Anatomy | Dermatome Connection | Dermatome Research | Dermatome Map | The Causes | A Cure? | MRI False Positives | Treatment | ESIs | The Odds | Risk Factors | Will I Recover? | The Outcome Studies| x

“Thou cold sciatica, cripple our senators, that their limbs may halt as lamely as their manners.” – William Shakespeare 1564.

As you may have gathered from the Shakespearian quote above, sciatica has been torturing mankind for years--probably since the time we evolved into upright creatures, which pressurized the intervertebral discs, in some cases, into failure. The first written reports of back pain and sciatica surfaced in the ancient medical text The Edwin Smith Surgical Papyrus, which was written in 1550 BC [10]. And, there has even been biblical mention of this disease [6]. I can personally attest to the horror, frustration, and true evil of this awful affliction--it was responsible for ending my hard sought Olympic metal in the late 80s and, more recently, my medical school journey in 2012.

Sciatica is a term that refers to a burning, stinging, and/or numbing pain that is felt in the buttock, thigh, leg, and/or foot; it may or may not be associated with low back pain but almost always travels below the knee and into the foot. (Note: other types of "referred pain" can mimic sciatica as it travels into the thigh and sometimes even the leg. Common sources of referred pain include the disc, the facet joints, and SI joints).

Sciatica affects approximately 5 to 10 of every 1000 people on an annual basis [3, 5, 33 ]. However, the life time prevalence of true below-the-knee sciatic was found to have affected 5% of men and 4% of women in a large population study[14].

The good news for those affected by sciatica for the first time (which may or may not be accompanied with lower back pain) is that 60% to 80% will recover to a nondisabling level within a period of 6 weeks (5,49). However, the recurrence rate (meaning that the chances that the sciatica will return) is approximately 10% to 15% [21]. So for some of you (like me), the problem will be an ongoing battle.

Some more grim statistical news: for those in whom suffer severe sciatica (bad enough to necessitate a trip to the hospital), more likely than not that pain will still be bothering you at the one-year time-point. More specifically, Balague et al. [22] demonstrated that only 29% of patients in whom suffered severe sciatica fully recovered at the 12 month time point. And 33% were lost to surgery within that 12 month period [22].

And what is the cause? In layman's terms, sciatica is caused by a pinching and/or irritation of one of the three lowest lumbar nerve roots that make up the giant sciatic nerve (that glowing red thing to the right). Any pinching / irritation of these delicate nerve roots may not only may cause lower back pain but may also ignite the entire sciatica nerve into a pain state!

Fig.#1 shows the general location of the giant sciatica nerve (yellow) which is the thickest and longest nerve in the human body. When this nerve gets aggravated (red), there is often a lot of pain involved over a large portion of the body (the lower limb). Note that there are three main 'spinal nerve roots' (within the lower back) that leave the spine and blend together within the pelvis and form the sciatic nerve. These are labeled L4, L5, and S1.

Not all lower extremity pain is classified as 'true sciatica': Sciatic pain may be classified as radicular pain (true sciatica) - pain radiating from the low back, past the knee, and into the dermatome (L4, L5, and/or S1) of the affected lumbar nerve root; or as non-radicular pain - pain radiating in the lower limb (usually not past the knee) in a non-dermatomal pattern (29). Bogduk defines radicular pain as a burning and/or numbing pain that presents in a band-like dermatomal pattern below the knee (7).

Now, if you already know the anatomy and understand what dermatomes are, you may jump over the anatomy lessons and continue here : The Causes of Sciatica

QUICK ANATOMY LESSION: The Formation of the Sciatic Nerve.

Fig.#3 Illustrates the anatomy of the origin of the sciatica nerve in greater detail; the backs of the vertebrae (posterior ring) have been cut away in order to see how the sciatic nerve is formed from the L4, L5 and S1nerve roots.

Spinal Nerve Roots: one motor root and one sensory root, leave the cauda equina and course towards their respective intervertebral foramen (IVF). As they 'transverse' towards the IVF, they come in close contact with the posterior surface of the intervertebral disc. Herniations of the disc can directly compress the passing spinal nerve root and cause back pain and sciatica.

Within the IVF the two spinal nerve roots blend into one larger nerve; this nerve is now called the 'Spinal Nerve'. The Spinal nerve quickly splits into a 'Ventral Rami', and 'Dorsal Rami'. The Dorsal Rami courses to the skin and muscle of the lower back and butt, the Ventral Rami courses downward to form the Sciatica nerve.

The only thing you really need to understand is that the L4, L5, and S1 Spinal Nerve Roots make up the sciatica nerve. Irritation to anyone of these nerve roots may ignite sciatica. For a better lesson and picture of real nerve roots, go to my 'Disc Anatomy' page and click the tab 'Real Nerve Anatomy'.

DERMATOMES & RADICULAR PAIN: Which Flavor of Sciatica do you have?

The first order of business is to clear-up some terminology issues: The terms Sciatica, Radicular Pain, Radiculopathy, Radiculopathic Pain, and Root Pain are all synonymous (mean the same). I prefer the term 'Radicular Pain' since it more accurately denotes that the patients 'pain' is coming from the spinal root level ('radic' indicates spinal nerve root) as opposed to a referred pain from a facet joint, SI joint, or other spinal structure. The term 'sciatica' is not very specific and only indicates that the patient has lower limb pain, which may or may not be caused from nerve root compression/irritation.

Since there are three possible nerve roots to irritate, and each of these nerve roots are connected to different regions of the 'skin' (sensory) and 'muscle' (motor) in the lower limbs, sciatica come in 'three different flavors': S1 radicular pain, L5 radicular pain, or L4 radicular pain (fairly rare). L3, L2, and L1 radicular pains (aka: radiculopathy) are also possible with high lumbar disc herniations; however, since these are not nearly as common and DON'T involve the sciatic nerve, they will not be discussed here.

Dermatome Research:

Did you know that most of the dermatome charts floating around the internet and on the walls of doctors' offices were based on investigations made over 35 years ago at best (31), and over 90 years ago at worst (30). Heck, some investigation date back to the 1800s. (32) Although in 1948 Keegan et al. had the right idea for developing dermatome charts (33), in that he studies and mapped the effects of disc herniations on the skin in the extremities, his results still couldn't confirm any of the prior work.

