CLINICAL NOTE Breathlessness Associated With Abdominal Spastic Contraction in a Patient With C4 Tetraplegia: A Case Report Isabelle Laffont, MD, Marie-Christine Durand, MD, Celia Rech, MD, Annie Perez De La Sotta, MD, Nicholas Hart, MD, Olivier Dizien, MD, Fre ´de ´ric Lofaso, MD, PhD ABSTRACT. Laffont I, Durand M-C, Rech C, Perez De La Sotta A, Hart N, Dizien O, Lofaso F. Breathlessness associated with abdominal spastic contraction in a patient with C4 tetraplegia: a case report. Arch Phys Med Rehabil 2003;84: 906-8. A tetraplegic patient with C4 cervical cord injury reported breathlessness during episodes of spastic contraction of the abdominal muscles. To determine the mechanism, we per- formed electrophysiologic testing of the phrenic nerves. We measured abdominal pressure, esophageal pressure, and trans- diaphragmatic pressure (Pdi) during a maximal inspiratory effort (Pdi max), a maximal sniff maneuver (sniff Pdi) during resting breathing, and during the episodes of breathlessness. Electrophysiologic testing of the phrenic nerves showed axonal neuropathy on the left. Sniff Pdi and Pdi max were 38cmH 2 O and 42cmH 2 O, respectively. Transient spastic contractions of abdominal muscles were associated with an increase in abdom- inal pressure greater than 30cmH 2 O, with a decrease in abdom- inal volume; this rise in abdominal pressure was transmitted to the esophageal pressure. Inspiration became effective only when esophageal pressure fell below the resting baseline value. Achieving this decrease required an increase in inspiratory effort, characterized by swings in esophageal pressure and Pdi of 30cmH 2 O and 40cmH 2 O (approximately 100% of Pdi max), respectively. During these periods, minute ventilation was markedly reduced. This is the first report that spastic abdominal muscle contractions can impose a significant load on the dia- phragm, uncovering moderate diaphragmatic weakness. This has important clinical implications; abolition of the spastic abdominal muscle contraction in this patient completely re- solved her intermittent respiratory symptoms. Key Words: Case report; Dyspnea; Rehabilitation; Respi- ratory insufficiency; Respiratory muscles. © 2003 by the American Congress of Rehabilitation Medi- cine and the American Academy of Physical Medicine and Rehabilitation T ETRAPLEGIA CAUSED by transection of the cervical cord severely compromises some inspiratory muscles and most expiratory muscles. 1,2 The main physiologic consequence of expiratory muscle paralysis is an impaired cough, 3 which is frequently associated with respiratory complications such as mucus plugging, atelectasis, and pneumonia, 4 a major cause of mortality in this population. 3 After the initial stage of spinal shock has passed, patients with tetraplegia may develop abnormal spinal reflexes that involve the abdominal muscles 5 ; spastic contraction of those muscles is relatively common. 5 This spastic contraction re- duces the elastic properties of the abdominal compartment of the respiratory system, which, in turn, can increase the load imposed on the diaphragm. A study 6 that investigated the impact of abdominal muscle spastic contraction by placing weights on the abdomen showed that patients with cervical cord injury below C4 had an increase in diaphragmatic activ- ity. 6 However, there are no data in the literature that describe the effect of abdominal muscle spasm on ventilation in patients with tetraplegia. In this report, we present a patient with a C4 cervical cord injury who was referred to our hospital for management of dyspnea associated with episodes of spastic contraction of the abdominal muscles. We hypothesized that the physiologic basis for such a phenomenon could be the result of an excess load imposed on the diaphragm. To inves- tigate this hypothesis, we studied the changes in pulmonary mechanics during quiet breathing and during the episodes of breathlessness. CASE DESCRIPTION The patient was a 45-year-old woman with American Spinal Injury Association class A 7 posttraumatic tetraplegia at the C4 level on the left and the C8 level on the right. At the initial stage of the tetraplegia, she had no thoracic traumatism but needed a tracheostomy because of her neurologic level; it was removed 2 months later. She was reviewed 4 years after injury when she developed a recurrent dislocation of the left hip that was associated with severe spasticity of the adductors; she also experienced breathlessness during episodes of abdominal spas- tic contractions. These episodes occurred during spontaneous hip reduction (when moving from the supine to the sitting position), or when the left hip was passively moved into abduction, extension, and external rotation. Static lung volumes were assessed while she was in sitting and supine positions, according to standard guidelines. 8 Elec- trophysiologic testing of the phrenic nerves was performed with a Neuropack Sigma electromyography device a and the Newsome Davis method. 9 The patient was seated in a chair with head up at 60°. Flow was measured by using a Fleisch No. 2 pneumotachograph, b and esophageal pressure (Pes) and gastric pressure (Pga) were recorded with a catheter-mounted transducer. c Thoracic and abdominal movements were assessed by using uncali- brated inductive plethysmography. Transdiaphramatic pressure (Pdi=Pga-Pes) was measured during maximal inspiratory ef- forts (Pdi max) and during maximal sniffs (sniff Pdi), 10 both performed at functional residual capacity. Spastic contractions of abdominal muscles were induced by reducing the dislocated left hip. From the Unite ´ de Me ´decine Physique et de Re ´adaptation (Laffont, Rech, Dizien) and Service de Physiologie-Explorations Fonctionnelles (Durand, Perez De La Sotta, Lofaso), Ho ˆpital Raymond Poincare ´, Garches, France; Respiratory Muscle Labora- tory, Royal Brompton Hospital, London, UK (Hart); and Institut National de la Sante ´ et de la Recherche Me ´dicale, Ho ˆpital Henri Mondor, Cre ´teil, France (Lofaso). No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the author(s) or upon any organization with which the author(s) is/are associated. Correspondence to Fre ´de ´ric Lofaso, MD, PhD, Service de Physiologie-Explora- tions Fonctionnelles, Ho ˆpital Raymond Poincare ´, 92380 Garches, France, e-mail: f.lofaso@rpc.ap-hop-paris.fr. Reprints are not available. 0003-9993/03/8406-7518$30.00/0 doi:10.1016/S0003-9993(02)04898-0 906 Arch Phys Med Rehabil Vol 84, June 2003