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    Old 06-10-2004, 08:56 AM   #1
    conniej
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    Question Degenerative Stenosis and Degenerative Disc Disease

    My MRI results show Degenerative Disc Disease in the L5-S1 and to a much lesser degree at the L3-4 level, also Degenerative stenosis at the C5-6 level. I was hit by a military vehicle(I was a pedestrian) while in Desert Storm and have had severe back problems, headaches (including migraines)for over ten years and hand pain. Can anyone interpret what the MRI scan means and what type of treatment is offered for it? Thanks

     
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    Old 06-10-2004, 05:41 PM   #2
    Brooke79
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    Re: Degenerative Stenosis and Degenerative Disc Disease

    Hey There

    Here's a bit of information that may help you in understanding what degenerative disc disease is.

    Part of the confusion probably comes from the term "degenerative", which implies that it will get worse with age. While the disc degeneration is likely to progress over time, the associated pain usually does not get worse and in fact usually gets better over time.

    Another source of confusion is probably created by the term "disease", which is actually a misnomer. Degenerative disc disease is actually not a disease at all, but rather a degenerative condition that at times can produce pain from a damaged disc. It is quite variable in its nature and severity. With age, all people will exhibit changes in their discs consistent with degeneration. However, not all people will develop symptoms.

    Finally, some of the confusion probably comes from the medical community, as few medical professionals have yet to agree on what the term describes. Because few practitioners agree on what does and does not constitute a diagnosis of degenerative disc disease, very few medical textbooks even attempt to give an accurate description. Therefore, while many practitioners believe that degenerative disc disease is a common cause of low back pain in young adults, very few agree on the implications.

    The lumbar disc is a unique and well-designed structure in the spine. It is strong enough to resist terrific forces in multiple different planes of motion, yet it is still very mobile. The disc functions as a shock absorber between the vertebral bodies.

    The lumbar disc has been likened to a "jelly donut" and is comprised of:
    A firm, tough outer layer (annulus fibrosus)
    A soft inner core (nucleus pulposus)

    There is minimal blood supply to the disc, so the disc lacks any significant reparative powers. Unlike muscles, which have good blood supply, once a disc is injured it cannot repair itself.

    Annulus Fibrosus
    Nerves to the disc space only penetrate into the very outer portion of the annulus fibrosus. Even though there is little innervation to the disc, it can become a significant source of pain if a tear in the annulus reaches the outer portion and the nerves become sensitized.

    Nucleus pulposus
    The nucleus pulposus contains a great deal of very inflammatory proteins. If this inner disc material comes in contact with a nerve root, it will inflame the nerve root and create pain down the leg (sciatica or a radiculopathy). In the same manner, if any of the inflammatory proteins within the disc space leak out to the outer annulus and touch the pain fibers in this area it can create a lot of back pain.

    In the 1970’s, Kirkaldy-Willis first described the "degenerative cascade". He postulated that after an individual suffers a torsional (twisting) injury to the disc, the disc would degenerate in three general stages.

    First, there is significant dysfunction caused by the acute pain of the injury
    Next is a long phase of relative instability at that particular vertebral segment and the patient will be prone to intermittent bouts of back pain.
    Finally, the body re-stabilizes the segment and the patient experiences fewer episodes of back pain.
    Based on the observation that demographic studies show less back pain in elderly adults (over 60 years) than in younger adults (30 to 50 year-olds), he also concluded that this process happened over a period of 20 to 30 years.

    While this summary is a simplification of Kirkaldy-Willis’s extensive work, it lays the framework for what is known today. We do know that lumbar disc degeneration is a very common and natural process.

    The natural history of lumbar degenerative disc disease is relatively benign. The pain tends to be intermittent, and although at times the pain may seem to be getting worse, the painful symptoms are generally not progressive. While the degeneration will progress, the symptoms do not tend to get worse with the progression of the degeneration.

