Category: Traumatic Brain Injury

CDC defines TBI as a disruption in the normal function of the brain that can be caused by a bump, blow, or jolt to the head, or penetrating head injury. TBI is typically classified as focal (confined to a specific location), diffused (comprises a widespread area) or mixed injury (combination of both focal and diffused). Different aspects including TBI ethology, severity, brain region affected, and patient gender direct contribute to a unique brain pathology with a widely varying clinical outcome.

TBI pathophysiology is commonly classified into primary and secondary injury. Primary injury corresponds to the mechanical forces involved at impact moment inducing bone fractures, tissue and vascular damage as well as immediate cell death. As result, multiple pathophysiological mechanisms resulting in further brain damage are observed over hours or even years following the inciting TBI event, giving rise to term secondary injury(Ng & Lee, 2019). Secondary injury initially comprises multiple neurotoxic events including excitotoxicity, calcium influx, mitochondrial dysfunction, oxidative stress, neuronal death, inflammation and cerebral edema. Acute neurochemical changes observed in the first hours following TBI may be associated with the emergence of early behaviour impairments including motor deficit. On the other hand, long-term progression of secondary injury is followed by several changes underlying brain network reorganization. Thus, TBI patients may develop long-term neuropsychiatry complications including memory deficit and anxiety. In the next sections we are going to discuss the potential use of GUO on the acute/long-term progression of secondary injury and behaviour impairments following TBI.

Glutamate is considered the major excitatory neurotransmitter in the CNS playing an essential role on neuronal development, plasticity, memory and learning. Despite that, excessive levels of this amino acid in neuronal synapses may also result in neuronal death by excitotoxic mechanisms. Thereby, the precise balance of glutamate release and uptake are crucial to maintain the fine-tune of brain function.

A common TBI feature is the abrupt spreading depolarization of neurons at the damage epicentre resulting in a massive and disseminated glutamate release in the synaptic cleft (Katayama, Becker, Tamura, & Hovda, 1990). In addition, the glutamate clearance mainly performed by excitatory amino acid transporters GLAST and GLT1 in astrocytes are impaired during the initial stage following TBI (Dobrachinski et al., 2017). Preclinical studies show that a single GUO injection 15 or 40 min following FPI in rats, restore the glutamate uptake activity in hippocampal and cortical slices 3 and 8 hours upon TBI (Dobrachinski et al., 2017; R. D. R. Gerbatin et al., 2017). In addition, GUO prevents the FPI-induced downregulation on expression levels of glutamate transporters GLAST and GLT1 (Dobrachinski et al., 2017). Thus, GUO likely restore the glutamate uptake function by maintaining the suitable protein levels of glutamate transporters in astrocytes.

Glutamate uptake function is also tightly dependent of extracellular gradients of Na+ and cytoplasmic K+ sustained in equilibrium by the transmembrane enzyme Na+ K+-ATPase (Danbolt, 2001). GLT1 and GLAST drive the extracellular glutamate into astrocytes by a cotransport of high affinity of 3Na+ ions in the exchange of 1K+ ion (Danbolt, 2001). However, FPI results in loss of Na+ K+-ATPase activity leading to a breakdown of Na+ and K+ electrochemical gradients across membranes resulting in potential disruption of glutamate uptake function (R. D. R. Gerbatin et al., 2017). Interestingly, GUO protects against the loss on Na+ K+-ATPase activity in rats submitted to FPI (R. D. R. Gerbatin et al., 2017). This GUO effect likely reflects not only on maintenance of glutamate uptake function but also in cell osmotic equilibrium preventing astrocytic swelling induced by TBI.

Glutamate delivered into astrocytes is converted into glutamine by action of glutamine synthetase enzyme (GS) (Danbolt, 2001). Thereby, GS has an essential role for glutamate recycling sustaining this neurotransmitter below toxic levels in the CNS. FPI in rats results in failure of GS activity indicating a possible reduction of glutamate recycling in astrocytes exacerbating the harmful glutamate effects in the brain(R. D. R. Gerbatin et al., 2017). In contrast, GUO treated rats show a significant protection against the loss on GS activity 8 hours after FPI (R. D. R. Gerbatin et al., 2017). Thus, GUO seems to restore the glutamate recycling in astrocytes attenuating the glutamate toxicity in CNS.

Changes in the cellular redox state may also represents another important factor for the raise of glutamate levels observed following TBI. Oxidative damage targeting proteins such as GLT1, GLAST, Na+ K+-ATPase and GS may disrupt its function resulting in failure of precise synchrony between glutamate uptake and recycling in astrocytes (Hachimori et al., 1975; Morel, Tallineau, Pontcharraud, Piriou, & Huguet, 1998; Trotti, Danbolt, & Volterra, 1998). Interestingly, GUO shows protective effects against FPI-induced protein carbonyl content in rats (R. D. R. Gerbatin et al., 2017). The finding suggests GUO might also control the glutamate homeostasis in CNS by attenuating the TBI-induced oxidative damage to proteins involved in glutamate uptake/recycling in astrocytes.

Increased levels of glutamate in the synaptic cleft following TBI are associated with a massive Ca2+ and Na+ influx into neuronal and glial cells resulting from an overstimulation of NMDA and AMPA receptors (Ng & Lee, 2019). Cytoplasmic Ca2+ homeostasis in these cells is constantly maintained by mitochondria through Ca2+ sequester into the mitochondrial matrix compartment (Ng & Lee, 2019). However, Ca2+ overload into this compartment may results in mitochondrial swelling. Mitochondrial swelling following FPI in rats has been associated with loss of mitochondrial potential (ΔΨm), ROS generation and unbalance of redox system (Dobrachinski et al., 2017). In a closed-head model of mild TBI in rats, mitochondrial bioenergetic function evaluated by high-resolution respirometry (HRR) was also found compromised after TBI (Courtes et al., 2020). In both TBI models, all parameters related to mitochondrial respiration were restored by a single GUO treatment following TBI (Courtes et al., 2020; Dobrachinski et al., 2017; R. D. R. Gerbatin et al., 2017). In addition, such GUO effect on mitochondrial function was associated with the modulation of A1 adenosine receptor (R. R. Gerbatin, Dobrachinski, Cassol, Soares, & Royes, 2019). Thus, GUO likely sustain the suitable balance of mitochondrial function across different TBI models by reducing mitochondrial calcium overload in a dependent manner of A1 adenosine receptor modulation.

Mitochondrial disfunction is also associated with cell death by necrotic (lack of ATP) or apoptotic events following TBI (Ng & Lee, 2019). The opening of the mitochondrial permeability transition pore (MPTP) and release of cytochrome C may lead to caspase 3 activation (Ng & Lee, 2019). As a main effector apoptotic protein, caspase 3 initiates the programmed cell death from mitochondrial (intrinsic pathway) or cytoplasmic signalling (extrinsic pathway) (Ng & Lee, 2019). In contrast, GUO treatment after FPI attenuates the spread of neuronal loss around the injury site and protects against an increase in the levels of caspase 3 (R. D. R. Gerbatin et al., 2017). The finding suggests GUO may effectively counteract the progress of neurotoxic events associated to TBI.

