The treatment in the case of sudden bleeding is focused on restoration of vital function. Anticonvulsant medications such as phenytoin are often used to control seizure; medications or procedures may be employed to relieve intracranial pressure. Eventually, curative treatment may be required to prevent recurrent hemorrhage. However, any type of intervention may also carry a risk of creating a neurological deficit.

In the U.S., surgical removal of the blood vessels involved (craniotomy) is the preferred curative treatment for most types of AVM. While this surgery results in an immediate, complete removal of the AVM, risks exist depending on the size and the location of the malformation.

Radiation treatment (radiosurgery) has been widely used on smaller AVMs with considerable success. The Gamma Knife, developed by Swedish physician Lars Leksell, is one apparatus used in radiosurgery to precisely apply a controlled radiation dosage to the volume of the brain occupied by the AVM. While this treatment is non-invasive, two to three years may pass before the complete effects are known. Complete occlusion of the AVM may or may not occur, and 8%-10% of patients develop long term neurological symptoms after radiation.

Embolization, that is, occlusion of blood vessels with coils or particles or glue introduced by a radiographically guided catheter, is frequently used as an adjunct to either surgery or radiation treatment. However, embolization alone is rarely successful in completely blocking blood flow through the AVM.

The benefit of invasive treatment for unruptured AVMs has never been proven, as the risk of intervention may be as high as the spontaneous bleeding risk. An international study is currently under way to determine the best therapy for patients with unruptured AVMs (ARUBA—A Randomized Trial of Unruptured Brain AVMs).^[1]

References

[1] Hartmann A, Mast H, Choi JH, Stapf C, Mohr JP (2007). “Treatment of arteriovenous malformations of the brain”. Current neurology and neuroscience reports 7 (1): 28–34. doi:10.1007/s11910-007-0018-2. PMID 17217851.

Who Gets Spinal Stenosis?

This disorder is most common in men and women over 50 years of age. However, it may occur in younger people who are born with a narrowing of the spinal canal or who suffer an injury to the spine.

What Structures of the Spine Are Involved?

The spine is a column of 26 bones that extend in a line from the base of the skull to the pelvis (see fig. 1). Twenty-four of the bones are called vertebrae. The bones of the spine include 7 cervical vertebrae in the neck; 12 thoracic vertebrae at the back wall of the chest; 5 lumbar vertebrae at the inward curve (small) of the lower back; the sacrum, composed of 5 fused vertebrae between the hip bones; and the coccyx, composed of 3 to 5 fused bones at the lower tip of the vertebral column. The vertebrae link to each other and are cushioned by shock-absorbing disks that lie between them.

The vertebral column provides the main support for the upper body, allowing humans to stand upright or bend and twist, and it protects the spinal cord from injury. Following are structures of the spine most involved in spinal stenosis (see figs.1, 2, 3, and 7).

• Intervertebral disks—pads of cartilage filled with a gel-like substance which lie between vertebrae and act as shock absorbers.
• Facet joints—joints located on the back of the main part of the vertebra. They are formed by a portion of one vertebra and the vertebra above it. They connect the vertebrae to each other and permit backward motion.
• Intervertebral foramen (also called neural foramen)—an opening between vertebrae through which nerves leave the spine and extend to other parts of the body.
• Lamina—part of the vertebra at the back portion of the vertebral arch that forms the roof of the canal through which the spinal cord and nerve roots pass.
• Ligaments—elastic bands of tissue that support the spine by preventing the vertebrae from slipping out of line as the spine moves. A large ligament often involved in spinal stenosis is the ligamentum flavum, which runs as a continuous band from lamina to lamina in the spine.
• Pedicles—narrow stem-like structures on the vertebrae that form the walls of the front part of the vertebral arch.
• Spinal cord/nerve roots—a major part of the central nervous system that extends from the base of the brain down to the lower back and that is encased by the vertebral column. It consists of nerve cells and bundles of nerves. The cord connects the brain to all parts of the body via 31 pairs of nerves that branch out from the cord and leave the spine between vertebrae.
• Synovium—a thin membrane that produces fluid to lubricate the facet joints, allowing them to move easily.
• Vertebral arch—a circle of bone around the canal through which the spinal cord passes. It is composed of a floor at the back of the vertebra, walls (the pedicles), and a ceiling where two laminae join.
• Cauda equina—a sack of nerve roots that continues from the lumbar region, where the spinal cord ends, and continues down to provide neurologic function to the lower part of the body. It resembles a “horse’s tail” (cauda equina in Latin).

What Causes Spinal Stenosis?

The normal vertebral canal (see fig. 4) provides adequate room for the spinal cord and cauda equina. Narrowing of the canal, which occurs in spinal stenosis, may be inherited or acquired. Some people inherit a small spinal canal (see fig. 5) or have a curvature of the spine (scoliosis) that produces pressure on nerves and soft tissue and compresses or stretches ligaments. In an inherited condition called achondroplasia, defective bone formation results in abnormally short and thickened pedicles that reduce the diameter (distance across) of the spinal canal.

Acquired conditions that can cause spinal stenosis are explained in more detail in the sections that follow.

Degenerative Conditions

Spinal stenosis most often results from a gradual, degenerative aging process. Either structural changes or inflammation can begin the process. As people age, the ligaments of the spine may thicken and calcify (harden from deposits of calcium salts). Bones and joints may also enlarge: when surfaces of the bone begin to project out from the body, these projections are called osteophytes (bone spurs).

When the health of one part of the spine fails, it usually places increased stress on other parts of the spine. For example, a herniated (bulging) disk may place pressure on the spinal cord or nerve root (see fig. 6). When a segment of the spine becomes too mobile, the capsules (enclosing membranes) of the facet joints thicken in an effort to stabilize the segment, and bone spurs may occur. This decreases the space (neural foramen) available for nerve roots leaving the spinal cord.

[Fig 6]

Spondylolisthesis, a condition in which one vertebra slips forward on another, may result from a degenerative condition or an accident, or, very rarely, may be acquired at birth. Poor alignment of the spinal column when a vertebra slips forward onto the one below it can place pressure on the spinal cord or nerve roots at that place.

Aging with secondary changes is the most common cause of spinal stenosis. Two forms of arthritis that may affect the spine are osteoarthritis and rheumatoid arthritis.¹

Osteoarthritis—Osteoarthritis is the most common form of arthritis and is more likely to occur in middle-aged and older people. It is a chronic, degenerative process that may involve multiple joints of the body. It wears away the surface cartilage layer of joints, and is often accompanied by overgrowth of bone, formation of bone spurs, and impaired function. If the degenerative process of osteoarthritis affects the facet joint(s) and the disk, the condition is sometimes referred to as spondylosis. This condition may be accompanied by disk degeneration, and an enlargement or overgrowth of bone that narrows the central and nerve root canals.

Rheumatoid Arthritis—Rheumatoid arthritis usually affects people at an earlier age than osteoarthritis does and is associated with inflammation and enlargement of the soft tissues (the synovium) of the joints. Although not a common cause of spinal stenosis, damage to ligaments, bones, and joints that begins as synovitis (inflammation of the synovial membrane which lines the inside of the joint) has a severe and disrupting effect on joint function. The portions of the vertebral column with the greatest mobility (for example, the neck area) are often the ones most affected in people with rheumatoid arthritis.

Other Acquired Conditions

The following conditions that are not related to degenerative disease are causes of acquired spinal stenosis:

• Tumors of the spine are abnormal growths of soft tissue that may affect the spinal canal directly by inflammation or by growth of tissue into the canal. Tissue growth may lead to bone resorption (bone loss due to overactivity of certain bone cells) or displacement of bone.
• Trauma (accidents) may either dislocate the spine and the spinal canal or cause burst fractures that produce fragments of bone that penetrate the canal.
• Paget’s disease of bone is a chronic (long-term) disorder that typically results in enlarged and abnormal bones. Excessive bone breakdown and formation cause thick and fragile bone. As a result, bone pain, arthritis, noticeable bone structure changes, and fractures can occur. The disease can affect any bone of the body, but is often found in the spine. The blood supply that feeds healthy nerve tissue may be diverted to the area of involved bone. Also, structural problems of the involved vertebrae can cause narrowing of the spinal canal, producing a variety of neurological symptoms. Other developmental conditions may also result in spinal stenosis.
• Fluorosis is an excessive level of fluoride in the body. It may result from chronic inhalation of industrial dusts or gases contaminated with fluorides, prolonged ingestion of water containing large amounts of fluorides, or accidental ingestion of fluoride-containing insecticides. The condition may lead to calcified spinal ligaments or softened bones and to degenerative conditions like spinal stenosis.
• Ossification of the posterior longitudinal ligament occurs when calcium deposits form on the ligament that runs up and down behind the spine and inside the spinal canal (see fig. 7). These deposits turn the fibrous tissue of the ligament into bone. (Ossification means “forming bone.”) These deposits may press on the nerves in the spinal canal.

What Are the Symptoms of Spinal Stenosis?

The space within the spinal canal may narrow without producing any symptoms. However, if narrowing places pressure on the spinal cord, cauda equina, or nerve roots, there may be a slow onset and progression of symptoms. The neck or back may or may not hurt. More often, people experience numbness, weakness, cramping, or general pain in the arms or legs. If the narrowed space within the spine is pushing on a nerve root, people may feel pain radiating down the leg (sciatica). Sitting or flexing the lower back should relieve symptoms. (The flexed position “opens up” the spinal column, enlarging the spaces between vertebrae at the back of the spine.) Flexing exercises are often advised, along with stretching and strengthening exercises.

People with more severe stenosis may have problems with bowel and bladder function and foot disorders. For example, cauda equina syndrome is a severe, and very rare, form of spinal stenosis. It occurs because of compression of the cauda equina, and symptoms may include loss of control of the bowel, bladder, or sexual function and/or pain, weakness, or loss of feeling in one or both legs. Cauda equina syndrome is a serious condition requiring urgent medical attention.

How Is Spinal Stenosis Diagnosed?

The doctor may use a variety of approaches to diagnose spinal stenosis and rule out other conditions.

• Medical history—the patient tells the doctor details about symptoms and about any injury, condition, or general health problem that might be causing the symptoms.
• Physical examination—the doctor (1) examines the patient to determine the extent of limitation of movement, (2) checks for pain or symptoms when the patient hyperextends the spine (bends backwards), and (3) checks for normal neurologic function (for instance, sensation, muscle strength, and reflexes) in the arms and legs.
• X ray—an x-ray beam is passed through the back to produce a two-dimensional picture. An x ray may be done before other tests to look for signs of an injury, tumor, or inherited problem. This test can show the structure of the vertebrae and the outlines of joints, and can detect calcification.
• MRI (magnetic resonance imaging)—energy from a powerful magnet (rather than x rays) produces signals that are detected by a scanner and analyzed by computer. This produces a series of cross-sectional images (“slices”) and/or a three-dimensional view of parts of the back. An MRI is particularly sensitive for detecting damage or disease of soft tissues, such as the disks between vertebrae or ligaments. It shows the spinal cord, nerve roots, and surrounding spaces, as well as enlargement, degeneration, or tumors.
• Computerized axial tomography (CAT)—x rays are passed through the back at different angles, detected by a scanner, and analyzed by a computer. This produces a series of cross-sectional images and/or three-dimensional views of the parts of the back. The scan shows the shape and size of the spinal canal, its contents, and structures surrounding it.
• Myelogram—a liquid dye that x rays cannot penetrate is injected into the spinal column. The dye circulates around the spinal cord and spinal nerves, which appear as white objects against bone on an x-ray film. A myelogram can show pressure on the spinal cord or nerves from herniated disks, bone spurs, or tumors.
• Bone scan—an injected radioactive material attaches itself to bone, especially in areas where bone is actively breaking down or being formed. The test can detect fractures, tumors, infections, and arthritis, but may not tell one disorder from another. Therefore, a bone scan is usually performed along with other tests.