Nitta et al: Finally, Nitta et al. published the first investigation that was of high scientific design. (2) In 1992, this group of investigators successfully mapped the sensory-dermatomal distribution of the L4, L5, and S1 nerve roots. They gathered 71 patients, who were suffering disc herniation-associated radicular pain, and 'blocked' (anesthetized) their problematic nerve root with Xylocain; this was done under fluoroscopy to ensure the correct nerve roots were blocked. Next they carefully marked (aka: mapped) the areas on the patients skin that were numbed by the Xylocain nerve blocks. The results were tabulated and are shown below; however, the bottom line is this: "The L4 nerve root innervates (connects, gives-life-to) the medial side (inside) of the lower leg in 88% of the patients tested. The L5 nerve root innervates the side of the first digit (big toe) on the dorsum (top) of the foot in 82% of the patients. The S1 nerve root innervates the side of the fifth digit of the foot in 83% of the individuals." (2) I've based all of my dermatome maps on this investigation. (see below)

Although the majority of patients seem to share the same 'nerve root dermatomal distributions' (wiring), this investigation has clearly demonstrated that the neural anatomy of the lumbar spine does have some degree of variation, i.e., some 20% of the patients did NOT have the typical 'nerve root dermatomal distributions'. For example, in some patients, a L5 nerve root block would result in numbness of the S1 dermatome and not the anticipated L5 dermatome (2).

Kortelainen et al: In another giant study of radicular pain patterns, Kortelainen et al. also found that spinal nerve root irritation (via disc herniation) did NOT always project pain into the classic dermatomal regions; this was especially true of the S1 dermatome (1). After studying the radicular pain patterns of 403 disc herniation-induced radicular pain patients - all of whom eventually underwent discectomy surgery - they found the following:

In summary, sciatic pain projection into the L5 dermatome (top of the foot) was caused by the anticipated L4 disc herniation in 79% of the cases; by the unexpected L5 disc herniation in 18% of the cases; and by the really unexpected L3 disc herniation in 1.8% of the cases.
Pain project in into the S1 dermatome was caused by the anticipated L5 disc herniation in only 63% of the cases, and by a unexpected L4 disc herniation in 34% of the cases! As you can see by these results, S1 dermatomal pain (pain on the side of the foot) is not very accurate at predicting the level of nerve root compression/irritation (1) (I would note that the Kortelainen study was not as 'scientific' as the Nitta study, and we can only assume that the disc herniations all caused compression of the descending nerve root and NOT the transcending root. There was no mention of this very important factor in the paper!)

So, I hope I didn't loose too many of you in that last discussion! The bottom line is that you can't always trust the presence of pain in a dermatome to indicate which disc has herniated in the spine, although its still a moderately accurate method.

Let's go over where patients typically feel nerve root pain.

Dermatome Mapping: (Word of Warning: these pain patterns do have variability, and it is common for patients not to present exactly like these pictures depict--this is just another piece of the puzzle of pain.)

Without question, Nitta et al. has published the highest quality investigation on dermatomes (2); therefore, only his work will be reflected on the following dermatome maps:

S1 RADICULAR PAIN:

If the L5 disc herniates into the 'lateral recess' (which is where it usually does) and compresses / irritates the descending S1 nerve root, the patient may suffer an S1 radicular pain (aka: S1 root-pain, or S1 Sciatica). Fig.#4 shows the regions in the lower limb where the patient will most likely suffer the symptoms of S1 sciatica (2). As you can see, the majority of patients (75%) suffer the burning, stinging, and numbing pain of sciatica in the lateral foot, posterolateral leg, thigh, and butt, as well as, the bottom, outer 1/2 of the foot. These pains are the result of damage and irritation to the 'sensory portion' (portion of the nerve root which connects to skin) of the nerve root.

If the 'motor portion' (portion of the nerve root which connects to muscle) of the S1 nerve root is damaged or irritated by the disc herniation, the patient my suffer weakness and/or atrophy in the Gastrocnemius muscle (the calf), the peroneal muscles (foot evertors), and/or the muscles which flex or curl the 'big toe'. The Achilles' Reflex and Plantar Reflex may also be diminished or absent. If severe, the patient will be unable to do 'calf raises' with the effected foot. Calf raising is the 'gold standard' muscle test for S1.

L5 RADICULAR PAIN:

If the L4 disc herniates into the 'lateral recess' (which is where it usually does) and compresses / irritates the descending L5 nerve root, the patient may suffer an L5 radicular pain (aka: L5 root-pain, or L5 Sciatica). Fig. # 5 shows the regions in the lower limb where the patient will most likely suffer the symptoms of L5 sciatica (2). As you can see, the majority of patients (75%) suffer the burning, stinging, and numbing pain of sciatica in the top and inner surface (dorsum) of the foot, the outer-front of the leg, and the bottom of the big toe. These pains are the result of damage and irritation to the 'sensory portion' (portion of the nerve root which connects to skin) of the nerve root.

If the 'motor portion' (portion of the nerve root which connects to muscle) of the L5 nerve root is damaged or irritated by the disc herniation, the patient my suffer weakness in the Extensor Hallusis Longus muscle (muscle that lifts the big toe - classic finding) or the muscles that dorsi-flex the foot (lift the foot up) upward. If severe, the patient will be unable to 'walk on their heals' with their toes and ball-of-the-foot off the ground. There is no reliable reflex test for this nerve root.

L4 RADICULAR PAIN:

If the L3 disc herniates into the 'lateral recess' (which is where it usually does) and compresses / irritates the descending L4 nerve root, the patient may suffer an L4 radicular pain (aka: L4 root-pain, or L4 Sciatica). Fig. # 6 shows the regions in the lower limb where the patient will most likely suffer the symptoms of L4 sciatica (2). As you can see, the majority of patients (75%) suffer the burning, stinging, and numbing pain of sciatica in the top and inner surface (dorsum) of the foot, the outer-front of the leg, and the bottom of the big toe. These pains are the result of damage and irritation to the 'sensory portion' (portion of the nerve root which connects to skin) of the nerve root.

If the 'motor portion' (portion of the nerve root which connects to muscle) of the L4 nerve root is damaged or irritated by the disc herniation, the patient my suffer weakness in the quadriceps muscle (muscle that extend the knee). If severe, the patient will be unable to perform a squat or get out of a chair because. If the problem is severe, the patient will often have a diminished or absent Patellar Reflex (aka: knee jerk).

THE CAUSES OF SCIATICA: [ | Disc Herniation | The Conundrum | Discogenic Sciatica | Chemical Radiculopathy | Autoimmune Attack | ]

Now that we know what sciatica is, it's time to try and explain why it occurs--a task easier said than done!

As I see it, there are three possible "causes" of acute sciatica--excluding the more exotic forms: (1) disc herniation induced sciatica; that is, the posterior of the disc herniates into the adjacent sciatica nerve root, which in turn physically compresses and irritates that nerve root into a painful state; (2) grade V annular tear induced sciatica; that is, the disc rips open and allows biochemical (cytokines) to leak out and soak the adjacent sciatica nerve root(s), which in turn inflammes the sciatica nerve root into a painful state; and (3) discogenic sciatica; that is, the patient may experience a "referred" pain (that often is dermatomal) down the lower limb from severe irritation of the tiny sensory nerve fibers (sinuvertebral nerve) that live within the outer 1/3 of the annulus of the disc. This is NOT an irritation of the actual sciatica nerve but simply the patient's preception of sciatic nerve irritation--like the left arm pain felt by someone suffering a heart attack.