TBI-induced breakdown of blood brain barrier and cellular damage results in an immediate neuroinflammatory response characterized by several inflammatory mediators including TNFα and IL- β (Ng & Lee, 2019). Exacerbated levels of both pro-inflammatory mediators is critically related with apoptotic events and formation of cerebral edema resulting in extension of neuronal loss (R. D. R. Gerbatin et al., 2017; Ng & Lee, 2019). GUO treatment 40 min following FPI seems to reduce the levels of TNFα and IL-1 beta 8 hours after TBI in rats. This GUO effect was associated with reduction of edema in the perilesional area of TBI what potentially contributes to the preservation of neurological functions.

A typical behaviour impairment observed immediately following TBI comprehend the motor deficit. Motor function is mediated from cortex to spinal cord reaching the skeletal muscle through a precise signalling involving several brain regions including cortex, sensorimotor cortex, subcortical nuclei, cerebellum and brainstem (Fujimoto et al., 2004). Thereby, lacerations or typical neurochemical changes previously mentioned in any of these brain regions may disrupt the complex signalling to coordinate the movement. FPI in rats results in an early reduction of spontaneous locomotion activity characterized by a decrease in the number of crossing, rearing, velocity and distance travelled in the open field. On the other hand, GUO treatment upon FPI restores all parameters related to spontaneous locomotion to control levels. Furthermore, the motor coordination deficit observed following the mild TBI (closed-head model) and FPI in rats, was also prevented with a single GUO treatment. Taken together, GUO neuroprotective effects against early TBI-induced motor deficit may reflect the ability of GUO to blunt multiple neurotoxic pathways underlying the secondary injury following TBI.

The progression of secondary injury into a chronic phase may result in several neuropsychiatry complications including memory deficit and anxiety. Rats submitted to FPI show anxiety-like behaviour and memory deficits at 14 and 21 days following TBI, respectively (Dobrachinski et al., 2019). In contrast, GUO daily treatment after FPI prevents the development of anxiety-like behaviour traits and loss of memory performance (Dobrachinski et al., 2019).

Such long-term behaviour impairments following TBI may result from molecular and morphological changes underlying synapse network reorganization in different brain regions. In fact, changes in CREB-BDNF signalling in the hippocampus may compromise the synaptic plasticity of hippocampal neurons resulting in cognitive and emotional disorders. FPI in rats induces a long-term downregulation of BDNF and CREB in hippocampal neurons 21 days after TBI (Dobrachinski et al., 2019). Chronic GUO treatment over the same period prevents such decrease of both genes (Dobrachinski et al., 2019). In addition, GUO blunts the FPI-induced decrease of a calcium-binding protein found in the membrane of synaptic vesicles in hippocampus (synaptophysin). However, GUO did not show any effect on the expression levels of GAP-43, a protein related with synapse repair (Dobrachinski et al., 2019). Therefore, these data suggest that GUO prevents emotional problems and memory deficits following TBI by attenuating synaptotoxicity in hippocampal neurons.

From a morphological perspective, synapse function may be also negatively affected by reactive gliosis triggered by TBI (Sajja, Hlavac, & VandeVord, 2016). Gliosis is characterized by long-term morphological changes in astrocytes and microglia, which is thought to also contribute for mood swings and cognitive decline after TBI (Sajja et al., 2016). Accordingly, FPI in rats induces a reactive astro- and micro-glioses in the hippocampus while chronic GUO treatment counteracted these morphological changes (Dobrachinski et al., 2019). Taken together, GUO shows an ability in preventing molecular and morphological changes in hippocampus associated to emotional problems and memory deficits following TBI. Interestingly, GUO neuroprotective effects in TBI seems to be dependent on the modulation of A1 adenosine receptors (Dobrachinski et al., 2019). In the next section we are going to discuss the involving of purinergic signalling on the neuroprotective effects of GUO.

Traumatic Brain Injury also referred to as TBI is by definition a form of acquired brain injury, occurs when a sudden trauma causes damage to the brain. TBI can be the result of when the head violently hits an object, or when an object is pierced into the skull and enters brain tissue. Symptoms of TBI can differ from the severity of the injury depending on the extent of damage that occurred to the brain. Two main causes of TBIs are “in car accidents when the head hits the windshield and in bicycle accidents when the head hits the ground”. Whereas many milder TBIs can be caused while participating in physical activity, for example many athletes experience concussions which is considered to be a mild TBI.

There are many different characteristics separated into four different categories of Medical/Neurological Symptoms, Behavior/Emotional Symptoms, Cognitive Symptoms, and Social Skills Developments. Within those categories they each have a list of possible symptoms for children with Traumatic Brain Injury which can be a resource for those who do not have a knowledge in TBIs. Primary and secondary are the way that medical professionals describe two types of brain damage. The differences between primary and secondary are that primary damage is a direct outcome of an initial impact to the brain, whereas secondary damage develops overtime as the brain responds to initial trauma. In Individuals with Disabilities Act, it states that traumatic brain injury can result in total or partial functional disability or psychosocial impairment, or in some cases both which can affect a student’s educational performance because it can cause impairments in many areas, for example, memory, attention, motor skills, etc. Head injuries causing disabilities can also affect a student’s information processing, social behaviors, memory capacities, and many other factors.

Looking at statistics relating with traumatic brain injury is eye-opening. Statistics show that about 2.5 million people sustain TBIs each year, of this number about 50,000 individuals die, and 280,000 are hospitalized. Children between the ages of zero and fourteen years old sustain about 475,000 TBIs, along with about 180 per 100,000 children under the age 15 experiencing TBIs, and of that number about five to eight percent experience a severe TBI. As stated earlier TBIs are often caused from physical activity or sports and recreational activities, which had led to the rate of TBI caused by sports and recreational related injuries increased 57% in just eight years for children under the ages of nineteen or younger. As well as more than 229,000 military personnel being diagnosed with a TBI between 2000 and 2011. Sadly, TBI is a common injury for veterans of Iraq and Afghanistan wars. It is currently estimated that 5.3 million children and adults in the United States alone are living with the consequences of sustaining a TBI, 40% of which involve children.

It is believed that the number of TBIs would decrease in children and others if seat belts and other child restraint devices were consistently used, as well as decreasing the number of accidents caused by driving under the influence of alcohol and other substances. As well as, children and others should wear the proper safety gear when bicycling, skateboarding, skiing, snowboarding, horseback riding, and similar activities. Children should not have to be reminded to put on their safety gear, it should be a habit for them, just like putting on a seat belt should be a habit every time they get into a car. With all of the statistics that are shown, it is an increasing concern regarding the number of TBIs in not only children but also in adults.

Traumatic Brain Injuries are not like other disabilities it is hard to diagnose because there is no set test or examination that can be done to prove how severe the injury is, it can only truly be diagnosed from a medical professional by symptoms the patient is experiencing (Hardman,382). As well as there being no set time frame where a TBI can be diagnosed, for some they feel the symptoms almost immediately, whereas others might take a couple days to start seeing the symptoms.

