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National Institutes of Health (US). Office for Medical Applications of Research. NIH Consensus Statements [Internet]. Bethesda (MD): National Institutes of Health (US); 1977-2002.

  • This publication is provided for historical reference only and the information may be out of date.

This publication is provided for historical reference only and the information may be out of date.

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NIH Consensus Statements [Internet].

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56The Utility of Therapeutic Plasmapheresis for Neurological Disorders

National Institutes of Health Consensus Development Conference Statement June 2-4, 1986

Introduction

Therapeutic plasmapheresis or therapeutic plasma exchange (TPE) is a method for removing toxic elements from the blood. It is performed by removing blood, separating the plasma from the formed elements, and reinfusing the formed elements together with a plasma replacement.

TPE has been used to remove unwanted substances from the blood. These include toxins, metabolic substances, and plasma constituents implicated in disease, such as complement or antibodies. The ability to remove antibody and other immunologically active substances from the blood has led to the use of TPE as a therapy for neurological conditions in which autoimmunity is believed to play a role. It is estimated that one-half of the 20,000 to 30,000 TPE procedures performed annually at present in the United States are done on patients with neurologic disorders.

Reports regarding use of TPE in the medical literature have generated both enthusiasm and controversy. Clinical trials to assess efficacy of TPE have now been completed. In several neurological disorders, conflicting interpretations of their results have occurred.

To resolve these conflicts, the National Institute of Neurological and Communicative Disorders and Stroke, the Clinical Center, and the NIH Office of Medical Applications of Research convened a Consensus Development Conference on the Utility of Therapeutic Plasmapheresis for Neurological Disorders on June 2-4, 1986. Experts from North America and Europe presented data regarding the risks and benefits of TPE for the treatment of myasthenia gravis, Eaton-Lambert syndrome, Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy, paraproteinemic neuropathies, amyotrophic lateral sclerosis, and multiple sclerosis. They also discussed alternative therapies. Additionally, experts presented information regarding the appropriate techniques for performing TPE.

The consensus panel considered scientific evidence and addressed the following questions:

  • Is therapeutic plasmapheresis of benefit for neurological diseases? If so, for which diseases and under what circumstances?
  • What are the risks of plasmapheresis?
  • If effective, what are the mechanisms of action?
  • Is efficacy influenced by technique?
  • What is the relationship of plasmapheresis to other therapies?
  • What insights has plasmapheresis provided to suggest relevant clinical or basic research strategies?

Is Therapeutic Plasmapheresis of Benefit for Neurological Diseases? If So, for Which Diseases and Under What Circumstances?

Myasthenia Gravis (MG)

A considerable body of experimental animal and human clinical data has implicated an antibody-mediated attack on the acetylcholine receptor (AChR) in the pathogenesis of MG. Although the factors that trigger this antibody response are not understood, recent therapy has been directed toward lowering the levels of antibodies against the AChR.

The rationale for the use of TPE in MG is clear. Despite several open uncontrolled clinical trials suggesting that TPE induces short-term improvement in patients with MG and numerous anecdotal reports of dramatic improvement, a controlled trial of TPE in MG has never been done. Nonetheless, the panel is persuaded that TPE can be useful in strengthening patients with MG before thymectomy and during the postoperative period. It can also be valuable in lessening symptoms during the initiation of immunosuppressive drug therapy (ISDT) and during an acute crisis.

Eaton-Lambert Syndrome (ELS)

ELS seems to be an immune-mediated disease of the myoneural junction. It is characterized by weakness that may decrease with exercise and by specific electromyographic abnormalities. The evidence that it is an immune-mediated process comes from its association with other autoimmune diseases, presence of organ-specific autoantibodies, and the fact that the electrophysiologic features of the disease can be passively transferred to animals by immunoglobulin. Sixty-five percent of patients have an associated small cell carcinoma of the lung.

The rationale for the use of TPE in ELS is based on the presence of a serum antibody that blocks the release of neurotransmitter from the presynaptic membrane. Only a limited number of patients with ELS have had TPE. The data at hand, from a single uncontrolled trial, while suggestive, cannot be taken as definitive. Nonetheless, these preliminary data, taken in conjunction with the antibody-mediated pathogenesis of the disease, persuade the panel that TPE may well have a role in the treatment of this syndrome.

