Memory Deficit in Traumatic Brain Injury | Report

Memory deficit in traumatic brain injury
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Memory deficit in traumatic brain injury
Introduction
According to the World Health Organization (2008), traumatic brain injury is a great
public health concern due to its largest cause of brain injury leading to high morbidity and
mortality rates globally. The severity of traumatic brain injury often depends on various
factors such as injury type diffuse or focal, location and extension leading to damages. Head
injury entails a broad array of damage which entail structure of the scalp and the skull.
Traumatic Brain injury can lead to the development of physical, cognitive, social, emotional
and other behavioral aspects. The occurrence of memory issues occur among people with
moderate to severe traumatic brain injury, it has effects on the short term memory which
handles learning and remembering.
Description of the etiology
Traumatic Brain injury is assessed using the Glasgow Coma Scale which is the most
widely used tool to evaluate the severity. The frontal lobes and the temporal lobes have
shown particular interests in the development of lesions occasioned from the localization of
neuroanatomical locations. Key neuropsychological disorders caused by the this entails mild
to the moderate occurrence of traumatic brain injury, information reduction processing speed
and has been attributed to attention deficits, affecting other states such as self-monitoring,
flexibility, and problem-solving, this state’s lead to effects such as loss of memory and
attention. At the end of post-traumatic amnesia, severe TBI patients can present with memory
disorders in varying intensity leading to damages of both long term and short (Hillary, et al.,
2011).

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Traumatic brain injury results from external force onto the brain. Traumatic brain injury
is categorised with respect to severity, anatomical state, and mechanism. The classification of
the TBI entails closed and penetrating head injuries (Kasahara, et al., 2011). TBI has effects
on the memory processes, the kind f memory affected by TBI entails long term and short
memory processes. Prospective memory can also be affected by TBI, this entails a failure to
have a memory of intentions and plans to initiate actions. The occurrence of the injury
memory can also occur among the subjects. Victims often are confused coupled with the
inability to have memory storage thus leading to post-traumatic amnesia (Marquand et al.,
2011).
Characteristics of Traumatic Brain Injury
Brain injury effects can often be many and complex, having an understanding of how a
brain works are critical. Varying effects of head injury can occur in an individual. Behavioral
changes and personality have been linked to traumatic brain injury. These entail motivation
reduction loss of self-esteem, empathy difficulties, emotional processions, insight loss,
depression, post-traumatic stress disorders, anxiety and elevated fatigue levels (Miotto et al.,
2010).
Various effects of traumatic brain injury have been shown to have varying effects on an
individual; however, the majority of the injuries can result in some degree of impairment.
Brain injuries can lead to memory deficits, cognitive impairments, communication and
language functions impairments, psychosocial behaviors which entail aspects such as
depressions, denial, frustrations, anxiety euphoria, liability, and apathy (Harris et al., 2013).
Treatment and medication

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Memory is a fundamental aspect of everyday activity and cognitive related
impairments, injuries arising from a traumatic brain injury can have devastating effects. A
contributing factor is memory function which characterized by alteration of neural circuit
deficit linked to memory function (Paterno, Folweiler & Cohen, 2017). Cognitive impairment
aspects such as memory loss are due to traumatic brain injury and other forms of disability.
Across various levels, TBI severity, attention levels, speed processing, memory episodes, and
executive function are affected. The differential treatments for posttraumatic impairment are
broad and entail behavioural, emotional and physical problems and substance abuse, medical
conditions and self-prescribed medications. Undertaking a neuropsychiatric assessment is
crucial for managing cognitive impairments. First-line treatment for cognitive impairment
often entails nonpharmacological management. This entails education, realistic expectation,
lifestyle modification, and cognitive rehabilitation process.
Administration of pharmacotherapy entails the adoption of uncompetitive N-methyl-D-
aspartate receptor antagonists. Medications which have direct antagonism, medications which
have a direct augment on the cerebral acetylcholinergic and catecholaminergic ability. During
an immediate phase of the post-injury period, management with N-methyl-D-aspartate leads
to a reduction of unconsciousness duration. This mechanism is effected through the
involvement of attenuation of neurotrauma induced glutamate which is mediated by exciting
toxicity in the injured brain (Luo et al., 2017).
In the subacute or post-injury period, medication augment entails an effect on cerebral
acetylcholinergic which can have an improvement on the declarative memory, the secondary
treatment management effect entails increased processing speed, neurotransmitters, attention
and comorbid depression states. Many of the medications useful for the management of
cognitive impairment for the post-traumatic disorder, however despite this; those having
sufficient evidence are limited. Initiation of medication management entails an approach for

