Sciatica. GRRRR!!
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Doc2012
Senior Member
Dealing with a lot of sciatic nerve patients when I was with the grunts, I've see people do anything from lay around and slowly stretch it out, to people using Icy Hot patches to relax the muscle, to people doing yoga.
What have you tried? How did you injure it?
*****DISCLAIMER******
I am NOT a Doctor. I am a Corpsman. I have experience with this, but if you have tried the aforementioned stuff, I would go see a Chiropractor or your regular doctor.
What have you tried? How did you injure it?
*****DISCLAIMER******
I am NOT a Doctor. I am a Corpsman. I have experience with this, but if you have tried the aforementioned stuff, I would go see a Chiropractor or your regular doctor.
Quatre Coureur
New member
I had it pretty bad about 8 years ago. 600mg Naproxen. Worked for me. I know how painful it can be. Hope u feel better soon.
wheese88
New member
SO has it and she can hardly walk sometimes so I can empathize. Buy a heating pad the kind you plug into a wall (will save you money in the long run) Place in on the left butt cheek. After that, once the muscle is loose you'll want to do trigger pressure point massages Massage Therapy for Back Pain, Hip Pain, Sciatica
Had it done at the chiropractor's office and felt amazing afterwards, not a cure but more of a type of management.
Not a Dr, former pre-med, now just a hippie of sorts (biologist).
BEST OF LUCK!
Had it done at the chiropractor's office and felt amazing afterwards, not a cure but more of a type of management.
Not a Dr, former pre-med, now just a hippie of sorts (biologist).
BEST OF LUCK!
hikenbike
New member
Thanks all. Don't know how it happened......probably hiking up a heavy backpack or some normal activity like that. I've tried the hot patches, massages, and I try to stretch a lot. A couple of years ago I had something similar and stretching really helped but this is more severe and stretching aggravates it further. Been taking Aleve twice a day and it helps somewhat but it's very temporary. Seated its fine. Standing or walking is killer. I rode my bike 25 miles on Saturday and felt absolutely nothing. Great ride. As soon as I got off the bike, lots of pain.
Haven't been to a doctor so I think that's next.
Haven't been to a doctor so I think that's next.
JB.
New member
I'm in my 50s and very active. Have dealt with episodes all my life and am, in fact, dealing with a mild one right now.
Here's the place I've come to on the subject.
1. Back (and related) pain that's not the result of specific injury is very common and nearly always physically benign. ("Psychics" often happily utilize this fact). It seems there may be a tradeoff to walking upright.
2. Get any idea of slipped discs, damage, etc, out of your head. You're way better off not feeling fragile and, for me anyway, that means staying away from a Chiropractor or, in fact, becoming a patient of any kind.
3. I now stretch religiously every single day but use common sense on pushing particular moves too far if they hurt.
4. Heat is great but I have long since given up on poking around, massaging, etc, the area as my experience seems to indicate it doesn't help and only seems to make things worse. I have also decided that pain medication is not helpful in the long run either.
5. Even in cases where sitting feels better, I still like to get up often, if only to not become psychologically bound to the chair. I try to find ways to break up any routine and do some fresh activity that involves being on my feet. As a very general rule, I try to respond to sciatica by doing more (but different) rather than doing less.
Good luck.
Here's the place I've come to on the subject.
1. Back (and related) pain that's not the result of specific injury is very common and nearly always physically benign. ("Psychics" often happily utilize this fact). It seems there may be a tradeoff to walking upright.
2. Get any idea of slipped discs, damage, etc, out of your head. You're way better off not feeling fragile and, for me anyway, that means staying away from a Chiropractor or, in fact, becoming a patient of any kind.
3. I now stretch religiously every single day but use common sense on pushing particular moves too far if they hurt.
4. Heat is great but I have long since given up on poking around, massaging, etc, the area as my experience seems to indicate it doesn't help and only seems to make things worse. I have also decided that pain medication is not helpful in the long run either.
5. Even in cases where sitting feels better, I still like to get up often, if only to not become psychologically bound to the chair. I try to find ways to break up any routine and do some fresh activity that involves being on my feet. As a very general rule, I try to respond to sciatica by doing more (but different) rather than doing less.
Good luck.
Last edited:
Clone of the Mean
New member
I swear by acupuncture. I had a bad neck injury a few years ago. I went to PT for 2.5 years before I finally gave up. I went to a chiropractor who refused to touch me (imagine that) and recommended someone.
Twice a week for 6 weeks. That was over 10 years ago. It gives me trouble now and then but I have no complaints.
Twice a week for 6 weeks. That was over 10 years ago. It gives me trouble now and then but I have no complaints.
preacher35
New member
I am not a doctor, but I am a former physical therapist specializing in back injuries. I am not sure what you do for a living, but one of the "recurring" causes of sciatica, that I noticed in practice, was how patients would stagnate recovery or worse, exacerbate the sciatica by sitting all day at work. This was so insanely common, that I had to start asking referring docs to order their patients to take time off of work so that they were not sitting in a bad office chair all day. It is extremely important that you TAKE YOUR TIME TO RECOVER. That means you have got to be damned careful about how you bend over, sitting too long, picking stuff up. Good luck and I wish you the best.
MyHigh
New member
Many great ways to "deal" with the pain. Basically find out what's causing it, for me it was a herniated l-4- l-5 disc, for many people it's the periformus (sp) muscle a good stretch is to lay on your back knees bent, cross left ankle over right knee. Pull gently on left knee ( knee that is crossed) for about 15 sec. Do that three times. Next with leg still crossed push left knee forward very gentle same amount of time and reps. Repeat with other leg. Sometimes you get a better stretch if you place your feet against a wall while lying on your back make almost a 90degree angle. The periformus muscle kinda overlays the sciatic nerve as it shoots out the hip skeleto system. For some people either heat or cold help, everyone is different just remember to only do both no more then 20 minutes at a time. Also take some OTC inflammation drugs.
