Volume 4, Issue 4 (Autumn 2018)                   Iran J Neurosurg 2018, 4(4): 185-198 | Back to browse issues page


XML Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Ramezani S, Reihanian Z, Hosseini Nejad M, Yousefzadeh-Chabok S. Neuropsychological and Neuropsychiatric Deficits Following Traumatic Brain Injury: Common Patterns and Neuropathological Mechanisms. Iran J Neurosurg 2018; 4 (4) :185-198
URL: http://irjns.org/article-1-161-en.html
1- Neuroscience Research Center, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran.; Guilan Road Trauma Research Center, Guilan University of Medical Sciences, Rasht, Iran
2- Guilan Road Trauma Research Center, Guilan University of Medical Sciences, Rasht, Iran.; Department of Neurosurgery, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran
3- Department of Neurology, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran
4- Guilan Road Trauma Research Center, Guilan University of Medical Sciences, Rasht, Iran
Full Text [PDF 755 kb]   (1830 Downloads)     |   Abstract (HTML)  (4610 Views)
Full Text:   (3548 Views)
1. Introduction
raumatic Brain Injury (TBI) is a major cause of morbidity and disability in developing countries [1-6], which disrupts the health status of patients and jeopardizes their functional independence and quality of life [7-11]. Today, health policy-makers tend to mainly focus on preventive programs to reduce the occurrence of TBI as well as optimal management and the early rehabilitation of individuals suffering TBI. Therefore, a growing number of neuroscience studies have been assessing the behavioral, cognitive and emotional consequences of TBI to discover the underlying neuropathological mechanisms and the various risk factors of the related complications [12-19]. Evidently, varying complications that are attributable to the mentioned aspects may occur following TBI in different types and severities of the neural lesion [20-29].
Disabilities caused by focal lesions have symptoms similar to those of stroke, specific to the impaired anatomic brain region. In such disabilities, considering the injured part of the brain structure and the severity and extent of the lesion, the underlying neural function that controls the behavior is disturbed which in turn leads to local disability [30]. However, the disabilities that originate from diffuse lesions can extensively disrupt the networks and neural circuits [30, 31], contributing to deficiencies in information processing speed and information integrity which are fundamental for performing high-level cognitive and emotional functions [32-35]
Focal lesions are mainly caused by the impact of the brain with the intracranial bones. Hence, the frontal and temporal bridges are very vulnerable to these lesions, due to their proximity to the sharp edges of the sphenoid bone. Though the anterior regions of the brain, the junction of white and gray matter, and the rostral areas of the brain stem are the most vulnerable areas to diffuse lesions due to the shearing and compression of the brain tissue and axons after linear and angular acceleration and deceleration of the brain [17, 36].
In minor TBI, post-traumatic disorders often happen despite the lack of a visible brain abnormality on CT scans or conventional MRIs. However, the existence of these disorders in mild TBI patients may be associated with the subtle impairments of brain structures and functions represented by the advanced neuroimaging techniques. Therefore, an early diagnosis and accurate prognosis of the post-traumatic neuropsychological and neuropsychiatric deficits might, at least partly, assign a proper detection of neural substrates correlated to each disorder. Fundamentally, neuroscientists attribute cognitive, emotional and behavioral disabilities to the presence of maladaptive neuroplasticities which are known to increase and decrease the power of the synapse in adjacent and distant regions of the lesion, disturbing the normal networking inside the brain [37].
This compensatory neuroplasticity is probably induced by secondary insults promoted through neuropathological processes that may initiate from the first few minutes post TBI and remain for a long time [38, 39]. Thus, it is suggested that early rehabilitative interventions accompanied by non-invasive brain stimulations may modulate these compensatory neuroplasticities, leading to potent clinical improvement [40].
In this regard, identifying TBI-induced abnormal neural networks involved in post-TBI deficits in order to target them using neuromodulatory approaches is necessary . The purpose of this narrative review is to provide a brief overview of the common patterns of neuropsychological and neuropsychiatric disorders after TBI and to present the disrupted neural circuits and imbalanced neurochemical or neurotransmitter systems that are the underlying mechanisms of these disorders, according to human brain mapping and preclinical data in TBI subjects. 
2. Common cognitive disorders after TBI
Cognitive disorders following TBI include reduced processing speed of visual and verbal information, attention and working memory deficits, retrograde and anterograde amnesia, communicative deficits and poor executive function [41]. Depending on the TBI severity, the deficits can have varying severities [18]. In severe injuries, the disorders occur in the first phase and may persist days or months after the event of the TBI [29]. Acute mild TBIs may produce early cognitive impairments [42]. However, the prevalence of constant cognitive problems in patients with mild TBI is under 20% [23].
Factors such as the level of cognition before the injury [43-45] and the presence of psychiatric or somatic symptoms accompanied by cognitive deficits after TBI [46] are involved in the sustainability of cognitive impairment. According to results from previous studies, major changes in the concentrations of brain metabolites such as N-Acetyl Aspartate (NAA), glutamine, lactate, myoinositol and Choline (Cho) as well as neural function, especially in the ventromedial Prefrontal Cortex (vmPFC) and the Dorsolateral Prefrontal Cortex (DLPFC), is presumed to be related to post-traumatic cognitive deficits and recovery [47-54]. Likewise, the tractography data in these patients indicated that the reduced integrity of neural fibers such as fronto-striato-thalamic circuits, the corpus callosum, and fornix are associated with cognitive impairments after TBI [55-59].
In recent decades, neuroscientists have found the related evidence on the existence of these metabolic and functional alterations in the brain in the early phase of minor TBI, despite the manifestation of normal findings in CT and conventional MRI [53], insisting the necessary utilization of advanced imaging techniques in order to identify patients at risk for post-concussion syndrome which may occur long after a mild TBI. 
3. Attention and working memory deficits
Evidently, attention and working memory deficits usually occur together. The involved neural substrates are the cortical areas in the middle temporal gyrus, parietal cortex, cingulate gyrus, and DLPC. According to the evidence, neurotransmitter systems that are mainly involved in attention deficit and working memory include catecholaminergic and cholinergic systems. Reduced concentration of acetylcholine, dopamine, and norepinephrine in neural synapses of these areas have found to be correlated with post-TBI cognitive deficits [16]. Therefore, drugs which increase acetylcholine in central synapses such as anticholinesterases (e.g. donepezil), and catecholamines (e.g. methylphenidate) have been recommended to improve cognitive potential in TBI patients [60].
Post-traumatic attention deficit depends on the severity of the lesion(s). In patients with severe lesions whose Ascending Reticular Activating System (ARAS) is also damaged, the attentional bottom-up processing and arousal state are disrupted [61]. In mild traumatic injuries, generally the top-down attentional processing is disrupted [62] which weakens various forms of attention including selective, sustained, alternative, and comprehensive attention [63]. Studies have shown that the reduction of fractional anisotropy of cingulum fiber in Diffusion Tensor Imaging (DTI) during the acute phase of mild TBI is associated with enduring attention deficits in the acute and chronic phases [64].
Besides, studies on PET scans have revealed that the glucose reduction in the frontal cortex, posterior cingulate cortex, and cerebellum are associated with working memory impairment after TBI [65]. Based on findings from MR spectroscopy studies, the decreased concentration of NAA metabolite and increased choline, myoinositol and lactate in the splenium of the corpus callosum are related to impaired attention and working memory [66].
4. Executive function deficit
Another cognitive domain that is disturbed by TBI is the executive function [67], mediated by a neural network called Executive Control Network (ECN) [68]. The network consists of several nodes connected by axons, the most important of which are DLPFC and Posterior Parietal Cortex (PPC). Furthermore, intact executive function appears to be controlled by Default Mode Network (DMN) constituted by some neural regions including vmPFC, precuneus, Posterior Cingulate Cortex (PCC) and white matter fibers connecting those together. Particularly, ECN has an inverse relationship with the DMN [69]. Hence, the majority of the neuroscientists believe that after TBI, the activity of DMN is excessive, which inhibits the ECN network and causes subsequent poor performance of the patients in relevant cognitive tasks [70].
TBI patients with poor ECN have problems in high-level cognitive activities that tie with everyday activities like problem-solving skills, abstract thinking, judgment, decision-making, self-monitoring, flexibility, and planning [6]. These cognitive dysfunctions not only impair the patient’s personal life but also heavily affect their social life and participation in the community [71]. It seems that executive dysfunction and verbal communication disabilities in the initial phase of lesion formation are the most important predictors of long-term neuropsychiatric disorders after TBI [19].
