Piriformis Syndrome


Piriformis Syndrome

The sciatic nerve, the biggest in the body, forms behind the sacrum and exits the pelvis beneath the piriformis muscle. At times the over-tight muscle, and rarely, anatomical irregularities will compress the nerve, creating severe sciatic pain that is usually worse with sitting. Some people have this extremely painful condition for years before it is diagnosed, and it can be disabling.

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The usual causes are prolonged sitting at the computer or elsewhere, over-exertion in sports or working out, and trauma, such as an automobile accident or a backward fall.

At the right is the sciatic nerve exiting the pelvis just below the piriformis muscle, seenin its usual environment, the anatomy book (Clemente CD. Anatomy: A Regional Atlas of the Human Body. 3rd Ed.Urban and Schwartzenberg. Munich; 1987: fig 430.)  The tightened muscle presses the nerve into the sharp edge of the ischiofemoral ligament that lies just below it.

A physical exam is the first step to diagnosing piriformis syndrome. Electrodiagnosis testing the delay of reflexes along the sciatic nerve when the piriformis muscle is stretched across it makes the diagnosis definitive and helps to monitor the efficacy of [Hypertext: treatment].  A special MRI (neural scan) is also often helpful.

We performed a controlled, double blinded, randomized crossover study designed to assess the effects of botulinum injection into the piriformis muscle after diagnosing it with the FAIR-test (described below).  It proved quite successful, as per the graph that represents the patients’ response to a measure of their pain, the visual analogue scale (VAS). Level of pain was estimated every two weeks for three months following either botulinum injection (blue) or placebo (red) in a double blinded study of 58 patients.

Piriformis Syndrome Diagnostic Quiz

Just answer the questions below: the increase or decrease in odds represents the increased or decreased probability that conservatively treating the individual for piriformis syndrome will be helpful in relieving their pain at least 50%.*

Years of pain:
Positive Fair Test?
Overuse?
Tender Piriformis / sciatic nerve junction?
Solheim Sign?
Pain is worse when sitting (vs. standing)?
Female gender / high weight?
Illiotibial Band Syndrome?
Injection?
Non-sciatic Denervantion?
Peroneal Polyphasics?
Non-sciatic Polyphasics?
Relative Risk:

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Diagnosis and Treatment of Piriformis Syndrome

 

Piriformis syndrome has been estimated to cause 6% of sciatica in the past, but contemporary electrodiagnostic and imaging techniques find it significantly more common. Its prevalence is raised in the general U.S. population because it has been underdiagnosed and undertreated. The following outline is intended to summarize elements of the history and physical findings that suggest piriformis syndrome, and the electrophysiological methods for documenting its presence, injection technique and physical therapy. It includes an empirically-based interactive means to determine the probability that a given case of sciatica is due to piriformis syndrome. Finally, there is a section on outcome, alternative treatments, and our current clinical research protocol.

Diagnosis

The patient with piriformis syndrome typically complains of sciatic pain, tenderness in the buttock, and more difficulty sitting than standing. The pain usually arises from overuse: health club, athletics, heavy work, or prolonged sitting, though traumatic causes are also reasonably common, including automobile accidents, falls, and penetrating wounds.

Physical findings include tenderness of the buttock region, increased pain with adduction, internal rotation and flexion of the affected thigh while the patient is in the contralateral decubitus position (after Solheim), weakened abduction of the flexed thigh (after Pace), and frequently sacroiliac joint derangement and/or iliotibial band syndrome.

EMG findings include positive FAIR-test (increased H-reflex latency with Flexion, Adduction and Internal Rotation), signs of denervation (acute or chronic) in the pattern of the posterior tibial or the peroneal nerves, as opposed to a radicular distribution, reduced CMAPs and particularly sural SNAP on the affected side, and usually normal paraspinal EMG.

While standard MRI findings may describe either an atrophic or hypertrophic piriformis muscle in an affected buttock, newer neuroimaging techniques are more diagnostic and informative for future surgical intervention. See Aaron Filler, et. al.