Pray to god that it's something this easy to fix, surgery helped me but that was a last resort cure, I tried for a year to get better and nerver did, till I got surgery I hadent stood straight or walked more the 50 yards at a time,
It sucks really, really, really bad it can't be explained to someone who hasn't experienced that type of pain before, I feel for you man!
Good luck
Pray to god that it's something this easy to fix, surgery helped me but that was a last resort cure, I tried for a year to get better and nerver did, till I got surgery I hadent stood straight or walked more the 50 yards at a time,
It sucks really, really, really bad it can't be explained to someone who hasn't experienced that type of pain before, I feel for you man!
Good luck
VoodooTitan
New member
I am not a licensed physician. Any information I provide you is generalized. Any suggestions is in a hypothetical situation. Information provided is from a web-based medical database. I am not evaluating you, diagnosing you, or suggesting any treatment. This response is strictly to provide you with more indepth information on a common pathology routinely seen outpatient practice.
Back pain is a common problem and a leading reason for all physician visits. Most cases are attributed to musculoligamentous (where muscles connect to bone) injury or skeletal degenerative changes, although the differential diagnosis is broad.
I am not evaluating you. Hypothetically if you were a patient of mine, I would ask the following:
1. How severe is your pain on a scale from 1 to 10? 1 being minor, 10 being the worst pain in your life.
2. Does your pain radiate? Is it positional or constant? Do you experience numbness, tingling, or a loss of sensation in your lower extremities?
3. Did you recently sustain an injury? What and how?
4. Is there a family history of degenerative disk disease, cancer, or any other musculoskeletal related health problem?
5. Are your symptoms worse in the morning, afternoon, or at night, or are they constant?
6. Do you experience any weakness in your extremities?
Following this, I would perform a physical exam. Some things you can do at home, by yourself or with your spouse is test strength, mobility, range of motion, and measurements.
1. Observe symmetry of your body. Look in the mirror an make sure your shoulders are level with each other. Have someone look at you from behind with your shirt off and examine your spine. They should look to make sure your spine is in good alignment and doesn't have the shape of an S. Looking from the side, there should be a slight S shape to your spine from head to hips. This is testing for scoliosis, kyphosis, and lordosis which can participate in lower back pain symptoms. Perform a standing toe touch, someone should observe the muscles of your back for symmetry. Asymmetry could mean inflammation which could be causing pain. It could also reveal where weakness may be present in the back.
Measure your legs. If there is a minor difference in length, this could attribute to your symptoms. Physiologically, the shorter leg vs the longer leg would cause a minute shift in pace, strength, and what should be normal movement. Your body with compensate, if there is a drastic enough compensation, injury could occur, or a change significant enough to be noticeable.
2. Check strength against resistance. Have someone press on your shins and kick out while seated. Then pull in. Essentially test your range or motion, testing all the muscles in the lower leg.
3. Trendelenburg test. Google it or youtube it.
4. If you notice any positive findings, see a doctor and request some imaging studies. An X-ray of your Lumbar Spine should suffice.
Remember, it's not sciatica unless it's diagnosed. So don't go to a doctor saying you have sciatica. Then they'll begin "looking" for that, or seeking those symptoms, rather than diagnosing you yourself. You can say you'd like to rule out the possibility of it, but don't say you have it unless it's been previously diagnosed and treatment failed.
Pharmacological options are as follows.
1. Non-steroidal anti inflammatories: Motrin, Naprosyn/Naproxen, or Meloxicam are the most common and least expensive. Primarily used to act on non-selective and COX-2 selective receptors to reduce focal inflammation at site where receptors are active.
2. Acetaminophen: Tylenol. Primarily used for pain.
3. Skeletal muscle relaxants: Cyclobenzaprine and Methocarbamol are common with low noted side effects. Act by relaxing the skeletal muscle system by acting on the central nervous system. Most common side effect is drowsiness.
4. opiods: Morphine, etc. Severe pain management. Basically make it so you don't feel the pain, the problem is still there, but the pain is gone.
5. corticosteroids or Glucocorticoids. naturally occurring in the body. Anti-inflammatory properties. Used to reduce gross inflammation. Typically in allergic reactions and things more severe. Commonly used in Internal Medicine and Emergency Medicine.
Here's more info... if interested in reading.
ANATOMY — The lumbar spine consists of five movable lumbar vertebral bodies, numbered L1 to L5 (figure 1). The sacrum is made up of five developmentally fused vertebral levels (S1 to S5), followed by a terminal bony prominence, the coccyx. The entire region is commonly described as the lumbosacral spine.
Directly beneath each lumbar and sacral vertebra, there is a pair of neural foramina with the same number designation, such that the L1 neural foramina are located just below the L1 vertebral body. Neural foramina are bounded superiorly and inferiorly by pedicles, anteriorly by the intervertebral disc and vertebral body, and posteriorly by facet joints (figure 1).
Through each neural foramen passes the same numbered spinal nerve root, recurrent meningeal nerves, and radicular blood vessels. On each side there are five lumbar, five sacral, and one coccygeal spinal nerve roots.
