eMedicine Specialties > Neurology > Inflammatory and Demyelinating Diseases

Neurosarcoidosis

Author: Gabriel Bucurescu, MD, MS, Staff Neurologist, Neurology Service, Philadelphia Veterans Affairs Medical Center
Coauthor(s): Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Contributor Information and Disclosures

Updated: Jul 29, 2009

Introduction

Background

Sarcoidosis is a multisystem disease process whose pathogenesis involves formation of an inflammatory lesion known as a granuloma. Most patients with sarcoidosis do not have any symptoms; the disease often is detected on routine chest radiograph. Symptoms, if present, include cough, shortness of breath, and arthritis. The lungs are affected most frequently, but the eyes, nervous system, heart, kidneys, bones, and joints also may be affected.

Sarcoidosis is a disease of unknown etiology. Involvement of the central nervous system is referred to as neurosarcoidosis. Neurosarcoidosis is an uncommon but severe, sometimes life-threatening, manifestation of sarcoidosis. It generally occurs only if the disease has had substantial systemic involvement, and signs of neurologic involvement usually are seen in patients known to have active disease. Strictly neurologic forms are seen in fewer than 10% of patients.

Pathophysiology

Histologically, neurosarcoidosis is characterized by formation of granulomas in the central nervous system. The lesion consists of lymphocytes and mononuclear phagocytes surrounding a noncaseating epithelioid cell granuloma. These granulomas represent an autoimmune response to central nervous system tissues.

Frequency

United States

  • The prevalence of sarcoid varies widely, but generally it is more common in African Americans.
  • The prevalence is much higher in both blacks and whites in the southeastern United States than in the rest of the country.
  • In New York, the prevalence is 30 cases per 100,000 population
  • It is also seen in the Puerto Rican population, reaching a prevalence as high as 175 cases per 100,000 population in one retrospective study.
  • In Los Angeles, Mexican immigrants constituted 7% of the observed cases, compared to 82% for blacks.
  • The frequency of neurologic involvement is generally 5% of all cases of sarcoid1 , but in some series it was noted to vary from 5-16%. A recent prospective study identified neurologic complications to occur in 32 of 123 (26%) patients who had sarcoidosis. These figures are considered to be underestimated because of the usually silent manifestation of the disease and unavailability of tissue diagnosis in all cases.

International

The incidence of sarcoid varies from 0.04 case per 100,000 population in Spain to 64 cases per 100,000 population in Sweden. The prevalence in London was found to be 27 cases per 100,000 population for patients born in the United Kingdom, 97 cases per 100,000 population among Irishmen, and 200 cases per 100,000 population in men from the West Indies (5%). One study done in Paris showed that 13% of individuals from Martinique were affected with sarcoid. In Asia it is extremely rare, being almost unknown in Chinese and Southeast Asians. Data from Japan showed native Japanese to be affected.

Mortality/Morbidity

About two thirds of patients with neurosarcoidosis have a self-limited monophasic illness, and the rest have a chronic remitting relapsing course. With treatment, death from neurologic disease is unusual.

Neurological involvement is a major cause of disability in sarcoidosis.

Race

Neurosarcoidosis is more common in Africans, including those living in the West Indies, than any other people. The ratio in the United States of affected blacks to affected whites ranges from 10:1 to 17:1. In Europe, however, the disease affects mostly whites. It is very uncommon in Chinese, Southeast Asians, Inuits, Canadian Indians, and New Zealand Maoris.

Sex

Slightly more common in women than men, one study found 55% of the subjects were women.

Age

  • Neurosarcoidosis commonly occurs in adults aged 25-50 years.
  • Neurosarcoidosis is uncommon in children, but when it occurs, it affects children aged 9-15 years. Sarcoidosis of early childhood ( <8 y), when it does occur, has a different clinical manifestation than in adults, characterized by the triad of cutaneous nodules, arthritis, and uveitis. The rate of ocular involvement was reported to reach 100% in these patients; iritis and/or anterior vitreitis was observed in almost all cases. Children older than 8 years have a clinical picture similar to that of adults.

