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Neurological Findings in Myeloproliferative Neoplasms

Year 2013, Volume: 38 Issue: 2, 157 - 169, 01.06.2013

Abstract

Myeloproliferative neoplasms (MPN) arise from genetic deficiencies at the level of pluripotent stem cells. Each of these neoplasms is a clonal stem cell disorder with specific phenotypic, genetic and clinical properties. Age is one of the most important factors in the development of symptoms and complications associated with MPNs.High white blood cell counts in chronic myelocytic leukemia also known as leukocytosis may lead to central nervous system findings. Tumors developing outside the bone marrow named as extramedullary myeloid tumors (EMMT) could be detected at the initial diagnosis or during the prognosis of the disease, which may cause neurological symptoms due to pressure of leukemic cell mass on various tissues along with spinal cord. Central nervous system involvement and thrombocytopenic hemorrhage may lead to diverse neurological symptoms and findings.Transient ischemic attack and thrombotic stroke are the most common symptoms in polycythemia vera. Besides thrombosis and hemorrage, transformation to acute leukemia can cause neurological symptoms and findings. Transient ischemic attack, thrombotic stroke and specifically hemorrage can give rise to neurological symptoms similar to MPN in essential thrombocytosis.Extramedullary hematopoiesis refers to hematopoietic centers arise in organ/tissues other than bone marrow in myelofibrosis. Extramedullar hematopoietic centers may cause intracranial involvement, spinal cord compression, seizures and hydrocephalia. Though rare, extramedullary hematopoiesis can be detected in cranial/spinal meninges, paraspinal tissue and intracerebral regions. Extramedullary hematopoiesis has been reported in peripheral neurons, choroid plexus, pituitary, orbits, orbital and lacrimal fossa and in sphenoidal sinuses.

References

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Miyeloproliferatif Neoplazilerde Nörolojik Bulgular

Year 2013, Volume: 38 Issue: 2, 157 - 169, 01.06.2013

Abstract

Miyeloroliferatif neoplaziler (MPN) pluripotent kök hücre düzeyinde genetik bozukluklardan kaynaklanan, her biri kendine özgü fenotipik, genetik ve klinik özellikleri olan klonal kök hücre hastalıklarıdır. MPN"li olgularda ortaya çıkan semptom ve komplikasyonlarda özellikle nörolojik olaylarda yaş önemli bir faktördür.Kronik miyelositik lösemi olgularında beyaz küre sayısının çok fazla olmasına bağlı (lökostaz) santral sinir sistemi (SSS) bulgularına yol açabilir. İlk tanıda veya hastalığın seyri sırasında kemik iliği dışında yani ekstra medüller alanlarda ekstramedüller miyeloid tümörler (EMMT) olarak isimlendirilen ve lösemik hücrelerin oluşturduğu kitleler diğer doku ve organların yanı sıra gerek SSS"inde gerekse spinal korda bası etkisine yol açan kitleler nedeniyle nörolojik semptom ve bulgulara yol açar. Santral sinir sistemi tutulumu ve trombositopenik kanamalar nörolojik semptom ve bulgulara yol açabilir.Polisitemia verada geçici iskemik atak ve trombotik inme en sık bulgulardır. Tromboz ve hemoraji yanısıra akut lösemiye transfromasyon nörolojik bulgu ve belirtilere yol açabilir. Esansiyel trombositozda geçici iskemik atak, trombotik inme ve zellikle hemoraji diğer MPN"lerdekine benzer nörolojik semptomlara yol açabilir. Miyelofibroziste ekstramedüller hematopoez vücutta yaklaşık her organ/dokuda ortaya çıkan kemik iliği dışındaki kan yapımı odaklarıdır. EMH odakları intrakranyal bası yapan kitle ve spinal kord kompresyonuna, nöbetlere, hidrosefaliye yol açabilir. Nadir olmakla birlikte kranyal/spinal meninkslerde, paraspinal dokuda ve intraserebral lokalizasyonda EMH saptanabilir. Santral ve periferik sinirlerde, koroid pleksusta, pituiter bezde, orbitada, orbital ve lakrimal fossada, sfenoid sinusta EMH rapor edilmiştir.

