scholarly journals Not all Explanations are Equal: Only Explanations Invoking a Change from the true self Mitigate Responsibility

2020 ◽  
Author(s):  
John Protzko ◽  
Nick Buttrick ◽  
Charles R. Ebersole ◽  
Sebastian Lundmark ◽  
Jonathan Schooler

When do people believe that biological explanations, such as genes, brain damage, or abnormal hormones, mitigate punishment for crimes? We propose the way in which biology is viewed as impacting the true self of the actor—who the actor really is, deep down—is the key element for predicting biologically-based mitigation. Across four preregistered studies, 4,066 American adults learned of different biological explanations for crimes and judged punishment, fault, and blame. We show, while some biological explanations mitigate punishment and responsibility, general ascriptions to genes do not. Participants viewed external events like traumatic brain injury as a disconnect between the true self and the peripheral self, whereas they did not for genetic ascriptions. People interprete general genes-based explanations for crimes as indicating that the perpetrators true self was violent or dangerous, while other biological explanations did not impugn the actor’s true self. Only when genetic bases are described as mutations do genes become mitigating factors. In these latter cases, the actor is not judged as harshly because the violent crime could be attributed to aspects peripheral to the true self. Therefore, biological explanations differ in the extent to which they implicate the true self. These results help to clear up when biological explanations do and do not appear to mitigate responsibility for crimes: When the aspect of biology in question is viewed as part of the true self, it will not mitigate blame; but when the biological aspect is viewed as more peripheral, the blame seems to be mitigating.

2012 ◽  
Vol 33 (2) ◽  
pp. 311-318 ◽  
Author(s):  
Nicole A Terpolilli ◽  
Seong-Woong Kim ◽  
Serge C Thal ◽  
Wolfgang M Kuebler ◽  
Nikolaus Plesnila

Ischemia, especially pericontusional ischemia, is one of the leading causes of secondary brain damage after traumatic brain injury (TBI). So far efforts to improve cerebral blood flow (CBF) after TBI were not successful because of various reasons. We previously showed that nitric oxide (NO) applied by inhalation after experimental ischemic stroke is transported to the brain and induces vasodilatation in hypoxic brain regions, thus improving regional ischemia, thereby improving brain damage and neurological outcome. As regional ischemia in the traumatic penumbra is a key mechanism determining secondary posttraumatic brain damage, the aim of the current study was to evaluate the effect of NO inhalation after experimental TBI. NO inhalation significantly improved CBF and reduced intracranial pressure after TBI in male C57 Bl/6 mice. Long-term application (24 hours NO inhalation) resulted in reduced lesion volume, reduced brain edema formation and less blood–brain barrier disruption, as well as improved neurological function. No adverse effects, e.g., on cerebral auto-regulation, systemic blood pressure, or oxidative damage were observed. NO inhalation might therefore be a safe and effective treatment option for TBI patients.


2021 ◽  
Vol 19 ◽  
Author(s):  
Denise Battaglini ◽  
Dorota Siwicka-Gieroba ◽  
Patricia RM Rocco ◽  
Fernanda Ferreira Cruz ◽  
Pedro Leme Silva ◽  
...  

: Traumatic brain injury (TBI) is a major cause of disability and death worldwide. The initial mechanical insult results in tissue and vascular disruption with hemorrhages and cellular necrosis that is followed by a dynamic secondary brain damage that presumably results in additional destruction of the brain. In order to minimize deleterious consequences of the secondary brain damage-such as inflammation, bleeding or reduced oxygen supply. The old concept of the -staircase approach- has been updated in recent years by most guidelines and should be followed as it is considered the only validated approach for the treatment of TBI. Besides, a variety of novel therapies have been proposed as neuroprotectants. The molecular mechanisms of each drug involved in inhibition of secondary brain injury can result as potential target for the early and late treatment of TBI. However, no specific recommendation is available on their use in clinical setting. The administration of both synthetic and natural compounds, which act on specific pathways involved in the destructive processes after TBI, even if usually employed for the treatment of other diseases, can show potential benefits. This review represents a massive effort towards current and novel therapies for TBI that have been investigated in both pre-clinical and clinical settings. This review aims to summarize the advancement in therapeutic strategies basing on specific and distinct -target of therapies-: brain edema, ICP control, neuronal activity and plasticity, anti-inflammatory and immunomodulatory effects, cerebral autoregulation, antioxidant properties, and future perspectives with the adoption of mesenchymal stromal cells.