Clinical

History

Onset of neurosarcoidosis is most often in the fourth or fifth decade of life, but the disease affects children and the elderly as well. In patients known to have sarcoid, the appearance of neurologic symptoms usually poses no diagnostic problems, but the possibility of unrelated disease must be kept in mind, especially infections. When nervous disease complicates systemic sarcoidosis, it usually does so within 2 years of onset. Symptoms can include the following:

  • Mononeuropathy - Cranial nerve involvement
    • Facial palsy (the most commonly affected cranial nerve), either unilaterally or bilaterally - Heerfordt syndrome is characterized by fever, uveitis, swelling of the parotid gland, and facial nerve palsy and represents a type of neurosarcoidosis. The lesion site has been controversial, but direct nerve compression by parotid gland swelling or by a lesion within the facial canal has been assumed, in light of observations of accompanying taste disturbance.
    • Impaired taste and smell
    • Blindness, blurry vision, double vision, visual field defects, pupillary abnormalities, dry and sore eyes
    • Slurred speech, impaired swallowing, hoarseness
    • Vertigo, sensorineural deafness, tinnitus
    • Weakness of trapezius and sternocleidomastoid muscles
    • Tongue deviation and atrophy
  • Peripheral nerve involvement - Mononeuropathy, mononeuropathy multiplex, polyneuropathy
    • Sensory neuropathy - Characterized by loss of sensation and abnormal sensation (eg, tingling, numbness, extremity pain, low back pain, painful patches over the thorax, stocking/glove deficits)
    • Motor neuropathy - Characterized by weakness, leading to immobility and joint stiffness
  • Central nervous system involvement may affect the hypothalamus/pituitary gland, cerebral cortex, cerebellum, and spinal cord (rarely), resulting in the following:
    • Polydipsia
    • Polyuria
    • Diabetes insipidus
    • Changes in appetite
    • Changes in sleep cycle (somnolence)
    • Impaired temperature regulation (hyperthermia, hypothermia)
    • Obesity
    • Alveolar hypoventilation
    • Impotence
    • Change in menstrual period
    • Galactorrhea
    • Amenorrhea
    • Generalized confusion
    • Dementia
    • Amnesia, both short term and long term
    • Loss of judgment
    • Acalculia
    • Generalized fatigue
    • Headache
    • Meningitis
    • Corticospinal signs
    • Cerebellar signs
    • Brainstem signs
    • Focal seizures
  • Generalized or localized muscle weakness, muscle soreness

Physical

Patient may have signs of the following:

  • Mononeuropathy, mononeuropathy multiplex, plexopathy
  • Polyneuropathy
    • Sensory neuropathy
    • Motor neuropathy
    • Sensorimotor neuropathy
  • Space-occupying lesion of brain: Although necrotizing sarcoidosis has been reported most commonly in the lungs and rarely in other organ systems, sarcoidosis and its necrotizing variant should be considered in the differential diagnosis of an agranulomatous mass lesion involving the CNS, particularly in the context of a history of systemic disease.
  • Hypopituitarism
  • Optic neuritis leading to optic atrophy (see Media files 1-2)

    Atrophic right optic disc of a 37-year-old man wi...

    Atrophic right optic disc of a 37-year-old man with neurosarcoidosis and involvement of both optic nerves. Vision was lost. The disc is pale with sharp borders.

    [ CLOSE WINDOW ]
    Atrophic right optic disc of a 37-year-old man wi...

    Atrophic right optic disc of a 37-year-old man with neurosarcoidosis and involvement of both optic nerves. Vision was lost. The disc is pale with sharp borders.



    Atrophic left optic disc of a 37-year-old patient...