In a general sense, disc herniation (25, 70) and/or stenosis are by far the most frequent causes of compressive sciatica (67-70), there are, however, other more exotic causes of sciatica; such as, Spondylolisthesis, Piriformis Syndrome, Obturator Syndrome, Far-Out Syndrome, Synovial Cysts, Hypertrophied Epidural Vessels, Gas-containing Ganglion cysts, and Tumors. These rare causes are beyond the scope of this paper.

And before we dig deeping into the phenomenon of sciatica, here is another important fact that need be remembered: the mechanism of lower limb pain (sciatica) is most likely VERY complex and is not nearly as simple as the disc herniates, pinches the nerve, and you get pain. There are many other factors (some of which that are still unknown) that contribute to the pain of sciatica. In fact, recently we have learned from the work of Karppinen et al. that neither the amount of nerve root compression nor the size of the disc displacement (posterior outpouching of the disc) relates to the amount of pain (VAS) or disability (Oswestry) the patient suffers (70). Those 'other factors' are still being debated within the research community, but proinflammatory cytokines (especially TNF-alpha) are certainly involved (96-99). Pain 'referred' directly from the disc may also have a role in the sensation of sciatica (11,12).

Let talk a moment about the number one cause of sciatica: The disc herniation.

The Lumbar Disc Herniation:

It has been known for years and is generally accepted that a compressive lumbar disc herniation is a common cause of sciatica (25,70), and the patients symptoms will usually depend upon which spinal nerve root is involved. Since 95% of lumbar disc herniations occurs at either the L4 or L5 disc level (290), it's not at all surprising that sciatica is so very commonly. This high frequency of L4 and L5 disc herniation is also the reason why most EMG-confirmed radiculopathy occurs in the L5 or S1 root (290).

I'm not going to go into the mechanism of disc herniation on this page since it has been covered in depth on the 'Disc Herniation Page'. But, figure #3 depicts how this mechanism works:

Fig. #3 demonstrates a paracentral herniation (pink) of the L5 disc that is located within a region called the lateral recess. The herniation is compressing the right S1 nerve root which may cause 'radicular pain' in this patient's S1 dermatome (right lateral foot). This patient may also have a loss of 'motor function' in the right lower limb. More explicitly, a loss of muscle strength in gastrocnemius (calf), and peroneal muscles. There might also be a lost Achilles' reflex.

THE SCIATICA-HERNIATION CONUNDRUM:

So you think you've got this sciatica thing figured out? It's easy right: the disc herniates, pinches the sciatica nerve root, and pain occurs in the distribution of the sciatica nerve. NOT SO FAST!

Although disc hernation-induced sciatica certainly does occur, it's common knowledge that not all disc herniations cause sciatica. Some people have severe sciatica without any evidence of compressive disc herniation at all!

In a recent investigation by Karppinen et al. [Karppinen], it was demonstrated that 20% of severely acute sciatica patients had no compressive disc herniation on MRI; all MRI images were negative for protrusion, extrusion, and/or sequestration, yet these patients were suffering from severe back and leg pain! (70) These researchers concluded that the severity of sciatica and back pain are NOT related to the amount of the disc displacement (size of the herniation) or the amount of spinal nerve root compression! VAS and Oswestry scores were virtually the same for both disc herniations patients (disc herniation = protrusion, extrusion, & sequestration) as they were for disc bulge or normal disc patients! (I would add that patients who were applying for early retirement were removed from this study which enhances its validity). (70)

So, if its not a compressive disc herniation that's causing the suffering, then what it?

One possible explanation was put forth by both Ohnmeiss et al. (619,620) and Milette et al. (621) These investigators experimentally demonstrated that disruptions within the substance of the disc (anular tears) not only caused low back pain but also caused ‘referred pain’ into the lower limb; we may call this referred lower limb pain ‘discogenic sciatica’.   [Ohnmeiss Paper & Milette Paper]

Another explanation is based upon the investigations of Olmarker et al.   This group has repeatedly demonstrated that the application of nucleus pulposus upon the spinal nerve root can create marked morphological change (axon damage) and functional change (decreased conduction speed) to the micro-anatomy of that nerve root, as well as cause ‘pain-related behaviors’ to occur within the test animals (790-795).  

Therefore, if this nucleus pulposus get ‘loose’ in the epidural space (most likely from a grade 5 posterior anular disc tear), it may well cause the pathological spinal nerve root changes described by Olmarker (790-795) and result in a painful sciatica syndrome without nerve root compression.   Researchers have termed this phenomenon “Chemical Radiculopathy” (788,789).

The final theory on non-compression induced sciatica implicates the activation of the patients own immune system against the nucleus pulposus-soaked nerve root (800,801). This ‘auto-immune’ type reaction may help perpetuate the syndrome of chronic sciatic pain.

Whatever the cause, it is clear that non-compressive disc defects (bulges and contained herniations) are just as painful and disabling as the classic large compressive disc herniation.   Therefore the symptoms of sciatic patients without disc herniation in MRI should not be dismissed by the doctor.  

DISC HERNIATIONS IN NORMAL ASYMPTOMATIC PEOPLE:

It's common knowledge that not all compressive disc herniations (as seen on MRI and CT scan) will result in back pain and/or sciatica and are commonly found in completely asymptomatic people (40-47). I've got a page on the phenomenon of disc herniations in asymptomatic people ( here: Abnormal MRI in Pain-Free People ) , but would like to give you all an example and then the 'bottom line' of my research into MRI false positives:

The Bottom-line on the 'False Positives' of MRI:

If I were to gather a group of middle age folks (45 average age) who have NEVER had back pain before and shoot MRIs on them all, here's what we would find: 38% would have disc bulges, 37% disc protrusions (aka: contained herniations), 11% disc extrusions (aka: non-contained herniations), 0% disc sequestrations (aka: free fragments) and 4% nerve root compression by the disc herniation. (40-43)

Here's a recap of the main investigations of accuracy of MRI: See the full page here: (Abnormal MRI in pain-free people)

The below chart shows the percentages of false positive MRI readings for each type of disc herniations (bulge, protrusion, or extrusion) and for nerve root compression for a disc herniation. Remember, none of the below patients had ever had lower back pain before yet about 3/4 of them had some type of abnormal disc presentation:

And finally, another well known conundrum: the fact that patients radicular symptoms, clinical neurological presentation, and pain presentation do NOT always match the level of disc herniation (291)!

So you see, when it comes to diagnosing the cause of disc herniation-associated sciatica, sometimes things are not always so 'black and white'!

Discogenic Sciatica: Referred pain from the Disc mimics radicular pain.

