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Spinal Stenosis Medication

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

Medication Summary

First-line pharmacotherapy for lumbar spinal stenosis (LSS) includes nonsteroidal anti-inflammatory drugs (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. NSAIDs retain a dose-related analgesic ceiling point, above which larger doses do not confer further pain control.

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 (COX) isomer type 2 (COX-2) NSAID inhibitors reduce such toxicity. Tramadol and acetaminophen confer analgesia but do not affect inflammation.

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. 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.

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.

Oral opioids may be prescribed on a scheduled short-term basis. Consequently, co-treatment 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 1 practitioner, 1 pharmacy, scheduled medication use, no unscheduled refills, and no sharing or selling of medication.

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Nonsteroidal Anti-inflammatory Drugs

Class Summary

First-line pharmacotherapy for lumbar spinal stenosis (LSS) includes nonsteroidal anti-inflammatory drugs (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.

Ibuprofen (Motrin, Advil, Addaprin, Caldolor, NeoProfen, I-Prin, IBU-200)

 

Ibuprofen is the drug of choice for patients with mild to moderate pain. Ibuprofen inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Naproxen (Naprosyn, Aleve, Anaprox, Anaprox DS, Naprelan)

 

Naproxen is used for the relief of mild to moderate pain. Naproxen inhibits inflammatory reactions and pain by decreasing activity of COX, which is responsible for prostaglandin synthesis.

Diclofenac (Zipsor, Zorvolex, Cambia, Voltaren-XR, Cataflam)

 

Diclofenac is believed to inhibit the enzyme COX, which is essential in the biosynthesis of prostaglandins. Diclofenac has anti-inflammatory, analgesic, and antipyretic properties.

Etodolac

 

Etodolac is a short-acting indole NSAID with an intermediate half-life and is approved for analgesic use. Etodolac inhibits prostaglandin synthesis by decreasing activity of the enzyme, COX, which results in decreased formation of prostaglandin precursors. This, in turn, results in reduced inflammation. Has lower risk of producing GI complications and, as result, is especially well tolerated in elderly patients. Used for relief of mild to moderate pain.

Celecoxib (Celebrex)

 

Celecoxib is a nonsteroidal anti-inflammatory that selectively inhibits COX-2. COX-2 inhibitors have a lower incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, when compared with nonselective NSAIDs.

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Analgesics

Class Summary

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

Acetaminophen (Tylenol, FeverAll, Acephen, Valorin)

 

Acetaminophen may be used for pain control in patients who have documented hypersensitivity to aspirin or NSAIDs, who have upper GI disease, or who are taking oral anticoagulants.

Tramadol (Ultram, Ultram ER, Conzip, Rybix)

 

Tramadol mechanism not entirely known. It binds to opioid receptors and inhibits reuptake of serotonin and norepinephrine.

Hydrocodone bitartrate and acetaminophen (Vicodin, Lortab, Norco, Zamicet, Xodol)

 

Opioid analgesic that is indicated for moderate to severe pain. Binds to opioid receptors in the CNS and inhibits synthesis of prostaglandins. Oral opioids may be prescribed on a scheduled short-term basis.

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Muscle Relaxants

Class Summary

Muscle relaxants may be used to potentiate NSAID analgesia. Sedation from muscle relaxation promotes 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.

Cyclobenzaprine (Fexmid, Amrix)

 

Acts centrally and reduces motor activity of tonic somatic origins, influencing both alpha and gamma motor neurons. Acts to provide relief of muscle spasms associated with painful musculoskeletal conditions.

Methocarbamol (Robaxin)

 

Methocarbamol reduces nerve impulse transmission from spinal cord to skeletal muscle, providing pain relief for musculoskeletal conditions.

Carisoprodol (Soma)

 

Carisoprodol is a short-acting medication that may have depressant effects at spinal cord level. Skeletal muscle relaxants have modest short-term benefit as adjunctive therapy for nociceptive pain associated with muscle strains and, used intermittently, for diffuse and certain regional chronic pain syndrome.

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Anticonvulsants

Class Summary

Use of certain antiepileptic drugs, such as the GABA analogue Neurontin (gabapentin), has proven helpful in some cases of neuropathic pain.[49] 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.

Gabapentin (Neurotonin, Gralise)

 

Gabapentin has anticonvulsant properties and antineuralgic effects; however, the exact mechanism of action is unknown. It is structurally related to GABA but does not interact with GABA receptors.

Carbamazepine (Tegretol, Tegretol-XR, Carbatrol, Epitol)

 

Carbamazepine inhibits nerve impulses by decreasing cell membrane sodium ion influx.

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Antidepressant, Tricyclic

Class Summary

The tricyclic antidepressants are a complex group of drugs that have central and peripheral anticholinergic effects and sedative effects. They have central effects on pain transmission, and they block the active reuptake of norepinephrine and serotonin.

Amitriptyline

 

Amitriptyline has an analgesic effect for certain chronic and neuropathic pain. It blocks reuptake of norepinephrine and serotonin, which increases concentration in the CNS. Amitriptyline also decreases pain by inhibiting spinal neurons involved in pain perception. It is highly anticholinergic and is often discontinued because of somnolence and dry mouth. Cardiac arrhythmia, especially in overdose, has been described; monitoring the QTc interval after reaching the target level is advised. Up to 1 month may be needed to obtain clinical effects.

Nortriptyline (Pamelor)

 

Nortriptyline has demonstrated effectiveness in the treatment of chronic pain. By inhibiting the reuptake of serotonin and/or norepinephrine by the presynaptic neuronal membrane, this drug increases the synaptic concentration of these neurotransmitters in the central nervous system.

Clomipramine (Anafranil)

 

Clomipramine is useful for neuropathic pain because of its central effects on pain transmission. It inhibits the membrane pump mechanism responsible for uptake of norepinephrine and serotonin in adrenergic and serotonergic neurons.

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Corticosteroids

Class Summary

Epidural steroid injection (ESI) provides aggressive conservative treatment for patients with lumbar spinal stenosis (LSS) 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. Corticosteroids may also block nociceptive transmission in C fibers.

Triamcinolone (Kenalog)

 

Triamcinolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Dexamethasone

 

Dexamethasone decreases inflammation by suppressing the production of inflammatory mediators and neutrophil migration. The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of inflammatory cells into affected areas.

Methylprednisolone (A-Methapred, Solu-Medrol)

 

Methylprednisolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Hydrocortisone (Solu-Cortef, A-Hydrocort)

 

Hydrocortisone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

Acknowledgements

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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