All lumbar and sacral spinal nerve roots originate at the T10 to L1 vertebral level, where the spinal cord ends as the conus medullaris. A dorsal (somatic sensory) root from the posterolateral aspect of the spinal cord and a ventral (somatic motor) root from the anterolateral aspect of the cord join in the spinal canal to form the spinal nerve root (figure 1). The roots then course down through the intraspinal canal, forming the cauda equina, until they exit at their respective neural (intervertebral) foramina. Thus, the lumbosacral nerve roots exit the spinal canal at a lower level than where they arise. A potential consequence of this arrangement is that intraspinal pathology may affect roots at higher levels than the level where the roots exit [2,3].
Cell bodies of the motor nerve fibers are located in the ventral (anterior) horns of the spinal cord, while those of the sensory nerve fibers are in a dorsal root ganglion at each lumbar and sacral level. Dorsal root ganglia (DRG) tend to be located within the neural foramina, and are therefore not strictly speaking intraspinal (ie, within the lumbar canal). However, at the low lumbar and sacral levels there is a tendency for DRG to reside proximal to the neural foramina, within the intraspinal canal, as found in 11 to 38 percent of cases at L5 and 71 percent at S1 [4,5]. The dorsal root ganglia are attached to the vertebral body on the transverse process [6]. Compressive radicular disease typically occurs proximal to this.
As noted above, the spinal cord normally terminates at the conus medullaris within the lumbar intraspinal canal between the T10 and L1 vertebral levels. Exceptions include patients with congenital spinal deformities known as spina bifida, in which the fetal conus is tethered to ligamentous or bony structures, causing lengthening of the spinal cord during development. In such patients, the conus medullaris can be displaced downward to the middle or lower lumbar spine.
Rami — Just distal to the neural foramen, the nerve root divides in two, forming the dorsal and ventral primary rami.
The small dorsal (posterior) primary ramus supplies motor innervation to the paraspinal muscles and cutaneous innervation to the skin of the trunk and back
The large ventral (anterior) primary ramus supplies motor and sensory innervation to the legs and trunk, including abdominal wall muscles
The dorsal rami of the spinal nerves also supply the apophyseal joints and the paraspinal muscles. They innervate structures both above and below the level of the nerve. Clinical evaluation of injury to the dorsal rami is difficult because of the overlap in areas innervated by these nerves and because of the limited ability to clinically evaluate individual paraspinal muscles. However, electromyography can be helpful in determining the distribution of disease.
The ventral rami innervate the extremities and the trunk. These branches can be evaluated by assessing the motor and sensory functions of the different myotomes and dermatomes, respectively. However, variability to the dermatomal and myotomal distribution of innervation exists [7,8].
Myotomes and dermatomes — The collection of muscles with significant innervation from a single root is called a myotome. Similarly, the sensory distribution of a single root is labeled a dermatome.
The primary manifestations of lumbosacral root disease can be broken up into dysfunction of two distinct systems: motor and sensory. Motor dysfunction from a root lesion may cause weakness in some or all muscles innervated by that root. However, many muscles have innervation from multiple roots, which may result in preserved strength despite significant involvement of a single root.
Although there are classic descriptions for the distributions of myotomes and dermatomes, substantial variability exists in these distributions from person to person [7,8]. Sensory fields have considerable overlap, but there are areas that are exclusively served by individual nerves. These areas are called autonomous zones. The most important of these in the evaluation of lumbosacral radiculopathies include the sole of the foot (S1), dorsum of the foot (L5), medial calf (L4), and anterior thigh (L2 and 3) [9].
Lumbosacral myotomes are listed in the Table (table 1).
Sinuvertebral nerves — The sinuvertebral nerves are sensory nerves that innervate various structures within the spine, such as ligamentous structures, the dura, periosteum, and blood vessels [10]. They originate distal to the dorsal root ganglia and extend to communicate with branches from radicular levels both above and below the level of entry, as well as the contralateral side, making it difficult to localize pain from involvement of these nerves.
Irritation of the sinuvertebral nerves may result in low back pain. Because they arise distal to the nerve root, however, involvement of sinuvertebral nerves or their branches without involvement of the rest of the nerve root is not considered to be radicular in nature.
PATHOPHYSIOLOGY AND ETIOLOGY — The most common etiology of lumbosacral radiculopathy is nerve root compression caused by a disc herniation or spondylosis (ie, spinal stenosis due to degenerative arthritis affecting the spine). Additional etiologies include nonskeletal causes of nerve root compression and noncompressive mechanisms such as infection, inflammation, neoplasm, and vascular disease.
Pain generators in the lumbosacral spine — A number of tissues making up the low back contain nerve fibers with pain receptors. These are listed in the Table (table 2). Of note, intervertebral disc material does not contain significant numbers of pain fibers.
Classic radiating pain from spinal nerve injury is mediated through proximal spinal nerves. Compression of a spinal nerve root by disc or arthritic spur leads to local edema, ischemia, and inflammation. These factors contribute to production of pain impulses through the spinal nerves. The pain from acute disc herniation or spondylotic spinal nerve entrapment reflects a combination of pain generation within the nerve root itself, as well as the pain from neighboring tissues whose pain fibers are activated by the effect of disc herniation on dura, ligaments, and surrounding vasculature.
Localized lumbosacral pain is thought to arise from intraspinal structures. These pain impulses arise from the blood vessels, dura mater, and longitudinal ligaments, and travel in the sinuvertebral nerves through the neural foramina, connecting via rami communicantes with the extraspinal sympathetic chain.
Nonlocalized, nonradiating pain is thought to arise from muscle, bone, and ligament outside the spinal canal. Interconnected ventral and dorsal nerve plexuses surround the vertebral column [11]. The ventral nerve plexus serves the anterior longitudinal ligament and has bilateral innervation. Many branches from the sympathetic trunk, rami communicantes, and perivascular nerve plexuses join to form the ventral nerve plexus. The dorsal nerve plexus arises from the sinuvertebral nerves and serves the posterior longitudinal ligament.