Recently, we have learned that the intervertebral disc itself may ‘refer’ pain down into the lower limbs in a dermatomal like pain pattern (11, 621). The theory of Discogenic Sciatica is complex and still controversial but can be explained as follows: just as a person who is having a heart attack will often suffer a 'referred pain' down the left arm, a person with massive pain generation within a disrupted and/or diseased lumbar disc may also suffer a referred pain down into the leg, often in a dermatomal-like pain pattern. Ohnmeiss et al. has extensively investigated this theory and has done a good job at proving its existence (11). This phenomenon can make it very difficult to ascertain just exactly what is causing a patient’s sciatica: Is it from a disc herniation compressing the adjacent nerve-root, or from a severely internally disrupted disc referring pain, or a combination of both? This ‘referred pain’ from the disc into the lower back and/or lower limbs is called ‘Discogenic Pain’ or as I like to call it, ‘Discogenic Sciatica’.

Milette et al. has also investigated the phenomenon of discogenic referred pain and demonstrated that disruptions within the disc can indeed refer pain into the back and down the leg. Read the full paper here: (Milette - 1995: Discogenic Sciatica)

I will be devoting an entire page to this theory in the near future and will be presenting some real cases of 'Discogenic Sciatica' from an upcoming investigation that I will be writing with Dr. Jinfu Lin of Taiwan China.

Chemical Radiculopathy: A leaking disc may result in radicular pain.

Another possible cause of sciatica is called Chemical Radiculopathy (257,258). This is believed to occur when the disc rips open and leaks without disc bulge or herniation.   It has been proposed that certain biochemicals (especially proinflammatory cytokines) may ‘leak’ from a completely disrupted disc (a disc with a hole in it), soak the adjacent nerve root and cause a 'Biochemical irritation' to that nerve root, hence inducing radicular pain(153,155.550). Again we have a situation where radicular pain may occur without the presence of a disc herniation!

Although this theory is relatively new, I'm convinced that it happens all the time. Not only have I seen this time and time again in my own clinical practice, I've just recently seen it occur in two of our local medical doctors who I personally know (one's a neurosurgeon and the other's a neurologist). Both had come down with real root-related sciatica (confirmed by EMG) despite having a completely normal looking MRI!

Numerous animal investigations has confirmed that the presence of nucleus pulposus on spine nerve roots is a 'bad thing'(551,553-558,560)! Nucleus pulposus and the biochemical Tumor Necrosis Factor - alpha have been linked to some truly damaging effects on spinal nerve-roots, such as: Wallerian degeneration of the axons within the nerve root; a characteristic myelin injury to the axon (551,553-555); a local increase in vascular permeability with the nerve root (556,557); intravascular coagulation within the nerve root (551,558); reduced intraneural blood flow within the nerve root(560); leukotaxis (558); macrophage recruitment within the nerve root; and a splitting of the myelin sheath from the axon (140, 141).

AUTOIMMUNE ATTACK:

The final theory on non-compression induced sciatica implicates the activation of the patients own immune system against the nucleus pulposus-soaked nerve root (800,801). This ‘auto-immune’ type reaction may help perpetuate the syndrome of chronic sciatic pain. Again, this is a very complex subject, and I will be devoting an entire page to it in the near future.

RISK FACTORS FOR THE DEVELOPMENT OF SCIATICA:

Beside having bad genetics for disc building material, which is probably the number-one risk factor for disc herniation-associated sciatica, the line of work that you choose may significantly increase or decrease your livelihood of developing disc herniation-associated sciatica. Research has indicated that 'heavy manual labor' and 'sedimentary work' are the two types of employment most frequently associated with the development of sciatica (195). More explicitly, investigations have demonstrated that frequent heavy lifting, (193,194) frequent twisting and bending, (193,194) exposure to vibration,(192,193) and sedentary activity (192,195) [190] all increase the risk of developing sciatica.

It seems the 'safest' type of work (the work in which less people develop sciatica) is that which combines a combination of sitting standing and physical activity (195).

A CURE FOR SCIATICA? INFLIXIMAB & ETANERCEPT (False hope: 2005 update )

It is currently believed by some investigators that the cytokine 'Tumor Necrosis Factor - alpha' (TNF-a) is one of the "smoking guns" of sciatica as it has been shown to be directly involved in nucleus pulposus-induced nerve root damage (4). It has been experimentally demonstrated in both the animal and human that the chimeric antibody 'Infliximab' stops and minimizes nerve root damage after the application of nucleus pulposus upon a nerve root (animal studies) and significantly decreases the lower limb pain in acute sciatica sufferers (140). Although the use for Infliximab looks promising to combat sciatica, a larger randomized study is desperately needed to confirm the results of Karppinen's initial pilot study of 2003 (140) and recent 2005 one year follow-up on these 10 patients (900).

Although Infliximab has already been proven safe and effective for the treatment of other diseases of the body, such as rheumatoid arthritis (144,145), plaque-type psoriasis (146), active ankylosing spondylitis (147), and Crohn’s disease (148), further investigation is needed before sciatica can be added to the list of indications for the drug Infliximab (140).

UPDATE (2005) Unfortunately, It would now appear that Infliximab is no more effective than placebo for the treatment of disc herniation related sciatica. In a larger randomized controlled investigation, Karppinen et al. discovered that patients given placebo (fake) injections obtained just as much sciatic pain releif as those who got the injection of the "ultra-expensive" infliximab:

UPDATE 2007:

Now, Etanercept, another TNF-a inhibitor (a fusion protein) has been shot down by a grade "A" randomized placebo-controlled double blind trial. In 2007, John Hopkins School of Medicine's SP Cohen, et al published the results of their investigation into the off-lable use of Etanercept for the treatment of sciatica. Unfortunately, they discovered that this very expensive treatment is no better than that of a placebo (suger pill). They concluded, "A single low dose of intradiscal etanercept does not seem to be an effective treatment for chronic radicular or discogenic low back pain."

TREATMENT OPTIONS: [Surgery Timing | Surgery Indications | Treatment Guidelines | Epidural Steroid Injections ]

Without question, the best treatment for non-complicated, non-emergency sciatica is passage of TIME. Even the worst cases of sciatica may spontaneously resolve with time (albeit a long time), and even some very large disc extrusions may completely be reabsorbed by the body (23), hence decompressing the nerve root naturally. BUT, if you are a candidate for surgery and are not improving with care at all, then delaying the surgery seems to decrease your chances for a successful surgical out come (305).

FOUR INDICATIONS FOR SURGERY:

The American Academy of Orthopedic Surgeons and Alf Nachemson – who is the number one spine researcher in the world - (18) recommends the following conditions be met before decompressive surgery is offered:

The only ABSOLUTE indication for surgical intervention, however, is if the patient develops a loss of bowl or bladder control (cauda equina syndrome); if the patient develops severe progressive motor loss in the lower limbs, such as foot-drop; or if the patients has severe debilitating pain.  

