerve conduction velocity study, which is an electrical stimulation test. In recent years, diagnostic ultrasonography and MRI scans have been used to help diagnose CTS and exclude other causes of hand and wrist symptoms.
46. How is carpal tunnel syndrome treated?
Medication such as acetaminophen and nonsteroidal anti-inflammatory drugs can be used for symptom relief. Splinting the wrist, especially at night, helps keep the wrist straight during the night and thus decreases the pressure on the median nerve. These splints, which are available in most drug stores, may relieve symptoms, especially in milder cases.
A cortisone injection into the carpal tunnel area is often helpful in relieving symptoms for weeks to months and can be repeated. If there is an underlying disease, such as hypothyroidism (under active thyroid) or rheumatoid arthritis, causing the carpal tunnel syndrome, then treatment of the specific disease may also relieve symptoms.
When the above measures fail to relieve symptoms, surgical opening of the tunnel to relieve the pressure on the median nerve, known as a carpal tunnel release, is appropriate.
Spinal stenosis is a narrowing of one or more areas of the spine. This narrowing, which occurs most often in lumbar region (lower back) can put pressure on the spinal cord or nerves branching out from the compressed areas.
Typically, a person with spinal stenosis complains about developing tremendous pain in the legs or calves and lower back after walking. Pain comes on more quickly when walking up hills. This is usually very reproducible and immediately relieved by sitting down, or leaning over. When the spine is bent forward, more space is available for the spinal cord, causing a reduction in symptoms.
48. What causes spinal stenosis?
Unless the individual is born with a small spinal canal (congenital stenosis), spinal narrowing most commonly results from progressive degenerative changes. This “acquired spinal stenosis” can occur from the narrowing of the space around the spinal cord due to bony overgrowth from osteoarthritis combined with thickening of one of the ligaments in the back, and a bulge of the intervertebral discs.
Conditions that can cause spinal stenosis include:
- Osteoarthritis and osteophytes (bony spurs) associated with aging
- Inflammatory spondyloarthritis
- Spinal tumors
- Paget's disease of the bone
- Previous surgery
49. How is spinal stenosis diagnosed?
Your doctor will ask about your symptoms and medical history, and perform a physical exam if spinal stenosis is suspected.
Additional tests conducted to confirm and assess the diagnosis may include:
- An X-ray of the spine to check for abnormalities in the bones of the back including osteoarthritis, bone spurs and obvious narrowing of the spinal canal.
- A computed tomography (CT) scan to take images of the bony architecture of the back. This helps to evaluate the spinal canal.
- A magnetic resonance imaging (MRI) scan of the spine to make pictures of soft tissues such as the spinal cord and the spinal nerves inside the back.
- An EMG which may show active and chronic neurological changes.
50. How is spinal stenosis treated?
Although there is no cure for spinal stenosis, various therapies are available, one of the most important being exercise. Keeping the hip and thigh muscles from developing atrophy helps increase stability and the ability to walk.
Medications such as NSAIDs also may be helpful in pain relief. Cortisone injections into the epidural space (the area around the spinal cord) can give tremendous temporary or permanent relief.
For severe cases, surgery may be considered. However, adequate decompression of the neural elements and maintenance of bony stability are necessary for a good surgical outcome for patients with spinal stenosis. Decompression laminectomy, which is the removal of a build-up of bony spurs or increased bone mass in the spinal canal, can free space for the nerves and the spinal cord. Spinal fusion to fuse two vertebrae together to provide stronger support for the spine almost always follows a decompression laminectomy.