Who Treats Spinal Stenosis?

Nonsurgical treatment of spinal stenosis may be provided by internists or general practitioners. The disorder is also treated by specialists such as rheumatologists, who treat arthritis and related disorders; and neurologists, who treat nerve diseases. Orthopaedic surgeons and neurosurgeons also provide nonsurgical treatment and perform spinal surgery if it is required. Allied health professionals such as physical therapists may also help treat patients.

What Are Some Nonsurgical Treatments for Spinal Stenosis?

In the absence of severe or progressive nerve involvement, a doctor may prescribe one or more of the following conservative treatments:

• Nonsteroidal anti-inflammatory drugs, such as aspirin, naproxen (Naprosyn)², ibuprofen (Motrin, Nuprin, Advil), or indomethacin (Indocin), to reduce inflammation and relieve pain.
• Analgesics, such as acetaminophen (Tylenol), to relieve pain.
• Corticosteroid injections into the outermost of the membranes covering the spinal cord and nerve roots to reduce inflammation and treat acute pain that radiates to the hips or down a leg.
• Anesthetic injections, known as nerve blocks, near the affected nerve to temporarily relieve pain.
• Restricted activity (varies depending on extent of nerve involvement).
• Prescribed exercises and/or physical therapy to maintain motion of the spine, strengthen abdominal and back muscles, and build endurance, all of which help stabilize the spine. Some patients may be encouraged to try slowly progressive aerobic activity such as swimming or using exercise bicycles.
• A lumbar brace or corset to provide some support and help the patient regain mobility. This approach is sometimes used for patients with weak abdominal muscles or older patients with degeneration at several levels of the spine.

² Brand names included in this fact sheet are provided as examples only. Their inclusion does not mean that these products are endorsed by the National Institutes of Health or another government agency. Also, if a particular brand name is not mentioned, this does not imply that the product is unsatisfactory.

What Are Some Alternative Therapies for Spinal Stenosis?

Alternative (or complementary) therapies are diverse medical and health care systems, practices, and products that are not presently considered to be part of conventional medicine. Some examples of these therapies used to treat spinal stenosis follow:

• Chiropractic treatment—This treatment is based on the philosophy that restricted movement in the spine reduces proper function and may cause pain. Chiropractors may manipulate (adjust) the spine to restore normal spinal movement. They may also employ traction, a pulling force, to help increase space between the vertebrae and reduce pressure on affected nerves. Some people report that they benefit from chiropractic care. Research thus far has shown that chiropractic treatment is about as effective as conventional, nonoperative treatments for acute back pain.
• Acupuncture—This treatment involves stimulating certain places on the skin by a variety of techniques, in most cases by manipulating thin, solid, metallic needles that penetrate the skin. Research has shown that low back pain is one area in which acupuncture has benefited some people.

More research is needed before the effectiveness of these or other possible alternative therapies can be definitively stated. Health care providers may suggest these therapies in addition to more conventional treatments.

When Should Surgery Be Considered and What Is Involved?

In many cases, the conditions causing spinal stenosis cannot be permanently altered by nonsurgical treatment, even though these measures may relieve pain for a period of time. To determine how much nonsurgical treatment will help, a doctor may recommend such treatment first. However, surgery might be considered immediately if a patient has numbness or weakness that interferes with walking, impaired bowel or bladder function, or other neurological involvement. The effectiveness of nonsurgical treatments, the extent of the patient’s pain, and the patient’s preferences may all factor into whether or not to have surgery.

The purpose of surgery is to relieve pressure on the spinal cord or nerves and restore and maintain alignment and strength of the spine. This can be done by removing, trimming, or adjusting diseased parts that are causing the pressure or loss of alignment. The most common surgery is called decompressive laminectomy: removal of the lamina (roof) of one or more vertebrae to create more space for the nerves. A surgeon may perform a laminectomy with or without fusing vertebrae or removing part of a disk. Various devices may be used to enhance fusion and strengthen unstable segments of the spine following decompression surgery.

Patients with spinal stenosis caused by spinal trauma or achondroplasia may need surgery at a young age. When surgery is required in patients with achondroplasia, laminectomy (removal of the roof) without fusion is usually sufficient.

What Are the Major Risks of Surgery?

All surgery, particularly that involving general anesthesia and older patients, carries risks. The most common complications of surgery for spinal stenosis are a tear in the membrane covering the spinal cord at the site of the operation, infection, or a blood clot that forms in the veins. These conditions can be treated but may prolong recovery. The presence of other diseases and the physical condition of the patient are also significant factors to consider when making decisions about surgery.

What Are the Long-Term Outcomes of Surgical Treatment for Spinal Stenosis?

Removal of the obstruction that has caused the symptoms usually gives patients some relief; most patients have less leg pain and are able to walk better following surgery. However, if nerves were badly damaged before surgery, there may be some remaining pain or numbness or no improvement. Also, the degenerative process will likely continue, and pain or limitation of activity may reappear after surgery. NIAMS-supported researchers have published results from the Spine Patient Outcomes Research Trial (SPORT), the largest trial to date comparing surgical and non-surgical interventions for the treatment of low back and associated leg pain caused by spinal stenosis. The study found that for patients with spinal stenosis, surgical treatment was more effective than non-surgical treatment in relieving symptoms and improving function. However, the functional status of patients who received non-surgical therapies also improved somewhat during the study.

What Research on Spinal Stenosis Is Being Supported by the NIAMS?

The National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), a part of the Department of Health and Human Services’ National Institutes of Health, is supporting several research projects on spinal stenosis. For example, in a 5-year clinical trial involving 11 sites throughout the country, researchers are attempting to determine whether surgical or nonsurgical treatment is more effective at treating spinal stenosis and other back problems. Another project will try to find out if specific MRI findings will help physicians determine if they can identify groups who will fare better with surgical or nonsurgical treatments. For example, follow up of patients in SPORT will provide important insights into the long-term outcomes and cost-effectiveness of treatment options for spinal stenosis.

Source: National Institutes of Health, NIAMS

http://www.niams.nih.gov/Health_Info/Spinal_Stenosis/default.asp

Tears are almost always posterior-ipsilateral in nature owing to the presence of the posterior longitudinal ligament in the spinal canal. This tear in the disc ring may result in the release of inflammatory chemical mediators which may directly cause severe pain, even in the absence of nerve root compression (see “chemical radiculitis” below). This is the rationale for the use of anti-inflammatory treatments for pain associated with disc herniation, protrusion, bulge, or disc tear.

It is normally a further development of a previously existing disc protrusion, a condition in which the outermost layers of the annulus fibrosus are still intact, but can bulge when the disc is under pressure.

Terminology

Normal situation and spinal disc herniation in cervical vertebrae. (Wikimedia)

Some of the terms commonly used to describe the condition include herniated disc, prolapsed disc, ruptured disc and the misleading expression “slipped disc”. Other terms that are closely related include disc protrusion, bulging disc, pinched nerve, sciatica, disc disease, disc degeneration, degenerative disc disease, and black disc.

The popular term “slipped disc” is misleading, as an intervertebral disc, being tightly sandwiched between two vertebrae to which the disc is attached, cannot actually “slip”, “slide”, or even get “out of place”.

The disc is actually grown together with the adjacent vertebrae and can be squeezed, stretched and twisted, all in small degrees. It can also be torn, ripped, herniated, and degenerated, but it cannot “slip”.^[1] “The term ‘slipped disc’ may be harmful as it leads to a false idea of what is happening and therefore of the likely outcome.”^[2][3] However, one vertebral body can slip relative to an adjacent vertebral body. This is called spondylolisthesis and can damage the disc between the two vertebrae.

The spelling “disc” is based on the Latin root discus. Most English language publications use the spelling “disc” more often than “disk”. Nomina Anatomica designates the structures as “disci intervertebrales” [plural form] and Terminologia Anatomica as “discus intervertebralis/intervertebral disc”, [singular form].^[4]

Regional distribution

Frequency

Stages of spinal disc herniation. (Wikimedia)

Disc herniation can occur in any disc in the spine, but the two most common forms are lumbar disc herniation and cervical disc herniation. The former is the most common, causing lower back pain (lumbago) and often leg pain as well, in which case it is commonly referred to as sciatica.

Lumbar disc herniation occurs 15 times more often than cervical (neck) disc herniation, and it is one of the most common causes of lower back pain. The cervical discs are affected 8% of the time and the upper-to-mid-back (thoracic) discs only 1 – 2% of the time.^[5]

The following locations have no discs and are therefore exempt from the risk of disc herniation: the upper two cervical intervertebral spaces, the sacrum, and the coccyx.

Most disc herniations occur when a person is in their thirties or forties when the nucleus pulposus is still a gelatin-like substance. With age the nucleus pulposus changes (“dries out”) and the risk of herniation is greatly reduced. After age 50 or 60, osteoarthritic degeneration (spondylosis) or spinal stenosis are more likely causes of low back pain or leg pain.

Cervical disc herniation

Cervical disc herniations occur in the neck, most often between the fith & sixth (C5/6) and the sixth and seventh (C6/7) cervical vertebral bodies. Symptoms can affect the back of the skull, the neck, shoulder girdle, scapula,^[6] shoulder, arm, and hand. The nerves of the cervical plexus and brachial plexus can be affected.^[7]

Thoracic disc herniation

Thoracic discs are very stable and herniations in this region are quite rare. Herniation of the uppermost thoracic discs can mimic cervical disc herniations, while herniation of the other discs can mimic lumbar herniations.^[8]

Lumbar disc herniation

Lumbar disc herniations occur in the lower back, most often between the fourth and fifth lumbar vertebral bodies or between the fifth and the sacrum. Symptoms can affect the lower back, buttocks, thigh, and may radiate into the foot and/or toe. The sciatic nerve is the most commonly affected nerve, causing symptoms of sciatica. The femoral nerve can also be affected^[9] and cause the patient to experience a numb, tingling feeling throughout one or both legs and even feet or even a burning feeling in the hips and legs.

Causes

Narrowed space between L5 and S1 vertebrae, indicating probable prolapsed intervertebral disc - a classic picture. (Wikimedia)

Disc herniations can occur from general wear and tear, such as jobs that require constant sitting, but especially jobs that require lifting. Traumatic (quick) injury to lumbar discs commonly occurs from lifting while bent at the waist, rather than lifting while using the legs with a straightened back. Minor back pain and chronic back tiredness is an indicator of general wear and tear that makes one susceptible to herniation on the occurrence of a traumatic event from bending to pick up a pencil or a traumatic injury from a fall. When the spine is straight, such as standing or lying down, internal pressure is equalized on all parts of the discs. While sitting or bending to lift, internal pressure on a disc can move from 17 psi (lying down) to over 300 psi (lifting with a rounded back).

Herniation of the contents of the disc into the spinal canal often occurs when the front side (stomach side) of the disc is compressed while sitting or bending forward, and the contents (nucleus pulposus) get pressed against the tightly stretched and thinned membrane (annulus fibrosis) on the rear (back side) of the disc. The combination of membrane thinning from stretching and increased internal pressure (200 to 300 psi) results in the rupture of the confining membrane. The jelly-like contents of the disc then move into the spinal canal, pressing against the spinal nerves, thus producing intense and usually disabling pain and other symptoms.

There is also a strong genetic component. Mutation in genes coding for proteins involved in the regulation of the extracellular matrix, such as MMP2 and THBS2, has been demonstrated to contribute to lumbar disc herniation.^[10]

Symptoms

Symptoms of a herniated disc can vary depending on the location of the herniation and the types of soft tissue that become involved. They can range from little or no pain if the disc is the only tissue injured, to severe and unrelenting neck or low back pain that will radiate into the regions served by affected nerve roots that are irritated or impinged by the herniated material. Often, herniated discs are not diagnosed immediately, as the patients come with undefined pains in the thighs, knees or feet. Other symptoms may include sensory changes such as numbness, tingling, muscular weakness, paralysis, paresthesia, and affection of reflexes. If the herniated disc is in the lumbar region the patient may also experience sciatica due to irritation of one of the nerve roots of the sciatic nerve. Unlike a pulsating pain or pain that comes and goes, which can be caused by muscle spasm, pain from a herniated disc is usually continuous or at least is continuous in a specific position of the body.

