Important Topics - Please Review This Thread.

[dansdad]

this is a great IDEA!!!!!!!!!!! sure will save all the extra research,for us lazy guys.well what would you expect from a old,old man. :) B) thanks rentalguy......

[dansdad]

btw im in the process of puting together a back claim after the last MRI with ivds written all over it! ill talk more later

[rentalguy1]

this is a great IDEA!!!!!!!!!!! sure will save all the extra research,for us lazy guys.well what would you expect from a old,old man. :) B) thanks rentalguy......

LOL...I put it together out of my own laziness...I got tired of searching for my old posts.

[rentalguy1]

Here's a scholarly article that I included in my claim:

http://www.emedicine.com/PMR/topic133.htm

Author: Michael B Furman, MD, MS, Fellowship Director, Clinical Assistant Professor, Department of Physical Medicine and Rehabilitation, Orthopedic and Spine Specialists

Michael B Furman is a member of the following medical societies: Alberta Medical Association, American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, International Spine Intervention Society, North American Spine Society, Pennsylvania Medical Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation

Coauthor(s): Kirk M Puttlitz, MD, Consulting Staff, Pain Management and Physical Medicine, Arizona Neurological Institute; Robert Pannullo, MD, Interventional Spinal Care Fellow, Department of Physical Medicine and Rehabilitation, KDV Orthopaedics and Rehabilitation Ltd; Jeremy Simon, MD, Interventional Spine Fellow, Department of Physical Medicine and Rehabilitation, Orthopaedics and Spine Specialists, Ltd

Editors: J Michael Wieting, DO, MEd, Professor, Department of Physical Medicine and Rehabilitation, Director, Physical Medicine and Rehabilitation Residency Training, Michigan State University College of Osteopathic Medicine, Medical Director, Rehabilitation Center, Ingham Regional Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain (Tailbone Pain, Coccydynia) Service, UMDNJ-New Jersey Medical School; Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center; Rene Cailliet, MD, Professor-Chairman Emeritus, Department of Rehabilitation Medicine, University of Southern California School of Medicine; Former Director, Department of Rehabilitation Medicine, Santa Monica Hospital Medical Center

Synonyms and related keywords: central stenosis, , , , lateral gutter stenosis, lateral recess stenosis, stenosis, subarticular stenosis, subpedicular stenosis, , neurogenic claudication, NC, , LSS, neural compression, , ligamentum flavum hypertrophy, facet hypertrophy of cephalad vertebra, vertebral body osteophytosis, , HNP, , incomplete vertebral arch closure, , segmentation failure, , , early vertebral arch ossification, , shortened pedicles, thoracolumbar kyphosis, apical vertebral wedging, anterior vertebral beaking, Morquio syndrome, , zygapophyseal joint hypertrophy, , laminectomy, , , fluorosis, , , disc desiccation, , DDD, , bilateral neurogenic claudication, cauda equinamicrovascular ischemia, intraneuralfibrosis,

Background

Lumbar spinal stenosis (LSS) implies spinal canal narrowing with possible subsequent neural compression. LSS is classified by anatomy or etiology. Anatomic subclassifications include central canal and lateral recess stenosis. The classification of lumbar stenosis is important because of the implications of the underlying etiology and because it affects the therapeutic strategy, specifically the surgical approach.

• Central canal stenosis, commonly occurring at an intervertebral disk level, defines midline sagittal spinal canal diameter narrowing that may elicit neurogenic claudication (NC) or pain in the buttock, thigh, or leg. Such stenosis results from ligamentum flavum hypertrophy, inferior articulating process (IAP), facet hypertrophy of the cephalad vertebra, vertebral body osteophytosis, vertebral body compression fractures and herniated nucleus pulposus (HNP). Abnormalities of the disk usually do not cause symptoms of central stenosis in a normal-sized canal. In developmentally small canals, however, a prominent bulge or small herniation can cause symptomatic central stenosis. Large disk herniations can compress the dural sac and compromise its nerves, particularly at the more cephalad lumbar levels where the dural sac contains more nerves.
  
• Lateral recess stenosis (ie, lateral gutter stenosis, subarticular stenosis, subpedicular stenosis, foraminal canal stenosis, intervertebral foramen stenosis) is defined as narrowing (less than 3-4 mm) between the facet superior articulating process (SAP) and posterior vertebral margin. Such narrowing may impinge the nerve root and subsequently elicit radicular pain. This lateral region is compartmentalized into entrance zone, mid zone, exit zone, and far-out stenosis.
  • The entrance zone lies medial to the pedicle and SAP, and, consequently, arises from facet joint SAP hypertrophy. Other causes include developmentally short pedicle and facet joint morphology, as well as osteophytosis and HNP anterior to the nerve root. The lumbar nerve root compressed below SAP retains the same segmental number as the involved vertebral level (eg, L5 nerve root is impinged by L5 SAP).
    
  • The mid zone extends from the medial to the lateral pedicle edge. Mid-zone stenosis arises from osteophytosis under the pars interarticularis and bursal or fibrocartilaginous hypertrophy at a spondylolytic defect.
    
  • Exit-zone stenosis involves an area surrounding the foramen and arises from facet joint hypertrophy and subluxation, as well as superior disk margin osteophytosis. Such stenosis may impinge the exiting spinal nerve.
    
  • Far-out (extracanalicular) stenosis entails compression lateral to the exit zone. Such compression occurs with far lateral vertebral body endplate osteophytosis and when the sacral ala and L5 transverse process impinge on the L5 spinal nerve.
    
    
    
    Amundsen and colleagues found concomitant lateral recess stenosis in all cases of central canal stenosis; consequently, in his study, pure central stenosis without lateral stenosis failed to exist.
    
