An Unexpectedly Progressed Lumbar Herniated Disk

To the Editor:

After reading the case report by Lipton and McLeod¹ in the December 2013 issue of The Journal of the American Osteopathic Association, I have some concerns. I believe the history and physical examination findings in this patient are consistent with that of a patient who has pain and dysfunction in the left lower extremity and back caused by somatic dysfunctions in the lumbar spine, pelvis, and lower extremity. In my experience, the findings of Lipton and McLeod¹ are not consistent with a patient who has nerve damage in the spinal canal that caused pain of a perceived radicular nature in the foot. The injury to the left foot, which caused the fracture of the fifth metatarsal bone, could have caused somatic dysfunction of the ankle and lower leg and may have caused or exacerbated somatic dysfunction of the sacroiliac region.

The authors¹ explain that the patient was treated 6 months before presentation for a fracture of the left fifth metatarsal bone and that she wore a boot and walked with crutches for 8 weeks after the injury. However, details as to how this injury occurred are lacking. The physical examination findings are incomplete and, I believe, do not support a diagnosis of the clinical syndrome of lumbar spinal stenosis. A posteriorly rotated left anterior superior iliac spine (ASIS) and a physiologic short left leg were palpated. A right-on-right sacral torsion was noted. Physical findings that would corroborate the diagnosis of pain radiating into the foot from a proximal source are nonexistent. A lower extremity that has been locked in a boot for 8 weeks that occurred 6 months before presentation would be worthy of a detailed physical examination.

The posteriorly rotated left ASIS (classically described as a superior ASIS in osteopathic literature) is most commonly seen in the diagnosis of a left posterior innominate somatic dysfunction.² This diagnosis would require the finding of an inferior left PSIS (posterior superior iliac spine). During the normal walking cycle, when the left leg is forward, the left innominate is rotated posteriorly and the sacrum is in a right-on-right torsion.³ Patients who have diagnoses of a combination of these somatic dysfunctions have been shown to have a gait abnormality in which the stride length is reduced and the left step length is significantly longer than the right step length.⁴ It has also been shown that osteopathic manipulative treatment can result in not only a lengthened stride length but also in an equalization of the step length in a patient with these diagnoses.⁴

A patient whose sacroiliac region is stuck in this position has several restrictions to overcome when attempting to move the right leg forward. A left posterior innominate somatic dysfunction does not allow the left innominate to rotate anterior sufficiently to close the left sacroiliac joint. Similarly, with right-on-right sacral somatic dysfunction, the left sacral base has rotated rightward about a right oblique axis; it is stuck in this position and therefore cannot rotate posteriorly about this axis to close the left sacroiliac joint.⁴ When the patient tries to step forward with the right leg, the left sacroiliac joint is unable to contribute to this motion of the body. Therefore, the patient cannot shift the center of gravity physiologically to the left and efficiently swing the right leg forward maximally.

I have found that in patients with these somatic dysfunctions, the left lower extremity often has somatic dysfunctions involving the normal motions of the bones in the positions found physiologically with this forward position of the leg. The ankle may have a plantar somatic dysfunction, the tibia is often internally rotated, and the fibular head is posterior, which can cause hypertonicity of the lateral head of the biceps femoris muscle and the iliotibial band on the affected side. In my experience, this condition is frequently misdiagnosed as sciatica.

The overall management of the case described by Lipton and McLeod¹ raises several questions. The authors state that during the first 45 days of follow up in the physical medicine and rehabilitation department, the patient experienced relief of pain after osteopathic manipulative treatment sessions (changing from 7 to 0 on a 10-point scale). In late February 2012, they reported that she was “now aware that she had had a disk herniation at L4-5 2 years earlier that was diagnosed by [magnetic resonance (MR) imaging].”¹ Because of this revelation, a repeat MR image of the lumbar spine was ordered. The authors provide a figure that lists 10 reasons to order an MR image in a patient with low back pain. None of these include a patient having a prior MR image of the lumbar spine that demonstrates a herniated disk. Another reference cited by Lipton and McLeod to support ordering this test clearly states, “Decisions about repeated imaging should be based on development of new symptoms or changes in current symptoms.”⁵

This patient's condition was diagnosed as “severe stenosis” and was “successfully referred for surgical treatment despite her apparently unremarkable presentation.” A review of the medical literature suggests that the diagnosis of severe spinal stenosis is dependent on the history and physical examination before radiographic findings. Akuthota et al state, “The conundrum of spinal stenosis, like many spinal conditions, is that putative ‘pathologic’ anatomy does not equate with pain.”⁶ The diagnosis of the clinical syndrome of lumbar spinal stenosis requires specific history and physical examination findings.⁷ The classic presenting symptom is leg pain with walking, spinal extension, or standing, which is termed neurogenic intermittent claudication (NIC). A patient may also have radicular pain, which is a sharp band-like pain that radiates in a dermatomal distribution correlating with the nerve root that is being compressed and radiculopathy; the pain occurs when the compression is sufficient to cause objective signs such as weakness, sensation loss, and reflex loss.^6,7 Binder et al⁸ stated, “surgical decompression is indicated when back and leg pain initiated and exacerbated by standing and walking becomes disabling or intolerable or when progressive neurologic deficits develop.” In a meta-analysis of the diagnosis of lumbar spinal stenosis in asymptomatic adults, Kent et al⁹ found abnormalities on computed tomographic or MR images in 4% to 28% of cases. The decision to send a patient with spinal stenosis for surgical intervention is clearly dependent on the history and physical examination findings, not on the radiographic findings alone.

I believe the history and physical examination in this patient are consistent with a patient who has pain in the low back and left lower extremity caused by somatic dysfunctions in the lumbar spine, pelvis, and lower extremity. They are not consistent with a patient who has nerve damage in the spinal canal causing perceived pain of a radicular nature in the foot. I believe that as osteopathic physicians we should agree that conservative measures primarily in the form of osteopathic manipulative medicine must be thoroughly exhausted before a patient is subjected to the extensive trauma and subsequent loss of normal body function inherent in the use of invasive spinal surgery.