Although there are education support services for students who suffer from even a mild TBI but can be more extensive for the more severe injuries. Educational supports are there to focus on the student’s environmental changes that affect there day to day living and to help transition back into their appropriate school setting. For students who have TBIs, they can develop individualized education programs that can be written for short periods of time, for example for six to eight weeks, which gives the ability to make changes depending on progress and growth that is being made. It is common to see the most growth from students in the first year following the injury, with little progress made after that point which makes flexibility and responsiveness from teacher and support staff a necessity for the success of the student.

When thinking about the student’s success, it is beneficial to provide them with accommodations and modification to help ease them back into the workload depending on the severity of the injury. Some of the more common accommodations and modifications offered are a study guide or course outline, scribe or not taker, modify work amounts, having a classroom aid, and developing a routine and schedule. It is important to be able to provide resources for a student who is reintegrating back into the community, some services that may be recommended by medical professions or offered by the school are counseling and therapy to guide the students back into school.

For the students who decide that they want to continue their education after high school, there are resources out there to support them. There are interdisciplinary team members who contributed a great amount to help with the transition process, including the difficult factors of physical accessibility of the campus, living arrangements, academic achievement support, social and personal support systems, and training and placement for careers.. Whereas for students who find it difficult to continue their education after high school, the planning for the transition to employment is essential. Throughout high school, students with TBI should have developed skills associated with filling out job applications, interviewing, and participating in supervised work experiences. There are state agencies that provide assistance to young people to TBIs when looking to apply for jobs and some that even offer services related to aptitude assessment, training opportunities, and trial job placements.

It is important for people with TBIs to understand the benefits of collaboration and cooperation because they are key factors to success. Most children and youth with a TBI leave rehabilitations or hospital settings without preparation for the demands that come with returning to home and educational environments. As well as many educators are not prepared to provide the resources and services needed to a student with a TBI who has different cognitive, academic, and behavioral needs compared to other students. It is imperative that the appropriate teaching activities are given to help students with TBIs to have many opportunities throughout life.

Onе of thе lеast undеrstood, but most common injuriеs in sports is MTBI – mild traumatic brain injury – othеrwisе known as a concussion. An еstimatеd 3. 8 million rеcrеation- and sport-rеlatеd concussions occur in thе Unitеd Statеs еach yеar (Halstеad 599). Whilе most attributе youth rеlatеd concussions to high-contact sports such as football; concussions arе also prеvalеnt in sports such as soccеr, wrеstling, baskеtball, vollеyball, basеball, and softball (Gеssеl 497). Furthеr, an еlеvеn-yеar study of twеlvе high-school sports found that еvеry singlе sport saw an incrеasе in concussion ratеs bеtwееn 1997 and 2008 (Lincoln 960) making it a major public hеalth concеrn and thе focus of an еvеr incrеasing intеrеst in sports mеdicinе. Thе idеal solution would bе 100% prеvеntion of MTBI through pеrsonal protеction and implеmеntation of playеr safеty rulеs.

For football, this includеs improvеd hеlmеt dеsign, thе rеquirеd usе of mouthpiеcеs, and thе pеnalization of hеad-to-hеad contact. Yеt, as Graham еt al. rеportеd, at prеsеnt thеsе protеctivе dеvicеs in youth sports havе shown littlе еvidеncе in rеducing thе risk of MTBI, although thеy havе bееn shown to rеducе othеr injuriеs – е. g. , skull fracturеs – and should bе promotеd. Furthеr, sports such as soccеr, baskеtball, and wrеstling which havе dеmonstratеd a propеnsity for MTBI do not rеquirе any such protеctivе dеvicеs (IOM and NRC 272). Thеrеforе, for youth sports, thе еmphasis of concussion protocol rеsts with assеssmеnt and managеmеnt. Whilе MBTI occurrеncе and associatеd risks in profеssional sports has garnеrеd nationwidе еmphasis, with an еvеr incrеasing numbеr of athlеtеs еnding carееrs еarly as opposеd to risking longtеrm hеalth issuеs associatеd with MTBI, a glaring dеarth of knowlеdgе with rеgards to concussions еxists for youth sports.

Within this parеnt and voluntееr dominatеd еnvironmеnt, thе sеvеrity of this injury is oftеn dismissеd and is еuphеmizеd as a bеll-ringеr or “ding”. This lack of rеcognition lеads to a gross undеr-rеporting of MTBI in thе sporting arеna (Llеwеllyn 76). Young athlеtеs possеss an incrеdiblе amount of motivation to win, dеsirе to advancе within thеir sport, and longing for thеir tеammatеs’ accеptancе. Somеtimеs thеsе qualitiеs outwеigh thеir dеcision to play safе and rеport potеntial MTBI. McCrеa еt al. found that ovеr 15% of football playеrs sustainеd a concussion during a givеn sеason, but lеss than 50% of playеrs rеportеd thеir injury. Thе most common rеasons for concussion not bеing rеportеd includеd a playеr not thinking thе injury was sеrious еnough to warrant mеdical attеntion, motivation not to bе withhеld from compеtition, and lack of awarеnеss of probablе concussion.

Yеt, thеsе samе athlеtеs arе at an incrеasеd risk of catastrophic consеquеncеs duе to an immaturе nеrvous systеm, dеcrеasеd myеlination, thinnеr frontal and tеmporal bonеs, a largеr hеad body ratio, and wеakеr nеck musculaturе (Karlin S370). Thе lack of MTBI acknowlеdgеmеnt and incrеasеd risk factors can rеsult in SIS – sеcondimpact syndromе – a rarе but dangеrous rеsult of sеcond concussion that occurs whilе thе brain is still hеaling from a prеvious concussion. SIS may causе dangеrous brain swеlling and blееding rеsulting in dеath or pеrmanеnt disability and may occur еvеn days to wееks aftеr a first concussion is diagnosеd.

In 2006, Zackеry Lystеdt suffеrеd a lifе thrеatеning brain injury whilе playing middlе school football. Coachеs rеturnеd him to play, without an еvaluation by a licеnsеd hеalth carе profеssional. Hе collapsеd on thе fiеld at thе еnd of thе gamе and rеquirеd еmеrgеncy brain surgеry rеsulting in pеrmanеnt disability (MicCool). In 2009, thе statе of Washington passеd a law, in his namе, prohibiting thе rеturn to practicе or gamе of a youth athlеtе suspеctеd of sustaining a concussion without a licеnsеd hеalth-carе providеr’s writtеn approval.

