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Absence of secondary phrenic motoneuron (PhMN) loss following lateralized cervical contusion
Author(s) -
Little Lydia Nicole,
Hussey Shaunn,
GonzalezRothi Elisa J,
Mercier Lynne M,
Sanchez Deevee,
Osteen Barbara,
Fuller David,
Lane Michael,
Reier Paul
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb48
Subject(s) - medicine , diaphragm (acoustics) , hypercapnia , phrenic nerve , anesthesia , spinal cord injury , spinal cord , respiratory system , ventilation (architecture) , neuroprotection , peripheral , mechanical engineering , physics , psychiatry , acoustics , loudspeaker , engineering
Cervical spinal cord injuries (cSCI) are often accompanied by respiratory complications, due to compromised integrity of the phrenic nucleus (C3–C5/6) and loss of diaphragm function. This study utilized a lateralized C3/4 contusion to characterize temporal changes in diaphragm activity (EMG) and ventilatory function following cSCI, pairing EMG recordings with whole‐body plethysmography. A second goal was to determine secondary PhMN loss to guide future neuroprotective strategies. Initial studies demonstrated diaphragm electromyographic (diaEMG) activity was immediately and markedly reduced, but showed recovery under baseline conditions within 2 days post‐injury. In contrast, diaEMG was persistently attenuated during hypercapnia. Conversely, ventilation was unaffected at baseline and only transiently affected by hypercapnic challenge. Other preliminary results indicate 63% initial loss of PhMNs after injury without evidence of further loss at 4 weeks post‐injury. This suggests persistence of normal ventilatory patterns most likely reflects compensatory plasticity in other spinal respiratory circuits. The absence of secondary PhMN loss challenges the concept of neuroprotection at least in this motor system. Whether impaired diaphragm activity is due to primary PhMN loss, reduced innervation of PhMNs caudal to the injury, or loss of other phrenic circuit constituents remains unknown.