References

  • Baxter EJ, Scott LM, Campbell PJ, East C, Fourouclas N, Swanton S, Vassiliou GS, Bench AJ, Boyd EM, Curtin N, Scott MA, Erber WN, Green AR; Cancer Genome Project. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet. 2005; 365: 1054-61.
  • Kralovics R, Passamonti F, Buser AS, Teo SS, Tiedt R, Passweg JR, Tichelli A, Cazzola M, Skoda RC. A gain-of- myeloproliferative disorders. N Engl J Med. 2005; 352: 1779-90.
  • Levine RL, Wadleigh M, Cools J, et al. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. Cancer Cell. 2005; 7: 387-97.
  • Harrison CN. Platelets and Thrombosis in Myeloproliferative Diseases. Hematology. 2005; 409- 15.
  • Giona F, Teofili L, Moleti ML, Martini M, Palumbo G, Amendola A, Testi AM, , Pignoloni P, Mazzucconi MG, Orlando SM, Capodimonti S, Nanni M, Leone G, Larocca LM, Foa R. Thrombocythemia and polycythemia in patients younger than 20 years at diagnosis: clinical and biologic features, treatment, and long-term outcome. Blood. 2012; 119: 2219-27.
  • Scherber R, Dueck AC, Johansson P, Barbui T, Barosi G, Vannucchi AM, Passamonti F, Andreasson B, Ferarri LM, Rambaldi A, Samuelsson J, Birgegard G, Tefferi A, Harrison CN, Radia D, Mesa RA. The Myeloproliferative Neoplasm SymptomAssessment Form (MPN-SAF): International Prospective Validation and Reliability Trial in 402 patients. Blood. 2011; 118: 401-08.
  • Vardiman J, Hyjek E. World Health Organization ClassiŞcation, Evaluation, and Genetics of the Myeloproliferative Neoplasm Variants. Hematology. 2011; 250-56.
  • Tefferi A. How I treat myeloŞbrosis. Blood. 2011; 117: 3494-04.
  • Pavlovsky C, Kantarjian H, Cortes JE. First-line therapy for chronic myeloid leukemia: past, present, and future. Am. J. Hematol. 2009; 84: 287–93.
  • Krupinski A, Zdunczyk A, Banan L, Kałuza J. Central nervous system and organ infiltration in the chronic phase of chronic myelogenousleukemia: a case report. Wiad Lek. 1999; 52: 508-12.
  • Bug G, Anargyrou K, Tonn T, Bialleck H, Seifried E, Hoelzer D, Ottmann OG. Impact of leukapheresis on early death rate in adult acute myeloid leukemia presenting with hyperleukocytosis. Transfusion. 2007; 47: 1843–50.
  • Rowe JM, Lichtman MA. Hyperleukocytosis and leukostasis: common features of childhood chronic myelogenous leukemia. Blood. 1984; 63; 1230–34.
  • Chekol SS, Bhatnagar B, Gojo I, Hess JR. Leukopheresis for profound hyperleukocytosis. Transfusion and Apheresis Science. 2012; 46: 29– 31.
  • Muss HB, Moloney WC. Chloroma and other myeloblastic tumors. Blood. 1973; 42: 721–28.
  • Paydas S, Zorludemir S, Ergin M. Granulocytic sarcoma: 32 cases and review of the literature. Leuk Lymphoma. 2006; 47: 2527–41.
  • Imrie KR, Kovacs MJ, Selby D, et al. Isolated chloroma: the effect of early antileukemic therapy. Ann Intern Med. 1995; 123: 351–53.
  • Seok JH, Park J, Kim SK, Choi JE, Kim CC. Granulocytic sarcoma of the spine: MRI and clinical review. AJR Am J Roentgenol. 2010; 194: 485–89.
  • Smidt MH, de Bruin HG, van’t Veer MB, van den Bent MJ. Intracranial granulocytic sarcoma (chloroma) may mimic a subdural hematoma. J Neurol. 2005; 252: 498–99.
  • Shah RS, Shin RK, Castellani RJ. Granulocytic sarcoma mimicking HSV encephalitis. Neurologist 2010; 16: 319–21.
  • Bryant BJ, Alperin JB, Elghetany MT. Paraplegia as the Presenting Manifestation Extramedullary Megakaryoblastic Transformation of Previously Undiagnosed Chronic Myelogenous Leukemia. Am J Hematol. 2007; 82: 150–54.
  • Chalhoub-Hachem BR, Kattan JG, Ghosn MG, Abadjian GA, Okais NM. Granulocytic sarcoma with spinal cord compression in chronic myelogenous leukemia: a case report. J Med Liban. 2003; 51: 117- 19.
  • Niedermayer I, Schmitt-Graeff A, Kölbel CB, Hertel F, Feiden W. Granulocytic sarcoma (so-called chloroma) as a possible cause of spinal cord compression. Case report and differential diagnosis Pathologe. 2000; 21: 82-5.