    Parenthetically, Keim and colleagues mention the following simplistic LSS anatomical classification scheme:
    
    
    
    
    • Lateral, secondary to SAP hypertrophy
      
    • Medial, secondary to IAP hypertrophy
      
    • Central, due to hypertrophic spurring, bony projection, or ligamentum flavum/laminar thickening
      
    • Fleur de lis (clover leaf), from laminar thickening with subsequent posterolateral bulging
      
      
      LSS arises from the following primary and secondary etiologies:
      
      
      
      
      • Primary stenosis encompasses congenital malformations and developmental flaws. Congenital malformations include incomplete vertebral arch closure (spinal dysraphism), segmentation failure, achondroplasia, and osteopetrosis. Developmental flaws include early vertebral arch ossification, shortened pedicles, thoracolumbar kyphosis, apical vertebral wedging, anterior vertebral beaking (Morquio syndrome), and osseous exostosis. Primary stenosis is uncommon, occurring in only 9% of cases.
        
      • Secondary (acquired) stenosis arises from degenerative changes, iatrogenic causes, systemic processes, and trauma. Degenerative changes include central canal and lateral recess stenosis from posterior disk protrusion, zygapophyseal joint and ligamentum flavum hypertrophy, and spondylolisthesis. Iatrogenic changes result following surgical procedures such as laminectomy, fusion, and diskectomy. Systemic processes that may be involved in secondary stenosis include Paget disease, fluorosis, acromegaly, neoplasm, and ankylosing spondylitis.
        
        
        
        Pathophysiology
        Disk desiccation and degenerative disk disease (DDD) with resulting loss of disk height may induce segmental instability. Such instability incites vertebral body and facet joint hypertrophy. Cephalad vertebral body IAP hypertrophy promotes central spinal canal stenosis. Further canal volume loss results from HNP, ligamentum flavum hypertrophy, and disk space narrowing.
        
        Alternatively, the caudal vertebral body SAP contributes to lateral recess and foraminal stenosis. Indeed, facet hypertrophy between L4 and L5 vertebrae may impinge the L4 nerve root in the foramen and the L5 proximal nerve root sheath in the lateral recess.
        
        Jenis and An eloquently describe foraminal stenosis pathoanatomy, characterized by disk desiccation and DDD, which narrows disk height, permitting the caudad SAP to sublux anterosuperiorly. Such subluxation decreases foraminal space. Continued subluxation with resulting biomechanical disruption provokes osteophytosis and ligamentum flavum hypertrophy, further compromising foraminal volume. Anteroposterior (transverse) stenosis ultimately results from narrow disk height and hypertrophy anterior to the facet; specifically, the SAP and posterior vertebral body transversely trap the nerve root. Furthermore, in vertical (craniocaudal) stenosis, posterolateral vertebral endplate osteophytes and a lateral HNP may impinge the spinal nerve against the superior pedicle.
        
        The 2 lower motion segments (L3-L4, L4-L5) are most commonly affected by degenerative stenosis. These segments are in a transition zone from the rigid sacrum to the mobile lumbar spine. Also, the posterior joints in this area have less of a sagittal orientation, which affords more rotation, and are therefore more vulnerable to rotatory strains.
        
        Dynamic foraminal stenosis implies intermittent lumbar extension-provoked nerve root impingement from HNP, osteophytosis, and vertebral body slippage. Such dynamic stenosis with associated intermittent position-dependent symptoms may not manifest on imaging studies, thereby confounding diagnosis. Other factors promoting development of LSS include shortened gestational age, and synovial facet joint cysts with resulting radicular compression. Adult degenerative scoliosis, secondary to DDD-induced instability with subsequent vertebral rotation and asymmetric disk space narrowing, promotes facet hypertrophy and subluxation in the curve concavity. Degenerative spondylolisthesis, when combined with facet hypertrophy, causes both central canal and lateral recess stenosis.
        
        
        Frequency
        
        United States
        LSS remains the leading preoperative diagnosis for adults older than 65 years who undergo spine surgery. The cost of more than 30,000 LSS surgeries performed in 1994 exceeds 1 billion dollars.
        
        The incidence of lateral nerve entrapment is reportedly 8-11%. Some studies implicate lateral recess stenosis as the pain generator for 60% of patients with symptomatology of failed back surgery syndrome.
        
        Incidence of foraminal stenosis increases in lower lumbar levels because of increased dorsal root ganglion (DRG) diameter with resulting decreased foramen (ie, nerve root area ratio). Jenis and An cite commonly involved roots as L5 (75%), L4 (15%), L3 (5.3%), and L2 (4%). The lower lumbar levels maintain greater obliquity of nerve root passage, as well as higher incidence of spondylosis and DDD, further predisposing patients to L4 and L5 nerve root impingement.
        
        
        Mortality/Morbidity
        In their review of LSS, Fritz and colleagues cite several studies suggesting that many patients show symptomatic and functional improvement or remain unchanged over time. For example, they mention Porter and colleagues' study in which 90% of 169 untreated patients with suspected lateral recess stenosis improved symptomatically after 2 years. Additionally, they report Johnsson and colleagues' 4-year study of 32 patients treated conservatively for moderate stenosis, of whom only 16% worsened clinically and 30% reported diminished walking tolerance.
        
        
        Race
        No known correlation exists between incidence of LSS and race.
        
        
        Sex
        Patients typically are male.
        
        
        Age
        Patients with LSS due to degenerative causes generally are aged at least 50 years; however, LSS may be present at earlier ages in cases of congenital malformations.
        