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start low, go slow but go approach. This is supported by a frequent assessment of benefits and
side effects as well as other drug monitoring for interactions. Often medication intolerance
needs to be completed first before discontinuing other treatment avenues (Wortzel &
Arciniegas, 2012).
Search strategy
The search strategy employed by this study entails application Boolean operators on the
key words of the topic. The key words used entail ‘Memory’ AND ‘deficit’ AND ‘traumatic
brain injury’ OR ‘TBI’. Cinahal , Cochrane and PubMed databases were used. Search filter
employed entailing limiting to those studies below five years.
Literature review
Traumatic brain injury often results from the external mechanical force which
accelerates rapidly, causing an impact in the head. Brain function can be altered by the extent
of this damage, as it can lead to temporal or permanent injury and structural changes on the
head. Traumatic brain injury can occur from acquired brain injury or nontraumatic brain
injury such as strokes. Traumatic injuries entail head injuries. Injury to the brain falls under
two categories that are those under the central nervous system and neurotrauma. The severity
state of traumatic brain injury is based on anatomical features of the injury and causative
mechanism. The mechanism factors are categorized into closed and penetrating head-related
injuries. Closed injury normally occurs with a blunt object while a penetrating injury pierces
the skull and enters the dura mater membrane (Silver, McAlliste, & Arciniegas, 2018).
The severity of brain injuries is classified into mild, moderate and severe. Based on
Glasgow Coma Scale-GCS, grading of persons’ level of consciousness is done on a scale of
3-15 verbal assessment, motor and eye-opening abilities to external stimuli. The general

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assessment of the GCS score traumatic brain injury of 13 and above is mild, 9-12 is moderate
levels and below 8 is severe (Carney et al., 2017).
Pathological features of traumatic brain injury are based on lesions observance which
can be extra-axial or intra-axial. Damage occurring can be either focal or diffuse which is
confined to any specific area.
Focal injuries produce symptoms likely to be linked to damaged area functions.
Research has shown that most common focal lesions occurring through nonpenetration of
traumatic brain are those of the orbitofrontal cortex and those of the anterior temporal lobes
(). These are concerned with aspects of social behavior, olfaction and decision processes.
They are more of social and judgment deficits which can alter memory states.
Epidemiological data have shown that about 57 million people globally have
experienced any form of traumatic brain injury. The majority of these cases about 80% are
mild, though it is not attributed to any mortality cause, it contributes to neurological deficits
such as confusion, impairment and memory deficits. Research and evidence have shown that
increased episodes of traumatic brain injury can lead to severe neural psychological
disabilities and increase the overall risks of neurodegenerative diseases such as Alzheimer’s
and Parkinson's diseases (Dewan et al., 2018).
Cognitive impairment aspects have been focussed in reviewing brain imaging with
traumatic brain injury, key fundamental aspects have often emerged; patients of memory
deficit traumatic injury may not be admitted, secondly, the difference brain imaging may not
show case any signs and symptoms while long term such as mild memory decline is often
underscored.

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Studies have demonstrated the application of animal-based model studies which have
shown that short term effects of traumatic brain injury. Initial and early-stage changes may
not always reflect long term effects. A study by Luo et al (2017) aimed at assessing the short
term and long term factors linked to traumatic brain injury using animal models. Results
demonstrated that increased memory loss was evident between the 2,8 and 12 weeks post-
injury. Microarray assessment demonstrated that traumatic brain injury has a significant
alteration of 87 genes expression which are crucial in apoptosis, metabolism, transcription,
stress response and plasticity of the synapse. This result demonstrates an underlying
mechanism of induced neurological deficits and the chronic impairment of memory. There is
a need for long term monitoring and observation of traumatic brain injury patients for
effective memory recovery and reduction of neurodegenerative disease.
The inherent relation occurring between traumatic brain injury and the dysfunction of
the memory has been established over the decade study undertaken by Paterno, Metheny &
Cohen (2018) explored an association between memory deficit after mild traumatic brain
injury and link with branched-chain amino acid dietary therapy. This study assessed how
traumatic brain injury can affect spatial episodic memory. Using mice, running specific
recognition tasks demonstrated that there was specific performance after 3 minutes interval;
however, the traumatic brain injury mice had a spatial delay of 1 hour. An assessment of
traumatic specific injury impairment is liked to decreased exploratory behavior. The
behavioral deficit is associated with branched-chain amino acid dietary therapy which can
restore memory ability and enhance the normal exploratory behavior. These findings
demonstrated that branched-chain amino acid therapy has the potential to manage mild
traumatic brain injury and declined memory ability is associated with exploratory behavior
deficit crucial in the encoding process.

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An assessment by Manktelow et al (2017) on working memory after traumatic injury
showed fundamental findings. The study focused on the abnormality nature in terms of the
underlying connectivity and activity towards working memory of traumatic brain injury and
how they relate to memory improvement. Further, this study focused on the correlation of
working memory after the administration of methylphenidate. Results demonstrated that
traumatic brain injury can reduce effectively the activation levels and strength of connectivity
between fundamental areas of working memory. Further administration of methylphenidate
improves significantly cognitive outcomes on the memory task, hence the recommended
mode of treatment towards improving the working memory ability.
Conclusion
Traumatic brain injury plays a critical role in the rise and impairment of cognitive
deficits such as memory deficits. Increased occurrence often leads to an increased incidence
of neuropsychological disabilities which raises the overall ability to developed
neurodegenerative disorders. There is no known specific pharmacology treatment, however
uncompetitive N-methyl-D-aspartame has shown direct antagonisms in managing the decline
of memory. In addition to this application of branched-chain amino acid, therapy has been
shown to have positive effects. Management using methylphenidate has shown significant
improvements in memory recovery. Given this, there is a need for close monitoring of the
intervention to achieve intended outcomes.

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