It is possible to have a herniated disc without any pain or noticeable symptoms, depending on its location. If the extruded nucleus pulposus material doesn’t press on soft tissues or nerves, it may not cause any symptoms. A small-sample study examining the cervical spine in symptom-free volunteers has found focal disc protrusions in 50% of participants, which shows that a considerable part of the population can have focal herniated discs in their cervical region that do not cause noticeable symptoms.^[11][12]

Typically, symptoms are experienced only on one side of the body. If the prolapse is very large and presses on the spinal cord or the cauda equina in the lumbar region, affection of both sides of the body may occur, often with serious consequences.

There is now recognition of the importance of “chemical radiculitis” in the generation of back pain.^[13] A primary focus of surgery is to remove “pressure” or reduce mechanical compression on a neural element: either the spinal cord, or a nerve root. But it is increasingly recognized that back pain, rather than being solely due to compression, may also be due to chemical inflammation.^{[13][14][15][16]} There is evidence that points to a specific inflammatory mediator of this pain.^[17][18] This inflammatory molecule, called tumor necrosis factor-alpha (TNF), is released not only by the herniated disc, but also in cases of disc tear (annular tear), by facet joints, and in spinal stenosis.^{[13][19][20][21]} In addition to causing pain and inflammation, TNF may also contribute to disc degeneration.^[22]

Diagnosis

Diagnosis is made by a practitioner based on the history, symptoms, and physical examination. At some point in the evaluation, tests may be performed to confirm or rule out other causes of symptoms such as spondylolisthesis, degeneration, tumors, metastases and space-occupying lesions as well as evaluate the efficacy of potential treatment options.

Physical examination

Straight leg raise

The Straight leg raise may be positive; this finding has low specificity, however it has high sensitivity. Thus the finding of a negative SLR sign is an important in helping to “rule out” the possibility of a lower lumbar disc herniation. A variation is to lift the leg while the patient is sitting.^[23] However, this reduces the sensitivity of the test.^[24]

Imaging

• X-ray: Although traditional plain X-rays are limited in their ability to image soft tissues such as discs, muscles, and nerves, they are still used to confirm or exclude other possibilities such as tumors, infections, fractures, etc.. In spite of these limitations, X-ray can still play a relatively inexpensive role in confirming the suspicion of the presence of a herniated disc. If a suspicion is thus strengthened, other methods may be used to provide final confirmation.
• Computed tomography scan (CT or CAT scan): A diagnostic image created after a computer reads x-rays. It can show the shape and size of the spinal canal, its contents, and the structures around it, including soft tissues.
  1. Patient education on proper body mechanics^[31]
  2. Physical therapy, which may include ultrasound, massage, conditioning, and exercise programs^[31]
  3. Massage therapy^[31]
  4. Non-steroidal anti-inflammatory drugs (NSAIDs)^[31]
  5. Oral steroids (e.g. prednisone or methylprednisolone)^[31]
  6. Epidural (cortisone) injection^[31]
  7. Intravenous sedation, analgesia-assisted traction therapy (IVSAAT)
  8. Weight control^[31]
  9. Lumbosacral back support^[31]
  1. Spinal manipulation: A 2006 review of published research stated: “Contradictions in the literature exist in terms of the use of spinal manipulation in the management of disc herniation, with some authors advocating its usefulness, and others suggesting it is contraindicated.”^[32] According to the WHO, in their guidelines on chiropractic practice, when there is a “frank disc herniation with accompanying signs of progressive neurological deficit”, it is absolutely contraindicated.^[33]
  1. Non-surgical spinal decompression: A 2007 review of published research on this treatment method found shortcomings in most published studies and concluded that there was only “very limited evidence in the scientific literature to support the effectiveness of non-surgical spinal decompression therapy.”^[34] It’s use and marketing have been very controversial.^[35]
  1. ^ Slipped discs: “they do not actually ‘slip’…”
  2. ^ Prolapsed disc
  3. ^ Ehealthmd.com FAQ: “…the entire disc does not ‘slip’ out of place.”
  4. ^ Terminology
  5. ^ MedlinePlus Encyclopedia Herniated nucleus pulposus Frequency
  6. ^ “Neck and Shoulder Blade Pain”. http://www.treatment-for.com/shoulder-blade-pain-treatment.htm.
  7. ^ Cervical herniation at eMedicine
  8. ^ Thoracic herniation at eMedicine
  9. ^ Lumbar herniation at eMedicine
  10. ^ Yuichiro Hirose et al. (May 2008). “A Functional Polymorphism in THBS2 that Affects Alternative Splicing and MMP Binding Is Associated with Lumbar-Disc Herniation”. American Journal of Human Genetics 82 (5): 1122–1129. doi:10.1016/j.ajhg.2008.03.013. PMID 18455130. PMC 2427305. http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B8JDD-4SDFHH8-1-B&_cdi=43612&_user=10&_coverDate=05%2F09%2F2008&_sk=%23TOC%2343612%232008%23999179994%23688977%23FLA%23display%23Volume_82,_Issue_5,_Pages_1023-1226_(9_May_2008)%23tagged%23Volume%23first%3D82%23Issue%23first%3D5%23date%23(9_May_2008)%23&view=c&_gw=y&wchp=dGLzVtb-zSkzV&_valck=1&md5=368f7507ed0a5e28a15ca8290a854b0c&ie=/sdarticle.pdf.
  11. ^ Robert E Windsor (2006). “Frequency of asymptomatic cervical disc protrusions”. Cervical Disc Injuries.. eMedicine. http://www.emedicine.com/sports/byname/Cervical-Disc-Injuries.htm. Retrieved 2008-02-27.
  12. ^ Ernst CW, Stadnik TW, Peeters E, Breucq C, Osteaux MJ (Sep 2005). “Prevalence of annular tears and disc herniations on MR images of the cervical spine in symptom free volunteers”. Eur J Radiol 55 (3): 409–14. doi:10.1016/j.ejrad.2004.11.003. PMID 16129249.
  13. ^ ^{a b c} Peng B, Wu W, Li Z, Guo J, Wang X (Jan 2007). “Chemical radiculitis”. Pain 127 (1-2): 11–6. doi:10.1016/j.pain.2006.06.034. PMID 16963186.
  14. ^ Marshall LL, Trethewie ER (Aug 1973). “Chemical irritation of nerve-root in disc prolapse”. Lancet 2 (7824): 320. doi:10.1016/S0140-6736(73)90818-0. PMID 4124797.
  15. ^ McCarron RF, Wimpee MW, Hudkins PG, Laros GS (Oct 1987). “The inflammatory effect of nucleus pulposus. A possible element in the pathogenesis of low-back pain”. Spine 12 (8): 760–4. doi:10.1097/00007632-198710000-00009. PMID 2961088.
  16. ^ Takahashi H, Suguro T, Okazima Y, Motegi M, Okada Y, Kakiuchi T (Jan 1996). “Inflammatory cytokines in the herniated disc of the lumbar spine”. Spine 21 (2): 218–24. doi:10.1097/00007632-199601150-00011. PMID 8720407. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=21&issue=2&spage=218.
  17. ^ Igarashi T, Kikuchi S, Shubayev V, Myers RR (Dec 2000). “2000 Volvo Award winner in basic science studies: Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology. Molecular, histologic, and behavioral comparisons in rats”. Spine 25 (23): 2975–80. doi:10.1097/00007632-200012010-00003. PMID 11145807. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=25&issue=23&spage=2975.
  18. ^ Sommer C, Schäfers M (2004). “Mechanisms of neuropathic pain: the role of cytokines”. Drug Discovery Today: Disease Mechanisms 1 (4): 441–8. doi:10.1016/j.ddmec.2004.11.018.
  19. ^ Igarashi A, Kikuchi S, Konno S, Olmarker K (Oct 2004). “Inflammatory cytokines released from the facet joint tissue in degenerative lumbar spinal disorders”. Spine 29 (19): 2091–5. doi:10.1097/01.brs.0000141265.55411.30. PMID 15454697. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=29&issue=19&spage=2091.
  20. ^ Sakuma Y, Ohtori S, Miyagi M, et al. (Aug 2007). “Up-regulation of p55 TNF alpha-receptor in dorsal root ganglia neurons following lumbar facet joint injury in rats”. Eur Spine J 16 (8): 1273–8. doi:10.1007/s00586-007-0365-3. PMID 17468886.
  21. ^ Sekiguchi M, Kikuchi S, Myers RR (May 2004). “Experimental spinal stenosis: relationship between degree of cauda equina compression, neuropathology, and pain”. Spine 29 (10): 1105–11. doi:10.1097/00007632-200405150-00011. PMID 15131438. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=29&issue=10&spage=1105.
  22. ^ Séguin CA, Pilliar RM, Roughley PJ, Kandel RA (Sep 2005). “Tumor necrosis factor-alpha modulates matrix production and catabolism in nucleus pulposus tissue”. Spine 30 (17): 1940–8. doi:10.1097/01.brs.0000176188.40263.f9. PMID 16135983. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=30&issue=17&spage=1940.
  23. ^ Waddell G, McCulloch JA, Kummel E, Venner RM (1980). “Nonorganic physical signs in low-back pain”. Spine 5 (2): 117–25. doi:10.1097/00007632-198003000-00005. PMID 6446157.
  24. ^ Rabin A, Gerszten PC, Karausky P, Bunker CH, Potter DM, Welch WC (2007). “The sensitivity of the seated straight-leg raise test compared with the supine straight-leg raise test in patients presenting with magnetic resonance imaging evidence of lumbar nerve root compression”. Archives of physical medicine and rehabilitation 88 (7): 840–3. doi:10.1016/j.apmr.2007.04.016. PMID 17601462.
  25. ^ Vroomen PC, de Krom MC, Knottnerus JA (Feb 2002). “Predicting the outcome of sciatica at short-term follow-up”. Br J Gen Pract 52 (475): 119–23. PMID 11887877. PMC 1314232. http://openurl.ingenta.com/content/nlm?genre=article&issn=0960-1643&volume=52&issue=475&spage=119&aulast=Vroomen.
  26. ^ ^{a b} Carragee EJ (May 2005). “Clinical practice. Persistent low back pain”. N Engl J Med. 352 (18): 1891–8. doi:10.1056/NEJMcp042054. PMID 15872204.
  27. ^ Fredman B, Nun MB, Zohar E, et al. (Feb 1999). “Epidural steroids for treating “failed back surgery syndrome”: is fluoroscopy really necessary?”. Anesth Analg. 88 (2): 367–72. doi:10.1097/00000539-199902000-00027. PMID 9972758. http://www.anesthesia-analgesia.org/cgi/pmidlookup?view=long&pmid=9972758.
  28. ^ Landau WM, Nelson DA, Armon C, Argoff CE, Samuels J, Backonja MM (Aug 2007). “Assessment: use of epidural steroid injections to treat radicular lumbosacral pain: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology”. Neurology 69 (6): 614; author reply 614–5. doi:10.1212/01.wnl.0000278878.51713.c8. PMID 17679685.
  29. ^ Abbasi A, Malhotra G, Malanga G, Elovic EP, Kahn S (Sep 2007). “Complications of interlaminar cervical epidural steroid injections: a review of the literature”. Spine 32 (19): 2144–51. doi:10.1097/BRS.0b013e318145a360. PMID 17762818.
  30. ^ ^{a b c} Tobinick EL, Britschgi-Davoodifar S (Mar 2003). “Perispinal TNF-alpha inhibition for discogenic pain”. Swiss Med Wkly 133 (11-12): 170–7. doi:2003/11/smw-10163 (inactive 2008-11-18). PMID 12715286.
  31. ^ ^{a b c d e f g h} “Rush University Medical Center”. http://www.rush.edu/rumc/page-1160429743543.html. Retrieved 2009-04-22.
  32. ^ Snelling, Spinal manipulation in patients with disc herniation: A critical review of risk and benefit, International Journal of Osteopathic Medicine, Volume 9, Issue 3, Pages 77-84.
  33. ^ {http://www.who.int/medicines/areas/traditional/Chiro-Guidelines.pdf WHO guidelines on basic training and safety in chiropractic. “2.1 Absolute contraindications to spinal manipulative therapy”, p. 21]. WHO
  34. ^ Dwain M Daniel, Non-surgical spinal decompression therapy: does the scientific literature support efficacy claims made in the advertising media?, Chiropractic and Osteopathy, 2007, 15:7
  35. ^ Be Wary of Spinal Decompression Therapy with VAX-D or Similar Devices, Stephen Barrett
  36. ^ Stern, Scott D.; Adam S. Cifu, Diane Altkorn (2006). “Back Pain”. in Janet Foltin, Harriet Lebowitz, Karen Davis. Symptom to Diagnosis: An Evidence-Based Guide. New York: Lange Medical Books/McGraw-Hill. pp. 67–81. ISBN 0071463895.
  37. ^ Weinstein JN, Tosteson TD, Lurie JD, et al. (2006). “Surgical vs nonoperative treatment for lumbar disk herniation: the Spine Patient Outcomes Research Trial (SPORT): a randomized trial”. JAMA 296 (20): 2441–50. doi:10.1001/jama.296.20.2441. PMID 17119140.
  38. ^ Weinstein JN, Lurie JD, Tosteson TD, et al. (2006). “Surgical vs nonoperative treatment for lumbar disk herniation: the Spine Patient Outcomes Research Trial (SPORT) observational cohort”. JAMA 296 (20): 2451–9. doi:10.1001/jama.296.20.2451. PMID 17119141.
  39. ^ Peul WC, van Houwelingen HC, van den Hout WB, et al. (2007). “Surgery versus prolonged conservative treatment for sciatica”. N Engl J Med. 356 (22): 2245–56. doi:10.1056/NEJMoa064039. PMID 17538084. http://content.nejm.org/cgi/content/short/356/22/2245.
  40. ^ Minimally invasive procedures to treat herniated disk
  41. ^ Li J, Yan DL, Zhang ZH (2008). “Percutaneous cervical nucleoplasty in the treatment of cervical disc herniation.”. Eur Spine J. 17 (12): 1664–96. doi:10.1007/s00586-008-0786-7. PMID 18830638.
  42. ^ Sommer C, Schäfers M, Marziniak M, Toyka KV (Jun 2001). “Etanercept reduces hyperalgesia in experimental painful neuropathy”. J Peripher Nerv Syst. 6 (2): 67–72. doi:10.1046/j.1529-8027.2001.01010.x. PMID 11446385. http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=1085-9489&date=2001&volume=6&issue=2&spage=67.
  43. ^ Olmarker K, Rydevik B (Apr 2001). “Selective inhibition of tumor necrosis factor-alpha prevents nucleus pulposus-induced thrombus formation, intraneural edema, and reduction of nerve conduction velocity: possible implications for future pharmacologic treatment strategies of sciatica”. Spine 26 (8): 863–9. doi:10.1097/00007632-200104150-00007. PMID 11317106. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=26&issue=8&spage=863.
  44. ^ Murata Y, Onda A, Rydevik B, Takahashi K, Olmarker K (Nov 2004). “Selective inhibition of tumor necrosis factor-alpha prevents nucleus pulposus-induced histologic changes in the dorsal root ganglion”. Spine 29 (22): 2477–84. doi:10.1097/01.brs.0000144406.17512.ea. PMID 15543058. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=29&issue=22&spage=2477.
  45. ^ US patent 6537549 and others
  46. ^ Tobinick E, Davoodifar S (Jul 2004). “Efficacy of etanercept delivered by perispinal administration for chronic back and/or neck disc-related pain: a study of clinical observations in 143 patients”. Curr Med Res Opin 20 (7): 1075–85. doi:10.1185/030079903125004286. PMID 15265252.
  47. ^ Myers RR, Campana WM, Shubayev VI (Jan 2006). “The role of neuroinflammation in neuropathic pain: mechanisms and therapeutic targets”. Drug Discov Today 11 (1-2): 8–20. doi:10.1016/S1359-6446(05)03637-8. PMID 16478686.
  48. ^ Üçeyler N, Sommer C (2007). “Cytokine-induced Pain: Basic Science and Clinical Implications”. Reviews in Analgesia 9 (2): 87–103. doi:10.3727/000000007783992807. http://www.ingentaconnect.com/content/cog/ria/2007/00000009/00000002/art00003.
  49. ^ Leung VY, Chan D, Cheung KM (Aug 2006). “Regeneration of intervertebral disc by mesenchymal stem cells: potentials, limitations, and future direction”. Eur Spine J 15 Suppl 3: S406–13. doi:10.1007/s00586-006-0183-z. PMID 16845553.
  • Magnetic resonance imaging (MRI): A diagnostic test that produces three-dimensional images of body structures using powerful magnets and computer technology. It can show the spinal cord, nerve roots, and surrounding areas, as well as enlargement, degeneration, and tumors. It shows soft tissues even better than CAT scans.
  • Myelogram: An x-ray of the spinal canal following injection of a contrast material into the surrounding cerebrospinal fluid spaces. By revealing displacement of the contrast material, it can show the presence of structures that can cause pressure on the spinal cord or nerves, such as herniated discs, tumors, or bone spurs. Because it involves the injection of foreign substances, MRI scans are now preferred in most patients. Myelograms still provide excellent outlines of space-occupying lesions, especially when combined with CT scanning (CT myelography).
  • Electromyogram and Nerve conduction studies (EMG/NCS): These tests measure the electrical impulse along nerve roots, peripheral nerves, and muscle tissue. This will indicate whether there is ongoing nerve damage, if the nerves are in a state of healing from a past injury, or whether there is another site of nerve compression.
  • The Spine Patient Outcomes Research Trial (SPORT)
    • Patients studied. “intervertebral disk herniation and persistent symptoms despite some nonoperative treatment for at least 6 weeks…radicular pain (below the knee for lower lumbar herniations, into the anterior thigh for upper lumbar herniations) and evidence of nerve-root irritation with a positive nerve-root tension sign (straight leg raise–positive between 30° and 70° or positive femoral tension sign) or a corresponding neurologic deficit (asymmetrical depressed reflex, decreased sensation in a dermatomal distribution, or weakness in a myotomal distribution)
    • Conclusions. “Patients in both the surgery and the nonoperative treatment groups improved substantially over a 2-year period. Because of the large numbers of patients who crossed over in both directions, conclusions about the superiority or equivalence of the treatments are not warranted based on the intent-to-treat analysis”^[37][38]
  • The Hague Spine Intervention Prognostic Study Group^[39]
    • Patients studied. “had a radiologically confirmed disk herniation…incapacitating lumbosacral radicular syndrome that had lasted for 6 to 12 weeks…Patients presenting with cauda equina syndrome, muscle paralysis, or insufficient strength to move against gravity were excluded.”
    • Conclusions. “The 1-year outcomes were similar for patients assigned to early surgery and those assigned to conservative treatment with eventual surgery if needed, but the rates of pain relief and of perceived recovery were faster for those assigned to early surgery. “
  • Chemonucleolysis – dissolves the protruding disc ^[40]
  • IDET (a minimally invasive surgery for disc pain)
  • Discectomy/Microdiscectomy – to relieve nerve compression
  • Laminectomy – to relieve spinal stenosis or nerve compression
  • Hemilaminectomy – to relieve spinal stenosis or nerve compression
  • Lumbar fusion (lumbar fusion is only indicated for recurrent lumbar disc herniations, not primary herniations)
  • Anterior cervical discectomy and fusion (for cervical disc herniation)
  • Disc arthroplasty (experimental for cases of cervical disc herniation)
  • Dynamic stabilization
  • Artificial disc replacement, a relatively new form of surgery in the U.S. but has been in use in Europe for decades, primarily used to treat low back pain from a degenerated disc.
  • Nucleoplasty^[41]
  • Back pain
  • Degenerative disc disease
  • Low back pain
  • Sciatica
  • Vertebral column
  • Spinal stenosis
  • Failed back syndrome