        
        
        
        
        History
        LSS classically presents as bilateral NC. Unilateral radicular symptoms may result from severe foraminal or lateral recess stenosis. Patients, typically aged more than 50 years, report insidious-onset NC manifesting as intermittent, crampy, diffuse radiating thigh or leg pain with associated paresthesias. Indeed, leg pain affects 90% of patients with LSS.
        
        In a retrospective review of 75 patients with radiographically confirmed LSS, reports of weakness, numbness or tingling, radicular pain, and NC were in almost equal proportions. The most common symptom was numbness or tingling of the legs.
        
        NC pain is exacerbated by standing erect and downhill ambulation and is alleviated with lying supine more than prone, sitting, squatting, and lumbar flexion. Getty and colleagues documented 80% pain diminution with sitting and 75% with forward bending. Lumbar spinal canal and lateral recess cross-sectional area increases with spinal flexion and decreases with extension. Furthermore, cross-sectional area is reduced 9% with extension in the normal spine and 67% with severe stenosis. The Penning rule of progressive narrowing implies that the more narrowed the canal by stenosis, the more it narrows with spinal extension. Schonstrom and colleagues have shown that spinal compressive loading from weight bearing reduces spinal canal dimensions.
        
        NC, unlike vascular claudication, is not exacerbated with biking, uphill ambulation, and lumbar flexion and is not alleviated with standing. LSS patients compensate for symptoms by flexing forward, slowing their gait, leaning onto objects (eg, over a shopping cart) and limiting distance of ambulation. Unfortunately, such compensatory measures, particularly in elderly osteoporotic females, promote disease progression and vertebral fracture. Pain radiates downward in NC and, in contrast, upward in vascular claudication. Hall and colleagues note the presence of radiculopathy in 6% and NC in 94% of LSS patients.
        
        Distinguishing between neurogenic and vascular claudication is important because the treatments, as well as the implications, are quite different. Vascular claudication is a manifestation of peripheral vascular disease and arteriosclerosis. Other vessels, including the coronary, vertebral, and carotid, are also often affected. Further complicating diagnosis and treatment in some patients, both neurogenic vascular and claudication may occur together. This is because both conditions frequently occur in the elderly population.
        
        Proposed mechanisms for development of NC include cauda equina microvascular ischemia, venous congestion, axonal injury, and intraneural fibrosis. Ooi and colleagues myeloscopically observed ambulation-provoked cauda equina blood vessel dilation with subsequent circulatory stagnation in LSS patients with NC. They propose that ambulation dilates the epidural venous plexus, which, amidst narrow spinal canal diameter, increases epidural and intrathecal pressure. Such elevation of pressure ultimately compresses the cauda equina, compromises its microcirculation, and causes pain.
        
        Another pain generator may be the DRG, which contains pain-mediating neuropeptides, such as substance P, that possibly increase with mechanical compression. The DRG varies spatially within the lumbosacral spine, with L4 and L5 DRG in an intraforaminal position and S1 DRG located intraspinally. Such foraminal placement may predispose to stenotic compression with subsequent radicular symptomology.
        
        Lastly, severe radiologic stenosis in otherwise asymptomatic individuals suggests inflammation, not just mechanical nerve root compression. Specific inflammation generators may include HNP, ligamentum flavum, and facet joint capsule.
        
        Katz and colleagues report that the historical findings most strongly associated with LSS include advanced age, severe lower extremity pain, and absence of pain when the patient is in a flexed position. Fritz and colleagues contend that the most important elements involve the postural nature of the patient's pain, stating that absence of pain or improvement of symptoms when seated assists in ruling in LSS. Conversely, LSS cannot be ruled out when sitting is the most comfortable position for the patient and standing/walking is the least comfortable.
        
        
        Physical
        Physical examination findings frequently are normal in patients with LSS. Nevertheless, review of the literature suggests diminished lumbar extension appears most consistently, varies less, and constitutes the most significant finding in LSS. Other positive findings include loss of lumbar lordosis and forward-flexed gait. Charcot joints may be present in long-standing disease. Radiculopathy may be noted with motor, sensory, and/or reflex abnormalities. Asymmetric muscle stretch reflexes and focal myotomal weakness with atrophy occur more with lateral recess than central canal stenosis. Some report objective neurologic deficits in approximately 50% of LSS cases. Provocative maneuvers include pain reproduction with ambulation and prone lumbar hyperextension. Pain alleviation occurs with stationary biking and lumbar flexion.
        
        Patients may also have a positive result from the stoop test, which was described by Dyck in 1979. This is performed by having the patient walk with an exaggerated lumbar lordosis until NC symptoms appear or are worsened. The patient is then told to lean forward. Reduction of NC symptoms is a positive result and is suggestive of NC.
        
        Negative findings in the physical examination include skin color, turgor, and temperature; normal distal lower extremity pulses; and an absence of arterial bruits. Importantly, remember the 5 Ps of vascular claudication in the assessment of these patients: pulselessness, paralysis, paraesthesia, pallor, and pain. The absence of these problems, excluding pain and paraesthesias, which are common to both neurogenic and vascular claudication, should give the clinician confidence in the diagnosis of NC. Please refer to the excellent eMedicine article Peripheral Vascular Disease for more information on peripheral vascular disease and vascular claudication.
        
        Dural tension signs should be unremarkable. Lumbar segment mobilization often fails to reproduce pain, and palpation locates no trigger points.
        
        Katz and colleagues report physical examination findings most strongly associated with LSS include wide-based gait, abnormal Romberg test, thigh pain following 30 seconds of lumbar extension, and neuromuscular abnormalities; however, Fritz and colleagues state physical examination findings do not seem helpful in determining the presence or absence of LSS.
        
