The　early　clinical　features　of　nitrous　oxide　(N2O)-induced　neuropathy　were　mimicking　that　of　Guillain-Barre　syndrome　(GBS).　We　aimed　to　explore　clinical　and　laboratory　characteristics　of　N2O-induced　neuropathy　in　comparison　with　GBS.　We　retrospectively　reviewed　data　of　15　patients　with　N2O-induced　neuropathy　and　compared　them　with　15　GBS　patients.　The　age　of　the　N2O-induced　neuropathy　group　was　significantly　younger　than　that　in　the　GBS　group　(22　+/-　5　vs　45　+/-　17).　Paresthesia　was　more　common　in　N2O-induced　neuropathy　group　(100%　vs　53.3%).　The　proportion　of　distal　upper　limbs　weakness　was　lower　than　that　in　GBS　group　(20.0%　vs　93.3%).　There　was　no　significant　difference　in　the　distal　weakness　of　the　lower　limbs　(100%　vs　80.0%).　The　incidence　of　motor　conduction　block　and　compound　muscle　action　potential　amplitude　reduction　in　upper　limbs　was　lower　than　that　in　GBS　group　(6.7%　vs　60.0%;　26.7%　vs　80.0%).　The　sensory　nerve　action　potential　amplitude　drop　in　the　lower　limbs　was　more　severe　than　that　in　GBS　group　(53.3%　vs　0).　The　increase　of　Mean　corpuscular　volume　(MCV)　was　more　pronounced　compared　to　GBS　group　(96.97　+/-　6.00　vs　88.55　+/-　5.41).　High　homocysteine　levels　were　more　common　in　N2O-related　group　[29.80(11.60,　70.50)　vs　14.35(9.22,　19.30)].　Typical　clinical　features　of　the　acute　N2O　neuropathy　appears　to　be　a　myeloneuropathy,　affecting　the　lower　limbs　more　than　the　upper　limbs,　mixed　axonal-demyelinating　electrophysiological　performance,　higher　homocysteine　level,　and　larger　MCV　and　common　posterior　spinal　cord　involvement　in　cervical　segment.