Guillain-Barre Syndrome Medication
- Author: Michael T Andary, MD, MS; Chief Editor: Milton J Klein, DO, MBA more...
Immunomodulatory therapy, such as plasmapheresis or the administration of intravenous immunoglobulins (IVIGs), is frequently used in patients with Guillain-Barré syndrome (GBS). The efficacy of plasmapheresis and IVIGs appears to be about equal in shortening the average duration of disease.[112, 113, 114, 115, 136] Combined treatment has not been shown to produce a further, statistically significant reduction in disability.
A study by Lin et al indicated that the pretreatment severity score has the strongest association with therapeutic outcome in patients with GBS who undergo double-filtration plasmapheresis, with a higher score being linked to a poorer outcome. The study involved 60 GBS patients who underwent first-line therapy with the procedure.
The decision to use immunomodulatory therapy is based on the disease's severity and rate of progression, as well as on the length of time between the condition's first symptom and its presentation. Risks, such as thrombotic events associated with IVIG, should be taken into consideration.[138, 139] Patients with severe, rapidly progressive disease are most likely to benefit from treatment, with faster functional recovery.
These medications are used to improve the clinical and immunologic aspects of GBS. They may decrease autoantibody production and increase the solubilization and removal of immune complexes.
Intravenous immunoglobulin (Bivigam, Carimune NF, Gammagard S/D, Gamunex-C, Hizentra, Octagam, Privigen)
IVIG is derived from fractionated, purified human plasma collected from a large pool of multiple donors. The product is treated with solvents and detergents to inactivate any blood-borne virus. IVIG may work via several mechanisms, including the blockage of macrophage receptors, the inhibition of antibody production, the inhibition of complement binding, and the neutralization of pathologic antibodies.
Low Molecular Weight Heparin
Low ̶ molecular-weight heparin (LMWH) is used in the prophylaxis of deep venous thrombosis (DVT). The first LMWH to become available in the United States was enoxaparin (Lovenox). LMWH has been used widely in pregnancy, although clinical trials are not yet available to demonstrate that it is as safe as unfractionated heparin.
Reversible elevation of hepatic transaminase levels occurs occasionally. Heparin-associated thrombocytopenia has been observed with LMWH.
Enoxaparin enhances the inhibition of factor Xa and thrombin by increasing antithrombin III activity. It also slightly affects thrombin and clotting time and preferentially increases the inhibition of factor Xa.
This agent has a wide therapeutic window; the prophylactic dose is not adjusted based on the patient's weight. Enoxaparin is safer and more effective than unfractionated heparin for prophylaxis of venous thromboembolism. The average duration of treatment is 7-14 days.
Dalteparin is an LMWH with antithrombotic properties. It enhances the inhibition of Factor Xa and thrombin by increasing antithrombin. It has a minimal effect on activated partial thromboplastin time (aPTT).
Tinzaparin is an LMWH with antithrombotic properties. It enhances the inhibition of Factor Xa and thrombin by increasing antithrombin. It has a minimal effect on aPTT.
Pain medications may be required in inpatient and outpatient settings. A tiered pharmacologic approach that starts with nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen, with narcotic agents added as needed, is usually recommended.
Acetaminophen is the drug of choice for the treatment of pain in patients with documented hypersensitivity to aspirin or NSAIDs, as well as in those with upper GI disease or who are taking oral anticoagulants.
Ibuprofen inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. It is used to provide relief of cervical myofascial pain.
Indomethacin is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.
Naproxen is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.
Diclofenac inhibits prostaglandin synthesis by decreasing COX enzyme activity, which, in turn, decreases formation of prostaglandin precursors.
Ketoprofen is used for relief of mild to moderate pain and inflammation. Small dosages are indicated initially in small patients, elderly patients, and patients with renal or liver disease. Doses higher than 75 mg do not increase the therapeutic effects. Administer high doses with caution, and closely observe the patient's response.
Celecoxib primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek the lowest dose of celecoxib for each patient. It is extensively metabolized in liver primarily via cytochrome P450 2C9.
Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.
Anticonvulsants may be used to alleviate painful dysesthesias, which frequently accompany peripheral neuropathies. Although they have many different mechanisms of action, their use for alleviating neuropathic pain probably depends on their general tendency to reduce neuronal excitability.
Gabapentin is a membrane stabilizer, a structural analogue of the inhibitory neurotransmitter gamma-amino butyric acid (GABA), which paradoxically is thought not to exert an effect on GABA receptors. Gabapentin appears to exert action via the alpha(2)delta1 and alpha(2)delta2 auxiliary subunits of voltage-gaited calcium channels
It is used to manage pain and provide sedation in neuropathic pain.
Carbamazepine is a sodium channel blocker that typically provides substantial or complete relief of pain in 80% of individuals with some forms of painful paresthesia. It reduces sustained, high-frequency, repetitive neural firing and is a potent enzyme inducer that can induce its own metabolism. Due to potentially serious blood dyscrasias, undertake benefit-to-risk evaluation before the drug is instituted.
Tricyclic antidepressants are effective in painful paresthesias. Whereas the drugs in this category are administered in similar dosages, their sedative properties vary. Amitriptyline may be given if the patient suffers from insomnia, whereas nortriptyline and desipramine are better choices when sedation becomes a problem.
Amitriptyline is an analgesic for certain chronic and neuropathic pain. It blocks the reuptake of norepinephrine and serotonin, which increases their concentration in the CNS. Amitriptyline decreases pain by inhibiting spinal neurons involved in pain perception. It is highly anticholinergic. The drug 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 CNS.
Pharmacodynamic effects such as the desensitization of adenyl cyclase and down-regulation of beta-adrenergic receptors and serotonin receptors also appear to play a role in its mechanisms of action.
This is the original TCA used for depression. These agents have been suggested to act by inhibiting reuptake of noradrenaline at synapses in central descending pain-modulating pathways located in the brainstem and spinal cord.
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