summary Lumbar Spinal Stenosis is a degenerative spinal condition characterized by the narrowing of the lumbar spinal canal due to a variety of bony or soft tissues structures. Diagnosis is made with MRI studies of the lumbar spine. Treatment is a trial of nonoperative management with NSAIDs and physical therapy. Surgical laminotomy and discectomy is indicated for progressive disabling pain that has failed nonoperative management, and/or progressive neurological deficits. Epidemiology Incidence most common reason for lumbar spine surgery in patients > 65 years old seen in 20-25% Demographics slightly more common in males (1.5:1) average age at presentation is 65 years old Anatomic location most commonly occurs at L4-5 (91%) Risk factors Caucasian race increased BMI congenital spine anomalies (20%) failure of posterior elements to develop, leading to short pedicles and laminae Etiology Mechanism Narrowing of the lumbar spinal canal can be due to bony structures facet osteophytes uncinate spur (posterior vertebral body osteophyte) spondylolisthesis soft tissue structures herniated or bulging discs hypertrophy or buckling of the ligamentum flavum synovial facet cysts Pathophysiology cell, water, and proteoglycan content in the nucleus pulposus decreases with age degeneration of the intervertebral disk leads to diminished disk height and buckling/bulding of the anulus fibrosus anterior spinal column begins to have decreased ability to absorb stress, leading to an abnormal transfer of force to the posterior elements increased stress through the facets leads to facet joint hypertrophy, osteophyte formation, and ligamentum flavum buckling and hypertrophy combined changes lead to a narrowing of the spinal canal and compression of the neural elements Associated conditions degenerative spondylolisthesis degenerative scoliosis cauda equina syndrome rare Anatomy Osteology anterior vertebral body posterior arch formed by pedicles pedicles project posteriorly from posterolateral corners of vertebral bodies lamina lamina project posteromedially from pedicles, join in the midline spinous process transverse process mammillary processes separate ossification centers project posteriorly from superior articular facet pars interarticularis mass of bone between superior and inferior articular facets site of spondylolysis Articulations intervertebral disc act as an articulation above and below facet joint (zygapophyseal joint) formed by superior and inferior articular processes that project from junction of pedicle and lamina facet orientation facets become more coronal as you move inferior Nerve roots nerve root exits foramen under same numbered pedicle central herniations affect traversing nerve root far lateral herniations affect exiting nerve root Blood Supply segmental arteries dorsal branches supply blood to the dura & posterior elements Classification Etiologic classification acquired degenerative/spondylotic changes (most common) post-surgical post-traumatic (vertebral fractures) inflammatory (ankylosing spondylitis) secondary to systemic diseases (Paget disease, acromegaly, fluorosis) congenital short pedicles with medially placed facets can be subdivided into idiopathic developmental (achondroplasia) Anatomic classification central stenosis cross sectional area <100mm2 or <10mm A-P diameter on axial CT caused by ligamentum hypertrophy directly under the lamina posteriorly and the bulging disc anteriorly results in thecal sac compression presents with nonspecific root compression or symptoms of lower nerve root (at the L4/5 level, the root of L5 is affected) lateral recess stenosis (subarticular recess) caused by facet joint arthropathy and osteophyte formation overgrowth of the superior articular facet is usually the primary culprit results in nerve root compression presents with symptoms of descending nerve root (at the L4/5 level, the root of L5 is affected) foraminal stenosis occurs between the medial and lateral border of the pedicle caused by a substantial loss of disk height, foraminal disk protrusions or osteophytes, or angulation in the setting of degenerative scoliosis results in nerve root compression by the ventral cephalad overhang of the superior facet and the bulging disc presents with symptoms of exiting nerve root (at the L4/5 level, the root of L4 is affected) extraforaminal stenosis located lateral to the lateral edge of the pedicle caused by far lateral disc herniations presents with symptoms of exiting nerve root (at the L4/5 level, the root of L4 is affected) Presentation Symptoms back pain referred buttock pain leg pain often unilateral neurogenic claudication pain worse with extension (walking, standing upright) pain relieved with flexion (sitting, leaning over shopping cart, sleeping in fetal position) weakness bladder disturbances recurrent UTI present in up to 10% due to autonomic sphincter dysfunction cauda equina syndrome (rare) Physical exam Kemp