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Journal articles on the topic 'Neurosarcoidosis'

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Author: Grafiati

Published: 10 March 2023

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1

Lord, Jennifer, M. Mateo Paz Soldan, Jonathan Galli, Karen L. Salzman, Jacob Kresser, Rae Bacharach, L. Dana DeWitt, et al. "Neurosarcoidosis." Neurology - Neuroimmunology Neuroinflammation 7, no. 4 (May 13, 2020): e743. http://dx.doi.org/10.1212/nxi.0000000000000743.

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ObjectiveTo characterize patients with neurosarcoidosis within the University of Utah healthcare system, including demographics, clinical characteristics, treatment, and long-term outcomes.MethodsWe describe the clinical features and outcomes of patients with neurosarcoidosis within the University of Utah healthcare system (a large referral center for 10% of the continental United States by land mass). Patients were selected who met the following criteria: (1) at least one International Classification of Diseases Clinical Modification, 9th revision code 135 or International Classification of Diseases Clinical Modification, 10th revision code D86* (sarcoidosis) and (2) at least one outpatient visit with a University of Utah clinician in the Neurology Department within the University of Utah electronic health record.ResultsWe identified 56 patients meeting the study criteria. Thirty-five patients (63%) were women, and most patients (84%) were white. Twelve patients (22%) met the criteria for definite neurosarcoidosis, 36 patients (64%) were diagnosed with probable neurosarcoidosis, and 8 patients (14%) were diagnosed with possible neurosarcoidosis. A total of 8 medications were used for the treatment of neurosarcoidosis. Prednisone was the first-line treatment in 51 patients (91%). Infliximab was the most effective therapy, with 87% of patients remaining stable or improving on infliximab. Treatment response for methotrexate and azathioprine was mixed, and mycophenolate mofetil and rituximab were the least effective treatments in this cohort.ConclusionsThis is a comprehensive characterization of neurosarcoidosis within a single healthcare system at the University of Utah that reports long-term response to treatment and outcomes of patients with neurosarcoidosis. Our results suggest the use of infliximab as a first-line therapy for neurosarcoidosis.

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2

Tetikkurt, Cuneyt. "Neurosarcoidosis." Journal of Neurology & Neuromedicine 3, no. 4 (July 1, 2018): 108–12. http://dx.doi.org/10.29245/2572.942x/2018/4.1190.

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3

Brola, Waldemar, Renata Pejas-Dulewicz, Jarosław Wasiński, and Małgorzata Fudala. "Neurosarcoidosis." Medical Studies 1 (2014): 51–56. http://dx.doi.org/10.5114/ms.2014.42002.

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4

Ramazanov, G. R., E. V. Shevchenko, L. I. Idilova, V. N. Stepanov, E. V. Nugaeva, and S. S. Petrikov. "Neurosarcoidosis." Russian neurological journal 25, no. 5 (December 16, 2020): 45–50. http://dx.doi.org/10.30629/2658-7947-2020-25-5-45-50.

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The article represents the discussion of sarcoidosis involving the cranial nerves and meninges. It’s a rare disease diﬃcult to diagnose. This form of the disease is a progressive lesion of the nervous system, characterized by granulomatous inflammation of the membranes and /or tissue of cerebrum or spinal cord, cranial and /or peripheral nerves. Clinical signs of the nervous system disorder found in sarcoidosis, are detected only in 5–15% of patients. They are often represented by symptoms of cranial nerve damage, meningeal syndrome and epileptic seizures. X-ray computed tomography and magnetic resonance imaging of the brain do not reveal specific changes, however, they allow to exclude other structural lesions of the central nervous system and to identify neuroimaging signs, most common in the course of this disease. Diagnosis of neurosarcoidosis is possible in the presence of neurological symptoms, signs of multisystem lesions, and histological confirmation of non-caseous granulomatous inflammation in one or more organs. The article also represents a clinical observation of a patient with neurosarcoidosis, manifested by acute bilateral neuropathy of the facial nerves, unilateral neuropathy of the trigeminal nerve and meningism syndrome. The neuroimaging signs, often found in this disease, were revealed: the accumulation of contrast agent by the membranes of the brain and the tissue of cavum Meckeli. The course of the disease and diagnostic search, which made it possible to detect signs of multisystem lesion, are described. The diagnosis was confirmed by histological examination of the biopsy material of the intrathoracic lymph node. The results of neurosarcoidosis anti-inflammatory therapy are presented. The peculiarities influencing the choice of this type of treatment terms, are indicated.