        Johnsson and colleagues' single study of the natural course of LSS reports unchanged symptoms in 70% of patients, improvement in 15%, and worsening in 15% after a 49-month observation period. Walking capacity improved in 37% of patients, remained unchanged in 33%, and worsened in 30%.
        
        
        Causes
        See sections on Background and Pathophysiology.
        
        
        [Lumbar Degenerative Disc Disease]
        Achilles Tendon Injuries and Tendonitis
        Cancer and Rehabilitation
        Chronic Pain Syndrome
        Diabetic Lumbosacral Plexopathy
        Diabetic Neuropathy
        Fibromyalgia
        Lumbar Compression Fracture
        Lumbar Facet Arthropathy
        Lumbar Spondylolysis and Spondylolisthesis
        Mechanical Low Back Pain
        Myofascial Pain
        Neoplastic Lumbosacral Plexopathy
        Osteoarthritis
        Osteoporosis (Primary)
        Osteoporosis (Secondary)
        Piriformis Syndrome
        Radiation-Induced Lumbosacral Plexopathy
        RheumatoidArthritis
        Scheuermann Disease
        Spondylolisthesis
        Trochanteric Bursitis
        
        
        
        Other Problems to be Considered
        
        
        
        
        Rheumatologic
        
        Ankylosing spondylitis/spondyloarthropathy
        Diffuse idiopathic skeletal hyperostosis (DISH)
        
        Infectious
        
        Epidural, subdural, intradural abscess
        Diskitis
        Pott's Disease
        
        Metabolic
        
        Osteomalacia
        Parathyroid disease
        Vitamin B-12 or folic acid deficiency
        
        Traumatic
        
        Lumbar strain
        
        Developmental/Congenital
        
        Scoliosis
        
        Vascular
        
        Peripheral vascular disease (with vascular claudication)
        Abdominal aortic dissection
        
        Psychogenic Conversion disorder
        Malingering
        
        
        
        
        
        Lab Studies
        
        
        
      • Lab studies are not necessary to support the diagnosis of LSS.
        
        
        
    
    Imaging Studies
    
    
    
    • Plain radiograph (x-ray)
      • Nonspecific plain radiographic findings possibly implicating LSS include the following:
        • Disk space narrowing
          
        • Facet hypertrophy and arthrosis
          
        • Spondylosis
          
        • Degenerative scoliosis and spondylolisthesis
          
        • Osteochondrosis
          
        • Transitional segmentation
          
        • Spinous process settling
          
        • Shortened interpedicular distance
          
          
        • Interpedicular distance, considered subnormal if less than 18 mm, commonly increases from upper to lower lumbar segments.
          
        • Some sources define pure absolute central canal stenosis as a mid-sagittal canal diameter of less than or equal to 10 mm, pure relative at 10-12 mm, and mixed as a combination thereof. Mid-sagittal canal diameter less than 15 mm and transverse diameter less than 20 mm usually are considered abnormal.
          
        • Posterior disk height of 4 mm or less and foraminal height of 15 mm or less may suggest foraminal stenosis; nevertheless, clinical correlation is required. No convincing correlation has been found between clinical symptoms and radiologic findings in a study of 100 symptomatic patients with LSS. Similarly, no correlation has been shown between physical function and radiologic findings.
          
          
        • CT scan
          • CT scan provides excellent central canal, lateral recess, and neuroforaminal visualization. Additionally, CT scan offers contrasts between intervertebral disk, ligamentum flavum, and thecal sac. Unfortunately, CT scan, like MRI, yields a high false-positive rate (35.4% when correlated with surgically proven LSS).
            
          • Parasagittal reconstructed CT scan findings suggesting stenosis include posterolateral vertebral body or facet osteophytosis extending into the foramen.
            
            
          • MRI
            • MRI remains the imaging modality of choice for LSS. Fritz and colleagues maintain that MRI effectively rules LSS in or out anatomically.
              • Advantages include nonionizing radiation and superior multiplanar soft tissue visualization without osseous artifact. A trefoil-shaped central spinal canal may provoke more symptoms than a round or oval canal by depressing the lateral recess.
                
              • Sagittal T1-imaged adipose tissue outlines neuroforaminal nerve root segments and dorsal root ganglia. Therefore, parasagittal MRI findings suggesting foraminal stenosis include paucity of T1-weighted perineural adipose tissue surrounding the nerve root and diminished foraminal size. Unfortunately, MRI abnormalities have been documented in 20% of asymptomatic subjects.
                
                
                
              • Myelography
                • This test effectively documents central canal stenosis and remains superior in evaluating lumbar disk herniation. Predictive value of myelography versus CT scan has been reported as 83% versus 72%, respectively, for lumbar disk herniation, and 93% versus 89% for LSS. Furthermore, myelography images the entire lumbar spinal canal, and enhances stenotic segments due to hyperextension during imaging; however, it may miss lateral stenosis and HNP because the dural sac terminates at the lateral mid zone, preventing contrast spread to the distal nerve root sheath.
                  
                • Myelography is less sensitive and specific than CT scan or MRI.
                  
                • Procedural complications include spinal headache, seizure, allergic reaction, and nausea.
                  
                  
                • If vascular claudication is suspected, referral to an internist for a workup is indicated. This includes a serum cholesterol level, arterial Doppler studies, ankle-brachial index values, and, in some cases, arteriography.
                  
                  
                  
                  Other Tests
                  
                  
                  
                • Electrodiagnosis (EDX), including needle electromyography (EMG), nerve conduction studies (NCS), and somatosensory evoked potentials (SSEP), evaluates nerve root and peripheral nerve function.
                  