    Atrophic left optic disc of a 37-year-old patient with neurosarcoidosis and involvement of both optic nerves. The disc is pale with sharp borders. Vision was largely preserved.

    [ CLOSE WINDOW ]
    Atrophic left optic disc of a 37-year-old patient...

    Atrophic left optic disc of a 37-year-old patient with neurosarcoidosis and involvement of both optic nerves. The disc is pale with sharp borders. Vision was largely preserved.

  • Eye involvement leading to blindness, including uveitis, iritis, choroiditis, and cyclitis
  • Meningitis, rarely recurrent meningitis, especially basal brain involvement, leading to cranial nerve deficits, hydrocephalus, cauda equina signs, ependymitis, and encephalopathy
  • Heerfordt syndrome, which consists of the combination of fever, uveitis, parotid gland enlargement, and facial nerve palsy, is a rare manifestation.2
  • Peripheral signs of sarcoidosis, such as erythema nodosum
  • Cerebral infarct or transient ischemic attack due to vasculitis
  • Spinal cord lesions are rare, affecting 0.3-0.4% of patients with systemic sarcoidosis. Intramedullary lesions resembling demyelinating disease may possibly respond to steroids, as does demyelinating disease. Extramedullary sarcoid lesions are even rarer than intramedullary ones, but have been reported.
  • Myopathy is characterized by atrophy, tenderness, muscles feeling "hard" on palpation, and weakness.
  • Brain stem (sarcoid brainstem encephalitis) and cerebellar involvement: This is rare and can manifest as demyelination, hemorrhagic infarction, or parenchymal infiltration by granulomatous masses. A recently reported case of sarcoid brainstem encephalitis showed nemaline rods in every muscle examined (see Workup).
  • Seizures may be the first manifestation of neurosarcoidosis. Generally, seizures indicate a chronic course with poor prognosis. Cases associated with isolated mass lesions and simple partial or complex partial seizures (with or without secondary generalization) may be associated with better outcomes than patients with generalized tonic-clonic seizures only.
  • A recent case of neurosarcoidosis presenting as complicated sinusitis was reported, but the incidence of sinonasal cases is rare, ranging from 1-4% of patients. Head and neck manifestations occur in approximately 10-15% of patients with sarcoid.3  
  • Two cases of sudden death have been attributed to cardiac sarcoidosis and hypothalamic infiltration.4  

Causes

The causes of sarcoidosis are not clear. The present evidence suggests that active sarcoidosis results from an exaggerated cellular immune response to either foreign or self-antigens. T-helper cells proliferate, resulting in an exaggerated response. The T-helper lymphocytes undergo differentiation to a Th1-type cell under the influence of interleukin-4 (IL-4) and co-stimulator CD28. The Th1 cell induces IL-2 and interferon gamma (IFN-gamma) on the macrophages, followed by a cascade of chemotactic factors that promote formation of granuloma. IFN-gamma increases the expression of major histocompatability class (MHC) class II on macrophages, and activated macrophages receptors carry an Fc receptor of immunoglobulin G (IgG) which potentiates their phagocytosis function. Tissue destruction results and granuloma formation is thought to be a secondary process.

Several hypotheses have been proposed to explain the mechanism: (1) a persistent antigen (either foreign or self) triggers the T-helper cell response; (2) response of the suppressor arm of the immune response is inadequate, preventing T-helper cells from shutting down; or (3) a possible inherited or acquired (genetic) difference in response genes leads to the exaggerated response.

In addition to the exaggerated cellular immune response, active sarcoid shows hyperglobulinemia, with antibodies against several infectious agents (eg, Mycobacterium tuberculosis) as well as IgM anti–T-cell antibodies. However, no evidence exists to suggest that these antibodies play a role in disease pathogenesis; rather, their presence seems to be due to a nonspecific polyclonal stimulation of B cells by activated T cells at the site.

