HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Harraf, F. Articles by Kalra, L. Search for Related Content PubMed Articles by Harraf, F. Articles by Kalra, L. Related Collections Medical care All Cerebrovascular disease/Stroke TMS Motor Control Motor cortex

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

From the Departments of Stroke Medicine (F.H., K.W., L.K.), Asthma, Allergy and Respiratory Science (F.H., K.W., W.M., G.R., J.M.), and Clinical Neurophysiology (K.M.), King's College London; and Department of Respiratory Medicine (M.P.), The Royal Brompton Hospital, London, UK.

Address correspondence and reprint requests to Dr. Lalit Kalra, Dept. of Stroke Medicine, Academic Neuroscience Centre, PO Box 41, IOP, London SE4 8AF, UK lalit.kalra{at}kcl.ac.uk

Background: Expiratory muscle weakness due to cerebral infarction may contribute to reduced airway clearance in stroke patients.

Methods: Transcranial magnetic stimulation (TMS) at the vertex and over each hemisphere and magnetic stimulation over the T_10-11 spinal roots (Tw T₁₀) 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, TwT₁₀, and BAMPS. Regression models were used to assess determinants of peak voluntary cough flow rates (PCFR).

Results: 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 H₂O, p = 0.0003 and 8.7 ± 3.3 vs 16.7 ± 11.5 cm H₂O, p = 0.023, respectively). There were no differences in TwT₁₀ P_gas (25.2 ± 7.8 vs 29.4 ± 12.4 cm H₂O, p = 0.153) or BAMPS P_di (21.6 ± 7.2 vs 19.2 ± 3.4 cm H₂O, p = 0.163). TMS P_gas was lower (4.1 ± 2.8 vs 6.1 ± 1.9 cm H₂O, 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).

Conclusion: Ischemic cortical injury is associated with expiratory muscle weakness and may contribute to cough impairment in stroke patients.

BAMPS = bilateral anterolateral magnetic phrenic stimulation; EO = external oblique; MEP = motor evoked potential; NIHSS = NIH Stroke Scale; P_di = transdiaphragmatic pressure; P_es = esophageal pressure; P_gas = intragastric pressure; PCFR = peak voluntary cough flow rates; PE_max = maximum static expiratory pressure; POE = point of optimal excitability; RA = rectus abdominis; TMS = transcranial magnetic stimulation.

Received June 2, 2008. Accepted in final form September 15, 2008.

Funded by the Stroke Association, UK (Grant TSA 2004/05).

Disclosure: The authors report no disclosures.