2018 ◽  
Author(s):  
Jessica Bruijel ◽  
Sven Z Stapert ◽  
Annemiek Vermeeren ◽  
Jennie L Ponsford ◽  
Caroline M van Heugten

BACKGROUND Fatigue and sleep problems are common after a traumatic brain injury (TBI) and are experienced as highly distressing symptoms, playing a significant role in the recovery trajectory, and they can drastically impact the quality of life and societal participation of the patient and their family and friends. However, the etiology and development of these symptoms are still uncertain. OBJECTIVE The aim of this study is to examine the development of fatigue and sleep problems following moderate to severe TBI and to explore the changes in underlying biological (pain, brain damage), psychological (emotional state), and social (support family, participation) factors across time. METHODS This study is a longitudinal multicenter observational cohort study with 4 measurement points (3, 6, 12, and 18 months postinjury) including subjective questionnaires and cognitive tasks, preceded by 7 nights of actigraphy combined with a sleep diary. Recruitment of 137 moderate to severe TBI patients presenting at emergency and neurology departments or rehabilitation centers across the Netherlands is anticipated. The evolution of fatigue and sleep problems following TBI and their association with possible underlying biological (pain, brain damage), psychological (emotional state), and social (support family, participation) factors will be examined. RESULTS Recruitment of participants for this longitudinal cohort study started in October 2017, and the enrollment of participants is ongoing. The first results are expected at the end of 2020. CONCLUSIONS To the authors’ knowledge, this is the first study that examines the development of both post-TBI fatigue and sleep longitudinally within a biopsychosocial model in moderate to severe TBI using both subjective and objective measures. Identification of modifiable factors such as mood and psychosocial stressors may give direction to the development of interventions for fatigue and sleep problems post-TBI. CLINICALTRIAL Netherlands Trial Register NTR7162; http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=7162 (Archived by WebCite at http://www.webcitation.org/6z3mvNLuy) INTERNATIONAL REGISTERED REPOR RR1-10.2196/11295


2015 ◽  
pp. 1147-1160 ◽  
Author(s):  
Aric F. Logsdon ◽  
Brandon P. Lucke-Wold ◽  
Ryan C. Turner ◽  
Jason D. Huber ◽  
Charles L. Rosen ◽  
...  

2020 ◽  
Vol 51 (1) ◽  
pp. 28-35
Author(s):  
E. G. Sorokina ◽  
Zh. B. Semenova ◽  
N. S. Averianova ◽  
O. V. Karaseva ◽  
E. N. Arsenieva ◽  
...  

2013 ◽  
Vol 19 (6) ◽  
pp. 664-671 ◽  
Author(s):  
Yifat Levi ◽  
Yuri Rassovsky ◽  
Eugenia Agranov ◽  
Michal Sela-Kaufman ◽  
Eli Vakil

AbstractTraumatic brain injury (TBI) is the most common cause of brain damage, resulting in long-term disability. The “reserve” construct has been proposed to account for the reported mismatch between brain damage and its clinical expression. Although numerous studies have used various measures thought to reflect this construct, few studies have examined its underlying structure in clinical populations, and no studies have systematically studied this construct in TBI. In the present study, structural equation modeling technique was used to evaluate several models hypothesized to represent cognitive reserve (CR) in TBI. A broad range of data typically reported in the literature as representing CR was collected from 89 individuals who sustained moderate-to-severe TBI. Analyses revealed a best fitting model that consisted of three separate factors representing premorbid intelligence, socioeconomic status and leisure activity, with distinct pattern of associations among the three factors. Findings provide empirical support for the notion of a multi-factorial CR and suggest a coherent framework for further investigation. (JINS, 2013,19, 1–8)


2013 ◽  
Vol 34 (3) ◽  
pp. 503-531 ◽  
Author(s):  
Stefania Mondello ◽  
Kara Schmid ◽  
Rachel P. Berger ◽  
Firas Kobeissy ◽  
Domenico Italiano ◽  
...  

Author(s):  
Troy Rondinone

This chapter first describes the physical toll boxing took on boxers such as Gaspar Ortega and Emile Griffith. Research shows that boxers suffer disproportionally from neurological damage. The scientific term for it is chronic traumatic brain injury. The results are permanent and progressive. Symptoms include Parkinsonism, dementia, personality changes, and cerebellum dysfunction. Gaspar began suffering from nightmares. Griffith exhibited brain damage while Don Jordan lost his mind as well. The remainder of the chapter details Gaspar's life and activities after retiring from boxing. The brain damage that wiped the joy out of the golden years of so many of this boxing cohort did not strike Gaspar. He attributes this to his defensive, slippery style. Though he is occasionally off balance when he walks, that is minor compared to the devastation that brought such misery to so many other retired fighters.


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