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

CIDP is thought to be an immune-mediated process. It is characterized by a progressive or a relapsing course. Motor and sometimes sensory function are compromised or lost, as are reflexes.

As shown in a randomized double-blind sham pheresis trial of severely affected patients, a brief course of TPE may produce benefit but only for some manifestations of the disease and only transiently. Approximately one-third of patients showed benefit in this trial; it was not possible to predict who would respond. Results from uncontrolled trials have been comparable. The role of TPE in patients with mild CIDP has not been explored. There may be a place for repeated courses of TPE in CIDP.

Guillain-Barré Syndrome (GBS)

GBS is an acute monophasic demyelinating neuropathy characterized by loss of motor strength, loss of reflexes, and variable sensory loss. TPE appears to be of benefit in GBS based on the results of multicenter randomized clinical trials comparing TPE with supportive care. The panel notes that no trial comparing TPE with sham TPE has been done. Benefit has been seen in patients with severe disease and when TPE has been started early in the course of the illness, preferably within 2 weeks of onset of symptoms. Under these circumstances, TPE may shorten duration of motor weakness sufficiently to reduce hospital stay. For patients able to breathe without ventilatory support at the time of the first plasma exchange, TPE may also reduce the time spent on a respirator if ventilatory assistance is subsequently needed.

TPE is recommended only for GBS patients with, at a minimum, severe weakness at the time of the first plasma exchange. Severe weakness is defined as the ability to walk only with support. It is unclear whether patients able to walk without support will benefit from TPE.

The efficacy of TPE in GBS has been demonstrated using a schedule of 40 to 50 cc/kg per exchange (approximately one plasma volume) for a total of three to five exchanges over a 7- to 14-day period. The volume, frequency, and number of exchanges to achieve optimal benefit remain to be established. Because these exchanges involve seriously ill patients (many on respirators), it is recommended that TPE be done in hospitals with personnel experienced in performing this procedure on critically ill patients.

Paraproteinemia

Neuropathy can occur in patients with both malignant and nonmalignant paraproteinemia. The neuropathy seems to be associated with binding of immunoglobulin to peripheral nerve myelin. Most frequently, binding occurs with myelin-associated glycoprotein and with glycolipids. In most patients, the immunoglobulin is IgM. These paraproteinemias comprise a clinically and immunologically heterogeneous group of disorders. Whether TPE should play a role in treating these disorders has not been demonstrated by the studies conducted to date.

Amyotrophic Lateral Sclerosis (ALS)

ALS is characterized by progressive degeneration of motor neurons with consequent weakness, atrophy, and fasciculations. It may be associated with signs of corticobulbar or corticospinal tract involvement. Based on the evidence at hand, the panel concludes that TPE is of no benefit in treating this disorder.

Multiple Sclerosis (MS)

The etiology and mechanism of central nervous system myelin breakdown in MS is unknown. There is reason to believe that immune processes play an important role in pathogenesis. The rationale for TPE in MS includes changes in T cell regulation, immunoglobulin in the CSF, and a profound lymphocytic infiltrate in the active MS lesion. Other perturbations of the immune response involving both humoral and cell-mediated immunity are less clearly defined but could also provide a rationale for TPE.

There is no established treatment that alters the course of MS. Adrenocorticotropic hormone (ACTH) has been shown to lessen symptoms during acute exacerbations but not to alter the course over the longer term. Most current experimental treatment protocols distinguish among the various expressions of the disease. Thus, trials have been carried out in exacerbating-remitting MS and in progressive MS. A number of controlled trials involving diverse experimental protocols are under way currently, and the state of MS treatment is in flux.

