Lumbar Stenosis. Lumbar Stenosis Pathophysiology. Lumbar Stenosis. Lumbar Spinal Stenosis. Carole A. Miller, MD, FACS.

Transcription

1 Lumbar Spinal Stenosis Carole A. Miller, MD, FACS Professor, Department of Neurosurgery Director Neurosurgery Residency Training Program Director, Ohio State Comprehensive Spine Center Pathophysiology Decreased volume of the spinal canal due to osteoarthritis of the disc and facet joints Less space available for the neural elements Mechanical irritation can incite a local inflammatory response Vascular and conduction changes of neural elements are thought to be responsible for the symptoms Chronic neural compression leads to edema, demyelization and wallerian degeneration of the afferent and efferent fibers Substance P has been proposed as a pain modulator related to involvement of the nerve root and dorsal root ganglion. In the lumbar spine developmental, acquired, or a combined disease may lead to lumbar spinal stenosis with significant neurological sequelae. Developmental stenosis in the lumbar region may involve an isolated segment, causing a ring like constriction of the region or it may involve multiple levels of the entire lumbar segment. However, developmental stenosis in and of itself rarely causes symptoms. Combined stenosis is the most common form of lumbar spinal stenosis giving rise to clinical disease, and it is more common in the lumbar spine than in the thoracic or cervical spine. Pathophysiology Central Stenosis Ligamentum flavum buckling or hypertrophy Superior facet process hypertrophy or osteophyte formation Intervertebral disc protrusion or osteophyte formation Later recess stenosis Entrance zone: hypertrophy of the superior articular process Mid zone: Fibrocartilage overgrowth of the pars interarticularis defect Foraminal stenosis: Pedicular kinking from scoliosis, foraminal disc herniations, or foraminal collapse secondary to collapse of disc space 1

2 Central canal stenosis: Narrowing of the AP dimension of the spinal canal. The reduction in canal size may cause local neural compression and/or compromise of the blood supply to the cauda equina Foraminal stenosis: Narrowing of the neural foramen Lateral recess stenosis Key points in : Caused by hypertrophy of the facets and ligamentum flavum, may be exacerbated by disc bulging or spondylolisthesis, may be superimposed on congenital narrowing Most common at L4-5 and then L3-4 Symptomatic stenosis produces gradually progressive back and leg pain with standing walking that is relieved by sitting or lying (neurogenic claudication) Generally occurs in patients with congenitally shallow lumbar canal with superimposed acquired degeneration Symptoms differentiated from vascular claudication which is usually relieved at rest regardless of position Usually responds to surgery; fusion may be an adjunct Central Canal Stenosis Congenital as in achondroplastic dwarf Acquired most commonly superimposed on congenital Important* Stenosis in the lumbar region causes the syndrome of neurogenic claudication In the cervical region cervical myelopathy and ataxia (from spinocerebellar tract compression) may be present In 5%, lumbar and cervical stenoses are symptomatic simultaneously Symptomatic spinal stenosis in the thoracic region is rare. The transverse diameter can be determined on conventional x-rays sagittal diameter required myelography, CT or MRI Lumbar spinal stenosis in the adult is indicated ay an AP diameter of <13 mm or a transverse diameter of <20 mm measured on the CT 2

3 Lumbar Spinal Stenosis Often presents as neurogenic claudication (NC) aka pseudoclaudication. Ischemia of LS nerve roots and increased metabolic demand from exercise together with vascular compromise of the nerve root due to pressure from surrounding structures Must be differentiated from vascular claudication aka intermittent claudication, resulting form ischemia of exercising muscles Differential Diagnosis Vascular insufficiency Trochanteric bursitis Lumbar or Thoracic Disc Herniation Juxtafacet cyst Ganglion cyst Synovial cyst Arachnoiditis Intraspinal tumor Functional etiologies Diabetic neuritis pain Clinical features distinguishing neurogenic from vascular claudication Feature Sensory loss Inciting factors Relief with rest Claudicating distance Peripheral pulses Discomfort on lifting or bending Foot pallor on elevation Skin temp feet Neurogenic claudication dermotomal Dermatomal Exercise with maintenance of a given posture (65% have pain with standing at rest); coughing produces pain (38%) Slow often > 30 min; usually positional; *standing and resting usually not sufficient Varies day to day in 62% Normal Common (67%) None Normal Vascular claudication Muscular group (sclerotomal) Stocking distribution Reliably reproduced with fixed amount of exercise; rare at rest Almost immediate not dependent on posture (relief of walking induced symptoms with standing is a key differentiating feature Constant day to day in 88% Decreased or absent Infrequent (15%) marked decreased Associated Conditions Congenital Achondroplasia Congenitally narrowed canal Acquired Spondylolisthesis Acromegaly Post-traumatic Paget s Disease Ankylosing spondylitis Ossification of the yellow ligament 3