Several high quality outcome assessment investigations have shown that even patients with confirmed radiculopathy (nerve root damage) that meet the 'four criteria' for surgery often do 'well' with non-surgical treatment (77 - Saal & Saal); furthermore, although patients who undergo discectomy seem to get better faster (rarely 100% better), in the long-run (4 to 7 years) the non-surgical patients obtain nearly the same improvement in terms of pain relief and functional outcome. (78 - Weber)

SURGERY TIMING: When to "Pull the Trigger" and Try Surgery?

It is generally agreed upon, assuming the patient is NOT improving, that one should not wait too long before undergoing decompression via discectomy. The the experts can't seem to agree upon is how long the patient should be allowed to suffer. The forthcoming investigations all yield different opinions on when surgery should be performed; however, they all agree that a suffering patient should not wait longer than one year. The average time is currently 4.6 months, so waiting longer than this might decrease your chances of having a successful discectomy. I would seem to be living proof of this, i.e., I waited 15 months and my surgery failed miserably.

Treatment Guide-lines:

I’ve read a tremendous amount of research and picked-the-brain of many a doctor during my own battle with sciatica. Based on my research and personal experience I've developed some recommendations for the treatment of sciatica (*remember, these are to be discussed with your primary treating physician and this is not to be construed as medical/car practical advice):

Epidural Steroid Injections:

We know that it is not all about physical compression (via disc herniation) of the nerve root. It is well-established that an inflammatory process (sparked by biochemicals called cytokines) has just as much to do with the pain syndrome of sciatica. And the best way to stop the damaging inflammation cascade is at the first step in the cycle [membrane phospholipids --> Arachidonic acid has catalyzed by phospholipase A2 ( PLA2)]. More specifically, the injected cortisone will inhibit the enzymes PLA2, as well as COX2, which in turn will snuff out the damaging inflammatory cycle that most likely is occurring within the adjacent nerve roots.

Although many medical clinics are injecting corticosteroids epidurally (between the lamina), the evidence for this administration route is still lacking [48]. Therefore, I continue to suggest that epidural steroid injections be performed only transforaminally under the guidance of fluoroscopy.

Also, make sure that lidocaine (the stuff that deadens your nerves at the dentist office) is included with this steroid injection. This can be extremely diagnostic, for the lidocaine will immediately blot out the patient's pain if that is indeed the nerve root that is swollen and inflamed. The patient should notice almost immediate pain relief following the injection, which will initially wear off (much to the patient's chagrin) after several hours. Make sure the patient keeps a pain journal and give them a heads-up for that crucial few hours postinjection. The steroid component of the injection will kick in after a few days to relieve the pain again and this time the relief should be for a few months if not longer. But remember, it is the injection of that lidocaine and its effect for the first three hours that is diagnostically important for this procedure; the more permanent pain relief will occur because of the steroid in a day or two following the injection.

WHAT ARE MY CHANCES OF GETTING SCIATICA?

For the answer to this question, we must turn the giant population based survey studies which are mostly flawed with respect to sciatica, for they don’t differentiate between true root related sciatica, and fake sciatica (referred lower limb pains from the SI joint, intraspinal ligaments, and/or facet joints etc).

From these less specific studies we have learned that the life-time chance (prevalence) for developing ‘generic sciatica’ (sciatica of unknown cause) is about 35%; this number has been pretty well substantiated in other investigations as well (181,183-186).   Over the course of each year, about 1% of the North American population will suffer an attack of sciatica (9); that equates to about 4.9 MILLION cases per year!

Only two groups of investigators has had the intelligence to address the life-time prevalence of true root-related sciatica: Heliovaara et al. found that 5% of men and 4% of women will develop nerve root-related sciatica at some point in there life (181).   These numbers were later confirmed by Manninen P, et al in 1995 (182).  

The differentiation between the life-time chances of generic sciatica (35%) and true root-related sciatica (5%) demonstrates that true root-based sciatica is a relatively rare phenomenon.  (Don’t we feel special?)

There are no studies that have investigated the prevalence for ‘discogenic pain/sciatica’ in the population, but I’m guessing it to be around 1% or 2%.

WILL I RECOVER FROM SCIATICA? [ Pertinent Research outcome ]

The short answer: probably not 100% if your sciatica is a true radiculopathy confirmed by EMG and/ or severe.

Unlike lower back pain, sciatica has a more prolonged and less certain recovery period. For the general non-radiculopathic sciatica, 40% to 50% of those affected will completely recovery within 4 weeks (19,20), and 88% will recovery within 6 months (8); however, 5% to 10% will not recover and require surgical decompression (9).

For us patients with 'real' disc herniation-associated radicular pain (radiculopathy), the outcome is less favorable, as has been demonstrated by several well-written investigations: Only 37% will completely recovery from there radicular pain (sciatica) by 3.5 years! This number was derived by averaging out all the complete recovery patient from the major five outcome studies of our time. (here)

The Outcome Studies:

The Saal Study:

The Saal brothers’ 1989 outcome study is undoubtedly the best paper to date on the recovery-rates for radiculopathy-related sciatica:   the Saals followed 58 patients who had confirmed disc herniation-induced radiculopathy (via MRI & EMG). They had all failed ‘passive conservative care’ and were put through the authors aggressive conservative care program, which included special exercises, medications, epidural steroid injection and physical therapy.   After 2 ½ years, only 30% of the patients reported a full recovery and 10% were lost to surgery.   The good news - if you’re not an athlete - is that 90% of the patients returned to their original work and recovered enough to at least be able to perform some limited recreational activities (77).

The Atlas Study:

Atlas et al. followed 220 patients that were treated surgically for disc herniation-induced sciatica and 183 patients who were non-surgically treated for the same. At five years only 28% of the surgically treated patients reported that their pains were completely gone. The conservatively treated group faired even worse, in that only 12% reported a complete resolution of their symptoms (15).

The Nykvist Study:

Another outcome study by Nykvist et al. found that after five years of either surgical or non-surgical treatment; 82% of the non-surgically treated group and 62% of the surgically treated group still suffered with at least some degree of sciatica (17)!

The Weber Study #1:

Weber et al. studied the outcome for a group of 208 non-surgically treated patients, all of whom had “root symptoms” associated with sciatica. After one year, 30% of the patients had reduced capacity in work, and restrictions of leisure activity and only 50% reported no pain at work or leisure (19).