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5

Lacomis, David. "Neurosarcoidosis." Current Neuropharmacology 9, no. 3 (September 1, 2011): 429–36. http://dx.doi.org/10.2174/157015911796557975.

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6

Bradshaw, Michael J., Siddharama Pawate, Laura L. Koth, Tracey A. Cho, and Jeffrey M. Gelfand. "Neurosarcoidosis." Neurology - Neuroimmunology Neuroinflammation 8, no. 6 (October 4, 2021): e1084. http://dx.doi.org/10.1212/nxi.0000000000001084.

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Although often regarded as a protean illness with myriad clinical and imaging manifestations, neurosarcoidosis typically presents as recognizable syndromes that can be approached in a rational, systematic fashion. Understanding of neurosarcoidosis has progressed significantly in recent years, including updated diagnostic criteria and advances in treatment. The diagnosis of neurosarcoidosis is established by the clinical syndrome, imaging and histopathological findings, and exclusion of other causes. Mounting evidence supports the use of tumor necrosis factor inhibitors as an important addition to the therapeutic armamentarium, along with glucocorticoids and steroid-sparing cytotoxic immunosuppressants. In this narrative review, we summarize recent advances in the diagnosis and treatment of neurosarcoidosis.

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7

Williams, Daniel W., Allen D. Elster, and Stephen I. Kramer. "Neurosarcoidosis." Journal of Computer Assisted Tomography 14, no. 5 (September 1990): 704–7. http://dx.doi.org/10.1097/00004728-199009000-00004.

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8

Minagar, A., M. Hardjasudarma, and R. E. Kelley. "Neurosarcoidosis." Neurology 59, no. 3 (August 13, 2002): 477. http://dx.doi.org/10.1212/wnl.59.3.477.

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9

Oksanen, Virpi. "Neurosarcoidosis." Seminars in Respiratory and Critical Care Medicine 13, no. 06 (November 1992): 459–67. http://dx.doi.org/10.1055/s-2007-1006296.

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10

Schooff, Michael. "NEUROSARCOIDOSIS." Southern Medical Journal 86, Supplement (September 1993): 35. http://dx.doi.org/10.1097/00007611-199309001-00089.

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11

Hoyle, J. Chad, Courtney Jablonski, and Herbert B. Newton. "Neurosarcoidosis." Neurohospitalist 4, no. 2 (January 14, 2014): 94–101. http://dx.doi.org/10.1177/1941874413519447.

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12

Zajicek, John P. "Neurosarcoidosis." Current Opinion in Neurology 13, no. 3 (June 2000): 323–25. http://dx.doi.org/10.1097/00019052-200006000-00016.

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13

Scott, Thomas F. "Neurosarcoidosis." Neurology 43, no. 1 Part 1 (January 1993): 8. http://dx.doi.org/10.1212/wnl.43.1_part_1.8.

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14

Ribeiro Neto, Manuel, Brandon Moss, Mary Willis, and Daniel Culver. "Neurosarcoidosis." Seminars in Respiratory and Critical Care Medicine 38, no. 04 (July 27, 2017): 499–513. http://dx.doi.org/10.1055/s-0037-1604165.

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AbstractNeurosarcoidosis is an uncommon but clinically significant manifestation that will be routinely encountered in sarcoidosis specialty clinics. Overall, neurologic involvement is recognized in 5 to 10% of individuals with sarcoidosis. Neurologic symptoms will be the presenting manifestation of sarcoidosis in approximately one-half of those with neurosarcoidosis. The clinical and imaging features of neurosarcoidosis vary widely, largely depending on the anatomic distribution of the disease. The likelihood of spontaneous resolution is lower than for sarcoidosis in general, and residual functional deficits are not uncommon. Therefore, most patients with neurosarcoidosis require immunosuppressive therapy. Small fiber neuropathy, a recently recognized nongranulomatous parasarcoidosis syndrome, is prevalent in chronic sarcoidosis. The variety of neurologic manifestations, broad differential diagnosis, and complexity of management render neurosarcoidosis an area best served by multidisciplinary teams. Sarcoidologists, neurologists, radiologists, neurosurgeons, endocrinologists, urologists, physiatrists, and physical/occupational therapists all potentially have important roles.