Within 5 yеars, similar laws wеrе passеd in all 50 statеs and thе District of Columbia rеsulting in a dеcrеasеd ratе of MTBI rеcurrеncе (Yang 1916). For mе, thе issuе is dееply pеrsonal. In 2013, playing youth football, I was concussеd. Furthеr, duе to my cognitivе impairmеnt and ovеrall poor undеrstating of MTBI of all involvеd – i. е. coachеs, parеnts, and mе – I coaxеd my way back to thе playing fiеld. Fortunatеly, shortly thеrеaftеr it bеcamе apparеnt to thе rеfеrееs that I was impairеd and I was rеmovеd from thе fiеld. I was rеquirеd to obtain a doctor’s writtеn approval bеforе rеturning to practicе or gamеs, which involvеd computеd tomography or CT scans, providing mе thrее wееks of rеcovеry timе. If this sеason had occurrеd prior to Florida’s passing of thе Zachary Lystеdt law – April 27, 2012 – I would havе likеly rеturnеd to full contact immеdiatеly and would havе bееn at significant risk of SIS. еvеn so, I havе only just rеcеntly bеcomе awarе of thе pеrmanеnt damagе that occurs with rеpеtitivе concussions by pеrsonally rеsеarching thе topic. Furthеr, from my timе in youth and high school athlеtics, I havе witnеssеd an еxtrеmе lack of concеrn from fеllow compеtitors with rеgards to MTBI. This ignorancе of rеpеrcussions is thе rеal dangеr of concussions in youth sports.

For anyone who is familiar with rugby and other contact sports it is common knowledge that these sports are not always safe and have the potential to go incredibly wrong. It has been stated by Hosea, H (2012) “sports activities cause an estimated 20% of all TBIs among youths and young adults” which results in an estimated 300,000 cases per year. Repeated disturbances to the brain are not healthy to the individual and I believe it is important that these long-term effects are left out in the open so people can become aware of the effects of these frequently occurring injuries. Therefore, during this essay I decided to investigate Traumatic Brain injuries (TBI’s) further. To determine the long-term effects they have on us, their side effects and how these affects could impact our future generation as they grow up.

The first side effect I have researched is the link between Alzheimer’s Disease (AD) and TBI’s. Lou, D., et al. (2018) used a weight drop method equip with a hollow Plexiglas tube and acrylic stick which they tested on mice to simulate a TBI like concussion. They then accessed the chemical changes within the brains of the mice. Whereas the second article by Jasmeet, P.H., et al. (2017) used a sample of 160 nonHispanic veterans who were neuro-scanned by a Siemens 3 T TIM Trio. This is a device used for cardiac and neuro imaging studies to investigate disturbances in brains and bodies. The disadvantage of the first article by Lou. D. at al., (2018) is that it is not certain if these effects will directly translate into humans because it is not being conducted on humans. That would be unethical. It is also unethical to induce these types of injuries onto animals on purpose, to pursue an investigation.

The first researched side effect I have found is the link between TBI’s and Alzheimer’s disease (AD). The studies posted by Jasmeet, P.H., et al. (2017) and Lou. D. et al., (2018) both test for a link between TBI and Alzheimer’s disease but produce slightly different, but also similar results. According to Jasmeet, P.H., et al. (2017) traumatic brain injuries have shown a link to cross-sectional cortical thinning. This is a term used to describe the thickness of the brains cortex’s which may only vary a few millimeters. When this cortical thinning occurs in Alzheimer’s disease vulnerable regions of the brain it can be a mechanism of memory performance reduction and neurodegeneration for patients with a high genetic risk of AD. However, Lou. D. Et al., (2018) states that TBI’s put the brain under oxidative stress which initiates amyloid beta processing which is a significant part of AD. Amyloid beta processing is the dying of neurons in the brain, essentially neurodegeneration as Jasmeet, P.H., et al. (2017) also stated. In extreme cases this neurodegeneration can snowball affect into diseases such as AD which is defined as “chronic neurodegenerative disease” by Wikipedia. This is a significant problem for individuals with TBI’s because when neurons are lost, they are lost forever. These outcomes were slightly different due to the fact Jasmeet, P.H., et al. (2017) had access to the Siemens 3 T TIM Trio brain scanning devise and Lou. D. Et al., (2018) conducted their investigation on mice and were unable to see cortical thinning occurring in the brains of the mice.

The second neurological side effect of traumatic brain injuries is on the individuals sensory skills. The first article I am using is published by William, M.P., Micheal, J.L., Vonetta, M.D., & Kiesa, G.K. (2006) which conducted an experiment on 14 healthy patients and 15 patients with TBI’s and recorded how well they did on 2 tasks. The first task required the patients to read aloud numerous sentences where they had to remember the last word of each of these sentences. The second test was cued-stoop response ask where patients were presented an instructional cue, for example “which word reads the color red” and they needed to pair it with a visual stimulus. This tested how fast they could register stimulus and relate it to the real-life object. This was made more difficult by having the word red, written in blue. Their reaction times were recorded. The second research article I will be using was done by Siriluck, K., Achara, S., Suparat, W., Chawapornpan. C. (2015) and was done on 2 subjects with TBI’s and six of their closest care givers. The purpose of the experiment was to see if sensory stimulation (SS) in a real life context had an impact on the patient’s ability to recover from the TBI. A major difference between these 2 studies is that the sample size is very different. The study done by William, M.P et al., (2006) utilizes results from 29 different individual whereas the study conducted by Siriluck, K. et al., (2015) only discuses findings from 2. This difference in sample size means findings made by William, M.P et al., (2006) could be more valid because they have more trials to test for a similar outcome, whereas Siriluck, K. et al., (2015) only concludes findings off 2 . Siriluck, K. et al., (2015) concluded in their trials that the brain lesions (brain damage) induced by the TBI, restricted the signaling pathways for the neurons to the brain. This meant that more complex sensory signals were unable to properly translate into a cognitive function. Therefor patients would receive the stimulus but not know what it meant nor what to do with it. William, M.P., Micheal, J.L., Vonetta, M.D., & Kiesa, G.K. (2006) also found evidence similar to these results in their trial due to finding that the patients with TBI injuries produced dramatically more poorly in the trials tasks then the control group of unaffected individuals. This occurred through longer reaction times in the cued-stoop test and more frequent errors in the memory activity. Indicating the stimulus was present but the higher cognitive function was nonexistent or prolonged on some individuals.

The purpose of this essay was to research and analyse the side effects of Traumatic brain injuries to determine the severity of the issue which faces thousands of teenage and middle age people playing higher contact sports. The findings were as I predicted and show us that TBI’s should not be taking lightly, and that extra care to try and prevent TBI’s should be even more encouraged. In all sports and activities. Side effects of TBI’s in extreme cases can include mental degradation also known as Alzheimer’s disease, and other cognitive defects including brain pathway defects. This make higher cognitive function like registering a stimulus and completing a simple task difficult to complete for individual having had a TBI. These side effects can translate into difficulties in real life, not only in the controlled environment of an investigation. These side effects can affect the individuals in their workplace and when completing everyday tasks like talking with friends and family and going to the supermarket. Making almost any communicative and thinking task a challenge for TBI victims to complete.

There are many focal areas of neuropsychological disturbance associated with mild traumatic brain injury (mTBI). These include; impaired verbal retrieval, attentional deficits, and emotional distress. Equally other domains can be affected, for example, processing speed and memory, however, descriptions of mTBI most commonly include the first three. These issues may not present until a number of days after the insult. This may be due to the presence of other distracting injuries or because of cessation of normal duties due to visceral complaints of headaches and dizziness.