The proper role of TPE in the treatment of MS has not been defined. A controlled study of TPE in acutely exacerbating MS has not been completed. One double-blind randomized sham controlled study of TPE in progressive MS has been published. In this trial, prednisone, low-dose cyclophosphamide, and immunoglobulin were given together with TPE and the TPE was continued once weekly for 5 months. Benefit was reported, but the study has not been confirmed. Until confirmation of the benefit of TPE in progressive MS is forthcoming, the panel feels that TPE in MS should be viewed as an investigative procedure.

What Are the Risks of Plasmapheresis?

No systematic data have been collected to quantify the risks of TPE. Fifty fatal reactions associated with TPE between 1978 and 1983 have been reported worldwide. Of these, 16 were cardiac and 14 respiratory. Other deaths resulted from anaphylaxis, pulmonary thromboembolism, vascular perforation, hepatitis, systemic hemorrhage with disseminated intravascular coagulation, and sepsis. It is estimated that there were three deaths per 10,000 procedures. The risk of serious or fatal reactions may be greater when plasma is used as the replacement fluid.

Risk factors that have been identified for all apheresis procedures may be classified as device- or procedure-related. Device-related risk factors that are potentially major include red cell hemolysis, overheating of blood, and inaccurate delivery of anticoagulant and/or replacement fluids.

Procedure risk factors considered to have potential for major complications include:

  • Citrate-induced hypocalcemia.
  • Replacement with fluids depleted of coagulation factors, proteins, or electrolytes.
  • Replacement fluids containing plasma. These have the capacity to transmit infection (e.g., hepatitis, CMV, HTLV-III).
  • Allergic reactions leading to anaphylaxis.
  • Hemorrhage secondary to systemic anticoagulants.
  • Activation of coagulation, complement, fibrinolytic cascades, and/or aggregation of platelets.
  • Fluid imbalance.
  • Problems with vascular access.

These potential complications make it necessary to reserve TPE for situations of expected major benefit. Because it is necessary to define properly number, extent, and frequency of procedures to be performed, the total duration of the treatment, and the factors (laboratory, vital signs, etc.) to be monitored and interpreted during the procedure and postprocedure period, TPE should only be performed in an apheresis unit experienced with such matters.

If Effective, What Are the Mechanisms of Action?

In six conditions (MG, ELS, GBS, CIDP, paraproteinemic neuropathy, and MS), patients have been shown to benefit or possibly benefit from TPE. The response or failure to respond to TPE could help clarify disease mechanisms. Several immunopathogenic mechanisms exist for neural tissue injury. To the extent that TPE improves the course of the disorders considered at this conference, specific or nonspecific soluble factors are likely to mediate, be responsible for, or contribute to target organ damage. Criteria to establish that TPE removes one or more specific pathogenic substances are:

  1. TPE leads to a demonstrable, even if brief, improvement in function in the treated patients.
  2. Plasma removed by TPE ideally produces, on passive transfer, a comparable disease in animals.
  3. Purification of one or more of the plasma components removed by TPE and a demonstration that the component(s) is effective in passively transferring the disease identifies the component(s) as a mediator of the disease.

As a control, plasma from patients with the same target tissue damaged by a different mechanism should not produce the effect. This would eliminate the possibility of an epiphenomenon.

Using the three criteria listed above, the diseases considered in this conference can be compared. The response of patients with MG and ELS to TPE has contributed to the understanding of those disease mechanisms. In both diseases, TPE removes a pathogenic antibody. Whether comparable understanding will be generated by TPE studies of patients with GBS, CIDP, paraproteinemic neuropathy, or MS remains to be seen.

TPE also may work by removing nonspecific factors such as mediators of inflammation and lymphokines that contribute to the severity of a process without being its root cause. Optimally, efficacy of TPE should be rigorously tested against a sham TPE control for each disease for which a trial is carried out.

Is Efficacy Influenced by Technique?

TPE offers the capability of removing molecules of different molecular weights that have accumulated in the intravascular space. It is not known to have any effect on ablating primary pathologic processes. For TPE to be accepted as an effective therapy, relationships must be established between removal of some pathologic factor and reversal of morbidity or mortality. Under ideal circumstances, this implies that the molecular constituents of the pathological factor(s) are known; their intravascular and extravascular distributions are known; and something is known of their rates of synthesis, kinetics of diffusion across the capillary membrane, and the minimal quantity that must be removed to produce an observable response.

