Category: Brain

Brain plasticity, or neuroplasticity, refers to the ability of the brain to change the existing connections within it and make adjustments if necessary. For any brain, this ability allows for smooth development from the point of infancy to adulthood while also helping to recover from injury. Unlike a computer, the human brain is special because it is capable of processing both motor and sensory signals in parallel (Cobb, 2020). With the help of a multitude of neural pathways, which make it possible to replicate the functions of one another, the brain can correct small errors or short-term function limitations through pathway signals rerouting. Significant issues, however, can appear when the errors in functioning are long-term of that development issues are caused by such severe health complications as the Zika virus or a stroke. Even during such complications, given the appropriate conditions, the brain is capable of overcoming adversity to recover some functions due to its plasticity.

The anatomy of the brain is such that it makes sure that specific areas have specific purposes and functions, which is usually something that is genetically pre-determined. For instance, there is an area that is responsible for the functioning of a left leg, and damage to this area will have an adverse effect on the movement of the leg. Although, because a different part of the brain is responsible for transmitting sensation from the leg, it is possible to feel it but not move it. It is essential to note that one brain section cannot take on new roles and extend its functions to include additional ones. Therefore, despite its tremendous value for the restoration of brain functioning, neuroplasticity should not be confused with the infinite malleability of the brain.

The connections between sleep and memory have been extensively studied by researchers due to the potential of developing strategies for both long- and short-term restoration and recovery. Research evidence suggests that sleep helps both learning and memory in different ways. First, a person that does not get enough sleep cannot exhibit the optimal level of focus and attention, and, therefore, cannot learn efficiently. Second, in itself, sleep plays a memory consolidation role, which is imperative for learning new information and storing it. While the exact mechanisms involved have not been discovered yet, learning and memory are often described through such functions as acquisition, consolidation, and recall, all of which are essential for proper memory functioning.

Sleep is essential for maintaining the health of the brain by eliminating the toxins that accumulate during the day as a result of regular functions. Brain Recovery and restoration are facilitated by the removal of the toxic protein beta-amyloid by microglial cells (Clayton, Van Enoo, & Ikezu, 2017). As a result of this, the unnecessary synapses are removed while the neural wiring of the brain is repaired to prepare it for an active period. Sleep is mostly responsible for the memory consolidation function during which the neural connections strengthen to form memories. Although the research on how the brain forms memories is limited, it has been suggested that certain attributes of brainwaves during different sleep stages are connected to the formation of particular memory types. In the case of sleep deprivation, the microglial cells begin attacking functioning tissues, which can lead to impaired brain functioning if they remained unaddressed.

References

Clayton, K. A., Van Enoo, A. A., & Ikezu, T. (2017). Alzheimer’s Disease: The role of microglia in brain homeostasis and proteopathy. Frontiers in Neuroscience, 11, 680. Web.

Cobb, M. (2020). Why your brain is not a computer. The Guardian. Web.

Introduction

The brain is one of the most amazing organs of the body. Its manner of operation and coordination with other major body systems is filled with so much detail that it its creation can be indubitably described as perfect. It is part of the Nervous System, specifically the Central Nervous System (CNS), and it works in conjunction with the spinal cord and the Peripheral Nervous System (PNS). The former is the second part of the CNS and the latter is composed of the nerves and the autonomic nervous system that has organs for furnishing the activities of the nervous system (Boeree 2003, p. 1). The collaboration of the brain with the mentioned parts helps us run our day-to-day activities, both involuntary and voluntary. They control activities like blinking, breathing, and even memorization. The main function of the brain in this alliance is the interpretation of messages. This is enabled by the perfect organization of the components of the brain (Swanson 2002, pp. 23- 30).

Parts of the brain

The brain is composed of several parts that work together to give its control and power over the human body. The brain has three major constituent parts. These are the hindbrain, the midbrain, and the forebrain. The diencephalon (thalamus and the hypothalamus) and the cerebrum make the forebrain while the midbrain characteristic of its hearing and visual function has the tectum and tegmentum. The hindbrain, on the other hand, has the medulla, pons, and cerebellum. The first two and the midbrain are collectively known as the brainstem. The brain is surrounded by three membranous envelopes known as the meninges. They work in conjunction with cerebrospinal fluid to give physical protection to the CNS. As the name suggests, the cerebrospinal fluid fills the spinal cord and the ventricles of the brain (Leiner 1997, p. 1).

The forebrain

Let us have a closer look at the parts of the forebrain. The cerebrumm is the Latin word for brain and it constitutes approximate 87.5 % of the weight of the brain. It is also known as cerebral hemispheres. It is in the cerebrum that things like thought, judgment, decision, and imagination take place. It also performs motor roles and processes sensory signals. To achieve its surface (cerebral cortex) is heavily convoluted into the parental, the occipital, the temporal, and the frontal lobes. These accommodate approximate 10 billion neurons and 50 trillion synapses. The neurons are conductors of impulses that are used to send messages/information while the synapses are intermediaries between neurons. The other parts of the cerebrum are the basal ganglia, the limbic system, and the olfactory bulb. The basal ganglia are made up of nuclei that transmit signals related to motion and learning. The limbic system carries out functions related to emotions. It is comprised of the hippocampus for memory and the amygdala for common emotions like anxiety. The olfactory bulb carried out interpretation of smell and chemical information (Boeree 2003, p. 1).

The thalamus is visible at the top of the brainstem as the large structure with two lobes. It passes along sensory signals and forms an important part of motor, sensory and other sub cortical pathways. Its interconnection with the cortex plays an important role in the generation of rhythmic patterns and perception. The hypothalamus is found in the same area as the thalamus. It controls the pituitary gland and thus influences the secretion of hormones into the bloodstream. This means that it can influence behaviors related to the endocrine function like appetite, emotions, temperature etcetera (Leiner 1997, p. 1).

The brainstem

The midbrain is a base for auditory and visual information relays. Its functions are performed by the pons, medulla, and midbrain. Let us first look at the midbrain. It is composed of the tectum and the tegmentum. The tectum is found in the dorsal area of the midbrain. It is known for its auditory and visual functions. The tegmentum is found at the base of the brainstem. Its functions include control over motor functions, regulation of attention, awareness, and some autonomic functions. The motor function of the tegmentum is enabled by the presence of the red nucleus and the substantia nigra found in the tegmentum. The other parts of the brainstem are classified as the hindbrain. They include the pons and the medulla oblongata (Swanson 2002, p. 57).

The pons is located below the midbrain and its functions includ: input in the control of autonomic functions, arousal, sleep, and relay of sensory information between the cerebrum and the cerebellum. The final part of the brainstem is the medulla oblongata. This forms the lower part of the brainstem and is also referred to as the myelencephalon. It protrudes at the end of the spinal cord forming a swelling-like structure. It is a very important part of the brain due to its ability to control autonomic functions. This includes cardiovascular and respiratory functions. It controls a variety of body secretions, reflexes, and even swallowing. The medulla forms an interface between the brain and spinal cord for the relay of nerve signals. Its strategic position between the pons and the spinal cord is also very instrumental in the critical role it plays in the function of the brain (Swanson 2002, p. 92).

The Cerebellum

The cerebellum is a part of the hindbrain whose importance in the functions of the brain has been negligently underestimated for very long. It is located at the skull base over the brainstem. Its unction’s include equilibrium control, muscle tone, balance, and the coordination of voluntary movements. The last function enables it to fluency and dexterity which are, arguably, the most difficult functions of the brain save for memory. This could be extended to an explanation of how we learn movement-based skills such as riding a bicycle. The cerebellum is appropriately featured to perform its special function. For instance, as small as it is, it has a larger number of neurons than the rest of the brain combined. It is additionally able to process information very fast and thus beats all other parts of the brain in rapidness of action. It also receives a large amount of information from the cortex. This is evidenced by the 40 million nerve-fiber connection between the cerebellum and the cortex (Swanson 2002, p. 63).

Diseases related to the brain

An interruption of the proper functioning of the brain could prove to be quite disastrous. It may lead to psychological disorders such as epilepsy, schizophrenia which is characterized by thought disorder, hallucinations, and delusions, Alzheimer’s disorder that is characterized by memory loss, and mood disorders that could be signified by irrational passions and depression. Many of the above-mentioned disorders may occur due to a fault in the transmission of nerve impulses and they are genetic. An example of such genetic brain disease is the Alzheimer’s disease. The most common brain diseases are caused by inflammations in the brain and they include vision loss, paralysis, and weakness. When a stroke occurs, the victim may lose brain cells and this may affect the ability of the victim to think well. Brain tumors can also interfere with the proper functioning of the brain by pressing nerves. The treatment and appearance of symptoms of brain diseases depend on the problem the victim is suffering from. In some cases, symptoms may be invisible while in other cases, misleading symptoms may be evident. Treatments like therapy, medication, and surgery are used to improve or treat brain diseases (Leinner 1997, p. 1).

Conclusion

The effectiveness with which a human brain functions is amazing. However, what should be more amazing is the detail exercised in the choice and the arrangement of the parts of the brain. As explained in the body of the essay, its parts are perfectly chosen to perform various functions and each of them is equipped with different strengths to help it in performing its function. The coordination of the brain with the nervous system is also commendable. Although the brain is a very powerful organ, its sensitivity is very disadvantageous. An injury to the brain is normally fatal or it may lead to a life-long problem (Leinner 1997, p. 1). In a nutshell, the brain is, arguably, the most complex part of the body in terms of its anatomy and function.

References

Boeree, G. (2003). “The Cerebrum.” Web.

Leiner, H. (1997). “The treasure at the bottom of the brain.” Web.

Swanson, L. (2002). Understanding the Basic Plan. New York. Oxford University Press.

Abstract

It is often difficult for pathogens to penetrate the brain-blood barrier. However, some of them do. Toxoplasma Gondii, Naegleria Fowleri, and Taenia Solium are common pathogenic elements that could successfully penetrate this barrier. However, there is scanty medical literature explaining the mechanisms used by these pathogens to penetrate this blood-brain barrier. This paper bridges this research gap by giving more insight into how pathogens penetrate the barrier. However, the scope of this analysis is limited to the three pathogens mentioned – Toxoplasma Gondii, Naegleria Fowleri, and Taenia Solium. The research aims to find out if Naegleria Fowleri, Taenia Solium, and Toxoplasma Gondii use the same mechanism to cross the blood-brain barrier. A comprehensive assessment of existing research studies shows that Naegleria Fowleri, Taenia Solium, and Taxoplasma Gondii do not use the same mechanism to cross the blood-brain barrier. This assertion supports the main research hypothesis, which claims that Naegleria Fowleri, Taenia Solium, Taxoplasma Gondii use different mechanisms to cross the blood-brain barrier. Furthermore, this paper shows that pathogens use different mechanisms to minimize the effect of the host’s immune system.

Introduction

The blood-brain barrier plays an important function in the proper functioning of the central nervous system because it separates the blood system from the brain’s extracellular fluid (Velázquez-Moctezuma, Domínguez-Salazar, & Gómez-González, 2014). Indeed, for the central nervous system to work properly, the molecules passing across the blood-brain barrier are often tightly regulated (Manno, 2012). The blood-brain barrier does so by binding the cerebral endothelial cells together to prevent the flow of infectious molecules between the blood system and the brain (Velázquez-Moctezuma et al., 2014). The same mechanism prevents the diffusion of molecules between the endothelial cells and the brain (Pardridge, 2006). Masocha and Kristensson (2012) further explain this structural barrier by saying, “The cerebral endothelial cells have low levels of pinocytotic activity or transcytosis and form a functional barrier by selectively transporting only specific molecules into the brain parenchyma” (p. 202). This way, a key function of this permeable membrane is preventing parasites and pathogens from infiltrating brain tissues. Therefore, the blood-brain barrier only allows the selected permeability of molecules that are important to the human neurological function to pass the blood-brain barrier. It could also allow for the entry of water and specific gases into the brain tissue (Masocha & Kristensson, 2012). However, using different mechanisms, intracellular and extracellular parasites could still invade the central nervous system (Khan, 2008). Such infections could cause neurological damage or disturbances that could be fatal to victims. However, host-derived immune molecules fight such attempts. Nonetheless, some of these blood-borne pathogens have derived unique mechanisms for invading the blood-brain barrier, thereby undermining the host’s immune response (Davson, 1993). In light of this observation, Masocha and Kristensson (2012) says,

“The Th1 immune response, which is directed against intracellular pathogens, can be inhibited during infections with certain microbes in which the Th2 response, which is directed against extracellular pathogens, instead, is promoted; the two arms of the immune response being mutually inhibitory” (202).

