eMedicine Specialties > Neurology > Movement and Neurodegenerative Diseases

Multiple System Atrophy: Treatment & Medication

Author: André Diedrich, MD, PhD, Research Associate Professor of Medicine, Research Assistant Professor of Biomedical Engineering, Autonomic Dysfunction Center, Vanderbilt University School of Medicine
Coauthor(s): David Robertson, MD, Director, Clinical Research Center, Professor of Medicine, Pharmacology, and Neurology, Vanderbilt University
Contributor Information and Disclosures

Updated: Sep 4, 2009

Treatment

Medical Care

The cause of MSA remains unknown, and no current therapy can reverse or halt progression of the disease. The extrapyramidal and cerebellar aspects of the disease are debilitating and difficult to treat, but the earliest symptom that brings patients to medical attention usually is orthostatic hypotension. Orthostatic hypotension leads to curtailing of physical activity, with all the attendant problems of deconditioning that occur in consequence. Without an adequate upright BP, keeping patients active and on an exercise regimen is extremely difficult; therefore, management of orthostatic hypotension is one of the major tasks in the treatment of patients with MSA.

  • Nonpharmacologic management in MSA
    • Orthostatic hypotension: Mechanical maneuvers, such as leg-crossing, squatting, abdominal compression, bending forward, and placing 1 foot on a chair, can be effective to prevent episodes of orthostatic hypotension. Wearing a tight-waisted external support garment improves venous return and preload to the heart during standing but loses effectiveness if the patient is supine. Increased salt and fluid intake and tilted sleeping with the head elevated increase the circulatory plasma volume.
    • Postprandial hypotension: Small, frequent meals prevent BP drop after eating. Intake of water half an hour before meals or drinking coffee can counteract postprandial hypotension.
    • Supine hypertension: The management of patients with orthostatic hypotension and supine hypertension can be challenging, but adequate blood pressure control is often achieved following the treatment strategy:
        • Use of over-the-counter medication with pressor effects.
        • Avoid fluid intake at bedtime.
        • Avoid using elastic stockings when supine.
        • Avoid the use of pressor agents before bedtime.
        • Raise the head of the bed 6-9 inches.
        • Rest on a semirecumbent chair with feet on the floor during the day.
        • Snacks before bedtime are encouraged.
    • Urinary incontinence: Intermittent self-catheterization or suprapubic or urethral catheterization can improve symptoms of urinary incontinence.
    • Constipation: A high-fiber diet, bulk laxative, lactulose, and suppositories can prevent constipation.
    • Stridor: Speech therapy is often useful to improve swallowing and communication.
    • Deconditioning: Physical therapy and an aquatic exercise program (hypotension does not occur while patients are in water) prevent physical deconditioning of the patient unless the movement disorder aspect of the illness so impairs balance that this is not advisable.
  • Pharmacologic management in MSA: Please see the Medication section for a discussion of pharmacologic management.

Surgical Care

Surgical care may be necessary.

  • An atrial pacemaker rarely benefits patients but may be tried in patients with profound bradycardia to prevent orthostatic hypotension.
  • Consider tracheostomy with the utmost care for intermittent respiratory stridor.
  • Cricopharyngeal myotomy or gastrostomy has been used in patients with severe dysphagia, but its value is uncertain.

Consultations

Physical therapists, occupational therapists, speech therapists, and social works offer considerable practical help.

Diet

An essentially normal diet is recommended, with the following guidelines:

  • Increased salt and fluid intake maintains plasma volume.
  • Frequent and small meals may help those for whom postprandial hypotension is a significant problem.
  • A high-fiber diet, bulk laxatives, and suppositories prevent constipation.

Activity

Exercise of muscles of the lower extremities and abdomen, water aerobics at hip level (not swimming, as it causes polyuria), and postural training, in combination with drug therapy, are useful.