MRI Scan of lumbar disc herniation between fourth and fifth lumbar vertebral bodies. (Wikimedia)

Treatment

The majority of herniated discs will heal themselves in about six weeks and do not require surgery. One study found that “After 12 weeks, 73% of patients showed reasonable to major improvement without surgery.” ^[25]

If pain due to disc herniation, protrusion, bulge, or disc tear is due to chemical radiculitis pain, then prior to surgery it may make sense to try an anti-inflammatory approach. Often this is first attempted with non-steroidal anti-inflammatory medications, but the long-term use of NSAIDS for patients with persistent back pain is complicated by their possible cardiovascular and gastrointestinal toxicity; and NSAIDs have limited value to intervene in tumor necrosis factor-alpha (TNF)-mediated processes.^[26] An alternative often employed is the injection of cortisone into the spine adjacent to the suspected pain generator, a technique known as “epidural steroid injection”.^[27] Although this technique began more than a decade ago for pain due to disc herniation, the efficacy of epidural steroid injections is now generally thought to be limited to short term pain relief in selected patients only. ^[28] In addition, epidural steroid injections, in certain settings, may result in serious complications. ^[29] Fortunately there are now emerging new methods that directly target TNF. ^[30] These TNF-targeted methods represent a highly promising new approach for patients with chronic severe spinal pain, such as those with failed back surgery syndrome. ^[30] Ancillary approaches, such as rehabilitation, physical therapy, anti-depressants, and, in particular, graduated exercise programs, may all be useful adjuncts to anti-inflammatory approaches. ^[26]

Conservative treatment

Non-surgical methods of treatment are usually attempted first, leaving surgery as a last resort. Pain medications are often prescribed as the first attempt to alleviate the acute pain and allow the patient to begin exercising and stretching.

There are a variety of other non-surgical methods used in attempts to relieve the condition after it has occurred, often in combination with pain killers. They are either considered indicated, contraindicated, relatively contraindicated, or inconclusive based on the safety profile of their risk-benefit ratio and on whether they may or may not help:

Indicated

Contraindicated

Inconclusive

Surgery

Surgery should only be considered as a last resort after all conservative treatments (non-surgical therapy) have been tried, that did not alleviate the pain and heal the disc herniation.

Surgery is indicated if a patient has a significant neurological deficit.^[36] The presence of cauda equina syndrome (in which there is incontinence, weakness and genital numbness) is considered a medical emergency requiring immediate attention and possibly surgical decompression.

Regarding the role of surgery for failed medical therapy in patients without a significant neurological deficit, a meta-analysis of randomized controlled trials by the Cochrane Collaboration concluded that “limited evidence is now available to support some aspects of surgical practice”. More recent randomized controlled trials refine indications for surgery

Surgical options include:

Surgical goals include relief of nerve compression, allowing the nerve to recover, as well as the relief of associated back pain and restoration of normal function.