Pathogenic infections to the brain are often rare. However, when they occur, they could cause serious damage to the brain. Indeed, as Masocha and Kristensson (2012) observe, parasitic infections in the brain usually have serious medical consequences. In fact, in most cases, they are fatal (Masocha & Kristensson, 2012). Such fatalities often occur because the parasites prevent antibodies from circulating in the brain, thereby causing disturbances in the brain cycle (Masocha & Kristensson, 2012). This is why many patients who suffer from parasitic infections also suffer from other conditions, such as seizures or epilepsy (Masocha & Kristensson, 2012). However, a patient’s immune system could help to minimize these effects.

Some common parasites have a propensity to invade the immune system. For example, Toxoplasma gondii, Naegleria Fowleri, and Taenia Solium have a strong propensity to invade the blood-brain barrier and sabotage the host’s immunity (Velázquez-Moctezuma et al., 2014; Roy et al., 2014). Some parasite-derived molecules may support the invasion of these blood-borne pathogens in the brain. Recent medical studies have explored how bacterial infections could occur through the blood-brain barrier (Khan, 2008). Most of their assessments have not specifically focused on how blood-borne pathogens could similarly infiltrate the central nervous system, but they have explored how various microbes spread across the system (Masocha & Kristensson, 2012). Therefore, there is little information known regarding how blood-borne pathogens cross the blood-brain barrier and cause such infections. There is also scanty information to explain how the immune system controls these parasites. To fill this research gap, this review explores the mechanisms used by Naegleria Fowleri, Taenia Solium, and Toxoplasma Gondii to cross the blood-brain barrier.

Comparison/Contrast

Mechanism of Naegleria Fowleri

Naegleria Fowleri is among a few known parasites that affect the central nervous system and penetrate the blood-brain barrier (see figure 2) (Cardona, Restrepo, Jaramillo, & Teale, 1999). Naegleria Fowleri occurs naturally and causes primary amebic meningoecephalitis (PAM) (Chávez-Munguía et al., 2014). This condition has a high fatality rate of 97% (Masocha & Kristensson, 2012). Certain conditions cause this amoeba to thrive. For example, warm and moist environments aid its spread. Usually, these non-pathogenic elements are in the soil or water bodies. There is no clear explanation showing why Naegleria Fowleri targets the brain because its non-pathogenic nature makes it a less likely infiltrative element (Toney & Marciano-Cabra, 1994). However, its invasive mechanism stems from how amoeba enters its host. The common mode of exposure, for human beings, is swimming in freshwater bodies, which exposes them to the amoeba. Entry usually occurs through the nasal cavity. This point of entry allows it to attach to the nasal mucosa (Masocha & Kristensson, 2012). Later, it moves through the olfactory nerves and invades the brain tissue through the olfactory epithelium and the cribriform plate (Burri et al., 2012). After penetrating the brain tissue, Naegleria Fowleri destroys the central nervous system by penetrating through the brain vasculature (Masocha & Kristensson, 2012). This entry gives it access to the frontal lobes of the brain after reaching the meninges region. This infection mechanism greatly relies on adhesion because the amoeba has a surface protein that improves its bonding to fibronectin (Masocha & Kristensson, 2012; Burri et al., 2012). Researchers have always said that this surface protein is similar to the human integrin-like receptor (Chávez-Munguía et al., 2014). Nonetheless, the exceptional bonding with fibronectin becomes part of the matrix of the host’s cells. Naegleria Fowleri incapacitates the host’s immune system because it has efficient locomotive skills. Its relatively direct access to the site of infection also incapacitates the immune system from preventing an attack on the central nervous system (Chávez-Munguía et al., 2014).

How does it cope with the Immune System?

Few kinds of literature explain how CNS infective amoeba copes with the human immune system. However, there is enough medical evidence to show that Naegleria Fowleri has developed efficient mechanisms for evading the immune system. To explain how it does so, Stanford University (2015) says, “The amoeba attacks cells by tragocytosis and the release of a plethora of cytolitic enzymes, including aminopeptidases, hydrolases, esterases, acid, and alkaline phosphatases and dehydrogenases” (p. 7). The ability of Naegleria Fowleri to penetrate the blood-brain barrier also stems from its highly cytopathic effect. It contributes to the amoeba’s virulence by damaging impeding cells (Stanford University, 2015). Although the host’s immune system may produce cytolytic molecules to impede the destruction of the brain tissue, Naegleria Fowleri could defeat its attempts by creating a strong resistance to lysis (Chávez-Munguía et al., 2014). Regarding this analysis, Stanford University (2015) says, “Research suggests eukarytoic cells, such as mammalian erythrocytes, neutrophils, and tumor cells utilize complement-regulatory proteins to protect themselves from lysis by the complement system of the innate immune system” (p. 8). Naegleria Fowleri has also created strong resistance to the host’s immune system by adapting to carrying complementary regulatory proteins. The ability of Naegleria Fowleri to shed the membrane attack complexes also prevents the host’s immunity from destabilizing its infection mechanism (Chávez-Munguía et al., 2014). Based on these adaptive mechanisms, scientific research has yet to prove that the human immune system has any effect on Naegleria Fowleri’s attack mechanism (Stanford University, 2015). However, research has affirmed the presence of Naegleria Fowleri antibodies among people who suffer from amoeba exposure (Stanford University, 2015). However, there are usually a small number of these antibodies, thereby making it difficult to detect them during the pathogenic analysis (Burri et al., 2012). This failure leaves the host’s immune system as having the best mechanism to prevent infections by Naegleria Fowleri. However, the amoeba has developed elusive adaptations to evade its mechanisms, thereby leaving the host exposed to brain infections. However, this assessment does not mean that the host’s immune system is helpless to brain infections by Naegleria Fowleri because the amoeba has several vulnerabilities as well.

The Vulnerabilities of Naegleria Fowleri’s Invasive Mechanism

Although the above section of this paper shows the adaptations of Naegleria Fowleri, the amoeba is still vulnerable to some facets of the host’s innate immune system. This vulnerability comes from the amoeba’s weakness to neutrophils. The host’s immune system usually produces macrophages and microglia (before the amoeba’s infiltration) and prevents the parasite from causing damage to the brain cells (Chauhan et al., 2014). However, Stanford University (2015) says the host’s immune system usually creates a buildup of cytokines and other cytolitic molecules, which may not add to its immune function because Naegleria Fowleri is vulnerable to it (Burri et al., 2012). The Stanford University (2015) says the creation of cytokines abate the penetration of the blood-brain barrier because the production of cytokines and other cytolitic molecules

“Could cause lysis of nearby neuronal cells, a further collection of organic debris and further immune response, hyper inflammation and a breakdown of the blood-brain barrier, and in doing so aid the pathogenicity of the amoeba more than help control it” (Stanford University, 2015, p. 12).

The immune response of Naegleria Fowleri is usually shorter because of the host’s response system to invasions by Naegleria Fowleri. Although these immune attacks are real, there is little medical evidence to explain whether Naegleria Fowleri could replicate faster than the host’s immune system destroys it (Chauhan et al., 2014). However, studies on animals have shown that Naegleria Fowleri could replicate faster than the host’s immunity could kill it (Stanford University, 2015; Chauhan et al., 2014). Human-based evidence is scanty.

Mechanism of Toxoplasma Gondii

Toxoplasma Gondii is a protozoan that commonly occurs in many types of environments (Harker et al., 2013). Toxoplasma Gondii could be both extra-cellular and intracellular (see figure one). However, studies have shown that it is predominantly intracellular (Feustel, Meissner, & Liesenfeld, 2012). A patient’s immune system is always critical in making sure there is a low risk of pathogenic infections from Toxoplasma Gondii because, unlike other pathogenic subspecies, such as T. b. gambiense and T. b. rhodesiense, Toxoplasma Gondii could be dormant within a patient’s system for a long time (Feustel et al., 2012). However, an immunity compromise is likely to activate it. When it attacks, it could have a high prevalence among the infected population (Masocha & Kristensson, 2012). For example, studies in Europe and Africa have shown that the parasite could have a prevalence of up to 90% (Stanford University, 2015). Comparatively, studies based in Australia and Japan show that its prevalence could be exceptionally low (Stanford University, 2015). Infections by Toxoplasma Gondii usually show no known symptoms, but patients who have compromised immunity could suffer some of its worst effects (Berenreiterova, Flegr, Kubena, & Nemec, 2011). This group of patients also suffers a high risk of infection to the central nervous system (CNS). Patients who have congenital disorders are also likely to suffer a high risk of CNS infection (Carey, Westwood, Mitchison, & Ward, 2004). Encephalitis and other neurological diseases are common effects of advanced stages of CNS infection (Stanford University, 2015). Deleterious effects are also synonymous with CNS infections (Carey et al., 2004). Another common cause of infection is the immunosuppressing effect of HIV and AIDS. This condition usually reactivates latent infections.

Mechanism of Penetration through the Blood-brain Barrier

When Toxoplasma Gondii penetrates the blood-brain barrier, it usually causes cysts (Stanford University, 2015). However, before this process occurs, the protozoon usually invades its host through absorption via the small intestine (Coombes et al., 2013). Thereafter, it affects macrophages to make sure that the host’s immune system is incapacitated. The macrophage host cell is usually instrumental in preventing Toxoplasma Gondii infection because it helps in killing the protozoa through an oxidative burst, occasioned by nitric oxide production (Stanford University, 2015). However, Toxoplasma Gondii prevents this process from occurring by infecting the macrophages (Masocha & Kristensson, 2012). Nonetheless, infected monocytes are immune from this action because they could still produce nitric oxides and kill the parasite intracellularly (Stanford University, 2015). Lymphokines are also immune to the efficient macrophage-killing mechanism of Toxoplasma Gondii. This way, they could activate macrophages and other cells to attack Toxoplasma Gondii (Stanford University, 2015). Toxoplasma Gondii also risks elimination by the immune system through its invasive intuition mechanism, through the small intestine, which could damage the intestinal epithelium, thereby causing an inflammatory response. This outcome could easily trigger a full-blown immune response from the host’s body (Coombes et al., 2013). To minimize the possibility of elimination, Toxoplasma Gondii has to develop better biological responses that would not trigger the immune system, or prevent its elimination by protecting itself from a full-blown immunological response. Stanford University (2015) says the presence of gram-negative bacteria is the main trigger of the full-blown immunological response. Lipopolysaccharide production usually characterizes this response (Coombes et al., 2013). Toxoplasma Gondii prevents its elimination by possessing a gene that suppresses lipopolysaccharide production (Zhou et al, 2005). Cytokine production is usually the product of such a process. Such defensive mechanisms usually allow Toxoplasma Gondii to thrive by reproducing and penetrating the blood-brain barrier (Coombes et al., 2013).

Despite the above explanations regarding how Naegleria Fowleri penetrates the blood-brain barrier, researchers do not fully understand the mechanisms used by Toxoplasma Gondii to penetrate the blood-brain barrier (Stanford University, 2015; Siddiqui & Khan, 2014). However, preliminary reports show that the protozoa use two primary methods – attachment to white blood cells and attachment to endothelial cells (Carey et al., 2004). By attaching itself to white blood cells, Toxoplasma Gondii could penetrate the blood-brain barrier because white blood cells have a free passage through this barrier (Stanford University, 2015). However, this process is difficult for the Toxoplasma Gondii to accomplish because the presence of macrophages could complicate its attempt. Experts say the infiltration of the blood-brain barrier through the endothelial cells contributes to the highest cases of Toxoplasma Gondii brain infections, compared to infiltration through the white blood cells (Coombes et al., 2013). However, the host’s innate and acquired immune responses are likely to suppress attempts to penetrate the blood-brain barrier (Stanford University, 2015). To counter this response, Toxoplasma Gondii produces tachyzoites that form immune-resistant pseudocysts (Carey et al., 2004). These cysts usually assume a dormant nature until reactivation occurs. Usually, the host’s innate immune system prevents these cysts from activating. Indeed, the medical evidence shows that these cysts attempt to rapture and multiply, but the host’s immune system prevents them from doing so (Masocha & Kristensson, 2012). Usually, this process happens under normal conditions, but experts still do not know the mechanism used by the host’s immune system to prevent this action (Lachenmaier, Deli, Meissner, & Liesenfeld, 2011).