Verbal retrieval deficits may be unveiled through difficulty in recalling words readily, whether those be names, places, or objects. This dysnomia may produce misnamings or paraphasias with the substitution of similar semantically linked words, for example saying,” car,” instead of,” drive” (1) Such a presentation may be misconstrued as a memory failing, and yet it can be differentiated by utilizing cueing techniques. These can allow the patient to show their ability to know the word that they have difficulty recalling spontaneously. Hence, there is not infrequently a complaint of memory problems from this patient cohort which is actually attributable to an attentional and retrieval deficit rather than a memory problem per se. (2)

Slowed processing will present itself as an attentional deficit. This means that patients may be highly distractable, of poor concentration, and may have little ability to work in tandem at parallel tasks. There can be seen a tendency to underestimate time intervals and when there are severe attentional issues, the patient may experience disconcerting disorientation and even confusion.

During the first weeks following injury, in particular, activities that were previously automatic, such as mental calculations, reading, planning daily tasks, etc. require an intense focus. This loss of automaticity results from diffuse microscopic loci of damage throughout the whiter matter and upper brain stem. These increased requirements for concentrations, lead to a pervasive sense of fatigue. This symptom can be particularly disabling and is reinforced by the emotional dysregulation that is another feature of mTBI. In any illness, fatigue and tiredness will produce increased irritability levels and frustration, and this syndrome is no different. In fact, fatigue, mental inefficiency, and emotional dysregulation can be seen as a positive feedback loop, increasing the effect of the others. Education regarding these possible outcomes is essential in managing mTBI. Otherwise, the typical post-concussion syndrome can spiral into anxiety and depression. (3)

A comprehensive neuropsychological evaluation is a non-standardized entity. In a study looking at the current evaluation of patients with suspected mTBI, Blostein and Jones audited 35 trauma centers in the United States. They discovered that fewer than half had a standardized protocol for assessing patients. (6) This is likely a major contributing factor to the 50-90% of patients who go undiagnosed at presentation (7) These patients have a poorer prognosis due to the lack of follow-up or psychoeducation that can be afforded to them. An appropriate battery of testing would include the following areas; processing speed (Trail making test A), language (Boston Naming Test), visuospatial (Rey Complex Figure Test), executive functions (Trail Making Test B), memory (Story learning), attention (Continuous Performance Test of Attention). These tests will be compared to a premorbid estimate of functioning.

Whilst the features of neuropsychological impairment in this syndrome are well typified, consensus regarding the expected course of the disease process is heterogeneous. Most individuals would be expected to recover normal neuropsychological function within 1 to 3 months. A systematic review of meta-analyses was carried out by Karr et al, which demonstrated a resolution of cognitive impairment at 90 days (8) However, some studies have suggested that subtle aspects of attention and working memory could be seen to be impaired even at 5 years post-injury (4). The minority of patients that report deleterious problems months after injury (a phenomenon known as a post-concussive syndrome) have polarised opinions among healthcare professionals. One side of this dichotomy attributes symptoms to neurological damage sustained from the injury itself. Others have theorized that chronic complaints of cognitive dysfunction have etiology in psychogenic factors such as pre-morbid personality or the acquisition of monetary gains that may be afforded to injured parties. (5) A number of studies have demonstrated a correlation between pre-morbid psychological vulnerabilities and the development of post-concussive symptoms (9) This would support the latter argument. This must be balanced by the evidence of studies, which shows that the severity of the injury is a strong predictor of future PCS development. (10)

There are relatively sparse volumes of literature on the utility of early neuropsychological interventions in preventing post-concussive syndrome. The best-supported practices are education on post-concussive symptoms, the likely course of illness, and reassurance that recovery is expected to be complete for the majority of patients. Advice regarding a period of rest before an incremental return to activities is another important piece of advice. These early psycho-educational interventions are supported by a number of systematic reviews (11) Such evidence would support the integration of educational sessions as part of the standard of care for those who have sustained mTBI. This is particularly true for populations that are at higher risk of PCS, for example, lower socio-economic groups, older persons, and those with pre-existing disabilities.

Treatment options for those with established PCS are largely extrapolated from existing modalities used for specific symptoms that are frequently reported in those with the syndrome. This is due to a lack of data regarding the minority of patients who have long-term problems following mTBI. The two main arms of treatment for these patients can be described as cognitive rehabilitation and psychotherapy. A systematic review of outcomes in a military population who undertook cognitive rehabilitation following mTBI has supported their efficacy in improving function. (12) Therapy in this domain can be applied to treat attention dysregulation which is a common feature of PCS, impacting concentration, functional memory, and task orientation. Examples of interventions with consensus backing include Time Pressure Management and Attention Process Training. The impact of this can be strengthened with education on strategies of compensation to manage attentional capacity.

Executive dysfunction can have a particularly far-reaching negative influence and can be challenging to ameliorate. Traditionally there will be a graded approach taking in a number of stages. Initially, there must be a development of awareness, which will allow for visualization of possible obstacles in relation to a task. This will facilitate the execution of tasks that must be followed by an evaluation of performance. One such therapeutic framework is the Cognitive Orientation to Occupational Performance.

Interventions for memory deficits can be internal or external. Visualization association techniques can allow the individual to tack on new information to that which is already familiar. Converting complex new information into more manageable blocks is useful as is utilizing acronyms. External techniques are myriad in the modern age and can include the use of alarms, calendars, and memory apps available on smartphones.

Cognitive rehabilitation should be integrated with psychological interventions addressing the emotional distress associated with PCS. Possible strategies include CBT, mindfulness sessions, or talk therapy. The greatest evidence exists for the utility of CBT in this domain.

References

1. Murdoch, G.E. (1990). Acquired speech and language disorders. A neuroanatomical and functional neurological approach. New York. Chapman and Hall
2. Lezak, M.D. (1992). Assessment of mild, moderate, and severe traumatic brain injury. In N. Von Steinbuchel, D. Y. von Cramen and E. Poppel. Neuropsychological Rehabilitation. Berlin: Springer-Verlag.
3. Varney, N.R. and Sheperd, J.S. (1991) Minor head injury and the post-concussive syndrome. Neuropsychology and the Law. New York: Springer.
4. VANDERPLOEG, R., CURTISS, G., & BELANGER, H. (2005). Long-term neuropsychological outcomes following mild traumatic brain injury. Journal of the International Neuropsychological Society, 11(3), 228-236
5. Binder, L.M. (1986) Persisting symptoms after mild head injury: A review of the postconcussive syndrome. Journal of Clinical and Experimental Neuropsychology, 8, 323-346
6. Blostein, Paul & Jones, Susan. (2003). Identification and Evaluation of Patients with Mild Traumatic Brain Injury: Results of a National Survey of Level I Trauma Centers. The Journal of trauma. 55. 450-3.
7. McCrea, Michael & Nelson, Lindsay & Guskiewicz, Kevin. (2017). Diagnosis and Management of Acute Concussion. Physical Medicine and Rehabilitation Clinics of North America. 28. 10.1016/j.pmr.2016.12.005.
8. Karr, J. E., Areshenkoff, C. N., & Garcia-Barrera, M. A. (2014). The neuropsychological outcomes of concussion: A systematic review of meta-analyses on the cognitive sequelae of mild traumatic brain injury. Neuropsychology, 28(3), 321-336
9. Katz, Douglas & Cohen, Sara & Alexander, Michael. (2015). Chapter 9. Mild traumatic brain injury. Handbook of clinical neurology. 127C. 131-156
10. Wäljas, Minna & Iverson, Grant & Lange, Rael & Hakulinen, Ullamari & Dastidar, Prasun & Huhtala, Heini & Liimatainen, Suvi & Hartikainen, Kaisa & Ohman, Juha. (2014). A Prospective Biopsychosocial Study of the Persistent Post-Concussion Symptoms Following Mild Traumatic Brain Injury.. Journal of neurotrauma.
11. Snell DL, Surgenor LJ, Hay-Smith EJ, Siegert RJ A systematic review of psychological treatments for mild traumatic brain injury: an update on the evidence; J Clin Exp Neuropsychol. 2009 Jan 31(1):20-38.
12. Cooper D.B., Bunner A.E., Kennedy J.E., Ballin V., Tate D.F., Eapen B.C., Jaramillo C.A. Treatment of persistent post-concussive symptoms after mild traumatic brain injury: A systematic review of cognitive rehabilitation and behavioral health interventions in military service members and Veterans. Brain Imaging Behav. 2015;9:403–420.