Emerging treatment options

The identification of tumor necrosis factor-alpha (TNF) as a central cause of inflammatory spinal pain now suggests the possibility of an entirely new approach to selected patients with severe pain due to disc herniation, protrusion, bulge, or disc tear. Specific and potent inhibitors of TNF became available in the U.S. in 1998, and were demonstrated to be potentially effective for treating sciatica in experimental models beginning in 2001. ^[42][43][44] Targeted anatomic administration of one of these anti-TNF agents, etanercept, a patented treatment method,^[45] has been suggested in published pilot studies to be effective for treating selected patients with severe pain due to disc herniation, protrusion, bulge, or disc tear. ^[30][46] The scientific basis for pain relief in these patients is supported by the most current review articles. ^[47][48] In the future new imaging methods may allow non-invasive identification of sites of neuronal inflammation, thereby enabling more accurate localization of the “pain generators” responsible for symptom production.

Investigational treatments

Future treatments may include stem cell therapy. Doctors Victor Y. L. Leung, Danny Chan and Kenneth M. C. Cheung have reported in the European Spine Journal that “substantial progress has been made in the field of stem cell regeneration of the intervertebral disc. Autogenic mesenchymal stem cells in animal models can arrest intervertebral disc degeneration or even partially regenerate it and the effect is suggested to be dependent on the severity of the degeneration.”^[49]

References

1. ^ Slipped discs: “they do not actually ‘slip’…”
2. ^ Prolapsed disc
3. ^ Ehealthmd.com FAQ: “…the entire disc does not ‘slip’ out of place.”
4. ^ Terminology
5. ^ MedlinePlus Encyclopedia Herniated nucleus pulposus Frequency
6. ^ “Neck and Shoulder Blade Pain”. http://www.treatment-for.com/shoulder-blade-pain-treatment.htm.
7. ^ Cervical herniation at eMedicine
8. ^ Thoracic herniation at eMedicine
9. ^ Lumbar herniation at eMedicine
10. ^ Yuichiro Hirose et al. (May 2008). “A Functional Polymorphism in THBS2 that Affects Alternative Splicing and MMP Binding Is Associated with Lumbar-Disc Herniation”. American Journal of Human Genetics 82 (5): 1122–1129. doi:10.1016/j.ajhg.2008.03.013. PMID 18455130. PMC 2427305. http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B8JDD-4SDFHH8-1-B&_cdi=43612&_user=10&_coverDate=05%2F09%2F2008&_sk=%23TOC%2343612%232008%23999179994%23688977%23FLA%23display%23Volume_82,_Issue_5,_Pages_1023-1226_(9_May_2008)%23tagged%23Volume%23first%3D82%23Issue%23first%3D5%23date%23(9_May_2008)%23&view=c&_gw=y&wchp=dGLzVtb-zSkzV&_valck=1&md5=368f7507ed0a5e28a15ca8290a854b0c&ie=/sdarticle.pdf.
11. ^ Robert E Windsor (2006). “Frequency of asymptomatic cervical disc protrusions”. Cervical Disc Injuries.. eMedicine. http://www.emedicine.com/sports/byname/Cervical-Disc-Injuries.htm. Retrieved 2008-02-27.
12. ^ Ernst CW, Stadnik TW, Peeters E, Breucq C, Osteaux MJ (Sep 2005). “Prevalence of annular tears and disc herniations on MR images of the cervical spine in symptom free volunteers”. Eur J Radiol 55 (3): 409–14. doi:10.1016/j.ejrad.2004.11.003. PMID 16129249.
13. ^ ^{a b c} Peng B, Wu W, Li Z, Guo J, Wang X (Jan 2007). “Chemical radiculitis”. Pain 127 (1-2): 11–6. doi:10.1016/j.pain.2006.06.034. PMID 16963186.
14. ^ Marshall LL, Trethewie ER (Aug 1973). “Chemical irritation of nerve-root in disc prolapse”. Lancet 2 (7824): 320. doi:10.1016/S0140-6736(73)90818-0. PMID 4124797.
15. ^ McCarron RF, Wimpee MW, Hudkins PG, Laros GS (Oct 1987). “The inflammatory effect of nucleus pulposus. A possible element in the pathogenesis of low-back pain”. Spine 12 (8): 760–4. doi:10.1097/00007632-198710000-00009. PMID 2961088.
16. ^ Takahashi H, Suguro T, Okazima Y, Motegi M, Okada Y, Kakiuchi T (Jan 1996). “Inflammatory cytokines in the herniated disc of the lumbar spine”. Spine 21 (2): 218–24. doi:10.1097/00007632-199601150-00011. PMID 8720407. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=21&issue=2&spage=218.
17. ^ Igarashi T, Kikuchi S, Shubayev V, Myers RR (Dec 2000). “2000 Volvo Award winner in basic science studies: Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology. Molecular, histologic, and behavioral comparisons in rats”. Spine 25 (23): 2975–80. doi:10.1097/00007632-200012010-00003. PMID 11145807. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=25&issue=23&spage=2975.
18. ^ Sommer C, Schäfers M (2004). “Mechanisms of neuropathic pain: the role of cytokines”. Drug Discovery Today: Disease Mechanisms 1 (4): 441–8. doi:10.1016/j.ddmec.2004.11.018.
19. ^ Igarashi A, Kikuchi S, Konno S, Olmarker K (Oct 2004). “Inflammatory cytokines released from the facet joint tissue in degenerative lumbar spinal disorders”. Spine 29 (19): 2091–5. doi:10.1097/01.brs.0000141265.55411.30. PMID 15454697. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=29&issue=19&spage=2091.
20. ^ Sakuma Y, Ohtori S, Miyagi M, et al. (Aug 2007). “Up-regulation of p55 TNF alpha-receptor in dorsal root ganglia neurons following lumbar facet joint injury in rats”. Eur Spine J 16 (8): 1273–8. doi:10.1007/s00586-007-0365-3. PMID 17468886.
21. ^ Sekiguchi M, Kikuchi S, Myers RR (May 2004). “Experimental spinal stenosis: relationship between degree of cauda equina compression, neuropathology, and pain”. Spine 29 (10): 1105–11. doi:10.1097/00007632-200405150-00011. PMID 15131438. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=29&issue=10&spage=1105.
22. ^ Séguin CA, Pilliar RM, Roughley PJ, Kandel RA (Sep 2005). “Tumor necrosis factor-alpha modulates matrix production and catabolism in nucleus pulposus tissue”. Spine 30 (17): 1940–8. doi:10.1097/01.brs.0000176188.40263.f9. PMID 16135983. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0362-2436&volume=30&issue=17&spage=1940.
23. ^ Waddell G, McCulloch JA, Kummel E, Venner RM (1980). “Nonorganic physical signs in low-back pain”. Spine 5 (2): 117–25. doi:10.1097/00007632-198003000-00005. PMID 6446157.
24. ^ Rabin A, Gerszten PC, Karausky P, Bunker CH, Potter DM, Welch WC (2007). “The sensitivity of the seated straight-leg raise test compared with the supine straight-leg raise test in patients presenting with magnetic resonance imaging evidence of lumbar nerve root compression”. Archives of physical medicine and rehabilitation 88 (7): 840–3. doi:10.1016/j.apmr.2007.04.016. PMID 17601462.
25. ^ Vroomen PC, de Krom MC, Knottnerus JA (Feb 2002). “Predicting the outcome of sciatica at short-term follow-up”. Br J Gen Pract 52 (475): 119–23. PMID 11887877. PMC 1314232. http://openurl.ingenta.com/content/nlm?genre=article&issn=0960-1643&volume=52&issue=475&spage=119&aulast=Vroomen.
26. ^ ^{a b} Carragee EJ (May 2005). “Clinical practice. Persistent low back pain”. N Engl J Med. 352 (18): 1891–8. doi:10.1056/NEJMcp042054. PMID 15872204.
27. ^ Fredman B, Nun MB, Zohar E, et al. (Feb 1999). “Epidural steroids for treating “failed back surgery syndrome”: is fluoroscopy really necessary?”. Anesth Analg. 88 (2): 367–72. doi:10.1097/00000539-199902000-00027. PMID 9972758. http://www.anesthesia-analgesia.org/cgi/pmidlookup?view=long&pmid=9972758.
28. ^ Landau WM, Nelson DA, Armon C, Argoff CE, Samuels J, Backonja MM (Aug 2007). “Assessment: use of epidural steroid injections to treat radicular lumbosacral pain: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology”. Neurology 69 (6): 614; author reply 614–5. doi:10.1212/01.wnl.0000278878.51713.c8. PMID 17679685.
29. ^ Abbasi A, Malhotra G, Malanga G, Elovic EP, Kahn S (Sep 2007). “Complications of interlaminar cervical epidural steroid injections: a review of the literature”. Spine 32 (19): 2144–51. doi:10.1097/BRS.0b013e318145a360. PMID 17762818.
30. ^ ^{a b c} Tobinick EL, Britschgi-Davoodifar S (Mar 2003). “Perispinal TNF-alpha inhibition for discogenic pain”. Swiss Med Wkly 133 (11-12): 170–7. doi:2003/11/smw-10163 (inactive 2008-11-18). PMID 12715286.
31. ^ ^{a b c d e f g h} “Rush University Medical Center”. http://www.rush.edu/rumc/page-1160429743543.html. Retrieved 2009-04-22.
32. ^ Snelling, Spinal manipulation in patients with disc herniation: A critical review of risk and benefit, International Journal of Osteopathic Medicine, Volume 9, Issue 3, Pages 77-84.
33. ^ {http://www.who.int/medicines/areas/traditional/Chiro-Guidelines.pdf WHO guidelines on basic training and safety in chiropractic. “2.1 Absolute contraindications to spinal manipulative therapy”, p. 21]. WHO
34. ^ Dwain M Daniel, Non-surgical spinal decompression therapy: does the scientific literature support efficacy claims made in the advertising media?, Chiropractic and Osteopathy, 2007, 15:7
35. ^ Be Wary of Spinal Decompression Therapy with VAX-D or Similar Devices, Stephen Barrett
36. ^ Stern, Scott D.; Adam S. Cifu, Diane Altkorn (2006). “Back Pain”. in Janet Foltin, Harriet Lebowitz, Karen Davis. Symptom to Diagnosis: An Evidence-Based Guide. New York: Lange Medical Books/McGraw-Hill. pp. 67–81. ISBN 0071463895.
37. ^ Weinstein JN, Tosteson TD, Lurie JD, et al. (2006). “Surgical vs nonoperative treatment for lumbar disk herniation: the Spine Patient Outcomes Research Trial (SPORT): a randomized trial”. JAMA 296 (20): 2441–50. doi:10.1001/jama.296.20.2441. PMID 17119140.
38. ^ Weinstein JN, Lurie JD, Tosteson TD, et al. (2006). “Surgical vs nonoperative treatment for lumbar disk herniation: the Spine Patient Outcomes Research Trial (SPORT) observational cohort”. JAMA 296 (20): 2451–9. doi:10.1001/jama.296.20.2451. PMID 17119141.
39. ^ Peul WC, van Houwelingen HC, van den Hout WB, et al. (2007). “Surgery versus prolonged conservative treatment for sciatica”. N Engl J Med. 356 (22): 2245–56. doi:10.1056/NEJMoa064039. PMID 17538084. http://content.nejm.org/cgi/content/short/356/22/2245.
40. ^ Minimally invasive procedures to treat herniated disk
41. ^ Li J, Yan DL, Zhang ZH (2008). “Percutaneous cervical nucleoplasty in the treatment of cervical disc herniation.”. Eur Spine J. 17 (12): 1664–96. doi:10.1007/s00586-008-0786-7. PMID 18830638.
42. ^ Sommer C, Schäfers M, Marziniak M, Toyka KV (Jun 2001). “Etanercept reduces hyperalgesia in experimental painful neuropathy”. J Peripher Nerv Syst. 6 (2): 67–72. doi:10.1046/j.1529-8027.2001.01010.x. PMID 11446385. http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=1085-9489&date=2001&volume=6&issue=2&spage=67.
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Source: Wikipedia

http://en.wikipedia.org/wiki/Spinal_disc_herniation

Employment change. Employment of physicians and surgeons is projected to grow 22 percent from 2008 to 2018, much faster than the average for all occupations.

