Temperature effects on accommodative processes in simulated amyotrophic lateral sclerosis in the physiological range.

The present study investigates the temperature dependence of electrotonic potentials in mathematically-simulated myelinated axons with one of three increasingly-severe type of amyotrophic lateral sclerosis (ALS) pathology, termed as ALS1, ALS2 and ALS3, respectively, in the physiological range (30-37∘C). These potentials were elicited by long-lasting (100 ms) subthreshold polarizing current stimuli (±40% of the threshold). Numerical solutions were computed using our temperature-dependent multi-layered model.

Theoretical predication of temperature effects on accommodative processes in simulated amyotrophic lateral sclerosis during hypothermia and hyperthermia.

Electrotonic potentials allow the accommodative processes to long-lasting subthreshold polarizing stimuli to be assessed. The present study investigates such potentials in previously simulated cases of amyotrophic lateral sclerosis, termed as ALS1, ALS2 and ALS3, respectively, when the temperature is changed during hypothermia ([Formula: see text]C) and hyperthermia ([Formula: see text]C). The ALS cases are modeled as three progressively severe uniform axonal dysfunctions along the human motor nerve fiber which is simulated by our temperature-dependent multi-layered numerical model.

Theoretical predication of temperature effect on conducting processes in simulated amyotrophic lateral sclerosis at 20-40[Formula: see text]C.

The present study investigates action potential abnormalities in previously simulated cases of amyotrophic lateral sclerosis, termed as ALS1, ALS2 and ALS3, respectively, when the temperature is changed from 20[Formula: see text]C to 42[Formula: see text]C. These ALS cases are modeled as three progressively severe axonal abnormalities. The effects of temperature on the kinetics of currents, defining action potentials in the normal and abnormal cases, are also given and discussed.

Electrotonic potentials in simulated chronic inflammatory demyelinating polyneuropathy at 20°C-42°C.

Threshold electrotonus changes have been studied following warming to 37°C and cooling to 25°C in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). To extend the tracking of these changes also during hypothermia (≤ 25°C) and hyperthermia (≥ 40°C), and to explain their mechanisms, we investigate the effects of temperature (from 20°C to 42°C) on polarizing nodal and internodal electrotonic potentials and their current kinetics in previously simulated case of 70% CIDP. The computations use our temperature-dependent multi-layered model of the myelinated human motor nerve fiber.

Conducting processes in simulated chronic inflammatory demyelinating polyneuropathy at 20°C-42°C.

Decreased conducting processes leading usually to conduction block and increased weakness of limbs during cold (cold paresis) or warmth (heat paresis) have been reported in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). To explore the mechanisms of these symptoms, the effects of temperature (from 20°C to 42°C) on nodal action potentials and their current kinetics in previously simulated case of 70% CIDP are investigated, using our temperature dependent multi-layered model of the myelinated human motor nerve fiber. The results show that potential amplitudes have a bifid form at 20°C.