5. Communicative disorders
It is important to note that post-TBI communicative disorders are observed in most TBI cases and are fundamentally cognitive where a patient’s interactions are disturbed both verbally and non-verbally. Following TBI, a large spectrum of communication deficits can be manifested. Patients with TBI with verbal impairment show flight of ideas due to sustained attention deficit. They lose the coherence of thought and the message and intention of the conversation [72]. Indeed, linguistic deficits after TBI are mostly characterized by deficits in lexical, syntax, semantic and pragmatic dimensions of language. Hence, the typical pattern of linguistic dysfunction after TBI is similar to the lingual profile represented in the fluent aphasia. Highly prevalent in this group of patients, anomia inhibits patients to express their verbal message [14].
Moreover, exploring the non-verbal dimensions has proved that pragmatic skills are restrained in TBI patient. . Thus, the patient is unable to understand the feelings and emotions of the other person (partner) through the prosody of the speech and the gesture of the face and body language and does not observe turn-taking in conversation [71, 73, 74]. These verbal and non-verbal communication disabilities are rooted in weak high-level cognitive functions, which require the integrated function of neural networks in temporal, parietal, and frontal lobes [14].
These disabilities occur with higher probability in patients with damages to the fronto-temporal lobe and multiple damages including contusions co-occurring with subdural or intracortical hemorrhage [14]. According to tractography data, the arcuate fasciculus, uncinate fasciculus and corpus callosum are particularly vulnerable to TBI and their disruption appears to be related to the linguistic deficit after TBI [75]. It seems that a decrease in the concentration of NAA/Cho in the left frontal lobe is correlated to post-traumatic linguistic dysfunction regardless of the lesion side [76]. Given that the linguist problems after TBI is mainly generated from deficient sustained attention and executive function [77], it is suggested that increased activity of DMN may be associated with a perturbation of cognitive elements involved in language processing after TBI [70, 78]
6. Amnesia
Post-Traumatic Amnesia (PTA) is mostly observed following TBI in which patients cannot remember the events which have occurred after the incident. They may even forget their personal information [79]. PTA may last from less than an hour to more than a week and even a month. A high proportion of TBI patients have PTA for longer than one week or even one month [80]. Given the evidence, PTA duration is able to predict the length of the hospital, risk of early and late epilepsy, and post-traumatic cognitive function status [79]. Likewise, research has shown a positive correlation between the duration of PTA and retrograde amnesia [81, 82]. Based on neuroscience knowledge, individuals with lesions in the anterior temporal and frontal lobes are at risk of retrograde amnesia, in which long-term declarative memory including semantic and episodic memories, as well as dimensions of procedural memory may be impaired [83].
Sometimes post-TBI amnesia is anterograde, which in most cases accompanies retrograde amnesia. Usually, in the anterograde amnesia, neural lesions which have been caused by trauma are observed in the middle regions of the temporal cortex and the papez circuit with a gray matter composed of the anterior thalamus nucleus and mammillary body of the hypothalamus, and the cingulate gyrus, the entorhinal complex, the parahippocampus and hippocampus [83, 84]. Based on the data obtained from DTIs, disruption of the white matter fibers of the brain, including fornix, mammillothalamic tract and thalamocortical tracts is usually observed in people with anterograde amnesia after TBI [83, 85, 86]
7. Common emotional and neuropsychiatric disorders after TBI
The most common abnormal emotional behaviors after TBI include impulsivity, irritability, aggression, physical/verbal outbursts [87-89], affective instability, intolerance, apathy [90, 91], rigidity and inflexibility, risky behaviors [92], lack of empathy [93], and lack of motivation/initiative [94]. Data supports the predisposing role of executive function impairment during the acute phase of TBI on the subsequent appearance of impulsive and anti-social behaviors [27, 28]. Based on previous studies, the most common chronic psychiatric disorders after brain trauma include aggression, apathy, depression, and PTSD which can strongly be predicted by factors such as TBI severity, subcortical lesions and early post-traumatic linguistic dysfunction [6]. However, the development of post-traumatic neuropsychiatric disorders depends on multiple factors including baseline patients’ characteristics and preexisting medical conditions such as past psychiatric diagnosis, premorbid behavioral problems, and the history of neurological disorder and substance abuse [95].
Essentially, the most important neural substrates involved in the emotional and motivational behaviors are the ventromedial prefrontal-striatum-ventral thalamus [96, 97] which require a strong interaction between glutamatergic, GABAergic and dopaminergic neurotransmitter systems for normal functioning [98]. The dopaminergic projections of the Ventral Tegmental Area (VTA) of the midbrain to the thalamus nuclei and ventral striatum are vital for modulating the activity of this circuit [99, 100]. Damage to the structure and function of this circuit leads to a defect in motivation-related behaviors such as akinetic mutism, abulia, and apathy [101].
Empirical studies have demonstrated that damage to dopaminergic, serotonergic and adrenergic, mesolimbic and mesocortical projections is generally the neuropathological cause of emotional disorders after TBI [102]. These disorders are developed from all TBI severity. Human brain mapping investigations have indicated that the probability of occurrence of post-traumatic neuropsychiatric disorders is correlated with a reduction of functional connectivity in the anterior DMN following minor TBI.
8. Aggression
Aggression is typically characterized by signs such as physical and verbal outbursts, akathisia, maladaptive behavior, explosive anger, and irritabilit. The prevalence of aggression after TBI has been reported to be from 37% to 71% [103]. Based on the evidence, it seems that variables such as age, gender, and TBI severity have not influenced the risk of aggression after TBI. However, psychosocial impairment and dependence in daily life activities after TBI appear to be the main risk factors of post-traumatic aggression appearance [88]. Furthermore, a wide range of factors including environment, patient’s medical history [104], genetics [105], and neuroendocrine and neurochemistry functions [106] may be associated with aggression in TBI patients. Aggressive behaviors negatively affect recovery rate during inpatient and outpatient rehabilitation interventions [107, 108].
Thus, medical management for the recovery of post-traumatic aggression, especially in a high-risk population, is a serious priority. . Literature supports the effectiveness of beta-blockers and anticonvulsants for the treatment of agitation and aggressive behaviors after TBI [109]. However, due to their troublesome side effects, they are not widely accepted to be prescribed to this population by clinicians [110]. So far, the neuropathogenesis of aggression is not well elucidated. The few studies that have been done to understand the neural correlates of aggression use human brain mapping techniques. Furthermore, the findings of a resting-state functional MRI study has revealed that an elevation of functional connectivity between the right hippocampus and mid-cingulate cortex may be associated with aggression after mild TBI [111].
Recent preclinical data have suggested that the reduction of the serotonin release by the serotonergic projections of Raphe nuclei to DLPFC may be related to anti-social behavior and aggression. Based on this dysregulation, the activity of DLPFC and consequently the loss of the inhibiting control of the prefrontal cortex on the emotional processing of the limbic network result causes uncontrolled, illogical, automatic, and emotional outputs [112]. Hence, it seems that aggressive patients with this pattern of neural dysfunction may benefit from SSRIs [89]. However, in the last decade, the association between SSRI use and aggression has been considered [113, 114]. Undoubtedly, it is a controversial matter that requires further accurate investigations, especially for this population. 
9. Depression
Depression commonly develops in the first post-TBI year [115]. Depressive disorders after TBI may be usually associated with anxiety disorders and aggression [89, 116]. Various factors including genetic, demographic, developmental, and psychosocial variables appear to influence the risk factors of depression development following TBI [116]. It seems that the female gender, pre-injury depression, post-injury unemployment, and lower brain volume increase the risk of major depression following TBI [117]. However, evidence on the demographic risk factors of post-TBI depression has not provided a definitive conclusion [118-120]. From a neuropathological point of view, the serotonergic and adrenergic projections, which originate from the locus coeruleus and Raphe nuclei, reach the subcortical limbic and prefrontal ventromedial cortex, which play an important role in regulating the mood [121], are disturbed in patients with depression after TBI [122].
Investigations of the neural function imaging of patients with persistent post-TBI neuropsychiatric disorders such as depression support the increased function of DMN [123]. The study on resting network integrity following TBI has indicated that integrity within the Anterior Cingulate Cortex (ACC), insula, and thalamus may determine post-traumatic depression severity. Furthermore, an increase in the connectivity between the insula and superior temporal lobe and a connectivity decline between thalamus and DLPFC may be associated with depressive symptomatology of TBI patients [124]. So far, antidepressants and Selective Serotonin Reuptake Inhibitors (SSRIs) have been used for the remediation of mood disorders after TBI [125, 126].
Recently, it is suggested that after TBI the dysregulation of pro-inflammatory cytokines, like Tumor Necrosis Factor (TNF) which may lead to an increase in activity of serotonin transporter and consequently a decrease in serotonin at the synapse, are the neuropathogenic basis of depression after TBI [127]. Accordingly, pharmacological targeting of pro-inflammatory cytokines may be recommended as a new option for the treatment of post-traumatic depression. 
