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Severe disinhibition due to injuries of neural tracts related to emotion circuit in a patient with traumatic brain injury: A case report

RATIONALE: Approximately 30% of patients with traumatic brain injury (TBI) develop disinhibition, a condition that involves several brain structures, including the amygdala, orbitofrontal cortex (OFC), and anterior cingulate cortex (ACC). Using diffusion tensor tractography (DTT), we report on a pat...

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Autores principales: Jang, Sung Ho, Kwon, Hyeok Gyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer Health 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6392766/
https://www.ncbi.nlm.nih.gov/pubmed/29384946
http://dx.doi.org/10.1097/MD.0000000000009493
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author Jang, Sung Ho
Kwon, Hyeok Gyu
author_facet Jang, Sung Ho
Kwon, Hyeok Gyu
author_sort Jang, Sung Ho
collection PubMed
description RATIONALE: Approximately 30% of patients with traumatic brain injury (TBI) develop disinhibition, a condition that involves several brain structures, including the amygdala, orbitofrontal cortex (OFC), and anterior cingulate cortex (ACC). Using diffusion tensor tractography (DTT), we report on a patient with severe disinhibition and injuries of the amygdala, OFC, and ACC following TBI. PATIENT CONCERNS: A 27-year-old male patient suffered an in-car accident. DIAGNOSES: Since the onset of the TBI, the patient showed severe disinhibition including violence, as follows: 1) he sometimes attacked therapists and nurses with no provocation, 2) while he was laying on a bed, he shouted and kicked the bed when asked questions, and 3) during therapy with a difficult task, he behaved violently to a therapist. The subscale of disinhibition in Neuropsychiatric Inventory scored three points for severity and for distress. INTERVENTIONS: N/A. Outcomes: On 10-month DTT, the connectivity of amygdala to the prefrontal cortex including the medial prefrontal cortex and OFC had decreased in both hemispheres. In the prefronto-thalamic tracts, the orbitofronto-thalamic tractshad narrowed (the right hemisphere), and were non-reconstructed (the left hemisphere). Discontinuations of both anterior cingulums were observed in both hemispheres. LESSONS: Using DTT, concurrent injuries of the amygdala, OFC, and ACC were demonstrated in a patient with severe disinhibition following TBI. Our result suggests the need to assess these neural structures in patients with disinhibition after brain injury.
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spelling pubmed-63927662019-03-15 Severe disinhibition due to injuries of neural tracts related to emotion circuit in a patient with traumatic brain injury: A case report Jang, Sung Ho Kwon, Hyeok Gyu Medicine (Baltimore) Research Article RATIONALE: Approximately 30% of patients with traumatic brain injury (TBI) develop disinhibition, a condition that involves several brain structures, including the amygdala, orbitofrontal cortex (OFC), and anterior cingulate cortex (ACC). Using diffusion tensor tractography (DTT), we report on a patient with severe disinhibition and injuries of the amygdala, OFC, and ACC following TBI. PATIENT CONCERNS: A 27-year-old male patient suffered an in-car accident. DIAGNOSES: Since the onset of the TBI, the patient showed severe disinhibition including violence, as follows: 1) he sometimes attacked therapists and nurses with no provocation, 2) while he was laying on a bed, he shouted and kicked the bed when asked questions, and 3) during therapy with a difficult task, he behaved violently to a therapist. The subscale of disinhibition in Neuropsychiatric Inventory scored three points for severity and for distress. INTERVENTIONS: N/A. Outcomes: On 10-month DTT, the connectivity of amygdala to the prefrontal cortex including the medial prefrontal cortex and OFC had decreased in both hemispheres. In the prefronto-thalamic tracts, the orbitofronto-thalamic tractshad narrowed (the right hemisphere), and were non-reconstructed (the left hemisphere). Discontinuations of both anterior cingulums were observed in both hemispheres. LESSONS: Using DTT, concurrent injuries of the amygdala, OFC, and ACC were demonstrated in a patient with severe disinhibition following TBI. Our result suggests the need to assess these neural structures in patients with disinhibition after brain injury. Wolters Kluwer Health 2017-12-29 /pmc/articles/PMC6392766/ /pubmed/29384946 http://dx.doi.org/10.1097/MD.0000000000009493 Text en Copyright © 2017 the Author(s). Published by Wolters Kluwer Health, Inc. http://creativecommons.org/licenses/by-nc-nd/4.0 This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0
spellingShingle Research Article
Jang, Sung Ho
Kwon, Hyeok Gyu
Severe disinhibition due to injuries of neural tracts related to emotion circuit in a patient with traumatic brain injury: A case report
title Severe disinhibition due to injuries of neural tracts related to emotion circuit in a patient with traumatic brain injury: A case report
title_full Severe disinhibition due to injuries of neural tracts related to emotion circuit in a patient with traumatic brain injury: A case report
title_fullStr Severe disinhibition due to injuries of neural tracts related to emotion circuit in a patient with traumatic brain injury: A case report
title_full_unstemmed Severe disinhibition due to injuries of neural tracts related to emotion circuit in a patient with traumatic brain injury: A case report
title_short Severe disinhibition due to injuries of neural tracts related to emotion circuit in a patient with traumatic brain injury: A case report
title_sort severe disinhibition due to injuries of neural tracts related to emotion circuit in a patient with traumatic brain injury: a case report
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6392766/
https://www.ncbi.nlm.nih.gov/pubmed/29384946
http://dx.doi.org/10.1097/MD.0000000000009493
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