Skip Over Navigation Links jump over navigation bar
NIH Consensus Development Program Homepage
jump over navigation barHome Page for the NIH Consensus Development ProgramPrevious Conference Statements from the NIH Consensus Development Program

The programs listed are provided for reference purposes only. They were current when produced, but are no longer maintained and may now be outdated. Persons with disabilities having difficulty accessing information on this page may contact us for assistance. Please select the ODP's home page to access current information.
 

Neurofibromatosis

National Institutes of Health
Consensus Development Conference Statement
July 13-15, 1987

Conference artwork, human figure showing fibromas on the torso and arms.

This statement is more than five years old and is provided solely for historical purposes. Due to the cumulative nature of medical research, new knowledge has inevitably accumulated in this subject area in the time since the statement was initially prepared. Thus some of the material is likely to be out of date, and at worst simply wrong. For reliable, current information on this and other health topics, we recommend consulting the National Institutes of Health's MedlinePlus http://www.nlm.nih.gov/medlineplus/.

This statement was originally published as: Neurofibromatosis. NIH Consens Statement 1987 Jul 13-15;6(12):1-19.

For making bibliographic reference to the statement in the electronic form displayed here, it is recommended that the following format be used: Neurofibromatosis. NIH Consens Statement Online 1987 Jul 13-15 [cited year month day];6(12):1-19.

Introduction

The neurofibromatoses are genetic disorders that primarily affect cell growth of neural tissues. These disorders can cause tumors to grow on the nerves at any location and at any time. Some manifestations are progressive and may result in significant morbidity or mortality. Two distinctive forms are recognized, but variant forms may exist. A variety of names have been used to describe all forms; subsequent information has made these names technically inaccurate or incomplete. To avoid these historical legacies and to conform to current nosology in other diseases, the
Consensus Panel adopted a numbered classification.

The most common type, neurofibromatosis 1 or NF-1 (previously known as von Recklinghausen's neurofibromatosis or peripheral neurofibromatosis) is an autosomal dominant disorder affecting about 1 in 4,000 individuals. Multiple hyperpigmented areas (caf�-au-lait macules) and neurofibromas are characteristic.

Neurofibromatosis 2 or NF-2 (previously known as bilateral acoustic neurofibromatosis or central neurofibromatosis) is an autosomal dominant disorder occurring in about 1 in 50,000 individuals. Eighth nerve tumors are characteristic, but other intracranial and intraspinal tumors are common.

There is a considerable variation of manifestations even within a family, confounding classification in some patients. This variability affects management because it is often not possible to predict the course in an individual patient. Other forms of neurofibromatosis may exist, but their precise classification is not possible at the present time.

The NF-1 gene has just been localized to chromosome 17, and the NF-2 locus is probably on chromosome 22. Continued rapid scientific progress is expected in the molecular genetics of both NF-1 and NF-2. This will directly influence classification, patient care, counseling of families, and research.

There are no cures for the neurofibromatoses, and treatment consists of amelioration of the clinical symptoms. Many short- and long-term management issues were addressed by the
Consensus Conference, leading to recommendations for care at diagnosis and during routine followup and for research.

This NIH Consensus Development Conference on Neurofibromatosis was convened by the National Institute of Neurological and Communicative Disorders and Stroke, the National Cancer Institute, and the National Institutes of Health Office of Medical Applications of Research, on July 13-15, 1987, to address issues concerning the diagnosis and management of the neurofibromatoses. The conference brought together a wide range of scientists and medical experts, including specialists in neurology, pediatric neurology, neurosurgery, pediatrics, genetics, and other relevant fields. Presentations were made by experts, and discussions with the audience and the
Consensus Panel followed each presentation. Questions addressed by the panel were as follows:

  • What are the various clinical types of neurofibromatosis, and what are their frequencies and diagnostic criteria?
  • What are the recommendations for care of patients and their families at diagnosis and during routine followup?
  • What are the management options for major manifestations of neurofibromatosis?
  • What are the key research areas that will improve our knowledge about prevention, diagnosis, and treatment of neurofibromatosis?

The first three questions were addressed separately for NF-1, NF-2, and variant forms.  