There appeared to be reasonable standardization of steroid and immunosuppressive drug regimens in protocols reviewed by the panel. There was great variability, however, among the TPE protocols relative to (1) the volume processed per exchange, (2) the frequency with which the procedure was performed, (3) the total number of procedures performed, and (4) the duration of the total TPE treatment. How much this variability contributed to the outcome of the studies, either positively or negatively, is not clear. Standardization of TPE regimens within trials is desirable and is recommended, with consideration given to calculated patient plasma volume.

In addition to the physiologic and scientific issues related to the patient, each TPE device has its own individual geometry that influences plasma separation efficiency. Both this device variable and the expertise of the apheresis device operator introduce technique variables that could alter the efficacy of the treatment. Another dynamic factor that may contribute to the efficacy of TPE is the extent of binding of the pathogenic factor to the target tissue.

What Is the Relationship of Plasmapheresis to Other Therapies?

Myasthenia Gravis

Treatment modalities in MG have included anticholinesterases, thymectomy, corticosteroids, ACTH, ISDT, and TPE. Most clinicians currently agree that the mainstay of therapy (particularly in younger patients) is thymectomy. This is sometimes coupled with the administration of corticosteroids and (in severely affected refractory patients) ISDT. TPE appears to be useful in patients with chronic MG who either do not respond to or have deleterious side effects from corticosteroids or ISDT. It is also useful in patients who demonstrate acute deterioration either because of the disease process itself or the steroid therapy. TPE also appears to be helpful in preparing patients for thymectomy. The duration of clinical improvement induced by a course of TPE in MG patients is generally 4 to 6 weeks.

Eaton-Lambert Syndrome

The treatment of ELS has consisted of corticosteroids and ISDT. Short-term improvement in muscular weakness can be effected by TPE. This is particularly useful in those patients with small cell carcinoma of the lung. It also is useful when ISDT is not indicated. Long-term clinical improvement seems to be sustained better, however, by corticosteroids and ISDT than by TPE. No information is available about the use of TPE by itself without concomitant corticosteroids.

Guillain-Barré Syndrome

The treatment of GBS in the past has been supportive only. No clear benefits have been demonstrated so far with corticosteroids or ISDT. Current studies of the role of TPE in GBS suggest that TPE is effective when used early in the disease for severely affected individuals. Concurrent use of corticosteroids has not been shown to have any additional demonstrable beneficial effect.

Chronic Inflammatory Demyelinating Polyneuropathy

TPE may be useful in patients with CIDP, particularly those who have failed to respond to corticosteroids and ISDT. Repeated courses of TPE may be required to sustain benefits. Whether long-term ISDT should be given in conjunction with repeated courses of TPE remains unknown.

Multiple Sclerosis

In the only controlled trial of TPE in MS, TPE was used in conjunction with corticosteroids, ISDT, and immunoglobulin. There is no information available about the use of TPE alone in MS patients from controlled trials.

What Insights Has Plasmapheresis Provided To Suggest Relevant Clinical or Basic Research Strategies?

Myasthenia Gravis

The discovery that antibodies directed against the AChR are present in MG preceded experimental trials of TPE in this disease. Trials of TPE in MG flowed naturally from this discovery. On the other hand, a putative beneficial effect of TPE in ELS preceded the demonstration of antibodies directed against the terminal axon in this disease. Similarly, in patients with a myasthenia-like clinical presentation but no antibodies to the AChR, a successful trial of TPE spurred a search for disease-relevant antibodies and ultimately their discovery. From these observations, the following conclusions can be drawn: (1) When an antibody is found in a disease of unknown cause that could be relevant to its pathogenesis, a circumscribed trial of TPE may provide supporting evidence, albeit indirect, that the antibody in question is disease-related, and (2) trials of TPE may be worthwhile in certain neurologic diseases of unknown cause because they may provide clues to pathogenesis. Criteria for selecting a disease for study might include fluctuations (indicating a potential for recovery) and available outcome measures that are simple, sensitive, and readily quantified.