    Many patients worry that if they are in a lot of pain when they are only 35 years old, it will become much worse and they may be in a wheelchair by the time they’re in their sixties. However, if patients can find a way to manage their pain and maintain their function, the natural history is really quite favorable. With continued degeneration, all the inflammatory proteins within the disc space will eventually burn out, and the disc will usually become stiffer, thus decreasing micro-motion. In fact, someone who is 65 years old is actually less likely to have discogenic back pain than someone who is 35 years old.

    The natural degenerative process
    When we are born, the disc is comprised of about 80% water, which gives it its spongy quality and allows it to function as a shock absorber. As we age, the water content decreases and the disc becomes less capable of acting as a shock absorber.

    The proteins within the disc space also change composition, and most of us will develop tears into the annulus fibrosus (the outer hard core of the disc). We can all expect to have some level of disc degeneration by our sixth decade, yet we do not all have back pain.

    Magnetic Resonance Imaging (MRI scan) has contributed a great deal to our understanding of lumbar degenerative disc disease and the natural degenerative process. With the advent of MRI technology, good anatomic detail of the disc can be imaged and correlated with the individual’s back pain. Through studies with MRI scans, it was found that:

    A large number of young patients with chronic low back pain had evidence of disc degeneration on their MRI scans, and;

    Up to 30% of young healthy adults with no back pain had disc degeneration on their MRI scans.

    Therefore, degeneration on an MRI scan cannot be used as the sole diagnostic tool for lumbar degenerative disc disease. Disc degeneration present on an MRI scan is not synonymous with a diagnosis of degenerative disc disease and low back pain.

    It’s not exactly clear why some degenerated discs are painful and some are not. As with many common causes of back pain, there is probably a variety of reasons that discs can become painful. Some theories are:

    If a disc is injured, it may become painful because of the resultant instability from the disc injury, which in turn can lead to an inflammatory reaction that results in low back pain.

    Some people seem to have nerve endings that penetrate more deeply into the outer annulus than others, and this is thought to make the disc susceptible to becoming a pain generator

    Common symptoms
    Along with MRI scan results that show disc degeneration, there are some common symptoms that are fairly consistent for people with low back pain from degenerative disc disease.

    The typical individual with degenerative disc disease is an active and otherwise healthy person who is in their thirties or forties.

    Common symptoms include:

    The pain is generally made worse with sitting, since in the seated position the lumbosacral discs are loaded three times more than standing

    Certain types of activity will usually worsen the pain, especially bending, lifting and twisting

    Walking, and even running, may actually feel better than prolonged sitting or standing

    Patients will generally feel better if they can change positions frequently, and lying down is usually the best position since this relieves stress on the disc space

    Most patients will have some underlying chronic low back pain, with intermittent episodes of severe low back pain. The exact cause of these severe episodes of pain is not known, but it has been theorized that it is due to abnormal micro-motion in the degenerated disc that spurs an inflammatory reaction. In an attempt to stabilize the spine and decrease the micro-motion, the body reacts to the disc pain with muscle spasms. The reactive spasms are what make patients feel like their back has "gone out".

    The severe episodes of back pain will generally last from a few days to a few months before the patient goes back to their baseline level of chronic pain. The amount of pain is quite variable and can range from a nagging level of irritation to severe and disabling pain.

    In addition to low back pain, there may be leg pain, numbness and tingling. Even without pressure on the nerve root (a "pinched nerve"), other structures in the back can refer pain down the buttocks and into the legs. The nerves can become sensitized with inflammation from the proteins within the disc space and produce the sensation of numbness/tingling. Generally, the pain does not go below the knee.

    These sensations, although worrisome and annoying, rarely indicate that there is any ongoing nerve root damage. However, any weakness in the leg muscles (such as foot drop) is an indicator of some nerve root damage.

