Using threshold tracking, differences have been established between large myelinated sensory and α motor axons in humans. Major differences are that sensory axons are relatively depolarised at rest such that they have a greater persistent Na⁺ current, and have greater activity of hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels. Sensory axons may thereby be protected from hyperpolarising stresses, and are less likely to develop conduction block. However, the corollary is that sensory axons are more excitable and more likely to become ectopically active.

Citations

• Strength-duration properties and excitability of motor and sensory axons across different target thresholds
  Yoshimitsu Shimatani, Cindy Shin-Yi Lin, José Manuel Matamala, Matthew C. Kiernan
  Journal of Neurophysiology.2023; 129(6): 1434.     CrossRef
• Does Essential Tremor Alter the Axonal Excitability Properties of Lower Motor Neurons?
  Yerim Kim, Young Eun Kim, Joo Young Lee, Hyeo-Il Ma, Soon Kyung Shim, Sun min Yoon, Jong Seok Bae
  Journal of Clinical Neurophysiology.2022; 39(6): 492.     CrossRef
• Autonomic and Somatic Nerve Functions in Type 2 Diabetes Mellitus Patients: Electrophysiological Aspects
  Anca Motataianu, Laura Barcutean, Zoltan Bajko, Adina Stoian, Smaranda Maier, Septimiu Voidazan, Rodica Balasa
  Diagnostics.2021; 11(11): 2005.     CrossRef
• Simulating perinodal changes observed in immune-mediated neuropathies: impact on conduction in a model of myelinated motor and sensory axons
  Boudewijn T. H. M. Sleutjes, Maria O. Kovalchuk, Naric Durmus, Jan R. Buitenweg, Michel J. A. M. van Putten, Leonard H. van den Berg, Hessel Franssen
  Journal of Neurophysiology.2019; 122(3): 1036.     CrossRef

Multifocal motor neuropathy (MMN) is a chronic immune-mediated peripheral myelinopathy. The major clinical features include slowly progressive, painless, and asymmetric weakness, usually of distal limb muscle. Early in the course of the disease, weakness is not necessarily associated with muscle trophy, owing to the initial primary involvement of peripheral myelin. Chronic progressive weakness is often associated with some degree of concurrent axonal loss and subsequent muscle atrophy. Sensory symptoms are usually mild or absent, and involvement of cranial and respiratory muscles in rare. The findings of multifocal motor conduction block, abnormal temporal dispersion, and focal conduction slowing at segments not at risk for common entrapment or compression injury, associated with normal sensory conduction studies along the same segments, are the hallmark electrophysiologic features of MMN. The slow progression and absence of upper motor neuron signs are the major clinical points that separate MMN from amyotrophic lateral sclerosis. The role of GMI antibodies, found in high titers in 22~84% of MMN patients, remains uncertain. The contention that MMN is an autoimmune disorders is largely based on the often dramatic improvement in symptoms following the administration of intravenous of immunoglobulin or cyclophosphamide.

We present a case with stepwise weakness and sensory involvement of both hands for more than 2 months. His nerve conduction study findings revealed prolonged terminal latencies, decreased motor and sensory conduction velocities and conduction blocks of both ulnar nerves, more severely on left side. And there were other abnormalities manifested with mononeuropathy multiplex. Increased cerebrospinal fluid protein was found. We diagnosed him as Lewis-Sumner syndrome and tried high dose oral steroid therapy for 2 months. He showed improvement of motor functioning with persistent conduction block.

A 33-year-old women developed weakness in all limbs 3 days prior to admission. Motor examination showed decreased strength in all limbs, but sensory examination was normal. Deep tendon reflexes were areflexia. Electrophysiological examination showed conduction blocks with nearly normal conduction velocities and terminal latencies in motor nerves and normal amplitudes and velocities in sensory nerves. Her serum was positive for IgG antibodies to gangliosides GM1, GD1b, and galactocerebroside. Acute motor conduction block neuropathy may be another variant of Guillain-Barre