Sciatica –
Definition: Pain along the course of the sciatic nerve, originating from
irritation of or trauma to its fibers above the knee.
It is a symptom-with-a-range-of-causes:
In the literature of 15th Century Florence, the term sciatica described pain
at the ischial tuberosity. Tuberculosis and arthritis were cited as suspected
causes. Historically, a broad and varying definition suggested unclear
pathogenesis. Distal pedal pain due to intermittent claudication and nerve
entrapment at the fibular head are now termed “pseudo-sciatica” and “peroneal
palsy,” respectively, but they have often been mistaken for sciatica. More
recently, similar symptoms deriving from thalamic cerebrovascular accident,
multiple sclerosis, thoracic spinal fracture, and “phantom limb” phenomena have
been called sciatica because they share a similar distribution of pain. Symptoms
from these causes differ from our core concept in that they involve only the upper
motor neuron. While a patient may accurately describe the pain as “sciatic,” the
word would describe only the symptom and not the common pathophysiology.
We suggest that a CVA in the conus medullaris might be a limiting example of
true sciatica if it involved the lower motor and sensory neurons, but question
whether anything more rostral could be true sciatica. Another borderline case
would be a (rare) mononeuropathy multiplex involving the proximal sciatic nerve.
A study of 700 surgical cases performed under local anesthesia confirmed
the utility of this definition, finding symptoms were reproduced only when the
sciatic nerve or its involved roots were stimulated, stretched or compressed.
Regardless of other tissue involvement or injury, the closer the stimulus to the
site of nerve compression or tension, the greater the pain suffered by the patient.
This pain could always be eliminated by injection of Xylocaine beneath the nerve
sleeve proximal to the site of compression.1
Due to variance in definition, studies putting the lifetime prevalence of
‘generic sciatica’ at 35% must be interpreted cautiously.2 3 4 Two independent
studies with more precise definitions similar to ours yield lifetime prevalence of
true nerve-related sciatica at 5% in men and 4% in women.5 6 It is thought that
back pain affects approximately 14% of adults annually; about 1-2% also have
sciatica. 7 This amounts to 13% of 40,000,000 back pain cases per year: more
than 5,000,000 cases annually.
Three pathogenic groups contain the common causes of sciatica. There are also
a number of infrequent causes as well as a short list of habitual impostors.
Neuroforaminal
One level:
Laterally HNP/bulging disc
Spondylolisthesis
Multiple levels:
Arthritis
Intramedullary:
One level:
Medially HNP/bulging disc
Spondylosisthesis
Multiple levels:
Boney/Ligamentum flavum
Extraspinal
Piriformis syndrome:
Overuse/sitting
Traumatic
Anatomical
Ischial tunnel:
Overuse
Traumatic
Uncommon causesInfectious: e.g., Tuberculosis
Autoimmune: e.g., Lupus Erythematosis,
Lumbosacral plexus
Neuropathy: e.g., Mononeuropathy Monoplex
Neoplastic
Trauma:
Fracture
Gunshot
.
Impostors:
Sacroiliac joint derangement
Intermittent claudication
Thalamic CVA
Peroneal palsy
Morton’s neuroma
Differential diagnosis begins with the location of the pain and the accompanying
symptoms and signs.
Sciatica
Goes below the knee
No
Yes
Yes
Piriformis
Syndrome
Tender Buttock
Weak Abduction
Painful Adduction
No
Radiculopathy
Spinal Stenosis
Polyarthritis
Clinical Tests
Worst Sitting
Weak abduction,
painful adduction
of flexed thigh
Tender midbuttock
Pain with sex (F)
Lab Tests
EMG (FAIR-test)
Neural Scan
Clinical Tests
Numbness
Paraesthesias
Weakness
Incontinence
Reduced reflexes
Sacroiliac
Derangement
Clinical Tests
Pain getting up
Shifts side
Gaenslen’s sign
No Numbness
No Paraesthesias
No Weakness
No incontinence
Lab Test
HLA-B27
for Psoriatic
Arthritis
Lab Tests
EMG
MRI
L1
L2
L3
L4
L5
S1
S2
S3
S4
The problem is at one or more of these levels. See below to determine which ones.