Referred spine pain may arise from the abdominal viscera that share the same spinal level of innervation. Organs that can potentially refer pain to the spine include the aorta, pancreas, duodenum, colon, rectum, kidney, ureter, bladder, and pelvic organs. Systemic illness can refer pain to the bony spine or can produce bony disease that generates spine pain. The major categories and clues to their diagnosis are listed in the Table (table 3).
Degenerative changes — Damage to spinal nerve roots occurs as the result of degenerative change involving three main structures, which are:
The intervertebral discs
The uncovertebral joints
The zygapophyseal (facet) joints
Resulting bony overgrowth (osteophytes) or disc herniation at these points may directly impinge on spinal nerve roots or the spinal cord, or their effect may be primarily to produce instability and misalignment of the spine (ie, degenerative spondylolisthesis) that in turn produces pain and neurologic deficits. It is not known whether changes in these different structures are causally related or occur independently.
Degenerative spondylotic changes are common with aging and usually do not result in radiculopathy. Low back pain associated with degenerative changes is distinct from radicular pain and is much more frequent. Given the inability to ascertain the exact cause, it is commonly referred to as nonspecific low back pain.
One school of thought suggests that degenerative spondylotic change is led by age-related change in the nucleus pulposus of the disc. With age there is gradual narrowing of the disc space coincident with changes in disc proteoglycan composition. Later, cracks develop in the disc, and deposits of gas and calcification may form. Eventually the disc material becomes desiccated and friable. Age-related changes also occur in the annulus fibrosus, which becomes more fibrotic and less elastic. Fissures develop, and calcium is deposited. As the disc shrinks and the intervertebral disc space narrows, the annulus tends to buckle out.
Accompanying this disc degeneration are changes at the vertebral body endplates adjacent to the disc. The marrow undergoes fibrovascular change or fatty marrow replacement. Finally, endplate sclerosis develops. Osteophyte formation occurs at the margins of the vertebral bodies. What triggers osteophyte formation is unclear, although spinal movement at ligamentous attachment sites and loss of buffering tissues between bony surfaces likely play roles. Osteophyte production appears to slow as advancing spondylosis leads to decreasing spinal movement.
Uncovertebral joints are not true joints, but they may represent a slit in the intervertebral disc at the point where the uncinate process makes contact with the disc and vertebral body above. As disc substance decreases, there is more contact between the uncinate process and adjacent bone, leading to osteophyte formation. Dorsal protrusion of these osteophytes narrows the adjacent neural foramen.
Facet joint degeneration may not be directly related to spondylotic changes, but often coexists. Disc degeneration is likely to put additional weight-bearing strains on facet joints, which are not weight-bearing structures. With unnatural movement of the spine, the synovial joint bears more structural burden, degenerates, and develops osteophytes. These osteophytes grow into the posterior aspect of the neural foramen (image 1).
Disc protrusion and level of injury — The relationship between disc disease and lumbosacral radiculopathy was first identified in 1934 [12]. Disc protrusion can give rise to different anatomic levels of nerve root compression depending on the orientation of spinal nerve roots as they exit from the spinal cord. As noted earlier, all lumbar and sacral spinal nerve roots are constituted at the T12-L1 vertebral level, where the spinal cord ends as the conus medullaris. The roots then course down the canal as the cauda equina, until they exit at their respective neural foramina.
Depending upon the nature and location of intraspinal compression, roots may be injured at any disc level, from the L1-2 level to the level of their exit into their neural foramina. For example, the L5 root can be compressed by a central disc protrusion at the L2-3 or L3-4 level, a lateral disc protrusion at the L4-5 level (image 2), or disc protrusion into the foramen at the L5-S1 level (image 3). Because of the presence of multiple spinal nerve roots in the cauda equina, there is increased likelihood of multiple, bilateral simultaneous nerve root compressions.
Nerve root injury may be complete or only partial and thus may involve all or only a subset of root fibers. With partial injury, incomplete myotomal involvement may result, making the distinction between a radiculopathy and a peripheral nerve injury more challenging.
The lumbosacral spine is susceptible to disc herniations because of its mobility from flexion, extension, and torsion. Seventy-five percent of flexion and extension occurs at the lumbosacral joint [13]. This level, on the other hand, has limited torsion. Twenty percent of flexion and extension occurs at L4-L5. The remaining 5 percent occurs between L1 and L3 [13]. As the L4-L5 and L5-S1 levels are most susceptible to injuries from routine movements of the spine, about 90 to 95 percent of compressive radiculopathies occur at these levels [14]. The incidence of radiculopathies is split somewhat evenly between L4-L5 and L5-S1, as the lack of torsion at L5-S1 helps to increase its stability despite its higher degree of flexion and extension [15]. Next in frequency is L4. Other levels are uncommon.
Far lateral herniations are seen more often at the L2-4 levels. They may affect the rostral root. This is rare, as only 10 percent of far lateral herniations will result in nerve root compression [5]. Pain from the far lateral disc herniations may be more severe due to compression of the dorsal root ganglia [16].
Other skeletal causes — Congenital abnormalities of the bony spinal column or its contents occur in 25 to 50 percent of the general population [17]. Congenital narrowing of the canal is not uncommon as a substrate upon which spondylosis may result in neurologic disease; this is especially true of younger adults. Other developmental abnormalities include tethered cord or diastematomyelia and spina bifida. They may lead to radicular dysfunction due to injuries resulting from traction of the root.