    Chronic pain versus acute pain
    One very important tenet in chronic pain is that the level and extent of pain does not equal tissue damage. Severely degenerated discs may not produce much pain at all, and discs with little degeneration can produce severe pain.

    In this manner, chronic pain is very different from acute pain. With acute pain, the severity of pain directly correlates to the level of tissue damage. This provides us with a protective reflex, such as the reflex to remove your hand immediately if you put it on something hot. In chronic pain, the pain does not have the same meaning – it is not protective and does not mean there is any ongoing tissue damage.

    Hopefully this has helped with your understanding but I'm wondering who orderedyou MRI initally? Did they interpret or explain the course of action to you?

    Hope this helps

    Brooke
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    October 2003 PLIF for L5S1 Spondy
    May 2004 PLIF revision RHBMP2

     
    Old 06-10-2004, 06:22 PM   #3
    julzntx
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    Re: Degenerative Stenosis and Degenerative Disc Disease

    Hi Brooke, I found that very helpful...do you have any additional information about foot drop?

    Juliet

     
    Old 06-10-2004, 09:34 PM   #4
    conniej
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    Re: Degenerative Stenosis and Degenerative Disc Disease

    [COLOR=Magenta]Thanks Brooke you are an Angel![/COLOR]

    Last edited by conniej; 06-10-2004 at 09:35 PM.

     
    Old 06-10-2004, 10:25 PM   #5
    Brooke79
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    Re: Degenerative Stenosis and Degenerative Disc Disease

    Hey There Julzntx,

    Sure, no probs, here's a bit on foot drop for you.

    Foot drop can be defined as a significant weakness of ankle and toe dorsiflexion. The foot and ankle dorsiflexors include the tibialis anterior, extensor hallucis longus, and extensor digitorum longus. These muscles help the body clear the foot during swing phase and control plantar flexion of the foot on heel strike. Weakness in this group of muscles results in an equinovarus deformity. This is sometimes referred to as steppage gait, because the patient tends to walk with an exaggerated flexion of the hip and knee to prevent the toes from catching on the ground during swing phase. During gait, the force of heel strike exceeds body weight, and the direction of the ground reaction vector passes behind the ankle and knee center. This causes the foot to plantar flex, and if uncontrolled, to slap the ground. Ordinarily, eccentric lengthening of the anterior tibialis, which controls plantar flexion, absorbs the shock of heel strike. Injury to the dorsiflexors, or to any point along the neural pathways that supply them, can result in foot drop.


    Frequency: Peroneal neuropathy caused by compression at the fibular head is the most common compressive neuropathy in the lower extremity. Foot drop is its most notable symptom. All age groups are affected equally, but it is more common in males (male-to-female ratio 2.8:1). Ninety percent of peroneal lesions are unilateral, and they can affect the right or left side with equal frequency.

    A foot drop of particular concern to orthopedic surgeons is a peroneal nerve palsy seen after total knee arthroplasty or proximal tibial osteotomy. Foot drop has an estimated prevalence of 0.3-4% after total knee arthroplasty and a 3-13% occurrence rate after proximal tibial osteotomy. Ischemia, mechanical irritation, traction, crush injury, and laceration can cause intraoperative injury to the peroneal nerve. Correction of a severe valgus or flexion deformity also has been suggested to stretch the peroneal nerve and lead to palsy. Postoperative causes of peroneal nerve palsy include hematoma or constrictive dressings.

    In a study, the relative risk of palsy was 2.8 times greater for patients who had received epidural anesthesia for total knee arthroplasty than for those who received general or spinal anesthesia. One postulation is that epidural anesthesia likely decreased proprioception and sensation, continuing to some extent postoperatively, allowing the limb to rest in an unprotected state susceptible to local compression. In addition, intraoperative neurological damage may not have been readily apparent in the immediate postoperative period due to ongoing effects of epidural anesthesia. In this same study, the relative risk of palsy was 6.5 times greater in patients who had a prior lumbar laminectomy.

