USING MEG TO DEVELOP A PASSIVE MOTOR MAPPING PROTOCOL FOR PEDIATRIC EPILEPSY PATIENTS
Abstract number :
2.169
Submission category :
5. Neuro Imaging
Year :
2012
Submission ID :
16128
Source :
www.aesnet.org
Presentation date :
11/30/2012 12:00:00 AM
Published date :
Sep 6, 2012, 12:16 PM
Authors :
M. H. McManis, E. Darrow, A. Hernandez, S. Malik, S. Perry, A. Childers, R. Ross, E. Guevara, K. Mooneyham
Rationale: Magnetoencephalography (MEG) has become a regular tool for functional mapping in cases of epilepsy requiring surgery. However, in cases involving patients who need sedation for the MEG procedures, functional mapping is limited by the patient's inability to perform the necessary tasks. For these patients, there is a need to develop tasks that activate the necessary brain regions associated with the function using passive tasks that don't require any voluntary activities on the part of the patient. There is growing evidence that passive peripheral motor flexion induces activation of the motor cortex, thus making it possible passively map the motor cortex. As part of our clinical practice, we have developed a protocol for sedating children using intravenous (IV) dexmedetomidine sedation in conjunction with a passive flexion of the patient's index fingers. Methods: Three children with intractable epilepsy were seen in the Cook Children's Medical Center MEG laboratory as part of their presurgical evaluation. The children ranged in age from 4 - 11 years old. Sedation was required for the patients to complete the MEG scans. Motor mapping was done as part of a larger set of MEG scans for presurgical evaluation. Sedation: The patients were brought to the radiology preparation area and received the anxiolytic agent midazolam, orally or intravenously. Patients were then brought to the MEG scanner anteroom where they received inhalational nitrous oxide 70% and an IV catheter was placed. Patients were then given a bolus dose of dexmedetomidine (1 mcg/kg) over ten minutes. Following the bolus, patients received a continuous infusion of dexmedetomidine (0.2-0.4 mcg/kg/hr) for the duration of the MEG scan. Motor activation: Motor cortex activation was achieved by having a technician manually manipulate the index fingers on the left and right hands of the patient, using a fiber optic device to indicate each movement to the recording computer. Approximately 125 individual movements were made on each index finger at a rate averaging 2 movements every 3 seconds. Data were filtered and averaged and the resulting evoked magnetic field waveform was analyzed using the equivalent current dipole model. The peak of the response was localized and plotted on an MRI image. Results: For all cases, the sedation procedure was well tolerated and we were able to localize the motor cortex in both hemispheres. Analysis of the passive flexion responses shows that the peak in the motor cortex does not appear to be inhibited by dexmedetomidine, allowing for the mapping of the motor cortex in patients requiring sedation to complete their MEG scans. Conclusions: We conclude that a sedation protocol using dexmedetomidine makes it possible to do functional mapping of the motor cortex in patients who require sedation to complete their MEG scans. The present case series shows that children undergoing evaluation for epilepsy surgery can receive the benefits of MEG functional mapping, when appropriately sedated. Additional discussion includes the use of sedation in a pediatric MEG center for other functional modalities.
Neuroimaging