Root avulsion is a rare cause of lumbosacral radiculopathy that may occur with fractures of the sacroiliac joint or with diastasis of the symphysis pubis or the pubic rami
If you experience any saddle numbness (numbness in the groin area), difficulty transitioning from a seated to standing position, or vice versa (typically noted when using the toilet), constant numbness or loss of sensation, or notable weakness in your lower extremities, loss of bowel or urine, or episodes or paralysis; immediate seek emergency medical attention.
Back pain is a common problem and a leading reason for all physician visits. Most cases are attributed to musculoligamentous (where muscles connect to bone) injury or skeletal degenerative changes, although the differential diagnosis is broad.
I am not evaluating you. Hypothetically if you were a patient of mine, I would ask the following:
1. How severe is your pain on a scale from 1 to 10? 1 being minor, 10 being the worst pain in your life.
2. Does your pain radiate? Is it positional or constant? Do you experience numbness, tingling, or a loss of sensation in your lower extremities?
3. Did you recently sustain an injury? What and how?
4. Is there a family history of degenerative disk disease, cancer, or any other musculoskeletal related health problem?
5. Are your symptoms worse in the morning, afternoon, or at night, or are they constant?
6. Do you experience any weakness in your extremities?
Following this, I would perform a physical exam. Some things you can do at home, by yourself or with your spouse is test strength, mobility, range of motion, and measurements.
1. Observe symmetry of your body. Look in the mirror an make sure your shoulders are level with each other. Have someone look at you from behind with your shirt off and examine your spine. They should look to make sure your spine is in good alignment and doesn't have the shape of an S. Looking from the side, there should be a slight S shape to your spine from head to hips. This is testing for scoliosis, kyphosis, and lordosis which can participate in lower back pain symptoms. Perform a standing toe touch, someone should observe the muscles of your back for symmetry. Asymmetry could mean inflammation which could be causing pain. It could also reveal where weakness may be present in the back.
Measure your legs. If there is a minor difference in length, this could attribute to your symptoms. Physiologically, the shorter leg vs the longer leg would cause a minute shift in pace, strength, and what should be normal movement. Your body with compensate, if there is a drastic enough compensation, injury could occur, or a change significant enough to be noticeable.
2. Check strength against resistance. Have someone press on your shins and kick out while seated. Then pull in. Essentially test your range or motion, testing all the muscles in the lower leg.
3. Trendelenburg test. Google it or youtube it.
4. If you notice any positive findings, see a doctor and request some imaging studies. An X-ray of your Lumbar Spine should suffice.
Remember, it's not sciatica unless it's diagnosed. So don't go to a doctor saying you have sciatica. Then they'll begin "looking" for that, or seeking those symptoms, rather than diagnosing you yourself. You can say you'd like to rule out the possibility of it, but don't say you have it unless it's been previously diagnosed and treatment failed.
Pharmacological options are as follows.
1. Non-steroidal anti inflammatories: Motrin, Naprosyn/Naproxen, or Meloxicam are the most common and least expensive. Primarily used to act on non-selective and COX-2 selective receptors to reduce focal inflammation at site where receptors are active.
2. Acetaminophen: Tylenol. Primarily used for pain.
3. Skeletal muscle relaxants: Cyclobenzaprine and Methocarbamol are common with low noted side effects. Act by relaxing the skeletal muscle system by acting on the central nervous system. Most common side effect is drowsiness.
4. opiods: Morphine, etc. Severe pain management. Basically make it so you don't feel the pain, the problem is still there, but the pain is gone.
5. corticosteroids or Glucocorticoids. naturally occurring in the body. Anti-inflammatory properties. Used to reduce gross inflammation. Typically in allergic reactions and things more severe. Commonly used in Internal Medicine and Emergency Medicine.
Here's more info... if interested in reading.
ANATOMY — The lumbar spine consists of five movable lumbar vertebral bodies, numbered L1 to L5 (figure 1). The sacrum is made up of five developmentally fused vertebral levels (S1 to S5), followed by a terminal bony prominence, the coccyx. The entire region is commonly described as the lumbosacral spine.
Directly beneath each lumbar and sacral vertebra, there is a pair of neural foramina with the same number designation, such that the L1 neural foramina are located just below the L1 vertebral body. Neural foramina are bounded superiorly and inferiorly by pedicles, anteriorly by the intervertebral disc and vertebral body, and posteriorly by facet joints (figure 1).
Through each neural foramen passes the same numbered spinal nerve root, recurrent meningeal nerves, and radicular blood vessels. On each side there are five lumbar, five sacral, and one coccygeal spinal nerve roots.
All lumbar and sacral spinal nerve roots originate at the T10 to L1 vertebral level, where the spinal cord ends as the conus medullaris. A dorsal (somatic sensory) root from the posterolateral aspect of the spinal cord and a ventral (somatic motor) root from the anterolateral aspect of the cord join in the spinal canal to form the spinal nerve root (figure 1). The roots then course down through the intraspinal canal, forming the cauda equina, until they exit at their respective neural (intervertebral) foramina. Thus, the lumbosacral nerve roots exit the spinal canal at a lower level than where they arise. A potential consequence of this arrangement is that intraspinal pathology may affect roots at higher levels than the level where the roots exit [2,3].
Cell bodies of the motor nerve fibers are located in the ventral (anterior) horns of the spinal cord, while those of the sensory nerve fibers are in a dorsal root ganglion at each lumbar and sacral level. Dorsal root ganglia (DRG) tend to be located within the neural foramina, and are therefore not strictly speaking intraspinal (ie, within the lumbar canal). However, at the low lumbar and sacral levels there is a tendency for DRG to reside proximal to the neural foramina, within the intraspinal canal, as found in 11 to 38 percent of cases at L5 and 71 percent at S1 [4,5]. The dorsal root ganglia are attached to the vertebral body on the transverse process [6]. Compressive radicular disease typically occurs proximal to this.