10. Post- Traumatic Stress Disorder (PTSD)
Post-Traumatic Stress Disorder (PTSD) is categorized in the anxiety disorders after trauma which, as a result of traumatic events, can cause horror and intense fear and helplessness in persons. ICD-10 criteria for detecting PTSD include the re-experience of the traumatic event to form the hallucination, visualization, illusion, or nightmares,, to forego a reminder of the traumatic event plus hypervigilance, hyperarousal states, and a decrease in concentration and increased irritability lasting for more than a month [128, 129]. According to available data, the prevalence of PTSD after road traffic accidents varies from 20% to 58% [130-132].
Several studies have investigated the risk factors and predictors of PTSD in pediatric and adult patients with TBI. It has been disclosed that personal variables such as age, gender, education level, and work status may predict the appearance of PTSD following TBI [130]. Apparently, shorter PTA, early post-traumatic symptoms [117] and TBI severity [95] appear to be risk factors of PTSD in TBI patients. Recently, it has been revealed that the sustained attention deficit after pediatric TBI may be a key predictor of PTSD appearance, especially in children with mild TBI [133]. Human brain mapping studies have indicated that there is a decrease in functional connectivity between PCC and hippocampus in PTSD patients and the degree of connectivity between these two neural regions is negatively correlated to avoidance symptoms [134]. Likewise, it is found that the reduction of functional connectivity strength within DMN may increase PTSD severity [135, 136].
PTSD seems to be related with hyperactivity of the amygdala-based fear processing pathways and its projections to the cortex. Amygdala is a key mediator of emotional memory stabilization [137, 138]. Increasing the strength and durability of memories fixed in the presence of a severe fear may predispose people to other anxiety disorders, including agoraphobia [139]. Although antidepressants are suggested and used to resolve PTSD [140, 141], in most patients, the need for cognitive-behavioral therapy is emphasized as an auxiliary or alternative therapy [142, 143].
11. Sleep-wake disturbances after TBI
According to literature, the prevalence of sleep disorders is between 30% and 80% after trauma [26, 144-146]. Insomnia and Excessive Daytime Sleepiness (EDS) are the most common types of sleep disorders after TBI. They are usually associated with chronic fatigue and neuropsychiatric disorders [26]. Clinical manifestations of sleep disturbances after trauma occur in different degrees and phases after TBI [147] and interfere with the restoration of the nervous system and the process of primary neural recovery. As the sleep disturbances sustain, patients become unable to take part in rehabilitation programs [148, 149]. According to previous reports, sleep disturbance after trauma is associated with mood disorders and fatigue throughout the day and nighttime pain after TBI [150, 151]. The severity of brain damage seems to be associated with the likelihood of hypersomnia long after the onset of TBI [144].
In addition, low levels of orexin in the Cerebrospinal Fluid (CSF) in the early hours and 6 months after TBI is strongly correlated with EDS after the trauma [152]. However, findings concerning the prognostic role of the severity and location of the lesion in the occurrence of sleeping-awakening cycle problems after TBI are inconsistent [26, 144, 148, 150-152]. It is worth noting that sleep disturbances after brain trauma negatively affect cognitive and emotional functions [18, 29] and, as a risk factor for chronic traumatic encephalopathy, play a role in the onset and exacerbation of its symptoms, including poor cognition, aggression, and impulsivity [30, 31]
Several observations have also proposed that sleep disorders may be the cause of cognitive impairment and Alzheimer’s disease [32, 33]. However, others suggest that patients with neuropsychological deficits in the early phase of TBI are more likely to be at risk of post-TBI persistent sleep disorders [26]. From the neuro-pathophysiological point of view, the imbalance between the neural function of the centers which regulate the sleep/wake cycle in the brain stem and hypothalamus induced by TBI underpin the sleep disorders. Neuroscience findings have supported the dysfunction of neural pathways involved in the sleep/wake cycle after TBI.
It seems that the disruption of the inhibitory projections of the ventricular hypothalamus nucleus on locus coeruleus nucleus belonging to ARAS [153] and the lack or reduction of the basal forebrain cholinergic outputs for the modulation of the function of the sleep/wake cycle centers in the hypothalamus underlie pathobiological insomnia. Furthermore, brain stem lesions are particularly associated with symptoms of hypersomnia and EDS [154]. Insomnia is thought to be associated with overactivation of DMN [155] which appears to be unbalanced after TBI [156]. Indeed, it is thought that the lack of DMN deactivation during rest may cause insomnia [155].
Based on a classical hypothesis, hyperarousal is a possible explanation for the etiology of insomnia [157]. It is suggested that primary insomnia may be related to a decrease in functional connectivity between DMN and medial temporal gyrus, insula, and thalamus which are core regions of the Salience Network (SN) [158]. Hence, it seems that aberrant functional connectivity among neural networks occurred after TBI, especially between DMN and SN [31], may be the underlying neuropathological mechanism of post-traumatic insomnia. In order to increase the understanding of the neural signatures of post-traumatic sleep disorders, the investigation of the correlation between abnormal neural networks and types of sleep disturbances after TBI deserves further attention in the future. 
12. Conclusion 
Neuropsychological and neuropsychiatric impairments after TBI are detrimental to the health of patients. These deficits interact or exacerbate each other and bring about major problems in personal and social settings. A wide range of personal, educational, occupational, social and medical variables may be associated with the risk of appearance of these disorders. From a neuroscience perspective, the emergence and persistence of any undesirable cognitive and emotional outcomes following TBI can be detected and predicted by early employment of advanced imaging techniques that evaluate the brain metabolites and structural and functional integrity.
Evidently, the dysfunction of cortico-striato-thalamo-cortical circuits from the prefrontal cortex appears to be responsible for the common post-traumatic cognitive and emotional deficits. Furthermore, abnormal activity of DMN and/or other neural networks correlated to that may be characterized as a possible neuropathogenesis mechanism(s) of the majority of these disorders. TBI-induced aberrant neural networks may serve as the diagnostic and prognostic biomarkers of post-TBI neuropsychological and neuropsychiatric disorders and their severity even in cases with minor TBI could be potentially helpful in developing neural circuit-based therapeutic approaches. Neuromodulatory techniques attempt to modify abnormal inter or/and intra-networks connectivities due to compensatory neuroplasticity following injury. Therefore, understanding the neuropathophysiology and patterns of neural dysfunction after TBI, from which post-TBI neuropsychological and neuropsychiatric defects may originate, is a major priority for achieving optimal efficacy by neuromodulation-based therapies. 
Ethical Considerations
Compliance with ethical guidelines

This article does not contain any studies with animal or human participants performed by any of the authors.
Funding
This project was funded by Guilan University of Medical Sciences, Guilan Road Trauma Research Center (Grant number: 971208.61).
Authors' contributions
Conceptualization & writing original draft: Sara Ramezani; Review and editing: Zoheir Reihanian, Mozafar Hosseinin Nejad; Supervision: Shahrokh Yousefzadeh Chabok.
Conflict of interest
The authors declared no conflict of interest.
Acknowledgements
The authors are grateful to the staff at Guilan Road Trauma Research Center, Poursina General Hospital, Rasht, Iran especially Ms. Fattemeh Javadi for translating the manuscript.