  • Zha Y, Li M, Yang Y. Dynamic Contrast Enhanced Magnetic Resonance Imaging of Diffuse Spinal Bone Marrow Infiltration in Patients with Hematological Malignancies. Korean J Radiol. 2010; 11: 187-94.
  • Graff-Radford J, Fugate JE, Wijdicks EFM, Lachance DH, Rabinstein AA. Extramedullary tumors and leukemia. A diagnostic pitfall for the neurologist. Neurology. 2012; 79: 85–91.
  • Janssen JJWM, Berendse HW, Schuurhuis GJ, Merle PA, Ossenkoppele GJ. A 51-Year-Old Male CML Patient With Progressive Hearing Loss, Confusion, Ataxia And Aphasia During Imatinib Treatment. Am J Hematol. 2009; 84: 679-82
  • Kim HJ, Jung CW, Kim K, Ahn JS, Kim WS, Park K, Ko YH, Kang WK, Park K. Isolated Blast Crisis in CNS in a Patient With Chronic Myelogenous Leukemia Maintaining Major Cytogenetic Response After Imatinib. J Clin Oncol. 2006; 24: 4028-29.
  • Rajappa S, Uppin SG, Raghunadharao D, Rao IS, Surath A. Isolated central nervous system blast crisis in chronic myeloid leukemia. Hematol Oncol. 2004; 22: 179-81.
  • Matsuda M, Morita Y, Shimada T, Miyatake J, Hirase C, Tanaka M, Tatsumi Y, Maeda Y, Kanamaru A. Extramedullary blast crisis derived from 2 different clones in the central nervous system and neck during complete cytogenetic remission of chronic myelogenous leukemia treated with imatinib mesylate. Int J Hematol. 2005;81: 307-09.
  • Schocket LS, Massaro-Giordano M, Volpe NJ, Galetta SL. Bilateral optic nerve infiltration in central nervous system leukemia. Am J Ophthalmol. 2003; 135: 94-96.
  • Leis JF, Stepan DE, Curtin PT, Ford JM, Peng B, Schubach S, Druker BJ, Maziarz RT. Central nervous system failure in patients with chronic myelogenous leukemia lymphoid blast crisis and Philadelphia chromosome positive acute lymphoblastic leukemia treated with imatinib (STI- 571). Leuk Lymphoma. 2004; 45: 695-98.
  • Wolff NC, Richardson JA, Egorin M, Ilaria RL. The CNS is a sanctuary for leukemic cells in mice receiving imatinib mesylate for Bcr/Abl-induced leukemia. Blood. 2003; 101: 5010-13.
  • Altintas A, Cil T, Kilinc I et al. Central nervous system blastic crisis in chronic myeloid leukemia on imatinib mesylate therapy: a case report. J Neurooncol. 2007; 84: 103-05.
  • Alimena G, Breccia M, Latagliata R, Carmosino I, Russo E, Biondo F, Diverio D, Mancini M, Nanni M, Mandelli F. Sudden blast crisis in patients with Philadelphia chromosome-positive chronic myeloid leukemia who achieved complete cytogenetic remission after imatinib therapy. Cancer. 2006; 107: 1008-13.
  • Aichberger KJ, Herndlhofer S, Agis H Sperr WR, Esterbauer H, Rabitsch W, Knöbl P, Haas OA, Thalhammer R, Schwarzinger I, Sillaber C, Jäger U, Valent P. Liposomal cytarabine for treatment of myeloid central nervous system relapse in chronic myeloid leukaemia occurring during imatinib therapy. Eur J Clin Invest. 2007; 37: 808-13.
  • Neville K, Parise RA, Thompson P, Aleksic A, Egorin MJ, Balis FM, McGuffey L, McCully C, Berg SL, Blaney SM. Plasma and cerebrospinal fluid pharmacokinetics of imatinib after administration to nonhuman primates. Clin Cancer Res. 2004; 10: 2525-29.
  • Prcha JT. Philadelphia Chromosome–Negative Myeloproliferative Disorders: An Historical Perspective. Hematology. 2008; 68.
  • Ohta Y, Shichinohe H, Nagashima K. Spinal cord compression due to extramedullary hematopoiesis associated with polycythemia rubra vera. Neurol Med Chir. 2002; 42: 40-43.
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There are 71 citations in total.

Details

Primary Language Turkish
Journal Section Research
Authors

Semra Paydaş This is me

Publication Date June 1, 2013
Published in Issue Year 2013 Volume: 38 Issue: 2

Cite

MLA Paydaş, Semra. “Miyeloproliferatif Neoplazilerde Nörolojik Bulgular”. Cukurova Medical Journal, vol. 38, no. 2, 2013, pp. 157-69.