The Volvo Award Winning Weber Study:

In the only quality ‘randomized’ outcome study to date, Henrik Weber followed a group of 126 sciatica patients who were ‘randomly’ assigned to either surgery or non-surgical care. All of these patients were considered ‘boarder-line’ surgical candidates and were followed for over 10 years. Over that 10 year period, only 5% of the patients were lose, which gives this Volvo Award Winning study excellent predictive value. At four years post ‘treatment’, only 66% of the surgical patients were “completely satisfied” with their outcomes, versus only 52% of the conservatively treated group. At 10 years, only 58% of the surgical group were completely satisfied (some had worsened), and 56% of the conservative group were completely satisfied. At 10 years only 2% of both groups reported residual lower limb pains (sciatica), which was greatly improved from the 37% and 23% residual sciatica reported sciatica at 4 years (16).

The Balague Study of 1999: (126) This group of Swiss and American investigators study the outcomes of 82 'severe sciatica patients' - patients were hospitalized because of the severity of their sciatica. 33% of the patients were lost during the one year follow-up period to surgery, although they were still followed up. As for the recovery of this cohort, the authors stated the following, "...a substantial percentage of patients with acute severe sciatica had not recovered by 1 year after discharge." More explicitly, only 21 (29%) of the all 82 patients were "essentially" pain free at one year. Interestingly, only 74% of these patients had disc herniation on MRI, and only 62% had a positive EMG!

The Bottom Line:

Top | Home |

REFERENCES:

1) Kortelainen P, et al. “Symptoms and signs of sciatic and their relation to the location of the lumbar disc herniation.” Spine – 1985; 10:88-92

2) Nitta H, et al. "Study on dermatomes by means of selective lumbar spinal nerve root block." Spine 1993;18:1782-

3) Anderson GBJ. "The epidemiology of spinal disorders." In: Fermoyer JW, ed. The adult spine. New York:Raven Press:1997

4) Igarashi T. et al. "Volvo Award Winner 2000: Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology: Molecular, histologic, and behavioral comparisons in rats." Spine 2000; 25:2975-80

5) Van de Velden J, de Bakker DH. Basisrapport: morbiditeit in de huisartsenpraktijk. Utrecht: Nivel;1990

6) Fardon D. “Biblical pain:   Did Jacob have Sciatica?” Spine J 2002; 2(3):228

7) Bogduk N. "Clinical Anatomy of the Lumbar Spine and Sacrum. New York: Churchill Livingstone, 1997.

8) Hakelius A, “Prognosis in sciatica: a clinical follow-up of surgical and non-surgical treatment.” Acta Orthop Scand 1970; Suppl 129

9) Frymoyer J, “Back pain and sciatica.” N Engl J Med – 1988; 318:291-300

10) Breasted JH (1930) Edwin Smith Surgical Papyrus, in Facsimile and Hieroglyphic Transliteration and with Translation and Commentary, 2 vols. Chicago: University of Chicago Oriental Publications.

11) Ohnmeiss DD, et al. "Degree of disc disruption and lower extremity pain" Spine 1997; 22(14):1600-1605

12) Ohnmeiss DD, et al. "Relation between pain location and disc pathology: a study of pain drawings and CT/discography." Clin J Pain 1999;15:210-7.

14) Herkowitz HN, Dvorak K, Bell G, et al. "The Lumbar Spine-3rd edition." Lippincott Williams & Wilkins 2004; Philadelphia, PA

15) Atlas SJ, et al. "Surgical & nonsurgical management of sciatica secondary to a lumbar disc herniation: Five year outcomes from the Maine Lumbar Spine Study." Spine - 2001; 26(10):1179-1187

16) Henrik Weber, '1982 Volvo Award in Clinical Science' "Lumbar Disc Herniation: A controlled, Prospective Study with Ten Years of Observation." Spine - 1983; 8(2):131-140

17) Nykvist F, et al. "A prospective 5-year follow-up study of 276 patients hospitalized because of suspected lumbar disc herniation" Int. Disabil. Studies - 1989; 11(2):61-67

19) Weber H, et al. "The Natural Course of Acute Sciatica with Nerve Root Symptoms in a Double-Blind Placebo-Controlled Trial" Spine 1993; 18(11):1433-1438

20) Andersson GJB et al. “The intensity of work recovery in low back pain.” Spine 1983; 8:880-884

21) Biering-Sorensen F, Thomson C (1986) "medical, social and occupational history as risk indicators for low back trouble in the general population." Spine 11:720-5

22) Balague F, Nordin M, et al. "recovery from severe sciatica." Spine 1999; 24:2516-24.

23) Saal JA, et al. “The natural history of lumbar intervertebral disc extrusions treated nonoperatively.” Spine – 1990; 15:683-686

25) Mixter WJ, Barr JS. “Rupture of the intervertebral disc with involvement of the spinal canal.” N Engl J Med 1934; 211:210-5

29) van Akkerveeken PF. “Pain patterns and diagnostic blocks.” In: Wiesel SW, Weinstein JN, Herkowitz H, eds. The Lumbar Spine. Philadelphia: W.B. Saunders Company, 1996:105-22.

30) Foerster O: "Zur kenntniss der spinalen segmentinnervation der muskelin." Neurol Zbl 32:1202-1214, 1913

31) Uihlein A, et al. "neurologic changes, surgical treatment, and post operation evaluation. Symposium: Low back and sciatic pain." J Bone Joint Surg 50A:1, 1968

32) Bolk L. "Die Segmentaldifferenzigrung des menschlichen Rumpfes und seiner Extremitaten." morphol Jahrb 1898 - 1899; 25:465-543; 26:91-211; 27:630-711; 28:105-46

33) Konstantinou K, Dunn KM. "sciatica: review of epidemiological studies and prevalence estimates." Spine 2008; 33:2464-2472.

40) Jensen MC, et al. “MRI imaging of the lumbar spine in people without back pain.” N Engl J Med – 1994; 331:369-373

41) Boden SD et al. “Abnormal magnetic resonance scans of the lumbar spine in asymptomatic subjects: A prospective investigation.” J Bone Joint Surg Am 1990; 72A:403-408

42) Weishaupt D et al. “MRI of the lumbar spine: Prevalence of intervertebral disc extrusion and sequestration, nerve root compression and plate abnormalities, and osteoarthritis of the fact joints in Asymptomatic Volunteers.” Radiology – 1998; 209:661-666

43) Boos N, et al. “1995 Volvo Award in clinical science: The diagnostic accuracy of MRI, work perception, and psychosocial factors in identifying symptomatic disc herniations.” Spine – 1995; 20:2613-2625

44) Powell MC, et al. “Prevalence of lumbar disc degeneration observed by magnetic resonance in symptomless women.” Lancer – 1986; 2:1366-7

45) Boos N, et al. “Natural history of individuals with asymptomatic disc abnormalities in MRI: Predictors of low back pain-related medical consultation and work incapacity.” Spine 2000; 25:1484

46) Borenstein G, et al. “The value of magnetic resonance imaging of the lumbar spine to predict low-back pain in asymptomatic individuals: A 7-year follow-up study. J Bone Joint [am] 2001; 83:320-34

47) Wiesel SW, et al. “A study of computer-associated tomography: I. The incidence of positive CAT scans in asymptomatic group of patients.” Spine 1984;9:549-51

48) Leonardi M, Pirrman CW, Boos N (2006). "injection studies in spine disorders." Clin Orthop Relat Res 443:168-82.

