PURPOSE: This study analyzed the direct short-term effect of vagus nerve stimulation (VNS) on respiratory sinus arrhythmia (RSA) in children with pharmacoresistant epilepsy. METHODS: RSA magnitude is calculated as the ratio between maximum and minimum heart rate for each respiratory cycle-before, during, and after the actual VNS period. In 10 children, changes in RSA magnitude were evaluated on polysomnographic recordings, including electrocardiography (ECG), electroencephalography (EEG), thoracoabdominal distension, nasal airflow, and VNS artifacts. Measurements during stimulation were compared with those at baseline, immediately preceding the VNS periods and individually for each patient. RESULT: During VNS, respiratory frequency increased and respiratory amplitude decreased with a variable effect on cardiac activity. The coupling between heart rate and respiratory rate was disturbed and RSA magnitude decreased significantly in 6 of 10 children during VNS. These changes in RSA magnitude varied from one child to another. The observed changes for respiratory and cardiac activity were concomitant with changes in RSA but were not correlated. CONCLUSION: Together with disorders of respiration, cardiac activity, and oxygen saturation (SaO(2)) described previously. VNS also modifies synchronization between cardiac and respiratory activity, resulting in poor optimization of oxygen delivery to tissues that can be regarded as an additive side effect, which should be considered in patients with already altered brain function. This interaction between the effects of VNS and potential autonomic nervous system (ANS) dysfunction already reported in epileptic patients should be considered to be potentially life-threatening. In addition, evaluation of changes in respiratory parameters can also provide reliable markers for further evaluation of the effectiveness of VNS.
PURPOSE: This study analyzed the direct short-term effect of vagus nerve stimulation (VNS) on respiratory sinus arrhythmia (RSA) in children with pharmacoresistant epilepsy. METHODS: RSA magnitude is calculated as the ratio between maximum and minimum heart rate for each respiratory cycle-before, during, and after the actual VNS period. In 10 children, changes in RSA magnitude were evaluated on polysomnographic recordings, including electrocardiography (ECG), electroencephalography (EEG), thoracoabdominal distension, nasal airflow, and VNS artifacts. Measurements during stimulation were compared with those at baseline, immediately preceding the VNS periods and individually for each patient. RESULT: During VNS, respiratory frequency increased and respiratory amplitude decreased with a variable effect on cardiac activity. The coupling between heart rate and respiratory rate was disturbed and RSA magnitude decreased significantly in 6 of 10 children during VNS. These changes in RSA magnitude varied from one child to another. The observed changes for respiratory and cardiac activity were concomitant with changes in RSA but were not correlated. CONCLUSION: Together with disorders of respiration, cardiac activity, and oxygen saturation (SaO(2)) described previously. VNS also modifies synchronization between cardiac and respiratory activity, resulting in poor optimization of oxygen delivery to tissues that can be regarded as an additive side effect, which should be considered in patients with already altered brain function. This interaction between the effects of VNS and potential autonomic nervous system (ANS) dysfunction already reported in epilepticpatients should be considered to be potentially life-threatening. In addition, evaluation of changes in respiratory parameters can also provide reliable markers for further evaluation of the effectiveness of VNS.
Authors: Suresh Kotagal; Cynthia D Nichols; Madeleine M Grigg-Damberger; Carole L Marcus; Manisha B Witmans; Valerie G Kirk; Lynn A D'Andrea; Timothy F Hoban Journal: Sleep Date: 2012-11-01 Impact factor: 5.849