Reduced muscle fiber excitability can explain low CMAP amplitudes in human beings with CIM and in animal models [17], [18], [19]

Reduced muscle fiber excitability can explain low CMAP amplitudes in human beings with CIM and in animal models [17], [18], [19]. mean dCMAP duration was improved in the ulnar nerve and dCMAP duration ideals more frequently reached the cut-offs for demyelination. In S-AIDP nerves, DML was normal or slightly long term, but not reaching the used cut-offs for demyelination, with increased dCMAP period happening eleven occasions more commonly than in C-AIDP. Atenolol Increased dCMAP period is considered a specific marker of demyelination that enhances the level of sensitivity of criteria employed in the electrodiagnosis of AIDP [2], [16]. CMAP is the summation of many MUAPs, and CMAP amplitude, period, and morphology are primarily determined by: (1) the distribution of conduction velocities of individual axons; (2) the distance between stimulating and recording electrodes; (3) the conduction velocity of the muscle mass fibers; (4) phase cancelation between individual MUAPs. Normally the individual MUAP has a bad maximum period of 5C6?ms overlapping that of the negative phase of dCMAP. Indeed, with distal nerve activation most MUAPs arrive at the recording electrodes in phase with each other and the producing CMAP is quite compact because of the restricted range of conduction velocities of axons (around 10?m/sec) and the short distance between the stimulating and recording electrodes. In the nerves of S-AIDP individuals with normal DML and improved dCMAP period at least some large diameter fast materials conduct normally and the improved dCMAP duration could be explained by preferential demyelination of slower conducting nerve materials or by conduction slowing of muscle mass fibers. Interestingly in critical illness myopathy (CIM), besides reduced dCMAP amplitudes, long term dCMAP durations (comparable to those found in S-AIDP nerves with normal or slightly long term DML) have been reported [1], [10], [11]. Reduced muscle mass dietary fiber excitability can clarify low CMAP amplitudes in humans with CIM and in animal models [17], [18], [19]. In an in vitro model, serum from CIM individuals applied to solitary muscle mass materials induced depolarization of resting membrane potential, reduced the action potential rise time, and improved inward sodium current maximum amplitude [7]. In individuals with CIM, mean muscle mass fiber conduction velocity was halved, the conduction velocity percentage between fastest and slowest materials doubled, and an Atenolol inverse relationship between conduction velocity of muscle mass materials and CMAP durations was shown [1]. It can be hypothesized that in CIM associated with sepsis and systemic inflammatory response syndrome, a depolarizing shift of muscle mass membrane potential, probably caused by inflammatory OBSCN cytokines, may induce sodium-channel inactivation, slowing of conduction velocity and even membrane inexcitability, and eventually muscle damage [7], [8]. Some COVID-19 patients present a so-called cytokine storm, an uncontrolled over-production of soluble inflammatory markers which, in turn, sustains an aberrant systemic inflammatory response [13]. In the cohorts reported here, patients with S-AIDP had more frequent respiratory failure and were more frequently admitted to ICU compared to C-AIDP, probably because of summation of the effects of COVID-19 and GBS. Specifically, all 11 patients with normal or slightly prolonged DML and increased dCMAP duration in at least two nerves had pneumonia with respiratory insufficiency and 72.7% were hospitalized in ICU. We hypothesize that in these patients the increased dCMAP duration with normal or slightly prolonged DMLs indicates an additional involvement of muscle fiber excitability, comparable to that described in CIM and likely due to the COVID-19 hyperinflammatory state. If increased dCMAP duration Atenolol is not, as previously thought, specific of demyelination[16] but may also be due to muscle conduction slowing, it is important to establish how much this abnormality might have influenced electrodiagnosis in the S-AIDP group. As a matter of fact in three (12.5%) patients, increased dCMAP duration in at least two nerves was decisive for the diagnosis. When the increased dCMAP durations were excluded, the electrodiagnosis changed in two patients to equivocal: in one patient who had one prolonged F wave and two slow CVs not reaching the demyelinating cut-off; in the other who had one increased p/d CMAP duration. However, in the latter patient, a control study after 17 days Atenolol showed two increased p/d CMAP duration, one prolonged F wave and one slow CV confirming the AIDP diagnosis. The third patient, a 47-year-old man, had severe COVID-19 pneumonia and very high titers of IL6 (6152?pg/ml, normal 3.4) at ICU admission when severe muscle weakness was noted. Five days later, the patient was in a.