Job growth will occur because of continued expansion of healthcare-related industries. The growing and aging population will drive overall growth in the demand for physician services, as consumers continue to demand high levels of care using the latest technologies, diagnostic tests, and therapies. Many medical schools are increasing their enrollments based on perceived new demand for physicians.

Despite growing demand for physicians and surgeons, some factors will temper growth. For example, new technologies allow physicians to be more productive. This means physicians can diagnose and treat more patients in the same amount of time. The rising cost of healthcare can dramatically affect demand for physicians’ services.

Physician assistants and nurse practitioners, who can perform many of the routine duties of physicians at a fraction of the cost, may be increasingly used. Furthermore, demand for physicians’ services is highly sensitive to changes in healthcare reimbursement policies. If changes to health coverage result in higher out-of-pocket costs for consumers, they may demand fewer physician services.

Job prospects. Opportunities for individuals interested in becoming physicians and surgeons are expected to be very good. In addition to job openings from employment growth, openings will result from the need to replace the relatively high number of physicians and surgeons expected to retire over the 2008-18 decade.

Job prospects should be particularly good for physicians willing to practice in rural and low-income areas because these medically underserved areas typically have difficulty attracting these workers. Job prospects will also be especially good for physicians in specialties that afflict the rapidly growing elderly population. Examples of such specialties are cardiology and radiology because the risks for heart disease and cancer increase as people age.

Source: Bureau of Labor Statistics

http://www.bls.gov/oco/ocos074.htm#outlook

Detailed Description

Somatotroph pituitary adenoma is the most frequent cause of acromegaly. A transsphenoidal removal of the tumor is used as the first line treatment. Somatostatin analogs are used as to whether recovery was not obtained after surgery or pituitary surgery was contraindicated. Previous studies with somatostatin analogs have shown a drop in plasma GH and IGF-1 levels and a reduction in adenoma size in 75 and 25% of patients respectively. Retrospective studies suggest that a treatment with somatostatin analogs performed before surgery may be of interest to improve anesthesic conditions and surgical outcome. The aim of present study is to prospectively evaluate the interest of a first line treatment with a long-acting somatostatin analog (Sandostatin) before performing a pituitary surgery in acromegalic patients with either a micro or a macroadenoma to improve peri-operative conditions and hopefully surgical outcome.

After informed consent, untreated acromegalic patients will be included and randomly assigned to one of the following treatment procedures : either pituitary surgery or a six month treatment with long-acting Sandostatin 30 mg monthly for 6 months before performing transsphenoïdal adenoma removal. The patients will be evaluated before any treatment, on months 3 and 6 of the treatment with Sandostatin (for the patients enrolled in this arm of the study) and on months 3 and 12 after pituitary neurosurgery. Each evaluation will include clinical data, hormone testing and radiological (MRI) investigation. The main endpoint will be the rate of recovery proved by a normalisation of GH secretion and plasma IGF-1 level. Secondary endpoints will include the evaluation of clinical, radiological, biological, anesthesic, surgical and pathological parameters. A comparison between the two arms will be performed at entry into the study, at the time of surgery and then on months 3 and 12 following the transsphenoidal removal of the somatotroph adenoma.

This study is currently recruiting participants.

Verified by University Hospital, Rouen, December 2009

First Received: December 7, 2009 Last Updated: December 8, 2009 History of Changes

Primary Outcome Measures:

• IGF1 plasma levels [ Time Frame: 3 months and 12 months after transphenoidal surgery ] [ Designated as safety issue: No ]

Secondary Outcome Measures:

• GH plasma levels [ Time Frame: 3 and 12 months after transphenoidal surgery ] [ Designated as safety issue: No ]
• Evaluation of the effects of the pre-operative treatment with Sandostatin on clinical, radiological, biological, anesthesic, surgical and pathological parameters. [ Time Frame: at transphenoidal surgery ] [ Designated as safety issue: No ]

Eligibility

Criteria

Inclusion Criteria:

• men and women
• 18-80 years old
• untreated acromegaly
• unsuppressed GH secretion after a glucose load and elevated IGF-1 plasma levels
• presence of a pituitary adenoma on MRI
• informed consent given.

Exclusion Criteria:

• acromegaly previously treated
• contraindication to pituitary surgery
• associated hyperprolactinemia above 200 ng/ml
• visual field defect needing rapid transsphenoidal surgery
• contraindication to a treatment with octreotide

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT01029275

Contacts

Locations

Sponsors and Collaborators

University Hospital, Rouen

Investigators

More Information
No publications provided

Keywords provided by University Hospital, Rouen:

Additional relevant MeSH terms:

Source: ClinicalTrials.gov – processed this record on March 25, 2010

http://clinicaltrials.gov/ct2/show/NCT01029275

What Are the Costs?
The Clinical Center does not charge patients for participation and treatment in clinical studies at NIH. In addition, in certain emergency circumstances, you may qualify for help with travel and other expenses.

Why Participate?

• Patients taking part in NIH Clinical Center studies are seen by a team of expert doctors, dentists, nurses, technicians, and support staff.
• Clinical Center patients often are first to receive promising new treatments before they become available in the community.
• Patients are helping others with the same disease, both today and in the future.

Risks and Benefits
It is important to understand that some risks are involved in clinical research, just as in routine medical care and activities of daily living. In thinking about the risks of research, it is helpful to focus on two things: the degree of harm that could result from taking part in the study, and the chance of any harm occurring. Most clinical studies pose risks of minor discomfort, lasting only a short time. Some volunteer subjects, however, experience complications that require medical attention. The specific risks associated with any research protocol are described in detail in the consent document, which you are asked to sign before taking part in research. In addition, the major risks of participating in a study will be explained to you by a member of the research team, who will answer your questions about the study. Before deciding to participate, you should carefully weigh these risks against possible benefits. You may or may not receive direct benefit for yourself and your condition as a result of participating in research, but in either case, you will know that the knowledge developed may help others.

Dealing with Fears
Many protections and safeguards for volunteer patients are built into the Clinical Research process. It may help alleviate some of your fears about participating in a clinical study to know what some of these are:

The Patient Bill of Rights. All patients who take part in studies at the Clinical Center are protected by the Patient Bill of Rights, developed by the American Hospital Association for use in hospitals across the country. The Patients’ Bill of Rights contains guidelines to ensure privacy and confidentiality of patients and their medical records.

Hospital Accreditation. As in any medical research facility, an institutional review board (IRB) must review and approve every new study at NIH before the study can begin. The IRB is made up of medical specialists, statisticians,nurses, social workers, medical ethicists, and members of the community. The IRB reviews protocols to ensure patient safety. In addition, The Joint Commission, periodically reviews the Clinical Center hospital to see if stringent standards, leading to Joint Commission accreditation, have been met.

Informed Consent. Before entering a Clinical Center study, it is important that you as the patient fully understand the study and what your involvement would mean. Clinical Center staff members will help by providing you with an informed consent statement, which has detailed information about the study, including the length of the study, the number of visits required, and medical procedures and medications included. It also provides expected outcomes, potential benefits, and possible risks.

Clinical Center staff will review the informed consent statement with you and answer your questions. If you decide to participate after reviewing the statement and talking with staff and family members, you will need to sign the informed consent statement. Your signature indicates that you understand the study and agree to participate voluntarily.

Who Participates?
People who take part in Clinical Center studies include:

Children and adults wishing to improve their own health. They may be patients with newly diagnosed medical problems. They may have had the problems over a period of time, or they may have a family history of a certain disease.

Healthy volunteers who seek to advance knowledge about causes, progress, and treatment of disease also can participate in clinical research. They provide important medical information to researchers by helping them compare how healthy people differ medically from those who have a specific disease.

To participate, patients and healthy volunteers must meet certain requirements, which are different for each study.

Information for Healthy Volunteers
There are about 300 studies available to healthy volunteers. You can find information on these studies at Search the Studies. (To search for studies accepting healthy volunteers, type in the keywords: ‘healthy’ and ‘normal’.)

Will I be compensated as a healthy volunteer? Yes. NIH compensates volunteers for their time and, in some instances, for the inconvenience of a procedure. There are standard compensation rates for the volunteer’s time; the study’s principal investigator determines inconvenience rates.

How can I volunteer? If you are considering volunteering, please call 301-496-4763 or 1-800-892-3276 to talk to a staff member. You will need to come to the CRVP office to register for participation in a study. More information about the Clinical Research Volunteer Program is available at Program for Healthy Volunteers.

What Are the Main Types of Studies?
There are four types of drug studies:

Phase 1 studies test a potential new drug with a small number of volunteers for best dosage and potential side effects.

Phase 2 studies test a drug with known dose and side effects with a larger number of volunteers to learn more about side effects, how the body uses the drug, and how the drug helps the condition.

Phase 3 and 4 studies compare the new drug with a commonly used drug.

Other research may provide only indirect benefit to the patient by giving researchers information that may be an important first step toward developing a treatment. For example, research may show how a disease progresses or how it affects others systems in the body.

Patients can take part in clinical studies covering a wide range of medical diseases, conditions, and rare disorders affecting both children and adults, including those relating to AIDS, aging, alcohol abuse and alcoholism, allergy, cancer, digestive and kidney problems, diabetes, eye disorders, infectious diseases, genetics, mental health, neurological disorders, stroke, and others. There is an online database of current studies.

Making the Decision
It is important that patients be well informed and feel confident and secure about participating. Before deciding to participate, you should talk with your own doctors, family members, and Clinical Center staff. Be sure you know the answers to the following questions before you make your decision:

• What is the purpose of the study?
• What is required of me?
• What is my role in the study — am I a healthy volunteer or a patient volunteer?
• Will the study directly benefit me?
• Will the study benefit others?
• Are there risks? If so, what are they and what are the chances that they will occur?
• What discomforts are involved?
• What is the total time involved?
• Are there other inconveniences?
• Have I discussed participation in the study with those who are important to me, such as family and friends?
• Do I wish to participate in this study?

To take part in studies at the Clinical Center, referral by a medical practitioner is preferable. However, in certain instances, self-referral may be appropriate.

Patients and volunteers become partners in a special relationship with members of the research team who are searching for better ways to understand and treat disease. Their participation is critical for improving health today and in future generations. Please call us at 1-800-411-1222, or e-mail us at prpl@mail.cc.nih.gov with any questions about how you or someone you know might participate.

Search the Clinical Studies here.

Source: National Institutes of Health, Clinical Center

http://www.cc.nih.gov/participate/studies.shtml

Biography

Cushing was born in Cleveland, Ohio, the son of Bessie Williams; and Kirke Cushing, a physician whose family came to Hingham, Massachusetts, as Puritans in the 17th century.^[2] Harvey Cushing was the youngest of ten children. He graduated with an A.B. degree in 1891 from Yale University, where he was a member of Scroll and Key and Delta Kappa Epsilon (Phi chapter). He studied medicine at Harvard Medical School and was given his M.D. degree in 1895. Cushing completed his internship at Massachusetts General Hospital and then did a residency in surgery under the guidance of a famous surgeon, William Stewart Halsted, at the Johns Hopkins Hospital, in Baltimore. During his medical career he was a surgeon at Johns Hopkins Hospital, at the Peter Bent Brigham Hospital in Boston. He married Katharine Stone Crowell on June 10, 1902. They had five children: William Harvey Cushing; Mary Benedict Cushing who married Vincent Astor and after a divorce married painter James Whitney Fosburgh ^[3]; Betsey Cushing, who married James Roosevelt and later John Hay Whitney^[4] ; Henry Kirke Cushing; and Barbara Cushing, the socialite wife of Stanley Grafton Mortimer and later William S. Paley.^[5] He became a professor of surgery at the Harvard Medical School starting in 1912.^[6] He served in the U.S. Army Medical Corps as a surgeon with the American Expeditionary Forces in Europe during World War I, attaining the rank of Colonel (O6). In that capacity, he treated Lt. Edward Revere Osler, the son of Sir William Osler, who was fatally wounded during the third battle of Ypres.^[7] From 1933 to 1937, when he retired, he worked at Yale University School of Medicine.^[6] Cushing died on October 7, 1939 in New Haven, Connecticut, from complications of a myocardial infarction.^[1][6] He was interred at Lake View Cemetery in Cleveland.^[8] Interestingly, an autopsy performed on Cushing revealed that his brain harbored a colloid cyst of the third ventricle.

