Acquired brain injuries (ABI) occur after birth and are not congenital, degenerative, hereditary or induced by birth trauma.
There are two types of ABI: traumatic (TBI) and non-traumatic. Sources of TBIs include falls (47.9%), blows to the head (17.1%) and vehicle accidents (13.2%).1 Non-traumatic brain injuries result from internal injuries due to a variety of etiologies including lack of oxygen, vascular events such as strokes, exposure to toxins and brain tumors.1
The Brain Injury Association of America states that at least 2.8 million Americans sustain a traumatic brain injury (TBI) each year.1 The Centers for Disease Control and Prevention reports that TBI is a major cause of death and disability, with about 166 Americans dying each day from a TBI-related injury (2019 data).2
Brain injuries change the brain’s neuronal activity through disruption of neuronal metabolism and/or physical integrity. This results in a functional disturbance of the nerve cells in the brain.
in addition to the neurologic examination, cranial computed tomography (CT) and magnetic resonance imaging (MRI) can identify space-occupying lesions and displacement of the brainstem.3. These methods, however, fail to provide information about cerebral activity.
Based on severity, TBIs can be classified into three groups: mild, moderate, and severe. Focusing on mild TBI (mTBI), there are no clear EEG and Quantitative EEG (qEEG) pathognomonic features related to mTBI; however there are important considerations for measuring cerebral activity in these cases.
Acute mTBI: Look for epileptiform activity characterized by high amplitude sharp waves or high frequency discharges followed by 1-2 minutes of cortical activity suppression with a subsequent diffuse slowing of EEG that returns to normal baseline within 10 minutes to 1 hour.4
qEEG shows a reduction of mean alpha frequency with increased theta and delta bandwidth or increased Theta:Alpha ratio.5
Subacute mTBI: Weeks to months after a mTBI, the posterior alpha rhythm starts to gain 1-2Hz increase in frequency which has been explained as a return to the original baseline from the post-traumatic slowing activity.6
Chronic mTBI: Despite controversies in the medical community about post-concussive syndrome, a higher power of delta band (1.5Hz-5Hz) and lower alpha band (8.5Hz-12Hz) compared with matched controls.5
The majority of the acute EEG abnormalities described resolve by the three-month mark, and 90% of the rest by one year after the head trauma.6 While most patients who suffer mild TBI appear to fully recover, some patients have poor long-term outcomes or do not follow a typical recovery pattern for reasons that are unclear. For those patients, pre-injury factors such as depression, stress, anxiety disorders, substance abuse, compromised cognitive function, advanced age or poor medical health may play a role in their level of recorvery.7 More research is warranted.
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References
1. Brain Injury Facts and Statistics.Brain Injury Association
of America.https://www.biausa.org/wp-content/uploads/MTMBI-Fact-Sheet-2021-Revised.pdf.
Accessed 2 March 2022.
2. Traumatic Brain Injury and Concusssion. Centers for
Disease Control and Prevention. https://www.cdc.gov/traumaticbraininjury/index.ht...
Accessed 2 March 2022.
3. Reich JB, Sierra J, Camp W, Zanzonico P, Deck MDF,
Plum F. Magnetic resonance imaging measurements and clinical changes
accompanying transtentorial and foramen magnum brain herniation. Ann Neurol.
1993;33(2):159-170. doi:10.1002/ANA.410330205
4. Williams D. The Electro-Encephalogram in Acute Head
Injuries.. J Neurol Psychiatry. 1941;4(2):107. doi:10.1136/JNNP.4.2.107
5. Ianof JN, Anghinah R. Traumatic brain injury: An EEG
point of view. Dement Neuropsychol. 2017;11(1):3.
doi:10.1590/1980-57642016DN11-010002
6. Nuwer MR, Hovda DA, Schrader LM, Vespa PM. Routine
and quantitative EEG in mild traumatic brain injury. Clin Neurophysiol.
2005;116(9):2001-2025. doi:10.1016/J.CLINPH.2005.05.008
7. Ruff RM, Iverson GL, Barth JT, Bush SS, Broshek DK.
Recommendations for diagnosing a mild traumatic brain injury: A national
academy of neuropsychology education paper. Arch Clin Neuropsychol. 2009;24(1):3-10.
doi:10.1093/arclin/acp006