Neuropsychological and Neuropsychiatric Deficits Following Traumatic Brain Injury: Common Patterns and Neuropathological Mechanisms

Ramezani, Sara; Reihanian, Zoheir; Hosseini Nejad, Mozafar; Yousefzadeh-Chabok, Shahrokh

doi:10.32598/irjns.4.4.185

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

‎ 10.32598/irjns.4.4.185

Neuropsychological and Neuropsychiatric Deficits Following Traumatic Brain Injury: Common Patterns and Neuropathological Mechanisms

Sara Ramezani ^*

¹, Zoheir Reihanian²

, Mozafar Hosseini Nejad³

, Shahrokh Yousefzadeh-Chabok⁴

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

Abstract: (4647 Views)

Traumatic Brain Injury (TBI) in all degrees of injury severity mainly induces deviant cognitive, emotional and behavioral alterations that lead to their respective disorders. This brief overview strives to define the variables that determine the risk of occurrence of these disorders and to describe the common patterns of these disorders and their relevant neuropathogenetic mechanism(s). In addition, post-traumatic deficits can interact and exacerbate the probability, persistence and severity of each variable relative to one another. Since, neural substrates and pathways further complicate these TBI sequels, identifying the neuropathogenetic basis of these deficits using human brain mapping techniques has been a milestone in the investigations of the TBI field. It has been found that TBI-induced functional disturbance of one or more specific neural networks may cause a distinct disorder. However, this matter is a topic of discussion in TBI research. Evidently, prevalent, unpleasant TBI consequences such as motivational deficits, antisocial behaviors, aggression, disability of inhibitory control and executive function are mostly associated with the disruption of neural circuits originated from separate parts of the prefrontal cortex connected to thalamic nuclei and basal ganglia. Evidence strictly emphasizes the abnormality of the Default Mode Network (DMN) either within the network or between it and other neural networks for a majority of cognitive, emotional and sleep disorders after TBI. Therefore, imbalanced neural circuits due to TBI may serve as diagnostic and prognostic biomarkers for post-traumatic neuropsychological and neuropsychiatric disorders as well as a guide for circuit-based neurotherapy.

Keywords: Traumatic brain injury, Intrinsic neural networks, Neurotransmitter systems, Behavior, Cognition, Emotion

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Highlights
● Cognitive, emotional and behavioral disorders may be induced by traumatic brain injury with all degrees of severity, and can cause them to interact with each other.
● Results showed the abnormality of the default mode network either within the network or between it, and other neural networks for a majority of cognitive, emotional and sleep disorders after traumatic brain injury.
● Traumatic brain injury-induced imbalance in neural circuits may serve as diagnostic and prognostic biomarkers of deficits after traumatic brain injury.
Plain Language Summary
Neuropsychological and neuropsychiatric deficits such as cognitive, verbal, emotional, and mental disorders may be caused Traumatic Brain Injury (TBI) under all severity levels. The most common patterns of these disorders include amnesia, executive dysfunction, verbal and nonverbal communication impairment at the pragmatic level of language, aggression, depression, different types of anxiety especially post-traumatic stress disorder, and sleep-wake cycle disorders. These deficits usually interact with each other. Various variables including age, sex, severity of injury, duration of post-traumatic amnesia, pre-injury cognitive and psychological functions, medical history, hormonal and chemical functions of brain, and genetic background may be accounted as the risk factors for development and persistence of post-TBI neuropsychological and neurological symptoms. One of the research areas in TBI is the identification of the pathogenesis of neuropsychological and neuropsychiatric deficits after TBI. Nowadays, neural circuits underlying the pathogenesis of these deficits have been partially identified using brain mapping techniques. It seems that anomalies in the neural circuits connecting the frontal lobe of brain and subcortical areas including thalamus and the basal ganglia play an important role in the development of antisocial behaviors, executive dysfunctions, and emotional deficits following TBI. Evidence-based metabolic, structural, and functional neural circuitry abnormalities, characterized by neural mapping techniques, may be useful as diagnostic, prognostic and therapeutic biomarkers, and guide clinicians in circuit-based neurotherapy.

Type of Study: Review | Subject: Neurotrauma

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