People who have suppressed immunities often suffer the highest risks of cyst reactivation (Masocha & Kristensson, 2012). This failure may allow a full-blown infection to occur. The lack of antibodies in the brain often worsens this situation because CNS infections are likely to persist (compared to when the infection would occur in a different organ or part of the body) (Stanford University, 2015). Based on these dynamics, acute infections among patients who suffer from suppressed immunities are likely to occur in the central nervous system (Lachenmaier et al., 2011). Such infections are likely to cause severe pathogenesis, which draws a strong link with taxoplasmosis (Stanford University, 2015). Relative to this observation, Stanford University (2015) says, “Toxoplasmosis in the brain often consists of necrotizing encephalitis and associated inflammation, to which microglia respond by forming nodules in attempts to contain the infection” (p. 20). Often, suppressed immunities compromise this process. When such a situation occurs, Toxoplasma Gondii replicates faster than the host’s immunity could control it (Stanford University, 2015). The clinical effects of such compromised immunity are usually severe in affected patients.

Mechanism of Taenia Solium

Taenia Soliumn is the main causative agent for epilepsy. It usually affects the central nervous system through the spread of intermediate larvae from the porcine tapeworm, Taenia Solium (Motarjemi, 2013). Unlike other parasites highlighted in this paper, there is sufficient evidence explaining how Taenia Solium penetrates the blood-brain barrier. However, before delving into the details surrounding its penetrative mechanism, it is pertinent to understand that most people get infected by Taenia Solium by eating contaminated food (usually pig products) (Velázquez-Moctezuma et al., 2014). Taenia solium usually penetrates the blood-brain barrier by entering the blood system through the small intestine (Sun et al., 2014). Although infections are asymptomatic, infected people become hosts of Taenia Soliumn cells that continue to multiply in their systems. When multiplication occurs and Taenia Solium proportions increase in the host’s circulatory system, they affect the central nervous system and the subcutaneous tissue (Singh & Prabhakar, 2002). The Taenia Soliumn lives in the patient’s immune system as cysts that could stretch between 10 to 20 millimeters (Quinones-Hinojosa, 2012). To evade the host’s immune system, the parasite usually modulates it.

Taenia Soliumn could penetrate the blood-brain barrier because it covers its cysts with host-derived molecules. At the same time, it usually secretes immunomodulatory enzymes to counter the effects of the host’s immune system. These penetrative mechanisms usually occur by passing through the lymphatic system and bloodstream. This penetrative mechanism differs from that of Toxoplasma Gondii and Naegleria Fowleri as discussed below.

Discussion

Although few parasites, or pathogens, could penetrate the blood-brain barrier, evidence from this paper shows that Toxoplasma Gondii, Naegleria Fowleri, and Taenia Solium employ some immunosuppressing techniques to minimize the effect of the host’s immune system. Furthermore, some of these pathogens have preventive mechanisms for stopping antibodies from attacking them. Their strength is further elevated when hosts are suffering from immunosuppressive conditions, such as HIV/AIDS, or when they are taking immunosuppressing drugs (Singh & Prabhakar, 2002). Although the mechanisms used by the pathogens to infiltrate the blood-brain barrier may vary, their target is the same – the central nervous system. This target is preferable because immunity (in this system) is low (based on the possibility of an inflammatory response) (Stanford University, 2015). However, minimized immunity does not mean that the pathogens do not have to manage the host’s immunity because they do. Based on this limitation, penetrating the blood-brain barrier is often a common challenge for these microscopic brain eaters. For those that can do so, evading the host’s immune system, or suppressing it, are usually common characteristics of their penetrative mechanism (Estanol, Juarez, Irigoyen, Gonzalez-Barranco, & Corona, 1989). Nonetheless, the mechanisms used by the three species studied are not common. For example, this paper has shown that these species use different invasive mechanisms to attack their hosts. Toxoplasma Gondii and Taenia Solium enter the host’s blood supply system through the small intestine. Comparatively, Naegleria Fowleri enters the host’s blood supply system through the host’s nasal cavity. Indeed, by attaching to the upper wall of the host’s nasal cavity, the pathogens gain access to the frontal lobes. This paper has also shown that these pathogens use different mechanisms to penetrate the blood-brain barrier. For example, it has been shown that Toxoplasma Gondii penetrates the blood-brain barrier by attaching to white blood cells and the host’s endothelial cells. Comparatively, Naegleria Fowleri penetrates its host’s blood-brain barrier through the olfactory epithelium and the cribriform plate. Lastly, Taenia Soliumn penetrates the host’s blood-brain barrier by covering its cysts with host-derived molecules. This assessment alone shows that the three pathogens do not use the same mechanisms to penetrate the blood-brain barrier (see table one). Another area showing the differences in mechanisms used by the three pathogens is how they manage the host’s immune systems. Indeed, evidence from this paper shows that these pathogens endure the immune attack from the host’s system by selectively using different characteristics of the host’s immune system for their posterity. This way, the parasites penetrate the blood-brain barrier usually at the expense of their hosts. For example, Taenia Soliumn protects itself from the host’s immune system by modulating it. Comparatively, Toxoplasma Gondii kills the macrophage host cell, which would have otherwise created antibodies to fight the pathogen. Furthermore, this pathogen evades the host’s immune system by disguising itself as one of the host’s cells. Comparatively, Naegleria Fowleri copes with the host’s immune system by damaging inhibitor cells. These different mechanisms show that the three pathogens use different mechanisms for penetrating the blood-brain barrier and staying there (see table 2). The only area of commonality among the three pathogens is their target (brain tissue). They attack it by penetrating the blood-brain barrier and infecting the central nervous system. Findings from this paper also show that although the host’s immune system may struggle to contain infections in the brain tissue, the pathogens could replicate themselves much faster than the immune system could kill them (Sun et al., 2014). These mechanisms are adaptive methods used by pathogens to damage the host’s brain cells (Sun et al., 2014). Immunosuppression creates the greatest vulnerability to such pathogens. Therefore, the risk of pathogenic infection across the blood-brain barrier remains low (for healthy people) (Paredes et al., 2013). Comprehensively, although the findings presented in this paper are factual, it is important to note that they are not comprehensive because they stem from existing literature, which has not fully explained the mechanisms used by the above-mentioned pathogens to penetrate the blood-brain barrier.

Comprehensively, the mechanisms for penetration, outlined in this paper could be instrumental in expanding medical knowledge about the mechanisms used by these parasites to invade the blood-brain barrier. Consequently, they could inform valuable medical interventions about the same. Similarly, this research could be useful in developing highly efficacious treatment methods. This process is the first step in developing preventive treatment methods for stopping these parasites from causing further harm to their host’s central nervous system. However, there is a need to undertake more research to fine-tune the results depicted in this study.

Tables and Figures

Table one: Differences in Invasive mechanisms for species

Table 2: Differences in coping mechanism for Species

References

Berenreiterova, M., Flegr, J., Kubena, A., & Nemec, P. (2011). The Distribution of Toxoplasma gondii Cysts in the Brain of a Mouse with Latent Toxoplasmosis: Implications for the Behavioral Manipulation Hypothesis. PLoS ONE, 6(12), 1-14.

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Introduction

Blood brain barrier is the membrane separating the blood from the cerebrospinal fluid in the nervous system; it is usually found in all capillaries. In this membrane there are cells which restrict the diffusion of external microscopic objects into the central nervous system. This barrier contains highly dense cells which restricts the passage of any foreign substance in the blood system (Langley, 2002). This system is there to prevent any infection of the brain from the bacteria’s and this justifies why brain diseases are very rare and when they occur it becomes very complicated to be treated. Common brain diseases are caused by virus which easily attaches themselves on circulating immune cells. This does not rule out bacteria infections to the brain, since some diseases like treponema pallidum and Lyme are caused by bacteria (Maccagnan, 2007).

Drugs which cross the blood brain barrier

Caffeine is one of these kinds of drugs, this drug is found in; cola drinks, tea and coffee, some of the medications taken can also have this drug. When this drug is consumed the user feels an increased heart rate and the blood pressure goes up. In every consumption of this drug, some of the amounts go to the brain which then causes the blood vessels to narrow. For minors, consumption of this drug in amount of 800 pounds is fatal (Langley, 2002).

When nicotine is used, it directly goes to the brain unlike other drugs, this drug is always found in tobacco. Most people consume the same because it increases attention, memory and concentration. Consumption of this drug inhibits the flow of oxygen in the blood stream thus causing cancer and other diseases. This drug affects the brain by stimulating receptors which are distributed on nerve cells in the brain (Maccagnan, 2007).

Another drug that crosses the blood brain barrier is Ritalin, which is used to treat attention, this drug is mostly prescribed for children under the age of six years, it prevents the brain from being distracted and excess use of this drug can cause negative side effects (Langley, 2002).

Aspirin when used, it directly acts on the brain; it is mostly used to treat pain.

Old age can cause the blood brain barrier to weaken thus increasing the chances of the brain affection. With advance in age the permeability of cell membranes is lost which then decreases the enzyme activity (Maccagnan, 2007).

Coronary Heart Disease

This is the lack of enough oxygen circulating in the cardiac muscle, it is mainly caused by the following:

• Diabetes
• Smoking
• Hypertension

The above causes usually make the lumen of the coronary artery to be obstructed hence restricting the flow of oxygen to the myocardium (Daniel, 2007).

Conclusion

The best cure of this problem is to do some physical exercise and quitting smoking. Physical exercise reduces the amount of chorestral in the body thus reducing the chances of the lumen being obstructed (Kolata, 2002). Lack of body exercise can lead to excess glucose in the muscle, which is then stored as fat.To prevent the amount of high density lipoprotein from deteriorating one is bound to do some physical exercise regularly (Daniel, 2007).

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Sickness behavior refers to non-specific adaptive response of the innate immune system and is an expression of a central motivational state (Dantzer and Kelly, 2007; Aubert at al., 1997). Thus, cytokine induced sickness behavior refers to a motivational state that belongs to the realm of physiology, similar to other motivational states, such as fear or hunger (Dantzer and Kelly, 2007).

Withdrawing from the environment to seek rest and care for the body is as normal in response to infectious agents as being able to shift to a state of increased arousal and readiness for action when confronted with a potential external threat. Sickness behavior refers to an adaptive response of the host to infectious microorganisms. In theory, cytokines released in response to infection or inflammation alert the brain of any real or potential threats and initiate behaviors that are important for survival (Frink et al, 2009).

The result of a hyperactive proinflammatory state marked by excess production of proinflammatory cytokines may contribute to the pathogenesis of various human diseases such as allergy, autoimmunity, obesity, depression and atherosclerosis (Sternberg, 2006). Some even refer to the ability of the immune system to alert or communicate with the brain as a “sixth sense” (Blalock & Smith, 2007). Sickness behavior is adaptive in that it forces an individual to rest and withdraw from activities so that physiological processes can effectively produce healing (Blalock & Smith, 2007; Kelley, Dantzer, Zhou, Shen, Jhonson & Broussard, 2003).

However, sickness behavior is no longer adaptive if it goes beyond the organism’s resources and/or out of proportion with the triggering contributory factors that initiated the adaptive response. This is prevalent during a variety of chronic inflammatory diseases (Dantzer and Kelly, 2007).

Proinflammatory cytokines released during infection, inflammation, injury and even psychological stress can signal the brain to initiate behavioral changes that facilitate adaptation to these threats. Cytokine-to-brain signaling leads to mood disorders, particularly depression that accompanies the illness (Dantzer, 2009: Dantzer et al, 2008). Cytokines signal the brain to induce sickness behaviors through neural, hormonal, and cellular pathways (Capuron and Miller, 2011).