              • Needle EMG diagnoses lumbosacral radiculopathy by detecting increased insertional activity, spontaneous potentials (eg, positive waves, fibrillations, fasciculations, chronic repetitive discharges), and decreased motor unit recruitment in paraspinal and lower extremity muscles innervated by the same nerve root. The presence of polyphasic motor unit potentials helps establish long-standing disease.
              • Limitations include inability to evaluate sensory and upper motor neurons.
                
            • Multisegmental muscle innervation may cause false negative results by preserving motor unit function despite nerve root compromise. Such innervation may elicit multilevel abnormalities in severe LSS.
              
          • Johnsson and colleagues have correlated myelographic LSS severity with multisegmental EMG abnormality.
            
            
        • NCS differentiates LSS from other confounding neuropathic conditions such as lumbosacral plexopathy, generalized peripheral neuropathy, and mononeuropathy (eg, peroneal neuropathy at the fibular head, tarsal tunnel syndrome).
        • Canal stenosis may compress the cauda equina with resulting polyradicular insults. Such multiple lumbosacral radiculopathies involve lower lumbosacral (especially S1) nerve roots, are often bilateral and asymmetric, and frequently may manifest NCS abnormalities. Such abnormalities include decreased or unelicitable posterior tibial and peroneal compound motor action potentials (CMAPs) reflecting axon loss, and unobtainable H reflexes signifying bilateral S1 compression. Sensory nerve action potentials (SNAPs) remain unaffected (unless impingement occurs distal to the dorsal root ganglion), but may not be detectable in older persons. F waves may also be absent or prolonged in persons with LSS
          
      • Wilbourn and Aminoff advocate measuring peroneal CMAP amplitude from tibialis anterior and M-wave amplitude during H-reflex testing to gauge the extent of L5 and S1 acute denervation, respectively.
        
    • Overall, Wilbourn and Aminoff report variable EDX findings, including multiple, bilateral lumbosacral radiculopathies in 50% of LSS patients, with prominent chronic motor unit action potential (MUAP) changes, and fibrillations solely in distal musculature. The remaining 50% of patients demonstrate varied abnormalities, with some manifesting 2 radiculopathies commonly as a single radicular insult in each lower extremity, either symmetrically (eg, bilateral L5) or asymmetrically (eg, left S1 and right L5). Other patients display isolated L5 or S1 radiculopathy. Limited nondiagnostic findings may be elicited, including bilaterally absent H reflexes with normal lower extremity needle EMG and sural SNAPs, as well as fibrillations in a single S1-innervated limb muscle. Lastly, many patients demonstrate normal EDX tests.
      
  • Diagnostically, EMG complements MRI in assessing radiculopathy. Specifically, EMG rarely presents false-positive results and carries high specificity (85%). Conversely, MRI carries high sensitivity and poor specificity (50%) and, consequently, demonstrates many false-positive asymptomatic abnormalities. Some advocate using highly specific EMG to determine whether structural abnormalities imaged on MRI carry functional and pathologic significance. Indeed, Robinson proposes that such use of needle EMG ultimately might prove helpful in avoiding costly and high-risk invasive interventions.
    
    
• Somatosensory evoked potentials (SSEPs) are dispatched through large dorsal column myelinated fibers that are affected earlier than smaller fibers. Peripheral nerve lesions prolong SSEP latency and duration, while nerve root and spinal cord pathology induce further morphologic alterations.
• Keim and colleagues have documented posterior tibial abnormalities in 95%, peroneal abnormalities in 90%, and sural abnormalities in 60% of LSS patients studied. A high incidence of L4, L5, and S1 nerve root involvement existed, amidst a paucity of upper lumbar segment abnormality (measured by the saphenous nerve). Bilateral lower limb changes were documented in 7 of 20 patients, suggesting that bilateral lower limb SSEPs can uncover previously unsuspected lesions. SSEPs are useful intraoperatively during decompressive surgery to assist the physician in diagnosis of LSS amidst equivocal clinical and imaging studies. SSEPs also appear to be more sensitive than other EDX approaches in evaluating LSS-provoked nerve root compression.
  

Kraft contends the best EDX technique for assessing LSS is dermatomal somatosensory evoked potentials (DSEPs). Insidious low-grade compression from LSS causes impaired nerve conduction, which is best appreciated by DSEPs (similar to nerve conduction study [NCS] slowing in carpal tunnel syndrome). Such pathology contrasts sharply with dramatic acute-onset HNP root compression, inducing axon loss with subsequent denervation best detected by needle EMG.
Using CT scan and MRI comparison standards, Kraft and colleagues demonstrated 78% sensitivity and 93% predictive value with DSEPs for an anatomical study positive for LSS when using multiple root disease (MRD) criteria. When criteria of multiple root disease and single root disease (SRD) were added, the sensitivity rose to 93%, with a positive predictive value of 94%. Kraft emphasized that the DSEP electrophysiologic signature of LSS is MRD, but SRD can suggest LSS, especially amidst applicable clinical history, physical examination, and positive EMG findings. Conversely, Dumitru found DSEPs to be of low sensitivity when compared to needle EMG-proven radiculopathies.



Rehabilitation Program

Physical Therapy
Patients with LSS often benefit from conservative treatment and participation in a physical therapy (PT) program. Lumbar extension exercises should be avoided in this population, as spinal extension and increased lumbar lordosis are known to worsen LSS. Flexion exercises for the lumbar spine should be emphasized, as they reduce lumbar lordosis and decrease stress on the spine. Spinal flexion exercises increase the spinal canal dimension, thus reducing NC. Williams' flexion-biased exercises target increased lumbar lordosis, paraspinal and hamstring inflexibility, and abdominal muscle weakness. These exercises incorporate knee-to-chest maneuvers, pelvic tilts, wall-standing lumbar flexion, and avoidance of lumbar extension.

