Anti-Myelin Associated Glycoprotein (anti-MAG) neurological involvement classically manifests as a peripheral neuropathy with prominent sensitive symptoms. We describe a case report of a patient with positive anti-MAG antibodies presenting with clinical and neurophysiological evidence of spinal cord impairment. A 69-year-old woman came to our attention with subacute onset of dysesthesias at lower limbs and ataxia. Blood routine tests and hematological work-up led to a diagnosis of monoclonal gammopathy of undetermined significance. High titers of anti-MAG antibodies was revealed (34,594.70 BTU/mL, normal range 0-1000). Nerve conduction studies (NCS) ruled out a polyneuropathy at lower limbs. Somatosensory evoked potentials (SSEPs) showed prolonged central conduction time (CTT) at lower limbs, suggesting a dorsal column damage. Brain and spinal cord Magnetic Resonance Imaging (MRI) did not reveal any significant lesion. Analysis of cerebrospinal fluid (CSF) evidenced an albumin-cytologic dissociation. She was treated with corticosteroids with temporary remission of sensory symptoms and normalization of CTT. Subsequently, she developed a multineuropathy which was successfully treated with Rituximab. We discuss the potential role of anti-MAG antibodies in the pathophysiology of dorsal column impairment and the clinical usefulness of SSEPs in monitoring the evolution of anti-MAG neuropathy.

Spinal cord impairment in anti-Mag neuropathy: evidence from somatosensory evoked potentials

Boscarino M;Tombini M;Di Lazzaro V;Assenza G
2020-01-01

Abstract

Anti-Myelin Associated Glycoprotein (anti-MAG) neurological involvement classically manifests as a peripheral neuropathy with prominent sensitive symptoms. We describe a case report of a patient with positive anti-MAG antibodies presenting with clinical and neurophysiological evidence of spinal cord impairment. A 69-year-old woman came to our attention with subacute onset of dysesthesias at lower limbs and ataxia. Blood routine tests and hematological work-up led to a diagnosis of monoclonal gammopathy of undetermined significance. High titers of anti-MAG antibodies was revealed (34,594.70 BTU/mL, normal range 0-1000). Nerve conduction studies (NCS) ruled out a polyneuropathy at lower limbs. Somatosensory evoked potentials (SSEPs) showed prolonged central conduction time (CTT) at lower limbs, suggesting a dorsal column damage. Brain and spinal cord Magnetic Resonance Imaging (MRI) did not reveal any significant lesion. Analysis of cerebrospinal fluid (CSF) evidenced an albumin-cytologic dissociation. She was treated with corticosteroids with temporary remission of sensory symptoms and normalization of CTT. Subsequently, she developed a multineuropathy which was successfully treated with Rituximab. We discuss the potential role of anti-MAG antibodies in the pathophysiology of dorsal column impairment and the clinical usefulness of SSEPs in monitoring the evolution of anti-MAG neuropathy.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12610/4658
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