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 Table of Contents  
REVIEW ARTICLE
Year : 2018  |  Volume : 19  |  Issue : 2  |  Page : 97-101

Impact of traumatic brain injury on cognitive functions


1 MD, Centro De Investigaciones Biomédicas, Cartagena Neurotrauma Research Group Research, Faculty of Medicine, University of Cartagena, Cartagena De Indias, Bogota, Colombia
2 MD (Biochemistry), MSc. (Medical Biochemistry): Faculty, Department of Biochemistry, Medical College, Kolkata, West Bengal, India
3 MD, PhD: Professor and Chair (Head), Department of Community Medicine, MGM Medical College and LSK Hospital, Kishanganj, Bihar, India
4 Assistant Professor, Department of Neurology, Narayana Medical College and Hospital, Nellore, Andhra Pradesh, India
5 Neurosurgery-Critical Care, RED LATINO Organización Latinoamericana De Trauma Y Cuidado Neurointensivo, Bogota, Colombia
6 Professor, Department of Neurosurgery, Narayana Medical College and Hospital, Nellore, Andhra Pradesh, India

Date of Web Publication31-Dec-2018

Correspondence Address:
Dr. Amit Agrawal
Department of Neurosurgery, Narayana Medical College and Hospital, Nellore, 524 003, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AMH.AMH_14_18

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  Abstract 


In this systematic review, we summarize the current understanding and controversies on cognitive sequelae after traumatic brain injury (TBI) to understand the cognitive deficits such as memory, attention, executive functions, and unawareness of their deficits in TBI patients. This review presents the cognitive sequel of patients with moderate-to-severe TBI by a comprehensive focused conglomeration of research publications by searching various resources. A search strategy with specific inclusion criteria was performed in PubMed, Cochrane, Web of Science, and the WHO Global Health Library. This review noted that TBI is related with increase of various neurological and non-neurological disorders including problems with attention, inability to concentrate, speech and language dysfunctions, learning and memory impairment, impaired reasoning, impaired planning and problem-solving. This review found that patients' cognitive deficits are common in victims of moderate to severe TBI often as the long-lasting sequalae. The present review suggests that there is a need for further research to develop unique rehabilitation methods that will help to enhance brain plasticity and process of recovery after TBI.

Keywords: Cognitive problems, rehabilitation, traumatic brain injury


How to cite this article:
Said PZH, Ghosh A, Pal R, Poli N, Moscote-Salazar LR, Agrawal A. Impact of traumatic brain injury on cognitive functions. Arch Ment Health 2018;19:97-101

How to cite this URL:
Said PZH, Ghosh A, Pal R, Poli N, Moscote-Salazar LR, Agrawal A. Impact of traumatic brain injury on cognitive functions. Arch Ment Health [serial online] 2018 [cited 2019 Jan 22];19:97-101. Available from: http://www.amhonline.org/text.asp?2018/19/2/97/248875




  Introduction Top


The traumatic brain injury (TBI) has to be observed as a chronic disease that is closely related to the increase of various neurological and nonneurological disorders with a huge downstream unforeseen significant health and socioeconomic problem for our community life due to a spectrum of morbidity with mortality and disability.[1] Cognitive impairments due to TBI that include different areas of cognition cause substantial degree of morbidity for the affected individuals and can have impact on their family members and society as well. The most common neurocognitive consequences at all levels of severity of TBI are attention, executive functioning, and memory deficits. Disturbances of memory and attention are particularly concerning. Disruption of basic cognitive functions might cause or increase supplementary disturbances in decision-making function, communication, and additional multifaceted intellectual functions. Following TBI, a systematic neuropsychiatric assessment of the patient is a precondition for any treatment of impaired cognition.[2]


  Methods Top


This manuscript presents a review of the main cognitive dysfunctions reported in literature of patients with TBI. We explored a comprehensive focused conglomeration of research publications by searching various resources; hospital-based studies, retrospective data mining, published surveys, presentations, meeting, and personal communications about recent surveys not included in previous analyses in which long-term cognitive sequel of traumatic brain injuries were reported. A search strategy with specific inclusion criteria was performed in: PubMed, Cochrane, Web of Science, and the WHO Global Health Library.