Medication

Drug therapy is directed mainly toward alleviation of symptoms of the movement disorder and orthostatic hypotension (see also Table 9). Medical therapy can be also applied for urinary incontinence, constipation, erectile dysfunction, and supine hypertension. Medical Therapy of Movement Disorder

The movement-disorder component of MSA is usually treated with levodopa, dopaminergic agonists, anticholinergic agents, or amantadine, but results are rarely as favorable in MSA as in classic Parkinson disease.

Other classes of drugs now uncommonly used are nonsteroidal anti-inflammatory drugs (NSAIDs), antihistamines, somatostatin analogues, and caffeine.

Medical therapy of orthostatic hypotension

Many agents have been advocated for the management of orthostatic hypotension. Table 9 shows some of the most widely used approaches. However, drug therapy of orthostatic hypotension is limited by supine hypertension, which affects about 60% of patients with MSA.

Table 9. Drugs Used to Manage Orthostatic Hypotension in MSA

Open table in new window

Table
ClassDrugDescription or Mechanism
FludrocortisoneFludrocortisone acetate (Florinef)Mineralocorticoid; sodium retention, primarily in extravascular compartment, causes tissue edema to venous capacitance bed in lower extremity. With this edema, venous bed accommodates decreased volume of blood in an upright posture (high doses, late effect); increases sensitivity to norepinephrine (even with small doses)
Sympathomimetic aminesMidodrine, dihydroxyphenylserineAlpha1-adrenoreceptor agonist acts directly on vasculature, causes venous and arteriolar vasoconstriction
Recombinant erythropoietin (EPO)Epoetin alfaIncreases sensitivity to pressor effects of angiotensin II; increases plasma endothelin level; increases cytosolic free calcium in vascular smooth muscle; increases intravascular volume
NSAIDsIndomethacin, ibuprofenInhibition of vasodilator prostaglandins proposed but not proven
AntihistaminesDiphenhydramine, cimetidineReduce vasodilatation caused by histamine release
Somatostatin analogsSomatostatin, octreotideReduce splanchnic capacitance
Vasopressin agonistsDesmopressin (DDAVP)Vasopressin analogs; no effect on V1 receptors, which are responsible for vasopressin-induced vasoconstriction; acts on V2 receptors on renal tubuli, which are responsible for antidiuretic effect; prevents nocturnal diuresis, raises BP in morning
Other sympathomimetics Other sympathomimeticsYohimbineAlpha2-adrenoreceptor antagonist, sympathomimetic
CaffeineAdenosine receptor antagonist, sympathomimetic
ClassDrugDescription or Mechanism
FludrocortisoneFludrocortisone acetate (Florinef)Mineralocorticoid; sodium retention, primarily in extravascular compartment, causes tissue edema to venous capacitance bed in lower extremity. With this edema, venous bed accommodates decreased volume of blood in an upright posture (high doses, late effect); increases sensitivity to norepinephrine (even with small doses)
Sympathomimetic aminesMidodrine, dihydroxyphenylserineAlpha1-adrenoreceptor agonist acts directly on vasculature, causes venous and arteriolar vasoconstriction
Recombinant erythropoietin (EPO)Epoetin alfaIncreases sensitivity to pressor effects of angiotensin II; increases plasma endothelin level; increases cytosolic free calcium in vascular smooth muscle; increases intravascular volume
NSAIDsIndomethacin, ibuprofenInhibition of vasodilator prostaglandins proposed but not proven
AntihistaminesDiphenhydramine, cimetidineReduce vasodilatation caused by histamine release
Somatostatin analogsSomatostatin, octreotideReduce splanchnic capacitance
Vasopressin agonistsDesmopressin (DDAVP)Vasopressin analogs; no effect on V1 receptors, which are responsible for vasopressin-induced vasoconstriction; acts on V2 receptors on renal tubuli, which are responsible for antidiuretic effect; prevents nocturnal diuresis, raises BP in morning
Other sympathomimetics Other sympathomimeticsYohimbineAlpha2-adrenoreceptor antagonist, sympathomimetic
CaffeineAdenosine receptor antagonist, sympathomimetic
Medical therapy of supine hypertension