sign unilateral radicular pain from foraminal stenosis made worse by back extension straight leg raise (tension sign) usually negative Valsalva test radicular pain not worsened by Valsalva as is the case with a herniated disc normal neurologic exam patients may have no focal deficits, as exam often takes place with patient seated and symptoms may be reproducible or exacerbated only with lumbar extension or ambulation Imaging Radiographs findings do not always correlate with clinical symptomatology standing AP and lateral may show nonspecific degenerative findings (disk space narrowing, osteophyte formation) degenerative scoliosis degenerative spondylolisthesis flexion/extension radiographs may show segmental instability and subtle degenerative spondylolisthesis myelogram plain film myelography provides dynamic information such as degree of cut off when a patient goes into extension an invasive procedure MRI imaging modality of choice findings central stenosis with a thecal sac <100mm2 obliteration of perineural fat and compression of lateral recess or foramen facet and ligamentum hypertrophy MRI findings of spinal stenosis may found in asymptomatic patients CT myelogram more invasive than MRI findings central and lateral neural element compression bony anomalies bony facet hypertrophy Differential Important to differentiate symptoms of neurogenic claudication from vascular claudication flexion improves symptoms in neurogenic claudication because this posture increases the limited area available for the neural elements in the spinal canal and foramen Neurogenic Claudication vs. Vascular Claudication Neurogenic Claudication Vascular Claudication Postural changes Yes No Walking upright Causes symptoms Causes symptoms Standing stationary Causes symptoms Relieves symptoms Sitting Relieves symptoms Relieves symptoms Stair climbing Up easier (back flexed) Down easier Stationary bicycle (back flexed) Relieves symptoms Causes symptoms Pulses Normal Abnormal Hip-spine syndrome presence of coexisting hip and spine pathology must determine primary pain generatory prior to surgical treatment may require diagnostic injections to aid in diagnosis Treatment Nonoperative oral medications, physical therapy, and corticosteroid injections indications first line of treatment modalities include NSAIDS, physical therapy, weight loss and bracing preoperative opioid use associated with prolonged hospital stays and increased postoperative pain steroid injections (epidural and transforaminal) found to be effective and may obviate the need for surgery Operative wide pedicle-to-pedicle decompression indications persistent pain for 3-6 months that has failed to improve with nonoperative management progressive neurologic deficits (weakness or bowel/bladder) outcomes results in better improvement in pain and function than nonsurgical treatment wide pedicle-to-pedicle decompression with instrumented fusion indications segmental instability (isthmic spondylolisthesis, degenerative spondylolisthesis, degenerative scoliosis) surgical instability created by complete laminectomy and/or removal of > 50% of facets risk of adjacent segment degeneration >30% at 10 years Techniques Wide pedicle-to-pedicle decompression technique a single level decompression at L4/5 would include resection of the inferior half of spinous process of L4 resection of the L4 lamina to the level of the insertion of the ligamentum flavum resection of the ligamentum flavum medial facetectomy and lateral recess decompression undercutting of facets and removal of ligamentum flavum from lateral recess exploration and decompression of the L4/5 and L5/S1 foramina palpate L4 and L5 pedicle (pedicle-to-pedicle) and be sure the nerve root is patent below it complications specific to this treatment infection dural tear epidural hematoma instability outcomes improved pain, function, and satisfaction with surgical treatment most common cause of failed surgery is recurrence of disease above or below decompressed level comorbid conditions are strongest predictor of clinical outcomes after decompression for lumbar spinal stenosis Wide decompression with posterolateral fusion instrumentation is controversial circumferential fusion (with PLIF or TLIF) is accepted but no studies showing its superiority Complications Complications increase with age, blood loss, and levels fused Major complications wound infection (10%) deep surgical infections are to be treated with surgical debridement and irrigation pneumonia (5%) renal failure (5%) persistent neurologic deficits (4%) Minor complications transient neurologic deficits (36%) genitofemoral nerve deficits common following a transpsoas approach at higher lumbar levels femoral and/or obturator nerve at risk with prolonged or excessive retraction during a transpsoas approach to the L4/L5 disc space UTI (34%) anemia requiring transfusion (27%) confusion (27%) dural tear failure for symptoms to improve