Legacy

In the beginning of the 20th century he developed many of the basic surgical techniques for operating on the brain. This established him as one of the foremost leaders and experts in the field. Under his influence neurosurgery became a new and autonomous surgical discipline.

• He considerably improved the survival of patients after difficult brain operations for intracranial tumors.
• He used x-rays to diagnose brain tumors.
• He used electrical stimuli for study of the human sensory cortex.
• He played a pivotal role in development of the Bovie electrocautery tool with W.T. Bovie, a physicist.
• He was the world’s leading teacher of neurosurgeons in the first decades of the 20th century.

Arguably, Cushing’s greatest contribution came with his introduction to North America of blood pressure measurement.

On visiting colleague Scipione Riva-Rocci, an Italian physician, Cushing was astonished at Riva-Rocci’s non invasive way to measure intra-arterial pressure. In 1896, Riva-Rocci developed a wall-mounted mercury manometer linked to a balloon-inflated cuff that would measure the pressure needed to compress arterial systolic pressure, i.e. systolic blood pressure measurement. Riva-Rocci’s design was based on a more primitive version developed by French physician Pierre Potain.

Cushing brought back a sample of Riva-Rocci’s sphygmomanometer, and blood pressure measurement became a vital sign and its use spread like wildfire across the US and western world as a direct contribution by Harvey Cushing. Its use remained until Russian physician Nikolai Korotkov included diastolic blood pressure measurement in 1920 (after he discovered the famed “Korotkoff sounds”) with his modern sphygmomanometer, which also replaced the mercury manometer with a smaller, round dial manometer.^[9] Cushing’s name is commonly associated with his most famous discovery – Cushing’s disease.

Harvey Williams Cushing, "Father of Neurosurgery." (Wikimedia)

In 1912 he reported in a study an endocrinological syndrome caused by a malfunction of the pituitary gland which he termed “polyglandular syndrome”. He published his findings in 1932, as “The Basophil Adenomas of the Pituitary Body and Their Clinical Manifestations pituitary Basophilism”. Cushing was also awarded the 1926 Pulitzer Prize for Biography or Autobiography for a book recounting the life of one of the fathers of modern medicine, Sir William Osler.^[10] In 1930, Cushing was awarded the Lister Medal for his contributions to surgical science. As part of the award, he delivered the Lister Memorial Lecture at the Royal College of Surgeons of England in July 1930.^[11][12] Cushing was elected to the Royal Swedish Academy of Sciences in 1934.

In 1988, the United States Postal Service issued a 45 cent postage stamp in his honor, as part of the Great Americans series.^[13] The Harvey Cushing/John Hay Whitney Medical Library^[14] at Yale University contains extensive collections in the field of medicine and the history of medicine. In 2005, the library released portions of its collection online, including the Peter Parker Collection which consists of a collection of portrait engravings and 83 mid-19th century oil paintings rendered by artist Lam Qua of Chinese tumor patients, and a biography of Harvey Cushing by John F. Fulton.

• Harvey Cushing (c.1900)
• Born     April 8, 1869(1869-04-08) Cleveland, Ohio
• Died     October 7, 1939 (aged 70) New Haven, Connecticut, United States
• Education Yale University Harvard Medical School
• Years active 1895-1935
• Known for Pioneering brain surgery
• Children William Harvey Cushing Mary Benedict Cushing Betsey Cushing Henry Kirke Cushing Barbara Cushing
• Parents Bessie Williams Kirke Cushing

Notes

Source: Wikipedia

http://en.wikipedia.org/wiki/Harvey_Cushing

There are two main types of brain cancer (also called Glioma or Meningioma). Primary brain cancer starts in the brain. Metastatic brain cancer starts somewhere else in the body and moves to the brain.

Brain tumors can be benign, with no cancer cells, or malignant, with cancer cells that grow quickly.

Brain tumors can cause many symptoms. Some of the most common are

• Headaches, usually worse in the morning
• Nausea and vomiting
• Changes in your ability to talk, hear or see
• Problems with balance or walking
• Problems with thinking or memory
• Muscle jerking or twitching
• Numbness or tingling in arms or legs

No one knows the exact causes of brain tumors. Doctors can seldom explain why one person develops a brain tumor and another does not.

Source: National Cancer Institute

http://www.nlm.nih.gov/medlineplus/braincancer.html

In cross-section, the peripheral region of the cord contains neuronal white matter tracts containing sensory and motor neurons. Internal to this peripheral region is the gray, butterfly-shaped central region made up of nerve cell bodies. This central region surrounds the central canal, which is an anatomic extension of the spaces in the brain known as the ventricles and, like the ventricles, contains cerebrospinal fluid.

The spinal cord has a shape that is compressed dorso-ventrally, giving it an elliptical shape. The cord has grooves in the dorsal and ventral sides. The posterior median sulcus is the groove in the dorsal side, and the anterior median fissure is the groove in the ventral side. Running down the center of the spinal cord is a cavity, called the central canal.

The three meninges that cover the spinal cord—the outer dura mater, the arachnoid mater, and the innermost pia mater—are continuous with that in the brainstem and cerebral hemispheres. Similarly, cerebrospinal fluid is found in the subarachnoid space. The cord is stabilized within the dura mater by the connecting denticulate ligaments, which extend from the enveloping pia mater laterally between the dorsal and ventral roots. The dural sac ends at the vertebral level of the second sacral vertebra.

The spinal cord is protected by three layers of tissue, called spinal meninges, that surround the cord. The dura mater is the outermost layer, and it forms a tough protective coating. Between the dura mater and the surrounding bone of the vertebrae is a space, called the epidural space. The epidural space is filled with adipose tissue, and it contains a network of blood vessels. The arachnoid is the middle protective layer. Its name comes from the fact that the tissue has a spiderweb-like appearance. The space between the arachnoid and the underlyng pia mater is called the subarachnoid space. The subarachnoid space contains cerebrospinal fluid (CSF). The medical procedure known as a “spinal tap” involves use of a needle to withdraw CSF from the subarachnoid space, usually from the lumbar region of the spine. The pia mater is the innermost protective layer. It is very delicate and it is tightly associated with the surface of the spinal cord.

Spinal cord segments

The human spinal cord is divided into 31 different segments. At every segment, right and left pairs of spinal nerves (mixed; sensory and motor) form. Six to eight motor nerve rootlets branch out of right and left ventro lateral sulci in a very orderly manner. Nerve rootlets combine to form nerve roots. Likewise, sensory nerve rootlets form off right and left dorsal lateral sulci and form sensory nerve roots. The ventral (motor) and dorsal (sensory) roots combine to form spinal nerves (mixed; motor and sensory), one on each side of the spinal cord. Spinal nerves, with the exception of C1 and C2, form inside intervertebral foramen (IVF). Note that at each spinal segment, the border between the central and peripheral nervous system can be observed. Rootlets are a part of the peripheral nervous system.

In the upper part of the vertebral column, spinal nerves exit directly from the spinal cord, whereas in the lower part of the vertebral column nerves pass further down the column before exiting. The terminal portion of the spinal cord is called the conus medullaris. The pia mater continues as an extension called the filum terminale, which anchors the spinal cord to the coccyx. The cauda equina (“horse’s tail”) is the name for the collection of nerves in the vertebral column that continue to travel through the vertebral column below the conus medullaris. The cauda equina forms as a result of the fact that the spinal cord stops growing in length at about age four, even though the vertebral column continues to lengthen until adulthood. This results in the fact that sacral spinal nerves actually originate in the upper lumbar region. The spinal cord can be anatomically divided into 31 spinal segments based on the origins of the spinal nerves.

Each segment of the spinal cord is associated with a pair of ganglia, called dorsal root ganglia, which are situated just outside of the spinal cord. These ganglia contain cell bodies of sensory neurons. Axons of these sensory neurons travel into the spinal cord via the dorsal roots.

Ventral roots consist of axons from motor neurons, which bring information to the periphery from cell bodies within the CNS. Dorsal roots and ventral roots come together and exit the intervertebral foramina as they become spinal nerves.

The gray matter, in the center of the cord, is shaped like a butterfly and consists of cell bodies of interneurons and motor neurons. It also consists of neuroglia cells and unmyelinated axons. Projections of the gray matter (the “wings”) are called horns. Together, the gray horns and the gray commissure form the “gray H.”

The white matter is located outside of the gray matter and consists almost totally of myelinated motor and sensory axons. “Columns” of white matter carry information either up or down the spinal cord.

Within the CNS, nerve cell bodies are generally organized into functional clusters, called nuclei. Axons within the CNS are grouped into tracts.

There are 33 (some EMS text say 25, counting the sacral as one solid piece) spinal cord nerve segments in a human spinal cord:

• 8 cervical segments forming 8 pairs of cervical nerves (C1 spinal nerves exit spinal column between occiput and C1 vertebra; C2 nerves exit between posterior arch of C1 vertebra and lamina of C2 vertebra; C3-C8 spinal nerves through IVF above corresponding cervica vertebra, with the exception of C8 pair which exit via IVF between C7 and T1 vertebra)
• 12 thoracic segments forming 12 pairs of thoracic nerves (exit spinal column through IVF below corresponding vertebra T1-T12)
• 5 lumbar segments forming 5 pairs of lumbar nerves (exit spinal column through IVF, below corresponding vertebra L1-L5)
• 5 (or 1) sacral segments forming 5 pairs of sacral nerves (exit spinal column through IVF, below corresponding vertebra S1-S5)
• 3 coccygeal segments joined up becoming a single segment forming 1 pair of coccygeal nerves (exit spinal column through the sacral hiatus).

Because the vertebral column grows longer than the spinal cord, spinal cord segments do not correspond to vertebral segments in adults, especially in the lower spinal cord. In the fetus, vertebral segments do correspond with spinal cord segments. In the adult, however, the spinal cord ends around the L1/L2 vertebral level, forming a structure known as the conus medullaris. For example, lumbar and sacral spinal cord segments are found between vertebral levels T9 and L2.

Although the spinal cord cell bodies end around the L1/L2 vertebral level, the spinal nerves for each segment exit at the level of the corresponding vertebra. For the nerves of the lower spinal cord, this means that they exit the vertebral column much lower (more caudally) than their roots. As these nerves travel from their respective roots to their point of exit from the vertebral column, the nerves of the lower spinal segments form a bundle called the cauda equina.

There are two regions where the spinal cord enlarges:

• Cervical enlargement – corresponds roughly to the brachial plexus nerves, which innervate the upper limb. It includes spinal cord segments from about C4 to T1. The vertebral levels of the enlargement are roughly the same (C4 to T1).

• Lumbosacral enlargement – corresponds to the lumbosacral plexus nerves, which innervate the lower limb. It comprises the spinal cord segments from L2 to S3 and is found about the vertebral levels of T9 to T12.

Embryology

The spinal cord is made from part of the neural tube during development. As the neural tube begins to develop, the notochord begins to secrete a factor known as Sonic hedgehog or SHH. As a result, the floor plate then also begins to secrete SHH, and this will induce the basal plate to develop motor neurons. Meanwhile, the overlying ectoderm secretes bone morphogenetic protein (BMP). This induces the roof plate to begin to secrete BMP, which will induce the alar plate to develop sensory neurons. The alar plate and the basal plate are separated by the sulcus limitans.