The presence of supine hypertension can complicate the pharmacologic management of patients with MSA, but a rational approach to its treatment is often successful. Simply avoiding the supine position is often enough to control hypertension during the day. Treatment of supine hypertension is required at nighttime. Elevating the head of the bed is useful but rarely sufficient. Short-acting vasodilators are effective in controlling hypertension. The management of patients with orthostatic hypotension and supine hypertension can be challenging, but adequate BP control is often achieved following the nonpharmacologic approach as described above combined with following medication:

  • Nitrates, transdermal nitroglycerin (0.1–0.2 mg/h)
  • Hydralazine (50 mg)
  • Nifedipine; short-acting calcium blocker (30 mg)
  • Minoxidil (2.5 mg)
  • Clonidine (0.1 mg), early in the evening

Drug List

The following drug list is categorized and compiled for MSA treatments.

Antiparkinson agents

Patients with MSA may have an initial response to levodopa. This response usually diminishes over time. Withdrawal of levodopa can cause the patient's condition to deteriorate, but this is much more prominent in Parkinson disease than in MSA. In modern practice, levodopa is administered in combination with a dopa decarboxylase inhibitor.


Levodopa/Carbidopa (Sinemet)

Levodopa plus dopa decarboxylase inhibitor. Levodopa administered alone, largely decarboxylated by intestinal mucosa or other peripheral sites rich in MAO, and little reaches cerebral circulation and CNS.

Adult

25/100 mg PO hs; increase q3-7d to total 100 mg/d levodopa or until adverse effects occur

Pediatric

Not established

Hydantoins, pyridoxine, phenothiazines, and hypotensive agents may decrease effects; antacids and MAOIs increase toxicity

Documented hypersensitivity; narrow-angle glaucoma; malignant melanoma; undiagnosed skin lesions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

With SR form, certain CNS adverse effects (eg, dyskinesias) may occur early and at low doses; caution with history of myocardial infarction, arrhythmias, asthma, or peptic ulcer disease; sudden discontinuation of levodopa may cause worsening of Parkinson disease; high-protein meals should be distributed throughout day to prevent fluctuations in levodopa absorption

These agents are alternatives to levodopa therapy in the late phase of the movement disorder. They selectively act on different subtypes of dopamine receptors throughout the brain. The mechanism is independent of the functional capacities of the nigrostriatal neurons and may be more effective than other drugs.


Pergolide (Permax)

Pergolide was withdrawn from the US market March 29, 2007, because of heart valve damage resulting in cardiac valve regurgitation. It is important not to abruptly stop pergolide. Health care professionals should assess patients' need for dopamine agonist (DA) therapy and consider alternative treatment. If continued treatment with a DA is needed, another DA should be substituted for pergolide. For more information, see FDA MedWatch Product Safety Alert and Medscape Alerts: Pergolide Withdrawn From US Market.

May exert therapeutic effect by directly stimulating postsynaptic dopamine receptors in nigrostriatal system. Agonist of D1 and D2 striatal dopamine receptors.

Adult

0.75-3 mg PO qd

Pediatric

Not established

Dopamine antagonists (eg, neuroleptics, phenothiazines, butyrophenones, thioxanthenes, metoclopramide) may diminish effectiveness; because >90% bound to plasma proteins, caution if coadministered with drugs known to affect protein binding

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause valvular heart disease (yearly echocardiograms recommended for patients on chronic therapy); inhibits secretion of prolactin; causes transient rise in serum concentrations of growth hormone and decrease in serum concentrations of luteinizing hormone; adverse effects include nausea, hypotension, hallucinations, and somnolence; use caution in patients who have been treated for cardiac dysrhythmias; may cause or exacerbate preexisting states of confusion and hallucinations or dyskinesia


Bromocriptine (Parlodel)

Strong agonist of D2 and partial agonist of D1 striatal dopamine receptors.

