DELTAMED 2001 NEUROLOGY QU



RNSH 2003 NEUROLOGY QU.2

70 yo vasculopath, prev MI. c/o bilat leg pain brought on by walking 150m, relieved by sitting. O/E carotid bruits, femoral bruits bilat BUT periph pulses present. Best test to Dx leg pain?

a) arterial duplex legs

b) CT lumbar spine

c) Arteriography

d) NCS

e) Bone scan

LUMBAR SPONDYLOSIS

The same pathologic changes that define cervical spondylosis may affect the lower spine. Here, however, the roots of the cauda equina are affected rather than the spinal cord. The spinal cord becomes narrow because of age-related degenerative changes that affect the vertebral column articulations, including disc bulging and spur formation, facet joint enlargement, and hypertrophy of the ligamenta flava and facet capsule. Encroachment is usually maximal at the disc spaces. Spinal stenosis is the term for this narrowing. Congenital stenosis makes a person more vulnerable to these changes.

The stenosis caused by spondylosis may be diffuse, but it is usually confined to one or two lumbar levels. Isolated L4-5 disorder with unilateral or bilateral L-5 radiculopathy is the most common syndrome. The L3-4 segment is less often affected either alone or in combination with L4-5 stenosis. Disorders at other levels are rare.

The resulting syndrome differs from acute herniation in many respects. Most patients are older than 40 years, and many are older than 60. Progression of symptoms is likely to be gradual rather than acute. Twisting of the back, lifting, or falling are precipitating factors in fewer than one-third of cases, and back pain is not the dominant symptom but may be reported by more than 50% of patients. Leg pain, when present, is as often bilateral as unilateral. Weakness of the legs and urinary incontinence are symptoms in a minority of patients, but many show weakness of isolated muscles and loss of reflexes on examination. Straight leg raising is limited in a few patients.

The characteristic symptom is pseudoclaudication, seen in almost all patients, and is defined as unilateral or bilateral discomfort in buttock, thigh, or leg on standing or walking that is relieved by rest. Patients use the words “pain,” “numbness,” or “weakness” to describe the discomfort, but there is often no objective sensory loss or focal muscle weakness. The discomfort is relieved by lying down, sitting, or flexing at the waist. Sometimes, pain persists in recumbency until the spine is flexed. Unlike vascular claudication, the pain persists if the patient stops walking without flexing the spine, and sometimes the discomfort is brought on by prolonged standing without walking.

The pathogenesis of pseudoclaudication is uncertain. Sometimes, myelography shows that hyperextension of the spine increases the protrusion of intervertebral discs, with relief of nerve root compression in flexed postures. In addition, blood flow to the lumbar spinal cord may increase when leg muscles are exercised. As a result, vessels on nerve roots dilate, but are then confined by the bony changes and thus compress the nerve roots. This is relieved by cessation of activity.

The diagnosis is made from the characteristic history, clinical findings, and radiography. Formerly, the syndrome was defined by changes in plain spine radiographs and by evidence of partial or complete subarachnoid block found by contrast myelography. Diagnosis was facilitated by the advent of computed tomography (CT), alone or with intrathecal contrast agents. Now, however, magnetic resonance imaging alone usually suffices to show the specific patterns and extent of compression. Electromyography can reveal that denervation is restricted to muscles innervated by lumbosacral roots. The cerebrospinal fluid protein level may be normal if the tap is performed above the level of the block, but values greater than 100 mg/dL may be found if there are multiple blocks.

The differential diagnosis includes intermittent claudication caused by peripheral arterial occlusive disease, which is recognized by the loss of pulses and characteristic trophic changes in the skin of the feet. Aortoiliac occlusive disease may spare peripheral pulses, but the femoral pulse is usually affected; it may cause claudication and wasting of leg muscles but does not cause postural claudication. The pain of aortoiliac disease is localized to exercising muscles. The radicular pattern of spinal claudication is not seen. The pain of aortoiliac disease persists as long as exercise is continued, regardless of body position. Vascular sonography may be in order.

Osteoarthritis of the hip joint may also cause activity-induced leg pain that is relieved by rest. The pain originates in the hip and usually radiates into the groin or anterior thigh, but does not extend below the knee. Pain and limitation of hip rotation are the usual findings. The diagnosis is confirmed radiographically.

The treatment of lumbar stenosis varies according to the severity of the symptoms. Mild symptoms often respond to nonsteroidal antiinflammatory drugs and physical therapy. The symptoms of lumbar stenosis may be episodic; even severe pain should be treated conservatively because a prolonged remission may ensue. Surgical treatment consists of decompressive laminectomy with medial facetectomy and resection of the ligamenta flava at the stenosed levels. Epidural injection of steroids does not relieve the pain of spinal claudication.

Surgery is reserved for patients who have pain and claudication severe enough to affect the quality of life and who do not respond to conservative therapy. Surgery is usually well tolerated and is highly effective; about two-thirds of the patients report considerable improvement that is sustained for years after surgery. In one study, the following features indicated a favorable prognosis for patients with weak legs: disc herniation, stenosis at one level, duration of leg weakness of less than 6 weeks, and age younger than 65. In another study, the radiographic severity of stenosis was the best predictor of long-term outcome regardless of therapy, surgical or nonsurgical. There have been no controlled trials of surgical treatment.

With such a restricted ET, I would have expected more clinical signs if it was vascular claudication, and the fact that they specify that the pain disappears on sitting (as opposed to general stopping) implies to me that they’re driving at spinal stenosis. According to the text, the best invx would be MRI, but since we can’t have that, I’ll go with B.

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