Introduction: Psychotic Disorder Following Traumatic Brain Injury (PDFTBI) is a relatively rare disorder that may provide clues to understanding schizophrenia and psychosis. The objective of this paper was to develop a conceptual framework describing how traumatic brain injury (TBI) can contribute to the development of a psychosis and potential neurobiological mechanisms that cause a psychosis in this population.
Methods: The literature on PDFTBI and previous conceptualisations of the disorder were reviewed. A model of psychosis was described as a context for a conceptualisation of PDFTBI.
Results: PDFTBI is associated with abnormalities to the temporal and frontal areas. The general presentation includes persecutory delusions and auditory hallucinations with an absence of negative symptoms. The mean onset is 4-5 years after TBI with the majority of cases occurring within 2 years. The progression and course of PDFTBI is variable. Neuroleptics appear to be the most efficacious medication. Previous conceptualisations of PDFTBI are varied and suggest that the relationship is not a simple one.
Conclusion: We propose that psychosis results from damage to the frontal and temporal areas and dysregulation of the dopaminergic system. Everyone is vulnerable to a psychotic disorder and psychosis will result when a threshold of damage to these areas are attained. Traumatic brain injury can be the primary cause of psychosis or contribute to the development of a psychosis through secondary seizure disorder, increasing biological and psychological risk, and triggering psychosis in vulnerable patients. The relationship may also be coincidental. Traumatic brain injury triggers pathophysiological processes that generally result in a psychosis after a delay of 1-5 years. Directions for future research includes prospective studies examining the impact of TBI on developing psychosis, retrospective studies examining TBI as a risk factor in schizophrenia or other populations at risk for secondary psychosis, and studies examining prevention of psychotic illness.
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http://dx.doi.org/10.1080/135468000143000131 | DOI Listing |
G3 (Bethesda)
January 2025
Department of Neurobiology, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093.
The conserved MAP3K DLKs are widely known for their functions in synapse formation, axonal regeneration and degeneration, and neuronal survival, notably under traumatic injury and chronic disease conditions. In contrast, their roles in other neuronal compartments are much less explored. Through an unbiased forward genetic screening in C.
View Article and Find Full Text PDFJ Neurol
January 2025
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Introduction: While cerebral amyloid angiopathy is likely responsible for intracerebral hemorrhage (ICH) occurring in superficial (grey matter, vermis) cerebellar locations, it is unclear whether hypertensive arteriopathy (HA), the other major cerebral small vessel disease (cSVD), is associated with cerebellar ICH (cICH) in deep (white matter, deep nuclei, cerebellar peduncle) regions. We tested the hypothesis that HA-associated neuroimaging markers are significantly associated with deep cICH compared to superficial cICH.
Patients And Methods: Brain MRI scans from consecutive non-traumatic cICH patients admitted to a referral center were analyzed for cSVD markers.
Eur J Trauma Emerg Surg
January 2025
Delray Medical Center, Division of Trauma and Critical Care Services, 5352 Linton Boulevard, Delray Beach, FL, 33484, USA.
Purpose: Many patients originally transported to non-trauma centers (NTC) require transfer to a trauma center (TC) for treatment. The aim was to analyze injury characteristics and outcomes of transfer patients and investigate the secondary overtriage (SOT).
Methods: Study included 2,056 transfers to an urban level 1 TC between 01/2016 and 06/2020.
Eur J Trauma Emerg Surg
January 2025
Department of Neurosurgery, Penn State Health Milton S. Hershey Medical Center, Hershey, PA, 17033, USA.
Background: The role of beta-blockers in severe, traumatic brain injury (TBI) management is debated. Severe TBI may elicit a surge of catecholamines, which has been associated with increased morbidity and mortality. We hypothesize administering propranolol, a non-selective beta-blocker, within 48 h of TBI will reduce patient mortality within 30 days of injury.
View Article and Find Full Text PDFEur J Trauma Emerg Surg
January 2025
Department of Emergency Medicine, Teikyo University of Medicine, 2- 11-1 Kaga, Itabashi-ku, Tokyo, 173-8606, Japan.
Purpose: D-dimer, a fibrinolysis indicator, may predict functional and life outcomes in traumatic brain injury (TBI) patients. We aimed to identify optimal D-dimer cutoff values for poor functional outcomes in severe TBI.
Methods: We used data from a multi-centre prospective observational cohort study that included patients with TBI with a Glasgow Coma Scale (GCS) score ≤ 8 within 48 h after injury or required neurosurgical procedures.
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