Adult

2.5-40 mg PO qd

Pediatric

Not established

Ergot alkaloids may increase toxicity; amitriptyline, butyrophenones, imipramine, methyldopa, phenothiazines, and reserpine may decrease effects

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic disease

These agents were widely used before levodopa was discovered.


Trihexyphenidyl (Artane)

Anticholinergic receptor agent affecting structures in neostriatum.

Adult

2-4 mg PO tid

Pediatric

Not established

Amantadine may increase anticholinergic adverse effects (resolve when dose reduced); haloperidol may worsen schizophrenic symptoms; may decrease haloperidol serum concentrations; may reduce pharmacologic and/or therapeutic actions of phenothiazines

Documented hypersensitivity; glaucoma; peptic ulcers; pyloric or duodenal obstruction; stenosing prostatic hypertrophy or bladder neck obstructions; achalasia; toxic megacolon

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Dose adjustment may be required in elderly patients; caution in tachycardia, cardiac hypotension, prostatic hypertrophy, arrhythmias, hypertension, or any tendency toward urinary retention, liver or kidney disorders, or obstructive disease of GI or GU tract; if dry mouth severe and impairs swallowing or speaking or if loss of appetite and weight, reduce dose or discontinue temporarily


Benztropine mesylate (Cogentin)

Anticholinergic receptor agent affecting structures in neostriatum.

Adult

2-4 mg PO tid

Pediatric

Not established

Decreases effects of levodopa; increases effects of narcotic analgesics, phenothiazines, quinidine, TCAs, and anticholinergics

Documented hypersensitivity; angle-closure glaucoma; stenosing peptic ulcers; prostatic hypertrophy; bladder neck obstructions; myasthenia gravis; pyloric or duodenal obstruction; achalasia (megaesophagus); megacolon

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate hypertension, tachycardia, cardiac arrhythmias, liver or kidney disorders, hypotension, prostatic hypertrophy, urinary retention, and obstructive disease of GI and/or GU tract; toxic psychosis may occur in extrapyramidal reactions due to phenothiazine to treat psychiatric conditions


Diphenhydramine hydrochloride (Benadryl)

Affects structures in neostriatum.

Adult

25-50 mg PO tid/qid

Pediatric

Not established

Potentiates effect of CNS depressants; because of alcohol content, do not give syrup to patient taking medications that can cause disulfiram-like reactions

Documented hypersensitivity; MAOIs

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, or urinary tract obstruction; xerostomia


Amantadine (Symmetrel)

May alter dopamine release or reuptake and actions at glutamate receptors.

Adult

100 mg PO bid

Pediatric

Not established

Drugs with anticholinergic or CNS stimulant activity increase toxicity; hydrochlorothiazide plus triamterene may increase plasma concentrations

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in liver disease, uncontrolled psychosis, eczematoid dermatitis, seizures, and use of CNS stimulants; reduce dose in renal disease in treating Parkinson disease; do not discontinue abruptly

Urinary antispasmodic agents

When detrusor hyperreflexia is the cause of the patient's urinary incontinence, peripherally acting anticholinergic agents (eg, oxybutynin chloride [Ditropan], tolterodine [Detrol], propantheline [Pro-Banthine]) can be applied.


Oxybutynin chloride (Ditropan)

Tertiary amine muscarinic receptor antagonist. Nonspecific relaxant on smooth muscles.

Adult

5-10 mg PO hs

Pediatric

Not established

CNS effects increase with concurrent CNS depressants

Documented hypersensitivity; glaucoma; partial or complete GI obstruction; myasthenia gravis; ulcerative colitis; toxic megacolon

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in urinary tract obstruction, reflux esophagitis, and heart disease; may worsen constipation


Tolterodine (Detrol)

Competitive muscarinic receptor antagonist for overactive bladder. Selective for urinary bladder over salivary glands; therefore, differs from other anticholinergics. High specificity for muscarinic receptors, minimal activity or affinity for other neurotransmitter receptors and other potential targets (eg, calcium channels).

