Spinal Stenosis Medication
- Author: John K Hsiang, MD, PhD; Chief Editor: Stephen Kishner, MD, MHA more...
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.
Nonsteroidal Anti-inflammatory Drugs
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 is the drug of choice for patients with mild to moderate pain. Ibuprofen inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
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 is believed to inhibit the enzyme COX, which is essential in the biosynthesis of prostaglandins. Diclofenac has anti-inflammatory, analgesic, and antipyretic properties.
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 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.
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 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 mechanism not entirely known. It binds to opioid receptors and inhibits reuptake of serotonin and norepinephrine.
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.
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.
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 reduces nerve impulse transmission from spinal cord to skeletal muscle, providing pain relief for musculoskeletal conditions.
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.
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.
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 inhibits nerve impulses by decreasing cell membrane sodium ion influx.
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 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 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 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.
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 decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.
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 decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Hydrocortisone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
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