Functional EMG testing

The FAIR-test compares the sum of M-wave plus H-reflex in the anatomical position with the sum of M-wave plus H-reflex in the Flexed, Adducted, Internally Rotated position, a provocative maneuver. In testing 88 normals, the standard deviation was 0.62 ms, with mean value of the H-reflex latency changing by -.01 ms. Therefore the positive FAIR-test’s H-reflex differs from the anatomical H-reflex by at least 1.86 ms, three standard deviations beyond the mean seen in normal.

The Positive FAIR test

The patient should be lying in contralateral decubitus, face toward the examiner. Though it is somewhat painful, the physician or assistant should flex, adduct and internally rotate the affected leg by grasping the ankle with one hand, and holding back the hip (to prevent the patient turning prone) with the other. See figure 1. One should be sure that the patient’s navel is facing above the horizontal, to prevent the patient from inadvertently lying prone, and ending up in abduction instead of adduction.

The physician should use caution not to injure the patient by overly vigorous adduction, internal rotation (the angle alpha in the figure above) or flexion, in that order. This is a provocative test, and indiscretion can bring about some harm. Both posterior tibial and peroneal nerves are tested, making four M-waves plus H-reflexes for each limb tested. For the posterior tibial nerve, the ground is placed just distal to the popliteal fossa, with active and reference electrodes placed over the soleus muscle in proximal to distal array, respectively. For the peroneal nerve, active and reference electrodes are placed in the same alignment four fingerbreadths distal to the fibular head. H-reflexes are studied in the anatomical position, and in flexion, adduction and internal rotation without moving the electrodes. Each limb serves as its own control. Therefore, if an alternative placement is used, there

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is a high likelihood of a meaningful result, provided the same montage is maintained for both the anatomical and FAIR H-reflex. In each case the anatomical (M + H) is subtracted from the FAIR (M + H).

H-reflex and M-wave are added because it is likely that the FAIR positioning moves the sciatic nerve’s fibres beneath the skin. Still, the sum of the reflex arc, from the soleus muscle up to the level of synapse at T-11 or T-12 and back down to the soleus muscle is a set distance. If the nerve moves proximally, then the sensory limb of the reflex becomes longer, and the M-wave shorter by the same amount. As illustrated below, if the point of stimulation (of the nerve, not the skin) moves from S1 to S2, then the motor fibres’ course down to the soleus (M-wave) is lengthened by exactly the same distance that the sensory limb of the H-reflex is shortened, (S1 – S2.)

These factors cancel each other, and the movement of the nerve poses no difficulty unless the motor and sensory nerve conduction velocities differ. Usually this is negligible. Assuming the nerve moves 5 cm. and that the motor nerve conduction velocity is 50 m/s while the sensory nerve conduction velocity is 40 m/s. Distance equals rate X time.

D = RT

D/R = T

0.05 m (divided by) 50m/s = .001s

0.05 m (divided by) 40m/s = .00125s

Difference of H-reflex latency = -.00025s

This is less than 0.5 standard deviation beyond the mean found in studies of normals.

In testing 88 normals, the mean standard deviation was 0.62 ms. In testing 1014 suspected legs, the mean maximum prolongation for all legs judged positive for piriformis syndrome on clinical criteria was 3.275 ms, or 5.28 standard deviations.

The prolongation of the H-reflex is reversible, doing no permanent damage to the nerve fibres, but producing a temporary neuropraxia that confirms significant pressure generated by the piriformis muscle on one or both portions of the sciatic nerve.

The delay in H-reflex is not subtle: any nerve conduction slowing brought about by stretching the piriformis muscle over the sciatic nerve and/or its divisions has an effect on both the ascending and descending limbs of the H-reflex arc, doubling any discrepancy that the stretch produces. After flexing the hip to 90 degrees, then as one increases adduction and internal rotation (the angle alpha in the drawing above), the H-reflex response is prolonged proportionally. As amount of adduction and internal rotation (the independent variable) increases, the prolongation of the H-reflex (the dependent variable) increases. There are cases in which flexion, adduction and internal rotation is so painful to the patient that one must look for changes in the dependent variable according to smaller increments and decrements of the independent variable in order to establish that piriformis syndrome is present. In these cases the responsiveness of the dependent variable (H-reflex latency) to changes in the independent variable (how much you stretch the muscle in flexion, adduction and internal rotation) is the best indicator of piriformis syndrome.

