|M.Sc Student||Marco Avihu|
|Subject||Why Post mTBI Accident Acute Pain Turns Chronic?|
An EEG Research
|Department||Department of Medicine||Supervisor||Professor David Yarnitsky|
|Full Thesis text|
to the world health organization, between 20 and 50 million people
suffer non-fatal injuries as a result of a road traffic crash every year. This kind of mild
motor vehicle crashes is characterized by sudden acceleration-deceleration mechanism, and as a result, a rapid change of head positioning transfers massive energy to the cervical spine and can be described as whiplash injury. Whiplash associated disorder and mild traumatic brain injury, with or without direct trauma to the head, cause patients, in the acute stage, various neurological symptoms. Up to 50% of whiplash injury patients will experience long-term persistent pain, and approximately 30% will report moderate to severe pain-related disability. The mechanisms underlying the chronification of pain are not known, and our ability to predict which of the patients will suffer chronic pain is very limited. This prospective observational cohort study aims to use electroencephalography (EEG) to investigate whether there is an electrophysiological biomarker that could help predict the presence of chronic pain one year after mild traumatic brain injury. Our hypothesis was that higher peak of a frequency in frontal or somatosensory regions at baseline EEG would serve as a predictor in patients that later present chronic pain, as opposed to those whose pain is relieved. 65 post accident patients, were recruited from the Rambam ER. Within 72 hours post-accident, they underwent psychophysical and psychological assessment as well as resting state EEG. Every patient was also asked to provide numeric ratings of his/her pain once a month for 12 months. Pain rated above 20 was considered significant. In order to best characterize the pain profile along the follow-up year, we divided our cohort based on rating above 20 in at least 4 out of 10 possible ratings into chronic pain group (P, NP=29) and pain-relived group (nP, NnP=36). EEG signals were processed and various spectra bands (q, a, b, g), were checked in different brain regions by averaging electrodes reflecting activity in relevant brain regions including; SI, SII, dorsolateral-prefrontal cortex, orbitofrontal cortex, insula, and cingulate cortex. Median tests with Bonferroni correction for multiple comparisons revealed a significant reduction of area under the curve of q band (p < 0.0076) and an increment of b and g wave`s AUC (p < 0.018 & p < 0.0036 respectively) in the left SII in the chronic pain group. No other significant results were found. It seems that neurophysiological activity in the SII region, differ in a statistical significant manner. In theory, this might be a reflection of variability in levels of neurotransmitters such as GABA or glutamate. Certain features of pain processing that determine the chances of pain chronification at least in the context of mild head injury might be a result of this difference. These findings might cast a new understanding of the role of SII in pain processing, as either a stand-alone brain region or as part of a larger brain network. While more research needs to be done in this field, these differences might be the beginning of new understanding on chronic pain chronification.