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Spinal Stenosis Clinical Presentation

  • Author: John K Hsiang, MD, PhD; Chief Editor: Stephen Kishner, MD, MHA  more...
Updated: Jun 13, 2016


The primary clinical manifestation of spinal stenosis is chronic pain. In patients with severe stenosis, weakness and regional anesthesia may result. Among the most serious complications of severe spinal stenosis is central cord syndrome. Central cord syndrome is the most common incomplete cord lesion. The presentation commonly is associated with an extension injury in a patient with an osteoarthritic spine. In hyperextension injury, the cord is injured within the central gray matter, which results in proportionally greater loss of motor function of upper extremities than loss of motor function of lower extremities, with variable sensory sparing.

Patients with spinal stenosis become symptomatic when pain, motor weakness, paresthesia, or another neurologic compromise causes distress. Spinal stenosis of the thoracic spine is more likely to directly affect the spinal cord because of the relatively narrow thoracic spinal canal.

Spinal stenosis of the cervical and thoracic regions may contribute to neurologic injury, such as development of a central spinal cord syndrome following spinal trauma. Spinal stenosis of the lumbar spine is associated most commonly with midline back pain and radiculopathy. In cases of severe lumbar stenosis, innervation of the urinary bladder and the rectum may be affected, but lumbar stenosis most often results in back pain with lower extremity weakness and numbness along the distribution of nerve roots of the lumbar plexus.

Spinal canal size is not always predictive of clinical symptoms, and some evidence suggests that body mass may play a role in limitations of function in this population.[27]

Severe radiologic stenosis in otherwise asymptomatic individuals suggests inflammation, not just mechanical nerve root compression. Specific inflammation generators may include herniated nucleus pulposus (HNP), ligamentum flavum, and facet joint capsule.

Metastatic and infectious processes that affect the spine may present with both regional pain and signs of central spinal canal narrowing. The regional pain may result from pathologic fractures or nerve root compression by the tumor or abscess. Long tract findings may result from bone fragments, a hemorrhage, an abscess, or a tumor compressing the spinal cord.

Cervical stenosis

Stenosis of the cervical spine causes the clinical syndrome of cervical spondylotic myelopathy (CSM). Initial symptoms may be subtle loss of hand dexterity and mild proximal lower extremity weakness, often without neck or arm pain. With progression, spastic quadriparesis results. Pathologic reflexes such as the Hoffman sign, clonus, and/or the Babinski reflex may augment the diffuse hyperreflexia. Some patients also have associated ataxia from compression of spinocerebellar tracts.[5, 11, 12, 28, 29]

If associated cervical root impingement exists, patients may experience sharp radicular pain into the affected arm, with associated paresthesias and weakness referable to the compressed root. Depending on the level, some upper extremity reflexes (biceps, triceps, brachioradialis) may be depressed or absent in such patients. Males older than 55 years most commonly are affected. Up to two thirds of patients with myelopathy have deteriorating or unchanging conditions. They are also at increased risk of spinal cord injury in the setting of minor trauma.

Lumbar stenosis

Katz and colleagues report that the historical findings most strongly associated with lumbar spinal stenosis (LSS) include advanced age, severe lower extremity pain, and absence of pain when the patient is in a flexed position.[30] 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.[23] Conversely, LSS cannot be ruled out when sitting is the most comfortable position for the patient and standing/walking is the least comfortable.

Patients with significant lumbar spinal canal narrowing report pain, weakness, numbness in the legs while walking, or a combination thereof. Onset of symptoms during ambulation is believed to be caused by increased metabolic demands of compressed nerve roots that have become ischemic due to stenosis. This is the hallmark of neurogenic claudication. The pain is relieved when the patient flexes the spine by, for example, leaning on shopping carts or sitting. Flexion increases canal size by stretching the protruding ligamentum flavum, reduction of the overriding laminae and facets, and enlargement of the foramina. This relieves the pressure on the exiting nerve roots and, thus, decreases the pain. The most common nerve affected is the L5, with associated weakness of extensor hallucis longus.

LSS classically presents as bilateral neurogenic claudication (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.[31]

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.[32] 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.[33]

NC, unlike vascular claudication, is not exacerbated with biking, uphill ambulation, and lumbar flexion and is not alleviated with standing. Patients with LSS 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 patients with LSS.[34]

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, neurogenic and vascular claudication may occur together. This is because both conditions frequently occur in the elderly population.