As noted above, the spinal cord normally terminates at the conus medullaris within the lumbar intraspinal canal between the T10 and L1 vertebral levels. Exceptions include patients with congenital spinal deformities known as spina bifida, in which the fetal conus is tethered to ligamentous or bony structures, causing lengthening of the spinal cord during development. In such patients, the conus medullaris can be displaced downward to the middle or lower lumbar spine.
Rami — Just distal to the neural foramen, the nerve root divides in two, forming the dorsal and ventral primary rami.
The small dorsal (posterior) primary ramus supplies motor innervation to the paraspinal muscles and cutaneous innervation to the skin of the trunk and backThe large ventral (anterior) primary ramus supplies motor and sensory innervation to the legs and trunk, including abdominal wall musclesThe dorsal rami of the spinal nerves also supply the apophyseal joints and the paraspinal muscles. They innervate structures both above and below the level of the nerve. Clinical evaluation of injury to the dorsal rami is difficult because of the overlap in areas innervated by these nerves and because of the limited ability to clinically evaluate individual paraspinal muscles. However, electromyography can be helpful in determining the distribution of disease.
The ventral rami innervate the extremities and the trunk. These branches can be evaluated by assessing the motor and sensory functions of the different myotomes and dermatomes, respectively. However, variability to the dermatomal and myotomal distribution of innervation exists [7,8].
Myotomes and dermatomes — The collection of muscles with significant innervation from a single root is called a myotome. Similarly, the sensory distribution of a single root is labeled a dermatome.
The primary manifestations of lumbosacral root disease can be broken up into dysfunction of two distinct systems: motor and sensory. Motor dysfunction from a root lesion may cause weakness in some or all muscles innervated by that root. However, many muscles have innervation from multiple roots, which may result in preserved strength despite significant involvement of a single root.
Although there are classic descriptions for the distributions of myotomes and dermatomes, substantial variability exists in these distributions from person to person [7,8]. Sensory fields have considerable overlap, but there are areas that are exclusively served by individual nerves. These areas are called autonomous zones. The most important of these in the evaluation of lumbosacral radiculopathies include the sole of the foot (S1), dorsum of the foot (L5), medial calf (L4), and anterior thigh (L2 and 3) [9].
Lumbosacral myotomes are listed in the Table (table 1).
Sinuvertebral nerves — The sinuvertebral nerves are sensory nerves that innervate various structures within the spine, such as ligamentous structures, the dura, periosteum, and blood vessels [10]. They originate distal to the dorsal root ganglia and extend to communicate with branches from radicular levels both above and below the level of entry, as well as the contralateral side, making it difficult to localize pain from involvement of these nerves.
Irritation of the sinuvertebral nerves may result in low back pain. Because they arise distal to the nerve root, however, involvement of sinuvertebral nerves or their branches without involvement of the rest of the nerve root is not considered to be radicular in nature.
PATHOPHYSIOLOGY AND ETIOLOGY — The most common etiology of lumbosacral radiculopathy is nerve root compression caused by a disc herniation or spondylosis (ie, spinal stenosis due to degenerative arthritis affecting the spine). Additional etiologies include nonskeletal causes of nerve root compression and noncompressive mechanisms such as infection, inflammation, neoplasm, and vascular disease.
Pain generators in the lumbosacral spine — A number of tissues making up the low back contain nerve fibers with pain receptors. These are listed in the Table (table 2). Of note, intervertebral disc material does not contain significant numbers of pain fibers.
Classic radiating pain from spinal nerve injury is mediated through proximal spinal nerves. Compression of a spinal nerve root by disc or arthritic spur leads to local edema, ischemia, and inflammation. These factors contribute to production of pain impulses through the spinal nerves. The pain from acute disc herniation or spondylotic spinal nerve entrapment reflects a combination of pain generation within the nerve root itself, as well as the pain from neighboring tissues whose pain fibers are activated by the effect of disc herniation on dura, ligaments, and surrounding vasculature.Localized lumbosacral pain is thought to arise from intraspinal structures. These pain impulses arise from the blood vessels, dura mater, and longitudinal ligaments, and travel in the sinuvertebral nerves through the neural foramina, connecting via rami communicantes with the extraspinal sympathetic chain.Nonlocalized, nonradiating pain is thought to arise from muscle, bone, and ligament outside the spinal canal. Interconnected ventral and dorsal nerve plexuses surround the vertebral column [11]. The ventral nerve plexus serves the anterior longitudinal ligament and has bilateral innervation. Many branches from the sympathetic trunk, rami communicantes, and perivascular nerve plexuses join to form the ventral nerve plexus. The dorsal nerve plexus arises from the sinuvertebral nerves and serves the posterior longitudinal ligament.Referred spine pain may arise from the abdominal viscera that share the same spinal level of innervation. Organs that can potentially refer pain to the spine include the aorta, pancreas, duodenum, colon, rectum, kidney, ureter, bladder, and pelvic organs. Systemic illness can refer pain to the bony spine or can produce bony disease that generates spine pain. The major categories and clues to their diagnosis are listed in the Table (table 3).Degenerative changes — Damage to spinal nerve roots occurs as the result of degenerative change involving three main structures, which are:
The intervertebral discsThe uncovertebral jointsThe zygapophyseal (facet) jointsResulting bony overgrowth (osteophytes) or disc herniation at these points may directly impinge on spinal nerve roots or the spinal cord, or their effect may be primarily to produce instability and misalignment of the spine (ie, degenerative spondylolisthesis) that in turn produces pain and neurologic deficits. It is not known whether changes in these different structures are causally related or occur independently.