More on Neurosarcoidosis

Overview: Neurosarcoidosis
Differential Diagnoses & Workup: Neurosarcoidosis
Treatment & Medication: Neurosarcoidosis
Follow-up: Neurosarcoidosis
Multimedia: Neurosarcoidosis
References
[ CLOSE WINDOW ]

References

  1. Motta M, Alongi F, Bolognesi A, Cozzarini C, Di Muzio N, Fazio F. Remission of refractory neurosarcoidosis treated with brain radiotherapy: a case report and a literature review. Neurologist. Mar 2008;14(2):120-4. [Medline].

  2. Petropoulos IK, Zuber JP, Guex-Crosier Y. Heerfordt syndrome with unilateral facial nerve palsy: a rare presentation of sarcoidosis. Klin Monatsbl Augenheilkd. May 2008;225(5):453-6. [Medline].

  3. Brigger MT, McLeod IK, Sorensen MP. Neurosarcoidosis presenting as complicated sinusitis: a case report and review. Ear Nose Throat J. Feb 2008;87(2):93-5. [Medline].

  4. Byard RW, Manton N, Tsokos M. Sarcoidosis and mechanisms of unexpected death. J Forensic Sci. Mar 2008;53(2):460-4. [Medline].

  5. Hammond ER, Kaplin AI, Kerr DA. Thalidomide for acute treatment of neurosarcoidosis. Spinal Cord. Dec 2007;45(12):802-3. [Medline].

  6. Aide N, Benayoun M, Kerrou K, Khalil A, Cadranel J, Talbot JN. Impact of [18F]-fluorodeoxyglucose ([18F]-FDG) imaging in sarcoidosis: unsuspected neurosarcoidosis discovered by [18F]-FDG PET and early metabolic response to corticosteroid therapy. Br J Radiol. Mar 2007;80(951):e67-71. [Medline].

  7. Benzagmout M, Boujraf S, Góngora-Rivera F, Bresson D, Van-Effenterre R. Neurosarcoidosis which manifested as acute hydrocephalus: diagnosis and treatment. Intern Med. 2007;46(18):1601-4. [Medline].

  8. Bos MM, Overeem S, van Engelen BGM, et al. A case of neuromuscular mimicry. Neuromuscular Disorders. 2006;16:510-513. [Medline].

  9. Brindeau C, Glacet-Bernard A, Roualdes B, et al. [Sarcoid optic neuropathy]. J Fr Ophtalmol. Dec 1999;22(10):1072-5. [Medline].

  10. Bullmann C, Faust M, Hoffmann A, et al. Five cases with central diabetes insipidus and hypogonadism as first presentation of neurosarcoidosis. Eur J Endocrinol. Apr 2000;142(4):365-72. [Medline].

  11. Bydder GM, Hajnal JV, Young IR. Use of the inversion recovery pulse sequence. In: Stark DD, Bradley WG Jr, eds. Magnetic Resonance Imaging. Vol 1. 3rd ed. St Louis: Mosby;1999:69-86.

  12. Cardonick EH, Naktin J, Berghella V. Neurosarcoidosis diagnosed during pregnancy by thoracoscopic lymph node biopsy. A case report. J Reprod Med. Jul 2000;45(7):585-7. [Medline].

  13. Chapelon-Abric C. [Neurologic forms of sarcoidosis]. Presse Med. Feb 19 2000;29(6):327-31. [Medline].

  14. Cohen JP, Lachman LJ, Hammerschlag PE. Reversible facial paralysis in sarcoidosis. Confirmation by serum angiotensin-converting enzyme assay. Arch Otolaryngol. Dec 1983;109(12):832-5. [Medline].

  15. Crystal RG. Sarcoidosis. In: Harrison's Principles of Internal Medicine. 15th ed. NY: McGraw-Hill;2000:1969-74.

  16. Cumming WJK, Fulthorpe JJ, Hudgson P. Inflammatory myopathies. In: Color Atlas of Muscle Pathology. Times Mirror International Publishers Ltd;1994:115.