Adult

2 mg PO hs

Pediatric

Not established

Patients treated with macrolide antibiotics or antifungals should not receive >1.0 mg bid

Documented hypersensitivity; urinary retention; gastric retention; uncontrolled narrow-angle glaucoma

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not give dosages >1.0 mg bid to patients with significantly reduced hepatic function; caution in renal impairment


Propantheline (Pro-Banthine)

Blocks action of acetylcholine at postganglionic parasympathetic receptor sites.

Adult

15-30 mg PO hs

Pediatric

Not established

Antacids decrease effects; disopyramide, tricyclic antidepressants, phenothiazines, corticosteroids, and bretylium increase toxicity

Documented hypersensitivity; ulcerative colitis; narrow-angle glaucoma; obstructive disease of GI or urinary tract

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic disease; may worsen constipation

Gastroprokinetic agents

If a special bulk-forming diet fails, lactulose occasionally is helpful. In rare cases, cisapride (Propulsid) may promote bowel movements.


Erythromycin (E.E.S., E-Mycin)

Macrolide antibiotic that duplicates action of motilin and is responsible for migrating motor complex activity, by binding to and activating motilin receptors. IV administration enhances emptying rate of liquids and solids. Effect can be seen with oral erythromycin. Enteric-coated form may be most tolerable.

Adult

250 mg PO 30 min ac initially

Pediatric

Not established

Theophylline, digoxin, carbamazepine, and cyclosporine may increase toxicity; may potentiate anticoagulant effects of warfarin; lovastatin and simvastatin increase risk of rhabdomyolysis

Documented hypersensitivity; hepatic impairment

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI side effects are common (give pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur

Agents for erectile dysfunction

MSA may respond to yohimbine with BP elevation; male erectile dysfunction occasionally improves. Yohimbine (Yohimex, Yocon) should be given 5.6 mg qd/tid. The effect of Viagra has not been determined in patients with autonomic failure. Other approaches include the use of mechanical devices, pumps, penile prostheses, or implants.


Yohimbine (Yohimex)

Blockade of alpha2-receptors in pontomedullary region of CNS increases sympathetic outflow.

Adult

2.7 -5.4 mg PO tid

Pediatric

Not established

Increases toxicity of antidepressants

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects include anxiety, tremor, palpitation, diarrhea, supine hypertension; not for use in patients with cardiorenal conditions

Mineralocorticoids

These agents have salt-retaining (mineralocorticoid) properties.


Fludrocortisone acetate (Florinef acetate)

Mainstay of therapy for last 40 years. Powerful mineralocorticoid largely devoid of glucocorticoid effect when administered in low-to-moderate doses (0.1-0.3 mg). Can initially increase blood volume, which tends to normalize after first week. Most patients gradually (over 2 wk) gain weight (usually 5-8 lb), with mild ankle edema, because of sodium retention, primarily in extravascular compartment.

Much benefit depends on support from tissue edema to venous capacitance bed in lower extremities. With edema, venous bed accommodates only low volume of blood in upright posture. Effect in turn improves blood return to heart and therefore functional capacity. In addition to direct effect of extravascular fluid accumulation, increases alpha1-adrenoreceptor sensitivity by about 50%. During therapy, renin-angiotensin system suppressed (as expected).

Adult

0.1-0.4 mg PO qd

Pediatric

Not established

Antagonizes effects of anticholinergics; rifampin, hydantoins, and barbiturates decrease effects of fludrocortisone; decreases salicylate levels

Documented hypersensitivity; systemic fungal infections; supine hypertension (eg, systolic BP >200 mm Hg)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypokalemia, hypomagnesemia, gain of weight, excessive fluid accumulation with excessive BP elevation in supine posture; supine hypertension in most patients, even without therapy (limits degree to which BP can be increased with drug); supine hypertension may increase risk of hemorrhage in MSA (reliable studies lacking)

Alpha-adrenergic agonists

These agents may reduce sympathetic outflow, which may reduce muscle tone.