Neurofibromatosis 1

What Are the Diagnostic Criteria

The diagnostic criteria for NF-1 are met in an individual if two or more of the following are found:

  • Six or more caf�-au-lait macules over 5 mm in greatest diameter in prepubertal individuals and over 15 mm in greatest diameter in postpubertal individuals.
  • Two or more neurofibromas of any type or one plexiform neurofibroma.
  • Freckling in the axillary or inguinal region.
  • Optic glioma.
  • Two or more Lisch nodules (iris hamartomas).
  • A distinctive osseous lesion such as sphenoid dysplasia or thinning of long bone cortex with or without pseudarthrosis.
  • A first-degree relative (parent, sibling, or offspring) with NF-1 by the above criteria.

Other disorders of pigmentation such as McCune-Albright or Watson syndrome can be confused with NF-1.

What Are the Recommendations for Care of Patients and Their Families at Diagnosis and During Routine Followup?

Once a diagnosis of NF-1 is made, the initial evaluation of patients without major complications can be made in a standard clinical setting.

  • History should focus on symptoms possibly associated with the disorder such as cognitive or psychomotor deficits, pain, vision problems, progressive neurologic deficit, and constipation.
  • Family history should include grandparents, great aunts and uncles, and their descendants. When possible, an effort should be made to locate medical records of affected first- and second-degree relatives.
  • Physical examination should give particular attention to possible manifestations of the disorder such as hypertension, scoliosis and other skeletal anomalies, macrocephaly, focal neurological deficits (impaired vision, ptosis, optic atrophy), developmental disabilities, proptosis, Lisch nodules, short stature, signs of precocious puberty or hypogonadism, cafe'-au-lait macules, and neurofibromas.
  • Tests should be dictated by findings on clinical evaluation. Laboratory tests in asymptomatic patients are unlikely to be of value, particularly computerized tomography (CT), magnetic resonance imaging (MRI), electroencephalography (EEG), and evoked potentials.
  • Counseling must be provided for all patients and their families and should include:
    • Prognosis. The natural history of the disorder is poorly understood but includes serious complications in some individuals. The probability of these serious complications has been overstated; an individual's risk is limited. Counseling should note the risks of progression during puberty or pregnancy.
    • Genetics. Each child born to an affected person has a 50-percent chance of having NF-1, but manifestations of the disorder vary among individuals within affected families. Genetic techniques will soon permit prenatal diagnosis.
    • Psychological and social adjustment. Issues to be addressed include anxieties regarding the uncertainties of the disorder's course and fear of possible disfigurement and of developing other severe complications.
    • Family members. Family members, particularly first-degree relatives, should be evaluated to determine whether they have NF-1. Appropriate counseling should accompany such assessments.
    • Followup. Annual visits (more often if indicated) should be scheduled with a clinician familiar with the disorder.
    • Resources for NF-1 patients. Patients should be offered the addresses and telephone numbers of specialized clinics that provide a broad array of relevant clinical expertise and of appropriate lay organizations that can give additional information and facilitate access to patient support groups.
  • A written report should summarize the clinical findings, test results, and information conveyed through the counseling.

Annual followup examination and counseling should parallel the initial assessment just described, with emphasis on new symptoms and progressive deficits.

Parents caring for a child with NF-1, and other family members, have a great need for accurate information, psychological support, and interaction with other affected families. Clinicians caring for patients with NF-1 should view involvement of family members as a major aspect of care.

What Are the Management Options for the Major Manifestations of Neurofibromatosis 1?

When symptoms suggest major manifestations of NF-1, the patient should be referred to the appropriate specialist and evaluated by x-ray, MRI, or laboratory tests. Surgical intervention and radiation therapy should be used sparingly and only when it is clear that they will contribute to the patient's well-being. The most common complications deserve special mention.

Optic Glioma

Optic glioma occurs in some patients with NF-1 and may cause progressive visual loss. However, most optic gliomas are nonprogressive and should be followed with annual ophthalmologic examinations. MR and CT imaging are the best methods to document their size, shape, and extension.

Because the visual impairment associated with optic glioma is probably not altered by intervention, surgical resection, radiation, or chemotherapy should only be used in special circumstances such as disfiguring orbital masses or large tumors that are compressing adjacent structures.

Other Neural Tumors

These tumors should be managed in NF-1 patients in the same manner as they are in the general population. When a focal, resectable lesion is identified that is causing progressive neurological deficit by compressing the brain or spinal cord, it should be surgically removed.

Tumors within the central nervous system are frequently not resectable, and therefore surgical therapy is not warranted unless they are causing increased intracranial pressure or distorting neighboring structures. When malignant change is suspected, biopsy, internal decompression, chemotherapy, or radiation therapy may be indicated.