Removal of antibody may not provide a total explanation for effects seen following TPE. Thus, even in MG, where anti-AChR antibody is held to cause the disease, disease severity may be influenced by other circulating factors at present unknown. Antibody presence correlates with MG, but antibody levels do not reflect disease severity nor predict response to TPE.

Guillain-Barré Syndrome

The apparent efficacy of plasmapheresis in GBS leads to several questions:

  1. What is the optimum TPE regimen in GBS? There is a suggestion that even one or two treatments can sometimes abort progression. This point requires clarification.
  2. Should mildly affected GBS patients be treated? A controlled trial is needed.
  3. Which patients should not be treated? Are those who already require respirator assistance or in whom illness has been present for more than 2 weeks less likely to benefit from TPE?
  4. What is the mechanism of action of TPE?

Removal of antibody alone may not explain the beneficial effect of plasmapheresis in GBS. Circulating lymphokines and circulating acute phase reactants (common after infectious illness) may contribute to disease progression, and their removal may have beneficial effects. It would be of interest to follow levels of these factors as well as antimyelin antibodies and relate them to the clinical response.

GBS following infection with Campylobacter jejuni may be more severe than GBS following other infections and perhaps less responsive to TPE. It will be important to develop data that predict patient response to TPE.

Multiple Sclerosis

Further studies are needed to clarify whether treatment with TPE benefits patients with multiple sclerosis.

Other Considerations

The possibility that sham pheresis is not merely a placebo should be tested. Optimal regimens have not been established for any neurologic condition in which TPE has a role in management.

Conclusion

TPE is a promising new mode of therapy for a limited number of neurologic diseases. Its effect, when seen, is relatively short-lived. This need not be a problem in monophasic diseases of short duration such as GBS but poses limitations in the management of chronic disease. In chronic diseases, its use should, in general, be viewed as a short-term expedient rather than as a definitive treatment. TPE has offered new insights into neurologic disease pathogenesis and can be expected to continue to do so.

Consensus Development Panel

  • Barry G. Arnason, M.D.
  • Professor and Chairman
  • Department of Neurology
  • University of Chicago
  • Chicago, Illinois
  • Judith Areen, J.D.
  • Professor of Law
  • Associate Dean
  • Georgetown University Law Center
  • Professor of Community and Family Medicine
  • Georgetown Medical Center
  • Washington, D.C.
  • Robert J. Baumann, M.D.
  • Associate Professor of Neurology
  • Head
  • Child Neurology Program
  • Department of Neurology
  • University of Kentucky
  • Lexington, Kentucky
  • S. Mitchell Freedman, M.D.
  • Private Practice
  • Raleigh Neurology Clinic
  • Raleigh, North Carolina
  • Judith D. Goldberg, A.B., S.M., Sc.D.
  • Department Head
  • Statistical Design and Analysis
  • Medical Research Division
  • American Cyanamid Company
  • Lederle Laboratories
  • Pearl River, New York
  • Vice Admiral Thor Hanson, U.S.N. (Ret.)
  • President and CEO
  • National Multiple Sclerosis Society
  • New York, New York
  • Jeane P. Hester, M.D.
  • Professor of Medicine
  • Chief, Pheresis Service
  • University of Texas System
  • Cancer Center
  • Houston, Texas
  • Nelson G. Richards, M.D.
  • Private Practice
  • Clinical Professor of Neurology
  • Medical College of Virginia
  • Virginia Commonwealth University
  • Attending Neurologist
  • McGuire Veterans Hospital
  • Richmond, Virginia
  • Paul J. Schmidt, M.D.
  • Director
  • Southwest Florida Blood Bank, Inc.
  • Professor of Pathology
  • University of South Florida
  • College of Medicine
  • Tampa, Florida
  • Donald H. Silberberg, M.D.
  • Professor and Chairman
  • Department of Neurology
  • University of Pennsylvania School of Medicine
  • Hospital of the University of Pennsylvania
  • Philadelphia, Pennsylvania
  • Parker A. Small, Jr., M.D.
  • Professor of Immunology
  • Professor of Pediatrics
  • University of Florida College of Medicine
  • Gainesville, Florida
  • Leslie P. Weiner, M.D.
  • Chairman
  • Department of Neurology
  • University of Southern California
  • Los Angeles, California
  • John N. Whitaker, M.D.
  • Professor and Chairman
  • Department of Neurology
  • University of Alabama at Birmingham
  • University Station
  • Birmingham, Alabama