Therefore, the purpose of this paper is to describe how cytokines signal access the brain, then describe the key evidence that supports the concept that cytokines signal the brain to induce sickness behaviors through shedding the light on the two crucial models; the Dantzer’s Motivational Model of Sickness Behavior and The Two Hit Model of Cytokine-induced-Depression. Finally, the paper will derive clinical implications.

Cytokine Signals access in the brain

Cytokines are relatively large molecules prohibited from passing through the blood brain barrier. However, evidence reveals that cytokines signal the brain through hormonal, neural and cellular pathways (Capuron and Miller, 2011).

Data has shown that activation of the specific mechanisms differentially mediates cytokine effects on the central nervous system. Within the brain, there is a cytokine network consisting of cells. The neural pathway of immune signals underlies the potent effects of peripheral proinflammatory cytokines on pathways involved in the pathophysiology of neuropsychiatric disorders, including the activation of the HPA axis and corticotrophin-releasing hormone and the alteration of the metabolism of key neurotransmitter, such as serotonin (Dantzer et al., 1999)

Cytokine signals the brain through humoral, neural and cellular pathways. Hormonal pathways refer to the activation of monocytes and macrophages, which release the proinflammatory cytokine and enter the brain through the choroid plexus region and circumventricular organs of the blood-brain barrier. However, in the brain, the activation of endothelial cells is responsible for the subsequent release of second messengers that act on specific brain targets (Capuron and Miller, 2011).

While the neural pathways refer to the activation of monocytes, macrophages stimulate primary afferent nerve fibers in the vagus nerve, which result in the release of proinflammatory cytokines. Then, this information gets to the brain by sensory afferents of the vagus nerve to specific brain regions through the activation of the nucleus of the tractus solitarius and postrema area (Capuron and Miller, 2011).

Lastly, D’Mello & Swain (2009) identified another new immune-to-central nervous system communication pathway in the setting of organ-centered peripheral inflammation. According to D’Mello & Swain (2009), evidence shows that there is a significant infiltration of activated monocytes into the brain in mice with hepatic inflammation (D’Mello & Swain, 2009). This cellular pathway refers to the stimulation of microglia by proinflammatory cytokines to produce monocyte chemoattractant protein-1, which in turn is responsible for the recruitment of monocytes into the brain (D’Mello & Swain, 2009).

The Dantzer’s Motivational Model of Sickness Behavior

The Origin of Motivational Model of Sickness Behavior

Dantzer’s proposition of sickness as a motivational state built on Bolles’ definition of motivations as central states that reorganize perception and action (Bolles and Fanselow, 1980). Bolles (1974) emphasized that a motivational state enables the individual to detach perception from action, which results in a selective appropriate strategy depending on the encountered state. In order for the body to deal with the invading infectious organism efficiently, sickness takes precedence over other behavioral activities as the infected organism is at the death stage (Dantzer & Kelley, 2007).

Bolles and Fanselow (1980) presented a fear motivation system, which by assumption, activates a unique class defensive behavior, such as freezing and flight from a frightening situation. This activation aims at defending the animal against predation of natural danger while reorganizing the perception of environmental events to facilitate the perception of danger and safety (Bolles and Fanselow, 1980). The following example illustrates the expression of sickness behavior as a motivational state:

First, Neal Miller (1964) conducted the first series of experimental investigation that demonstrated a differential effect of bacterial endotoxin on behavior. Endotoxin administration decreased bar pressing when it resulted in an appetitive stimulus like food or water, but endotoxin did not decrease when it resulted in the termination of an aversive event. Rats given an endotoxin injection increased bar pressing to stop the rotation of a drum, an aversive stimulus (Miller, 1964). Interestingly, these results revealed that the consequence of the behavior which, does not necessarily decrease following exposure to sickness-inducing agents, influences the effect of the sickness-inducing agent.

Second, Aubert, Goodall, and Dantzer (1995) compared the effects of cold and cytokines on spontaneous dietary self-selection of rats. First, they habituated rats to free access to carbohydrate, protein and fat diets for 4 hours a day for 10 days. Then they randomly received physiological saline, IL-1 beta injection or lipopolysaccharide (LPS), or exposed to cold (5 degrees C). Results revealed that LPS- and IL-1 beta-treated rats ate less, but ingested relatively more carbohydrates and less proteins whereas relative fat intake remained unchanged. The rats exposed to cold slightly increased their food intake, but in a non-significant manner.

They also increased their relative intake of fat but did not change their relative intake of carbohydrate and protein. These results reveal interesting pyrogenic and metabolic effects of cytokines, which provides a clear-cut example or behavioral reorganization in response to sickness (Aubert, Goodal, and Dnatzer, 1995). In a subsequent study, Aubert, Goodall, Dantzer, & Gheusi (1997) investigated the sensitivity to LPS injection in lactating mice. They found that nest building significantly decreased in LPS-treated mothers compared to saline-treated animals at an ambient temperature of 22 degrees C. Furthermore, they found that LPS-treated mice exposed to cold temperature (6 degrees C) expressed not only pup-retrieving but also nest-building activity. Therefore, these activities are a result of a motivational state to due to the cooler environment.

These differential results indicate that the maternal behavioral expressions of LPS-induced sickness are dependent on the comparative priority of the behavior under consideration (different components of maternal care under consideration). Apparently, sickness prevents mice from displaying motor activities (pup retrieving or nest building) and from evaluating the situation under consideration efficiently (Aubert, Goodall, Dantzer, & Gheusi, 1997).

Finally, Aubert Kelley, & Dantzer (1997) compared the effects of LPS on food intake and food hoarding. Rats underwent tests under different motivational levels for food hoarding (receiving food supplement to maintain stable body weight or did not receive such a supplement). Interestingly, they found that LPS-injection significantly decreased total food intake in rats in general whereas food hoarding suffered less in LPS-treated rats from those who did not receive a supplement.

The expression of a still salient secondary motivation in LPS-treated rats, which did not receive any food supplement, suggested the expression of an anticipatory feeding behavior along with a reduced immediate appetite. Their results demonstrated that LPS treatment disrupted food hoarding in a minor way when rats received all of their food from hoarding, compared to rats that had supplemental food in their home cages (Aubert, Kelley, & Dantzer, 1997). LPS-treated animals still appear able to adjust their defensive behavioral strategies with regard to their needs and capacities. These findings support the adaptive value of the behavioral changes displayed by LPS-treated animals (Aubert, Kelley, & Dantzer, 1997).

These evidences confirm the hypothesis that sickness behaviors reflect the expression of motivational changes and reorganizations of behavioral priorities (Dantzer, 2007). Additionally, Aubert, Kelley, & Dantzer (1997) confirm that environmental conditions can be determinants of the behavioral change induced by illness or cytokines, in other words, when there are possible adverse effects of behavioral depression, behavior is less likely to suffer disruptions by infections and cytokines.

Motivational aspect of sickness behavior

From the previous discussion of historical origin of the motivational model, it was clear that sickness has motivational properties that reorganize the function on the organism at subjective, behavioral, and visceral levels in order to cope with the threat encountered (Dantzer, 2009). The Motivational aspect of sickness behavior is a vital perspective in pathophysiology; it entails that the neural pathways underlie the expression of sickness behavior, activated by immune stimuli but could possibly receive activations from non-Immune stimuli (Dantzer, 1997).

Therefore, cytokines signal the brain by inducing sickness behavior as result expression of a motivational state triggered by activation of the peripheral innate immune system (Danzter, 2009). As mentioned earlier it is an adaptive normal response to the exposure to a threat of a predator rather than being pathologic. In theory, cytokines released in response to infection or inflammation alert the brain to any real or potential threats and initiate behaviors that are important for survival (Frink et al, 2009). Some even refer to the ability of the immune system to alert or communicate with the brain as a “sixth sense” (Blalock & Smith, 2007).

Sickness behavior is adaptive in that it forces an individual to rest and withdraw from activities so that physiological processes can more effectively produce healing (Blalock & Smith, 2007; Kelley, Dantzer, Zhou, Shen, Jhonson & Broussard, 2003). Proinflammatory cytokines released during infection, inflammation, injury and even psychological stress can signal the brain to initiate behavioral changes that facilitate adaptation to these threats.

However, similar to other responses, sickness behavior can become anomalous or pathologic outside its original context and in the absence of inflammatory stimulus which, when it happens over longer period of time (Dantzer, 2009). This pathologic state derives from several factors:

1. The hyperactive proinflammatory state marked by persistent excess production of proinflammatory cytokines like IL-1, IL-6 and TNF and IFN gamma (Dantzer, 2009), which may also contribute to the pathogenesis of various human diseases in addition to sickness behaviors, such as allergy, autoimmunity, obesity, depression and atherosclerosis (Sternberg, 2006).
2. The predominance of proinflammatory cytokines over anti-inflammatory cytokines (which normally down-regulate the activation of the proinflammatory cytokines of the sickness response), this mismatch result in the exaggerated sickness response due to the peripheral immune system or direct activation of the brain cytokine system (Dantzer, 2009).
3. The sensitization of the neuronal circuits: Activation of afferent nerve fibers by peripherally released cytokines represents the fast pathway of transmission of immune signals from the periphery to the brain. This neural pathway certainly sensitizes the brain target areas of inflammatory mediators to the action of brain-produced cytokines that relay and amplify the action of peripheral cytokines (Dantzer, 2001).

The Motivational Competition between Motivational States for Behavioral Output

Normally, hierarchal organization of motivational states is required for the expression of behaviors, along with continuous evaluation of the encountered internal context and external events occurrences (Dantzer, 2001). For example, if an individual is sick with a flu have generalized muscle weakness that result in bed rest for the whole day, this individual is more likely to overcome this illness in the case of an alarming emergency immediately in order to escape a threat/predator.

The effect of cytokines on maternal behavior provides more representative example of the competition of motivational states, in the sense that maternal behaviors are critical for the survival of the offspring. In the previously mentioned study by Aubert, Goodall, Dantzer, & Gheusi (1997) LPS-treated mice exposed to ambient temperature of 22 degrees C, compared to saline-treated mice, demonstrated pup retrieving but nest building was significantly decreased.

However, LPS-treated mice exposed to ambient cold temperature, compared to saline-treated mice, demonstrated pup-retrieving and nest-building activity. Interestingly, their results signify that the behavioral expression of LPS-induced sickness depends on the priority of the behavior under consideration (Aubert, Goodall, Dantzer, & Gheusi, 1997). In motivational terms, maternal behaviors compete with sickness, and maternal-motivated behavior takes superiority over sickness behavior. This observation provides a valuable example of the motivational competition between behaviors.

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Abstract

The rehabilitation after a head surgery is a complex process, the success of which is largely dependent on the degree of cooperation between the patient and the therapist. The present paper follows the rehabilitation period of Bobby Robson, a patient who was diagnosed with a brain damage after a car accident. The paper includes interview with Robson and his neurologist, Dr. Milton, tracing the recovery process and providing corresponding support from literature.

Bobby Robson, 36, was admitted to Northwestern Memorial Hospital in Chicago, Illinois, with a brain damage as a result of a car crash. Diagnosed with brain damage, injured tissues and labored oxygen flow, Dr. Milton, a neurologist, appointed a surgery for Robson, who lost consciousness several times after the accident. Robson, who was able to answer a few questions right after the accident, stated “I lost control of the car, and the next thing I saw was the rapidly approaching wall”. An examination of the injury as well as a description of the accident revealed that Robson hit a hard surface with his head. Head injuries are one of the major causes of brain damage, most of which are caused by road accidents, falls, and blast injuries. Head injuries are classified as ‘harm caused on the brain after the head is subjected to severe pressure.