Orthopedic Problems

The two most common orthopedic problems associated with NF-1 are kyphoscoliosis and tibial bowing. Both may benefit from early intervention and should be managed by an orthopedist familiar with the complications of NF-1. Patients with kyphoscoliosis should have MRI of the spine to investigate the possibility of focal spinal cord lesions. They should be fitted early with bracing, followed closely with spine x-rays, and if deformity progresses, undergo spinal fusion. Tibial bowing should be treated by bracing in an attempt to prevent fracture and subsequent pseudarthrosis.

Disfigurements

Disfigurements that may benefit from intervention are common, although the need for major surgery is less frequent. Removal of neurofibromas may contribute to maintenance of function and psychological well-being. Sphenoid dysplasia occurs in a small number of patients. The resulting facial asymmetry and exophthalmos may be improved by reconstructive surgery. Deformities secondary to large soft tissue masses are difficult to repair and have a tendency to recur.

Developmental Disabilities

Language disorders and learning disabilities mandate neuropsychologic assessment so as to provide therapists and educators with information upon which to base remediation.

Vascular Problems

Hypertension in patients with NF-1 must be fully evaluated with particular emphasis on identifying treatable causes such as pheochromocytoma and renal vascular stenosis. Other vascular disorders must be handled on an individual basis in the same manner as they would be in the general population.

Malignancy

Although malignancies are rare in NF-1, there is an increased incidence of sarcomas and leukemias, especially in childhood. When malignancies are detected, NF-1 patients should be evaluated and treated the same as other patients. Because NF-1 patients also have an increased incidence of second malignancies, they must have close, long-term followup.  

Neurofibromatosis 2

What Are the Diagnostic Criteria

The criteria for NF-2 are met by an individual who has:

  1. Bilateral eighth nerve masses seen with appropriate imaging techniques (e.g., CT or MRI), or
  2. A first-degree relative with NF-2 and either:
    1. unilateral eighth nerve mass, or
    2. two of the following:
      • neurofibroma.
      • meningioma
      • glioma.
      • schwannoma.
      • juvenile posterior subcapsular lenticular opacity.

What Are the Recommendations for Care of Patients and Their Families at Diagnosis and During Routine Followup?

Once a diagnosis of NF-2 is made, the initial evaluation of patients without major complications can be made in a standard clinical setting.

  • History should focus on symptoms possibly associated with the disorder such as hearing loss, tinnitus, dizziness, loss of balance, pain, headache, and seizures.
  • Family history should include grandparents, great aunts and uncles, and their descendants. When possible, an effort should be made to locate medical records of affected first- and second-degree relatives.
  • Physical examination should give particular attention to possible manifestations of the disorder such as cafe'-au-lait macules and neurofibromas. Neurological assessment should emphasize cranial nerves, balance, and coordination.
  • Tests must include an audiogram and brain stem auditory evoked responses (BAER). MRI is the neuroimaging procedure of choice to be used in patients with evidence of hearing impairments or abnormal BAER. Tests of vestibular function may be useful adjuncts to BAER screening because eighth nerve tumors develop on the vestibular division. If no MRI has been performed by puberty, it should be obtained. Other tests should be performed as dictated by findings on clinical evaluation.
  • Counseling must be provided for all patients and their families and should include:
    • Prognosis. The natural history of the disorder is unpredictable. The major risks for the patient are loss of hearing and vestibular function. Underwater activities and climbing pose particular risks. There is an increased risk of developing intracranial and intraspinal neoplasms.
    • Genetics. Each child born to an affected person has a 50 percent chance of having NF-2, but the manifestations of the disorder vary among individuals within affected families. Genetic techniques will soon permit prenatal diagnosis. Counseling should also note that pregnancy may accelerate the growth of eighth nerve tumors.
    • Psychological and social adjustment. Issues to be addressed include anxieties regarding the uncertainties of the disorder's course and fear of hearing loss and other complications. Counseling should also include a realistic discussion of the implication of possible hearing loss for schooling, career planning, and use of alternative communication methods.
    • Family members. Family members, particularly first-degree relatives, should be evaluated periodically to determine whether they have NF-2. Appropriate counseling should accompany such assessments.
    • Followup. Annual visits (more often if indicated) should be scheduled with a clinician familiar with the disorder.
    • Resources for NF-2 patients. Patients should be offered the addresses and telephone numbers of specialized clinics that provide a broad array of relevant clinical expertise and of appropriate lay organizations that can give additional information and facilitate access to patient support groups.
  • A written report should summarize the clinical findings, test results, and the information conveyed through counseling.