Two-stage treadmill testing has demonstrated longer walking times on an inclined treadmill, presumably due to promotion of spinal flexion. Conversely, level treadmill testing is thought to promote more spinal extension-induced NC and elicit earlier symptom onset and longer recovery time. Ancillary exercises to target weak gluteals, as well as shortened hip flexors and hamstrings, are indicated. Physical examination should be performed to assess for concurrent degenerative hip disease, which may mimic LSS. Traction harness-supported treadmill and aquatic ambulation to reduce compressive spine loading has been shown to improve lumbar range of motion (ROM), straight leg raising, gluteal and quadriceps femoris muscle force production, and maximal (up to 15 min) walking time.

Others advocate stationary cycling and abdominal muscle strengthening. Passive modalities such as heat, cold, transcutaneous electrical nerve stimulation (TENS), and ultrasound may provide transient analgesia and increased soft tissue flexibility in LSS patients.

The addition of a rolling walker is often necessary in many cases. The rolling walker provides some stability and promotes a flexed posture, which allows the afflicted patient to ambulate greater distances.


Medical Issues/Complications
In rare cases, central canal stenosis may provoke cauda equina syndrome with associated saddle anesthesia, bladder and/or bowel dysfunction and altered muscle reflexes. Additionally, patients with lateral recess stenosis-induced radiculopathy may manifest significant lower limb weakness or numbness. Lastly, intractable axial, radicular, or NC pain may result.


Surgical Intervention
LSS remains one of the most common conditions leading to lumbar spine surgery in adults aged 65 years and older. Increasing rates of LSS surgery among the Medicare population has been shown to be due possibly to imaging techniques that enable physicians to diagnose LSS more frequently. Other contributing factors may include improved surgical techniques that might allow patients previously managed conservatively to undergo surgery, as well as a philosophy that LSS surgery prevents future morbidity.



Widely agreed upon indications for LSS surgery do not exist. Typically, patients undergo elective surgery to improve walking tolerance and disabling leg and back pain. Preoperatively, such disability infrequently is measured in objective quantitative terms. Some suggest preoperative treadmill testing to facilitate objective selection of potential surgical candidates. Surgical emergencies (eg, cauda equina syndrome, rapid neurologic deterioration) rarely arise.
Surgical techniques include standard wide laminectomy and decompression, which first removes lamina and ligamentum flavum from the lateral borders of one lateral recess to the other and then decompresses entrapped nerve roots.
Foraminal enlargement surgery is used to address refractory foraminal stenosis-induced radicular pain. Other surgical decompressions include the following:Laminotomy
Medial facetectomy
Medial or lateral foraminotomy.

Midline interlaminar approaches are used to address concurrent central and foraminal stenosis.
The Wiltse approach with foraminotomy is used for isolated foraminal stenosis by providing the following:Widening the longissimus-multifidus muscle interval
Removing the lateral pars interarticularis and facet joint
Exposing the nerve root with subsequent decompression

[*]In addition to decompression and foraminal enlargement, some patients with segmental instability from facet joint removal and pain secondary to DDD may require fusion.

[*]Fusion stabilizes the intervertebral segment while maintaining lordosis and foraminal size.

[*]Additional options include arthrodesis and instrumentation.

[*]Surgical outcomes for patients with LSS vary.

[*]Surgical outcome literature is difficult to assess due to observer bias, inadequate outcome data categorization, vaguely defined outcome measures, and study design.

[*]Reports show widely varied outcomes (26-100% success and 31% dissatisfaction at 4.6 years), due to disparate research methodologies.

[*]Conservative versus surgical treatment for LSS remains controversial due to wide variations in outcome study type and quality.

[*]Johnsson and colleagues document improvement in 60% of surgically treated patients with 25% worsened, compared with improvement in 30% of conservatively treated patients and no change in 60%.

[*]Atlas and colleagues tracked 67 conservatively treated and 81 surgically treated patients over 12 months; surgically treated patients reported greater improvement in pain relief than those treated conservatively.

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[*]Treatment outcome predictors do not exist; specifically, severe spinal degenerative changes do not necessarily correlate with an unfavorable prognosis or mandate surgery.

[*]Simotas and colleagues cite that 12 of 49 patients treated conservatively with incorporation of analgesics, physical therapy, and epidural steroid injection, reported sustained improvement. Conservative and surgical treatments have not been subjected to rigorous well-designed study.

Consultations

[*]Consultation with an internal medicine specialist or subspecialty may be indicated when low back pain (LBP) suggests an underlying systemic illness such as malignancy, infection, or metabolic bone disease. Also, if the diagnosis of vascular claudication is in question, referral to an internist is indicated.

[*]Consultation with a rheumatologist may be considered when back pain suggests a rheumatologic condition such as ankylosing spondylitis, rheumatoid arthritis, osteoporosis, or fibromyalgia.

[*]Consultation with a surgeon is warranted for deteriorating neurologic status (eg, cauda equina syndrome), segmental instability, and/or intractable radicular or NC pain.

Other Treatment

Epidural steroid injection (ESI) provides aggressive-conservative treatment for LSS patients who demonstrate limited response to oral medication, physical therapy, and other noninvasive measures. Corticosteroids may inhibit edema formation from microvascular injury sustained by mechanically compressed nerve roots. Furthermore, corticosteroids inhibit inflammation by impairing leukocyte function, stabilizing lysosomal membranes, and reducing phospholipase A2 activity. Lastly, corticosteroids may block nociceptive transmission in C fibers. When using oral steroids (in rapid tapering fashion), remember that possible side effects may include fluid retention, skin flushing, and shakiness. Local anesthetic may be combined with corticosteroids to provide immediate pain relief and diagnostic feedback on the proximity of the injectate to the putative pain generator.