Using the FAIR-test to detect piriformis syndrome has the following sensitivity and selectivity.

 

Either Posterior Tibial or Peroneal

FAIR-test > 3 Standard Deviations (1.86ms)

Piriformis Syndrome*

Met Clinical Criteria Yes No Total
 

FAIR-test

Positive

 

512

 

69

 

581

Negative 26 129 155
Total 736**

 

Sensitivity = 0.881; Specificity = 0.832

*Clinically Determined

**240 additional cases were unjudged.

 

 

Either Posterior Tibial and Peroneal

FAIR-test > 2 Standard Deviations (1.24ms)

Piriformis Syndrome*

Clinical Crit              Yes            No              Total
Positive            568            19              587
Negative            107            49              156
Total              743**

 

Sensitivity = 0.986, Specificity = 0.686

*By Clinical Criteria

**237 additional cases were unjudged.

Given this means of diagnosis, (see Fishman and Zybert, 1992) and the neuroimaging techniques recently developed at UCLA, (see Filler, et. al. 2005) piriformis syndrome is no longer a diagnosis of exclusion. Authors of recent articles using these active diagnostic techniques, have found that piriformis syndrome is a common cause of sciatica, possibly as common or more common than the herniated disc. It is important, therefore, to recognize the clinical signs of piriformis syndrome, and obtain one of the reliable tests for it when the signs are present.

However, if there are signs of denervation of the hamstrings, glutei, tensa fascie lata, and/or the piriformis muscle itself, then, since the nerve supply for these muscles does not travel under or through the piriformis muscle with the sciatic nerve, there are likely to be other causes of these findings, and possibly other causes of the patient’s sciatica which may, naturally, coexist with piriformis syndrome in the same patient.

A discussion in the journal Muscle and Nerve included a criticism of our work by Dr. John D. Stewart of McGill University. He cast doubt on our findings since we did not isolate patients that had MRIs without evidence of spinal pathology, nor patients with normal electrophysiological examinations of the paraspinal muscles. (1) We feel that Dr. Stewart’s criticism was just, since it would help to distinguish patients in whom there was minimal suspicion of a spinal cause for their sciatica.

Since that time we have looked over the records of those same patients. Here are the statistics:

 

Outcomes of Patients with Piriformis Syndrome

by Lumbar MRI and Paraspinal EMG (n=449)

MRI (n) Improved 60% or more Average Improvement Years of Pain
 

Positive

 

129

 

74.7

 

62.3

 

6.9

Negative 320 74 61.5 5.8
 

Normal MRI + EMG

179 76 61.8 5.9

 

It appears that patients did very much the same whether their MRIs showed spinal pathology or not. This may be due to the fact that an individual may have more than one diagnosis. They may have piriformis syndrome and spinal pathology. The question is which one is the major cause of their pain. Since in our medical environment the herniated disc is generally recognized and treated first, the majority of the patients who have come to us with these two diagnoses are the ones in which the piriformis syndrome was the major cause of their sciatica.

In researching Dr. Stewart’s question, the FAIR-test appears able to determine if the piriformis impingement is an operant cause of sciatica in these cases. The patients with spinal pathology actually did (insignificantly) better than the others, but what may be significant is that they suffered more than one year longer. This is possibly due to the greater period of time clinicians spent treating the lower back in these patient, exactly because their MRIs were positive, but, as it turned out, irrelevant to their pain. In part, then, their suffering is a consequence of considering piriformis syndrome a diagnosis of exclusion.  We have recently (summer 2015) completed a double-blinded, randomized, controlled study in which we excluded patients with electromyographic signs of paraspinal denervation.  The data is currently with the statistician, but just eyeballing the data suggests that the treatment of the piriformis muscle in cases of positive FAIR-tests is effective well beyond what is seen in placebo treatment.