 

Annual followup examination and counseling should parallel the initial assessment just described.

Parents caring for a child with NF-2, and other family members, have a great need for accurate information, psychological support, and interaction with other affected families. Clinicians caring for patients with NF-2 should view involvement of family members as a major aspect of care.

What Are the Management Options for the Major Manifestations of Neurofibromatosis 2?

When eighth nerve tumors are found, patients need to be advised about the possibility of total hearing loss at some time in the future. A management strategy should be discussed and the patient referred to a center with experience in determining the best treatment plan for long-term preservation of hearing. Because the possibility of removing a tumor with minimal injury to the auditory nerve is much better when the tumor is small, consideration should be given to attempting to remove one progressive tumor while bilateral hearing remains. If the tumor is successfully removed with preservation of hearing on that side, consideration should be given to removing the second tumor. If hearing is not preserved by removing the first tumor, it may be better to follow the second tumor as long as possible and then perform a subtotal removal in an attempt to prevent deafness. An MRI scan of the cervical spine should be performed before surgery to detect intraspinal tumors that might damage the spinal cord during surgery. All surgery for eighth nerve tumors should use auditory and facial nerve monitoring in an attempt to minimize the possibility of nerve injury. Stereotactic radiation therapy may be a treatment option for these tumors.

Other intracranial or intraspinal tumors occur in many patients but should be surgically treated only when they can be implicated as the cause of progressive disease.

Other Forms

Some patients, particularly children, have insufficient findings to meet NF-1 and NF-2 criteria. These patients require annual followup evaluations. Molecular genetics may permit a diagnosis of NF-1 or NF-2 in these patients. This may require modification of current NF-1 or NF-2 diagnostic criteria. Patients who do not fit into the NF-1 or NF-2 group by clinical or genetic criteria may, in the future, constitute the basis for establishing additional types of NF. These patients may require referral for more precise diagnosis or treatment of specific complications.

What Are the Key Research Areas That Will Improve Our Knowledge About Prevention, Diagnosis, and Treatment of Neurofibromatosis?

Molecular Genetics and Cell Biology

Molecular genetics provides unique opportunities for research in the neurofibromatoses. The gene for NF-1 has just been mapped to a site on chromosome 17 using a number of large kindreds. Recent evidence has localized NF-2 to chromosome 22 through analysis of tumor DNA. The immediate issues that must be addressed for NF-1 and NF-2 are the possibility of genetic heterogeneity among families and the identification of useful DNA markers closely flanking the genes.

In the near future, it will be possible to accurately trace the NF-1 and NF-2 genes in families by genetic linkage. A consequence of the identification of closely linked markers will be the availability of prenatal diagnosis. Individuals with minimal expression can be definitively diagnosed. Those individuals demonstrated not to carry the NF genes can be removed from the at-risk category.

The isolation of the NF-1 and NF-2 genes can be accomplished by recombinant DNA technology. Because many questions about the pathophysiology of the neurofibromatoses can be addressed through knowledge of the structure of the relevant genes, strong support of this line of investigation is recommended. Culture studies using Schwann and other related cell types clearly will be important. Signals leading to modulation of NF gene expression and to the variable phenotypes seen in vivo may be revealed in this in vitro approach.

The analysis of tumor DNA from NF-2 patients has already demonstrated the value of direct studies of tumor material. The elucidation of the mechanistic basis of tumor formation in the neurofibromatoses is likely to have significant implications for other neoplastic disorders. Therefore, it is recommended that tumor tissue from NF patients continue to be made accessible to investigators who are attempting to identify the basis of abnormal growth control.

Appropriate animal models for NF-1 and NF-2 will be desirable for testing potential therapies under in vivo conditions and for extending cell culture findings. Molecular genetic techniques provide an avenue to the development of such animal models. The development of such models is strongly recommended.

Natural History and Treatment

It is important to determine the natural history of NF, including predictors of disease progression, site-specific risks for subsequent neoplasia, and survival patterns. A source of patients and family members for genetic studies is essential. Research protocols for evaluation of specific interventions are needed. Centralized reporting systems that are well conceived and organized will be required to address these issues.  