References
  1. Bryan-Hancock C, Harrison J. The global burden of traumatic brain injury: Preliminary results from the global burden of disease project. Injury Prevention. 2010; 16 (Suppl. 1):A17. [DOI:10.1136/ip.2010.029215.61] 
  2. Dewan MC, Rattani A, Gupta S, Baticulon RE, Hung YC, Punchak M, et al. Estimating the global incidence of traumatic brain injury. Journal of Neurosurgery. 2018; 130(4):1-18. [DOI:10.3171/2017.10.JNS17352] [PMID]
  3. Hyder AA, Wunderlich CA, Puvanachandra P, Gururaj G, Kobusingye OC. The impact of traumatic brain injuries: A global perspective. NeuroRehabilitation. 2007; 22(5):341-53. [PMID]
  4. Li M, Zhao Z, Yu G, Zhang J. Epidemiology of traumatic brain injury over the world: A systematic review. General Medicine: Open Access. 2016; 4(5):e275-e. [DOI:10.1177/0963689717714102] 
  5. Stewart KA, Groen RS, Kamara TB, Farahzad MM, Samai M, Cassidy LD, et al. Traumatic injuries in developing countries: Report from a nationwide cross-sectional survey of Sierra Leone. JAMA Surgery. 2013; 148(5):463-9. [DOI:10.1001/jamasurg.2013.1341] [PMID] [PMCID] 
  6. Wood RL, Worthington A. Neurobehavioral abnormalities associated with executive dysfunction after traumatic brain injury. Frontiers in Behavioral Neuroscience. 2017; 11:195. [DOI:10.3389/fnbeh.2017.00195] [PMID] [PMCID] 
  7. Dijkers MP. Quality of life after traumatic brain injury: A review of research approaches and findings. Archives of Physical Medicine and Rehabilitation. 2004; 85(Suppl. 2):21-35. [DOI:10.1016/j.apmr.2003.08.119] 
  8. Polinder S, Haagsma JA, Steyerberg EW, Van Beeck EF. Health-related quality of life in persons after traumatic brain injury: A systematic review of the literature. The Lancet. 2013; 381:S116. [DOI:10.1016/S0140-6736(13)61370-7] 
  9. Polinder S, Haagsma JA, Van Klaveren D, Steyerberg EW, Van Beeck EF. Health-related quality of life after TBI: A systematic review of study design, instruments, measurement properties, and outcome. Population Health Metrics. 2015; 13(1):4. [DOI:10.1186/s12963-015-0037-1] [PMID] [PMCID] 
  10. Vieira RDE C, Hora EC, Oliveira DV, Ribeiro MDO, de Sousa RM. Quality of life of victims of traumatic brain injury six months after the trauma. Revista Latino-Americana de Enfermagem. 2013; 21(4):868-75. [DOI:10.1590/S0104-11692013000400006] [PMID] 
  11. Yousefzade-Chabok S, Kapourchali SR, Reihanian Z, Kazemnezhad Leili E, Moghadam AD, Mohtasham Amiri Z. Predictors of Chronic Physical and Mental Quality of Life Following Traumatic Brain Injury. Health. 2014; 6(6):496-503. [DOI:10.4236/health.2014.66069] 
  12. Al-Sarraj S. The pathology of Traumatic Brain Injury (TBI): A practical approach. Diagnostic Histopathology. 2016; 22(9):318-26. [DOI:10.1016/j.mpdhp.2016.08.005] 
  13. Blennow K, Hardy J, Zetterberg H. The neuropathology and neurobiology of traumatic brain injury. Neuron. 2012; 76(5):886-99. [DOI:10.1016/j.neuron.2012.11.021] [PMID] 
  14. Chabok SY, Kapourchali SR, Leili EK, Saberi A, Mohtasham-Amiri Z. Effective factors on linguistic disorder during acute phase following traumatic brain injury in adults. Neuropsychologia. 2012; 50(7):1444-50. [DOI:10.1016/j.neuropsychologia.2012.02.029] [PMID] 
  15. Mateer CA, Sira CS. Cognitive and emotional consequences of TBI: Intervention strategies for vocational rehabilitation. NeuroRehabilitation. 2006; 21(4):315-26. [PMID]
  16. McAllister TW. Neurobiological consequences of traumatic brain injury. Dialogues in Clinical Neuroscience. 2011; 13(3):287-300. [PMID] [PMCID] 
  17. McKee AC, Daneshvar DH. The neuropathology of traumatic brain injury. In: Salazar AM, Grafman J, editors. Handbook of Clinical Neurology. Amesterdam: Elsevier; 2015. [DOI:10.1016/B978-0-444-52892-6.00004-0] [PMID] [PMCID] 
  18. Rabinowitz AR, Levin HS. Cognitive sequelae of traumatic brain injury. The Psychiatric Clinics of North America. 2014; 37(1):1-11. [DOI:10.1016/j.psc.2013.11.004] [PMID] [PMCID] 
  19. Yousefzadeh-Chabok S, Ramezani S, Reihanian Z, Safaei M, Alijani B, Amini N. The role of early posttraumatic neuropsychological outcomes in the appearance of latter psychiatric disorders in adults with brain trauma. Asian Journal of Neurosurgery. 2015; 10(3):173-80. [DOI:10.4103/1793-5482.161165] [PMID] [PMCID] 
  20. Danna-Dos-Santos A, Mohapatra S, Santos M, Degani AM. Long-term effects of mild traumatic brain injuries to oculomotor tracking performances and reaction times to simple environmental stimuli. Scientific Reports. 2018; 8(1):4583.[DOI:10.1038/s41598-018-25220-2] [PMID] [PMCID] 
  21. Finnanger TG, Olsen A, Skandsen T, Lydersen S, Vik A, Evensen KA, et al. Life after adolescent and adult moderate and severe traumatic brain injury: Self-reported executive, emotional, and behavioural function 2-5 years after injury. Behavioural Neurology. 2015; 2015:329241. [DOI:10.1155/2015/329241] [PMID] [PMCID] 
  22. Gagner C, Landry-Roy C, Bernier A, Gravel J, Beauchamp MH. Behavioral consequences of mild traumatic brain injury in preschoolers. Psychological Medicine. 2018; 48(9):1551-9. [DOI:10.1017/S0033291717003221] [PMID] 
  23. 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(4):e0174847. [DOI:10.1371/journal.pone.0174847] [PMID] [PMCID] 
  24. Mouzon BC, Bachmeier C, Ojo JO, Acker CM, Ferguson S, Paris D, et al. Lifelong behavioral and neuropathological consequences of repetitive mild traumatic brain injury. Annals of Clinical and Translational Neurology. 2018; 5(1):64-80. [DOI:10.1002/acn3.510] [PMID] [PMCID] 
  25. Muelbl MJ, Slaker ML, Shah AS, Nawarawong NN, Gerndt CH, Budde MD, et al. Effects of mild blast traumatic brain injury on cognitive-and addiction-related behaviors. Scientific Reports. 2018; 8(1):9941. [DOI:10.1038/s41598-018-28062-0] [PMID] [PMCID] 
  26. Ramezani S, Yousefzadeh-Chabok S. Identification of imaging and clinical markers predicting chronic sleep disturbances after traumatic brain injury in adults. Iranian Journal of Neurosurgery. 2019; 4(3):125-38. [DOI:10.32598/irjns.4.3.125] 
  27. Ruet A, Bayen E, Jourdan C, Ghout I, Meaude L, Lalanne A, et al. A detailed overview of long-term outcomes in severe traumatic brain injury eight years post-injury. Frontiers in Neurology. 2019; 10:120. [DOI:10.3389/fneur.2019.00120] [PMID] [PMCID] 
  28. Ruttan L, Martin K, Liu A, Colella B, Green RE. Long-term cognitive outcome in moderate to severe traumatic brain injury: A meta-analysis examining timed and untimed tests at 1 and 4.5 or more years after injury. Archives of Physical Medicine and Rehabilitation. 2008; 89(Suppl 12):S69-76. [DOI:10.1016/j.apmr.2008.07.007] [PMID] 
  29. 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. Behavioural Neurology. 2015; 2015:680308. [DOI:10.1155/2015/680308] [PMID] [PMCID] 
  30. Andriessen TM, Jacobs B, Vos PE. Clinical characteristics and pathophysiological mechanisms of focal and diffuse traumatic brain injury. Journal of Cellular and Molecular Medicine. 2010; 14(10):2381-92. [DOI:10.1111/j.1582-4934.2010.01164.x] [PMID] [PMCID] 
  31. Sharp DJ, Scott G, Leech R. Network dysfunction after traumatic brain injury. Nature Reviews Neurology. 2014; 10(3):156-66. [DOI:10.1038/nrneurol.2014.15] [PMID] 
  32. Manktelow AE, Menon DK, Sahakian BJ, Stamatakis EA. Working memory after traumatic brain injury: The neural basis of improved performance with methylphenidate. Frontiers in Behavioral Neuroscience. 2017; 11:58. [DOI:10.3389/fnbeh.2017.00058] [PMID] [PMCID] 
  33. Shim M, Im CH, Lee SH. Disrupted cortical brain network in post-traumatic stress disorder patients: A resting-state electroencephalographic study. Translational Psychiatry. 2017; 7(9):e1231. [DOI:10.1038/tp.2017.200] [PMID] [PMCID] 
  34. Tlustos SJ, Peter Chiu C, Walz NC, Wade SL. Neural substrates of inhibitory and emotional processing in adolescents with traumatic brain injury. Journal of Pediatric Rehabilitation Medicine. 2015; 8(4):321-33. [DOI:10.3233/PRM-150350] [PMID] [PMCID] 
  35. Wolf JA, Koch PF. Disruption of network synchrony and cognitive dysfunction after traumatic brain injury. Frontiers in Systems Neuroscience. 2016; 10:1-14. [DOI:10.3389/fnsys.2016.00043] [PMID] [PMCID]
  36. Hayes JP, Bigler ED, Verfaellie M. Traumatic brain injury as a disorder of brain connectivity. Journal of the International Neuropsychological Society. 2016; 22(2):120-37. [DOI:10.1017/S1355617715000740] [PMID] [PMCID] 
  37. Villamar MF, Santos Portilla A, Fregni F, Zafonte R. Noninvasive brain stimulation to modulate neuroplasticity in traumatic brain injury. Neuromodulation: Technology at the Neural Interface. 2012; 15(4):326-38. [DOI:10.1111/j.1525-1403.2012.00474.x] [PMID] 
  38. Hylin MJ, Kerr AL, Holden R. Understanding the mechanisms of recovery and/or compensation following injury. Neural Pplasticity. 2017; 2017:7125057. [DOI:10.1155/2017/7125057] [PMID] [PMCID] 
  39. Nudo RJ. Recovery after brain injury: Mechanisms and principles. Frontiers in Human Neuroscience. 2013; 7:887. [DOI:10.3389/fnhum.2013.00887] [PMID] [PMCID] 
  40. Dhaliwal SK, Meek BP, Modirrousta MM. Non-invasive brain stimulation for the treatment of symptoms following traumatic brain injury. Frontiers in Psychiatry. 2015; 6:119. [DOI:10.3389/fpsyt.2015.00119] [PMID] [PMCID] 
  41. Neumann D, Lequerica A. Cognitive problems after traumatic brain injury. Archives of Physical Medicine and Rehabilitation. 2015; 96(1):179-80. [DOI:10.1016/j.apmr.2013.06.003] [PMID] 
  42. De Freitas Cardoso MG, Faleiro RM, de Paula JJ, Kummer A, Caramelli P, Teixeira AL, et al. Cognitive impairment following acute mild traumatic brain injury. Frontiers in Neurology. 2019; 10:1-9. [DOI:10.3389/fneur.2019.00198] [PMID] [PMCID] 
  43. Donders J, Stout J. The influence of cognitive reserve on recovery from traumatic brain injury. Archives of Clinical Neuropsychology. 2019; 34(2):206-13. [DOI:10.1093/arclin/acy035] [PMID] 
  44. Leary J, Schwimmer C, Hussain U, Lopez K, McNally S, Dsurney J, et al. Cognitive Reserve and Preservation of Functioning Following Traumatic Brain Injury. American Academy of Neurology. 2015; 84(Suppl. 14):P7.188.
