Guillain-Barre Syndrome Complicating Multiple Myeloma
Authors: Iqbal Afsheen N , Le Quan , Motiwala Rajeev , Clay Leila J , Motiwala Tej , Lendvai Nikoletta , Siegel David S. , Goldberg Stuart L 
Published: April 2020

Abstract
Background: Although neuropathies complicating multiple myeloma (MM) are common as a result of medications and spinal cord compression, neuropathy as a consequence of cross reactivity between the paraprotein and neural tissues is rare. In CANOMAD syndrome (chronic ataxic neuropathy, ophthalmoplegia, M-protein, agglutination, anti-disialosyl antibodies) IgM paraproteins with shared reactivity between Campylocacter jejuni lipopolysaccharides and human peripheral nerve disialylated gangliosides including GQ1b have been described. In POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin changes) cerebral spinal fluid concentrations of vascular endothelial growth factor (VEGF) may be markedly elevated, similar to other inflammatory polyneuropathies. Guillain-Barre syndrome (GBS) is an acute inflammatory demyelinating polyradiculopathy yielding flaccid areflexic paralysis that, to our knowledge, has only been reported once as a complication of MM.
Case reports: At Hackensack University Medical Center we have observed 5 cases of GBS complicating MM since 2002 (approximate incidence &lt;0.5%). Details are described below. In all five cases, blood and cerebrospinal fluid cultures, anti-GQb1, anti-GM1, and anti-MAG antibodies were negative and radiographic imaging including computerized axial tomographic scan (CT) of the head and magnetic resonance imaging (MRI) of the brain were unrevealing. In four patients cerebrospinal fluid examination showed albumin/cytologic dissociation.
Conclusions: Our observation represents the first series of patients with GBS complicating MM, and suggests that GBS, although rare, should be considered as part of the neurologic complications of plasma cell dyscrasias.
Case Age Sex Type of Myeloma MM Therapy Presenting symptoms 1 68 M IIIB IgD lambda VAD, Mel 200 PBSC, month 9, recurring CN VI palsy, areflexia upper extremities, hyporeflexia lower extremities, paresthesias feet & side face 2 63 M IIIA IgA kappa Dex-Thal, Mel 200 PBSC, week 2 Parasthesias hands, legs, and feet. Motor weakness lower extremities ascending. 3 68 M IIIA IgG kappa Dex-Thal, CDEP, Mel 200 PSCT, wk 3 Bilateral facial, sternocleidomastoid, neck muscle weakness with sluggish gag reflex. Upper and lower muscles weak and hyporeflexic. 4 81 F III A IgA kappa + urine Dex-Lenolidomide Lower extremity weakness, with areflexia and severely ataxic gait. Sensory defects in LE. 5 25 M IgA lambda plasma-cytomas None (GBS presenting feature) Marked LE weakness CSF protein Motor Nerve Conductions Sensory Nerve Conductions Treatment & Response 1 126 mg/dl Prolonged median F wave latency Prolonged DSL superficial peroneal Plasmapheresis, dex, thalidomide (improved) 2 77 mg/dl Severely prolonged DML, Reduced CMAP amplitudes, Slow CV, Conduction block Absent SNAPs Plasmapheresis (no response), IVIG (improved) 3 76 mg/dl Prolonged F wave latencies, Slow CV, Reduced CMAP amplitudes Absent SNAPs IVIG (minimal response), plasmapheresis (slow improvement) 4 202 mg/dl Prolonged distal motor latencies, Reduced amplitudes of CMAPS in lower extremities, Prolonged F wave latencies, Slow CV in lower extremities Absent or reduced amplitudes of SNAPs IVIG (no response), plamapheresis (improved) 5 59 mg/dl Prolonged DML, Prolonged F wave latencies or absent F waves, Mild slowing CV, Mild reduction of CMAP amplitudes Normal IVIG and plasmapheresis (no response, paraplegia), Mel 200 PBSC X2 (improved)