Written By Shameel Asad
Introduction
A TBI or a 'Traumatic Brain Injury' is a sub-clinical term for representing a blow to the head or change in cognitive development of a person, in layman terms. It ranges from mild to severe brain injury resulting in mood swings and neurobiological deviations in the brain such as reduced neuronal activity or synaptic disassociation causing nerve cell death.
1.1 Traumatic brain injuries and their effects on cognition
Numerous mental and neurobehavioral issues are linked to traumatic brain injury (TBI). Attention has shifted to the cognitive, emotional, and behavioral comorbidities of injuries throughout the severity scale, which are frequently more incapacitating than lingering physical symptoms, as mortality rates for severe TBI have decreased. Personality changes, such as impulsivity, extreme anger, emotional instability, apathy(aversion to others’ feelings), and heightened insensitivity, can result after moderate to severe TBI. Now recognized to be linked to a variety of affective symptoms, suicidal ideation, and the worsening or new emergence of various psychiatric illnesses, including PTSD and major depressive disorder, mild traumatic brain injury was formerly thought to be a generally innocuous condition. It is currently thought that repetitive head hits, which often occur in sporting situations, can lead to a variety of emotional and behavioral shifts 1. A shock to the head has a chance of causing chemical imbalances in the brain while comorbidities such as depression, fatigue, and sudden behavioral shifts are observed 2.
1.2 Role of neuroimaging in treating traumatic brain injuries
Neural imaging apparatuses(fMRI, PET, MRI, CAT, and EEG) are diagnostically viable tools to assess the presence or absence of a visible deformity in the brain such as a tumor. The overview of several image analysis approaches aims to demonstrate how various neuroimaging techniques tap various elements of TBI-related neuropathology and to connect quantitative neuroimaging methods with neuropsychological outcome measures. The relationship between various neuropathologies and neuropsychological outcomes is also addressed by looking at how injury affects neural networks and brain connections 3. In Positron emission tomography scans (PET), areas having high metabolic activity are shown visibly regardless of the fact that it may not be cancerous but instead a brain trauma like surgery or a blow to the head etc. This example shows how functional imaging tools aid in Neuropsychological assessment.
Figure 1.2
Bigler, E. D. (2016). Systems biology, neuroimaging, neuropsychology, neuroconnectivity and traumatic brain injury. Frontiers in systems neuroscience, 10, 55.
The above illustration shows the difference between a standard brain injury and a more profound one. It is visible that the right cerebral hemisphere is undergoing neural degeneration by neuroinflammation3 .
1.3 The dark side of degenerative brain trauma
In this section, it is speculated that Traumatic brain injury can cause the Breakdown of Neural networks causing chemical or endocrinological issues since the pituitary gland is responsible for directing these processes is disturbed and hence inhibited till therapeutic intervention is done. In animals, however, TBI results in morbidly degenerated brain tissues resulting in the death of an animal4.
Taking the above experiment as an analogy, swift treatment post-concussion is prudent. Neurobiologically, the brain initiates a defense strategy when met with adversity in the form of a concussion by inflaming its tissues for repair(exactly how physical injuries elicit a secondary response by raising body temperature in order to maximize blood flow to that area and kill off any pathogen that may have entered). As of late, no neuroprotective therapy has been found and researchers dream of initiating the brain’s inflammation response artificially5.
2.1 Progressive neurodegeneration and brain swelling issues
Although little is known about the processes causing neural alterations, recent clinical investigations show that traumatic brain injury (TBI) causes persistent and progressive neurodegenerative changes that result in late neurologic impairment. After a TBI, neuroinflammation caused by neuroglia(neuron-supporting cells) is a significant secondary damage mechanism. In research on humans, it has been discovered that microglial activation lasts for many years after the original brain trauma, especially after moderate to severe TBI alluding to the idea that all brain trauma indeed has irreparable damage to the nervous system resulting in nerve cell loss progressively 6 . A similar mechanism is responsible for exacerbating the effects of Alzheimer's in the brain.
Figure 2.1
Afridi, R., Lee, W., & Suk, K. (2020). Microglia Gone Awry: Linking Immunometabolism to Neurodegeneration. Frontiers in Cellular Neuroscience, 14, 544757. https://doi.org/10.3389/fncel.2020.00246
The above diagram illustrates the contrast between healthy and dysfunctional glial cells(directly affecting neuronal activity) due to Traumatic Brain Injury 7 .
Conclusion
To sum the argument up, various neuroimaging techniques are responsible for adequate diagnosis and treatment of Brain injuries by allowing physicians to view neural networks and internal structures to spot any irregularities(tumors and aneurysms). Apart from shifts in cognition, patients who have undergone TBI often exhibit psychiatric ailments such as suicidal ideation, major depressive disorder and extensive cognitive distortion often paired with comorbidities such as apathy and emotional dysregulation. If we focus on the Neurological side of brains afflicted by TBI, it is visible that microglia cause irreparable and often acute Neuroinflammation which lingers in the body indefinitely, progressively resulting in Neural Degeneration and high mortality rates worldwide.
References:
Howlett, J. R., Nelson, L. D., & Stein, M. B. (2022). Mental health consequences of traumatic brain injury. Biological psychiatry, 91(5), 413-420.
Pavlovic, D., Pekic, S., Stojanovic, M., & Popovic, V. (2019). Traumatic brain injury: neuropathological, neurocognitive and neurobehavioral sequelae. Pituitary, 22, 270-282.
Bigler, E. D. (2016). Systems biology, neuroimaging, neuropsychology, neuroconnectivity and traumatic brain injury. Frontiers in systems neuroscience, 10, 55.
SMITH, D. H., CHEN, X. H., PIERCE, J. E., WOLF, J. A., TROJANOWSKI, J. Q., GRAHAM, D. I., & MCINTOSH, T. K. (1997). Progressive atrophy and neuron death for one year following brain trauma in the rat. Journal of neurotrauma, 14(10), 715-727.
Hellewell, S., Semple, B. D., & Morganti-Kossmann, M. C. (2016). Therapies negating neuroinflammation after brain trauma. Brain research, 1640, 36-56.
Loane, D. J., Kumar, A., Stoica, B. A., Cabatbat, R., & Faden, A. I. (2014). Progressive neurodegeneration after experimental brain trauma: association with chronic microglial activation. Journal of Neuropathology & Experimental Neurology, 73(1), 14-29.
Afridi, R., Lee, W., & Suk, K. (2020). Microglia Gone Awry: Linking Immunometabolism to Neurodegeneration. Frontiers in Cellular Neuroscience, 14, 544757. https://doi.org/10.3389/fncel.2020.00246
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