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15

Agnihotri, Shruti, Tarun Singhal, Barney Stern, and Tracey Cho. "Neurosarcoidosis." Seminars in Neurology 34, no. 04 (November 4, 2014): 386–94. http://dx.doi.org/10.1055/s-0034-1390387.

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16

Fels, C., A. Riegel, K. Javaheripour-Otto, and S. Obenauer. "Neurosarcoidosis." Clinical Imaging 28, no. 3 (May 2004): 166–69. http://dx.doi.org/10.1016/s0899-7071(03)00146-3.

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17

Ungprasert, Patompong, and Eric L. Matteson. "Neurosarcoidosis." Rheumatic Disease Clinics of North America 43, no. 4 (November 2017): 593–606. http://dx.doi.org/10.1016/j.rdc.2017.06.008.

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18

Sharma, Om P. "Neurosarcoidosis." Chest 100, no. 2 (August 1991): 301–2. http://dx.doi.org/10.1378/chest.100.2.301.

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19

Aksamit, Allen. "NEUROSARCOIDOSIS." CONTINUUM: Lifelong Learning in Neurology 14 (February 2008): 181–96. http://dx.doi.org/10.1212/01.con.0000299992.09447.2b.

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20

Tavee, Jinny O., and Barney J. Stern. "Neurosarcoidosis." CONTINUUM: Lifelong Learning in Neurology 20 (June 2014): 545–59. http://dx.doi.org/10.1212/01.con.0000450965.30710.e9.

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21

Segal, Benjamin M. "Neurosarcoidosis." Current Opinion in Neurology 26, no. 3 (June 2013): 307–13. http://dx.doi.org/10.1097/wco.0b013e3283608459.

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22

Chapelon, Catherine, Jean Marc Ziza, Jean Charles Piette, Yves Levy, Gilles Raguin, Bertrand Wechsler, Marc Olivier Bitker, et al. "Neurosarcoidosis." Medicine 69, no. 5 (September 1990): 261–76. http://dx.doi.org/10.1097/00005792-199009000-00001.

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23

Tamagno, Gianluca, Eugenio De Carlo, Chiara Martini, and Giovanni Murialdo. "Neurosarcoidosis." Journal of the Royal Society of Medicine 98, no. 10 (October 2005): 443. http://dx.doi.org/10.1177/014107680509801006.

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24

Seem, C. P. Chan, and E. G. Spokes. "NEUROSARCOIDOSIS." Lancet 326, no. 8468 (December 1985): 1363. http://dx.doi.org/10.1016/s0140-6736(85)92656-x.

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25

Gascón-Bayarri, J., J. Mañá, S. Martínez-Yélamos, O. Murillo, R. Reñé, and F. Rubio. "Neurosarcoidosis." European Journal of Internal Medicine 22, no. 6 (December 2011): e125-e132. http://dx.doi.org/10.1016/j.ejim.2011.08.019.

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26

STERN, BARNEY J., ALLAN KRUMHOLZ, and CAROL J. JOHNS. "Neurosarcoidosis." Annals of the New York Academy of Sciences 465, no. 1 Tenth Interna (June 1986): 722–30. http://dx.doi.org/10.1111/j.1749-6632.1986.tb18551.x.

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27

Marangoni, S., V. Argentiero, and B. Tavolato. "Neurosarcoidosis." Journal of Neurology 253, no. 4 (November 14, 2005): 488–95. http://dx.doi.org/10.1007/s00415-005-0043-5.

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28

Sharma, Om P. "Neurosarcoidosis." Chest 112, no. 1 (July 1997): 220–28. http://dx.doi.org/10.1378/chest.112.1.220.

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29

Terushkin, Vitaly, Barney J. Stern, Marc A. Judson, Mari Hagiwara, Bidyut Pramanik, Miguel Sanchez, and Stephen Prystowsky. "Neurosarcoidosis." Neurologist 16, no. 1 (January 2010): 2–15. http://dx.doi.org/10.1097/nrl.0b013e3181c92a72.

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30

Hughes, Betsy D., J. Ned Pruitt, and John R. Vender. "Neurosarcoidosis." Contemporary Neurosurgery 29, no. 3 (February 2007): 1–7. http://dx.doi.org/10.1097/00029679-200702150-00001.

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31

Tamagno, G. "Neurosarcoidosis." Journal of the Royal Society of Medicine 98, no. 10 (October 1, 2005): 443. http://dx.doi.org/10.1258/jrsm.98.10.443.