[*]Caudal ESI

[*]Caudal ESI entails needle placement through the sacral hiatus into the sacral epidural space.

[*]Advantages include ease of performance and low risk of dural puncture.

[*]Disadvantages include large injectate volumes (6-10 mL) necessary to ensure adequate medication spread to more cephalad pathology (ie, above L4-L5). Furthermore, such large volumes potentially may dilute the effect of the corticosteroid.

[*]Interlaminar ESI

[*]Interlaminar ESI entails needle passage through the interlaminar space, with subsequent injection directly into the epidural space. Consequently, delivery of medication occurs closer to the affected spinal segmental level than in caudal ESI.

[*]Disadvantages include greater potential for dural puncture, and, like caudal ESI, limited spread of medication to the target site if a midline raphe or epidural scarring exists. Furthermore, interlaminar injection delivers medication to the posterior epidural space with possible limited ventral diffusion to nerve root impingement sites.

[*]Transforaminal ESI

[*]Transforaminal ESI facilitates precise deposit of higher steroid concentrations closer to the involved spinal segment, and, consequently, might prove more efficacious in reducing pain.

[*]Transforaminal ESI may be used for unilateral radicular pain provoked by lateral recess or foraminal stenosis.

[*]Bilateral transforaminal ESI also may be used to treat bilateral central stenosis-induced NC pain when imaging studies demonstrate limited posterior epidural space, thereby precluding safe interlaminar ESI. Otherwise, interlaminar ESI may be used to treat bilateral or multilevel NC or radicular pain.

[*]Absolute contraindications to ESI include bleeding diathesis and anticoagulation therapy because of the increased risk of epidural hematoma. While the actual incidence of this complication is unknown, estimates in the literature suggest is occurs less than 1 in 150,000 outpatient epidural injections. Anticoagulation therapy (eg, warfarin, heparin) should be stopped a few days prior to injection. (Alternative methods of DVT prophylaxis, such as serial compression hose, should be instituted in the interim). In the case of patients taking coumadin, PT/INR should be drawn the day of the procedure. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) should be discontinued before the procedure in accordance with their half-life and hematologic profile.

[*]Other absolute contraindications include systemic infection, injectate allergy, and pregnancy (because of the teratogenicity of fluoroscopy). Relative contraindications include diabetes mellitus (DM) and congestive heart failure, given the hyperglycemic and fluid retention properties of corticosteroids, respectively. Other relative contraindications include adrenal dysfunction and hypothalamic-pituitary axis suppression.

[*]Serious complications, although rare, include infection (eg, epidural or subdural abscess) and epidural hematoma. Epidural hematoma has been associated with traumatic needle insertions, but this is neither sensitive nor specific for predicting development. Vandermeulen et al reported 61 case reports in the literature between 1904 and 1994 after central nervous blocks. Dural puncture (in 5% of lumbar interlaminar ESIs and 0.6% of caudal injections) with possible subsequent subarachnoid anesthetic/corticosteroid deposition may provoke neurotoxicity, sympathetic blockade with hypotension, and/or spinal headache; however, contrast-enhanced fluoroscopic guidance minimizes the possibility of dural puncture and intravascular injection.

[*]Therapeutic epidural steroid injection (ESI) techniques are performed ideally using fluoroscopic guidance and radiologic contrast dye enhancement to ensure delivery of injectate to the target site. Studies document misplacement of 40% of caudal and 30% of interlaminar injections performed without fluoroscopy, even by experienced injectionists.

[*]Transient corticosteroid dose-related side effects include facial flushing, low-grade fever, insomnia, anxiety, agitation, hyperglycemia, and fluid retention. Steroids may suppress the hypothalamic-pituitary axis for 3 months following the injection. Lastly, vasovagal reaction, nerve root injury, injectate allergy, and temporary pain exacerbation can occur as well.

[*]Recent studies assessing efficacy of fluoroscopically guided, contrast-enhanced ESI, even for HNP-induced radicular pain, appear promising, suggesting that a significant inflammatory component amenable to corticosteroid treatment may accompany HNP-nerve root pathology.

[*]Studies of ESI for LSS treatment demonstrate mixed results due to varying injection and guidance techniques, patient populations, follow-up periods and protocols, ancillary treatments (eg, physical therapy, oral medication), and outcome measures. This lack of consistency limits the ability to assess ESI efficacy for LSS.

[*]Some studies, nevertheless, suggest that, unlike HNP-provoked radicular pain, NC may be more mechanical or ischemic than inflammatory in nature. Consequently, corticosteroid anti-inflammatory properties may fail to provide designed long-term symptom relief. Studies report that 50% of patients with LSS or HNP-provoked radicular pain received temporary relief and that such results were close to those associated with the placebo effect.

[*]Because of concomitant lateral recess stenosis from facet hypertrophy or lateral HNP, patients may fail transforaminal ESI therapy for HNP-induced radicular pain. ESI may do little to relieve chronic lateral recess stenosis-related radicular pain. Additionally, studies show patients with a preinjection duration of symptoms greater than 24 weeks may respond to ESI as favorably as those with symptoms of less than 24 weeks' duration. This finding, may suggest that chronic nerve compression could induce irreversible neurophysiologic change that ultimately renders the nerve root refractory to ESI.

[*]Future studies require controlled design, contrast-enhanced fluoroscopic guidance, and objective validated outcome measures before definitive conclusions can be drawn regarding efficacy of ESI treatment of LSS.