Diagnosis from muscle weakness:
Flexing the thigh (with knee bent) – Dx: Radiculopathy at L 1 – 2
Extending the knee – Dx: Radiculopathy at L 3 – 4
Walking on the heels – Dx: Radiculopathy L 4 – 5
Walking on the toes – Dx: Radiculopathy L 5 – S1
Difficulty controlling the bowel or bladder – Dx: S 1 – 2 – 3
Note: Physical therapists often treat each of these conditions with McKenzie
exercises appropriate for the level and severity of injury.
Diagnosis from numbness and/or paraesthesias:
Inguinal region, including side of testicle, labia majoris: L1
Upper front and side of thigh: L2
Main region of front of thigh down to or including knee: L3
Inside of calf, top of foot: L4 – 5
First web space, very outside of foot, outside of calf: S1
Middle back of thigh: S2
Middle portion of testicles, penis, labia majora, anus: S3
Glans penis, clitoris: S4
*Adapted from Fishman LM, Ardman CA. Sciatica Solutions: Diagnosis,
treatment and cure of spinal and piriformis problems. W.W. Norton. New
York. 2006.
Prediagnostic treatment for sciatica:
Given the painful nature of sciatica, analgesia often precedes diagnostic
workup. Many patients have already started a pain control regimen with
ibuprofen or another over-the-counter non-steroidal anti-inflammatory by the time
they reach the doctor. Nonsteroidal analgesia can be used in ascending order of
potency: Tramadol (g of ultram), acetaminophen (g), meloxicam (g of mobic),
celecoxib (g of celebrex), ketorolac (g toradol), diclofenac (g of voltaren),
indomethacin (g). If ineffective, propoxyphene HCl (g of darvon),
acetaminophen/hydrocodone (g of vicodin), meperidine (g of Demerol), codeine,
acetaminophen/codeine (g of Tylenol #3), acetaminophen/oxycodone (g of
Percocet), Hydromorphone (g of dilaudid), and oxymorphone (g of Opana) can
be utilized. It should be noted that some common synthetic and semi-synthetic
opiates include enough acetaminophen to approach hepatotoxicity at prolonged
higher dosages.
Practical diagnosis:
The diverse etiology of sciatica makes it necessary to be comprehensive
and precise when evaluating a patient. Many clinicians rely on imaging early on
in a patient’s treatment. Plain radiographs are rarely useful in the initial
evaluation of non-geriatric acute back pain. They do not reveal herniated
intervertebral discs nor spinal stenosis, and the findings on plain films are often
unrelated to symptoms. E.g., spondylolisthesis can be seen in up to 5 percent of
normal subjects.8 Immediate X-ray of the lumbar spine should be reserved for
patients with alarm symptoms suggestive of infection, cancer, violent wounds or
fracture; however, a normal plain film itself does not rule out these conditions. In
general, MRI or CT and EMG are required for definitive diagnosis of many spinal
conditions. Nonetheless, these studies are not acutely necessary in patients
with sciatica unless major neurological deficits or severe pain are present.
Imaging studies may sometimes be deferred until 4-6 weeks of conservative
therapy have failed.
Once obtained, there can still be an issue of misdiagnosis. One wellknown study found that more than 30% of a group of pain-free subjects had
serious spinal abnormalities on their MRIs.9 If spinal pathology can be painless,
it can also coexist with sciatica that has a different cause. This prompts the
clinician to use EMG as an extension of the history and physical exam to confirm
the diagnosis.
Treatment for Radiculopathy and Spinal Stenosis by cause:
Herniated Nucleus Pulposus: Whether central or lateral, usual treatment
begins with analgesia and McKenzie and manual medical techniques, extension
exercises, paraspinal myofascial work, modalities, Alexander work, and/or Yoga.
Tapering oral steroids (starting dose often dexamethasone 8 – 16mg) over a 6day to 3 week period may dramatically lower a patient’s pain, enabling him or her
to tolerate an effective therapy program. Translaminar or transforaminal epidural
injections are sometimes beneficial, though studies demonstrating the efficacy of
these common practices are lacking.
True disc-related sciatica has a very high morbidity. This makes surgery
an appealing alternative to conservative treatment for some patients. Many
studies support surgery as the most efficient treatment. One analysis of
medication use, ability to return to work, leisure activity and pain score found that
after the first year of treatment, 30% of conservatively treated patients were
satisfied with their outcome, while 60% of surgically treated patients reported
satisfaction.10 Surgery continued to lead until differences became insignificant at
10 years and beyond. Another study found 99.99% identical outcomes in
surgical and non-surgical patients after 10 years.11 It should be noted that in
most studies the more severely involved patients tended to enter the surgical
group.