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32

Ullapalli, Dakshinamurty, and Lawrence H. Phillips. "Neurosarcoidosis." Current Neurology and Neuroscience Reports 4, no. 6 (December 2004): 441–47. http://dx.doi.org/10.1007/s11910-004-0066-9.

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33

Nozaki, Kenkichi, and Marc A. Judson. "Neurosarcoidosis." Current Treatment Options in Neurology 15, no. 4 (May 24, 2013): 492–504. http://dx.doi.org/10.1007/s11940-013-0242-9.

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34

Lower, Elyse E., and Kenneth L. Weiss. "Neurosarcoidosis." Clinics in Chest Medicine 29, no. 3 (September 2008): 475–92. http://dx.doi.org/10.1016/j.ccm.2008.03.016.

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35

Tavee, Jinny O., and Barney J. Stern. "Neurosarcoidosis." Clinics in Chest Medicine 36, no. 4 (December 2015): 643–56. http://dx.doi.org/10.1016/j.ccm.2015.08.007.

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36

Walker, Aljoeson, and William Tyor. "Neurosarcoidosis." Current Treatment Options in Neurology 3, no. 6 (November 2001): 529–35. http://dx.doi.org/10.1007/s11940-001-0015-8.

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37

Burns, Ted M. "Neurosarcoidosis." Archives of Neurology 60, no. 8 (August 1, 2003): 1166. http://dx.doi.org/10.1001/archneur.60.8.1166.

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38

Patel, Ashok V., David E. Stickler, and William R. Tylor. "Neurosarcoidosis." Current Treatment Options in Neurology 9, no. 3 (May 2007): 161–68. http://dx.doi.org/10.1007/bf02938405.

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39

Herrero-Morant, A., L. Sanchez-Bilbao, I. González-Mazón, D. Martínez-López, J. L. Martín-Varillas, R. Fernández-Ramón, M. Á. González-Gay, and R. Blanco. "POS1362 NEUROSARCOIDOSIS. STUDY OF 30 PATIENTS FROM A SERIES OF 384 SYSTEMIC SARCOIDOSIS FROM A TERTIARY UNIVERSITY HOSPITAL." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 963.1–963. http://dx.doi.org/10.1136/annrheumdis-2021-eular.3052.

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Background:Neurosarcoidosis is a serious and infrequent complication of sarcoidosis. Data on Biologic Therapy (BT) efficacy is scarce.Objectives:To assess in neurosarcoidosis a) its prevalence and associations of clinical clusters and b) efficacy and safety of BT.Methods:Study of neurosarcoidosis from a large cohort (n=384) of all consecutive patients diagnosed with sarcoidosis from January 1, 1999 to December 31, 2019 in a single University hospital.Results:30 (19 women/ 11 men) out of 384 (7.8%) patients had neurosarcoidosis. Mean age at diagnosis was 41.8±15.8 years. Clusters of clinical associations were lungs (n=23, 76.7%) and joints (n=15, 50.0%) (Figure 1). The underlying neurological manifestations were chronic headache (n=13, 43.4%), peripheral neuropathy (n=6, 20.0%), cranial neuropathy (n=5, 16.7%), spinal cord abnormalities (n=3, 10.0%) and aseptic meningitis (n=3, 10.0%). 26 (86.7%) patients received oral corticosteroids (mean maximum dose 50±19.2mg) and 7 (23.3%) iv corticosteroids. In addition, 18 (60.0%) patients received conventional immunosuppressants and 12 (40.0%) BT. 4 (13.3%) did not have any treatment. Table 1 shows the main clinical features and treatment.Figure 1.Clusters of clinical associations in neurosarcoidosis12 patients received treatment with 14 BT. Monoclonal anti-TNFα (n=10, 83.3%) was the most used BT. 10 (83.3%) patients treated with BT achieved clinical remission. No serious adverse effects were observed.Conclusion:Neurosarcoidosis was observed in 7.8% of systemic sarcoidosis. Most patients treated with BT, especially monoclonal anti-TNFα, achieved clinical remission.Table 1.Main clinical features and treatment of 30 patients with neurosarcoidosis.n (%)Conventional immunosuppressant, n (%)monoclonal anti-TNFα, n (%)Etarnecept, n (%)Tocilizu-mab, n (%)Secukinu-mab, n (%)Rituxi-mab, n (%)Chronic headache13 (43.4)5 (38.5)2 (15.4)0 (0)01 (7.7)1 (7.7)Peripheral neuropathy6 (20.0)4 (66.7)3 (50.0)1 (16.7)000Cranial neuropathy5 (16.7)4 (80.0)3 (60.0)0000Spinal cord abnormalities3 (10.0)1 (33.3)1 (33.3)0000Aseptic meningitis3 (10.0)2 (66.7)2 (66.7)01 (33.3)00Disclosure of Interests:Alba Herrero-Morant: None declared, Lara Sanchez-Bilbao: None declared, Iñigo González-Mazón: None declared, David Martínez-López: None declared, José Luis Martín-Varillas Grant/research support from: AbbVie, Pfizer, Lilly, Janssen, and Celgene, Raúl Fernández-Ramón: None declared, Miguel Á. González-Gay Speakers bureau: AbbVie, Pfizer, Roche, Sanofi, Lilly, Celgene and MSD, Grant/research support from: AbbVie, MSD, Jansen and Roche, Ricardo Blanco Speakers bureau: AbbVie, Pfizer, Roche, Bristol-Myers, Janssen, Sanofi, Lilly and MSD, Grant/research support from: AbbVie, MSD, and Roche