The literature search for TBI and downstream cognitive impairments in PubMed with specific subject headings related to “TBI” (MeSH Terms) OR AND “cognitive impairments” (All Fields), OR AND “injury” (All Fields),” head injury “(All Fields) AND “cognition” (MeSH Terms) was used as the search terms for each database. Every effort was made to identify all relevant articles that report data related to RTI from 1966 to 2017. Two independent reviewers (including corresponding author) have evaluated all reference titles obtained from the database. Any reference title that appeared to involve RTI and India was selected. The research works was further classified into clinical and epidemiological studies for better internalization. The main outcome variables were specific patterns of TBI and associated cognitive deficits from published reports.

Traumatic brain injury

The TBI is considered a public health problem[3] and one of the main causes of death and disability in adults in industrialized countries.[4],[5],[6],[7] Approximately 10 million people worldwide suffer a TBI.[3] In the US, more than 1.7 million occur annually and approximately 5.3 million Americans have disabilities after the TBI.[5] An incidence rate of 150/100,000 population has been reported in Bengaluru, India. However, in India, approximately 2 million people suffer brain injuries.[3] In China, approximately between 60 and 70 of every 100,000 inhabitants suffer from TBI and it has been estimated that 1 million people are victims of TBI annually.[8] Among the most common causes of TBI are automobile accidents, injuries with a firearm, wounded with a knife, falls, among others.[5]

Impact of traumatic brain injury

TBI can have a great impact on emotional stability, behavior, and confidence in people after the BIT. In addition, the stress and emotional burden on caregivers of these patients is very marked.[3] Cognitive dysfunctions generate in the patient difficulties to reintegrate into society, affect their interpersonal and intrapersonal relationships, affect their work environment, family, and have economic repercussions.[9] Most people after a TBI have a chronic disability of certain skills and abilities that negatively impact lifestyles and affect their behavior.[3]

These events cause damage to the brain parenchyma traumatically, producing mechanical deformations in the structures of the nervous system. The TBI is classified as a primary and secondary lesion. The primary lesion occurs when the parenchyma and vessels are damaged directly, causing a neurological alteration; and the secondary lesion includes alteration of the blood–brain barrier, excess of free radicals, excessive release of neurotransmitters, mitochondrial dysfunction, alteration of blood flow, among others.[7] In addition, the TBI can be mild, moderate, or severe, with the slight lesion being the most common representing approximately 70%–90% of the TBI.[10] However, the lesions may be focal or diffuse. The focal ones are produced by direct impact on the brain and include contusions, lacerations, and intracranial hemorrhages. The diffuse lesion refers to the stretching and tearing of the brain parenchyma, which are common after car accidents and the main form of injury, is the diffuse axonal injury, which may be the main cause that causes the decrease in levels of excitation and the severity of the posttraumatic neurological deficit. It has been considered that the disruption of the axonal and neuronal cell membranes results in an excessive release of neurotransmitters and ionic changes that include the increase of potassium, extracellular sodium, and intracellular calcium. The consumption of glucose increases as the pumps increase the activity to achieve the restoration of the ionic balance, exhausting the energy reserves. In addition, decreased blood flow and low glucose availability result in calcium endothelial accumulation causing a cell crisis.[9],[11]

Cognitive functions in patients with traumatic brain injury

The TBI is classified taking into account the level of consciousness, the Glasgow coma scale and Glasgow outcome scale, and the presence of posttraumatic amnesia and can present physiological, cognitive, social, emotional, and behavioral disabilities in the short and long term.[3],[7],[10],[11] This lesion may be related to marked retrograde amnesia depending on the degree of the injury.[6] Approximately 10%–25% of people with a mild TBI will have persistent cognitive symptoms.[7],[10] The TBI should be observed as a chronic disease that is closely related to the increase of various neurological and nonneurological disorders,[4],[12] being cognitive dysfunction the most common.[4] This dysfunction includes attention deficit, memory, executive functions,[3],[5],[10] learning, difficulties in information processing, speech and language;[7],[10] these dysfunctions can present a marked heterogeneity depending on the region of the cerebral parenchyma that is affected.[4],[5]