One study followed patients hospitalized for disc-related sciatica for five
years, comparing the 1/3 that refused surgery with the 2/3 that did not. At 5
years, 82% of the non-surgically treated patients still had pain in a sciatic
distribution, versus 68% of the surgically treated patients. More than 13% of the
surgical group required an additional operation for recurrent disc herniation.
Outcome studies of this small group of patients found 84% in the WHO 'Severe
handicap’ group. 12
Surgery may be an appealing option for many patients given the generally
more favorable outcome. However, a recent study found little risk of serious or
permanent injury when surgery for simple sciatica was delayed more than 7
months.13 Given this information, a rational approach to treating sciatica clearly
caused by a herniated disc is to attempt conservative treatment for 4-6 weeks. If
intractable pain persists, a microdiscectomy or similar procedure can reasonably
proceed.
Anterior spondylolisthesis, the most common form of spondylolisthesis, in
which the upper vertebra is moved forward relative to the one below, may cause
radiculopathy if it truncates neuroforamina, and/or spinal stenosis if the
intramedullary space is narrowed. It is graded I through IV by the quartiles of
vertebral body displacement. It is often successfully treated with an abdominal
binder or lumbosacral corset, abdominal strengthening and postural training (the
latter by a physical therapist or Alexander therapist). Yoga and Feldenkreis are
also helpful. Beyond grade II, be it antero- retro- or lateral listhesis, surgical
procedures that reestablish the proper alignment often utilize hardware such as
titanium cages, and usually meet with considerable, but sub-total improvement
that may not last more than 4-5 years. Studies of conservative medical,
chiropractic or surgical treatment of spondylolisthesis are few.
Arthritis may narrow neuroforamina to cause radiculopathy unilaterally or
bilaterally at one or more levels. Often, periodic episodes of increasing severity,
frequency and duration occur after age 65-70. Pain as well as motor and sensory
complaints will be gradual in onset, and at least early on, are often positional.
Conservative strategy reduces the attendant inflammation, lowers peripheral and
central sensitization, and increases range of motion at neighboring joints to
reduce compromise at the affected level(s).14 Non-steroidal and/or steroidal antiinflammatories, yoga, and physical therapy often accomplish these three goals,
respectively. 15 16 17 Although quite effective, steroids must be used with caution
in osteoporotic patients. More advanced or complicated cases of arthritis may
require surgery to remove deteriorated bone and disc material, osteophytes, or
other matter impinging on the nerves. In these refractory patients, an EMG is
helpful in identifying and characterizing the levels warranting treatment, and the
severity of impingement.
Boney growth and/or swelling of the ligamentum flavum may narrow the
lumbar intramedullary canal, causing single or multiple level spinal stenosis and
resultant sciatica. The former may have genetic or arthritic pathogenesis, the
latter inflammatory or traumatic. Conservative treatment aims to reduce the girth
of the canal’s contents: tapered oral or epidural steroids, traction, and postural
work by physical therapists, Alexander therapists and osteopathic physicians
have had success.
While ligamentous swelling may subside naturally, boney narrowing will
not. Surgical intervention, sometimes requiring stabilization procedures as well,
should be considered when a progressive boney thickening is documented, but
before emergent intervention is required. Cauda equina syndrome, a rare
complication of spinal stenosis in which ascending numbness or weakness and
bladder or bowel incontinence, results from extreme pressure on descending
rootlets within the intramedullary space, is one such surgical emergency.
In a recent study of nonemergent spinal stenosis surgery, outcome
comparison of control and intervention groups at 1 and 4 years favored surgical
treatment. After 8-10 years, a similar percentage of each group reported low
back pain was improved but sciatica relief continued to favor the surgical group.18
Because it is generally progressive, surgery for spinal stenosis may wisely occur
before it is utterly mandatory, since its necessity may arise after the patient is too
frail for it.19
Piriformis syndrome is an under-recognized cause of sciatica. This was
validated when 239 patients who failed conservative or surgical treatment for the
above causes underwent MR neurography. Piriformis involvement was found in
more than 2/3 of them.20 Symptoms arise from compression of the sciatic nerve
as it exits the buttock in relation to the piriformis muscle, due to spasm or
tightness in the muscle. The chief environmental causes are overuse at health
clubs, from running, outdoor activities, excessive sitting, trauma from auto
accidents and falls. Anomalous relationships between the sciatic nerve and the
inferior gluteal artery or vein at the greater sciatic foramen are uncommon but
demonstrated anatomic bases for pain.