Treatment

The prolongation of the H-reflex is reversible, doing no permanent damage to the nerve fibres, but producing a temporary neuropraxia that confirms significant pressure generated by the piriformis muscle on one or both branches of the sciatic nerve. There can be denervation, but it is usually mild, preserving adequate nerve fibre supply for reflexes, normal activity and the exuberant outbursts of energy that characterize most people’s lives.

Improvement of Piriformis Patients with Positive FAIR-tests

NERVE Improved 50% with PT (n) Improved 50% with surgery (n) Clinicians Seen (n) Years with Pain (n) Sural SNAP Reduced 50% (n)
P Tib. 71.2% (345) 70%  (43 ) 6.5 (345) 6.6 (345) About 30%
Peron. 71.0% (320) 70% (23) 6.6 (320) 5.8 (320) About 30%
Mean  

71.1% (665)

 

70%

(66)

 

6.55 (665)

 

6.2

(665)

About 30%

 

If overuse and trauma are the chief causes of piriformis syndrome, spasm and scarring are the main mechanisms by which pain is produced. Leg-length discrepancy, contracted iliopsoas muscle, prolonged sitting, poor seating and over-enthusiastic exercise can be countered with heel-lift, iliopsoas stretching and gait training, breaks in sitting, better chairs and vehicular seats, and cutting down on exercise programs, respectively. For simple spasm, the following program of physical therapy has brought 79% of the 1014 legs treated a minimum of 50% improvement or more.(See Fishman, et. al., 2001).

Improvement of Piriformis, non-Piriformis and Surgical Patients

Weight (n) Age (n) Average Months Followup (n) Average Improvement (n)
 

Piriformis Present

150.99 (671) 54 (671) 10.2 (671) .71 (671)
 

Piriformis Absent

149.57 (332) 57 (331) 9.9 (339) .55 (339)
 

Mean

 

149.12 (42)

 

49 (42)

 

10.1 (42)

 

.66 (42)

 

These exercises require a physical therapist or physician, and should not be attempted otherwise. They are dangerous and will harm people who have advanced osteoarthritis of the hip, sacroiliac joint derangement, lumbar hypermobility, hip or knee replacements, and a number of other conditions. For patients with piriformis syndrome and these other conditions, physicians must devise and supervise the safe practice of different exercises, often modifying what follows.

Physical Therapy for Piriformis Syndrome

  1. Place patient in contralateral decubitus and Flexed Adducted Internally Rotated (FAIR) position:**
  2. Ultrasound to piriformis muscle, while leg is placed in flexion, adduction and internal rotation (FAIR): 2.25-2.5 watts/cm2 for 10-14 minutes. Beware of patients with any hypoaesthesia or anaesthesia due to neurological or surgical causes in the dorsal lumbosacral region. Beware of cavitation in post-laminectomy patients.**
  3. Wipe off ultrasound gel.
  4. Hot packs or cold spray at the same location x 10 minutes.
  5. Stretch the piriformis muscle for 10-14 minutes by applying manual pressure to the muscle’s inferior border, being careful not to press downward, rather directing pressure tangentially, toward the ipsilateral shoulder.****

6. Myofascial release at lumbosacral paraspinal muscles.

  1. McKenzie exercises.
  2. Use lumbosacral corset when patient in the FAIR position.*****

Duration: 2-3 times weekly for one-two months.

*Patients usually require 2-3 months of biweekly therapy for 60-70% improvement.

**Because it is painful, patients often subtly shift to prone. This must be avoided because it works to place the affected leg in abduction, not adduction, greatly reducing the stretch placed on the piriformis muscle.

***Cavitation is unreported in more than 20,000 treatments

****Unless explicitly stated, therapists may tend to knead or massage the muscle, which is useless or worse. The muscle must be stretched perpendicular to its fibres, in a plane that is tangent to the buttock at the point of intersection of the piriformis muscle and the sciatic nerve, but approximately 3-4 of an inch deep to the buttock, (i.e., just below the gluteus maximus).

