Virginia Thornley, M.D., Neurologist, Epileptologist
March 10, 2018
Introduction
A concussion occurs commonly as high-speed vehicular accidents become more common in today’s fast-paced world. In addition, it occurs frequently in sports-related activity such as football or boxing. The brain is composed of millions of connections and though a patient may complain of several neurological complaints, it is not often manifest in neuroimaging studies, except perhaps diffusion tensor imaging. More often than not, a good clinician can diagnose symptoms of post-concussion syndrome based on neurological symptoms and a preceding event. During injury, there is shearing of thousands of axons diffusely throughout the brain. The contrecoup effect of the injury occurring over the frontotemporal poles produces damage causing a myriad of neurological symptoms. On EEG, non-specific changes can be found corresponding with the degree of injury. There is slowing of the posterior dominant rhythm and excessive theta rhythms which eventually clears after weeks or months of recovery (1). Some patients, however, are left with recurrent symptoms such as post-concussion headaches, or dizziness or sensations of discomfort. On EEG, some studies show post-concussion symptoms correlating with bursts of theta rhythms.
EEG findings in a few minutes spanning more than 6 months
In animal studies, the EEG shows high voltage sharp waves followed by diffuse background suppression which can last a few minutes. This is followed by diffuse slowing that normalizes after 15 minutes in one study occurring between 10-60 minutes (2). Over a few hours to weeks, there are increased theta and delta rhythms and reduced ratio of theta to alpha frequencies. there was an increase in delta activity in the posterior regions. There are brief periods of reduced delta: alpha ratios. In one study called the “Belfast studies,” amnesia was evaluated in 73 patients at 24 hours and 6-week follow-up with EEG and brainstem auditory evoked potentials (BAEP). It was found that amnesia did not have EEG correlate but correlated with abnormal BAEPs suggesting amnesia was derived from brainstem dysfunction rather than cortical dysfunction. Over weeks to months, there are reduced alpha and increased delta rhythms are noted. In the Belfast studies, there was more persistent left temporal slowing, which seemed to correlate with chronic symptoms when it persisted beyond 6 months. After more than 6 months, there were increased delta activity and fewer alpha rhythms (2).
Other EEG findings in closed head injury and part-seizure like activity
In one retrospective study of 3 groups of veterans at a Veteran Affairs Medical Center, 30 comprised of normal subjects with normal EEGs, 30 had EEG’s with non-paroxysmal theta delta slowing and 38 patients had theta bursts. The patients with episodes of theta bursts seemed to have corresponding partial seizure-like clinical symptoms. Patients with head injury reported episodic symptoms across all 3 groups. These findings conclude that clinicians may want to evaluate patients for seizure-like activity in the context of closed head injury and presence of bursts of theta activity (3).
Reference
- Nuwer, et al, “Routine and quantitative EEG in mild traumatic brain injury,” Clinical Neurophysiology, 2005, Sep., 116(9):2001-2025
- Haneef, et al, “Electroencephalography and quantitative electroencephalography in mild traumatic brain injury,” Journal of Neurotrauma, 2013, Apr., 30(8):653-656.
- Roberts, et al, “Theta bursts, closed head injury, and partial seizure-like symptoms: a retrospective study,” Applied Neuropsychology, 2001, 8(3):140-7.
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