Speakers

  • Stuart D. Cook, M.D.
  • "Pathophysiology of Guillain-Barré Syndrome and Rationale for Plasmapheresis"
  • Professor and Chairman
  • Department of Neurosciences
  • New Jersey Medical School
  • Newark, New Jersey
  • Marinos Dalakas, M.D.
  • "Plasmapheresis in the Treatment of Paraproteinemic Neuropathies"
  • Senior Investigator
  • Office of the Clinical Director
  • National Institute of Neurological and
  • Communicative Disorders and Stroke
  • National Institutes of Health
  • Bethesda, Maryland
  • Peter James Dyck, M.D.
  • "Plasmapheresis for Chronic Inflammatory Neuropathy"
  • Professor of Neurology
  • Mayo Medical School
  • Mayo Clinic
  • Rochester, Minnesota
  • George W. Ellison, M.D.
  • "Pathophysiology of Multiple Sclerosis and Rationale for Plasmapheresis"
  • Professor of Neurology
  • University of California at Los Angeles
  • Los Angeles, California
  • Douglas W. Huestis, M.D.
  • "Methodology and Risks"
  • Professor of Pathology
  • Chief of Immunohematology
  • University of Arizona College of Medicine
  • Tucson, Arizona
  • Richard A.C. Hughes, M.D., F.R.C.P.
  • "British Study"
  • Department of Medicine
  • Guy's Hospital Medical School
  • Comder Bridge
  • UNITED KINGDOM
  • John G. Humphrey, M.C., F.R.C.P.(C)
  • "Toronto Study"
  • Associate Professor of Medicine
  • Division of Neurology
  • Toronto General Hospital
  • Toronto, Ontario
  • CANADA
  • John Verrier Jones, B.M., F.R.C.P., F.R.C.P.(C)
  • "Rationale for Plasmapheresis"
  • Professor of Medicine
  • Department of Medicine
  • Dalhousie University
  • Halifax, Nova Scotia
  • CANADA
  • Norman Latov, M.D., Ph.D.
  • "Plasmapheresis in the Treatment of Paraproteinemic Neuropathies"
  • Assistant Professor of Neurology
  • Columbia University College of Physicians and
  • Surgeon
  • New York, New York
  • Jerry R. Mendell, M.D.
  • "Ohio State Study"
  • Professor of Neurology
  • Department of Neurology
  • Ohio State University College of Medicine
  • Professor of Pathology
  • Ohio State University Hospital
  • Columbus, Ohio
  • Guy M. McKhann, M.D.
  • "Plasmapheresis in Guillain-Barré Syndrome"
  • Professor and Head
  • Department of Neurology
  • Johns Hopkins University
  • Baltimore, Maryland
  • Michael P. McQuillen, M.D.
  • "Plasmapheresis in Multiple Sclerosis"
  • Professor and Chairman
  • Department of Neurology
  • Medical College of Wisconsin
  • Milwaukee, Wisconsin
  • John Newsom-Davis, M.D., F.R.C.P.
  • "Plasmapheresis in Myasthenia Gravis"
  • "Use of Plasmapheresis in Lambert-Eaton Syndrome"
  • Professor of Clinical Neurology
  • Department of Neurological Science
  • Royal Free Hospital School of Medicine
  • Institute of Neurology Queen South
  • London
  • ENGLAND
  • Forbes H. Norris, Jr., M.D.
  • "Amyotrophic Lateral Sclerosis"
  • Vice President and Clinical Director
  • Amyotrophic Lateral Sclerosis Center
  • Pacific Medical Center
  • San Francisco, California
  • Audrey S. Penn, M.D.
  • "Pathophysiology of Myasthenia Gravis and a Rationale for Plasmapheresis"
  • Professor of Neurology
  • Department of Neurology
  • Columbia Presbyterian Medical Center
  • New York, New York
  • Jean Claude Raphael
  • "French Study"
  • Professor
  • Department of Neurology and Intensive Care
  • Hospital Raymond Poincare
  • Garaches
  • FRANCE
  • Allan Ropper, M.D.
  • "Massachusetts General Hospital Study"
  • Director of Neurology
  • Neurosurgery Intensive Care Unit
  • Associate Neurologist
  • Massachusetts General Hospital
  • Associate Professor of Neurology
  • Harvard Medical School
  • Boston, Massachusetts
  • Allen D. Roses, M.D.
  • "Plasmapheresis in Myasthenia Gravis"
  • Professor and Chief
  • Division of Neurology
  • Director
  • Duke Neuromuscular Research Clinic
  • Duke University Medical Center
  • Durham, North Carolina
  • Richard S.A. Tindall, M.D.
  • "Chronic Inflammatory Neuropathy"
  • "Plasmapheresis in Myasthenia Gravis"
  • Associate Professor of Neurology
  • Director
  • Neuromuscular Treatment Center
  • Southwestern Medical School
  • Dallas, Texas
  • Klaus V. Toyka, M.D.
  • "Chronic Inflammatory Neuropathy"
  • Professor of Neurology
  • Department of Neurology
  • University of Dusseldorf
  • Dusseldorf
  • FEDERAL REPUBLIC OF GERMANY
  • Howard L. Weiner, M.D.
  • "Plasmapheresis in Multiple Sclerosis"
  • Robert L. Kroc Associate Professor of Neurology
  • Harvard Medical School
  • Center for Neurologic Diseases
  • Brigham and Women's Hospital
  • Boston, Massachusetts

