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Evaluation of diaphragmatic electromyography of cervical spinal cord hemi section in rat model


Samah Fouad
Basem Awad
Awad Rizk
Shaymaa Rezk
Esam Mosbah

Abstract

Objective: Estimation the degree of induced hemisection damage of the cervical segments of the two separately diaphragmatic pillars in rat model using Electromyography (EMG).


Design: Prospective controlled study.


Animals: Sixteen Sprague dawely rats were divided into 2 groups


Procedures: Cervical hemi lateral cord section below the cervical dorsal root number 2 was induced with micro scalpel. After 28 days post-injury, EMG record was done at the two diaphragmatic crural regions, followed by histopathological and immunohistochemical examinations.


Results: There was significant decrease in mean integrated EMG activity of LT diaphragmatic muscles than RT one in the hemi sectioned group P<0.05. Moreover, there was a significant decrease (P<0.05) in the integrated traces (mv) for peak burst area of LT diaphragmatic muscles activity. On histopathological examination, affected neurons of hemi-sectioned group appeared shrunken with chromatolysis, others were completely lost and replaced by cavities. The neutrophil adjacent to the necrotic neurons lost its homogeneous appearance and appeared vacuolated or edematous with significant decrease in the number of viable motor neurons compared to the control group (P < 0.05). On other hand, the astrocytosis become more evident and the number of astrocytes was significantly increased (P < 0.05). The surrounding white matter exhibited severs degeneration and demyelination. Glial fibrillary acidic protein (GFAP) immune expression for hemi-sectioned group was significantly increased than control group (P < 0.05)


Conclusion and clinical relevance: Parallel impairment of the diaphragmatic EMG occurred to the decrease in the number of viable motor neurons of the anterior horn of the cervical segment below the level of the cervical hemisection together with the disintegration of Nissl bodies and the developed astrocytosis.


Journal Identifiers


eISSN: 2682-2512
print ISSN: 1110-7219