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40

Kleinschmidt-Demasters, B. K., David Ormond, and Evan Winograd. "NIMG-61. UNUSUAL PRESENTATION OF NEUROSARCOIDOSIS: A CASE SERIES." Neuro-Oncology 22, Supplement_2 (November 2020): ii161. http://dx.doi.org/10.1093/neuonc/noaa215.674.

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Abstract INTRODUCTION Neurosarcoidosis is a rare diagnosis, and even with known systemic disease or history, often remains a diagnosis of exclusion. Typical imaging findings of neurosarcoidosis include white matter lesions coupled with meningeal enhancement, or “sugarcoating” near the skull base. Occasionally, imaging can be quite unusual and mimic other entities. Other diagnoses to rule out include neoplastic, autoimmune, or infectious pachymeningitis, neoplastic lesions, neurosyphilis or tuberculosis. METHODS Our neuropathology database was queried for neurosarcoidosis from January 2008 until December 2019. These cases were then reviewed for cases with unusual presentations for further review and discussion. RESULTS Here we present 16 cases of neurosarcoidosis with histories and/or imaging that did not conform to the typical appearance of neurosarcoidosis. Along with a rare radiographic presentation, these cases also lacked CSF, laboratory, or systemic findings to suggest a diagnosis of neurosarcoidosis. 15 of these cases presented intracranially while 1 case presented within the spinal cord. CONCLUSIONS Neurosarcoidosis presentations can vary greatly. A better understanding of some unique patient presentations can help improve noninvasive diagnosis, although biopsy often remains necessary for confirmation.

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41

Bui, Peter V. "Disseminated Histoplasmosis with Miliary Histoplasmosis, Neurohistoplasmosis, and Histoplasma capsulatum Bacteremia in Probable Neurosarcoidosis." Case Reports in Medicine 2018 (December 11, 2018): 1–3. http://dx.doi.org/10.1155/2018/3162403.

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Introduction. Neurosarcoidosis, either isolated or as part of systemic sarcoidosis, is an uncommon entity and has diagnostic uncertainty. Treatment for neurosarcoidosis can increase the risk of infections, including fungal infections such as disseminated histoplasmosis. Neurosarcoidosis may further predispose patients to infections of the central nervous system. Case Presentation. A 54-year-old male with a history of probable neurosarcoidosis on methotrexate and infliximab presented with encephalopathy, hypoxia, and reported fevers. The patient was found to have disseminated histoplasmosis involving the lungs (miliary histoplasmosis), central nervous system (neurohistoplasmosis), and bloodstream. The Histoplasma capsulatum infection was treated with amphotericin and then voriconazole. Discussion. Patients with neurosarcoidosis are suspected to have blood-brain barrier dysfunction. Lumbar puncture should be considered as part of initial investigative studies for infection. Empiric antimicrobial therapy for a patient with neurosarcoidosis on immunosuppressive agents may need to include antifungal agents.

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42

Sakuta, Manabu. "12. Neurosarcoidosis." Nihon Naika Gakkai Zasshi 99, no. 8 (2010): 1830–36. http://dx.doi.org/10.2169/naika.99.1830.

