Transcranial magnetic stimulation study of expiratory muscle weakness in acute ischemic stroke

Abstract

Expiratory muscle weakness due to cerebral infarction may contribute to reduced airway clearance in stroke patients. Transcranial magnetic stimulation (TMS) at the vertex and over each hemisphere and magnetic stimulation over the T(10-11) spinal roots (Tw T(10)) and the phrenic nerves bilaterally (BAMPS) were performed in 15 acute ischemic stroke patients (age 68.9 +/- 9.8 years) and 16 matched controls. Surface electrodes recorded motor evoked potentials (MEPs) in the rectus abdominis (RA) and external oblique (EO) muscles bilaterally. Respiratory muscle function was assessed by measuring maximum static expiratory pressure (PE(max)) and changes in intragastric (P(gas)) and transdiaphragmatic (P(di)) pressure after voluntary cough, TMS, TwT(10), and BAMPS. Regression models were used to assess determinants of peak voluntary cough flow rates (PCFR). PCFR, cough P(gas), and vertex TMS P(gas) were decreased in stroke patients compared with controls (203.6 +/- 151.1 vs 350.8 +/- 111.7 L/min, p = 0.004; 72.7 +/- 64.5 vs 163.4 +/- 55.8 cm H(2)O, p = 0.0003 and 8.7 +/- 3.3 vs 16.7 +/- 11.5 cm H(2)O, p = 0.023, respectively). There were no differences in TwT(10) P(gas) (25.2 +/- 7.8 vs 29.4 +/- 12.4 cm H(2)O, p = 0.153) or BAMPS P(di) (21.6 +/- 7.2 vs 19.2 +/- 3.4 cm H(2)O, p = 0.163). TMS P(gas) was lower (4.1 +/- 2.8 vs 6.1 +/- 1.9 cm H(2)O, p = 0.023) following TMS of the injured compared with the uninjured hemisphere in stroke patients. Age and gender adjusted PCFR correlated with P(gas) (r = 0.51, p = 0.009) and PE(max) (r = 0.46, p = 0.024). Stroke was an independent determinant of PCFR after adjusting for P(gas) and PE(max) (p = 0.031). Ischemic cortical injury is associated with expiratory muscle weakness and may contribute to cough impairment in stroke patients.