Introduction

Traumatic brain injury (TBI) is commonly defined as an insult to the brain from an external force that causes temporary or permanent impairment in functional, psychosocial, or physical abilities (Delgado, 2016). It is a significant cause of morbidity and mortality, and the leading cause of death and disability among young adults. Common causes of TBI include motor vehicle accidents, falls, sports injuries, and violence, and it is recognized increasingly in war zone injuries. According to Lozano (2015) “There are many types of TBI which includes concussions, contusions, diffuse axonal injury (DAI), traumatic subarachnoid hemorrhage (tSAH), and Hematoma”. According to (Talsky, 2011) “In the US, approximately 2 million people will sustain a TBI each year, one-quarter of whom will require hospitalization, leading to a conservative estimate of direct and indirect costs of $50 billion to $100 billion annually”. The side effects of a TBI can be mild, moderate, or severe, depending on the degree of harm to the brain (Delgado, 2016). In mild TBI the person is awake; eyes open. Symptoms can include confusion, disorientation, memory loss, headache, and brief loss of consciousness. In moderate TBI the person is lethargic; eyes open to stimulation. Loss of consciousness lasting 20 minutes to 6 hours. Some brain swelling or bleeding causes sleepiness, but still arousable. Whereas in severe TBI the person is unconscious; eyes do not open, even with stimulation. Loss of consciousness lasting more than 6 hours (Talsky, 2011).

Etiology

• Ground-level fall
• Elevated-level fall
• Low-speed motor vehicle collision (< 25 mph)
• High-speed motor vehicle collision (> 25 mph)
• Blunt trauma
• Sports-related
• Military-related (blast)Penetrating injury
• Acceleration–Deceleration injury
• “Shaken Baby” injury (Lozano, 2015)

Briefly explain how TBI is diagnosed.

TBI needs to undergo a systematic yet fast assessment in the emergency room. Cardiovascular and pulmonary function is assessed first. According to (Richardson, 2018) “Next, a speedy assessment of the entire body is performed, followed by a total neurological assessment”. The neurological examination includes an assessment utilizing the Glasgow Coma Scale (GCS). In addition to the GCS, the ability of the pupils to become smaller in bright light is also tested. In patients with large mass lesions or with high intracranial pressure (ICP), one or both pupils may be very wide or ‘blown’ (Richardson, 2018). The presence of a wide or dilated pupil on only one side suggests that a large mass lesion may be present on the same side as the dilated pupil. Brainstem reflexes including gag and corneal (blink) may also be tested (Richardson, 2018).

A computed tomography scan (CT or CAT scan) is the gold standard for the radiological evaluation of a TBI patient. According to (Richardson, 2018) “A CT scan is easy to perform and is an excellent test for recognizing the presence of blood and fractures, which are the most crucial lesions to identify in medical trauma cases”.

Describe the pathophysiology of traumatic brain injury

Traumatic brain injury (TBI) stays one of the main sources of morbidity and mortality among citizens and the military workforce internationally. Despite advances in our knowledge of the complex pathophysiology of TBI, the underlying mechanisms are yet to be fully elucidated (Yun, 2019). While initial brain insult involves acute and irreversible primary damage to the parenchyma, the ensuing secondary brain injuries often progress slowly over months to years, hence providing a window for therapeutic interventions. As per Lee ‘To date, hallmark occasions during deferred optional CNS harm incorporate Wallerian degeneration of axons, mitochondrial brokenness, excitotoxicity, oxidative pressure and apoptotic cell passing of neurons and glia’ (2019). Broad research has been coordinated to the recognizable proof of druggable targets related to these procedures. Moreover, huge exertion has been advanced to improve the bioavailability of therapeutics to CNS by formulating systems for the productive, explicit, and controlled conveyance of bioactive operators to cell targets (Yun, 2019).

The initial phases of cerebral damage after TBI are described by direct tissue harm and impaired regulation of CBF and metabolism. This ‘ischemia-like’ pattern leads to the accumulation of lactic corrosive because of anaerobic glycolysis, increased membrane permeability, and continuous edema development (Yun, 2019). Since the anaerobic metabolism is inadequate to maintain cellular energy states, the ATP stores deplete and failure of energy-dependent membrane ion pumps occurs. The second phase of the pathophysiological is described by terminal membrane depolarization alongside the excessive release of excitatory neurotransmitters (for example glutamate, aspartate), activation of N-methyl-D-aspartate, α-amino-3-hydroxy-5-methyl-4-isoxazole propionate, and voltage-dependent Ca2+- and Na+-channels (Yun, 2019). The sequential Ca2+-and Na+- influx leads to self-digesting (catabolic) intracellular processes. Ca2+ activates lipid peroxidases, proteases, and phospholipases which in turn increase the intracellular concentration of free fatty acids and free radicals. Furthermore, activation of caspases (ICE-like proteins), translocases, and endonucleases start dynamic basic changes of natural films and the nucleosomal (DNA fracture and restraint of DNA fix) (Yun, 2019). Together, these events lead to membrane degradation of vascular and cell structures and ultimately necrotic or programmed cell death (apoptosis).

What are the signs and symptoms associated with TBI?

The seriousness of manifestations relies upon whether the damage is mild, moderate, or severe. concussion either doesn’t cause unconsciousness or unconsciousness lasts for 30 minutes or less (Alzheimer’s Association, 2020). Mild traumatic brain injury symptoms may include:

Failure to recollect the reason for the damage or occasions that happened preceding or as long as 24 hours after it occurred:

• Perplexity and bewilderment.
• Trouble recollecting new data.
• Migraine.
• Unsteadiness.
• Foggy vision.
• Queasiness and spewing.
• Ringing in the ears.
• Inconvenience talking intelligently.
• Changes in feelings or rest designs (Alzheimer’s Association, 2020)

These side effects regularly show up at the hour of the damage or before long, yet at times may not produce for a considerable length of time or weeks. Mild traumatic brain injury manifestations are generally impermanent and clear up within hours, days, or weeks; be that as it may, once in a while, they can a month ago or more. According to Alzheimer’s Association, (2020). Mild traumatic brain injury causes obviousness enduring over 30 minutes yet under 24 hours, and serve traumatic brain injury causes obviousness for over 24 hours. Side effects of moderate and serve traumatic brain injury are like those of mild traumatic brain injury, yet progressively genuine and longer-enduring.