Midodrine (Pro- Amatine)

Prodrug with activity as alpha1-adrenoreceptor agonist that acts directly on vasculature. Also widely used to treat orthostatic hypotension in MSA. Acts directly on vasculature to increase BP and avoids electrolyte abnormalities associated with fludrocortisone. However, supine hypertension significant problem and limits enhancement of functional capacity in MSA.

Adult

10 mg PO tid

Pediatric

Not established

Drugs that stimulate alpha-adrenergic agonists may enhance or potentiate pressor effects; coadministration with cardiac glycosides may enhance or precipitate bradycardia, psychopharmacologic agents or beta-blockers, AV block, or arrhythmia

Documented hypersensitivity; supine hypertension (eg, systolic BP >200 mm Hg)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in diabetes or visual complications; discontinue and reevaluate if signs or symptoms of bradycardia occur

Sympathomimetics

These agents augment both coronary and cerebral blood flow. Agents such as phenylpropanolamine, ephedrine, and dihydroxyphenylserine have also been in MSA and share with midodrine the possible complication of excessive supine hypertension. The advantage of these short-acting pressors is that they can be given during the day if the patient does not lie down for the next 3-4 h. A late-afternoon dose should be avoided if possible.


Phenylpropanolamine (Propagest)

Recalled from US market. Sympathomimetic amine. Acts to directly release noradrenaline

Adult

12.5-25 mg PO bid with 12 oz of water

Pediatric

Not established

Theophylline, atropine, or MAO inhibitors may increase toxicity

Documented hypersensitivity; supine hypertension (eg, systolic BP >200 mm Hg)

Pregnancy

C-Safety for use during pregnancy has not been established.

Precautions

Reduced appetite, nervousness, tachycardia, supine hypertension, tachyphylaxis


Ephedrine (Ephedrine sulfate)

Sympathomimetic amine. Alpha- and beta-adrenergic agonist; peripheral vasoconstrictor

Adult

Starting: 25 mg PO tid

Pediatric

Not established

Theophylline, atropine, or MAO inhibitors may increase toxicity; alpha- and beta-blockers decrease vasopressor effects of ephedrine; cardiac glycosides and general anesthetics increase cardiac stimulation of ephedrine

Documented hypersensitivity; angle-closure glaucoma, and cardiac arrhythmias

Pregnancy

C-Safety for use during pregnancy has not been established.

Precautions

Caution in elderly, diabetes mellitus, hyperthyroidism, hypertension, cardiovascular disease, prostatic hypertrophy, or cerebrovascular insufficiency


Dihydroxyphenylserine (L-DOPS)

Sympathomimetic amine. Direct synthesis of NE from this drug in absence of dopamine beta- hydroxylase.

Adult

250-500 mg PO bid

Pediatric

Not established

Theophylline, atropine, or MAO inhibitors may increase toxicity

Documented hypersensitivity; severe hypertension or ventricular tachycardia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May not work in patients taking carbidopa (Sinemet) or benserazide

Colony-stimulating factor

These agents correct anemia associated with MSA.


Epoetin alfa (Epogen, Procrit)

Recombinant EPO recently shown to increase functional capacity of patients with MSA, particularly those with characteristic mild anemia. Up to 38% of patients with severe autonomic failure have anemia. Lack of sympathetic stimulation may lead to decreased EPO production and anemia. Sympathetic impairment and low plasma norepinephrine levels correlated with severity of anemia. Even low doses (25-50 units/kg SC 3 times/wk) successfully corrected anemia and improved upright BP. Biologic activity mimics human urinary EPO, which stimulates division and differentiation of committed erythroid progenitor cells and induces release of reticulocytes from bone marrow into bloodstream.

