Traumatic brain injury (TBI) is a major cause of death and disability in the United States. In 2014, about 2.87 million TBI-related emergency department (ED) visits, hospitalizations, and deaths occurred. 1 From 2006 to 2014, TBI-related emergency department visits increased by 54%1.
Neurodiagnostic procedures are critical assessment tools throughout the TBI patient’s journey. Evaluating the potential long-term impacts of TBI is challenging, though, particularly in the early days post-event. The Glasgow Coma Scale (GCS) is the standard clinical tool for assessing neurological functioning immediately after brain injury, but other objective neurodiagnostic measures also contribute valuable information related to the prognosis of patients with TBI.
The Role of Electroencephalography (EEG) in Prognosis
There are relatively few studies on EEG’s value in predicting recovery from chronic disorders of consciousness (DOCs ) following TBI, and those that exist tend to have small sample sizes.2 However, EEG’s role in prognostication post-TBI is worthy of additional research. For example, some indicators related to prognosis that are yielded in part by EEGs include the following:
- EEG reactivity. TBI patients with a transitory increase of slow waves or suppression to sensory stimulation seem to have better outcomes compared with those without reactive EEG.3
- Non-reactive EEG and pathological somatosensory evoked potentials together classified 70% of patients into an unfavorable outcome group, especially in patients with a GCS of ≤8.4
- In the acute setting, EEG recordings are used to detect non-convulsive status epilepticus or non-convulsive seizures that might explain patient's unresponsiveness. These types of seizures can be found in up to 30% of comatose patients in the neurological ICU.5 Epileptogenesis is common after moderate-severe TBI and typically begins within the first week after injury.6
- Seizures in TBI patients have been associated with higher early mortality.7 Routine EEG monitoring (e.g., 20-30 minutes long) may be insufficient to detect seizures in critically injured patients.8 (Continuous monitoring of at least 24 hours has been shown to detect 95% of critical events.9
Recent studies of continuous EEG in moderate-severe TBI demonstrate a high incidence of early seizures (25%) and interictal epileptiform activity (45-60%).6 When depth EEG is used, the rate of early seizures is over 60%.6 This suggests that EEG is can be used early on to identify those patients at high risk for post-traumatic epilepsy (PTE), which occurs in 15-55% of patients with severe TBI.6
The Role of Evoked Potentials in TBI Prognosis
Somatosensory Evoked Potentials
In a meta-analysis of SEP compared with other methods of neurologic testing, SEP were found superior to pupil examination, motor response, EEG, computed tomography, and GCS in predicting a negative outcome in coma.10
Nearly 40 years ago, Goldie et al showed that if the N20 signal is bilaterally absent in a comatose patient, the patient’s outcome will be very poor.11 A transient disappearance of N20 component might be secondary to focal midbrain dysfunction or focal cortical lesions in TBI patients.12,13 In children, however, the absence of an N20 signal does not necessarily indicate an irreversible loss of neural function.14
Given the importance of the N20 signal in indicating prognosis, facilitating accurate interpretation is key. Ensure the integrity of the peripheral input pathways though the presence of Erb (N9) and cervical components (N13).
Recent evidence also suggests that novel quantitative SEP methods (e.g., phase space area) in multimodal approaches may track cerebral recovery and might predict good outcomes.15
Auditory Evoked Potentials
Auditory evoked potentials (AEPs) can be used as sensitive tools in tracking physiological changes underlying physical and cognitive symptoms associated with TBI.
Mismatch negativity (MMN) was associated with awakening, especially in TBI patients with a positive predictive value (PPV) >90% for recovery, which was also confirmed in a sedated patient subset.16
Middle-latency auditory evoked potentials, particularly the applications of P3 component, have been employed for prognosis purposes with promising results elicited by the subject's own name.17 A detectable P3 at two to three months after TBI was associated with an increased chance of recovery within 12 months.17
The Research Continues
The prognostic utility of various modes of neurodiagnostic evaluation remains an area of continuing research. For example, more studies are needed to define the value of markers in quantitative EEG as well as the potential benefits of transcranial magnetic stimulation in TBI patients in both prognosis and rehabilitation as well as evaluating residual basic cognitive capacities. Accurate and reliable neurodiagnostic testing and evolving techniques will continue to provide even greater insights into appropriate care and treatment paths for TBI patients.
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References
1.https://www.cdc.gov/traumaticbraininjury/get_the_facts.html
2.Pauli R, O'Donnell A, Cruse D. Resting-State Electroencephalography for Prognosis in Disorders of Consciousness Following Traumatic Brain Injury. Frontiers in Neurology. 2020; 11.
3.Gütling E, Gonser A, Imhof HG, Landis T. EEG reactivity in the prognosis of severe head injury. Neurology 1995;45:915-8.
4.https://www.sciencedirect.com/science/article/abs/pii/S1388245718312835
5.Claassen J, Mayer SA, Kowalski RG, Emerson RG, Hirsch LJ. Detection of electrographic seizures with continuous EEG monitoring in critically ill patients. Neurology 2004;62:1743-8.
6.Duncan D, Vespa P, Toga AW. Detecting features of epileptogenesis in EEG after TBI using unsupervised diffusion component analysis. Discrete Continuous Dyn Syst Ser B. 2018 Jan;23(1):161-172.
7.Hesdorffer DC, Benn EKT, Cascino GD, Hauser WA. Is a first acute symptomatic seizure epilepsy? Mortality and risk for recurrent seizure. Epilepsia 2009;50:1102-8.
8.Pandian JD, Cascino GD, So EL, Manno E, Fulgham JR. Digital videoelectroencephalographic monitoring in the neurological-neurosurgical intensive care unit: clinical features and outcome. Arch Neurol 2004;61:1090-4.
9.Nguyen-Michel V-H, Dinkelacker V, Solano O, Levy P-P, Lambrecq V, Adam C, et al. 4h versus 1h-nap-video-EEG monitoring in an Epileptology Unit. Clin Neurophysiol 2016;127:3135-9.
10.Madl C, et al. Detection of non-traumatic comatose patients with no benefit of intensive care treatment by recording of sensory evoked potentials. Arch Neurol. 1996;53:512-516.
11.Goldie WD, Chiappa KH, Young RR, Brooks EB. Brainstem auditory and short-latency somatosensory evoked responses in brain death. Neurology 1981;31:248–56.
12.Zhang Y, Su YY, Ye H, Xiao SY, Chen WB, Zhao JW. Predicting comatose patients with acute stroke outcome using middle-latency somatosensory evoked potentials.Clin Neurophysiol 2011;122:1645-9.
13.Logi F, Fischer C, Murri L, Mauguière F. The prognostic value of evoked responses from primary somatosensory and auditory cortex in comatose patients. Clin Neurophysiol 2003;114:1615-27.
14.Carrai R, Grippo A, Lori S, Pinto F, Amantini A. Prognostic value of somatosensory evoked potentials in comatose children: a systematic literature review. Intensive Care Med 2010;36:1112-26.
15.Lachance B, Wang Z, Badjatia N, Jia X. Somatosensory evoked potentials and neuroprognostication after cardiac arrest. Neurocrit Care 2020;32:847-57.
16.Fischer C, Luaute J, Morlet D. Event-related potentials (MMN and novelty P3) in permanent vegetative or minimally conscious states. Clin Neurophysiol 2010;121:1032-42.
17.Li R, Song W, Du J, Huo S, Shan G. Electrophysiological correlates of processing subject's own name. NeuroReport 2015a;26:937-44.