Traumatic brain injury and spectrum of cognitive dysfunctions

Cognitive dysfunction is one of the most frequent consequences in patients suffering from TBI. This covers the deficit of memory, executive skills,[13] attention, memory, language and communication, and visuospatial perception.[3] These dysfunctions vary according to the anatomic location of the lesion.[13] Attention deficit is frequent in severe TBI including lack of concentration, distraction, and decreased processing speed. Memory is one of the dysfunctions that is recovered and is the main objective in cognitive rehabilitation therapies that include words, paragraph compression, images, and among others. Hemiasomatognosy, deterioration of the body schema and construction skills as visuospatial perception changes are common in severe TBI. Within the language and communication disorders are apraxia, aphasia, dysarthria, and cognitive communication disorder; the type of speech and language disorder depends on the extent and location of the brain injury. Finally, the deficiency of the executive function generates the person's inability to plan, solve problems, evaluate the performance, and may prevent the realization of daily activities.[3]

Traumatic brain injury severity and cognitive dysfunctions

The severity of cognitive dysfunction is related to the regions of the parenchyma that is affected by primary lesions that may or may not generate secondary lesions. However, when they generate secondary lesions that can cause ischemia due to the decrease in cerebral blood flow, generating neuronal loss and axonal degeneration, this together with a synaptic plasticity and an alteration in the neurotransmission systems important for the development of cognition contribute to a cognitive dysfunction.[5]

Mild traumatic brain injury and cognition

It has been reported that up to one-third of the patients with “mild” TBI may develop features of persistent postconcussion syndrome and more than half can have measurable cognitive deficit at the end of 1 year. In spite of growing literature on the cognitive consequences of mild TBI, predisposing risk factors to sustaining such injury is limited.[14] Nordström et al. in a cohort of more than 3 lakhs Swedish population examined the relations among an exposure to concussion, cognitive functions, academic attainment, and measures of social well-being.[10]

Cognitive impairment in the short term

The alteration of consciousness and posttraumatic amnesia (amnesia posttraumatica) are characteristic of mild TBI. When the latter is present, alterations in the wakefulness, agitation cycle can be observed,[9] mild confusion, attention deficit, and temporary loss of memory that may improve up to 3 months after the injury.[4] However, the mild TBI the patient may or may not present an alteration of the state of consciousness.[9] This can alter the structure and function of the white matter and the neurotransmitter activity of cognition functions.[4],[15]

Long-term cognitive impairment

Cognitive dysfunctions cause disability by generating difficulties for performing daily functions of the patient. The cognitive sequelae depend to some extent on the duration of the deterioration of consciousness, that is, the longer the duration of the deterioration, the greater the cognitive dysfunction. In moderate and severe injuries, cognitive dysfunction is associated with impaired memory, attention, decreased processing, executive function (various cognitive abilities of high order executed mainly by regions of the prefrontal cortex), communication, language, and intellectual capacity which can improve up to 5 years after the injury. Executive functioning refers to the acquisition and recovery of memory and planning (alteration of the dorsal lateral prefrontal cortex), behavior, apathy (subcortical lesions and dysfunction of the right hemisphere), decision-making and learning that can be seriously affected by a TBI. An alteration in behavior in patients with TBI leads to breaking rules and making inappropriate decisions that can bring problems in everyday life and even at work. When the injury worsens, patients may even be unaware that they suffered an injury.[9]

As can be seen, this cognitive dysfunction can persist chronically in patients with severe or moderate TBI, which may be accompanied by coma and vegetative state. This dysfunction may improve between 6 and 18 months after the injury. Up to 2 years can be seen improvement in some patients, in others it can develop dementia, this depends on the processes of repair of the organism before the TBI.[4]

Approach to management of cognitive dysfunctions

Cognitive rehabilitation seeks to improve the patient's ability to process and interpret information, achieving better results when there is a multidisciplinary group. Rehabilitation therapy includes the restorative approach that seeks to significantly improve the skills lost by the TBI through repeated exercises aimed at specific cognitive dysfunction; and the compensatory approach seeks to compensate the impaired function through the use of electronic devices or any technique that allows a reintegration of patients to their previous lifestyle[3],[9] and that is why cognitive rehabilitation therapy has been designed to address mainly problems of attention, communication, memory, and executive functioning.[9]