  45. Steward KA, Kennedy R, Novack TA, Crowe M, Marson DC, Triebel KL. The role of cognitive reserve in recovery from traumatic brain injury. The Journal of Head Trauma Rehabilitation. 2018; 33(1):E18-27. [DOI:10.1097/HTR.0000000000000325] [PMID] [PMCID] 
  46. Prince C, Bruhns M. Evaluation and treatment of mild traumatic brain injury: The role of neuropsychology. Brain Sciences. 2017; 7(8):105. [DOI:10.3390/brainsci7080105] [PMID] [PMCID] 
  47. Allen MD, Bigler ED, Larsen J, Goodrich-Hunsaker NJ, Hopkins RO. Functional neuroimaging evidence for high cognitive effort on the word memory test in the absence of external incentives. Brain Injury. 2007; 21(13-14):1425-8. [DOI:10.1080/02699050701769819] [PMID] 
  48. Babikian T, Freier MC, Ashwal S, Riggs ML, Burley T, Holshouser BA. MR spectroscopy: Predicting long‐term neuropsychological outcome following pediatric TBI. Journal of Magnetic Resonance Imaging: An Official Journal of the International Society for Magnetic Resonance in Medicine. 2006; 24(4):801-11. [DOI:10.1002/jmri.20696] [PMID] 
  49. Chen JK, Johnston KM, Collie A, McCrory P, Ptito A. A validation of the post concussion symptom scale in the assessment of complex concussion using cognitive testing and functional MRI. Journal of Neurology, Neurosurgery & Psychiatry. 2007; 78(11):1231-8. [DOI:10.1136/jnnp.2006.110395] [PMID] [PMCID] 
  50. Medaglia JD. Functional neuroimaging in traumatic brain injury: From nodes to networks. Frontiers in Neurology. 2017; 8:407. [DOI:10.3389/fneur.2017.00407] [PMID] [PMCID] 
  51. Scheibel RS. Functional magnetic resonance imaging of cognitive control following traumatic brain injury. Frontiers in Neurology. 2017; 8:352. [DOI:10.3389/fneur.2017.00352] [PMID] [PMCID] 
  52. Sivák Š, Bittšanský M, Grossmann J, Nosál’ V, Kantorova E, Sivakova J, et al. Clinical correlations of proton magnetic resonance spectroscopy findings in acute phase after mild traumatic brain injury. Brain Injury. 2014; 28(3):341-6. [DOI:10.3109/02699052.2013.865270] [PMID] 
  53. Veeramuthu V, Seow P, Narayanan V, Wong JHD, Tan LK, Hernowo AT, et al. Neurometabolites alteration in the acute phase of mild Traumatic Brain Injury (mTBI): An in vivo proton magnetic resonance spectroscopy (1H-MRS) Study. Academic Radiology. 2018; 25(9):1167-77. [DOI:10.1016/j.acra.2018.01.005] [PMID] 
  54. Yeo RA, Gasparovic C, Merideth F, Ruhl D, Doezema D, Mayer AR. A longitudinal proton magnetic resonance spectroscopy study of mild traumatic brain injury. Journal of Neurotrauma. 2011; 28(1):1-11. [DOI:10.1089/neu.2010.1578] [PMID] [PMCID] 
  55. Croall ID, Cowie CJ, He J, Peel A, Wood J, Aribisala BS, et al. White matter correlates of cognitive dysfunction after mild traumatic brain injury. Neurology. 2014; 83(6):494-501. [DOI:10.1212/WNL.0000000000000666] [PMID] [PMCID] 
  56. Hanks R, Millis S, Scott S, Gattu R, O’Hara NB, Haacke M, et al. The relation between cognitive dysfunction and diffusion tensor imaging parameters in traumatic brain injury. Brain Injury. 2019; 33(3):355-63. [DOI:10.1080/02699052.2018.1553073] [PMID] 
  57. Kraus MF, Susmaras T, Caughlin BP, Walker CJ, Sweeney JA, Little DM. White matter integrity and cognition in chronic traumatic brain injury: A diffusion tensor imaging study. Brain. 2007; 130(10):2508-19. [DOI:10.1093/brain/awm216] [PMID] 
  58. Narayana PA. White matter changes in patients with mild traumatic brain injury: MRI perspective. Concussion. 2017; 2(2):CNC35. [DOI:10.2217/cnc-2016-0028] [PMID] [PMCID] 
  59. Oehr L, Anderson J. Diffusion-tensor imaging findings and cognitive function following hospitalized mixed-mechanism mild traumatic brain injury: A systematic review and meta-analysis. Archives of Physical Medicine and Rehabilitation. 2017; 98(11):2308-19. [DOI:10.1016/j.apmr.2017.03.019] [PMID] 
  60. Dougall D, Poole N, Agrawal N. Pharmacotherapy for chronic cognitive impairment in traumatic brain injury. Cochrane Database of Systematic Reviews. 2015; 2015(12):CD009221. [DOI:10.1002/14651858.CD009221.pub2] [PMID]
  61. Robertson K, Schmitter-Edgecombe M. Focused and divided attention abilities in the acute phase of recovery from moderate to severe traumatic brain injury. Brain Injury. 2017; 31(8):1069-76. [DOI:10.1080/02699052.2017.1296192] [PMID] [PMCID] 
  62. Xu B, Sandrini M, Levy S, Volochayev R, Awosika O, Butman JA, et al. Lasting deficit in inhibitory control with mild traumatic brain injury. Scientific Reports. 2017; 7(1):14902. [DOI:10.1038/s41598-017-14867-y] [PMID] [PMCID] 
  63. Gazzaniga M, Ivry RB. Cognitive neuroscience: The Biology of the Mind, 4th edition. Manhattan: W. W. Norton & Company; 2013.
  64. Xiao H, Yang Y, Xi JH, Chen ZQ. Structural and functional connectivity in traumatic brain injury. Neural Regeneration Research. 2015; 10(12):2062-71. [DOI:10.4103/1673-5374.172328] [PMID] [PMCID] 
  65. Ricker JH, Hillary FG, DeLuca J. Functionally activated brain imaging (O-15 PET and fMRI) in the study of learning and memory after traumatic brain injury. The Journal of Head Trauma Rehabilitation. 2001; 16(2):191-205. [DOI:10.1097/00001199-200104000-00007] [PMID] 
  66. Wintermark M, Sanelli PC, Anzai Y, Tsiouris AJ, Whitlow CT, ACR Head Injury Institute, et al. Imaging evidence and recommendations for traumatic brain injury: Conventional neuroimaging techniques. Journal of the American College of Radiology. 2015; 12(2):e1-14. [DOI:10.1016/j.jacr.2014.10.014] [PMID] 
  67. Cicerone KD, Giacino JT. Remediation of executive function deficits after traumatic brain injury. NeuroRehabilitation. 1992; 2(3):12-22. [DOI:10.3233/NRE-1992-2304] 
  68. Lee MH, Smyser CD, Shimony JS. Resting-state fMRI: A review of methods and clinical applications. American Journal of Neuroradiology. 2013; 34(10):1866-72. [DOI:10.3174/ajnr.A3263] [PMID] [PMCID] 
  69. Menon V, Uddin LQ. Saliency, switching, attention and control: A network model of insula function. Brain Structure and Function. 2010; 214(5-6):655-67. [DOI:10.1007/s00429-010-0262-0] [PMID] [PMCID] 
  70. Bonnelle V, Ham TE, Leech R, Kinnunen KM, Mehta MA, Greenwood RJ, et al. Salience network integrity predicts default mode network function after traumatic brain injury. Proceedings of the National Academy of Sciences. 2012; 109(12):4690-5. [DOI:10.1073/pnas.1113455109] [PMID] [PMCID] 
  71. 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. 2017; 96(4):e5968. [DOI:10.1097/MD.0000000000005968] [PMID] [PMCID] 
  72. Hallowell B, Chapey R. Introduction to language intervention strategies in adult aphasia. In: Chapey R, editor. Language Intervention Strategies in Aphasia and Related Neurogenic Communication Disorders. Philadelphia: Lippincott Williams & Wilkins; 2008.