49) Vroomen PC, de Krom MC, Knottnerus JA. Predicting the outcome of sciatica at short-term follow-up. Br J Gen Pract. 2002; 52:119-123.

50) Nygaard OP, Kloster R, Solberg T. Duration of leg pain as a predictor of outcome after surgery for lumbar disc herniation: a prospective cohort study with one-year follow-up. J Neurosurg. 2000; 92 (2 supppl): 131-134.

51) Jannson KA, et al. health-related quality of life in patients before and after surgery for a herniated lumbar disc. J Bone Joint Surg Br. 2005; 87:959-964.

53) McCulloch JA (1996) Focus issure on lumbar disc herniation: macro-and microdiscectomy." Spine 21:45S-56S.

67) Coventry MB, et al. “The intervertebral disc: Its microscopic anatomy and pathology: Part II. Changes in the intervertebral disc concomitant with age.” J Bone Joint Surg 27A:233-252

68) Mixter WJ, Barr JS. “rupture of the intervertebral disc with involvement of the spinal canal.” N Engl J Med 211:210-214 1934

69) Vernon-Roberts B, Pirie CJ. “Degenerative changes in the intervertebral disc of the lumbar spine and their sequealae.” Rheum Rehab 16:13-21 1977

70) Karppinen J, et al. “Severity of Symptoms and Signs in Relation to Magnetic Resonance Imaging Findings Among Sciatic Patients.” Spine 2001; 26:E149-E154

77) Saal & Saal, "Nonoperative Treatment of Herniated Lumbar IVD with Radiculopathy: An outcome Study." Spine 1989; 14(4):431-437

78) Henrik Weber , '1982 Volvo Award in Clinical Science' "Lumbar Disc Herniation: A controlled, Prospective Study with Ten Years of Observation." Spine 1983; 8(2):131-140

80) Nakamura SI, Takahashi K, Takahashi Y, et al. "Origin of nerves supplying the posterior portion of lumbar Intervertebral discs in rats." Spine 1996; 21:917-924

81) Nakamura SI, Takahashi K, Takahashi Y, et al. "The afferent pathways of discogenic low-back pain. Evaluation of L2 spinal nerve infiltration." J Bone Jont Surg. 1996;78:606-612

95] Cooper RG, Freemont AJ, “TNF-a blockade for herniated intervertebral disc-induced sciatica: a way forward at last?” Rheumatology 2004; 43:119-121

96) Olmarker K, Rydevik B, et al. “Autologous nucleus pulposus induced's neurophysiologic and histologic changes in porcine cauda equina nerve roots.” Spine 1993; 18:1425-32

97) Olmarker K, et al. “Inflammatory properties of nucleus pulposus.” Spine 1995; 20:665-9

98) kayama S, Olmarker K, et al. “Incision of the annulus fibrosus induces nerve root morphological, vascular and functional changes: an experimental study.” Spine 1996; 21:2539-43

99) Olmarker K, Brisby H, et al. “The effects of normal, frozen and hyaluronidase-digested nucleus pulposus on nerve root structure and function.” Spine 1997; 22:471-5

126) Balague F, et al. "Recovery of Severe Sciatica." 1999; 24(23):2516-2524

140) Karppinen J, et al. “Tumor necrosis factor-alpha Monoclonal Antibody, Infliximab, Used to manage severe sciatica.” Spine; 28(8):750-753

141) Igarahi T, et al “Volvo Award Winner 2000” Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology: Molecular, histologic, and behavioral comparisons in rats.” Spine 2000; 25:2975-80

144) Blumenauer B, et al. “Infliximab for the treatment of rheumatoid arthritis.” Cochrane Database Syst Rev 2002; 3:CD003785

145) Maini R, et al. “Infliximab (Chimeric Antitumor necrosis factor-alpha monoclonal antibody) versus placebo in rheumatoid arthritis patients receiving concomitant methotrexate: A randomized phase III trial. ATTRACT Study Group. Lancet 1999; 354:1932-9.

146) Chaudhari U, et al. “Efficacy and safety of infliximab monotherapy for plaque-type psoriasis: A random trail. Lancet 2001; 357:1842-7

147) Braun J, et al. “Treatment of active ankylosing spondylitis with infliximab: A randomized controlled multicentre trial.” Lancet 2002; 359:1187-93

148) Hanauer SB, et al. “maintenance infliximab for Crohn’s disease: The ACCENT I randomized trial. Lancet 2002;359:1541-9

153) Olmarker K, Rydevik B, et al. “Autologous nucleus pulposus induces neurophysiologic and histologic changes on porcine cauda equina nerve roots.” Spine 1993 18:1425-1432

155) Olmarker K, Rydevik B, et al. “ultrastructural changes in spinal nerve roots induced by Autologous nucleus pulposus.” Spine 1996; 21:411-414

181) Heliovaara M, et al. “Lumbar disc syndrome in Finland.” J Epidemiol Commun Health 1987; 41:251-258

182) Manninen P, et al. “Incidence and risk factors of low-back pain in middle-aged farmers.” Occup med 1995; 45:141-146

183) Svensson HO, Andersson GBL. “Low back pain in forty to forty-seven year old men:   I Frequency of occurrence and impact on medical services.” Scand J Rehabil Med. 1982; 14:47-53

184) Svensson HO, Andersson GBL. “Low back pain in forty to forty-seven year old men:   work history and work environment factors.”Spine 1983 8:272-276

185) Svensson HO, Andersson GBL.   “The relationship of low back pain, work history, work environment, and stress: A retrospective cross-sectional study of 38- to 64-year old women.” Spine 1989; 14:517-522

186) Svensson HO, Andersson GBL. “A retrospective study of low back pain in 38- to 64 year old women: frequency and occurrence and impact on medical services.”   Spine 1988; 13:548-522

[190] Boos N, et al. “1995 Volvo Award in Clinical Sciences: The Diagnostic Accuracy of Magnetic Resonance Imaging, Work Perception, and Psychosocial Factors in Identifying Symptomatic Disc Herniations.” Spine 1995; 20:2613-2625

191) Spencer DL. Mechanisms of nerve root compression due to a herniated disc. In: Weinstein JN, Wiesel SW, International Society for the Study of the Lumbar Spine, eds. The Lumbar Spine. Philadelphia: WB Saunders, 1990:141-5.

192) Kelsey JL. An epidemiological study of the relationship between occupations and acute herniated lumbar intervertebral discs. Int J Epidemiol 1975;4:197-205.