Researchers in this field has been using battery of tests for TBI dedicated to cognitive dysfunction from mild[16]-to-severe TBI severities.[17] The tests assessed the significant cognitive domains frequently impaired in patients, also domains probable to be affected by medication. These tests exhibited the usefulness of the cholinesterase inhibitor rivastigmine in TBI cases having memory impairment.[18],[19] These tests are biologically pertinent, with TBI[20] and changes in task presentation over time associate with changes in brain edifice in TBI cases.[21]

In general, a neuropsychological evaluation is used to determine the severity of cognitive dysfunction[22] and it should be done in any patient with TBI. The interview is a fundamental tool for the assessment of cognitive dysfunction because it can assess the patient's perception, planning, the relationship with family members and friends, behavior, the alteration of their ability to care, among others. For the clinical investigation of the BIT, a tool of common elements of data (early childhood development) that includes basic and complementary cognitive tests has been determined. An adequate neuropsychological evaluation allows to observe the cognitive areas conserved by the patient.[9]

However, the quality of life, limitation of activity, and restriction of participation must be evaluated to observe the repercussions of the psychosocial problem after the injury, that is why this evaluation is important and should not only be limit the cognitive part.[23] The screen of the Barrow Neurological Institute for higher brain functions includes the evaluation of the level of excitation, basic communication, and cooperation used to discover cognitive and affective alterations.[12]

Rehabilitation

Certain drugs such as psychostimulants and some of the dopaminergic agents (e.g., levodopa/carbidopa, methylphenidate, bromocriptine, dextroamphetamine, and amantadine) diffidently improve arousal, swiftness of information dealing, decrease distractibility, and recover some of the executive functions. The system approach includes frequent consistent dosing, concurrent evaluation of effects, side effects, and monitoring drug reactions. Cognitive rehabilitation involves the treatment of memory losses following TBI. Cognitive rehabilitation mandates targeted solutions of diminished attention, interpersonal communication, and executive function in TBI cases on follow-up which are of utmost importance for TBI cases with mild-to-moderate cognitive impairments. These medical, vocational, social, and psychological rehabilitation efforts are also valuable for those TBI cases with relative independence in specific functions and are also motivated to involve in and repeat these specific strategies. The addition of psychotherapy (e.g., individual, group, and family levels cognitive, behavioral, and supportive,) is a vital component of interventions. For patients under medications need assistance from families, community, country with adjustment to permanent disability.[2]


  Conclusions Top


Disorders of attention and memory are key problems in the realm of cognitive dysfunctions along with physical, neurologic, and psychiatric syndromes following TBI. Neuropsychiatric assessments of these cases are mandatory to refine the provisional diagnosis of impaired cognition. Psychostimulants and dopaminergic pharmaceutically active molecules improve arousal and speed of processing of information. Cognitive rehabilitation is an integral part of the treatment of cognitive impairments following TBI. Psychotherapy is an important component of treatment to assist both patients and families with holistic concept of rehabilitation to cope up with the permanent disabilities.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Cristofori I, Levin HS. Traumatic brain injury and cognition. Handb Clin Neurol 2015;128:579-611.  Back to cited text no. 1
    
2.
Arciniegas DB, Held K, Wagner P. Cognitive impairment following traumatic brain injury. Curr Treat Options Neurol 2002;4:43-57.  Back to cited text no. 2
    
3.
Barman A, Chatterjee A, Bhide R. Cognitive impairment and rehabilitation strategies after traumatic brain injury. Indian J Psychol Med 2016;38:172-81.  Back to cited text no. 3
[PUBMED]  [Full text]  
4.
Wang ML, Li WB. Cognitive impairment after traumatic brain injury: The role of MRI and possible pathological basis. J Neurol Sci 2016;370:244-50.  Back to cited text no. 4
    
5.
Walker KR, Tesco G. Molecular mechanisms of cognitive dysfunction following traumatic brain injury. Front Aging Neurosci 2013;5:29.  Back to cited text no. 5
    
6.
Fujimoto ST, Longhi L, Saatman KE, Conte V, Stocchetti N, McIntosh TK, et al. Motor and cognitive function evaluation following experimental traumatic brain injury. Neurosci Biobehav Rev 2004;28:365-78.  Back to cited text no. 6
    