Physical Examination

Patients with cervical stenosis usually present with cervical radiculopathy, with or without myelopathy. Typically, the condition involves the lower cervical spine. Patients frequently complain of radiating arm pain with numbness and paresthesia in the involved dermatomes. Occasionally, associated weakness occurs in the muscles supplied by that nerve root. If the stenosis is severe enough, or if it is positioned centrally in the spine, patients may present with signs and symptoms of myelopathy (spinal cord dysfunction). Typically, these patients complain of finger numbness, clumsiness, and difficulty walking due to spasticity and loss of position sense. In more severe cases, the patients can have bowel and bladder control dysfunction. Upon examination, these patients have "long-tract signs" such as hyperreflexia, positive Hoffman sign, positive Babinski sign, and/or clonus.

Katz and colleagues report physical examination findings most strongly associated with lumbar spinal stenosis (LSS) include wide-based gait, abnormal Romberg test, thigh pain following 30 seconds of lumbar extension, and neuromuscular abnormalities[30] ; however, Fritz and colleagues state physical examination findings do not seem helpful in determining the presence or absence of LSS.[23]

Patients with LSS usually present with a constellation of symptoms that include lower back pain, radiating leg pain (unilateral or bilateral), and possible bladder and bowel difficulties. The classic presentation is radiating leg pain associated with walking that is relieved by rest (neurogenic claudication). When patients bend forward, the pain diminishes. Rarely, patients with LSS present with cauda equina syndrome (bilateral leg weakness, urinary retention due to atonic bladder).

Physical examination findings are frequently 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.[35] 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 P s of vascular claudication, as follows:

  • Pulselessness
  • Paralysis
  • Paresthesia
  • Pallor
  • Pain

The absence of these problems, excluding pain and paresthesias, which are common to neurogenic and vascular claudication, should give the clinician confidence in the diagnosis of NC. 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.

Dural tension signs should be unremarkable. Lumbar segment mobilization often fails to reproduce pain, and trigger points are typically not present.

Contributor Information and Disclosures

John K Hsiang, MD, PhD Director of Spine Surgery, Swedish Neuroscience Institute, Swedish Medical Center

John K Hsiang, MD, PhD is a member of the following medical societies: American Association of Neurological Surgeons, North American Spine Society, Sigma Xi, Society of Critical Care Medicine

Disclosure: Nothing to disclose.


Michael B Furman, MD, MS Physiatrist, Interventional Spine Care Specialist, Electrodiagnostics, Pain Medicine, Director, Spine and Sports Fellowship, Orthopaedic and Spine Specialists, Sinai Hospital of Baltimore

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

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kishner, MD, MHA Professor of Clinical Medicine, Physical Medicine and Rehabilitation Residency Program Director, Louisiana State University School of Medicine in New Orleans

Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.


Patrick M Foye, MD Director of Coccyx Pain Center, Associate Professor and interim Chair of Physical Medicine and Rehabilitation, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, University Hospital, Newark, New Jersey

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society

Disclosure: Nothing to disclose.

Robert Pannullo MD, Staff Physician at Ocean Medical Center, Central Jersey Surgical Center

Robert Pannullo is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Phi Beta Kappa

Disclosure: Nothing to disclose.

Paul L Penar, MD, FACS Professor, Department of Surgery, Division of Neurosurgery, Director, Functional Neurosurgery and Radiosurgery Programs, University of Vermont College of Medicine

Paul L Penar, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, Congress of Neurological Surgeons, and World Society for Stereotactic and Functional Neurosurgery

Disclosure: Nothing to disclose.

Kirk M Puttlitz, MD Consulting Staff, Pain Management and Physical Medicine, Arizona Neurological Institute

Kirk M Puttlitz, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Phi Beta Kappa

Disclosure: Nothing to disclose.

K Daniel Riew, MD Mildred B Simon Distinguished Professor of Orthopedic Surgery, Professor of Neurologic Surgery, Washington University School of Medicine; Chief, Cervical Spine Surgery, Department of Orthopedic Surgery, Barnes-Jewish Hospital

K Daniel Riew, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, AO Foundation, Cervical Spine Research Society, North American Spine Society, and Scoliosis Research Society

Disclosure: Medtronic Royalty Medtronic Vertex; Biomet Royalty Maxan anterior cervical plate; Osprey Royalty Interbody Graft; Osprey Stock Options None; SpineMedica None None; Synthes Consulting fee Other

Jeremy Simon, MD Attending Physician, Department of Physical Medicine, The Rothman Institute

Jeremy Simon, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, International Spine Intervention Society, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Amir Vokshoor, MD Staff Neurosurgeon, Department of Neurosurgery, Spine Surgeon, Diagnostic and Interventional Spinal Care, St John's Health Center

Amir Vokshoor, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, American Medical Association, and North American Spine Society

Disclosure: Nothing to disclose.