Conclusion

The clinical and genetic analyses of NF have now converged to provide a new framework for the understanding of NF. The assignment of individual patients to NF-1 and NF-2, based on distinctive clinical features, is now confirmed by localization of the genes to separate chromosomes. Clinical management differs for NF-1 and NF-2. We now recognize that NF-1 individuals often do not experience major complications requiring intervention. However, when present, these complications represent a major burden. Generally, complications can be recognized by history and examination, minimizing the need for routine laboratory testing. The major feature of NF-2, bilateral eighth nerve tumor leading to deafness, is frequent. Significant progress has been made in the surgical treatment of these lesions.

Research on the neurofibromatoses is at an exciting juncture. Isolation of the NF-1 and NF-2 genes can now proceed by well-established methods. Research opportunities include defining the natural history of the disorder, its complications, and the effects of their treatment; elucidating molecular genetic mechanisms; and clarifying the biological processes underlying the neoplastic lesions.  

Consensus Development Panel

David A. Stumpf, M.D., Ph.D.
Panel Chairperson
Professor of Pediatrics and Neurology
Vice Chairman
Department of Neurology
Northwestern University Medical School
Chief
Pediatric Neurology
Children's Memorial Hospital
Chicago, Illinois
John F. Alksne, M.D.
Professor and Chairman
Neurological Surgery
University of California, San Diego
San Diego, California
John F. Annegers, Ph.D.
Professor of Epidemiology
University of Texas
School of Public Health
Houston, Texas
Sarah S. Brown, M.P.H.
Study Director
Institute of Medicine
National Academy of Sciences
Washington, D.C.
P. Michael Conneally, Ph.D.
Professor of Medical Genetics and Neurology
Indiana University Medical Center
Indianapolis, Indiana
David Housman, Ph.D.
Professor
Department of Biology
Center for Cancer Research
Massachusetts Institute of Technology
Cambridge, Massachusetts
Mark F. Leppert, Ph.D.
Senior Research Associate
Howard Hughes Medical Institute
University of Utah Medical Center
Salt Lake City, Utah
J. Philip Miller, Ph.D.
Associate Professor
Division of Biostatistics
Washington University Medical School
St. Louis, Missouri
Melvin L. Moss, Ph.D.
Consultant and Former Director of Research
Muscular Dystrophy Association
National Advisory Board
Williams Syndrome Association
Verona, Pennsylvania
Anthony J. Pileggi, M.D.
Neurodevelopmental Pediatrics
Geisinger Medical Center
Danville, Pennsylvania
Isabelle Rapin, M.D.
Professor of Neurology and Pediatrics (Neurology)
Albert Einstein College of Medicine
Bronx, New York
Richard C. Strohman, Ph.D.
Professor of Human Biology
Department of Zoology
University of California, Berkeley
Berkeley, California
Larry W. Swanson, Ph.D.
Senior Member
The Salk Institute for Biological Studies
Investigator
Howard Hughes Medical Institute
Adjunct Professor
University of California, San Diego
La Jolla, California
Andrew Zimmerman, M.D.
Pediatric Neurologist
Knoxville Neurology Clinic
The University of Tennessee Medical
Center at Knoxville
Knoxville, Tennessee