    A series of patients who developed foot drop following primary hip arthroplasty were carefully examined and found to have spinal stenosis. Up to 70% of patients undergoing hip arthroplasty have electromyographic evidence of nerve injury, but they rarely have clinical symptoms. Patients with preexisting spinal stenosis are believed to be at increased risk for foot drop following hip arthroplasty due to this proximal compromise. This is the double-crush phenomenon described in more detail in the Pathophysiology section.

    Foot drop may be observed with direct injury to the dorsiflexors. A few cases of rupture of the tibialis anterior tendon leading to foot drop and suspicion of peroneal nerve palsy have been reported. This subcutaneous tendon rupture usually follows a minor trauma with the foot in plantar flexion.

    Compartment syndromes also may lead to foot drop. These are surgical emergencies and are not associated only with fracture or acute trauma. March gangrene, a form of anterior compartment syndrome, is thought to be due to edema and small hemorrhages in the muscles of the anterior compartment occurring after strenuous activity in individuals not accustomed to it. Deep posterior compartment syndrome also may result in foot drop as a late sequelae due to resultant contracture formation.

    Neurological causes of foot drop include mononeuropathies of the deep peroneal, common peroneal, or [B]sciatic nerves[/B]. Lumbosacral plexopathy, lumbar radiculopathy, motor neuron disease, or parasagittal cortical or subcortical cerebral lesions also can manifest as foot drop. These lesions can be differentiated through clinical and electrodiagnostic examinations.

    Foot drop also may be seen as a combination of neurologic, muscular, and anatomic dysfunction. Charcot foot is one example.


    Pathophysiology: The pathophysiology of nerve damage commonly causing foot drop is as follows:

    The functional integrity of an axon and its target depend on the continued supply of trophic substances synthesized in the neuronal perikaryon and transported down the axon, known as axoplasmic flow.

    A laceration interrupts this flow. A crush injury may compromise it as well.

    A double-crush phenomenon occurs when a proximal insult in a nerve root diminishes axoplasmic flow, making it more susceptible to injury.

    A distal lesion further compromises the flow, and clinical palsy results. This is the phenomenon thought to be responsible for the increased risk of foot drop after hip replacement in a patient with preexisting spinal stenosis. The spinal stenosis causes the proximal compromise, while intra-operative stretch of the sciatic nerve provides the distal insult.

    Whilst all this sounds technical it's only because all the anatomical sturctures have been listed in detail. Do you suffer with foot drop because of a leg injury or is it from sever nerve compression in the spine?

    Foot drop when talking about nerve compression from a vertebrae is simply the final progression from an untreated or too late treated nerve damage at a higher level (ie: not from the leg but the spine).

    Hope this helps

    Brooke
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    October 2003 PLIF for L5S1 Spondy
    May 2004 PLIF revision RHBMP2

     
    Old 06-10-2004, 10:27 PM   #6
    Brooke79
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    Re: Degenerative Stenosis and Degenerative Disc Disease

    Dear Conny,

    Thank you. I'm studying exercise physiology at uni and am a personal trainer..that and i have too much time on my hands i think. LOL..

    Brooke
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    October 2003 PLIF for L5S1 Spondy
    May 2004 PLIF revision RHBMP2

     
    Old 06-13-2004, 10:36 AM   #7
    skywater
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    Re: Degenerative Stenosis and Degenerative Disc Disease

    [QUOTE=Brooke79]Hey There

    Here's a bit of information that may help you in understanding what degenerative disc disease is.

    Part of the confusion probably comes from the term "degenerative", which implies that it will get worse with age. While the disc degeneration is likely to progress over time, the associated pain usually does not get worse and in fact usually gets better over time.

    Another source of confusion is probably created by the term "disease", which is actually a misnomer. Degenerative disc disease is actually not a disease at all, but rather a degenerative condition that at times can produce pain from a damaged disc. It is quite variable in its nature and severity. With age, all people will exhibit changes in their discs consistent with degeneration. However, not all people will develop symptoms.