J Michael Wieting, DO, MEd, FAOCPMR, FAAPMR Professor of Physical Medicine and Rehabilitation, Associate Dean, Consultant in Sports Medicine, Assistant Vice President of Program Development, Division of Health Sciences, Lincoln Memorial University-DeBusk College of Osteopathic Medicine

J Michael Wieting, DO, MEd, FAOCPMR, FAAPMR is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Osteopathic Academy of Sports Medicine, and Association of Academic Physiatrists

Disclosure: Nothing to disclose.

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Oblique view of the cervical spine demonstrates 2 levels of foraminal stenosis (white arrows) resulting from facet hypertrophy (yellow arrow) and uncovertebral joint hypertrophy.
Axial cervical CT myelogram demonstrates marked hypertrophy of the right facet joints (black arrows), which results in tight restriction of the neuroforaminal recess and lateral neuroforamen.
Short recovery time T1-weighted spin-echo sagittal MRI scan demonstrates marked spinal stenosis of the C1/C2 vertebral level cervical canal resulting from formation of the pannus (black arrow) surrounding the dens in a patient with rheumatoid arthritis. Long recovery time T2*-weighted fast spin-echo sagittal MRI scans better define the effect of the pannus (yellow arrow) on the anterior cerebrospinal fluid space. Note the anterior displacement of the upper cervical cord and the lower brainstem.
Posterior view from a radionuclide bone scan. A focally increased uptake of nuclide (black arrow) is demonstrated within the mid-to-upper thoracic spine in a patient with Paget disease.
T2-weighted sagittal MRI of the cervical spine demonstrating stenosis from ossification of the posterior longitudinal ligament, resulting in cord compression.
Severe cervical spondylosis can manifest as a combination of disk degeneration, osteophyte formation, vertebral subluxation, and attempted autofusion as depicted in this sagittal MRI. Also, note the focal kyphosis, which is typical in severe forms.
Lateral T2-weighted magnetic resonance imaging (MRI) scan demonstrating narrowing of the central spinal fluid signal (L4-L5), suggesting central canal stenosis.
Axial T2 magnetic resonance imaging (MRI) scan (L4-L5) in the same patient as in the above image, confirming central canal stenosis.
Trefoil appearance characteristic of central canal stenosis due to a combination of zygapophysial joint and ligamentum flavum hypertrophy.
Lumbar computed tomography (CT) myelogram scan demonstrates a normal central canal diameter.
Lateral and axial magnetic resonance imaging (MRI) scan demonstrating right L4 lateral recess stenosis secondary to combination of far lateral disk protrusion and zygapophysial joint hypertrophy.
Sagittal measurements taken of the anteroposterior diameter of the cervical spinal canal are highly variable in otherwise healthy persons. An adult male without spinal stenosis has a diameter of 16-17 mm in the upper and middle cervical levels. Magnetic resonance imaging (MRI) scans and reformatted computed tomography (CT) images are equally as effective in obtaining these measurements, while radiography is not accurate.
Oblique 3-dimensional shaded surface display CT reconstruction of right foraminal stenosis resulting from unilateral facet hypertrophy (black arrow). The volume of the reconstruction has been cut obliquely across the neuroforaminal canal.
Anterior view of a lumbar myelogram demonstrates stenosis related to Paget disease. Myelography is limited because of the superimposition of multiple spinal structures that contribute to the overall pattern of stenosis.
Lateral view of a lumbar myelogram performed in a patient who has been fused across the L4-L5 and the L5-S1 vertebral interspaces using transpedicular screws. Treatment of lumbar spinal stenosis may include decompression laminectomies, followed by the placement of transpedicular screws (yellow arrows) with a posterior stabilization bar.
Sagittal view of a 3-dimensional volume image of the lumbar spine in a patient with a posterior fusion using transpedicular screws in L4 and L5. Note that an interposition graft has been placed between L4 and L5 to maintain satisfactory
Lateral swimmer's radiographic view demonstrates compression of the anterior contrast-filled cervical thecal sac. The defect helps localize the stenosis; however, the pattern does not reflect lateral disc herniation or spondylosis directly.
Axial T2-weighted gradient echo MRI scan. Note the high-grade spinal stenosis resulting in severe upper cervical cord compression (arrows). This patient presented with a central spinal cord syndrome that improved following surgical decompression.
Sagittal T2-weighted MRI image demonstrates severe stenosis. Spinal stenosis is demonstrated at several levels (white and yellow arrows) resulting from a combination of disc annulus bulging (white arrow) and epidural soft-tissue thickening (yellow arrow).
Superior-to-inferior view of 3-dimensional volume reconstruction of central canal spinal stenosis resulting from chronic disc herniation. The patient presented with lower extremity weakness and loss of bladder control.