Speakers

Jonathan Buckley, Ph.D., M.B.B.S.
"Opportunities for Research on Etiology Within Cooperative Clinical Trials Groups"
Assistant Professor
Department of Preventive Medicine
Children's Cancer Research Group
Pasadena, California
John C. Carey, M.D., M.P.H.
"von Recklinghausen Neurofibromatosis: General, Historical, and Overview"
Chief
Division of Medical Genetics
Associate Professor of Pediatrics
University of Utah School of Medicine
Cancer Research Wing
Salt Lake City, Utah
Alvin H. Crawford, M.D.
"Management of Skeletal Complications in von Recklinghausen's Neurofibromatosis"
Director
Pediatric/Orthopedic Surgery
Children's Hospital Medical Center
Cincinnati, Ohio
Martha Bridge Denckla, M.D.
"von Recklinghausen's Neurofibromatosis: Neurological and Cognitive Assessment of Cognitive Functions in Neurofibromatosis"
Developmental Neurology Branch
Convulsive, Developmental, and Neuromuscular Disorders Program
National Institute of Neurological and Communicative Disorders and Stroke
National Institutes of Health
Bethesda, Maryland
Roswell Eldridge, M.D.
"Bilateral Acoustic Neurofibromatosis: Genetic Basis, Natural History, and Counseling"
Clinical Genetic Studies
Neuroepidemiology Branch
National Institute of Neurological and Communicative Disorders and Stroke
National Institutes of Health
Bethesda, Maryland
Thomas B. Fitzpatrick, M.D., Ph.D.
"The Melanocyte in von Recklinghausen's Neurofibromatosis"
Professor of Dermatology
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts
James F. Gusella, Ph.D.
"Genetics, von Recklinghausen's, and Bilateral Acoustic Neuroma"
Director for Neurogenetics Laboratory
Massachusetts General Hospital
Harvard Medical School
Neurogenetics Laboratory
Boston, Massachusetts
Judith Goslin Hall, M.D., F.A.A.P., F.R.C.P.(C),F.C.C.M.G., F.A.B.M.G.
"Penetrance, Variability, and Maternal Factors"
Professor, Medical Genetics
University of British Columbia
Grace Hospital
Vancouver, British Columbia
CANADA
William F. Hoyt, M.D.
"Optic Glioma"
Professor of Ophthalmology, Neurosurgery, and
Neurology
University of California, San Francisco
San Francisco, California
Susan M. Huson, M.B., Ch.B., M.R.C.P.
"Research Directions 1"
"Genetic Linkage Studies of von Recklinghausen Neurofibromatosis"
Senior Registrar in Clinical Genetics
Division of Inherited Metabolic Disease
Clinical Research Centre
Harrow, Middlesex
ENGLAND
Bruce R. Korf, M.D., Ph.D.
"Overall Summary: Management of VRNF"
Assistant Professor of Neurology
Director of Clinical Genetics
Harvard Medical School
Children's Hospital
Boston, Massachusetts
Edward Raymond Laws, Jr., M.D.
"The Neurosurgical Mangement of Optic Nerve Glioma"
Professor of Neurologic Surgery
Joseph I. and Barbara Ashkins Professor of Surgery
Mayo Clinic
Mayo Medical School
Rochester, Minnesota
G. Dean MacEwen, M.D.
"Management of Skeletal Complications in von Recklinghausen's Neurifibromatosis"
Chairman
Department of Pediatric Orthopedic Surgery
Professor of Orthopedics
Louisiana State University at New Orleans
New Orleans, Louisiana
Robert L. Martuza, M.D.
"Bilateral Acoustic Neurofibromatosis: Diagnosis and Natural History"
Associate Professor of Surgery
Harvard Medical School
Associate Visiting Neurosurgeon
Director
Neurofibromatosis Clinic
Massachusetts General Hospital
Boston, Massachusetts
Anna T. Meadows, M.D.
"Management of Malignancy in von Recklinghausen's Neurofibromatosis"
Professor of Pediatrics
University of Pennsylvania School of Medicine
Children's Hospital of Philadelphia
Philadelphia, Pennsylvania
John J. Mulvihill, M.D.
"Overview and Natural History of Neurofibromatosis"
Chief
Clinical Genetics Section
Clinical Epidemiology Branch
National Cancer Institute
Director
Interinstitute Medical Genetics Program
National Institutes of Health
Bethesda, Maryland
Georg Nor�n, M.D.
"Stereotactic Radiation Treatment in Bilateral Acoustic Neuroma"
Associate Professor
Department of Neurosurgery
Karolinska Hospital
Stockholm
SWEDEN
Robert G. Ojemann, M.D.
"Management of Patients with Bilateral Acoustic Neuroma"
Professor of Surgery
Harvard Medical School
Senior Neurosurgeon
Massachusetts General Hospital
Boston, Massachusetts
John A. Persing, M.D.
"Reconstructive Surgery of Patients With Neurofibromatosis"
Associate Professor of Plastic and Neurological
Surgery
Department of Plastic Surgery
University of Virginia Medical Center
Charlottesville, Virginia
David E. Pleasure, M.D.
"Biology of Neurofibroma Schwann-Like Cells"
Vice Chairman of Neurology
Professor of Neurology and Pediatrics
University of Pennsylvania
Director of Research of Pediatric Neurology
Joseph Stokes, Jr., Research Institute
Children's Hospital
Philadelphia, Pennsylvania
Albert L. Rhoton, Jr., M.D.
"General Management of Acoustic Neuromas"
Chairman
Department of Neurosurgery
R.D. Keene Family Professor
University of Florida College of Medicine
J. Hillis Miller Health Center
Gainesville, Florida
Vincent M. Riccardi, M.D.
"Alternative Forms of Nueofibromatosis"
Professor of Medicine
Baylor College of Medicine
Houston, Texas
Kenneth N. Rosenbaum, M.D.
"Management at Diagnosis and on Followup"
Director
Clinical Genetics
Children's Hospital National Medical Center
Washington, D.C.
Alonzo H. Ross, Ph.D.
"Biology of Neurofibromatosis Schwann-Like Cells"
Assistant Professor Wistar Institute
Assistant Professor of Neurology
Department of Neurology
University of Pennsylvania Medical School
Philadelphia, Pennsylvania
Allan E. Rubenstein, M.D.
"Neurofibromatosis: Other Forms"
Associate Professor of Neurology
Department of Neurology
Mount Sinai School of Medicine
New York, New York
Kenneth H. Sonnenfeld, Ph.D.
"Growth Factor-Receptors in Neurofibromatosis"
Fish & Neave
New York, New York
Sven Asger S�rensen, M.D.
"Morbidity and Mortality in Neurofibromatosis"
Associate Professor
Institute of Medical Genetics
University of Copenhagen
The Panum Institute
Copenhagen N
DENMARK
Mary H. Waziri, M.D.
"Psychosocial Aspects of von Recklinghausen Neurofibromatosis"
Associate
Department of Pediatrics
Division of Medical Genetics
University of Iowa Hospitals
Iowa City, Iowa

