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ANTI‐SULFATIDE IgM ANTIBODIES DETECTED IN A PATIENT DIAGNOSIS OF MOTOR NEURON DISEASE
Publication year - 2002
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1046/j.1529-8027.2002.7011_14.x
Subject(s) - medicine , fasciculation , motor neuron , multifocal motor neuropathy , pathology , anesthesia , disease , electroencephalography , mismatch negativity , psychiatry
D'Avino C., Del Corona A., Bacci A., Calabrese R., Siciliano G. Department of Neuroscience‐Clinical Neurology‐University of Pisa‐Italy Case report. The patient, a 66‐year‐old man with a 5‐year diagnosis of diabetes mellitus, in Sep. 2000 started complaining of language disturbances as rhinolalia. In Jan. 2001, because of generalized fatigue and difficulties in walking, he was hospitalized in Internal Medicine and a diagnosis of diabetic angiopathy and neuropathy was made. Since discharge patient clinical conditions gradually deteriorated and a neurological evaluation showed tongue atrophy, dysarthria, dysphagia, fasciculations in the four limbs, increased deep tendon reflexes with bilateral foot clonus and paraparetic spastic deambulation. He underwent spinal MRI that showed mild arthrosic abnormalities in cervical spinal cord and limb EMG that showed denervation spontaneous activity with neurogenic MUAP modifications, with normal sensory and motor conduction velocity. MEP showed bilateral pyramidal track involvement. A significantly increased anti‐sulphatide IgM antibodies titer (1:32,000) in the serum was detected. The diagnosis at discharge was “probable motor neuron disease” and the patient is under riluzole therapy at the moment. Discussion. Anti‐sulfatide IgM antibodies are currently associated with several subtypes of peripheral neuropathy. In most cases it is a chronic dysimmune sensory or sensorimotor neuropathy in which electrophysiological and morphological studies are usually con‐ sistent with a predominant demyelination frequently associated with prominent axonal loss. Although rare, an association between motor neuron disease and IgM anti‐sulfatide has been described in a recent paper by Latov and coworkers that reviewed electrophysiologic, morphologic and laboratory data of 25 patients with elevated antisulfatide antibodies. It seems interesting to follow‐up the clinical course of the patient, the response to therapy and its correlation to antibodies titer, while the opportunity of high dose IVIg therapy is under discussion at the moment.