Degenerative spondylotic changes are common with aging and usually do not result in radiculopathy. Low back pain associated with degenerative changes is distinct from radicular pain and is much more frequent. Given the inability to ascertain the exact cause, it is commonly referred to as nonspecific low back pain.
One school of thought suggests that degenerative spondylotic change is led by age-related change in the nucleus pulposus of the disc. With age there is gradual narrowing of the disc space coincident with changes in disc proteoglycan composition. Later, cracks develop in the disc, and deposits of gas and calcification may form. Eventually the disc material becomes desiccated and friable. Age-related changes also occur in the annulus fibrosus, which becomes more fibrotic and less elastic. Fissures develop, and calcium is deposited. As the disc shrinks and the intervertebral disc space narrows, the annulus tends to buckle out.
Accompanying this disc degeneration are changes at the vertebral body endplates adjacent to the disc. The marrow undergoes fibrovascular change or fatty marrow replacement. Finally, endplate sclerosis develops. Osteophyte formation occurs at the margins of the vertebral bodies. What triggers osteophyte formation is unclear, although spinal movement at ligamentous attachment sites and loss of buffering tissues between bony surfaces likely play roles. Osteophyte production appears to slow as advancing spondylosis leads to decreasing spinal movement.
Uncovertebral joints are not true joints, but they may represent a slit in the intervertebral disc at the point where the uncinate process makes contact with the disc and vertebral body above. As disc substance decreases, there is more contact between the uncinate process and adjacent bone, leading to osteophyte formation. Dorsal protrusion of these osteophytes narrows the adjacent neural foramen.
Facet joint degeneration may not be directly related to spondylotic changes, but often coexists. Disc degeneration is likely to put additional weight-bearing strains on facet joints, which are not weight-bearing structures. With unnatural movement of the spine, the synovial joint bears more structural burden, degenerates, and develops osteophytes. These osteophytes grow into the posterior aspect of the neural foramen (image 1).
Disc protrusion and level of injury — The relationship between disc disease and lumbosacral radiculopathy was first identified in 1934 [12]. Disc protrusion can give rise to different anatomic levels of nerve root compression depending on the orientation of spinal nerve roots as they exit from the spinal cord. As noted earlier, all lumbar and sacral spinal nerve roots are constituted at the T12-L1 vertebral level, where the spinal cord ends as the conus medullaris. The roots then course down the canal as the cauda equina, until they exit at their respective neural foramina.
Depending upon the nature and location of intraspinal compression, roots may be injured at any disc level, from the L1-2 level to the level of their exit into their neural foramina. For example, the L5 root can be compressed by a central disc protrusion at the L2-3 or L3-4 level, a lateral disc protrusion at the L4-5 level (image 2), or disc protrusion into the foramen at the L5-S1 level (image 3). Because of the presence of multiple spinal nerve roots in the cauda equina, there is increased likelihood of multiple, bilateral simultaneous nerve root compressions.
Nerve root injury may be complete or only partial and thus may involve all or only a subset of root fibers. With partial injury, incomplete myotomal involvement may result, making the distinction between a radiculopathy and a peripheral nerve injury more challenging.
The lumbosacral spine is susceptible to disc herniations because of its mobility from flexion, extension, and torsion. Seventy-five percent of flexion and extension occurs at the lumbosacral joint [13]. This level, on the other hand, has limited torsion. Twenty percent of flexion and extension occurs at L4-L5. The remaining 5 percent occurs between L1 and L3 [13]. As the L4-L5 and L5-S1 levels are most susceptible to injuries from routine movements of the spine, about 90 to 95 percent of compressive radiculopathies occur at these levels [14]. The incidence of radiculopathies is split somewhat evenly between L4-L5 and L5-S1, as the lack of torsion at L5-S1 helps to increase its stability despite its higher degree of flexion and extension [15]. Next in frequency is L4. Other levels are uncommon.
Far lateral herniations are seen more often at the L2-4 levels. They may affect the rostral root. This is rare, as only 10 percent of far lateral herniations will result in nerve root compression [5]. Pain from the far lateral disc herniations may be more severe due to compression of the dorsal root ganglia [16].
Other skeletal causes — Congenital abnormalities of the bony spinal column or its contents occur in 25 to 50 percent of the general population [17]. Congenital narrowing of the canal is not uncommon as a substrate upon which spondylosis may result in neurologic disease; this is especially true of younger adults. Other developmental abnormalities include tethered cord or diastematomyelia and spina bifida. They may lead to radicular dysfunction due to injuries resulting from traction of the root.
Root avulsion is a rare cause of lumbosacral radiculopathy that may occur with fractures of the sacroiliac joint or with diastasis of the symphysis pubis or the pubic rami
If you experience any saddle numbness (numbness in the groin area), difficulty transitioning from a seated to standing position, or vice versa (typically noted when using the toilet), constant numbness or loss of sensation, or notable weakness in your lower extremities, loss of bowel or urine, or episodes or paralysis; immediate seek emergency medical attention.
Hepar
New member
Sorry to hear. I've been dealing with sciatica since Dec 2005 when I was in a pretty bad car accident. Was lucky to walk away, but it seems like I now have this for life. I can live with the day to day pain and annoyances, but the biggest headache is that I literally get about 4-5hrs of sleep a night and it's seriously taking its toll. I'm ALWAYS tired. Sucks.