Planning Committee

  • Barry G. Arnason, M.D.
  • Professor and Chairman
  • Department of Neurology
  • University of Chicago
  • Chicago, Illinois
  • Michael J. Bernstein
  • Director of Communications
  • Office of Medical Applications of Research
  • National Institutes of Health
  • Bethesda, Maryland
  • Marinos Dalakas, M.D.
  • Senior Investigator
  • Office of the Clinical Director
  • National Institute of Neurological and
  • Communicative Disorders and Stroke
  • National Institutes of Health
  • Bethesda, Maryland
  • Mark Hallett, M.D.
  • Clinical Director
  • National Institute of Neurological and
  • Communicative Disorders and Stroke
  • National Institutes of Health
  • Bethesda, Maryland
  • Harvey G. Klein, M.D.
  • Chief
  • Department of Transfusion Medicine
  • Clinical Center
  • National Institutes of Health
  • Bethesda, Maryland
  • Henry F. McFarland, M.D.
  • Deputy Chief
  • Neuroimmunology Branch
  • National Institute of Neurological and Communicative Disorders and Stroke
  • Intramural Research Program
  • National Institutes of Health
  • Bethesda, Maryland
  • Dale E. McFarlin, M.D.
  • Chief
  • Neuroimmunology Branch
  • Intramural Research Programs
  • National Institute of Neurological and Communicative Disorders and Stroke
  • National Institutes of Health
  • Bethesda, Maryland
  • Alvaro Pineda, M.D.
  • Director
  • Apheresis Laboratory
  • Mayo Clinic Blood Bank and Transfusion Service
  • Rochester, Minnesota
  • William H. Pitlick, Ph.D.
  • Deputy Director
  • Convulsive, Development and Neuromuscular Disorders Program
  • National Institute of Neurological and
  • Communicative Disorders and Stroke
  • National Institutes of Health
  • Bethesda, Maryland
  • Martin Rose, M.D., J.D.
  • Chief Medical Officer
  • Office of Medical Applications of Research
  • National Institutes of Health
  • Bethesda, Maryland
  • Allen D. Roses, M.D.
  • Professor and Chief
  • Division of Neurology
  • Director
  • Duke Neuromuscular Research Clinic
  • Duke University Medical Center
  • Durham, North Carolina
  • Sylvia Schaffer
  • Chief
  • Office of Scientific and Health Report
  • National Institute of Neurological and Communicative Disorders and Stroke
  • National Institutes of Health
  • Bethesda, Maryland
  • Zekin A. Shakhashiri, M.Sc., M.D., M.P.H.
  • Senior Medical Advisor
  • Legislation Analysis Branch
  • Administration and Analysis
  • Office of the Director
  • National Institute of Neurological and Communicative Disorders and Stroke
  • National Institutes of Health
  • Bethesda, Maryland
  • Emanuel M. Stadlan, M.D.
  • Deputy Director
  • Demyelinating, Atrophic and Dementing Disorders Program
  • National Institute of Neurological and
  • Communicative Disorders and Stroke
  • National Institutes of Health
  • Bethesda, Maryland
  • Richard S. A. Tindall, M.D.
  • Associate Professor of Neurology
  • Director
  • Neuromuscular Treatment Center
  • Southwestern Medical School
  • Dallas, Texas

