Traumatic Brain Injury: Pathophysiology and Treatments

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Table of Contents

Presentation
Pathophysiology
Assessment
Diagnosis
Treatment
References

Presentation

Traumatic brain injury (TBI) is a non-congenital and non-generative condition, which may result from a wide range of injuries occurring when the brain is affected by an external mechanical force (a jolt or a blow to the head or an object penetrating the skull). It may result in temporary or permanent dysfunction of the brain (impairing physical, cognitive, and psychological functions of the patient), bleeding, tom tissues, bruising, or other complications, some of which might lead to death (Algattas & Huang, 2013). Due to the number of causes and inclusion criteria, the definition of TBI is often inconsistent and problematic.

Post-concussive syndrome (PCS) may appear as a result of a mild traumatic brain injury or concussion and has a number of lingering symptoms such as fatigue, dizziness, headache, etc. It may be referred to as a mild type of TBI, which makes the conditions similar in symptoms. However, the key difference is that it is not life-threatening even despite the fact that its consequences can be rather long-lasting and serious (Boyd, 2014). Both conditions imply a change in the normal brain function; yet, the degree of this change is different.

Pathophysiology

There are two key mechanisms of TBI: focal (laceration, contusion, hemorrhage) and diffuse (brain swelling) damage to the brain. The type determines the outcome of the injury for the patient. The primary impact of TBI is produced at the moment of contact with an external mechanic force while the secondary impact covers subsequent, delayed pathological processes including but not limited to intracranial hypertension and cerebral ischemia. At the first stage of its development, the condition may be characterized by evident tissue damage as well as distorted metabolism and CBF regulation, which makes it similar to ischemia. Increased membrane permeability, anaerobic glycolysis, and formation of edema make lactic acid accumulate in the body (Algattas & Huang, 2013). Due to this, anaerobic metabolism dysfunction occurs as it is no longer able to regulate and maintain energy in the cells. As a result, the energy-dependent membrane fails, and the stores of ATP deplete. At the second stage, the terminal membrane depolarizes, and an excessive amount of excitatory neurotransmitters is released; catabolic processes are launched owing to Ca2þ- and Naþ-influx. The amount of intracellular free radicals and fatty acids increases as a result of the activation of lipid proteases, peroxidases, and phospholipases. All these processes affect the nucleosomal DNA and cause membrane degradation and apoptosis (Diaz-Arrastia et al., 2014).

The situation is less clear with post-concussive syndrome. It is considered by some scholars to be different from TBI is that it is unclear whether it has an organic or psychological basis. Still, the majority of studies accept its organic nature. It appears after an excessive amount of aspartate and glutamate is released, which results in a calcium influx leading to neuronal toxicity and cell death (frequently referred to as excitotoxic reaction). In this respect, the conditions are similar (Boyd, 2014). However, some researchers argue that memory impairment, cognitive and other disturbances may be purely psychological.

Assessment

To diagnose TBI, a thorough assessment of the patient’s physical and neurological damage is required as well as his/her course of recovery. This necessitates implementing a multidisciplinary approach to exclude potential errors of judgment. If an individual reveals some swallowing, cognitive, or communication problems, he/she must be assessed comprehensively. The assessment includes the investigation of the individuals’ medical and socioeconomic status, education, job, background, motor, cognitive, auditory, and emotional status, vision, the integrity of speech, motor planning, swallowing, speaking, reading, and writing abilities, memory, etc.

As far as PCS is concerned, the mechanism of assessment is generally the same (as it often appears sequelae of TBM). However, the difference is there is no reliable quantitative method that would allow identifying patients who are likely to develop the condition after being inflicted a brain injury (Boyd, 2014). That makes it rather challenging to assess risks and identify risk groups.

Diagnosis

In cases of moderate or severe TBIs, it is rather easy to diagnose the condition since the damage is evident. However, if the patient has other serious injuries, it is possible that a closed TBI can go unnoticed. Therefore, a proper neurological examination is crucial for giving necessary evidence. It is performed via MRI, CAT scan, PET scan, and SPECT (Carney et al., 2017). The diagnosis should be supported by neuropsychologists, occupational, physical, and speech therapists.

PCS is different since it is harder to diagnose until the patient starts having problems with routine tasks, which he/she used to perform successfully. No scan or testing can prove the presence of PCS. This accounts for the fact that the condition is typically diagnosed by its symptoms (which are basically the same as those of TBI): dizziness, headache, irritability, fatigue, insomnia, anxiety, blurry vision, loss of memory or concentration, light hypersensitivity, ringing in the ears, etc. (Boyd, 2014).

Treatment

Depending on the severity of the condition, there can be several types of treatment for TBI. The initial treatment is aimed to stabilize the patient shortly after the brain was damaged. Its goal is to assess vital body functions and divert possible life-threatening changes. Then, rehabilitative care center treatment follows, which is aimed at restoring the individual’s daily life functions. Minimization of secondary injury is achieved through the acute treatment program. Finally, surgical treatment may be needed to deal with swelling and a lack of oxygen (Carney et al., 2017)

Unlike TBI, the treatment of PCS is not so complex. No medications, rehabilitation therapies, or surgical interventions are required. In the majority of cases, time is the best treatment even if the patient has certain cognitive problems as they usually pass away on the own with the course of time (Boyd, 2014).

References

Algattas, H., & Huang, J. H. (2013). Traumatic brain injury pathophysiology and treatments: Early, intermediate, and late phases post-injury. International Journal of Molecular Sciences, 15(1), 309-341.

Boyd, W. D. (2014). Post-Concussion Syndrome. Bloomington, IN: Xlibris Corporation.

Carney, N., Totten, A. M., O’Reilly, C., Ullman, J. S., Hawryluk, G. W., Bell, M. J.,… Rubiano, A. M. (2017). Guidelines for the management of severe traumatic brain injury. Neurosurgery, 80(1), 6-15.

Diaz-Arrastia, R., Wang, K. K., Papa, L., Sorani, M. D., Yue, J. K., Puccio, A. M.,… Maas, A. I. (2014). Acute biomarkers of traumatic brain injury: Relationship between plasma levels of ubiquitin C-terminal hydrolase-L1 and glial fibrillary acidic protein. Journal of Neurotrauma, 31(1), 19-25.

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