4 Radiographic Evaluation Myelogram Lumbo-sacral spine x-rays CT scan Myelogram MRI May show spondylolisthesis, AP diameter of canal is narrowed but interpedicular distance is normal Classically shows trefoil canal; also hypertrophied ligaments, facet arthropathy, and bulging discs; best for seeing bone Lateral shows washboard pattern AP shows wasp-waisting (narrowing of dye column. Impingement on neural structures and loss of CSF signal on T2WI at severely stenotic levels. Good for seeing nerve impingement. *Asymptomatic abnormalities are demonstrated in up to 33% of asymptomatic patients yrs old Lateral myelogram of 60 yo F complaints of both lower back and radiating leg pain > with activity. Segmental stenosis of severe degree from L-2 through L-5, with disc degeneration an posterior osteophyte formation CT Scan : Myelogram AP myelogram of an 83 yo F. At the level of L3-4 there is severe constriction with almost complete block, and at the L4-5 there is a mild narrowing on the left side. The nerve roots also are affected at the L3-4 level 4

5 : CT Scan MRI Scan : CT Scan Adjuncts to Radiographic Evaluation Bicycle test : patients with NC can usually tolerate longer periods of exercise on a bicycle than patients with intermittent vascular claudication because the position in bicycling flexes the waist Ratio of ankle to brachial blood pressure (A:B ratio: >1.0 is normal; mean of 0.59 in patients with intermittent claudication; 0.26 in patients with rest pain; <0,05 indicates impending gangrene Vascular lab studies (Doppler) may assist in identifying vascular insufficiency EMG with NCV may show multiple nerve-root abnormalities bilaterally; or may be normal 5

6 Natural History and Treatment Gary Rea, MD Treatment-Non Surgical Physical Therapy Flexion exercises-no extension Water aerobics Stationary bicycle, rowing, lifting weights while sitting Other-Cane, Walker, Scooter Natural History Radiographic stenosis-slowly progressive with degeneration process Clinical symptoms-5 years back pain-leg pain with intermittent deterioration Leg pain-progressively severe with neurogenic claudication Paralysis-not an issue, even with severe cases Non-Treatments Traction with computerized decompression apparatus $4000-insurance may not pay No randomized prospective studies to show it is better than natural history or other treatments 6

7 Invasive Treatments Epidural Steroids May help in mild to moderate cases Rarely help in severe patients To be considered successful, must improve pain for at least 3 months Laminectomy alone-addresses the stenosis, but does not address the instability inherent in the condition Best used in patients with normal lordosis, males, older patients Still a good treatment option in specific patients X-Stop-Acts to flex spine and open canal Can be done under local Most useful in very elderly and poor health Long term effectiveness is not clear May have real problems with osteoporosis Bilateral hemilaminectomy and fixation with facet screws Not a common procedure, but addresses the compression and the instability Less blood loss than fixation with pedicle screws, but less strong Best in patients with single level problems and in older patients 7

8 Lumbar Laminectomy and fusion/fixation Addresses stenosis and instability No large randomized studies to show its superiority BUT-many studies show the fusion/fixation improves outcome in back pain and pain Has some increased risk because of length of surgery and blood loss Summary-Treatment of Lumbar stenosis is a slowly progressive degenerative problem-rarely emergency Non-invasive treatments focus on flexion posture, sitting exercises, use of walking aids Decompressive therapy is unproven Steroid injections are reasonable, but often not effective in severe cases Laminectomy and Fusion/Fixation with Pedicle screws Problems-length of surgery, blood loss, osteoporosis, problems at other levels, complications Good News % significant improvement in symptoms-far greater than any other treatment in patients with neurogenic claudication Summary-Treatment of s X-Stop-newer treatment puts vertebrae in flexion-less invasive-elderly population Laminectomy-effective, but doesn t address instability-best in males without listhesis Bilateral hemilam with fixation with facet screws-smaller surgery, less strong, effective with single level disease 8

9 Summary-Treatment of Surgical treatments Lumbar laminectomy and fusion/fixation-addresses compression and instability > 60%success, but is big surgery in older population 9