In all types of, traumatic brain injury cognitive changes are among the most widely recognized, disabling, and long-lasting symptoms that can result directly from the injury. The capacity to learn and recall new data is often affected (Alzheimer’s Association, 2020). Other commonly affected cognitive skills include the ability to focus, arrange thoughts, plan effective strategies for finishing tasks and activities, and make sound decisions.

Outline the medical and surgical treatment of TBI

Medical Treatment

Before a surgical procedure is considered, medical management is typically attempted to reduce ICP. As indicated by (Knot, 2014) ‘Mannitol or hypertonic sodium chloride solution are typically the first-line treatments after pain and agitation have been dealt with and the patient is inappropriate body position as described before’. I.V. administration of hyperosmolar agents, including hypertonic sodium chloride solution and mannitol, makes an osmolar angle, drawing water across the blood-brain barrier and diminishing interstitial volume. This intervention has been shown to decrease ICP and improve CPP in patients with severe TBI (Knot, 2014).

Barbiturates are regularly used to treat ICP. There is no affirmation that barbiturates lessen mortality; it also causes low BP. Phenytoin is recommended to decrease posttraumatic seizures. Levetiracetam can be utilized as another option (Varghese, 2017). Sympathetic storming which includes posturing, dystonia, hypertension, tachycardia, dilatation of the pupils, sweating, hyperthermia, and tachypnea can occur within the first 24 h after injury until several weeks. As per (Varghese, 2017) ‘This can be caused after the cessation of sedatives and narcotics in the ICUs and ought to be treated based on their signs and symptoms by initiating planned medications to reduce the activities of the sympathetic nervous system”. The patients who receive erythropoietin show lower mortality and better neurological result and limited neuronal harm induced by TBI. Naloxone effectively reduces mortality and controls ICP in TBI (Varghese, 2017).

Surgical Management

Surgical evacuation is done on patients having a GCS score ≤8 with a huge lesion on non-contrast head CT scan. Depressed skull fractures are open or complicated and need surgical repair (Varghese, 2017). The available surgical options to control increased intracranial pressure and to limit secondary brain damage in the setting of severe traumatic brain injury (TBI) include decompressive craniectomy, cisternostomy, and other methods to divert cerebrospinal fluid (CSF) such as placement of an external ventricular drain (Giammattei, 2018).

Decompressive craniectomy (DC) had been used to control ICP associated with abnormal conditions, including intracranial neoplasm, ischemic disease, and diffuse edema from TBI (Moon,2017). The benefit of DC in the treatment of malignant infarction had been proved by previous studies. Although DC in TBI reduces ICP by evacuating hematoma and providing wider space for the brain, its improvement for the clinical outcome is not clear. DC must be extensive at all times because the benefits of DC are directly affected by surgical technique and the degree of decompression achieved (Moon,2017). According to Moon (2017), “Two main techniques widely used for DC in TBI are unilateral frontotemporoparietal craniectomy and bifrontal craniectomy”. Unilateral frontotemporoparietal craniectomy is especially useful for unilateral localized lesions, including traumatic hematoma, and brain swelling due to middle cerebral artery (MCA) infarction(Moon,2017).

The cisternostomy as a procedure can be either an outflow corridor for the cerebrospinal fluid (CSF) from the ventricular system to the cisternal subarachnoid space or an inflow corridor for the atmospheric pressure to be opened on the basal cistern and equalize cisternal and external pressure aiming for brain relaxation. As indicated by (Hoz, 2018) classify cisternostomy into two broad categories such as outflow corridor and inflow corridor. With the outflow corridor when the cisternostomy procedure provides a drainage pouch for the ventricular CSF and/or closed fluid-containing compartments. Theoretically, the inflow cisternostomy can be categorized into convexity and basal cisternostomy and the last can be partitioned into supratentorial and infratentorial, however, the ongoing proof considers the basal supratentorial cisternostomy is the cisternostomy appropriate.

External ventricular drains (EVDs) are generally utilized in neurosurgery in various conditions however frequently in the management of traumatic brain injury (TBI) to monitor and/or control intracranial pressure (ICP) by occupying cerebrospinal fluid (CSF). According to (Chau, 2019) ‘Their clinical viability, when utilized as a therapeutic ICP- lowering procedure in contemporary practice, stays vague’. No consensus has been reached regarding the drainage strategy and the optimal timing of insertion (Chau, 2019).

Three (3) classes of medications TBI

In 2008 a retrospective analysis was conducted on medications prescribed to brain injury patients. Charts of patients examined in the Raymond J. Greenwald Rehabilitation Center at the SUNY State College of Optometry from the years 2000 to 2003 were reviewed. As indicated by (Kapoor, 2008) ‘ The 4 most common classes of medication taken by TBI patients anti-anxiety/antidepressants (42.5%), anticonvulsants (26.9%), opiate/combination analgesics (23.8%), and cardiac/antihypertensive (23.1%). However, the top three (3) classes of medication used for patients with Traumatic Brain Injury will be elaborated on.

Anti-depressant

Anti-depressant medications are thought to work by affecting the levels of the brain’s natural chemical messengers, called neurotransmitters, and adjusting the brain’s response to them. Examples include citalopram, amitriptyline, paroxetine, and sertraline (CEMM Virtual Library, 2018).

Anti-depressants treat disorders such as:

• Anxiety
• Bulimia (eating disorder)
• Obsessive-compulsive disorder
• Panic disorders (CEMM Virtual Library, 2018).

Some possible side effects of Anti-depressants are:

• Blurred vision
• Cardiac palpitations
• Confusion
• Constipation
• DizzinessDrowsiness (CEMM Virtual Library, 2018).

Anti-convulsant

Anti-convulsant medications are used to suppress the rapid and excessive firing of neurons that start a seizure (CEMM Virtual Library, 2018). Anti-convulsants can sometimes prevent the spread of a seizure within the brain and offer protection against possible excitotoxic (excessive stimulation by chemicals in the nervous system) effects that may result in brain damage (CEMM Virtual Library, 2018). Examples include sodium valproate, gabapentin, topiramate, and carbamazepine.

Anticonvulsants treat different types of seizures such as:

• Absence seizures (formerly called petit mal seizures)
• Acute seizures
• Bipolar disorders
• Corticofocal seizures
• Generalized tonic-clonic seizures (CEMM Virtual Library, 2018).

Some possible side effects of Anti-convulsant are:

• Alopecia (hair loss)
• Amnesia (memory loss)
• Nausea
• Nystagmus (rapid, involuntary eye movements)
• Tremor
• Vomiting
• Weight gain (CEMM Virtual Library, 2018).