  73. Angeleri R, Bosco FM, Zettin M, Sacco K, Colle L, Bara BG. Communicative impairment in traumatic brain injury: A complete pragmatic assessment. Brain and Language. 2008; 107(3):229-45. [DOI:10.1016/j.bandl.2008.01.002] [PMID] 
  74. Nickelson RK. Traumatic Brain Injuries in Adults: Effects on Pragmatics [Internet]. 2014 [Updated Spring 2014]. Available from: https://pdfs.semanticscholar.org/0b28/4e4f7e7de86c655e3a27754a498f98a1f508.pdf
  75. Liégeois FJ, Mahony K, Connelly A, Pigdon L, Tournier JD, Morgan AT. Pediatric traumatic brain injury: Language outcomes and their relationship to the arcuate fasciculus. Brain and Language. 2013; 127(3):388-98. [DOI:10.1016/j.bandl.2013.05.003] [PMID] [PMCID] 
  76. Govind V, Gold S, Kaliannan K, Saigal G, Falcone S, Arheart KL, et al. Whole-brain proton MR spectroscopic imaging of mild-to-moderate traumatic brain injury and correlation with neuropsychological deficits. Journal of Neurotrauma. 2010; 27(3):483-96. [DOI:10.1089/neu.2009.1159] [PMID] [PMCID] 
  77. McDonald S, Code C, Togher L. Communication disorders following traumatic brain injury: London: Psychology Press; 2016. [DOI:10.4324/9781315539034] 
  78. Bonnelle V, Leech R, Kinnunen KM, Ham TE, Beckmann CF, De Boissezon X, et al. Default mode network connectivity predicts sustained attention deficits after traumatic brain injury. Journal of Neuroscience. 2011; 31(38):13442-51. [DOI:10.1523/JNEUROSCI.1163-11.2011] [PMID] [PMCID] 
  79. Marshman LA, Jakabek D, Hennessy M, Quirk F, Guazzo EP. Post-traumatic amnesia. Journal of Clinical Neuroscience. 2013; 20(11):1475-81. [DOI:10.1016/j.jocn.2012.11.022] [PMID] 
  80. Nakase-Richardson R, Sepehri A, Sherer M, Yablon SA, Evans C, Mani T. Classification schema of posttraumatic amnesia duration-based injury severity relative to 1-year outcome: Analysis of individuals with moderate and severe traumatic brain injury. Archives of Physical Medicine and Rehabilitation. 2009; 90(1):17-9. [DOI:10.1016/j.apmr.2008.06.030] [PMID] 
  81. Luoto TM, Iverson GL, Losoi H, Wäljas M, Tenovuo O, Kataja A, et al. Clinical correlates of retrograde amnesia in mild traumatic brain injury. Brain Injury. 2015; 29(5):565-72. [DOI:10.3109/02699052.2014.1002421] [PMID] 
  82. Roberts CM, Spitz G, Mundy M, Ponsford JL. Retrograde autobiographical memory from PTA emergence to six-month follow-up in moderate to severe traumatic brain injury. The Journal of Neuropsychiatry and Clinical Neurosciences. 2018; 31(2):112-122. [DOI:10.1176/appi.neuropsych.18010015] [PMID] 
  83. Cantu RC. Posttraumatic retrograde and anterograde amnesia: Pathophysiology and implications in grading and safe return to play. Journal of Athletic Training. 2001; 36(3):244-8. [PMID] [PMCID]
  84. Aggleton JP. Looking beyond the hippocampus: Old and new neurological targets for understanding memory disorders. Proceedings of the Royal Society B: Biological Sciences. 2014; 281(1786):pii20140565. [DOI:10.1098/rspb.2014.0565] [PMID] [PMCID] 
  85. Aggleton JP. Understanding anterograde amnesia: Disconnections and hidden lesions. The Quarterly Journal of Experimental Psychology. 2008; 61(10):1441-71. [DOI:10.1080/17470210802215335] [PMID] 
  86. Niogi SN, Mukherjee P, Ghajar J, Johnson CE, Kolster R, Lee H, et al. Structural dissociation of attentional control and memory in adults with and without mild traumatic brain injury. Brain. 2008; 131(12):3209-21. [DOI:10.1093/brain/awn247] [PMID] 
  87. Aaronson A, Lloyd RB. Aggression after traumatic brain injury: A review of the current literature. Psychiatric Annals. 2015; 45(8):422-6. [DOI:10.3928/00485713-20150803-08] 
  88. Rao V, Rosenberg P, Bertrand M, Salehinia S, Spiro J, Vaishnavi S, et al. Aggression after traumatic brain injury: Prevalence and correlates. The Journal of Neuropsychiatry and Clinical Neurosciences. 2009; 21(4):420-9. [DOI:10.1176/jnp.2009.21.4.420] [PMID] [PMCID] 
  89. Tateno A, Jorge RE, Robinson RG. Clinical correlates of aggressive behavior after traumatic brain injury. The Journal of Neuropsychiatry and Clinical Neurosciences. 2003; 15(2):155-60. [DOI:10.1176/jnp.15.2.155] [PMID] 
  90. Arnould A, Rochat L, Azouvi P, Van der Linden M. A multidimensional approach to apathy after traumatic brain injury. Neuropsychology Review. 2013; 23(3):210-33. [DOI:10.1007/s11065-013-9236-3] [PMID] 
  91. Worthington A, Wood RL. Apathy following traumatic brain injury: A review. Neuropsychologia. 2018; 118(Pt B):40-7. [DOI:10.1016/j.neuropsychologia.2018.04.012] [PMID] 
  92. Kennedy E, Cohen M, Munafo M. Childhood traumatic brain injury and the associations with risk behavior in adolescence and young adulthood: A systematic review. The Journal of Head Trauma Rehabilitation. 2017; 32(6):425-32. [DOI:10.1097/HTR.0000000000000289] [PMID] [PMCID] 
  93. De Sousa A, McDonald S, Rushby J, Li S, Dimoska A, James C. Understanding deficits in empathy after traumatic brain injury: The role of affective responsivity. Cortex. 2011; 47(5):526-35. [DOI:10.1016/j.cortex.2010.02.004] [PMID] 
  94. Jang SH, Kwon HG. Akinetic mutism in a patient with mild traumatic brain injury: A diffusion tensor tractography study. Brain Injury. 2017; 31(8):1159-63. [DOI:10.1080/02699052.2017.1288265] [PMID] 
  95. Ahmed S, Venigalla H, Mekala HM, Dar S, Hassan M, Ayub S. Traumatic brain injury and neuropsychiatric complications. Indian Journal of Psychological Medicine. 2017; 39(2):114-21. [DOI:10.4103/0253-7176.203129] [PMID] [PMCID] 
  96. Fettes P, Schulze L, Downar J. Cortico-striatal-thalamic loop circuits of the orbitofrontal cortex: Promising therapeutic targets in psychiatric illness. Frontiers in Systems Neuroscience. 2017; 11:25. [DOI:10.3389/fnsys.2017.00025] [PMID] [PMCID] 
  97. Hiser J, Koenigs M. The multifaceted role of the ventromedial prefrontal cortex in emotion, decision making, social cognition, and psychopathology. Biological Psychiatry. 2018; 83(8):638-47. [DOI:10.1016/j.biopsych.2017.10.030] [PMID] [PMCID] 
  98. Ikemoto S, Yang C, Tan A. Basal ganglia circuit loops, dopamine and motivation: A review and enquiry. Behavioural Brain Research. 2015; 290:17-31. [DOI:10.1016/j.bbr.2015.04.018] [PMID] [PMCID] 
  99. Haber SN. The place of dopamine in the cortico-basal ganglia circuit. Neuroscience. 2014; 282:248-57. [DOI:10.1016/j.neuroscience.2014.10.008] [PMID] [PMCID] 
  100. Haber SN. Corticostriatal circuitry. In: Pfaff DW, Voldow ND, editors. Neuroscience in the 21st Century. New York City: Springer; 2016. [DOI:10.1007/978-1-4614-6434-1_135-1] 
  101. Bonelli RM, Cummings JL. Frontal-subcortical circuitry and behavior. Dialogues in Clinical Neuroscience. 2007; 9(2):141-51. [PMID] [PMCID]
  102. Kawa L, Arborelius UP, Yoshitake T, Kehr J, Hökfelt T, Risling M, et al. Neurotransmitter systems in a mild blast traumatic brain injury model: Catecholamines and Serotonin. Journal of Neurotrauma. 2015; 32(16):1190-9. [DOI:10.1089/neu.2014.3669] [PMID] [PMCID] 