193) Kelsey JL, Githens PB, White AA. An epidemiologic study of lifting and twisting on the job and risk for acute prolapsed lumbar intervertebral discs. J Orthop Res 1984;2:61-6.

194) Mundt DJ, Kelsey JL, Golden AL, et al. An epidemiologic study of non-occupational lifting as a risk factor for herniated lumbar intervertebral disc. Spine 1993;18:595-602

195) Videman T, Nurminen M, Troup JD. 1990 Volvo Award in Clinical Sciences. Lumbar spinal pathology in cadaveric material in relation to history of back pain, occupation, and physical loading. Spine 1990;15:728-40.

257) Marshall LL, et al. “Chemical irritation of nerve root in disc prolapse.”   Lancet 1973; 2:320

258) Marshall LL, et al. “Chemical Radiculitis: A clinical, physiological and immunological study.   Clin Orthop 129:61-67, 1977

281) Monteiro A et al. “lateral decompression of a pathological disc in the treatment of lumbar pain & sciatica.” Clin Orthop 1989; 56-63

282) Schreiber A, et al. “Does percutaneous nucleotomy with discoscopy replace conventional discectomy? Eight years of experience and results in treatment of herniated lumbar disc.” Clin Orthop 1989; 35-42

[290] Kortelainen P, et al. “Symptoms and signs of sciatic and their relation to the location of the lumbar disc herniation.” Spine – 1985; 10:88-92

291) Hirsch C, Nachemson A. “The reliability of lumbar disc surgery.” Clin Orthop 1963; 29:189-194

301) Dauch WA, et al. "predictors of treatment success after microsurgical operation of lumbar intervertebral disc displacements" Zentralbl Neurochir - 1994; 55:144-155

302) Dvorak J, et al. "The outcome of surgery for lumbar disc herniation."   Spine -1988; 13:1418-22

303) Hurme M and Alaranta H "Factors predicting the result of surgery for lumbar intervertebral disc herniation.   Spine - 1987; 12:933-938

304) Postacchini F, "Management of herniation of the lumbar disc." J Bone Joint Surg - 1999; 81- B :567 -576

305) Rothoerl RD, et al. "When should conservative treatment for lumbar disc herniation be ceased and surgery considered?" Neurosurg Rev - 2002; 25:162-165

306) Davis RA, et al. “A long-term outcome analysis of 984 surgically treated herniated lumbar discs.” J Neurosurg – 1994; 80:415-21

307) Hakelius A, “Prognosis in sciatica: a clinical follow-up of surgical and non-surgical treatment.” Acta Orthop Scand 1970; Suppl 129

308) Salenius P, “Results of operative treatment of lumbar disc herniation. Acta Orthop Scand 1977; 48:630-4

309) Spengler DM, et al. “Elective discectomy for herniation of lumbar disc: additional experience with an objective method.” J Bone Joint Surg – 1990; 72A:230-237

550) Olmarker K, Larsson K. “Tumor necrosis factor alpha, and nucleus-pulposus-induced nerve root injury.” Spine 1998; 23:2538-2544

551) Kayama S, Olmarker K, et al. “Incision of the anulus fibrosus induces nerve root morphologic, vascular, and functional changes: An experimental study.” Spine 1996;21:2539-43

552) Olmarker K, Brisby H, Rydevik B, et al. “The effects of normal, frozen, and hyaluronidase-digested nucleus pulposus on nerve root structure and function.” Spine 1997; 22:471-5discussion 476

553) Olmarker K, Rydevik B, et al. “Effects of methylprednisolone on nucleus pulposus-induced nerve root injury.” Spine 1994; 19:1803-8

554) Olmarker K, Rydevik B, et al. “Ultrastructural changes in spinal nerve roots induced by autologous nucleus pulposus.” Spine 1996; 21:411-4

555) Olmarker K et al. “Autologous nucleus pulposus induces neurophysiologic and histologic changes in porcine cauda equina nerve roots [see comments] Spine 1993; 18:1425-32

556) Byrod G, Reydevik B, Olmarker K, et al. “Acute increase in endoneural vascular permeability induced by epidural application of nucleus pulposus on spinal nerve roots. Manuscript [550]

557) Otani K Olmarker K, et al. “Nucleus pulposus-induced increased in vascular permeability in the nerve root. Manuscript [550]

558) Olmarker et al. “Inflammatogenic properties of nucleus pulposus.” Spine 1995;20:665-9

619) Ohnmeiss DD, et al. "Degree of disc disruption and lower extremity pain" Spine 1997; 22(14):1600-1605

620) Ohnmeiss DD, et al. "Relation between pain location and disc pathology: a study of pain drawings and CT/discography." Clin J Pain 1999 ;15:210-7.

621) Milette PC, et al. “Radiating Pain to the Lower Extremities Caused by Lumbar Disk Rupture without Spinal Nerve Root Involvement.” AJNR Am J Neuroradiol 1995; 16:1605-1613

788) Marshall LL, et al. “Chemical irritation of nerve root in disc prolapse.” Lancet 1973; 2:320

789) Marshall LL, et al. “Chemical Radiculitis: A clinical, physiological and immunological study. Clin Orthop 129:61-67, 1977

790) Olmarker K, Rydevik B, et al. “Autologous nucleus pulposus induced neurophysiologic and histologic changes in porcine cauda equina nerve roots.” Spine 1993; 18:1425-32

791) Olmarker K, Rydevik B, et al. “ Ultrastructural changes in spinal nerve roots induced by autologous nucleus pulposus.” Spine 1996; 21:411-4

792) Olmarker K, et al. “Inflammatory properties of nucleus pulposus.” Spine 1995; 20:665-9

793) kayama S, Olmarker K, et al. “Incision of the annulus fibrosus induces nerve root morphological, vascular and functional changes: an experimental study.” Spine 1996; 21:2539-43

794) Olmarker K, Brisby H, et al. “The effects of normal, frozen and hyaluronidase-digested nucleus pulposus on nerve root structure and function.” Spine 1997; 22:471-5

795) Olmarker K, Larsson K. “Tumor necrosis factor alpha, and nucleus-pulposus-induced nerve root injury.” Spine 1998; 23:2538-2544

800) Brisby H, Rydevik B, et al. " Glycosphingolipid antibodies in serum in patients with sciatica." Spine 2002 ;27(4):380-6.

801) Chacur M, et al. "A new model of sciatic inflammatory neuritis (SIN): induction of unilateral and bilateral mechanical allodynia following acute unilateral peri-sciatic immune activation in rats." Pain 2001 ;94(3):231-4

900) Korhonen T, Karppinen J, et al. 'Efficacy of infliximab for disc herniation-induced sciatica: one-year follow-up.' Spine. 2004 Oct 1;29(19):2115-9

© Copyright 2002 – 2005 by Dr. Douglas M. Gillard DC - All rights reserved