Opiate/Combination analgesics

Pain management medications are used to control pain stemming from TBI, and the symptoms and effects related to the injury (CEMM Virtual Library, 2018). Examples include acetaminophen, ibuprofen, and naproxen sodium.

Opiate/Combination analgesics usually treat symptoms such as:

• Arthralgia (joint pain)
• Fever
• Headache
• Mild to moderate pain
• Myalgia (muscle pain)

Some possible side effect of Opiate/Combination analgesics are:

• Burning sensation
• Constipation
• Dizziness
• Gastrointestinal irritation and bleeding
• Heartburn
• Nausea (CEMM Virtual Library, 2018).

What are the nursing considerations/management for this patient?

Effective nursing management strategies for traumatic brain injury are still an amazing issue and a difficult task for neurologists, neurosurgeons, and neuro nurses. According to (Varghese, 2017) ‘Nurses are the health professionals who see the full effect of TBI and have what it takes that can alter the course of a patient’s recovery; it is significant for nurses to have a valuable resource with evidence-based”.

Temperature management

Hypothermia reduces ICP (40%) and cerebral blood flow (CBF, 60%), has effects on cerebral metabolism, and improves results for 3 months after injury. Hence, it limits secondary brain injury. Normothermia ought to be maintained with the utilization of antipyretic medication, surface cooling devices, or even endovascular temperature management catheters (Varghese, 2017).

Nutrition

Patients following damage may encounter a systemic and cerebral hypermetabolic state. Early enteral feeding should be initiated within 72 h of damage. By day 7 of postinjury, these patients ought to be given full caloric substitution (Varghese, 2017). After TBI, early initiation of nutrition is recommended.

Fluid therapy

Fluid therapy helps in restoring vascular capacity, tissue perfusion, and cardiac flow rate (Varghese, 2017). Hypertonic saline can be used for patients with complications of TBI and systemic shock.

Hyperventilation

Hyperventilation reduces PaCO2, CBF, and ICP through cerebral autoregulation. It can be used only if ICP >30 mmHg and CPP 70 mmHg but higher ICP >40 mmHg (Varghese, 2017).

Glucose management

Extremes of very high or low blood glucose levels should be managed accordingly. A target range of up to 140 mg/dL or possibly even 180 mg/dL may be appropriate (Varghese, 2017). Patients with hyperglycemia should be managed with insulin protocol in cases with values>200 mg/dl for improving the outcome.

Care Plan

A care plan for this patient offers a critically important basis for the person and his family to fully appreciate the seriousness of the acquired impairments, likely complications, implications for independence and quality of life, and long-term care needs, whether for clinical or litigation purposes. Two actual and one potential diagnosis for this patient includes:

Conclusion

In conclusion, Traumatic Brain Injury is a major health issue that affects the anatomy and functions of the brain. It’s as sudden damage to the brain caused by a blow or jolt to the head. Common causes include car or motorcycle crashes, falls, sports injuries, and assaults. Injuries can range from mild concussions to severe permanent brain damage. While treatment for mild TBI may include rest and medication, severe TBI may require intensive care and life-saving surgery. Those who survive a brain injury can face lasting effects on their physical and mental abilities as well as emotions and personality. Most people who suffer moderate to severe TBI will need rehabilitation to recover and relearn skills. TBI typically affects all aspects of a patient’s future life: domestic, recreational, vocational, social, and personal. Safety precautions in daily activities may help to avoid TBI.

Naturally, we all try and take care of our physical and mental health. Nevertheless, none of us are exempt from suffering the kind of accident that could affect our brains.

As a matter of fact, the most serious accidents tend to happen when we least expect them. Furthermore, the head is one of the most delicate areas of the body when it comes to injuries. These can range from a traumatic brain injury to other various kinds of damage. Their effects vary, depending on the severity of the contusion.

Most brain injuries are closed-head injuries. However, penetrating injuries in which an object enters the skull also occur frequently. It’s these that carry the most serious consequences. We should mention that after any blow to the head, as a safeguard, it’s always recommended to consult a doctor.

Traumatic Brain Injury

Traumatic brain injury (TBI) is an injury that directly affects the brain. It causes damage that, depending on the severity, can reach extremes such as coma or death. Furthermore, these kinds of injuries can occur at any time. For example, due to accidents, blows, falls, or even when you’re practicing your favorite sport.

Understanding the psychological effect of a traumatic brain injury is of great help in discerning if the contusion is mild, moderate, or severe. In fact, a blow to the head can completely change a person’s life. It can affect everything, from their mobility and their relationships to the way they feel and express their emotions.

What can cause traumatic brain injury?

It’s important to note that an impact on the head can cause anything from headaches and buzzing sounds to more serious consequences such as depression and anxiety. Therefore, you should always try and protect your body and not expose yourself to dangerous situations.

Here are some of the most common causes of brain injuries:

• Car accidents. In fact, they’re often made worse due to the appropriate safety measures not being taken.
• Being near the kind of explosion that could cause brain damage.
• Direct impact resulting from a fall on a hard surface.
• A blow to the head with a blunt and heavy object.
• Sudden loss of consciousness or fainting.

Psychological impacts of traumatic brain injury

People often experience emotional problems after a traumatic brain injury. Although most usually recover without any consequences, others present certain psychological changes. They usually develop problems in managing emotions and controlling mood swings.

Here are some of the main psychological and emotional consequences of a traumatic brain injury.

Attacks of irritability and personality changes

An article by Tessa Hart, a scientist at the Moss Rehabilitation Research Institute states that one of the main factors in traumatic brain injury concerns other issues surrounding the accident. For example, job loss, physical ailments, and difficulty concentrating. The sufferer may also feel frustrated due to their loss of independence.

“People with brain injuries can learn some basic anger management such as self-calming strategies, relaxation, and better communication methods. A psychologist or other mental health professional familiar with TBI can help”.

Anxiety and depression problems

Various investigations have shown that two of the main psychological impacts of a traumatic brain injury are depression and anxiety. As a matter of fact, these mental disorders are six times more likely to develop in this type of patient than in the general population. The symptoms can even persist for several years after the accident.

In fact, depending on its impact and the sufferer’s subsequent physical limitations, they may begin to have a negative view of their reality, post-trauma. This is because it can be quite a challenge for them to immediately make a complete return to the life they had before suffering the injury.

Manic syndrome and psychosis

As a rule, the kinds of alterations that completely change the life of the sufferer and the way they behave are among the less common consequences of a blow to the head. As for mania, studies have concluded that it usually has an incidence of around seven percent after a head injury.

With regards to psychosis, it’s believed that the most affected area that could be responsible for this condition after brain injury is the temporal lobe. Of course, personal histories, such as previous drug use or the development of post-traumatic epilepsy should also be considered. The condition may be treated with antipsychotics.

Traumatic brain injury can happen to anyone

As much as we take care of our bodies to lead mentally and physically healthy lives, we can’t legislate for the intervention of fate. Indeed, any one of us could suffer an accident when we least expect it.

It must always be remembered that, in the event of a traumatic brain injury, the support of family and loved ones is of vital importance. Of course, this is in addition to surgery, medications, and rehabilitation theories. Together, they’ll gradually heal any remaining physical and emotional damage.