  103. Deb S, Leeson V, Aimola L, Bodani M, Li L, Weaver T, et al. Aggression following traumatic brain injury: Effectiveness of risperidone (AFTER): Study protocol for a feasibility randomised controlled trial. Trials. 2018; 19(1):325. [DOI:10.1186/s13063-018-2601-z] [PMID] [PMCID] 
  104. Pryor J. What environmental factors irritate people with acquired brain injury? Disability and Rehabilitation. 2004; 26(16):974-80. [DOI:10.1080/09638280410001702397] [PMID] 
  105. Pardini M, Krueger F, Hodgkinson CA, Raymont V, Strenziok M, Amore M, et al. Aggression, DRD1 polymorphism, and lesion location in penetrating traumatic brain injury. CNS Spectrums. 2014; 19(5):382-90. [DOI:10.1017/S1092852914000108] [PMID] [PMCID] 
  106. Renner CI. Interrelation between neuroendocrine disturbances and medical complications encountered during rehabilitation after TBI. Journal of Clinical Medicine. 2015; 4(9):1815-40. [DOI:10.3390/jcm4091815] [PMID] [PMCID] 
  107. Levy M, Berson A, Cook T, Bollegala N, Seto E, Tursanski S, et al. Treatment of agitation following traumatic brain injury: A review of the literature. NeuroRehabilitation. 2005; 20(4):279-306. [PMID]
  108. Seel RT, Corrigan JD, Dijkers MP, Barrett RS, Bogner J, Smout RJ, et al. Patient effort in traumatic brain injury inpatient rehabilitation: Course and associations with age, brain injury severity, and time postinjury. Archives of Physical Mmedicine and Rehabilitation. 2015; 96(Suppl. 8):S235-44. [DOI:10.1016/j.apmr.2014.10.027] [PMID] [PMCID] 
  109. Luauté J, Plantier D, Wiart L, Tell L, SOFMER Group. Care management of the agitation or aggressiveness crisis in patients with TBI. systematic review of the literature and practice recommendations. Annals of Physical and Rehabilitation Medicine. 2016; 59(1):58-67. [DOI:10.1016/j.rehab.2015.11.001] [PMID] 
  110. Fleminger S. Managing agitation and aggression after head injury. British Medical Journal Publishing Group. 2003; 327(7405):4-5. [DOI:10.1136/bmj.327.7405.4] [PMID] [PMCID] 
  111. Dailey NS, Smith R, Vanuk JR, Raikes AC, Killgore WD. Resting-state functional connectivity as a biomarker of aggression in mild traumatic brain injury. NeuroReport. 2018; 29(16):1413-7. [DOI:10.1097/WNR.0000000000001127] [PMID] 
  112. Balázsfi D, Zelena D, Demeter K, Miskolczi C, Varga ZK, Nagyváradi Á, et al. Differential roles of the two raphe nuclei in amiable social behavior and aggression-an optogenetic study. Frontiers in Behavioral Neuroscience. 2018; 12:163. [DOI:10.3389/fnbeh.2018.00163] [PMID] [PMCID] 
  113. Rubin DH, Walkup JT. SSRIs, adolescents, and aggression: Tempering human implications regarding SSRI-induced aggression in hamsters: Comment on Ricci and Melloni (2012). Behavioral Neuroscience. 2012; 126(5):742-7. [DOI:10.1037/a0030069] [PMID] 
  114. Sharma T, Guski LS, Freund N, Gøtzsche PC. Suicidality and aggression during antidepressant treatment: Systematic review and meta-analyses based on clinical study reports. British Medical Journal. 2016; 352:i65. [DOI:10.1136/bmj.i65] [PMID] [PMCID] 
  115. Jorge RE, Arciniegas DB. Mood disorders after TBI. Psychiatric Clinics of North America. 2014; 37(1):13-29. [DOI:10.1016/j.psc.2013.11.005] [PMID] [PMCID] 
  116. Jorge RE, Robinson RG, Moser D, Tateno A, Crespo-Facorro B, Arndt S. Major depression following traumatic brain injury. Archives of General Psychiatry. 2004; 61(1):42-50. [DOI:10.1001/archpsyc.61.1.42] [PMID] 
  117. Cnossen MC, Scholten AC, Lingsma HF, Synnot A, Haagsma J, Steyerberg PEW, et al. Predictors of major depression and posttraumatic stress disorder following traumatic brain injury: A systematic review and meta-analysis. The Journal of Neuropsychiatry and Clinical Neurosciences. 2017; 29(3):206-24. [DOI:10.1176/appi.neuropsych.16090165] [PMID] 
  118. Deb S, Burns J. Neuropsychiatric consequences of traumatic brain injury: A comparison between two age groups. Brain Injury. 2007; 21(3):301-7. [DOI:10.1080/02699050701253137] [PMID] 
  119. Demakis GJ, Hammond FM, Knotts A. Prediction of depression and anxiety 1 year after moderate-severe traumatic brain injury. Applied neuropsychology. 2010; 17(3):183-9. [DOI:10.1080/09084282.2010.499752] [PMID] 
  120. Whelan-Goodinson R, Ponsford JL, Schönberger M, Johnston L. Predictors of psychiatric disorders following traumatic brain injury. The Journal of Head Trauma Rehabilitation. 2010; 25(5):320-9. [DOI:10.1097/HTR.0b013e3181c8f8e7] [PMID] 
  121. Venkatraman A, Edlow BL, Immordino-Yang MH. The brainstem in emotion: A review. Frontiers in Neuroanatomy. 2017; 11:15. [DOI:10.3389/fnana.2017.00015] [PMID] [PMCID] 
  122. Schwarzbold M, Diaz A, Martins ET, Rufino A, Amante LN, Thais ME, et al. Psychiatric disorders and traumatic brain injury. Neuropsychiatric Disease and Treatment. 2008; 4(4):797-816. [DOI:10.2147/NDT.S2653] [PMID] [PMCID] 
  123. Van der Horn HJ, Scheenen ME, De Koning ME, Liemburg EJ, Spikman JM, van der Naalt J. The default mode network as a biomarker of persistent complaints after mild traumatic brain injury: A longitudinal functional magnetic resonance imaging study. Journal of Neurotrauma. 2017; 34(23):3262-9. [DOI:10.1089/neu.2017.5185] [PMID] 
  124. Moreno-López L, Sahakian BJ, Manktelow A, Menon DK, Stamatakis EA. Depression following traumatic brain injury: A functional connectivity perspective. Brain Injury. 2016; 30(11):1319-28. [DOI:10.1080/02699052.2016.1186839] [PMID] 
  125. Jorge RE, Acion L, Burin DI, Robinson RG. Sertraline for preventing mood disorders following traumatic brain injury: A randomized clinical trial. JAMA Psychiatry. 2016; 73(10):1041-7. [DOI:10.1001/jamapsychiatry.2016.2189] [PMID] 
  126. Plantier D, Luauté J, SOFMER Group. Drugs for behavior disorders after traumatic brain injury: Systematic review and expert consensus leading to French recommendations for good practice. Annals of Physical and Rehabilitation Medicine. 2016; 59(1):42-57. [DOI:10.1016/j.rehab.2015.10.003] [PMID] 
  127. Bodnar CN, Morganti JM, Bachstetter AD. Depression following a traumatic brain injury: Uncovering cytokine dysregulation as a pathogenic mechanism. Neural Regeneration Research. 2018; 13(10):1693-1704. [DOI:10.4103/1673-5374.238604] [PMID] [PMCID] 
  128. Alway Y, Gould KR, McKay A, Johnston L, Ponsford J. The evolution of post-traumatic stress disorder following moderate-to-severe traumatic brain injury. Journal of Neurotrauma. 2016; 33(9):825-31. [DOI:10.1089/neu.2015.3992] [PMID] 
  129. Bryant R. Post-traumatic stress disorder vs traumatic brain injury. Dialogues in Clinical Neuroscience. 2011; 13(3):251-62. [PMID] [PMCID]
  130. Khodadadi-Hassankiadeh N, Dehghan Nayeri N, Shahsavari H, Yousefzadeh-Chabok S, Haghani H. Predictors of post-traumatic stress disorder among victims of serious motor vehicle accidents. International Journal of Community Based Nursing and Midwifery. 2017; 5(4):355-64. [PMID] [PMCID]