The only thing that has helped my symptoms is by getting my core as strong as possible. I find that the stronger my core is, the better my back feels. Hasn't cured it by any means, but it's something.
The only thing that has helped my symptoms is by getting my core as strong as possible. I find that the stronger my core is, the better my back feels. Hasn't cured it by any means, but it's something.
wallytoo
Member
welcome to the clulb. it's a cost of getting older as far as i'm concerned. i have good days and bad days as far as back pain, but i ignore it as best as possible. there are times when it pretty much floors me, but i get up, and keep doing whatever i was doing.
my job involves lots of walking, primarily over uneven ground, in the woods, and i typically cover 3 to 7 miles per day, with some long days that approach 15 miles of walking (not in any particular direction, just the cumulative distance of looking at trees in a property and evaluating them).
i've also noticed that i now get "vision" migraines, where i get almost tunnel-vision with very limited peripheral. at least, so far, no headache with it, and the episodes seem to last for about 5 minutes and then go away for weeks or months.
i split my cordwood by hand, too (with a maul, as opposed to a hydraulic lot splitter). sometimes splitting makes my back feel better. on the other hand, a few days ago, after splitting for about an hour, my back did start to throb, and pretty much hurt the rest of the day and into the evening. sitting or lying down didn't alleviate it at all. the solution was medication, specifically The Macallan single malt, and after that, i slept fine. woke up with no pain, either.
learn to deal with it, and accept that you will have some rough days.
my job involves lots of walking, primarily over uneven ground, in the woods, and i typically cover 3 to 7 miles per day, with some long days that approach 15 miles of walking (not in any particular direction, just the cumulative distance of looking at trees in a property and evaluating them).
i've also noticed that i now get "vision" migraines, where i get almost tunnel-vision with very limited peripheral. at least, so far, no headache with it, and the episodes seem to last for about 5 minutes and then go away for weeks or months.
i split my cordwood by hand, too (with a maul, as opposed to a hydraulic lot splitter). sometimes splitting makes my back feel better. on the other hand, a few days ago, after splitting for about an hour, my back did start to throb, and pretty much hurt the rest of the day and into the evening. sitting or lying down didn't alleviate it at all. the solution was medication, specifically The Macallan single malt, and after that, i slept fine. woke up with no pain, either.
learn to deal with it, and accept that you will have some rough days.
wake_rider
New member
Alright, I've been a sciatica patient since I was 13 and dealt with three fractured vertebras following a motocross accident. Now at 31, my back feels better than it did 5 years ago.
Now, if I go more than two weeks without preventative "rehab," all of my sciatica issues come straight back, so what I'm about to tell you is not a permanent fix, but rather constant treatment and preventative maintenance.
DO YOGA
No joke. I had tried every type of working out (I am a former collegiate athlete, and a current semi-pro sand volleyball player... not enough hours in the day with all my responsibilities to train for full-time touring), and every type of rehab and physical therapy. Some PT certainly helped, but nothing worked like yoga has.
My wife has been into yoga for years and she always tried to get me into it, but I was hardheaded and a bit judgmental of "yogi" types of dudes. Well, I finally gave it a shot and I was amazed with just how wiped out I felt after one at-home session. However, the next day, my sciatica was on fire. Both legs were hot, fiery and burning, and my lower back was almost so bad that it was giving out while I was walking. I thought I'd never to yoga again. I was pissed.
However, my wife talked about how yoga is 80% all the time, and never greater than 90%. I over did it trying to keep up with her, which was supremely ignorant. About two days went by and she had me practice with her again, focusing only on my breathing, correct form, and dialing it back on effort. haha. Being a competitive athlete my whole life, not dialing in 100% on effort is absolutely foreign to me. "Drop ego and focus on your breath," she kept telling me. What she was saying was, "if you're holding your breath in order to get into position because you're straining so hard, back off and focus on easy, full breathing." It's impossible to go more than 80% when you're breathing freely.
Well, fast forward about 2 weeks later, and I was laying in bed realizing that I had zero burning, but a nice warmth down my legs that I had not felt in bed in more than a decade. It was surreal. I had not had that kind of comfort in my lower back, glutes and legs in seriously a decade or so. That was about two years ago, and as long as I stick with at least a mild yoga practice of 30 minutes a day about 3 days a week, then I have no problems. However, if I go more than a week or two without practicing, the problems start to creep right back in. No bueno.
Now, this is not a pill you can cure yourself with overnight. It takes work, but it really does work. If you're in as bad of shape as I was, I was willing to do anything, and yoga did and has continued to work. If you're wanting to have the quick fix, well, look into pills your doctor can prescribe that will dull the symptoms but do nothing to fix the issue. Release that binding and compression in the lower back that causes swelling around the nerves that are flaring up, and you will deliver yourself from that lower-back burning...
hikenbike
New member
Thanks. I've heard this a few times now and I enjoyed yoga when I touched on it when doing P90x a couple of years back. It's not easy by any means but it does get you good and stretched.
hikenbike
New member
wake_rider
New member
Look into a few yoga studios in your area and go take an introductory level class. Now, I will preface this by stating that if you just go to any yoga studio, you might feel awkward because a good number of them cater to old women. However, if you can find an Ashtanga studio, they are the crunchy-granola types of studios where you can find a massive diversity in the students. Normally ashtanga classes are a good 50/50 split between guys and girls, and it's easy to blend in with the crowd. Having somebody show and correct your form, and showing adaptations/modifications for problematic areas is imperative, though. Incorrect form and/or pushing too hard will just end up injuring you worse...
Hepar
New member
I've been meaning to give yoga a go for a while now. This might just be what gets me into the door.
