Focal brain ischemia in mice does not cause electrophysiological signs of critical illness neuropathy

Methods

Focal brain ischemia was induced in adult male C57Bl/6 mice by a 60-minute MCAo followed by reperfusion. Nerve conduction function was measured in the ipsilateral sciatic nerve and muscle potentials were recorded in the ipsilateral gastrocnemius and quadriceps muscle with standard electroneurography/-myography on days 10, 22 and 44 after stroke. An additional crush-injury to the sciatic nerve was included in two sham-operated mice as internal positive control.

Results: MCAo/ reperfusion induced functional deficits with a maximum Bederson score of 2 on day 3 and marked hemispheric brain atrophy of -27 % in histological analysis. No significant difference in large-fiber conduction function was found between MCAo and sham-operated animals, nor was there an increase in spontaneous electromyographic activity in muscles of animals in the MCAo group. In contrast, sham-operated mice with an additional crush injury of the sciatic nerve (sham+) developed marked abnormalities: reduction of the compound motor action potential amplitudes (CMAP) and motor conduction velocities (MCV) in combination with pathologic spontaneous activity (PSA), all of which had largely recovered by day 44.

Conclusion: Mice showed no signs of systemic peripheral nerve dysfunction or axonal degeneration typical for a CIP-like phenotype after 60 min MCAo/ reperfusion.