Adult

25-50 U/kg body wt SC 3 times/wk

Pediatric

Not established

Documented hypersensitivity; uncontrolled hypertension

Pregnancy

C Safety for use during pregnancy has not been established.

Precautions

Caution in porphyria, hypertension, history of seizures; decrease dose if increase in hematocrit > 4 U in any 2-wk period; multidose preserved formulation contains benzyl alcohol and may increase risk of neurologic toxicity in infants (use preservative-free formulation); treatment results depend on adequate iron supplementation

Nonsteroidal Anti-inflammatory Drug (NSAID), Oral

These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation and various cell-membrane functions.


Indomethacin (Indocin)

Inhibits vasodilator prostaglandin synthesis.

Adult

25 mg PO tid ac; increase to 50 mg tid

Pediatric

Not established

Coadministration with aspirin increases risk of serious NSAID-related adverse effects; probenecid may increase concentrations and possibly toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when patient taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may increase when administered concurrently

Documented hypersensitivity; GI bleeding or renal insufficiency

Pregnancy

B-Usually safe but benefits must outweigh the risks

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia present)

Antihistamine

These agents prevent histamine response in sensory nerve endings and blood vessels. They are more effective in preventing histamine response than in reversing it.


Diphenhydramine (Benadryl, Benylin)

First-generation antihistamine with anticholinergic effects that binds to H1 receptors in CNS and body. Competitively blocks histamine from binding to H1 receptors. Significant antimuscarinic activity and penetrates CNS, which causes pronounced tendency to induce sedation. Approximately half of patients treated with conventional doses have some somnolence.

Adult

25-50 mg PO q6-8h prn; not to exceed 400 mg/d
10-50 mg IV/IM q6-8h prn; not to exceed 400 mg/d

Pediatric

Not established

Potentiates effect of CNS depressants; due to alcohol content, do not give syrup to patient taking medications that can cause disulfiram-like reactions

Documented hypersensitivity; MAO inhibitors

Pregnancy

C Safety for use during pregnancy has not been established.

Precautions

May exacerbate angle closure glaucoma, hyperthyroidism, peptic ulcer, or urinary-tract obstruction; xerostomia may occur

More on Multiple System Atrophy

Overview: Multiple System Atrophy
Differential Diagnoses & Workup: Multiple System Atrophy
Treatment & Medication: Multiple System Atrophy
Follow-up: Multiple System Atrophy
References

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Further Reading

Keywords

MSA, multiple-system atrophy, multisystem atrophy, Shy-Drager syndrome, striatonigral degeneration, MSA-P, sporadic olivopontocerebellar atrophy, MSA-C

Contributor Information and Disclosures

Author

André Diedrich, MD, PhD, Research Associate Professor of Medicine, Research Assistant Professor of Biomedical Engineering, Autonomic Dysfunction Center, Vanderbilt University School of Medicine
André Diedrich, MD, PhD is a member of the following medical societies: American Autonomic Society and American Heart Association
Disclosure: Nothing to disclose.

Coauthor(s)

David Robertson, MD, Director, Clinical Research Center, Professor of Medicine, Pharmacology, and Neurology, Vanderbilt University
David Robertson, MD is a member of the following medical societies: American Heart Association and Association of American Physicians
Disclosure: Nothing to disclose.

Medical Editor

Christopher Luzzio, MD, Clinical Assistant Professor, Department of Neurology, University of Wisconsin at Madison
Christopher Luzzio, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Nestor Galvez-Jimenez, MD, MSc, MHA, Chairman, Department of Neurology, Program Director, Movement Disorders, Department of Neurology, Division of Medicine, Cleveland Clinic Florida
Nestor Galvez-Jimenez, MD, MSc, MHA is a member of the following medical societies: American Academy of Neurology, American College of Physicians, and Movement Disorders Society
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

 
 
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