Planning Committee

Joseph S. Drage, M.D.
Planning Committee Chairperson
Chief
Developmental Neurology Branch
Division of Convulsive, Developmental, and Neuromuscular Disorders
National Institute of Neurological and Communicative Disorders and Stroke
National Institutes of Health
Bethesda, Maryland
Michael J. Bernstein
Director of Communications
Office of Medical Applications of Research
National Institutes of Health
Bethesda, Maryland
Patricia Duncan
Technical Publications Writer
Office of Scientific and Health Reports
National Institute of Neurological and Communicative Disorders and Stroke
National Institutes of Health
Bethesda, Maryland
Jerry M. Elliott
Program Analyst
Office of Medical Applications of Research
National Institutes of Health
Bethesda, Maryland
Harry Handelsman, D.O.
Health Science Analyst
Office of Health Technology Assessment
Rockville, Maryland
Robert L. Martuza, M.D.
Associate Professor of Surgery
Harvard Medical School
Associate Visiting Neurosurgeon
Director
Neurofibromatosis Clinic
Massachusetts General Hospital
Boston, Massachusetts
Manfred D. Muenter, Ph.D.
Associate Professor of Neurology
Department of Neurology
Mayo Medical School
Rochester, Minnesota
John J. Mulvihill, M.D.
Chief
Clinical Genetics Section
Clinical Epidemiology Branch
National Cancer Institute
Director
Interinstitute Medical Genetics Program
National Institutes of Health
Bethesda, Maryland
Ntinos C. Myrianthopoulos, Ph.D.
Research Geneticist
Developmental Neurology Branch
National Institute of Neurological and Communicative Disorders and Stroke
National Institutes of Health
Bethesda, Maryland
Martin Rose, M.D., J.D.
Former Chief Medical Officer
Office of Medical Applications of Research
National Institutes of Health
Bethesda, Maryland
Zekin A. Shakhashiri, M.D., M.Sc., M.P.H.
Senior Medical Advisor
National Institute of Neurological and Communicative Disorders and Stroke
National Institutes of Health
Bethesda, Maryland
David A. Stumpf, M.D., Ph.D.
Professor of Pediatrics and Neurology
Vice Chairman
Department of Neurology
Northwestern University Medical School
Chief
Pediatric Neurology
Children's Memorial Hospital
Chicago, Illinois

Conference Sponsors

National Institute of Neurological and Communicative Disorders and Stroke
Murray Goldstein, D.O.
Director
National Cancer Institute
Vincent T. DeVita, Jr., M.D.
Director
Office of Medical Applications Of Research
Itzhak Jacoby, Ph.D.
Acting Director

Privacy Notice | Disclaimer | Accessibility | Contact NIH
Department of Health and Human Services HomepageNational Institutes of Health Home PageFirstGov Home Page - The U.S. Government's Official Web Portal  National Guideline ClearingHouse - a public resource for evidence-based clinical practice guidelines