Which neurophysiologic findings are characteristic of ethylene-related toxic neuropathy?

Updated: Dec 06, 2017
  • Author: Jonathan S Rutchik, MD, MPH, FACOEM; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS  more...
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  • Neurophysiologic abnormalities in workers exposed to ethylene oxide

    • In 1993, Ohnishi and Murai reviewed polyneuropathy cases caused by EtO. Needle EMG revealed neurogenic changes in 8 of 11 patients. Conduction studies of limb nerves were abnormal in 8 of 10 patients. Relatively mild decreases of motor and sensory NCVs with decreases in the amplitudes of nerve and muscle action potentials indicated axonal degeneration of both motor and sensory nerve fibers. [50]

    • In 1983, Kuzuhara et al reported 2 patients with occupationally induced EtO polyneuropathy and their EMG and NCV results. In one patient, EMG of the limb muscles was normal except for long-duration and high-amplitude units recorded from the triceps. Motor NCVs were relatively well preserved. In the second patient, only an EMG was performed, which revealed denervation patterns in distal limb muscles. [24]

    • Finelli et al reported electrophysiological findings in 3 patients with EtO-induced neuropathy; they demonstrated mild slowing of motor conduction with positive sharp waves and fibrillation potentials on EMG during the active disease state, indicating axonal neuropathy. [25]

      • In patient 1, nerve conduction studies showed no response to stimulation of the left peroneal nerve, slowing of motor conduction over the right peroneal and the right posterior tibial nerves, and absence of the right tibial H reflex and the right sural nerve sensory potential. The EMG showed scattered positive sharp waves and fibrillation potentials with increased polyphasic activity in the intrinsic foot muscles and, to a lesser extent, in the leg muscles. Repeated examinations 5 weeks and 7 months later showed return of normal conduction velocity and disappearance of denervation potentials and the recording of giant potentials as signs of reinnervation. The left H reflex remained suppressed.

      • In patient 2, the EMG initially showed positive sharp-wave fibrillation potentials and small-amplitude motor unit potentials in leg and foot muscles. Follow-up studies showed the disappearance of the denervation potentials and the appearance of giant potentials indicating reinnervation.

      • Patient 3 showed absent potentials from the extensor digitorum brevis muscle on stimulation of the right peroneal nerve. Right tibial conduction was slowed, and the tibial H reflex was absent on the right and delayed on the left. The right sural nerve sensory potential amplitude was normal but delayed. Leg and foot muscle EMG studies showed denervation potentials. Repeat studies 7 months later showed mild slowing and active denervation on EMG with some polyphasic giant potentials.

    • In 1979, Gross et al reported 4 patients with EtO neurotoxicity and results of their nerve conduction studies. One patient had acute CNS symptoms and normal NCV. Another 2 had milder CNS symptoms with symptoms of a generalized sensorimotor polyneuropathy with fibrillations in the intrinsic muscles of the feet and abnormal NCVs (patient 2), and decreased numbers and increased amplitude and duration of motor unit potentials in the distal muscles (patient 3). Patient 4 was asymptomatic. Patients 2, 3, and 4 had decreased amplitudes of motor action potentials, moderately decreased NCVs, and signs of denervation compatible with axonal degeneration as the cause of neuropathy. [21]

    • In 1985, Schroeder et al also reported a case of EtO-induced polyneuropathy. This patient had nerve conduction study findings that showed slowed NCVs; the mean tibial NCV was 26 m/s, with normal amplitudes, 2.5 mV. [23]

    • Fukushima et al reported a 19-year-old patient with 20 days of EtO exposure who had numbness and weakness of his extremities and was noted to have a steppage gait on examination at the time of admission 1 month later. Nerve conduction study findings were abnormal; mean peroneal and tibial NCVs were 37.7 and 37.1 m/s (no normals were included), respectively. No latency potential was demonstrable for the right peroneal nerve. Neurogenic changes were demonstrated on EMG in the anterior tibial muscles. [22]

    • Deschamps et al reported a case of persistent asthma after accidental EtO exposure. They performed EMG and NCVs after an examination of the patient's lower extremities revealed abnormal findings. EMG and NCV findings were normal, but maximum amplitudes of the right and left H reflex responses were reduced significantly (ie, 6% and 2% of the maximum amplitude elicited from the direct response) without a decrease in the proximal conduction velocity. These results suggested axonal neuropathy. [51]

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