*****This is useful in patients that have had laminectomies, or in others to prevent lumbar hypermobility.

Calculate the Likelihood of Piriformis Syndrome

This brief interactive table is intended to estimate the likelihood that an individual’ will recover in treating them for piriformis syndrome via our protocol. The calculated odds may also indicate the individual’s likelihood of having piriformis syndrome, but since we have come to define piriformis syndrome using these very criteria, that would be circular. What is not a matter of definition is that people’s answers to these questions turns out to be a strong basis for predicting whether treating them for piriformis syndrome will help them significantly. This table does not diagnose anyone, but gives the added probability that each symptom provides.

The table is based on a careful study of more than 1000 cases of sciatica, most of which had no evidence of spinal injury, or had already had spinal surgery which did not benefit them.

Once again, it is intended as a means for a clinician or patient to determine the value of pursuing the diagnosis of piriformis syndrome further. It is not a means to diagnose in itself. One needs to see a person “in the flesh,” do a physical exam, review a good history, and perform tests to arrive at a diagnosis one can trust enough to act upon.

Now what percentage of the people with sciatica have piriformis syndrome in the first place? No one knows. We certainly don’t, since our population of patients is significantly skewed toward those people that have it! Twenty years ago doctors at the Mayo Clinic estimated piriformis syndrome to account for 6% of sciatica, (Hallin, 1983) but the incidence of the diagnosis in the county of the Mayo Clinic has gone up five-fold since then. (Fishman,2003) Comparing the number of MRIs done annually in the United States with the number of lumbar surgeries, a neurosurgeon at Cedars-Sinai Hospital in Beverly Hills, California estimated that piriformis syndrome may be as common a cause of sciatica as herniated disc. (Filler, 2005) All we can say is that based on current data, an individual’s chance of recovering from the therapy we outlined above is greater or lesser depending upon the factors we have isolated so far, and offer tests to confirm or exclude it.

Still, people with the lowest probablilty may, of course, have piriformis syndrome, just as a horse with long odds sometimes win the race, and people that currently have no spots may develop chicken pox! In the case of piriformis syndrome, as in just about everything in medicine, the history and physical, performed by a conscientious and informed clinician are the golden standard of care, and the royal road to diagnosis.

Just answer the questions below: the increase or decrease in odds represents the increased or decreased probablility that treating the individual for piriformis syndrome will be helpful in relieving their pain at least 50%.*

Years of pain: 1
Positive Fair Test?
Overuse?
Tender Piriformis / sciatic nerve junction?
Solheim Sign?
Pain is worse when sitting (vs. standing)?
Female gender / high weight?
Illiotibial Band Syndrome?
Injection?
Non-sciatic Denervantion?
Peroneal Polyphasics?
Non-sciatic Polyphasics?
Relative Risk: -0.0943 (baseline)

* Based on thorough history and physical and approximately 10 month follow-up of more than 1000 sciatica-sufferers.

 

Definitions and explanations:

 

Years of pain: Please use digits and decimals.

Positive FAIR-test: Nerve conduction test performed by physiatrists and neurologists in which the H-reflex is prolonged at least 1.86 ms when the leg with sciatica is stretched in flexion, adduction and internal rotation.

Overuse: More than 3 miles/day running, high-performance athletics such as tennis, fencing, pole-vaulting, or sitting for hours at a time are examples.

Tender piriformis/sciatic junction: Pain with digital or other pressure just below the mid-buttock. Occasionally this may induce or exaggerate the sciatica.

Solheim’s sign: Pain with adduction of the flexed thigh, which stretches the piriformis muscle against the sciatic nerve. We named after the Norwegian neurosurgeon that described it.

Pain is worse when sitting than standing: This may take 15 minutes to 1 hour to appear.

Female gender/high weight: Obese females, with body mass indices above 30, had lower recovery rates than others. This is the only negative factor on the list.

Iliotibial band syndrome: Pain and tenderness along the lateral edge of the affected thigh. A physician, physical therapist or chiropractor might help confirm this diagnosis.

