Postoperative Transient Neurologic Dysfunction: A Proposal for Pathophysiology.
10.3988/jcn.2018.14.3.393
- Author:
Ji Hoon PHI
1
;
Seung Jin LEE
;
Hyun Seung KANG
;
Jeong Eun KIM
;
Seung Ki KIM
;
Won Sang CHO
;
Seo Young LEE
Author Information
1. Division of Pediatric Neurosurgery, Seoul National University Children's Hospital, Seoul National University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
transient neurologic dysfunction;
cortical spreading depression;
postoperative;
migraine;
moyamoya disease;
encephalo-duro-arterio-synangiosis
- MeSH:
Brain;
Cerebrovascular Circulation;
Cortical Spreading Depression;
Depression;
Diffusion;
Dysarthria;
Electroencephalography;
Epilepsy;
Extremities;
Follow-Up Studies;
Humans;
Ischemia;
Ischemic Attack, Transient;
Magnetic Resonance Angiography;
Migraine Disorders;
Moyamoya Disease;
Neuroimaging;
Neurologic Manifestations*;
Paresis;
Perfusion Imaging;
Postoperative Period;
Seizures;
Tomography, Emission-Computed, Single-Photon
- From:Journal of Clinical Neurology
2018;14(3):393-400
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND AND PURPOSE: Sudden neurological deterioration which cannot be explained by structural change, ischemia or seizure is often observed among neurosurgical patients. We aimed to provide new insight into the pathophysiology of postoperative transient neurologic dysfunction. METHODS: We describe prolonged but fully reversible focal neurologic dysfunction of unknown origin based on the initial evaluation in 8 patients who had received encephalo-duro-arterio-synangiosis for moyamoya disease. We performed brain imaging, including diffusion weighted imaging and perfusion magnetic resonance imaging or single photon emission computed tomography, and electroencephalography (EEG) during the episodes and after resolution of the symptoms. RESULTS: The symptoms consisted of dysarthria, hemiparesis, or hemiparesthesia of limbs contralateral to the operated side. These symptoms developed between 12 hours and 8 days after surgery and lasted between 12 hours and 17 days. Structural imaging did not show any significant interval change compared with the immediate postoperative images. Perfusion imaging showed increased cerebral blood flow in the symptomatic hemisphere. EEG revealed low amplitude arrhythmic slowing in the corresponding hemisphere. Follow-up imaging and EEG after recovery did not show any abnormalities. CONCLUSIONS: Transient neurologic dysfunction can occur during the postoperative period of brain surgery. Although this may last more than usual transient ischemic attack or seizure, it eventually resolves regardless of treatment. Based on our observation, we propose that this is the manifestation of the transient cortical depression triggered by mechanical stimulation, analogous to migraine aura associated with cortical spreading depression.