  17. Dale JC, O''Brien JF. Determination of angiotensin-converting enzyme levels in cerebrospinal fluid is not a useful test for the diagnosis of neurosarcoidosis. Mayo Clin Proc. May 1999;74(5):535. [Medline].

  18. Delaney P. Neurologic manifestations in sarcoidosis: review of the literature, with a report of 23 cases. Ann Intern Med. Sep 1977;87(3):336-45. [Medline].

  19. DeRemee RA. Sarcoidosis and Wegener''s granulomatosis: a comparative analysis. Sarcoidosis. Mar 1994;11(1):7-18. [Medline].

  20. Ferriby D, de Seze J, Stojkovic T, et al. [Clinical manifestations and therapeutic approach in neurosarcoidosis]. Rev Neurol (Paris). Nov 2000;156(11):965-75. [Medline].

  21. Fery F, Plat L, van de Borne P, et al. Impaired counterregulation of glucose in a patient with hypothalamic sarcoidosis. N Engl J Med. Mar 18 1999;340(11):852-6. [Medline].

  22. Gaines JD, Eckman PB, Remington JS. Low CSF glucose level in sarcoidosis involving the central nervous system. Arch Intern Med. Feb 1970;125(2):333-6. [Medline].

  23. Garcia Berrocal JR, Trinidad A, Vargas JA, et al. [Sudden hearing loss and uveitis as a form of presentation of neurosarcoidosis]. Acta Otorrinolaringol Esp. Aug-Sep 1998;49(6):488-90. [Medline].

  24. Glocker FX, Seifert C, Lücking CH. Facial palsy in Heerfordt''s syndrome: electrophysiological localization of the lesion. Muscle Nerve. Sep 1999;22(9):1279-82. [Medline].

  25. Gott PS, Kumar V, Kadakia J, Sharma OP. Significance of multimodality evoked potential abnormalities in sarcoidosis. Sarcoidosis Vasc Diffuse Lung Dis. Sep 1997;14(2):159-64. [Medline].

  26. Hoitsma E, Faber CG, Drent M, Sharma OP. Neurosarcoidosis: a clinical dilemma. Lancet Neurol. Jul 2004;3(7):397-407. [Medline].

  27. Hoyle JC, Newton HB, Katz S. Prognosis of refractory neurosarcoidosis altered by thalidomide: a case report. J Med Case Reports. Jan 28 2008;2:27. [Medline].

  28. James DG. Life-threatening situations in sarcoidosis. Sarcoidosis Vasc Diffuse Lung Dis. Sep 1998;15(2):134-9. [Medline].

  29. Jarnier D, Seriès C. [Neurosarcoidosis. Review of the literature]. Neurochirurgie. Sep 1999;45(3):214-8. [Medline].

  30. Kadakia JK, Collette PM, Sharma OP. Role of magnetic resonance imaging in neurosarcoidosis. Sarcoidosis. Sep 1993;10(2):98-9. [Medline].

  31. Kang S, Suh JH. Radiation therapy for neurosarcoidosis: report of three cases from a single institution. Radiat Oncol Investig. 1999;7(5):309-12. [Medline].

  32. Kone-Paut I, Portas M, Wechsler B, et al. The pitfall of silent neurosarcoidosis. Pediatr Neurol. Mar 1999;20(3):215-8. [Medline].

  33. Kuks JB. [Neurosarcoidosis]. Ned Tijdschr Geneeskd. Apr 16 1994;138(16):805-7. [Medline].

  34. Leiba H, Siatkowski RM, Culbertson WW, Glaser JS. Neurosarcoidosis presenting as an intracranial mass in childhood. J Neuroophthalmol. Dec 1996;16(4):269-73. [Medline].