Conference Sponsors

  • National Institute of Neurological and Communicative Disorders and Stroke
  • Murray Goldstein, D.O., M.P.H.
  • Director
  • Clinical Center
  • National Institutes of Health
  • John L. Decker, M.D.
  • Director
  • Office of Medical Applications of Research
  • Itzhak Jacoby, Ph.D.
  • Acting Director

Supplemental Information for NIH Consensus Statement on the Utility of Therapeutic Plasmapheresis for Neurological Disorders

Since the NIH Consensus Statement on The Utility of Therapeutic Plasmapheresis for Neurological Disorders was issued, additional information has become available that supplements the original statement.

The NIH Consensus Statement on Intravenous Immunoglobulin: Prevention and Treatment of Disease was issued in May 1990. In addition, following information on Guillain Barré Syndrome and Paraproteinemia may be of assistance.

Guillain Barré Syndrome

In a multicenter study of 150 patients with Guillain Barré Syndrome (GBS) randomly assigned to receive either plasmapheresis or 0.4 gram/kg/day for 5 days of intravenous immunoglobulin (IVIG), the strength improved by one grade in 34 percent of patients treated with plasmapheresis as compared with 55 percent of those treated with gammaglobulin. The median time to improvement by one grade was 41 days with plasmapheresis and 27 days with IVIG. Fewer complications and less need for artificial ventilation were noted in the IVIG-treated group.

This study, published in the N Engl J Med (1992;326:1123-1129), provided convincing evidence that in acute GBS treatment with IVIG is at least as effective, and probably superior, to plasmapheresis. Because IVIG has fewer side effects, is easily available, and does not require equipment, it may have major advantages compared to plasmapheresis. IVIG should not be considered as a reasonable alternative, if not the treatment of choice, in patients with acute GBS.

Paraproteinemia

In a double blind, randomized, cross-over study comparing plasmapheresis with sham pheresis in 39 patients with IgG, IgA, or IgM paraproteinemic polyneuropathies, a mild improvement was noted in those patients who had IgA or IgG paraproteinemia (N Engl J Med 1991;325:1482-1486). Because the improvement was marginal, it remains still unclear whether therapeutic plasma exchange has a role in treatment of these neuropathies.

This statement was originally published as: The Utility of Therapeutic Plasmapheresis for Neurological Disorders. NIH Consens Statement 1986 Jun 2-4;6(4):1-7.

For making bibliographic reference to the statement in the electronic form displayed here, it is recommended that the following format be used: The Utility of Therapeutic Plasmapheresis for Neurological Disorders. NIH Consens Statement Online 1986 Jun 2-4 [cited year month day];6(4):1-7.

NIH Consensus Statements are prepared by a nonadvocate, non-Federal panel of experts, based on (1) presentations by investigators working in areas relevant to the consensus questions during a 2-day public session; (2) questions and statements from conference attendees during open discussion periods that are part of the public session; and (3) closed deliberations by the panel during the remainder of the second day and morning of the third. This statement is an independent report of the consensus panel and is not a policy statement of the NIH or the Federal Government.

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