: Sagittal T2 weighted fast spin-echo (FSE) MRI scan of a meningioma of the lower thoracic spine obtained without contrast enhancement. The effect of the mass is better seen because of the contrast between the mass and the cerebrospinal fluid (CSF). The anterior spinal canal is occupied by a mass that displaces and compresses the conus medullaris (C) at the T12 level. The mass (white arrow) is of intermediate increased signal brightness, compared to the normal spinal cord.
Sagittal T1-weighted spin-echo (SE) MRI scan of a meningioma of the lower thoracic spine obtained following IV gadolinium contrast enhancement. The mass is better seen because of the contrast enhancement within the meningioma (M). The anterior spinal canal is occupied by a mass that displaces and compresses (white arrows) the conus medullaris (C) at the T12 level. The mass (white arrow) is of intermediate increased signal brightness, compared to the normal spinal cord.
Normal findings in the thoracic spine as demonstrated by CT myelography. Note the detail of the spinal cord and the ventral and dorsal nerves surrounded by contrast.
nal-cut view of 3-dimensional reconstruction CT scan of the thoracic spine in tuberculosis spondylitis. Note the central spinal cavity (black arrow). The vertebral endplate has compressed downward (double blue arrows). The advantage of 3-dimensional reconstructions is the ability to better evaluate preoperatively the type of surgery needed to stabilize spinal compression fractures.
Paraspinal abscess aspiration biopsy. The stains were positive for mycobacteria (black arrows; acid-fast stain, magnification X100).
With the patient in a prone position and using CT localization, a bone biopsy and aspiration were performed from the area of greatest destruction within the vertebral endplate (arrow).
Aspergillosis organisms were recovered from a lumbar disc space abscess. The patient had received a renal transplant 12 months prior to the infection (hematoxylin and eosin, magnification X40).
Long recovery time T2*-weighted fat-suppressed sagittal MRI scan of the thoracic spine demonstrates subtle enlargement of a thoracic vertebral body (double white arrows) and a slightly increased degree of signal brightness within the vertebral body (yellow arrow).
Paget disease of the thoracic spine. Thoracic spinal CT scan demonstrates enlarged vertebral body endplates (black arrows). The axial image on the left demonstrates the characteristic thickening of the bony matrix of the vertebral body.
Axial lumbar CT scan demonstrates marked right-sided spinal canal stenosis (black arrow) resulting from advanced right-sided facet hypertrophy. Note the vacuum disc sign within the intervertebral disc (double yellow arrow). The vacuum disc sign is further indication of degenerative changes and spinal instability.
Pantopaque tracer in the epidural spaces. Pantopaque can remain in the epidural and facial spaces for years following a myelogram. Chronic inflammatory arachnoiditis has been associated with a combination of trauma (bleeding) with administration of Pantopaque.
Localization of thoracic lesion prior to surgical correction. A needle/wire localization technique is used to ensure the correct surgical level. Such preoperative localizations save time in the operating suite while reducing the need for intraoperative radiology.
Sagittal 3-dimensional CT reconstruction of the lumbar spine in a patient with multiple myeloma. The central portions of the vertebral bodies (yellow arrows) have been replaced by the nonossified tumor.
Biopsy (yellow arrow) of a multiple myeloma mass (black arrow) that has replaced the lumbar spinal canal (blue arrow) completely.
Multiple myeloma. Photomicrograph of an aspiration biopsy specimen.
Three-dimensional surface CT image of the lumbar spine following transpedicular screw placement across the L4-L5 interspace. Note how the tips of the screws project beyond the anterior margins of the L5 vertebral body.
Axial CT image taken through L5 in a patient in whom transpedicular screws have been placed. Note that the screws (black arrows) are too far lateral and anterior. The iliac veins lie just anterior to tips of the screws (white arrows). Both the angle of screw placement and the length of the screws must be tailored to the individual patient.
Spinal stenosis. Sagittal multiplanar reconstruction (MPR) image from a CT scan of the lumbar spine following posterior decompression and fusion of the L4-L5 interspace. The interposition graft (white arrow) is posterior to the desired position. The patient remained asymptomatic. Follow-up imaging should focus upon the stability of the posterior fusion, the position of the pedicle screws, and the position of the interposition graft.
Sagittal reformatted image from a CT of the cervical spine following anterior spinal decompression and fusion. Surgical treatment of spinal canal stenosis often involves anterior vertebrectomy and bone graft interposition. The goal in such cases is to restore cervical spinal alignment (white line) while securing anterior stability. In this patient, the bone graft (double black arrows) has migrated forward (double yellow arrows).
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