  35. Lexa FJ, Grossman RI. MR of sarcoidosis in the head and spine: spectrum of manifestations and radiographic response to steroid therapy. AJNR Am J Neuroradiol. May 1994;15(5):973-82. [Medline].

  36. Lieberman J, Bell DS. Serum angiotensin-converting enzyme as a marker for the chronic fatigue-immune dysfunction syndrome: a comparison to serum angiotensin-converting enzyme in sarcoidosis. Am J Med. Oct 1993;95(4):407-12. [Medline].

  37. Lower EE, Broderick JP, Brott TG, Baughman RP. Diagnosis and management of neurological sarcoidosis. Arch Intern Med. Sep 8 1997;157(16):1864-8. [Medline].

  38. Lower EE, Weiss KL. Neurosarcoidosis. Clin Chest Med. Sep 2008;29(3):475-92. [Medline].

  39. Matsubara S. Ultrastructural changes in granulomatous myopathy. Acta Neuropathol (Berl). 1980;50(2):91-6. [Medline].

  40. Matsumoto K, Awata S, Matsuoka H, et al. Chronological changes in brain MRI, SPECT, and EEG in neurosarcoidosis with stroke-like episodes. Psychiatry Clin Neurosci. Dec 1998;52(6):629-33. [Medline].

  41. McLean BN, Mitchell DN, Thompson EJ. Local synthesis of specific IgG in the cerebrospinal fluid of patients with neurosarcoidosis detected by antigen immunoblotting using Kveim material. J Neurol Sci. Nov 1990;99(2-3):165-75. [Medline].

  42. Nardone R, Venturi A, Buffone E, et al. Extramedullary spinal neurosarcoidosis: report of two cases. Eur Neurol. 2005;54:220-224. [Medline].

  43. Nishie M, Mori F, Suzuki C, et al. Disseminated intraparenchymal microgranulomas in the brainstem in central nervous system sarcoidosis. Neuropathology. 2005;25:361-364. [Medline].

  44. Nouri KH, Kevorkian CG, Nisbet JJ. Neurosarcoidosis presenting with lower-back and leg pain. Am J Phys Med Rehabil. Jan 2007;86(1):1-2. [Medline].

  45. Oh SJ. Nerve conduction in polyneuropathies. In: Clinical Electromyography. Baltimore: Williams & Wilkins;1993:628-9.

  46. Oksanen V. Neurosarcoidosis. Sarcoidosis. Mar 1994;11(1):76-9. [Medline].

  47. Pavese P, Brion JP, Chabre O, et al. [Neurologic involvement in sarcoidosis. Federation of Systemic Diseases of Grenoble]. Presse Med. Jan 30 1999;28(4):168-72. [Medline].

  48. Pickuth D, Heywang-Kobrunner SH. Neurosarcoidosis: evaluation with MRI. J Neuroradiol. Sep 2000;27(3):185-8. [Medline].

  49. Pickuth D, Spielmann RP, Heywang-Kobrunner SH. Role of radiology in the diagnosis of neurosarcoidosis. Eur Radiol. 2000;10(6):941-4. [Medline].

  50. Popli AP. Risperidone for the treatment of psychosis associated with neurosarcoidosis. J Clin Psychopharmacol. Apr 1997;17(2):132-3. [Medline].

  51. Radziwill A, Weder B. [Neurosarcoidosis of the central nervous system. Analysis of the long-term follow-up of 8 cases]. Nervenarzt. Dec 1995;66(12):915-22. [Medline].

  52. Sakakibara R, Hattori T, Uchiyama T, Yamanishi T. Micturitional disturbance in a patient with neurosarcoidosis. Neurourol Urodyn. 2000;19(3):273-7. [Medline].

  53. Salama B, Gicquel JJ, Lenoble P, Dighiero PL. Optic neuropathy in refractory neurosarcoidosis treated with TNF-alpha antagonist. Can J Ophthalmol. Dec 2006;41(6):766-8. [Medline].