Head Injuries

Head injuries is a serious risk for the population, where studies carried out to determine the number of Americans with head injuries or brain injuries have shown that 1.4 million Americans suffer from head injury every year that is a very disturbing outcome. To accommodate and rehabilitate such cases costs are estimated at around $40 billion. The volume of these prices are credited to behavioral and cognitive changes, still these changes are not properly understood due to DAI being widespread and hard to determine by using standard brain imaging methods. Toward that end, a program known as Traumatic Brain Injury offers an integrated solution and treatment program for patients having traumatic head injuries or diseases. This program deals with individual patient needs, including initial trauma, through physical and medical rehabilitation, behavioral grooming, and community re-entry (Centre for Neuro Skills).

A study conducted on patients who were suffering from diffuse axonal injury (DAI) explained the process of head injuries, where during accidents the victims head is banged on hard surfaces causing the brain to shake violently within the skull. This leads to widespread disconnection of the brain cells and subsequently a condition, which is defined as ‘brain damage’ (Baycrest Centre for Geriatric Care, 1).

An individual with brain injury is left with a number of unyielding impairments that continually interfere during the course of finding and keeping an occupation. These obstacles can be cognitive, that is they involve difficulties with memory, attention, reasoning, communicating, problem solving, etc. They also give rise to physical problems such weakness, vision impairment, sleeping disorder, fatigue, reduced coordination in arms and legs, etc. Brain injury also results into emotional breakdown, vulnerability to depression, increasing anger, or anxiety, and several behavioral problems (Koob et al).

Recovery

For the recovery process in Robson’s case was dependent on the cause of the injury. According to Brown, Lyons, and Rose (2006), the causes of traumatic injury can be classified as follows:

• In trauma; occurs when the brain is shaken violently causing multiple shears across the brain, especially when the brain collides with the skull during impact/period of incident.
• Brain swelling caused by initial injuries can cause secondary brain damage since the skull does not allow expansion/swelling.
• Neuron death due to blood vessel damage due to initial trauma/impact of accident that caused injury.
• Neuron death after brain swelling cause oxygen deficiency cutting off oxygen supply and subsequent neuron death in seconds.

The recovery process, as Robson described, was not easy,

After the surgery, it was like gradually discovering the pain. My main fears were about any consequences that the surgery might have had on my memory or my mental abilities. The pain was usually eased with pain killers and anesthetic procedures. However, I have to talk about memory losses.

Robson’s confusion is understandable, as most patients lack information on the state of their health and abilities, right after the surgery. The role of the staff might be seen in eliminating the risks of patients going to assumptions. Such problem was covered in Morris et al (2005), stating that the fundamental problem encountered during rehabilitation is that patients with brain injury lack awareness about their difficulties or impairments. Additionally, research into this development has often ignored the conditions of those affected by the trauma and do not present an insider’s viewpoint on the process by which a patient with a brain injury educates themselves about their difficulties. In other words, people having less visible, emotional, or behavioral disabilities may find it difficult to convince a VR counselor that they are impaired to qualify for services. Conventional VR system relies on the candidate who is applying for services to be “self-motivated” to work (High et al 31; Malec et al).

Dr. Milton’s position on Robson’s fears was twofold. On the one hand, Dr. Milton stated that the surgery itself went well, where post surgery examination revealed no complications. On the other hand, the case of Robson’s memory losses might require further examination.

We should understand that the rehabilitation is a sensitive period. Several conditions are temporary, and accordingly, I try to calm patients down. At the same time, I should comprehensively test all brain functions at this period. In Robson’s case, magnetic resonance imaging (MRI) was done for part of the testing.

Observation is an essential procedure during post-surgery periods, specifically in head injuries, where observation might indicate damages. Accordingly, the usage of MRI in order to assess brain activity is a common procedure (Baycrest Centre for Geriatric Care). Such procedure is performed to measure the ability to tackle mentally challenged tasks. Such tasks involve the control and manipulation of brain memory. Such level of cognitive operation is very important to help an organization realize full employee productivity. It is also essential in maintaining daily tasks especially when resolving commonplace organization and problem as explained by Brown (Brown et al 937-946).

Rehabilitation

For a period of 5 weeks after the surgery, Robson’s emotional condition was gradually improving. Several discussion sessions were held in order to assess Robson’s needs and fears. The approach widely used in such case by expert neurosurgeons is Interpretative Phenomenological Approach (IPA), which allows learning more about patient’s conditions, views, and hopes as they recover. Robson’s views on emotional state was not good in first sessions,

It is like gathering pieces together. The headaches are gone, although I still cannot remember all things about the accident. I think there is still something wrong with that.

A couple of sessions later, Robson’s mood started to gradually change, where being around family members, along with the treatments showed positive results. As more information was gathered through the sessions on the experience of the patient, the rehabilitation process improved. The insight from direct observation and interviews provide ideal clinical and rehabilitation settings. It also helps the set up of appropriate alternative interventions to treatment and rehabilitation. According to Eames & Wood, Twenty-four patients with severe brain injury who had disturbed behaviors preventing rehabilitation were used as cohorts to determine outcomes. Many neurosurgeons do the same to get result. The cohorts were under care in ordinary settings and provided treatment in a typical token economy (Eames & Wood, 613-619). A long-term follow-up study to observe behavioral trends in ‘post brain injury’ treatment period shows that post-traumatic behavior disorders are prevalent and can be treated. Eames and Wood propose lengthy rehabilitation and advice that it can have surprisingly good effects (Eames & Wood, 613-619). Doctors doing research on post-traumatic conditions single out psychiatric implications as commonplace outcomes. Reekum, Cohen, and Wong point out that traumatic brain injury (TBI) may cause psychiatric illness (Reekum, Cohen & Wong, 315-327). This evidence proves that there is a strong association between TBI and mood and anxiety disorders in posttraumatic brain injury and post rehabilitation periods (Reekum, Cohen & Wong, 315-327).

Dr. Milton comments on the rehabilitation and post-rehabilitation periods were largely positive. He admitted that a few problems existed at the start of the period, mainly related to diagnosis. As Dr. stated,

Diagnostics can be problematic when measuring brain damage right after the accident. Examining Robson, the main problem can be seen in vague descriptions of his state. General discomfort is common right after a brain surgery. The problem was to identify problems, which can be evident during examination and the rehabilitation period.

The statement of Dr. Milton largely conforms to the opinions on post-injury problems. According to Rice-Oxley and Turner-Stokes, both doctors in leading neurosurgical centers, the problems posed by conditions and the lack of diagnostic specifics as guides to what to measure when diagnosing range of brain damage after injury is a pitfall. However, this is now cushioned inside robust evidence for the effectiveness of rehabilitation of brain-injury cohorts (Rice-Oxley & Turner-Stokes, 7-24). Rice-Oxley and Turner-Stokes provide insight about how Meta analysis demonstrates clearly that stroke units, a procedural measure during treatment and rehabilitation of brain injury. Strokes units are believed to provide much better outcomes than general management of the process in a medical ward, though this applies only in a survival level, discharge destination, and reliance on assistance circumstances (Rice-Oxley & Turner-Stokes, 7-24).

Rice-Oxley and Turner-Stokes project that the advantages of the approach include the fact that out of every 100 patients treated four deaths are avoided. On the same level, two institutional admissions are avoided (Rice-Oxley & Turner-Stokes, 7-24). These benefits are because of good-quality acute management during and after treatment. In addition, the coordinated input of an efficient multidisciplinary team plays a pivotal role in making the results very effective (Rice-Oxley & Turner-Stokes, 7-24). Therapy programs commonly observed as rehabilitative measures provide clinicians an overview that rehabilitation programs are of greater benefit and are effective solutions for brain damage recovery (Rice-Oxley & Turner-Stokes, 7-24).

On the keys to success working with patients, Dr. Milton outlined the importance of information during that period. Cooperation during such period is essential, and in that regard, considering the situation, the responsibility lies also on the patient as much as on the therapist. He followed,

Lacking information is like working through a keyhole behind a closed door. It takes time the patient’s condition allows to give us the key to that door.

The importance of information is also outlined in Denton (2008), when discussing the applicability of the therapeutic approaches in stimulating memory resurfaces. Denton argues that every chunk of information (as observed earlier) is an essential stimulus. It will open a door somewhere in the brain that will eventually lead to something one may be conversant with. It takes time, if in rehabilitative conditions, encouragement and mentoring can significantly bring quality recovery (Denton 173-178). Therapeutic approaches work well as the posttraumatic stage ends. Mapping out specific areas of weakness and engaging compelling strategies like lessons, assuming very comfortable positions, and relaxing are essential in making recovery very possible and smooth. Many patients confess that relaxing and self-deep thinking has provided very significant progress in recovering memory and fully regaining one’s mental health.

Conclusion

It can be concluded that the rehabilitation period in the case of Bobby Robson was successful. The report outlined critical periods during and after the rehabilitation. Many expert neurologists insist that comprehensive rehabilitation is very essential in making recovery a success. The recovery process is aimed at correcting certain problems that come along with the head injury.

Works Cited

Brown, D.; Lyons, E.; Rose, D. “Recovery from brain injury: Finding the missing bits of the puzzle” Brain Injury 20.9 (2006). Web.

Centre for Neuro Skills. “Welcome to Centre for Neuro Skills.” Centre for Neuro Skills, 2010. Web.

Denton, Gail. Brainlash: Maximize Your Recovery from Mild Brain Injury . 3. 1. New York: Demos Medical Publishing, 2008. 173-178. Print.

Eames, P, and R Wood. “Rehabilitation after severe brain injury: a follow-up study of a behavior modification approach..”Journal of Neurology, Neurosurgery, and Psychiatry with Practical Neurology 48.7 (1985): 613-619. Web.

High, Walter, Angelle Sander, and Margaret Struchen. Rehabilitation for traumatic brain injury. New York: Oxford University Press, 2005.

Koob, A.; Colby, J.; and Richard B.. “Behavioral recovery from traumatic brain injury after membrane reconstruction using polyethylene glycol”. Journal of Biological Engineering. 2.9 (2008). Web.

Malec, James, and Rachel Scanlan. “Employment after Traumatic Brain Injury”. Brain Injury Association of America. Brain Injury Association of America, 2004. Web.

Morris, Paul et al. “Patients’ views on outcome following head injury: a qualitative study.”BMC Family Practice 6.30 (2005): 5-40. Web.

Reekum, Robert, Tammy Cohen, and Jenny Wong. “Can Traumatic Brain Injury Cause Psychiatric Disorders?.” Journal Neuropsychiatry Clinical Neuroscience 12. (2000): 316-327. Web.

Rice-Oxley, Margaret, and Lynne Turner-Stokes. “Effectiveness of brain injury rehabilitation.” Clinical Rehabilitation 13.1 (1999): 7-24. Web.

Santa Clara Valley Medical Center. “Traumatic Brain Injury”. Santa Clara Valley Medical Center. Santa Clara Valley Medical Center, 2008. Web.

Introduction

Violence in sports is a common phenomenon that occurs in diverse sports as a result of distinct factors. Sometimes the notion of violence may differ depending on the approach. As a result, sports-related head trauma has been prevalent in various professional sports. Although there is no recognized standard laboratory test conducted to establish the extent of these traumatic brain injuries, a common concern exists in the mental health statistics portrayed worldwide. In the last decade, there has been a surge in research on the consequences of repetitive head injuries on cognitive neurological performance of the brain associated with violence of all kinds in the sporting arena (Mizobuchi & Nagahiro, 2016). Violence is more prevalent in current generational sports than it used to be years ago, whether it is between players, spectators, or post-match riots. To some people, it is their way of expressing patriotism or fanaticism, while others use it to show dissent with authorities regulating matches. The problem of violence has had far-fetched consequences in the world. Therefore, it is important to understand what factors contribute to violence in professional sports, risk factors of repetitive brain injuries, preventive measures and the consequences of such injuries among players.

Head injuries are common in such games as mixed martial arts, where acts of kicking, punching, knee-striking, or use of pounds and ground to strike the head can accumulate into traumatic head injuries. Such encounters may result in debilitating conditions among the participants and endanger their psychological and cognitive health. Repeated traumatic brain injuries have the potential of causing future problems and may become fatal among player populations (Mizobuchi, & Nagahiro, 2016). Fares et al. (2020) assert that head injuries are attributable to routine punches, kicks, and strikes, which interfere with the structure of the skull, most common in martial arts and other contact games. Concurrently, the strains and the shock impact on the brain result in a potential long-lasting impairment, which then endangers one’s career for a lifetime.