Additionally, the floor plate also secretes netrins. The netrins act as chemoattractants to decussation of pain and temperature sensory neurons in the alar plate across the anterior white commissure, where they then ascend towards the thalamus.

Lastly, it is important to note that the past studies of Viktor Hamburger and Rita Levi-Montalcini in the chick embryo have been further proven by more recent studies which demonstrated that the elimination of neuronal cells by programmed cell death (PCD) is necessary for the correct assembly of the nervous system.

Overall, spontaneous embryonic activity has been shown to play a role in neuron and muscle development but is probably not involved in the initial formation of connections between spinal neurons.

Somatosensory organization

Somatosensory organization is divided into the dorsal column-medial lemniscus tract (the touch/proprioception/vibration sensory pathway) and the anterolateral system, or ALS (the pain/temperature sensory pathway). Both sensory pathways use three different neurons to get information from sensory receptors at the periphery to the cerebral cortex. These neurons are designated primary, secondary and tertiary sensory neurons. In both pathways, primary sensory neuron cell bodies are found in the dorsal root ganglia, and their central axons project into the spinal cord.

In the dorsal column-medial leminiscus tract, a primary neuron’s axon enters the spinal cord and then enters the dorsal column. If the primary axon enters below spinal level T6, the axon travels in the fasciculus gracilis, the medial part of the column. If the axon enters above level T6, then it travels in the fasciculus cuneatus, which is lateral to the fasiculus gracilis. Either way, the primary axon ascends to the lower medulla, where it leaves its fasiculus and synapses with a secondary neuron in one of the dorsal column nuclei: either the nucleus gracilis or the nucleus cuneatus, depending on the pathway it took. At this point, the secondary axon leaves its nucleus and passes anteriorly and medially. The collection of secondary axons that do this are known as internal arcuate fibers. The internal arcuate fibers decussate and continue ascending as the contralateral medial lemniscus. Secondary axons from the medial lemniscus finally terminate in the ventral posterolateral nucleus (VPL) of the thalamus, where they synapse with tertiary neurons. From there, tertiary neurons ascend via the posterior limb of the internal capsule and end in the primary sensory cortex.

The anterolateral system works somewhat differently. Its primary neurons enter the spinal cord and then ascend one to two levels before synapsing in the substantia gelatinosa. The tract that ascends before synapsing is known as Lissauer’s tract. After synapsing, secondary axons decussate and ascend in the anterior lateral portion of the spinal cord as the spinothalamic tract. This tract ascends all the way to the VPL, where it synapses on tertiary neurons. Tertiary neuronal axons then travel to the primary sensory cortex via the posterior limb of the internal capsule.

It should be noted that some of the “pain fibers” in the ALS deviate from their pathway towards the VPL. In one such deviation, axons travel towards the reticular formation in the midbrain. The reticular formation then projects to a number of places including the hippocampus (to create memories about the pain), the centromedian nucleus (to cause diffuse, non-specific pain) and various parts of the cortex. Additionally, some ALS axons project to the periaqueductal gray in the pons, and the axons forming the periaqueductal gray then project to the nucleus raphe magnus, which projects back down to where the pain signal is coming from andMotor organization

The corticospinal tract serves as the motor pathway for upper motor neuronal signals coming from the cerebral cortex and from primitive brainstem motor nuclei.

Cortical upper motor neurons originate from Brodmann areas 1, 2, 3, 4, and 6 and then descend in the posterior limb of the internal capsule, through the crus cerebri, down through the pons, and to the medullary pyramids, where about 90% of the axons cross to the contralateral side at the decussation of the pyramids. They then descend as the lateral corticospinal tract. These axons synapse with lower motor neurons in the ventral horns of all levels of the spinal cord. The remaining 10% of axons descend on the ipsilateral side as the ventral corticospinal tract. These axons also synapse with lower motor neurons in the ventral horns. Most of them will cross to the contralateral side of the cord (via the anterior white commissure) right before synapsing.

The midbrain nuclei include four motor tracts that send upper motor neuronal axons down the spinal cord to lower motor neurons. These are the rubrospinal tract, the vestibulospinal tract, the tectospinal tract and the reticulospinal tract. The rubrospinal tract descends with the lateral corticospinal tract, and the remaining three descend with the anterior corticospinal tract.

The function of lower motor neurons can be divided into two different groups: the lateral corticospinal tract and the anterior cortical spinal tract. The lateral tract contains upper motor neuronal axons which synapse on dorsal lateral (DL) lower motor neurons. The DL neurons are involved in distal limb control. Therefore, these DL neurons are found specifically only in the cervical and lumbosaccral enlargements within the spinal cord. There is no decussation in the lateral corticospinal tract after the decussation at the medullary pyramids.

The anterior corticospinal tract descends ipsilaterally in the anterior column, where the axons emerge and either synapse on lower ventromedial (VM) motor neurons in the ventral horn ipsilaterally or descussate at the anterior white commissure where they synapse on VM lower motor neurons contralaterally . The tectospinal, vestibulospinal and reticulospinal descend ipsilaterally in the anterior column but do not synapse across the anterior white commissure. Rather, they only synapse on VM lower motor neurons ipsilaterally. The VM lower motor neurons control the large, postural muscles of the axial skeleton. These lower motor neurons, unlike those of the DL, are located in the ventral horn all the way throughout the spinal cord.

Spinocerebellar tracts

Proprioceptive information in the body travels up the spinal cord via three tracts. Below L2, the proprioceptive information travels up the spinal cord in the ventral spinocerebellar tract. Also known as the anterior spinocerebellar tract, sensory receptors take in the information and travel into the spinal cord. The cell bodies of these primary neurons are located in the dorsal root ganglia. In the spinal cord, the axons synapse and the secondary neuronal axons decussate and then travel up to the superior cerebellar peduncle where they decussate again. From here, the information is brought to deep nuclei of the cerebellum including the fastigial and interposed nuclei.

From the levels of L2 to T1, proprioceptive information enters the spinal cord and ascends ipsilaterally, where it synapses in Clarke’s nucleus. The secondary neuronal axons continue to ascend ipsilaterally and then pass into the cerebellum via the inferior cerebellar peduncle. This tract is known as the dorsal spinocerebellar tract.

From above T1, proprioceptive primary axons enter the spinal cord and ascend ipsilaterally until reaching the accessory cuneate nucleus, where they synapse. The secondary axons pass into the cerebellum via the inferior cerebellar peduncle where again, these axons synapse on cerebellar deep nuclei. This tract is known as the cuneocerebellar tract.

Motor information travels from the brain down the spinal cord via descending spinal cord tracts. Descending tracts involve two neurons: the upper motor neuron (UMN) and lower motor neuron (LMN) ^[2]. A nerve signal travels down the upper motor neuron until it synapses with the lower motor neuron in the spinal cord. Then, the lower motor neuron conducts the nerve signal to the spinal root where efferent nerve fibers carry the motor signal toward the target muscle. The descending tracts are composed of white matter. There are several descending tracts serving different functions. The corticospinal tracts (lateral and anterior) are responsible for coordinated limb movements^[3].

Injury

Spinal cord injuries can be caused by trauma to the spinal column (stretching, bruising, applying pressure, severing, laceration, etc.). The vertebral bones or intervertebral disks can shatter, causing the spinal cord to be punctured by a sharp fragment of bone. Usually, victims of spinal cord injuries will suffer loss of feeling in certain parts of their body. In milder cases, a victim might only suffer loss of hand or foot function. More severe injuries may result in paraplegia, tetraplegia, or full body paralysis (called Quadriplegia) below the site of injury to the spinal cord.

Damage to upper motor neuron axons in the spinal cord results in a characteristic pattern of ipsilateral deficits. These include hyperreflexia, hypertonia and muscle weakness. Lower motor neuronal damage results in its own characteristic pattern of deficits. Rather than an entire side of deficits, there is a pattern relating to the myotome affected by the damage. Additionally, lower motor neurons are characterized by muscle weakness, hypotonia, hyporeflexia and muscle atrophy.

Spinal shock and neurogenic shock can occur from a spinal injury. Spinal shock is usually temporary, lasting only for 24-48 hours, and is a temporary absence of sensory and motor functions. Neurogenic shock lasts for weeks and can lead to a loss of muscle tone due to disuse of the muscles below the injured site.

The two areas of the spinal cord most commonly injured are the cervical spine (C1-C7) and the lumbar spine (L1-L5). (The notation C1, C7, L1, L5 refer to the location of a specific vertebra in either the cervical, thoracic, or lumbar region of the spine.)

Spinal cord genomic map

The Allen Institute for Brain Science, on July 16, 2008, launched the online “Allen Spinal Cord Atlas” (backed by Paul Allen). Its first release included 4000 sets of digital images, showing spatial expression patterns for various genes.^[4] When complete, it is planned to map 20,000 genes in adult and juvenile mouse spinal cords. The spinal cord atlas is organized like the Allen Institute’s earlier atlas of the mouse brain.^[5][6]

See also

• Cauda equina
• Conus medullaris
• Meninges
• Spinal nerves
• Lumbar puncture
• Neutral spine
• Brown-Sequard Syndrome

References

1. ^ Maton, Anthea; Jean Hopkins, Charles William McLaughlin, Susan Johnson, Maryanna Quon Warner, David LaHart, Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. pp. 132–144. ISBN 0-13-981176-1.
2. ^ Saladin. Anatomy and Physiology, 5th Ed.
3. ^ Saladin. Anatomy and Physiology, 5th Ed.
4. ^ “Gene Search :: Spinal Cord”. mousespinal.brain-map.org. http://mousespinal.brain-map.org/. Retrieved 2010-02-23.
5. ^ msnbc.msn.com, Gene map charts spinal cord mysteries
6. ^ sciencenews.org/view, MapQuest for the mouse spinal cord

http://en.wikipedia.org/wiki/Spinal_cord

Etymology

The term tumour / tumor is derived, from the Latin word for “swelling” tumor and has come to the english language via the Old French tumour (contemporary French : Tumeur). In Britain the spelling “Tumour” is commonly used, in the US it is shortened to “Tumor”.

In its medical sense it originally meant an abnormal swelling of the flesh. In contemporary English, tumor is synonymous with solid neoplasm,^[2] all other forms of swelling being called swelling.^[3] This usage is common also in medical literature, where the nouns tumefaction and tumescence, derived from the adjective tumefied, are the current medical terms for non-neoplastic swelling.

Context

According to medical literature there are 5 distinguishing characteristics of an abnormality (infection, or malformation)

   * tumor (swelling)
   * calor (heath : markable temperature difference with the surrounding tissue)
   * rubor (redness : difference in colour)
   * dolor (pain)
   * functio laesa (dysfunction : the inability to use a limb or organ fully).

Its important that a tumor can be benign or malign (usually measured on a shifting or continously graded scale).

Not every swelling is a tumor according to the definition, swelling can occur due to increased production of fluid (oedema), a cell groth or both. Examples :

• A bump after a fall is primarily oedema, perhaps combined with soem red bloodcell from a localised microscopic hemorrage.
• In case of a carbuncle the content is oedema, infectious bacteria, white cells and pus
• In a Sebaceous cyst the cavity is filled with tallow-like material.

• A wart is considered a tumor albeit benign.
• Finally there are malignent tumors that are of cancerous origin like the Glioblastoma Multiform

Cause

A neoplasm is an abnormal proliferation of tissues, usually caused by genetic mutations. Most neoplasms cause a tumor, with a few exceptions like leukemia or carcinoma in situ.

A tumor may be benign, pre-malignant or malignant. The nature of the tumor is determined by a pathologist after examination of the tumor tissues from a biopsy or a surgical excision specimen.

References

1. ^ Tumor at Dorland’s Medical Dictionary
2. ^ Tumor in MedlinePlus Medical Encyclopedia
3. ^ Swelling in MedlinePlus Medical Encyclopedia

http://en.wikipedia.org/wiki/Tumour