Neuromuskuläre Komplikationen nach allogener Knochenmarktransplantation

Abstract

Neuromuscular syndromes following allogeneic bone marrow transplantation (BMT), although occasionally described,were not the focus of studies concerning neurologic complications following bone marrow transplantation. In this study,we summarize different polyneuropathy syndromes following BMT and report on patients with myasthenia gravis and inflammatory neuromuscular disorders such as myositis or fasciitis. Concerning the etiology of neuropathies, a neurotoxicity of immunosuppressants,a preexisting disorder due to the underlying disease as well as an association with graft-versus-host disease (GVHD) is discussed.GVHD-associated polyneuropathies as well as muscular complications have been found to occur during the early BMT phase, while myasthenia gravis is a late neurologic complication of GVHD.

Muscle Cramps and Neuropathies in Patients with Allogeneic Hematopoietic Stem Cell Transplantation and Graft-versus-Host Disease

“…Few previous studies used electrodiagnostic tests to identify patients with peripheral nervous system complications. Padovan et al reported that 12 of 58 (21%) patients developed a de novo polyneuropathy after allo-HSCT and 14 (24%) distal muscular atrophy, associated with preceding severe acute GVHD, metabolic disturbances and prolonged immunosuppression [34]. In our study only two patients had a demyelinating pattern of neuropathy.…”

“…Often, they manifest as GBS- or CIDP-like disease (reviewed in [6], [7]), or as mild progressive neuropathy [16], [34]. The close temporal relationship with the occurrence of GVHD and improvement upon immunosuppression in some patients suggest that neuropathies indeed are part of GVHD.…”

Hemosiderin deposits in chronic graft‐vs.‐host disease related myopathy

“…It is often a great challenge to differentiate the muscular weakness of GVHD‐associated myositis or myopathy from that of steroid myopathy and peripheral neuropathy, particularly in patients presenting with a normal CK level and no lymphocytic infiltration in the muscle biopsy. Peripheral neuropathy and steroid myopathy are frequently induced in SCT patients by neurotoxic drugs like corticosteroids, cyclosporine, tacrolimus and thalidomide (10, 21).…”

“…Phenotyping experiments confirmed that donor oligoclonal T cells caused this inflammatory process resembling autoimmune polymyositis (8, 9). However, a few patients with cGVHD‐related myopathy have a normal CK, lack significant lymphocytic infiltration in the muscle biopsy and rarely respond to immunosuppressive drugs (6, 10).…”

“…cGVHD‐associated polymyositis or myopathy usually occurs 2–5 yr after SCT and is typically pronounced in the proximal lower limb (4, 6, 11–13). The majority of the patients show cGVHD‐involvement of organ systems other than the skeletal muscles (6, 14–16), but it seems that polymyositis or myopathy may occur as a unique manifestation of cGVHD (10, 17). Possible risk factors for developing polymyositis as a manifestation of cGVHD include aplastic anemia, certain recipient human leukocyte antigen (HLA)‐types like HLA DR52, and a female donor.…”