Consequences of Repetitive Brain Injuries in Professional Sport

To explicitly understand violence in professional sports, it is ideal to explore the meaning of the term itself. Violence, in this context, defines unnecessary harmful acts intentionally committed before, during, or after a game as motivated by the sporting event. Some of the key games where such behavior often manifests involve contact games such as boxing, American football, rugby, hockey, mixed martial arts, wrestling, and lacrosse, among others. Several factors often cause violence in such games. Such dynamics frequently range from personalities, environmental elements to a combination of other variables in play (Weinberg, 2016). Nonetheless, the occurrence of these events is a major worry for many authorities around the world. Concurrently, the occurrence of violent events in sports emanates from institutional and individual factors, which may require critical evaluation and research. There are varying study results from soccer, football, rugby, boxing, martial arts, and other multiple engagements in repetitive violence.

Acute traumatic brain injury may lead to long term damage of the brain functionalities. In many instances, individual exposure to injuries depends on the types of sporting activities. These competitions expose the participant’s brain to direct injuries because of physical contact with the opponents’ jabs. Recently, there has been a surge in consequential chronic traumatic injuries among athletes. According to Mizobuchi and Nagahiro (2016), there are several sport-related brain injuries initiated by continued violence in sporting behavior. Some of these acute conditions include concussion, subdural hematoma (ASDH), chronic traumatic encephalopathy, and traumatic cerebrovascular disease (Mizobuchi & Nagahiro, 2016). In essence, almost all of these conditions occur as a result of contact sporting events which often interfere with the normal brain performances of the sportsmen. The severity of these impacts depends on the nature of the sporting activity.

Subdural haematoma (ASDH) is the leading cause of death based on repeated sports-related brain injury. Mizobuchi and Nagahiro (2016) claim that the Judo survey revealed that more than 28% of accidents of injured players had headaches before engaging in these accidents. Thus, the players were susceptible to vein ruptures. According to Mizobuchi and Nagahiro (2016), the prevalence of severe head damage due to repeated exposure to contact sports, including American football and rugby which are mainly associated with Acute Subdural Hematoma (ASDHs) forming closely 90% of the cases. In Japan, this condition is often associated with Judo as the main sporting event.

Concussion defines diffuse brain injuries developed over time because of contact games. It often results in altered mental status, including shaking of brain that induces severe injuries to neurons and nerve fibers. Worldwide, 1.6 to 3.8 million people has reported concussions annually as a consequence of sport-related trauma (Mizobuchi & Nagahiro, 2016). Nonetheless, the symptoms and signs may not be clincially explained medically but may include lost consciousness, loss of memory and significant alteration of perceived judgment. Such trend is also evident in cases of traumatic cerebrovascular disease, where 80% of patients also had other conditions like ischemia or infarction and male dominated the list (Mizobuchi & Nagahiro, 2016). Concussions are often considered as mild traumatic brain injuries.

Chronic Traumatic Encephalopathy results from progressive neuro-functional degeneration that results from repeated brain injuries. Self-defense mechanisms employed by the athletes alongside their health status also determine the extent of brain damage during these repetitive exposures. Prominently, the figures vary depending on the type of sports and may cumulatively result in vivid complications among the victims at later ages. Following closely are the cases of traumatic cerebrovascular disease and concussions. Interestingly, male athletes are suffering more of these conditions than their female counterparts (Mizobuchi & Nagahiro, 2016). According to Mizobuchi and Nagahiro (2016), these conditions are correlated to several other individual factors among these players, including mental health status, family relations and economic classes.

Mixed martial art type of fight combines traditional martial arts with kickboxing and wrestling as a mode of competition between different gamers. Often, participants encounter repetitive head injuries with the potential to cause myriad problems within the peripheries of cognitive performances. However, there is minimal research conducted on this field to empower fighters with the right timely information on mental health implications. Primarily, this game entails knockout norms which replicate loss of stability upon the loser. In essence, it exposes the victim to high tension on the cranial cavity because of the jibes on the skull. Although it is a periodic form of engagement, routine fighters face multiple mental health challenges because the knockouts have the potentials to impair their mental performance for a lifetime (Mizobuchi & Nagahiro, 2016). Such perception vindicates the importance of understanding the value of repetitive trauma on mental health.

Repeated encounters of knockouts and technical knockouts have critical consequences on the functionality of the brain, even as they may mark the end of a match between two opponents. The purge on one’s cognitive capability in an enclosed ring may also mark the beginning of mental health struggle for such individuals. A study by Fares et al. (2020) reveals that losing during repetitive rounds of mixed martial arts may have impacts on the general psychological stability of such individuals for a long time in history. Thus, head injuries sustained during such events have become fundamental contributing factors in the rise of mental illnesses worldwide. The resulting state of being knocked out or undergoing a technical knockout indicates that the brain can no longer sustain the weight of the pressure endured during these games. Thus, the victim cannot withstand the injuries anymore, signaling medical concerns which may require immediate clinical care or continuous monitoring to avert severe impaction.

At the same time, the varying trends in gender difference also showcase the internal factors affecting mental health. Simultaneously, age factor is also an important aspect of self-intuition in repetitive traumatic injuries translating to differences among males as well. Several other reasons, such as psycho-social wellness and family values, also contribute to the variations in mental response to repetitive traumatic injuries. As traumatizing accidents or calamities, sporting trauma too can be devastating if not well-managed in the long run. As a result, finding the correlations between various variables in play can shape the way in which players respond to different situations. Practically, there is a significant correlation between social background and the psychological wellness of gamers (Weinberg, 2016). Thus, the continued link between players and their fans is a fundamental element of brain competence in the face of miseries and stress.

Epidemiological studies reveal that mixed martial arts, rugby, and American football are leading games marred by violence and repetitive head injuries. Fares et al. (2020) postulate the mixed martial arts entails critical fighting tactics which endanger the lives of perpetrators in various ways. Based on Fares et al.’s (2020) study, repeated traumas in sports constitute more than 35% of the head injuries among male players engaging in sanctioned games, athletic exposures. At the same time, female mixed martial artists showcased 23% chronic head injuries for the athletic exposure as recorded in Nevada State Athletic Commission (Fares et al., 2020). Such statistics may also have global trends in chronic head injuries among different players. Essentially, athletics and other contact games bear the burden of these numeric and replicate to the worrying trend of deteriorating cognitive health across the globe.

Moreover, the degenerative brain health among sports people may result in anti-social implications, including depressions, aggressiveness, poor impulse control as well as dementia. These consequences depend on the value of personal contribution towards their well-being. Ling et al. (2015) asserts that the traumatic injuries are progressive and irreversible, hence, require preventive measures instead of treatment procedures. When such norms are not adhered to or broken, there is always an evidential outburst of emotions among players, fans, and interested parties (Lockwood et al., 2018). Such state may indicate the initiation of brain damage.

The various forms of traumatic brain injuries cause axonal injury and functional disturbances, and not direct structural damage to the brain. Lin et al. (2015) asserts that the varieties of the consequences encountered by various players may develop temporary and permanent symptoms requiring the victim to seek intensive care. For concussions, some of the key indicators may include dizziness, nausea, reduced attention, amnesia and headache (Lin et al., 2015). The deviance from normal behavior becomes a major outcome, with a biased perception of events as they unfold (Weinberg, 2016). In essence, it is difficult to control the emotions of such charged folks within the field. Therefore, they often begin to suffer from different mental illnesses if no management program is initiated.

The other consequence of injuries includes the economic burdens. Technically, the functional neuroimaging, electrophysiological, neuropsychological and neurochemical assessments may require a lot of funds to conduct. As a result, some players may resort to living with these conditions to avoid such burdens while others can afford therapeutic procedures and manage their health effectively. The economic frustrations may then constitute to variance in cognitive health concerns. According to Weinberg (2016), individuals respond to social and psychological pressures differently. Similarly, players respond to field demands in distinctive patterns as some resort to violence against the opponent while others may accommodate the external pressure and play normal games. Such variance in behavioral theories portrays classical pattern in which the trend involving chronic mental health problems occur around the universe

Moreover, traumatic brain injuries portray different consequences among different ages. Ling et al. (2015) claim that young people with developing brains are more vulnerable to concussion than adults. Subsequently, children and adolescent players may develop complicated symptoms which last longer than those of older men and women in athletics. To curb the rise in vulnerable and susceptible populations, the international unions such as Federation Internationale de Football Association (FIFA) and World Anti-Doping Agency (WADA) have set rules guiding the conducts of players and fans on and off the pitch. As a governing body, their mandate is to govern the execution of matches and minimize violence among the athletes. Concurrently, they ensure that the playing grounds are safe and fit for healthy athleticism while harmonizing security for the safety of spectators in all activities. Such mechanisms prove pivotal in setting standards to avoid chronic harm among players in various games. The sole aim of these bodies is to set a level playing ground for all folks and promote sustainable mental health across all types of competitions. The prevalence in emerging cases of new chronic traumatic mental injuries may have farfetched implications for economic growth and development.

Personal Opinion and Recommendable Measures

There are no well-established diagnostic practices on how to handle mental injuries among athletes. Therefore, there is a need to ensure an integrated approach in handling the global prevalence of injuries among these players. On the one hand, there is no clear correlation between physical injuries and brain damages. The final cases of damages are an outcome of cumulative exposure to both physical violence and environmental injustice petted against sportsmen in different cadres. Lockwood et al. (2018) recommend that there is need for investment in medical strategies and elucidation of proper mechanism to ensure sustainable management of these injuries. Although injuries are common aspects of games, repetitive violent behavior may result in life-changing behaviors among the victims.

One of the ways to manage the challenge of violence and brain injuries is to optimize sporting environments. The participants should endure conducive surrounding which encourages them to be positive to one another and embrace sporting as an art and not an end of life encounter. Alongside building good infrastructures, there should be effective handling techniques and expertise to ensure sustained mental awareness. The relevant authorities and government agencies should promote commitment to human rights, paying sports people just any other employees in the corporate sector based on agreements. Succinctly, the current trend of an integrated approach to sporting activities will reduce violence in contact games and ensure sustainable recognition of talents in different areas.

Moreover, efficient awareness creation and behavior change communication on sportsmanship should be a major priority in athletics. As a game, athletics, including mixed martial art, should be enjoyable for the players, fans, and all interested parties to avert violence endured during these games. Thus, stakeholders should strategize a way of preventing repetitive knockout for medals and ensure protective mechanisms that shield both the loser and the winner in a game. In most cases, players struggle to acquire titles even by executing violence against their opponents. Concurrently, the organizers need to institute mechanisms through which all participants are recognized so that they are motivated and feel happy about their accomplishments.

In my view, investing in research targeting brain injuries and long-term neurodegenerative effects of repeated traumas will help to establish the best practices in tackling these challenges. Currently, there seems to be a minimal investment in mental health, especially sports-related outcomes. Thus, there is a need to explore mechanisms for providing sufficient protective environments, including well-trained field-side physicians who have diagnostic expertise in effectively treating traumatic brain injuries among players in all levels of games encounter. At the same time, there is a need for further research to expand on the accessibility of services and assessment of patients under different circumstances.

Conclusion

Repetitive brain injuries often result from risky contact games and may have severe short and long-term impacts on the cognitive performances of the victims in different ways. Although there is an evidential surge in the love of such sports, there is a need to design protective mechanisms which will help to harmonize the safety of the athletes first. Repetitive head injuries occur in almost all sectors of sport. However, people showcase differing severity based on exposure and care given in terms of protective gears and self-precautionary measures. In an ideal world, sporting events often culminate in passionate relations and long-term memories. In many ways, some individuals engage in athletics and other games to earn a living and entertaining their audience. Some of these folks may not understand the accumulative implications of the use of violent tactics against their opponents.

At the same time, the victims may fail to seek medical attention because they do not understand the extent of the impacts. Over time, these events prompt deteriorating mental health statuses which are sometimes life-threatening. As a result, there is a need for effective public education on behavioral change among players and fans. All sports agencies and governments worldwide should develop policies that harmonize and guide the conducts of players on and off the pitch. Alongside the World Anti-doping Agency (WADA), other bodies should be formed to monitor and implement healthy practices in all sectors of play.