7.
Lin W, Yang LK, Cai S, Zhu J, Feng Y, Yang L, et al. Cognitive function and biomarkers after traumatic brain injury: Protocol for a prospective inception cohort study. Asia Pac J Clin Trials Nerv Syst Dis 2016;1:170-6.  Back to cited text no. 7
  [Full text]  
8.
Zhang H, Zhang XN, Zhang HL, Huang L, Chi QQ, Zhang X, et al. Differences in cognitive profiles between traumatic brain injury and stroke: A comparison of the montreal cognitive assessment and mini-mental state examination. Chin J Traumatol 2016;19:271-4.  Back to cited text no. 8
    
9.
Rabinowitz AR, Levin HS. Cognitive sequelae of traumatic brain injury. Psychiatr Clin North Am 2014;37:1-1.  Back to cited text no. 9
    
10.
Nordström A, Edin BB, Lindström S, Nordström P. Cognitive function and other risk factors for mild traumatic brain injury in young men: Nationwide cohort study. BMJ 2013;346:f723.  Back to cited text no. 10
    
11.
Vincent AS, Roebuck-Spencer TM, Cernich A. Cognitive changes and dementia risk after traumatic brain injury: Implications for aging military personnel. Alzheimers Dement 2014;10:S174-87.  Back to cited text no. 11
    
12.
Stenberg M, Godbolt AK, Nygren De Boussard C, Levi R, Stålnacke BM. Cognitive impairment after severe traumatic brain injury, clinical course and impact on outcome: A Swedish-icelandic study. Behav Neurol 2015;2015:680308.  Back to cited text no. 12
    
13.
Di Paola M, Phillips O, Costa A, Ciurli P, Bivona U, Catani S, et al. Selective cognitive dysfunction is related to a specific pattern of cerebral damage in persons with severe traumatic brain injury. J Head Trauma Rehabil 2015;30:402-10.  Back to cited text no. 13
    
14.
Newcombe VF, Menon DK. Cognitive deficits and mild traumatic brain injury. BMJ 2013;346:f1522.  Back to cited text no. 14
    
15.
McInnes K, Friesen CL, MacKenzie DE, Westwood DA, Boe SG. Mild traumatic brain injury (mTBI) and chronic cognitive impairment: A scoping review. PLoS One 2017;12:e0174847.  Back to cited text no. 15
    
16.
Sterr A, Herron KA, Hayward C, Montaldi D. Are mild head injuries as mild as we think? Neurobehavioral concomitants of chronic post-concussion syndrome. BMC Neurol 2006;6:7.  Back to cited text no. 16
    
17.
Salmond CH, Chatfield DA, Menon DK, Pickard JD, Sahakian BJ. Cognitive sequelae of head injury: Involvement of basal forebrain and associated structures. Brain 2005;128:189-200.  Back to cited text no. 17
    
18.
Silver JM, Koumaras B, Chen M, Mirski D, Potkin SG, Reyes P, et al. Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology 2006;67:748-55.  Back to cited text no. 18
    
19.
Silver JM, Koumaras B, Meng X, Potkin SG, Reyes PF, Harvey PD, et al. Long-term effects of rivastigmine capsules in patients with traumatic brain injury. Brain Inj 2009;23:123-32.  Back to cited text no. 19
    
20.
Newcombe VF, Outtrim JG, Chatfield DA, Manktelow A, Hutchinson PJ, Coles JP, et al. Parcellating the neuroanatomical basis of impaired decision-making in traumatic brain injury. Brain 2011;134:759-68.  Back to cited text no. 20
    
21.
Newcombe VF, Correia MM, Ledig C, Abate MG, Outtrim JG, Chatfield D, et al. Dynamic changes in white matter abnormalities correlate with late improvement and deterioration following TBI: A diffusion tensor imaging study. Neurorehabil Neural Repair 2016;30:49-62.  Back to cited text no. 21
    
22.
Liu Z, Dong J, Zhao X, Chen X, Lippa SM, Caroselli JS, et al. Assessment of feigned cognitive impairment in severe traumatic brain injury patients with the forced-choice graphics memory test. Brain Behav 2016;6:e00593.  Back to cited text no. 22
    
23.
Sashika H, Takada K, Kikuchi N. Rehabilitation needs and participation restriction in patients with cognitive disorder in the chronic phase of traumatic brain injury. Medicine (Baltimore) 2017;96:e5968.  Back to cited text no. 23
    




 

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