Injection: 20 mg triamcinolone acetonide with 1.5 cc of 2%Lidocaine was used in our studies. We now use EMG guidance, and may use .5% Marcaine or up to 300 units of Botulinum neurotoxin Type A, or 12,500 units of Botulinum neurotoxin Type B, all of which improve the positive influence of this factor beyond what is represented here.

Non-sciatic denervation: EMG findings of nerve loss in muscles that are not innervated by the sciatic nerve improved people’s responsiveness for debatable reasons.

Peroneal polyphasics: EMG findings of chronic denervation with recovery may reflect a long-standing condition. Because of its underdiagnosis, piriformis may be more likely to be untreated for longer than other causes of sciatica with denervation.

Non-sciatic polyphasics: EMG findings of chronic nerve loss in muscles that are not innervated by the sciatic nerve improved people’s responsiveness. The explanation for this is not clear.

Yoga Therapy for Piriformis Syndrome

1. Janusirsasana
 2. Matsyendrasana
 3. Parivrtta Trikonasana 
4. Parivrtta Parsvakonasana 
5. Garudasana
6. Gomukhasana
 7. Kapotasana

There are many substitutes and fine points to the long-term yoga treatment of piriformis syndrome. Those interested find further information in Yoga for Back Pain. Fishman LM, Ardman CA. W.W. Norton 2006, Piriformis Syndrome. Fishman, LM ebook, 2014, and Healing Yoga, Fishman, LM, W.W. Norton 2015.

Injection of 20 mg. Triamcinolone Acetonide with 1.5cc of 2% lidocaine or 0.5% marcaine has been successful in relieving pain in the short run and enhancing patients’ recovery rates and overall improvement. Botulinum injections do not take effect for five to ten days, but have been shown to enhance overall improvement most reliably in the 2-6 month range. A detailed description of these injections can be seen in Current and Past Research. Physicians can e-mail loren@sciatica.org for further information.

 

 

Characteristics Favoring a Successful Outcome

p-value odds Ratio 95%   C.I.*
Positive Fair Test .001 2.225  

1.42-3.60

 

Overuse .001 2.05  

1.35-3.12

 

Tender Piriformis/sciatic .003 1.97  

1.20-2.82

 

Solhiem Sign .005 1.84  

2.25-4.90

 

Sitting worse than standing .007 1.77  

1.17-2.68

 

Male Gender .017 1.67  

1.10-2.50

 

Illiotibial Band Syndrome .028 1.67  

1.12-7.38

 

 

Injection

.030 1.55 1.05-2.31

 

* Confidence interval

Values are from logistic model (univariate analyses) and stepwise regression: receiver operating characteristic (ROC) = 6.92. Stepwise logistic regression model CI was larger but comparable. n = 651 patients, 514 successful outcomes ( 50% improvement or more.)

So What’s Really Going on Here?

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 well-known study found that more than 50% 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 Back Pain 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 6-day 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.  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.

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.  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.

Central Spinal Stenosis: although the symptoms may be literally identical, the treatment for is almost the opposite of what works for herniated disc. There is a large ligament at the back of the actual spinal canal which buckles with extension and actually narrows the space up to 63%. What works for spinal stenosis is flexion, something that for a herniated disc would be painful and possibly harmful!  We have developed electrophysiological techniques to determine whether spinal stenosis or herniated disc is really responsible for a person’s pain, invaluable tool when both conditions are present, as they frequently are. Once we found out what the main pain generator is, we can use yoga to teach people what they need you on their own, and free them from a dependence on medications and even physical therapy.

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 anti-inflammatories, yoga, and physical therapy often accomplish these three goals, respectively.  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.  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.

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.  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.  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.  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.  Neurovascular anomalies and ventral piriformis muscle scars require surgery which appears to benefit 60-80% of cases.

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 gIschial 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.  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, which considers certain diagnostic entities “diagnoses of exclusion”  is not recommended.  Considering a condition a diagnosis of exclusion logically cannot find those cases in which more than a single condition coexist.  Considering that piriformis syndrome, herniated disc and spinal stenosis, just to name three pathological entities that are independent and can occur together, it is logically impossible not to under-diagnose piriformis syndrome if it is considered a diagnosis of exclusion.

 

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