TY - JOUR
T1 - Clinical and serological features of acute sensory ataxic neuropathy with antiganglioside antibodies
AU - Rojas-García, Ricard
AU - Querol, Luis
AU - Gallardo, Eduard
AU - Salva, Noemi De Luna
AU - Juarez, Cándido
AU - Garces, Mercedes
AU - Fages, Eva
AU - Casasnovas, Carlos
AU - Illa, Isabel
PY - 2012/6/1
Y1 - 2012/6/1
N2 - There is as yet no consensus for considering pure acute sensory ataxic neuropathy (ASAN) as a variant of Guillain-Barré syndrome (GBS). Reactivity against gangliosides sharing disialosyl epitopes has been reported in these patients. The aim of this study was to determine the spectrum of reactivity against gangliosides in ASAN and to define the clinical pattern. From our database we identified patientswith suspicion of ASAN. We defined ASAN as the presence of ataxia of peripheral origin with loss of proprioception, and areflexia, absence of ophthalmoplegia and no or minimal muscle weakness. Patients who met these criteria were retrospectively reviewed for their spectrum of reactivity against gangliosides and clinical features. We identified 12 patients fulfilling pre-defined criteria for ASAN. Reactivity against gangliosides containing disialosyl epitopes was present in seven patients. Concomitant reactivity against other gangliosides was present in 6/7 patients. All patients presented good prognosis and an antecedent illness was present in nine. Our results support the previously described clinico-immunological association between ASAN and disialosyl specificity, and widen the spectrum of reactivity against gangliosides. The acute presentation with a monophasic course, and good prognosis in all cases, together with transient immunoglobulin G antiganglioside antibodies and infectious antecedent in 7/12 patients support the inclusion of ASAN as a GBS variant. © 2012 Peripheral Nerve Society.
AB - There is as yet no consensus for considering pure acute sensory ataxic neuropathy (ASAN) as a variant of Guillain-Barré syndrome (GBS). Reactivity against gangliosides sharing disialosyl epitopes has been reported in these patients. The aim of this study was to determine the spectrum of reactivity against gangliosides in ASAN and to define the clinical pattern. From our database we identified patientswith suspicion of ASAN. We defined ASAN as the presence of ataxia of peripheral origin with loss of proprioception, and areflexia, absence of ophthalmoplegia and no or minimal muscle weakness. Patients who met these criteria were retrospectively reviewed for their spectrum of reactivity against gangliosides and clinical features. We identified 12 patients fulfilling pre-defined criteria for ASAN. Reactivity against gangliosides containing disialosyl epitopes was present in seven patients. Concomitant reactivity against other gangliosides was present in 6/7 patients. All patients presented good prognosis and an antecedent illness was present in nine. Our results support the previously described clinico-immunological association between ASAN and disialosyl specificity, and widen the spectrum of reactivity against gangliosides. The acute presentation with a monophasic course, and good prognosis in all cases, together with transient immunoglobulin G antiganglioside antibodies and infectious antecedent in 7/12 patients support the inclusion of ASAN as a GBS variant. © 2012 Peripheral Nerve Society.
KW - Acute sensory ataxic neuropathy
KW - Antiganglioside antibodies
KW - Disialosyl
KW - Guillain-Barré syndrome
U2 - 10.1111/j.1529-8027.2012.00407.x
DO - 10.1111/j.1529-8027.2012.00407.x
M3 - Article
VL - 17
SP - 158
EP - 168
JO - Journal of the Peripheral Nervous System
JF - Journal of the Peripheral Nervous System
SN - 1085-9489
IS - 2
ER -