Publication Information: Klinisk neurofysiologi
Karolinska Inst, Sect Clin Neurophysiol, Dept Clin Neurosci, S-17177 Stockholm, Sweden.
Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden.
Karolinska Inst, Dept Clin Neurosci, Sect Neurosurg, S-17177 Stockholm, Sweden.
Karolinska Univ Hosp, Dept Pathol, S-17164 Stockholm, Sweden.
Karolinska Inst, Sect Clin Neurophysiol, Dept Clin Neurosci, S-17177 Stockholm, Sweden.;Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden.;Penn State Univ, Dept Biobehav Hlth, University Pk, PA 16802 USA.
MDPI
Abstract: Introduction. The acquired muscle paralysis associated with modern critical care can be of neurogenic or myogenic origin, yet the distinction between these origins is hampered by the precision of current diagnostic methods. This has resulted in the pooling of all acquired muscle paralyses, independent of their origin, into the term Intensive Care Unit Acquired Muscle Weakness (ICUAW). This is unfortunate since the acquired neuropathy (critical illness polyneuropathy, CIP) has a slower recovery than the myopathy (critical illness myopathy, CIM); therapies need to target underlying mechanisms and every patient deserves as accurate a diagnosis as possible. This study aims at evaluating different diagnostic methods in the diagnosis of CIP and CIM in critically ill, immobilized and mechanically ventilated intensive care unit (ICU) patients. Methods. ICU patients with acquired quadriplegia in response to critical care were included in the study. A total of 142 patients were examined with routine electrophysiological methods, together with biochemical analyses of myosin:actin (M:A) ratios of muscle biopsies. In addition, comparisons of evoked electromyographic (EMG) responses in direct vs. indirect muscle stimulation and histopathological analyses of muscle biopsies were performed in a subset of the patients. Results. ICU patients with quadriplegia were stratified into five groups based on the hallmark of CIM, i.e., preferential myosin loss (myosin:actin ratio, M:A) and classified as severe (M:A < 0.5; n = 12), moderate (0.5 <= M:A < 1; n = 40), mildly moderate (1 <= M:A < 1.5; n = 49), mild (1.5 <= M:A < 1.7; n = 24) and normal (1.7 <= M:A; n = 19). Identical M:A ratios were obtained in the small (4-15 mg) muscle samples, using a disposable semiautomatic microbiopsy needle instrument, and the larger (>80 mg) samples, obtained with a conchotome instrument. Compound muscle action potential (CMAP) duration was increased and amplitude decreased in patients with preferential myosin loss, but ...
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