Paraneoplastic Cerebellar Degeneration Medication

Updated: Jul 01, 2020
  • Author: Erika Lan, DO, MA; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
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Medication

Medication Summary

There is no specific medication approved for treatment of paraneoplastic cerebellar degeneration. Treatment is mainly directed at the underlying malignancy. However, immunotherapy may also be tried, such as the medications listed below. These may also be used in combination with plasmapheresis. 

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Immune Globulins

Class Summary

IVIg is a purified preparation of gamma globulin. It is derived from large pools of human plasma and is composed of 4 subclasses of antibodies, approximating the distribution of human serum.

Immune globulin IV (IVIG, Octagam, Gammagard, Bivigam)

Intravenous immune globulin neutralizes circulating myelin antibodies through anti-idiotypic antibodies. It downregulates proinflammatory cytokines (eg, interferon gamma), blocks Fc receptors on macrophages, suppresses inducer T and B cells, and augments suppressor T cells. IVIg also blocks the complement cascade and promotes remyelination. In addition, it may increase IgG in cerebrospinal fluid.

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Antineoplastics, Anti-CD20 Monoclonal Antibodies

Class Summary

Monoclonal antibodies are used to bind to specific antigens, thereby stimulating the immune system to target these antigens.

Rituximab (Rituxan, Rituximab-abbs, Truxima)

Rituximab is a monoclonal antibody directed against the CD20 antigen on B-lymphocytes. It is recommended as second-line therapy in immune tolerance induction regimens for patients with FVIII inhibitors, especially those with high inhibitor titers. This agent binds to, and mediates destruction of, B-cells, thereby decreasing production of FVIII inhibitors and autoimmunization.

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Corticosteroids

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli and inhibit the synthesis of tumor necrosis factor (TNF)-alpha, interleukin-2 (IL-2), IL-6, and interferon (IFN)-gamma. In addition, glucocorticoids modulate serum and leukocyte-bound levels of cell adhesion molecules.

Methylprednisolone (Solu-Medrol, Depo-Medrol, Medrol)

Methylprednisolone decreases inflammation by suppressing migration of PMNs and reversing increased capillary permeability. This agent is slightly more potent than prednisone; 4 mg of methylprednisolone is equivalent to 5 mg of prednisone.

Prednisolone (Orapred ODT, Millipred, Millipred DP)

Prednisolone decreases inflammation by suppressing migration of PMNs and reducing capillary permeability.

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Antineoplastics, Alkylating

Class Summary

Cancer chemotherapy is based on an understanding of tumor cell growth and on how drugs affect this growth. After cells divide, they enter a period of growth (G1 phase), followed by DNA synthesis (S phase). The next phase is a premitotic phase (G2 phase), then finally a phase mitotic cell division (M phase).

Rates of cell division vary for different tumors. Most common cancers grow slowly compared with normal tissues, and the rate may decrease further in large tumors. This difference allows normal cells to recover from chemotherapy more quickly than malignant ones. This is partly the rationale for current cyclic dosage schedules.

Cyclophosphamide

Exerts its cytotoxic effect by alkylation of DNA, which leads to interstrand and intrastrand DNA crosslinks, DNA-protein crosslinks, and inhibition of DNA replication.

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