  54. Salvage DR, Spencer JA, Batchelor AG, MacLennan KA. Sarcoid involvement of the supraorbital nerve: MR and histologic findings. AJNR Am J Neuroradiol. Oct 1997;18(9):1785-7. [Medline].

  55. Sharma OP. Effectiveness of chloroquine and hydroxychloroquine in treating selected patients with sarcoidosis with neurological involvement. Arch Neurol. Sep 1998;55(9):1248-54. [Medline].

  56. Sharma OP. Neurosarcoidosis: a personal perspective based on the study of 37 patients. Chest. Jul 1997;112(1):220-8. [Medline].

  57. Siltzbach LE, James DG, Neville E, et al. Course and prognosis of sarcoidosis around the world. Am J Med. Dec 1974;57(6):847-52. [Medline].

  58. Sponsler JL, Werz MA, Maciunas R, Cohen M. Neurosarcoidosis presenting with simple partial seizures and solitary enhancing mass: case reports and review of the literature. Epilepsy & Behavior. 2005;6:623-630. [Medline].

  59. Stern BJ. Neurological complications of sarcoidosis. Curr Opin Neurol. Jun 2004;17(3):311-6. [Medline].

  60. Strickland-Marmol LB, Fessler RG, Rojiani AM. Necrotizing sarcoid granulomatosis mimicking an intracranial neoplasm: clinicopathologic features and review of the literature. Mod Pathol. Aug 2000;13(8):909-13. [Medline].

  61. Tikoo RK, Kupersmith MJ, Finlay JL. Treatment of refractory neurosarcoidosis with cladribine. N Engl J Med. Apr 22 2004;350(17):1798-9. [Medline].

  62. Toth C, Martin L, Morrish W, Coutts S, Parney I. Dramatic MRI improvement with refractory neurosarcoidosis treated with infliximab. Acta Neurol Scand. Oct 2007;116(4):259-62. [Medline].

  63. Vital A, Lagueny A, Ferrer X, Louiset P, Canron MH, Vital C. Sarcoid neuropathy: clinico-pathological study of 4 new cases and review of the literature. Clin Neuropathol. Mar-Apr 2008;27(2):96-105. [Medline].

  64. Younus F, Wallach SL. Neurosarcoidosis presenting as syncope. Sarcoidosis Vasc Diffuse Lung Dis. Jun 2000;17(2):194. [Medline].

  65. Zajicek JP. Neurosarcoidosis. Curr Opin Neurol. Jun 2000;13(3):323-5. [Medline].

  66. Zajicek JP, Scolding NJ, Foster O, et al. Central nervous system sarcoidosis--diagnosis and management. QJM. Feb 1999;92(2):103-17. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

sarcoidosis of nervous system, sarcoidosis, granuloma, central nervous system, lymphocytes, mononuclear phagocytes, iritis, anterior vitreitis

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Gabriel Bucurescu, MD, MS, Staff Neurologist, Neurology Service, Philadelphia Veterans Affairs Medical Center
Gabriel Bucurescu, MD, MS is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society
Disclosure: Nothing to disclose.

Coauthor(s)

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Medical Editor

Amy A Pruitt, MD, Associate Professor of Neurology, University of Pennsylvania; Attending Neurologist, Hospital of the University of Pennsylvania
Amy A Pruitt, 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

Florian P Thomas, MD, MA, PhD, Drmed, Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Paraplegia Society, and National Multiple Sclerosis 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

B Mark Keegan, MD, FRCPC, Assistant Professor of Neurology, College of Medicine, Mayo Clinic; Master's Faculty, Mayo Graduate School; Consultant, Department of Neurology, Mayo Clinic, Rochester
B Mark Keegan, MD, FRCPC is a member of the following medical societies: American Academy of Neurology, American Medical Association, and Minnesota Medical Association
Disclosure: Neurology (Journal of the American Academy of Neurology)  Honoraria Section Editor

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.