First-line pharmacotherapy for LSS includes NSAIDs, which provide analgesia at low doses and quell inflammation at high doses. An appropriate therapeutic NSAID plasma level is required to achieve anti-inflammatory benefit.

Aspirin, which binds irreversibly to cyclo-oxygenase and requires larger doses to control inflammation, may cause gastritis; consequently, it is not recommended. Additionally, it may induce multiorgan toxicity, including renal insufficiency, peptic ulcer disease, and hepatic dysfunction. Cyclo-oxygenase isomer type 2 (COX-2) NSAID inhibitors reduce such toxicity. NSAIDs retain a dose-related analgesic ceiling point, above which larger doses do not confer further pain control.

Muscle relaxants may be used to potentiate NSAID analgesia. Sedation results from muscle relaxation, promoting further patient relaxation. Such sedative side effects encourage evening dosing for patients who need to get sufficient sleep but may limit safe performance of some functional activities.

Membrane-stabilizing anticonvulsants, such as gabapentin and carbamazepine, may reduce neuropathic radicular pain from lateral recess stenosis.

Tricyclic antidepressants (TCAs) are often given for neuropathic pain, but their adverse effects limit their use in elderly persons. These include somnolence, dry mouth, dry eyes, and constipation. More concerning are the possible arrhythmias that may occur when used in combination with other medications.

Tramadol and acetaminophen confer analgesia but do not affect inflammation.

Oral opioids may be prescribed on a scheduled short-term basis. Consequently, cotreatment with a psychologist or other addiction specialist is recommended for patients with a history of substance abuse. Patients may be asked to sign a medication contract restricting them to one practitioner, one pharmacy, scheduled medication use, no unscheduled refills, and no sharing or selling of medication.

Drug Category: Anticonvulsants

Use of certain antiepileptic drugs, such as the GABA analogue Neurontin (gabapentin), has proven helpful in some cases of neuropathic pain. These agents have central and peripheral anticholinergic effects, as well as sedative effects, and block the active reuptake of norepinephrine and serotonin. The multifactorial mechanism of analgesia could include improved sleep, altered perception of pain, and increase in pain threshold. Rarely should these drugs be used in treatment of acute pain, since a few weeks may be required for them to become effective.

Drug Category: Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who experience pain.

Drug Category: Tricyclic antidepressants

A complex group of drugs that have central and peripheral anticholinergic effects and sedative effects. They have central effects on pain transmission. They block the active reupdate of norepinephrine and serotonin.

<H3>Further Inpatient Care</H3>

[*]Inpatient care is necessary for patients with LSS who elect to undergo surgery. The length of stay in the hospital is dependent on the type of procedure performed, but, on average, the patient is released 2-5 days following surgery. Following the operation, it is important that these patients resume basic mobility, activities of daily living (ADL), and ambulation as soon as possible and become educated on proper body mechanics and back safety techniques prior to their dismissal. A short course of active physical therapy may be recommended after surgery for these patients to strengthen the lower back and abdominal muscles to speed recovery time. Ideally, an appropriate exercise program can be initiated before surgery and continued thereafter.

<H3>Further Outpatient Care</H3>

[*]Many patients with LSS choose to receive conservative treatment for back and leg pain. An active physical therapy program often is beneficial for these patients to improve flexibility and strength to maintain or improve their current activity levels. Other forms of treatment (eg, ESI) may be administered on an outpatient basis and used in conjunction with other medications and physical therapy. Please see the Physical Therapy and Other Treatment sections for further discussion of these treatments.

<H3>Deterrence</H3>

[*]No prevention exists for LSS.

<H3>Complications</H3>

[*]Complications that may develop in patients with LSS include the following:

[*]

[*]Cauda equina syndrome (in rare cases)

[*]Lower extremity weakness and numbness

[*]Intractable axial, radicular, or NC pain

[*]Disability and loss of productivity

Complications that may develop in patients after surgery include the following:

[*]Sustained axial and radicular pain

[*]Progressive spinal deformity

[*]Cerebrospinal fluid leak

[*]Epidural hematoma

[*]Pulmonary embolism (PE)

<li>Some authors report spondylolisthesis as a complication of lumbar decompression without arthrodesis, especially after total facetectomy. Preoperative risk factors for postoperative development or progression of L4 or L5 spondylolisthesis include the following:

[*]Absence of degenerative osteophytosis

[*]Small and sagittally oriented facets

[*]Well-maintained disk height

<li>Ciol and colleagues report a substantial reoperation rate following LSS surgery in the Medicare population, for reasons that remain unclear.

[*]Possible explanations may include the following:

[*]Failure of implanted devices

[*]Changed patient expectations

[*]Aggressive surgical philosophy

<H3>Patient Education</H3>

[*]Patients should be educated to avoid aggravating factors, such as excessive lumbar extension and downhill ambulation. Additionally, patients should be instructed on correct posture and a home exercise program (eg, flexion-biased lumbar stabilization, flexibility training, gluteal strengthening, aerobic conditioning).

[*]For excellent patient education resources, visit eMedicine's <A href=http://www.emedicinehealth.com/collections/CO1546.asp" target=_blank>Back, Ribs, Neck, and Head Center and Muscle Disorders Center. Also, see eMedicine's patient education articles, http://www.emedicinehealth.com/Articles/4563-1.asp' target="_blank">Back Pain<

[rentalguy1]

Here's a link to another one I used. It covers Degenerative Disc Disease. Pay particular attention to the "cascade of degenerative changes" that are discussed.

For some reason, I can't post the body of this article here?

[Tbird]

Please Do NOT post any personal identifying information on the forum. This is for your protection, make sure if you post anything or attach a file that none of your personal information is visible. The internet is a wide open place and we don't want anyone to use your information in a nefarious way.

Thanks