References

Fares, M. Y., Salhab, H. A., Fares, J., Khachfe, H. H., Fares, Y., Baydoun, H., & Alaaeddine, N. (2020). Craniofacial and traumatic brain injuries in mixed martial arts. The Physician and Sportsmedicine, 1-9. Web.

Ling, H., Hardy, J., & Zetterberg, H. (2015). Neurological consequences of traumatic brain injuries in sports. Molecular and Cellular Neuroscience, 66, 114-122. Web.

Lockwood, J., Frape, L., Lin, S., & Ackery, A. (2018). Traumatic brain injuries in mixed martial arts: A systematic review. Trauma, 20(4), 245-254. Web.

Mizobuchi, Y., & Nagahiro, S. (2016). A review of sport-related head injuries. Korean Journal Of Neurotrauma, 12(1), 1-5.

Weinberg, J. D. (2016). Consensual violence: Sex, sports, and the politics of injury. University of California Press.

Accident-Related Methods

Phineas Gage Technique

How itworks:

• Phineas Gage survived brain injury after a catastrophe with an iron rod.
• This technique scrutinizes the behavioral pattern of an individual after some brain damage caused by an accident (Nevid, 2008).

This method is a case study of Phineas Gage who survived a brain injury. It has very minimal control on experiments. However, circumstances that cannot be quantified in the laboratory can be handled using this method. Besides, the connection between the structure and function of the brain can be studied.

Lesions Technique

Mode of Operation:

• The behavioral characteristics of an individual is examined especially after undergoing damage of the brain owing to infections, psychosurgery or factors related to genes (Pinel, 2007).
• Entails removing or destroying a section of the brain (Baars & Gage, 2010).

Some parts of the brain structure is destroyed or lesion and then after the recovery of the individual, the degree of the damage is assessed against behavioral patterns.

EEG & Neuroimaging Techniques

Electroencephalogram (EEG)

How it works:

• The electrical activity taking place in the human brain can be recorded and then amplified for easy monitoring.
• The sensors are placed right on the scalp of the brain.
• Electrodes or sensors are used to capture waves emanating from the brain (Baars & Gage, 2010).

The resolution of this technique is temporarily high. Besides, the method is not invasive since the procedure is relatively painless. However, this brain study method has a poor spatial resolution.

Computerized Axial Tomography scan

Mode of operation:

• The three dimensional (3D) image of the structure of the brain is captured.
• This is done using rotating X-ray cameras positioned on the head of an individual under examination (Roe, 2009).

The method gives a very high resolution of the structure of the brain. The amount of radiation exposed to an individual should be regulated because it can lead to brain damage (killing of brain cells). The information on the function of the brain is not provided by this method.

Positron Emission Tomography (PET) scan

Mode of Working:

• Glucose that is radioactive in nature is an important component of the brain.
• In order to determine the level and rate of consumption of this radioactive glucose, Positron Emission Tomography (PET) scan is used (Baars & Gage, 2010)

The technique provides reliable information on the functioning of the brain. For instance, sections of the brain that consumes the most amount of energy can be analyzed or determined by researchers using Positron Emission Tomography scan. The machines that are required to make radioactive isotopes are expensive. In addition, the process is long and requires injection of the desired radiation.

Magnetic Resonance Imaging (MRI)

How it Works:

• There are countless atoms located in the brain.
• These atoms can be disoriented when exposed to a powerful magnetic field.
• Hence, MRI is used to produce signals emanating from soft brain tissues which are then analyzed for defects (Nevid, 2008).
• MRI produces stronger signals than that of X-rays.

The structure of the brain can be determined without the use of radiation. The procedure is not painful.

Functional Magnetic Resonance Imaging (fMRI)

How it Works:

• This type of Magnetic Resonance Imaging assists in determining the quantity of blood that flows through the brain at nay given time(Roe, 2009).
• Different parts of the brain are examined with this type of study.
• The amount of oxygen consumed is also imperative in studying the functioning of the brain using this technique.

The imaging process is quick and the technique also gives spatial resolution that is quite high. Although this method is painless, it may be uncomfortable to go through the experience.

References

• Baars, J.B. and Gage, M.N. (2010). “Cognition, Brain, and Consciousness: Introduction to Cognitive Neuroscience”, Burlington: Elsevier Ltd.
• Nevid, S.J. (2008). “Psychology: Concepts and Applications”, Boston: Houghton Mifflin Company.
• Pinel, J.P.J. (2007). “Basics of Biopsychology”, Boston: Allyn & Bacon.
• Roe, W.A. (2009). “Imaging the Brain with Optical Methods”, New York: Springer.

PICOT Question: “In Traumatic brain injuries on returning soldiers how effective is EEG Biofeedback medication of Traumatic Brain Injuries compared to computer medication in improving memory during the pretreatment to post-treatment time?”‘

P=Patient / Population and Problem

Traumatic Brain Injury (TBI) is an injury in cognitive functioning. TBI is a disruption of the brain functions as a result of sudden trauma to the head. Traumatic Brain Injury is caused by blast waves resulting from explosions in wars as well as direct impacts that result in severe head injuries. It is observed that TBI causes secondary injuries such as increased pressure within the skull as well as changes in cerebral blood flow that worsen the initial brain injuries that are caused by blast waves.

TBI is known to cause a lot of physical, behavioral as well as emotional problems that are not easily detectable. Research indicates that TBI is associated with causing accelerated hormone deficiency that triggers physiological, psychological and physical manifestations that are expressed in form of memory loss, anxiety, depression, anger, high blood pressure, loss of libido among others (Levine, Cabeza, McIntosh, Black, Grady& Stuss, 2002).

It is noted that those patients who suffer from TBI are mainly dependent on that part of the brain that is damaged. Soldiers have a high prevalence of being affected by TBI. Many soldiers are diagnosed with TBI after returning home from war as a result of being exposed to blast waves that originate from explosives that are used during the war. Many US military officers who were deployed in Iraq and Afghanistan showed signs of traumatic brain injury in a number of months or days after returning home from the war. This has shown that there might be long-term effects to this condition that may affect the returning soldiers over a long period of time.

The research established that most US military personnel who returned home from the Golf War in Iraq showed some symptoms of traumatic brain injury. Some of the symptoms noted included: concussion which is a condition that entails a brief loss of consciousness. Irritability which is the tendency of being easily annoyed by things that a normal person who is not exposed to brain damage cannot mind about. Many soldiers were noted to have difficulty remembering things.

Some soldiers were noted to have a problem recalling simple instructions or tasks. Others complained about prolonged headaches, migraines and having difficulty in concentration. There are some soldiers who lamented of having a problem in sleeping and companied of staying up all night. There are others who complained of feeling tired and at the same time having blurred vision that affected their sight. Lastly there are those soldiers who complained about difficulty in driving as a result of muscle weaknesses.

I=Intervention under Consideration (Change in Treatment Adopted)

EEG Biofeedback interventions are the most recent strategies for TBI rehabilitation. The approach entails operant conditioning of brainwave patterns through reinforcement. The feedback aims at returning fundamental electrophysiological function of the brain to its original normative form. The method entails four strategies that include: Flexyx Neurotherapy approach which is an improved EEG biofeedback technique that combines small radio frequency with conventional QEEG biofeedback. It does so in order to change QEEG patterns that are linked with cognitive dysfunction.

The standard quantitative QEEG strategy focuses on enhancing the strength of beta microvolt activity as well as reducing the strength of theta microvolt activity (Thatcher, 2000). The eye closed QEEG involve comparing the behavior of a patient’s who is resting with the eyes closed QEEG to a reference database. This is aimed at producing more protocols for patients. The last strategy which is the most recent advancement is the activation database QEEG-guided biofeedback. This approach assesses the brain functions of resting patients with their eyes closed (Lubar & Davidson, 2004).

C=Comparison: The Current Treatment Being Compared With Intervention

Many patients who are diagnosed with TBI are mainly treated through Cognitive Rehabilitation (CR). CR is considered as a systematic, functionally based approach of therapy that is founded on an evaluation and understanding of one’s brain behavior deficit. CR entails redirecting brain services in order to achieve changes in brain functioning by strengthening, reinforcing or reestablishing previously acquired behaviors.

Most physicians use computer interventions and strategy instruction in the treatment of TBI (Cappa, Benke, Clarke, Rossi, Stemmer & van, 2003). This method of treatment is designed in a manner to enhance attention of the patient. The patient is required to tab the bar of the computer every time a large red circle is displayed on the monitor. There are three strategies used in this method that entail; restorative cognitive rehabilitation that entail use of computer simulation that is designed to cause repetition in order to restore function (Guyatt & Rennie, 2008).The strategy aims at reinforcing, strengthening as well as reestablishing previously acquired patterns of behaviors.

However, very little success is achieved through this process. The second method is strategy cognitive rehabilitation that concentrates on developing conscious cognitive strategies by anticipating that improvements will generalize to daily activities through establishing new patterns of cognitive activity. However, research has shown high failure rate of this approach as patients fail to continue using the strategy during post treatment period.

The third method that is also widely employed in the treatment of TBI is compensatory cognitive rehabilitation that offers outside, prosthetic help for dysfunctions. This method is appraised by many scholars for its cost benefit effects. However, it does not result to any meaningful enhancement in a patient’s core cognitive skills (Cherek & Taylor, 2005; Ashley, Krych, & Lehr,1990).

O=Outcome: What is the effect of the “I” on “P?” What is desired outcome?

The use of computer interventions in the treatment of TBI is not associated with significant improvement in the memory, attention as well as problem solving skills for patients suffering from TBI. However, EEG biofeedback interventions are associated with great outcomes in acquisition of long term memory, attention and problem solving skills for those suffering from TBI.

T=Time

Traditionally, improvements as well as recovery of those suffering from TBI were considered to occur after a short time span following medication, although there is no evidence to support this claim. Nowadays, neurological function improvements for those suffering from TBI are noted a few weeks after medications for mild TBI (Belanger, Vanderploeg, Curtiss & Warden, 2007). However, for serious complications, improvements are observed after two or more years after patients start computer interventions. However, with the adoption of EEG biofeedback interventions, the recovery of those suffering from TBI is expected to reduce considerably (Cherek & Taylor, 2005).

Reference List

Ashley, M. J., Krych, D. K., & Lehr, R. P. (1990). Cost/Benefit analysis For post-Acut Rehabilitation of the Traumatically Brain-Injured Patient. Journal of Insurance Information. 22, 2, 156-161.

Belanger, H. G., Vanderploeg, R. D., Curtiss, G., & Warden, D. L. (2007). Recent Neuroimaging Techniques in Mild Traumatic Brain Injury. Journal of Neuropsychiatry, 5, 7, 78-89 and Clinical Neurosciences, 19(1), 5-20.

Cappa, S. F., Benke, T., Clarke, S., Rossi, B., Stemmer, B., & van, C. M. (2003). EFNS Guidelines on Cognitive Rehabilitation: Report of an EFNS Task Force. European Journal of Neurology. 10,1, 11-23.

Cherek, L., & Taylor, M. (2005). Rehabilitation, Case Management, and Functional Outcome: An Insurance Industry Perspective. Neurorehabilitation, 5,1, 87-95.

Guyatt, G. H., & Rennie, D. (Eds.). (2008). Users’ guide to the medical literature: Essentials of evidence-based clinical practice (2nd ed.). Chicago: AMA Press.

Levine, B., Cabeza, R., McIntosh, A. R., Black, S. E., Grady, C. L., & Stuss, D. T. (2002). Functional reorganization of memory after traumatic brain injury: a study With H2150 Positron Emission Tomography. Journal of Neurology, Journal of Neurosurgery & Psychiatry, 73, 2, 173-181.

Lubar, J.O., & Davidson, J.F. (2004). Electroencephalographic Biofeedback of SMR and Beta for Treatment of Attention Deficit Disorders in a Clinical Setting. Journal of Biofeedback and Self-Regulation, 9, 1, 1-23.

