Brain Advance Access originally published online on August 10, 2006
Brain 2006 129(9):2461-2470; doi:10.1093/brain/awl191
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Nerve excitability changes in critical illness polyneuropathy
1 Sobell Department of Neurophysiology, Institute of Neurology London, UK 2 Department of Clinical Neurophysiology, National Hospital for Neurology and Neurosurgery London, UK 3 Department of Neurology, St Thomas' Hospital London, UK 4 Intensive Care, St Thomas' Hospital London, UK 5 Department of Neurology, Inselspital University of Berne, Berne, Switzerland
Correspondence to: Prof. H. Bostock, Sobell Department of Neurophysiology, Institute of Neurology, Queen Square, London WC1N 3G, UK E-mail: h.bostock{at}ion.ucl.ac.uk
Patients in intensive care units frequently suffer muscle weakness and atrophy due to critical illness polyneuropathy (CIP), an axonal neuropathy associated with systemic inflammatory response syndrome and multiple organ failure. CIP is a frequent and serious complication of intensive care that delays weaning from mechanical ventilation and increases mortality. The pathogenesis of CIP is not well understood and no specific therapy is available. The aim of this project was to use nerve excitability testing to investigate the changes in axonal membrane properties occurring in CIP. Ten patients (aged 37–76 years; 7 males, 3 females) were studied with electrophysiologically proven CIP. The median nerve was stimulated at the wrist and compound action potentials were recorded from abductor pollicis brevis muscle. Strength–duration time constant, threshold electrotonus, current–threshold relationship and recovery cycle (refractoriness, superexcitability and late subexcitability) were recorded using a recently described protocol. In eight patients a follow-up investigation was performed. All patients underwent clinical examination and laboratory investigations. Compared with age-matched normal controls (20 subjects; aged 38–79 years; 7 males, 13 females), CIP patients exhibited reduced superexcitability at 7 ms, from –22.3 ± 1.6% to –7.6 ± 3.1% (mean ± SE, P 
0.0001) and increased accommodation to depolarizing (P < 0.01) and hyperpolarizing currents (P < 0.01), indicating membrane depolarization. Superexcitability was reduced both in patients with renal failure and without renal failure. In the former, superexcitability correlated with serum potassium (R = 0.88), and late subexcitability was also reduced (as also occurs owing to hyperkalaemia in patients with chronic renal failure). In patients without renal failure, late subexcitability was normal, and the signs of membrane depolarization correlated with raised serum bicarbonate and base excess, indicating compensated respiratory acidosis. It is inferred that motor axons in these CIP patients are depolarized, in part because of raised extracellular potassium, and in part because of hypoperfusion. The chronic membrane depolarization may contribute to the development of neuropathy.
Key Words: axonal excitability; intensive care; membrane potential
Abbreviations: BE, base excess; CIP, critical illness polyneuropathy; CMAP, compound muscle action potential; Er, resting potential; Ek, potassium equilibrium potential; SNAP, sensory nerve action potential
Received January 10, 2006. Revised June 15, 2006. Accepted June 17, 2006.
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