Diagnosis is made by EMG through delay of H-reflexes in flexion,
adduction and internal rotation (the FAIR-test). Comparing affected with
unaffected limbs helps rule out radiculopathy or spinal stenosis, and may be
used in the 90% of cases that are unilateral. 21 Neural scan imaging (NMR) will
show asymmetrical development of the affected piriformis muscle, and evidence
of inflammation or focal narrowing of the sciatic nerve. EMG and NMR will only
be positive if piriformis syndrome is present, and not in simple SI derangement
alone. However, these conditions occur together with some frequency. Since the
piriformis muscle arises in part from the sacroiliac joint, it is possible that SI joint
derangement causes piriformis muscle spasm in these cases.
Conservative treatment begins with EMG- or fluoroscopically-guided
steroid and Lidocaine/Marcaine injection of the piriformis muscle near its lateral
musculotendinous junction, as well as stretching and relaxing the muscle, using
ultrasound, myofascial release and spray/stretch techniques. Appropriate home
yoga therapy is often successful over time.22 Botulinum neurotoxin A or B, 300
or 12,500 units, respectively, in four locations throughout the muscle, are
reported to significantly relieve 60% to 90% of resistant cases.23 Neurovascular
anomalies and ventral piriformis muscle scars require surgery which appears to
benefit 60-80% of cases.24
Confusion resolved:
While the rare vascular and neurological abnormalites have been shown
to cause piriformis syndrome, the common variations in anatomy do not.
Piriformis syndrome is often attributed to one or both branches of the sciatic
nerve passing through the piriformis muscle, an anatomic “anomaly.” Cadaveric
studies show that approximately 15% of the population has at least one branch of
the sciatic nerve that travels such a course. Interestingly, in these people, the
anatomy is bilateral more than 90% of the time. The “anomaly” theory comes
into question in that complaints consistent with piriformis syndrome are bilateral
in less than 10% of patients. Further, at surgery only 15% of patients had
anatomy consistent with the “anomaly” theory, the same percentage that is seen
in the general population. 25
Ischial tunnel syndrome:
The FAIR test is occasionally positive when entrapment is at a site other
than the piriformis muscle. Four percent of sciatic nerve entrapment in the
buttock is due to entrapment as the nerve passes close to the ischium.26 The
pudendal nerve may be separately involved. Neural scan is the definitive
diagnostic tool for ischial tunnel syndrome. In these cases, treatment begins with
myofascial release, modalities, and postural re-training. Surgery is reported but
outcome studies lack sufficient numbers to be persuasive.
There are many other causes of sciatica, ranging from tumor and fracture
to gunshot wound. In all the pathogenetic mechanism and the diagnosis can be
understood on the anatomical bases that we have attempted to provide. Multiple
conditions can coexist in which the analytical “either – or” approach is not
recommended:
Proper initial treatment for a herniated disc is extension exercises, which
is contraindicated in spondylolisthesis and non-disc forms of spinal stenosis. For
these spinal stenosis and spondylolisthesis, flexion is standard, a treatment
which is contraindicated for most herniated discs. In the occurrence of both
conditions, lateral strengthening and spinal work such as the yoga pose
vasisthasana have proven useful in alleviating pain, with Fonar evidence of
anatomical improvement.28 To distinguish whether spinal stenosis or
neuroforaminal pathology is the major causative factor in a given patient’s pain,
other provocative tests, and functionally sensitive nerve-conduction are often
helpful, though currently at the experimental stage.
References
1
Kuslich SD, et al. "The Tissue Origin of Low Back Pain and Sciatica: A report of pain response
to tissue stimulation during operations on the lumbar spine using local anesthesia." Orthop Clinic
North Am 1991; 22:181-187.
Heliovaara M, et al. “Lumbar disc syndrome in Finland.” J Epidemiology Community Health
1987; 41:251-258.