Thatcher, R. W. (2000). EEG Operant Conditioning and Traumatic Brain Injury. Journal of Clinical Electroencephalography, 31, 1, 38-44.

The Purpose

For this session, we will try to:

• to examine the validity of the selected Patient Treatment Form [PTF] when used with Traumatic Brain Injury Patients.

Assessment

Assessment will be correlated with other well-normed and well researched rating scale:

• Neurobehavioral Cognitive Status Examination [Cognistat];
• Functional Independence Measure [FIM];
• Other NeuroCognitive Screening Tools.

Correlation

• Patient Treatment Form;
• Cognistat;
• other cognitive screening tools;
• FIM (valid for measuring the brain injured population).

Provide health professionals a useful clinical tool focused on cognitive functioning to use in treatment and vocational planning, and rehabilitation outcome assessments.

If it is found that the Patient Treatment Form is correlated to the Cognistat and other cognitive screening tools, and FIM (valid for measuring the brain injured population).

• this would provide health professionals a useful clinical tool focused on cognitive functioning to use in treatment and vocational planning, and rehabilitation outcome assessments.

PTF is a useful tool

• in offering a comprehensive conceptualization of functioning and disability associated with health conditions;
• incorporating evaluations from all staff members associated with the care of the patient on a weekly basis, instead of relying solely on the intake assessment of the FIM.

Cognition &Mental Status Exams

Mental status examinations are a series of detailed but simple questions designed to test cognitive ability, the patient’s state of:

• consciousness;
• appearance;
• general behavior;
• mood;
• content of thought.

Mental status examinations are a series of detailed but simple questions designed to test intellectual resources such as orientation with reference to:

• time,
• place, and
• person and
• comprehension (Koelfan, Freund, Dinter, & Schmidt, 1997).

The patient may be:

• asked to remember objects that had been listed earlier in the course of the exam,
• repeat sentences,
• solve simple mathematical problems, or
• copy a three-dimensional drawing.

When speech and language are tested:

• the examiner listens to the character and fluency of the speech,
• the patient’s ability to understand
• and carry out simple or complex commands,
• and to read and write.

In addition to specific questions that make up the actual mental status exam, it is also important that the examiner observes the patient’s general behavior during the examination (Showalter, & Netsky, 2000).

Patient Treatment Form

• developed as a rating scale for assessing cognitive issues of the brain injured patient;
• assist staff towards effective rehabilitation;
• developed and modified to conceptualize functioning;
• compliment the use of diagnostic labels;
• to portray a patient’s health as a dynamic interaction between functioning and disability.

The Patient Treatment Form is developed as a rating scale for assessing cognitive issues of the brain injured patient, thereby assisting staff towards effective rehabilitation.

The Patient Treatment Form was developed and modified to conceptualize functioning and compliment the use of diagnostic labels and to portray a patient’s health as a dynamic interaction between functioning and disability.

• rating scale is utilized weekly at patient staff meetings to evaluate the progress of the patient,
• and offer a standardized framework for communicating clinical assessments to professionals directly associated with the health of the patient, administrators, and health care providers.

Therefore, the patient’s functional status is a more reliable indicator of service needs and treatment outcomes than diagnosis alone, and diagnosis should not be the determining factor for considering the eligibility of psychologists to provide services aimed at improving functioning (Peterson, 2005).

PTF measures various areas of cognitive levels through items relating to the patient’s

• orientation,
• awareness,
• attention,
• memory,
• problem solving and
• reasoning,
• executive function,
• visual perception,
• comprehension,
• expression, and social / behavior emotional competencies.

Neurological Cognitive Status Examination

• is a screening assessment that is used to determine cognitive ability.
• First uses a variety of independent tests to assess a patient’s level of consciousness, attention, and orientation.
• then it evaluates the patient’s level of functioning in five cognitive ability areas.

The Neurological Cognitive Status Examination is a screening assessment that is used to determine cognitive ability.

This assessment first uses a variety of independent tests to assess a patient’s level of consciousness, attention, and orientation.

Then it evaluates the patient’s level of functioning in five cognitive ability areas:

5 cognitive ability areas:

• Language,
• Constructions,
• Memory,
• Calculations
• and reasoning.

Attention

• to devote mental power on the things happening around you.

Neurobehavioral examination

• typically assess your attention span by asking you to perform simple mental tasks.

Your ability to devote mental power on the things happening around you is called your attention.

This is a complex subject.

The neurobehavioral examination will typically assess your attention span by asking you to perform simple mental tasks.

For example, your ability to count or to recite the alphabet is very rudimentary skills requiring attention.

The digit span task requires that you repeat the numbers after your examiner calls out a short list.

A more complex skill, involving a great deal of concentration, is to recite a series of numbers or letters in reverse order (e.g., spelling a word backwards or reciting the days of the week or months of the year in reverse order).

Orientation

• The ability to pay attention is critical for gathering data: day of the week, month of the year, current year, and one’s present location. These data are classified under orientation.
• A person’s ability to orient self in the world, and to be able to pay attention to it are fundamental skills required for virtually all other aspects of one’s mental and cognitive life.

A person’s ability to pay attention is critical for gathering information such as the day of the week, month of the year, current year, and one’s present location.

This data are all classified under the heading Orientation.

A person’s ability to orient yourself in the world, and to be able to pay attention to it are fundamental skills required for virtually all other aspects of one’s mental and cognitive life.

Person’s ability to communicate

• one of the most important human qualities.
• Involuntary aspects of speech:

• • being able to make sounds;
  • holding your mouth in the proper position to form those sounds into meaningful parts of speech.

A person’s ability to communicate with others is one of the most important human qualities. There are involuntary aspects of speech, such as being able to make sounds, and holding your mouth in the proper position to form those sounds into meaningful parts of speech.

In speech output, the appropriateness can be judged in terms of:

• Content,
• Speed,
• Clarity,
• Other factors.

Once there is some evidence of speech output, the appropriateness of this output can be judged in terms of content, speed, clarity, and other factors.

Reading and writing ability patient should be able to:

• name objects in their environment;
• repeat words, phrases, or sentences;
• comprehend and answer questions;
• use reasonable grammar and syntax.

A person’s reading and writing ability may also need to be assessed. A patient should be able to name objects in their environment, to repeat words, phrases, or sentences, to comprehend and answer questions, and to use reasonable grammar and syntax, which are all important components of the language assessment.

Memory the ability to store and retrieve information of all types:

• Pictures,
• Movies,
• Sounds,
• other images in the patient’s brain,
• events,
• situations, all in the appropriate time-sequenced order,
• material that the person learned throughout a lifetime.

Memory includes the ability to store and retrieve information of all types. This can include pictures, movies, sounds, or other images in the patient’s brain.

It can also include events and situations, all in the appropriate time-sequenced order.

It might involve material that the person learned throughout a lifetime.

Neurobehavioral Examination

• Assess the memory in terms of its storage of new information, retrieval of information from memory that has been stored, and ability to recognize information that has not been retrieved properly.
• Passing the screening means skill is considered intact and no further testing of that specific skill is required.
• Upon failure, a series of questions asked will provide a quantitative evaluation of the level of disability.

The neurobehavioral examination will assess the memory in terms of its storage of new information, retrieval of information from memory that has been stored, and ability to recognize information that has not been retrieved properly.

If the patient passes the screening for a particular skill, then that skill is considered intact and no further testing of that specific skill is required.

If the patient fails, a series of questions asked that will provide a quantitative evaluation of the level of disability.

Cognistat

• Designed to focus on the degree of disability.
• A space is provided on the examination for the explanation of factors that may have affected the patient’s performance on the exam:

1. medications the patient is taking;
2. any sensory-motor deficits they may have;
3. performance anxiety.

The Cognistat was designed to focus on the degree of disability.

The test does not discriminate between average and superior performance, therefore, the range of scores within the non-disabled population is very small (Doninger, Bode, Heinemann, & Ambrose, 2000).

At the end of the examination, there is space provided for the examiner’s explanation of factors that may have affected the patient’s performance on the exam, such as medications the patient is taking, any sensory-motor deficits they may have, or performance anxiety.

Neurobehavioral Cognitive Status Examination

• A new approach to cognitive assessment designed to briefly provide an assessment of patients who are thought to be behaviorally disturbed.
• The examination has been revised six times since its implementation.
• The exam can be done by most physicians and is only part of the clinical examination process.

The Neurobehavioral Cognitive Status Examination is a new approach to cognitive assessment that was designed to briefly provide an assessment of patients who are thought to be behaviorally disturbed.

The examination has been revised a total of six times since its implementation.

The exam can be done by most physicians and is only part of the clinical examination process.

The Cognitive Status Exam refers to the component of the process that assesses the factors mentioned earlier.

Functional Independence Measure

• is well known through out the world of mental health and medicine.
• Used to assess the burden of care of patients suffering brain injury and may be unable to live without assistive care.
• Often used in hospitals and mental health facilities to help health care workers in setting goals for patients during their rehabilitation.

The Functional Independence Measure is well known through out the world of mental health and medicine.

It is used to assess the burden of care of patients who have suffered brain injury and may no longer be able to live without assistive care.

This measure is often recommended for use in hospitals and mental health facilities for helping health care workers in setting goals for patients during their rehabilitation.

• measures 18 items across 6 different domains:

1. Self care;
2. Sphincter control;
3. Mobility;
4. Locomotion;
5. Communication;
6. Social cognition.

The Functional Independence measure measures 18 items across 6 different domains.

These domains include self care, sphincter control, mobility, locomotion, communication, and social cognition. The individual is scored on an ordered scale of 7 down to 1 on each item in each domain. A score of 7 is achieved if the individual is able to perform the task independently and 1 indicates that the individual is fully dependent on another to complete the task.

Brain Injury (BI) Causes

• cell death;
• inhibition.

BI Symptoms

• Personality Changes;
• Borderline personality:

• • impulsive;
  • lack of empathy;
  • lack of a sense of self;
  • inability to self-monitor.

When a person experiences a BI, the symptoms seen are generally due to two physiological responses, cell death or inhibition.

Several different types of symptoms are associated with BI. Personality changes have been seen as the most significant problem, (Livingston, Brooks & Bond, 1985). Patients with frontal lobe dysfunction may exhibit Borderline personality traits such as impulsively, lack of empathy, lack of a sense of self, and inability to self-monitor. The individual may display a retardation of the maturation process, so that they seem childish.

BI Symptoms

“Chameleon” quality

Person assumes behavioral characteristics based on the individuals in the immediate environment.

• difficulty in perceiving social situation;
• difficulty with self-control and monitoring;
• stimulus bound;
• emotional changes;
• incapacity to learn from social experiences.

Symptoms associated with BI include Personality changes, (Livingston, Brooks & Bond, 1985).

In 1978, Lezak described several differences in personality following a TBI; difficulty in perceiving social situation, difficulty with self-control and monitoring, stimulus bound, emotional changes, and incapacity to learn from social experiences.

• difficulties with abstract thought;
• loss of a sense of humor;
• difficulty to maintain one set of information;
• perform a simultaneous comparison of another set of data;
• impairment in capacity to encode incoming data;
• language disturbances.

Frontal lobe injuries may result in difficulties with abstract though and a loss of a sense of humor. This may be due to a difficulty to maintain one set of information and perform a simultaneous comparison of another set of data (Andrews, 2001).
Memory usually suffers when a person experiences a TBI. Specifically, the impairment in capacity to encode incoming data resides in the hippocampus. This may be due to the location of the hippocampus, which resides in the anterior temporal lobe when upon impact may force tissue into the sphenodial ridge (Andrews, 2001; Lezak, 1995). Language disturbances are observed in 8%-85% of individuals following a TBI, (Groher, 1977).

Language Disturbances

• verbal memory;
• auditory processing;
• integration and synthesis of linguistic information;
• word retrieval;
• spelling;
• speech spontaneity.

Language disturbances are observed in 8%-85% of individuals following a TBI, (Groher, 1977). Patients usually experience problems with verbal memory, auditory processing, integration and synthesis of linguistic information, word retrieval and spelling. Individuals may also experience a difficulty in the spontaneity of speech (Damasio & Damasio, 2000).