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43

Ogawa, Yukari, Takeshi Saraya, Masachika Fujiwara, and Hajime Takizawa. "Massive Neurosarcoidosis." Internal Medicine 56, no. 18 (2017): 2537–38. http://dx.doi.org/10.2169/internalmedicine.8217-16.

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44

Ducloux, D., Y. Welker, J. Modai, and K. Lassoued. "Familial neurosarcoidosis." Journal of Internal Medicine 239, no. 1 (January 1996): 83–88. http://dx.doi.org/10.1046/j.1365-2796.1996.t01-1-439786000.x.

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45

Nozaki, Kenkichi, Thomas F. Scott, Mimi Sohn, and Marc A. Judson. "Isolated Neurosarcoidosis." Neurologist 18, no. 6 (November 2012): 373–77. http://dx.doi.org/10.1097/nrl.0b013e3182704d04.

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46

Giuffrida, S., A. Nicoletti, R. Saponara, S. Valvo, M. Malaguarnera, I. Chiaramonte, and F. Le Pira. "Primary Neurosarcoidosis." Rivista di Neuroradiologia 10, no. 1 (February 1997): 103–6. http://dx.doi.org/10.1177/197140099701000108.

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Neurosarcoidosis is primarily a disease of the leptomeninges although parenchymal involvement is less common. We describe a patient presenting with symptoms and signs of intracranial hypertension and diabetes insipidus. Brain CT scan showed periventricular and hypothalamic areas of increased density that enhanced after contrast administration. After steroid treatment, neurological symptoms resolved but diabetes insipidus persisted. MRI study performed 10 days later revealed a significant reduction of the previously demonstrated lesions, that were slightly hyperintense in T2-weighted images, while the hypothalamic lesions enhanced after Gd-DTPA administration. These lesions, due probably to infallamatory infiltration and/or oedema, were not present in a neuroradiological follow-up performed 2 and 3 months later. Two months after neurological onset the patient developed a systemic sarcoidosis. Primary neurosarcoidosis should be suspected in the presence of multiple intracranial lesions which improve after steroid therapy. MRI is the neuroradiological study of choice in the diagnosis and follow-up of this rare disease.

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Maskery, Mark Peter, Paul N. Cooper, and Adrian Pace. "Neurosarcoidosis associated with intracerebral haemorrhage: a challenge in diagnosis and management." Practical Neurology 18, no. 3 (January 23, 2018): 246–49. http://dx.doi.org/10.1136/practneurol-2017-001794.

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Sarcoidosis is an idiopathic multisystem granulomatous disorder of unknown cause. Nervous system involvement (central and/or peripheral) is uncommon, developing in 5%–10%. The presenting symptoms are variable, reflecting the level of involvement, and frequently fluctuate and progress. Diagnosing neurosarcoidosis in people with previously confirmed systemic disease may be relatively straightforward, but diagnosing primary neurosarcoidosis is challenging. Managing neurosarcoidosis is primarily consensus based; corticosteroid is its mainstay, alongside corticosteroid-sparing agents and emerging novel therapies. We describe a 39-year-old woman who presented with cranial neuropathy. Serial imaging, cerebrospinal fluid sampling and tissue biopsy gave a diagnosis of probable neurosarcoidosis. Her clinical course was complicated by intracerebral haemorrhage following intravenous corticosteroids for neurological relapse. This is a very rare complication of neurosarcoidosis; we discuss its possible causes and suggest ways to reduce its risk.

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48

Raza, Naheed, and Karisa C. Schreck. "Neurosarcoidosis Presenting With Recurrent Strokes." Neurohospitalist 7, no. 2 (July 7, 2016): 91–95. http://dx.doi.org/10.1177/1941874416656730.

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Neurosarcoidosis is a rare but important cause of stroke as it is treatable. Cases reported thus far have primarily been in young people who are relatively healthy. Here we report the case of a 73-year-old woman presenting with recurrent strokes and high-grade intracranial stenosis caused by probable neurosarcoidosis. This is unique as neurosarcoidosis is not usually considered as an etiology for recurrent strokes in our patient’s age-group. We review and categorize published cases of neurosarcoidosis causing stroke and describe a classification scheme for certainty of diagnosis. Given the implications of this diagnosis for secondary stroke prevention, we recommend that neurosarcoidosis be considered in the differential for patients with few vascular risk factors, recurrent strokes refractory to medical treatment, or possible vasculitis even in the elderly patients.

