Focal brain ischemia in mice does not cause electrophysiological signs of critical illness neuropathy
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RESEARCH NOTE
Focal brain ischemia in mice does not cause electrophysiological signs of critical illness neuropathy Petra Huehnchen1,2,3* , Klaus Viktor Toyka4, Karen Gertz1,5, Matthias Endres1,2,3,5,6,7† and Wolfgang Boehmerle1,2,3†
Abstract Objective: Critical illness polyneuropathy (CIP) is a common complication of severe systemic illness treated in intensive care medicine. Ischemic stroke leads to an acute critical injury of the brain with hemiparesis, immunosuppression and subsequent infections, all of which require extended medical treatment. Stroke-induced sarcopenia further contributes to poor rehabilitation and is characterized by muscle wasting and denervation in the paralytic, but also the unaffected limbs. Therefore, we asked whether stroke leads to an additional CIP-like neurodegeneration. Results: Focal brain ischemia was induced in adult mice by 60-min middle cerebral artery occlusion (MCAo) following reperfusion and led to functional deficits and marked hemispheric brain atrophy. Nerve conduction function and muscle potentials were measured in the ipsilateral sciatic nerve and gastrocnemius and quadriceps muscle with electroneurography/-myography on days 10, 22, 44 after stroke. An additional crush-injury to the sciatic nerve was included in two sham mice as positive control (sham +). We found no differences in nerve conduction function nor spontaneous electromyographic activity between MCAo and sham animals. Sham + mice developed marked reduction of the motor action potential amplitudes and conduction velocities with pathologic spontaneous activity. In conclusion, we found no peripheral nerve dysfunction/degeneration as signs of a CIP-like phenotype after MCAo. Keywords: Stroke, Axonal degeneration, Electromyography, Critical illness, Mice Introduction Critical illness polyneuropathy (CIP) is a frequent and severe neurological complication of intensive care treatment with up to one-third of critically ill patients being affected in clinical assessment (reviewed by [1]). CIP is characterized electrophysiologically by a decrease in the amplitudes of the compound motor nerve action *Correspondence: [email protected] † Matthias Endres and Wolfgang Boehmerle contributed equally to the present manuscript 1 Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Klinik und Hochschulambulanz für Neurologie, 10117 Berlin, Germany Full list of author information is available at the end of the article
potentials (CMAP) and sensory nerve action potentials (SNAP) while motor and sensory nerve conduction velocities (MCV, SCV) are only mildly altered [2]. Electromyography (EMG) shows fibrillations and positive sharp waves (PSW) as indicators of axonal degeneration. The underlying pathomechanisms of CIP remain largely elusive, but are multifactorial including abnormal microcirculation, hyperglycemia, mitochondrial dysfunction and inactivation of sodium channels. A catabolic stat
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