2
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.
3
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.
4
Heliovaara M, et al. “Lumbar disc syndrome in Finland.” J Epidemiol Commun Health 1987;
41:251-258.
5
Manninen P, et al. “Incidence and risk factors of low-back pain in middle-aged farmers.”
Occupational Medicine 1995; 45:141-146.
6
Deyo, RA, Tsui-Wu, YJ. “Descriptive Epidemiology of low back pain and its related medical
care in the United States.” Spine 1987; 12:264.
7
8
Rothman RH, Simeone FA: Spondylolisthesis. The Spine 1992; Volume 1: 913-969.
Jensen MC, Brant-Zawadzki MN, Obuchowski N, Modic MT, Malkasian D, Ross JS. “Magnetic
resonance imaging of the lumbar spine in people without back pain.” New England Journal of
Medicine; 1994:69-73.
9
10
Weber H , '1982 Volvo Award in Clinical Science' "Lumbar Disc Herniation: A controlled,
Prospective Study with Ten Years of Observation." Spine 1983; 8(2):131-140.
11
Agency for Health Care Policy and Research. Acute Low Back Problems in Adults. Clinical
Practice Guidelines no. 14. Rockville, Md., 1994, Publication 95-0642.
12
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.
13
Carragee E, “Surgical Treatment of Lumbar Disk Disorders.” JAMA 2006; 296:2485-2487.
Wolff CJ, Salter MW. “Neuronal Plasticity: increasing the gain in pain.” Science. 2000;
288:1765-1768.
14
Raghuraj P, Telles S. “Effect of yoga-based and forced uninostril breathing on the autonomic
nervous system.” Percept Mot Skills. 2003; 96(1):79-80.
15
Telles S, Hanumanthaiah BH, Nagarathna R, Nagendra HR. “Plasticity of motor control
systems demonstrated by yoga training.” Indian J Physiol Pharmacol. 1994;38(2):143-4.
16
17
Williams KA, Petronis J, Smith D, Goodrich D, Wu J, Ravi N, Doyle EJ Jr, Gregory Juckett R,
Munoz G, Kolar M, Gross R, Steinberg L. “Effect of Iyengar yoga therapy for chronic low back
pain.” Pain. 2005; 115(1-2):107-17.
18
Atlas SJ, Deyo RA, et al. 'Long-term outcomes of surgical and nonsurgical management of
sciatica secondary to a lumbar disc herniation: 10 year results from the maine lumbar spine
study.' Spine 2005 Apr 15; 30(8):927-35.
19
Agency for Health Care Policy and Research. Acute Low Back Problems in Adults. Clinical
Practice Guidelines no. 14. Rockville, Md., 1994, Publication 95-0642.
Papadopoulos, EC, Khan, SN. “Piriformis syndrome and low back pain: a new classification
and review of the literature.” Orthop Clin North Am 2004; 35:65.
20
Fishman LM, Zybert PA. “Electrophysiologic evidence of piriformis syndrome.” Arch Phys Med
Rehabil 1992 Apr; 73(4): 359-64.
21
22
Fishman L, Ardman C, Relief is in the Stretch. W.W. Norton. New York, 2005.
Fishman LM, Konnoth C, Rozner B. “Botulinum neurotoxin type B and physical therapy in the
treatment of piriformis syndrome: a dose-finding study.” Am J Phys Med Rehabil 2004 Jan; 83(1):
42-50.
23
Mizuguchi T. “Division of the piriformis muscle for the treatment of sciatica. Postlaminectomy
syndrome and osteoarthritis of the spine.” Arch Surg 1976 Jun; 111(6): 719-22.
24
Broadhurst NA, Simmons DN, Bond MJ. “ Piriformis syndrome: Correlation of muscle
morphology with symptoms and signs.” Arch Phys Med Rehabil 2004 Dec; 85(12): 2036-9.
25
Filler AG, Haynes J, Jordan SE, et al. “Sciatica of nondisc origin and piriformis syndrome:
diagnosis by magnetic resonance neurography and interventional magnetic resonance imaging
with outcome study of resulting treatment.” J Neurosurg Spine 2005 Feb; 2(2): 99-115.
26
27
Fishman LM and Saltonstall E. Yoga for Osteoarthritis W.W. Norton, New York. Scheduled for
publication in Spring 2008.