  131. Undavalli C, Das P, Dutt T, Bhoi S, Kashyap R. PTSD in post-road traffic accident patients requiring hospitalization in Indian subcontinent: A review on magnitude of the problem and management guidelines. Journal of Emergencies, Trauma, and Shock. 2014; 7(4):327-31. [DOI:10.4103/0974-2700.142775] [PMID] [PMCID] 
  132. Yohannes K, Gebeyehu A, Adera T, Ayano G, Fekadu W. Prevalence and correlates of post-traumatic stress disorder among survivors of road traffic accidents in Ethiopia. International Journal of Mental Health Systems. 2018; 12(50):1-8. [DOI:10.1186/s13033-018-0229-8] [PMID] [PMCID] 
  133. Guo X, Edmed SL, Anderson V, Kenardy J. Neurocognitive predictors of posttraumatic stress disorder symptoms in children 6 months after traumatic brain injury: A prospective study. Neuropsychology. 2017; 31(1):84-92. [DOI:10.1037/neu0000305] [PMID] 
  134. Miller DR, Hayes SM, Hayes JP, Spielberg JM, Lafleche G, Verfaellie M. Default mode network subsystems are differentially disrupted in posttraumatic stress disorder. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging. 2017; 2(4):363-71. [DOI:10.1016/j.bpsc.2016.12.006] [PMID] [PMCID] 
  135. Akiki T, Averill C, Wrocklage K, Scott JC, Alexander-Bloch A, Southwick S, et al. 581. The default mode network in Posttraumatic Stress Disorder (PTSD): A data-driven multimodal approach. Biological Psychiatry. 2017; 81(Suppl. 10):S235. [DOI:10.1016/j.biopsych.2017.02.451] 
  136. Viard A, Mutlu J, Chanraud S, Guenolé F, Egler PJ, Gérardin P, et al. Altered default mode network connectivity in adolescents with post-traumatic stress disorder. NeuroImage Clinical. 2019; 22:101731. [DOI:10.1016/j.nicl.2019.101731] [PMID] [PMCID] 
  137. Badura-Brack A, McDermott TJ, Heinrichs-Graham E, Ryan TJ, Khanna MM, Pine DS, et al. Veterans with PTSD demonstrate amygdala hyperactivity while viewing threatening faces: A MEG study. Biological Psychology. 2018; 132:228-32. [DOI:10.1016/j.biopsycho.2018.01.005] [PMID] [PMCID] 
  138. Koenigs M, Grafman J. Posttraumatic stress disorder: The role of medial prefrontal cortex and amygdala. The Neuroscientist. 2009; 15(5):540-8. [DOI:10.1177/1073858409333072] [PMID] [PMCID] 
  139. Mallya S, Sutherland J, Pongracic S, Mainland B, Ornstein TJ. The manifestation of anxiety disorders after traumatic brain injury: A review. Journal of Neurotrauma. 2015; 32(7):411-21. [DOI:10.1089/neu.2014.3504] [PMID] 
  140. Alexander W. Pharmacotherapy for post-traumatic stress disorder in combat veterans: Focus on antidepressants and atypical antipsychotic agents. Pharmacy and Therapeutics. 2012; 37(1):32-8. [PMID] [PMCID]
  141. Stein MB. Pharmacotherapy for post traumatic stress disorder in adults [Internet]. 2015 [Updated 2019 July 09]. Available from: https://www.uptodate.com/contents/pharmacotherapy-for-posttraumatic-stress-disorder-in-adults#H5614797
  142. Stein MB. Psychotherapy for posttraumatic stress disorder in adults [Internet]. 2017 [Updated 2019 May 24]. Available from: https://www.uptodate.com/contents/psychotherapy-for-posttraumatic-stress-disorder-in-adults#H1118664290
  143. Shubina I. Cognitive-behavioral therapy of patients with ptsd: Literature review. Procedia-Social and Behavioral Sciences. 2015; 165:208-16. [DOI:10.1016/j.sbspro.2014.12.624] 
  144. Castriotta RJ, Wilde MC, Lai JM, Atanasov S, Masel BE, Kuna ST. Prevalence and consequences of sleep disorders in traumatic brain injury. Journal of Clinical Sleep Medicine. 2007; 3(4):349-56. [PMID] [PMCID]
  145. Grima N, Ponsford J, Rajaratnam SM, Mansfield D, Pase MP. Sleep disturbances in traumatic brain injury: A meta-analysis. Journal of Clinical Sleep Medicine. 2016; 12(03):419-28. [DOI:10.5664/jcsm.5598] [PMID] [PMCID] 
  146. Mathias JL, Alvaro PK. Prevalence of sleep disturbances, disorders, and problems following traumatic brain injury: A meta-analysis. Sleep Medicine. 2012; 13(7):898-905. [DOI:10.1016/j.sleep.2012.04.006] [PMID] 
  147. Zuzuárregui JRP, Bickart K, Kutscher SJ. A review of sleep disturbances following traumatic brain injury. Sleep Science and Practice. 2018; 2:2. [DOI:10.1186/s41606-018-0020-4] 
  148. Kempf J, Werth E, Kaiser PR, Bassetti CL, Baumann CR. Sleep-wake disturbances 3 years after traumatic brain injury. Journal of Neurology, Neurosurgery & Psychiatry. 2010; 81(12):1402-5. [DOI:10.1136/jnnp.2009.201913] [PMID] 
  149. Rao V, Neubauer D, Vaishnavi S. Sleep disturbances after traumatic brain injury. Psychiatric Times. 2015; 32(9):30.
  150. Makley MJ, Johnson-Greene L, Tarwater PM, Kreuz AJ, Spiro J, Rao V, et al. Return of memory and sleep efficiency following moderate to severe closed head injury. Neurorehabilitation and Neural Repair. 2009; 23(4):320-6. [DOI:10.1177/1545968308325268] [PMID] 
  151. Ouellet MC, Beaulieu-Bonneau S, Morin CM. Insomnia in patients with traumatic brain injury: Frequency, characteristics, and risk factors. The Journal of Head Trauma Rehabilitation. 2006; 21(3):199-212. [DOI:10.1097/00001199-200605000-00001] 
  152. Hou L, Han X, Sheng P, Tong W, Li Z, Xu D, et al. Risk factors associated with sleep disturbance following traumatic brain injury: Clinical findings and questionnaire based study. PLOS One. 2013; 8(10):e76087. [DOI:10.1371/journal.pone.0076087] [PMID] [PMCID] 
  153. Samuels ER, Szabadi E. Functional neuroanatomy of the noradrenergic locus coeruleus: its roles in the regulation of arousal and autonomic function part I: Principles of functional organisation. Current Neuropharmacology. 2008; 6(3):235-53. [DOI:10.2174/157015908785777229] [PMID] [PMCID] 
  154. Hauw JJ, Hausser-Hauw C, De Girolami U, Hasboun D, Seilhean D. Neuropathology of sleep disorders: A review. Journal of Neuropathology & Experimental Neurology. 2011; 70(4):243-52. [DOI:10.1097/NEN.0b013e318211488e] [PMID] 
  155. Marques DR, Gomes AA, Caetano G, Castelo-Branco M. Insomnia Disorder and Brain’s Default-Mode Network. Current Neurology and Neuroscience Reports. 2018; 18(8):45. [DOI:10.1007/s11910-018-0861-3] [PMID] 
  156. Sharp DJ, Beckmann CF, Greenwood R, Kinnunen KM, Bonnelle V, De Boissezon X, et al. Default mode network functional and structural connectivity after traumatic brain injury. Brain. 2011; 134(8):2233-47. [DOI:10.1093/brain/awr175] [PMID] 
  157. Kalmbach DA, Cuamatzi-Castelan AS, Tonnu CV, Tran KM, Anderson JR, Roth T, et al. Hyperarousal and sleep reactivity in insomnia: Current insights. Nature and Science of Sleep. 2018; 10:193-201. [DOI:10.2147/NSS.S138823] [PMID] [PMCID] 
  158. Liu CH, Liu CZ, Zhang J, Yuan Z, Tang LR, Tie CL, et al. Reduced spontaneous neuronal activity in the insular cortex and thalamus in healthy adults with insomnia symptoms. Brain Research. 2016; 1648:317-24. [DOI:10.1016/j.brainres.2016.07.024] [PMID] 
Type of Study: Review | Subject: Neurotrauma

Add your comments about this article : Your username or Email:
CAPTCHA

Rights and Permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

© 2024 CC BY-NC 4.0 | Iranian Journal of Neurosurgery

Designed & Developed by: Yektaweb