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49

Arun, Tarunya, Laura Pattison, and Jacqueline Palace. "Distinguishing neurosarcoidosis from multiple sclerosis based on CSF analysis." Neurology 94, no. 24 (April 30, 2020): e2545-e2554. http://dx.doi.org/10.1212/wnl.0000000000009491.

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ObjectiveTo characterize a cohort of patients with neurosarcoidosis with particular focus on CSF analysis and to investigate whether CSF values could help in distinguishing it from multiple sclerosis (MS).MethodsThis retrospective cohort study enrolled 85 patients with a diagnosis of neurosarcoidosis (possible, probable, or definite). CSF total protein, white cell count, and angiotensin-converting enzyme levels were measured. CSF and serum oligoclonal immunoglobulin G (IgG) patterns were analyzed with the use of odds ratios and binary logistic regression.ResultsEighty patients had a probable (nonneural positive histology) or definite (neural positive histology) diagnosis of neurosarcoidosis. Most frequent findings on MRI were leptomeningeal enhancement (35%) and white matter and spinal cord involvement (30% and 23%). PET scan showed avid areas in 74% of cases. CSF analysis frequently showed lymphocytosis (63%) and elevated protein (62%), but CSF-selective oligoclonal bands were rare (3%). Serum ACE levels were elevated in 51% of patients but in only 14% of those with isolated neurosarcoidosis. Elevated CSF ACE was not found in any patient.ConclusionsLarge elevations in total protein, white cell count, and serum ACE occur in neurosarcoidosis but are rare in MS. The diagnostic use of these tests is, however, limited because minimal changes may occur in both. MS clinical mimics in neurosarcoidosis are not common, and intrathecal synthesis of oligoclonal IgG is a powerful discriminator because it is rare in neurosarcoidosis but occurs in 95% to 98% cases of MS. We suggest caution in making a diagnosis of neurosarcoidosis when intrathecal oligoclonal IgG synthesis is found.

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Otto, Carolin, Oliver Wengert, Nadine Unterwalder, Christian Meisel, and Klemens Ruprecht. "Analysis of soluble interleukin-2 receptor as CSF biomarker for neurosarcoidosis." Neurology - Neuroimmunology Neuroinflammation 7, no. 4 (May 11, 2020): e725. http://dx.doi.org/10.1212/nxi.0000000000000725.

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ObjectiveTo systematically analyze soluble interleukin-2 receptor (sIL-2R) in CSF as a diagnostic and disease activity biomarker in patients with sarcoidosis involving the CNS (neurosarcoidosis).MethodssIL-2R was determined by chemiluminescent immunoassays in CSF/serum samples from patients with neurosarcoidosis (n = 23), MS (n = 19), neurotuberculosis (n = 8), viral (n = 18) and bacterial (n = 9) meningitis, cerebral lymphoma (n = 15), Guillain-Barré syndrome (n = 8), and 115 patients with noninflammatory neurologic diseases (NINDs) as controls. The sIL-2R index was calculated by dividing the CSF/serum sIL-2R quotient (QsIL-2R) through the CSF/serum albumin quotient (QAlb). sIL-2R quotient diagrams were established by plotting QsIL-2R against QAlb. sIL-2R levels were correlated with clinical, MRI, and CSF disease activity markers of neurosarcoidosis.ResultsPatients with neurosarcoidosis had higher CSF sIL-2R, QsIL-2R, and sIL-2R index values than patients with NINDs (p < 0.0001 for all pairwise group comparisons). sIL-2R quotient diagrams demonstrated an intrathecal sIL-2R synthesis in >50% of neurosarcoidosis samples. Similar findings were observed in viral/bacterial meningitis, CNS lymphoma, and, most pronounced, in neurotuberculosis, but not in patients with MS. CSF sIL-2R parameters were associated with clinical disease activity, leptomeningeal gadolinium enhancement, and the CSF white cell count in patients with neurosarcoidosis.ConclusionsCSF sIL-2R parameters are elevated in patients with neurosarcoidosis, but this finding is not specific for neurosarcoidosis. Nevertheless, CSF sIL-2R parameters may help distinguishing neurosarcoidosis from MS and are associated with clinical, radiologic, and CSF disease activity markers of neurosarcoidosis.Classification of evidenceThis study provides Class II evidence that CSF sIL-2R parameters distinguish neurosarcoidosis from NINDs and MS.

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