    Finally, some of the confusion probably comes from the medical community, as few medical professionals have yet to agree on what the term describes. Because few practitioners agree on what does and does not constitute a diagnosis of degenerative disc disease, very few medical textbooks even attempt to give an accurate description. Therefore, while many practitioners believe that degenerative disc disease is a common cause of low back pain in young adults, very few agree on the implications.

    The lumbar disc is a unique and well-designed structure in the spine. It is strong enough to resist terrific forces in multiple different planes of motion, yet it is still very mobile. The disc functions as a shock absorber between the vertebral bodies.

    The lumbar disc has been likened to a "jelly donut" and is comprised of:
    A firm, tough outer layer (annulus fibrosus)
    A soft inner core (nucleus pulposus)

    There is minimal blood supply to the disc, so the disc lacks any significant reparative powers. Unlike muscles, which have good blood supply, once a disc is injured it cannot repair itself.

    Annulus Fibrosus
    Nerves to the disc space only penetrate into the very outer portion of the annulus fibrosus. Even though there is little innervation to the disc, it can become a significant source of pain if a tear in the annulus reaches the outer portion and the nerves become sensitized.

    Nucleus pulposus
    The nucleus pulposus contains a great deal of very inflammatory proteins. If this inner disc material comes in contact with a nerve root, it will inflame the nerve root and create pain down the leg (sciatica or a radiculopathy). In the same manner, if any of the inflammatory proteins within the disc space leak out to the outer annulus and touch the pain fibers in this area it can create a lot of back pain.

    In the 1970’s, Kirkaldy-Willis first described the "degenerative cascade". He postulated that after an individual suffers a torsional (twisting) injury to the disc, the disc would degenerate in three general stages.

    First, there is significant dysfunction caused by the acute pain of the injury
    Next is a long phase of relative instability at that particular vertebral segment and the patient will be prone to intermittent bouts of back pain.
    Finally, the body re-stabilizes the segment and the patient experiences fewer episodes of back pain.
    Based on the observation that demographic studies show less back pain in elderly adults (over 60 years) than in younger adults (30 to 50 year-olds), he also concluded that this process happened over a period of 20 to 30 years.

    While this summary is a simplification of Kirkaldy-Willis’s extensive work, it lays the framework for what is known today. We do know that lumbar disc degeneration is a very common and natural process.

    The natural history of lumbar degenerative disc disease is relatively benign. The pain tends to be intermittent, and although at times the pain may seem to be getting worse, the painful symptoms are generally not progressive. While the degeneration will progress, the symptoms do not tend to get worse with the progression of the degeneration.

    Many patients worry that if they are in a lot of pain when they are only 35 years old, it will become much worse and they may be in a wheelchair by the time they’re in their sixties. However, if patients can find a way to manage their pain and maintain their function, the natural history is really quite favorable. With continued degeneration, all the inflammatory proteins within the disc space will eventually burn out, and the disc will usually become stiffer, thus decreasing micro-motion. In fact, someone who is 65 years old is actually less likely to have discogenic back pain than someone who is 35 years old.

    The natural degenerative process
    When we are born, the disc is comprised of about 80% water, which gives it its spongy quality and allows it to function as a shock absorber. As we age, the water content decreases and the disc becomes less capable of acting as a shock absorber.

    The proteins within the disc space also change composition, and most of us will develop tears into the annulus fibrosus (the outer hard core of the disc). We can all expect to have some level of disc degeneration by our sixth decade, yet we do not all have back pain.

    Magnetic Resonance Imaging (MRI scan) has contributed a great deal to our understanding of lumbar degenerative disc disease and the natural degenerative process. With the advent of MRI technology, good anatomic detail of the disc can be imaged and correlated with the individual’s back pain. Through studies with MRI scans, it was found that:

    A large number of young patients with chronic low back pain had evidence of disc degeneration on their MRI scans, and;

    Up to 30% of young healthy adults with no back pain had disc degeneration on their MRI scans.

    Therefore, degeneration on an MRI scan cannot be used as the sole diagnostic tool for lumbar degenerative disc disease. Disc degeneration present on an MRI scan is not synonymous with a diagnosis of degenerative disc disease and low back pain.

    It’s not exactly clear why some degenerated discs are painful and some are not. As with many common causes of back pain, there is probably a variety of reasons that discs can become painful. Some theories are:

    If a disc is injured, it may become painful because of the resultant instability from the disc injury, which in turn can lead to an inflammatory reaction that results in low back pain.

    Some people seem to have nerve endings that penetrate more deeply into the outer annulus than others, and this is thought to make the disc susceptible to becoming a pain generator

    Common symptoms
    Along with MRI scan results that show disc degeneration, there are some common symptoms that are fairly consistent for people with low back pain from degenerative disc disease.

    The typical individual with degenerative disc disease is an active and otherwise healthy person who is in their thirties or forties.

    Common symptoms include:

    The pain is generally made worse with sitting, since in the seated position the lumbosacral discs are loaded three times more than standing

    Certain types of activity will usually worsen the pain, especially bending, lifting and twisting

    Walking, and even running, may actually feel better than prolonged sitting or standing

    Patients will generally feel better if they can change positions frequently, and lying down is usually the best position since this relieves stress on the disc space

    Most patients will have some underlying chronic low back pain, with intermittent episodes of severe low back pain. The exact cause of these severe episodes of pain is not known, but it has been theorized that it is due to abnormal micro-motion in the degenerated disc that spurs an inflammatory reaction. In an attempt to stabilize the spine and decrease the micro-motion, the body reacts to the disc pain with muscle spasms. The reactive spasms are what make patients feel like their back has "gone out".

    The severe episodes of back pain will generally last from a few days to a few months before the patient goes back to their baseline level of chronic pain. The amount of pain is quite variable and can range from a nagging level of irritation to severe and disabling pain.

    In addition to low back pain, there may be leg pain, numbness and tingling. Even without pressure on the nerve root (a "pinched nerve"), other structures in the back can refer pain down the buttocks and into the legs. The nerves can become sensitized with inflammation from the proteins within the disc space and produce the sensation of numbness/tingling. Generally, the pain does not go below the knee.

    These sensations, although worrisome and annoying, rarely indicate that there is any ongoing nerve root damage. However, any weakness in the leg muscles (such as foot drop) is an indicator of some nerve root damage.

    Chronic pain versus acute pain
    One very important tenet in chronic pain is that the level and extent of pain does not equal tissue damage. Severely degenerated discs may not produce much pain at all, and discs with little degeneration can produce severe pain.

    In this manner, chronic pain is very different from acute pain. With acute pain, the severity of pain directly correlates to the level of tissue damage. This provides us with a protective reflex, such as the reflex to remove your hand immediately if you put it on something hot. In chronic pain, the pain does not have the same meaning – it is not protective and does not mean there is any ongoing tissue damage.

    Hopefully this has helped with your understanding but I'm wondering who orderedyou MRI initally? Did they interpret or explain the course of action to you?

    Hope this helps

    Brooke[/QUOTE]

     
    Old 08-22-2005, 12:48 PM   #8
    P4ul
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    Re: Degenerative Stenosis and Degenerative Disc Disease

    Thank you very much 4 that Brooke79

    it was a great help, do you know why doctors try to blame back problems on DDD and in my case, although i never went to a doctor for back pain for 18 years they are now saying that since my accident, my MRI scan shows DDD and i would have had back problems in 3 years any way, why wouild i have back problems in 3 years, surley the problem is the damage to my nerve roots and disc protrusion, the tear in the thecal
    sac that is causing my back problems

     
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