scholarly journals Anhedonia following mild traumatic brain injury in rats: A behavioral economic analysis of positive and negative reinforcement

2019 ◽  
Author(s):  
Pelin Avcu ◽  
Ashley M. Fortress ◽  
Jennifer E. Fragale ◽  
Kevin M. Spiegler ◽  
Kevin C.H. Pang

AbstractPsychiatric disorders affect nearly 50% of individuals who have experienced a traumatic brain injury (TBI). Anhedonia is a major symptom of numerous psychiatric disorders and is a diagnostic criterion for depression. Recently, anhedonia has been divided into consummatory, motivational and decisional components, all of which may be affected differently in disease. Although anhedonia is typically assessed using positive reinforcement, the importance of stress in psychopathology suggests the study of negative reinforcement (removal or avoidance of aversive events) may be equally important. The present study investigated positive and negative reinforcement following a rat model of mild TBI (mTBI) using lateral fluid percussion. Hedonic value of and motivation for reinforcement was determined by behavioral economic analyses. Following mTBI, the hedonic value of avoiding foot shock was reduced. In contrast, the hedonic value of escaping foot shock or obtaining a sucrose pellet was not altered by mTBI. Moreover, neither motivation to avoid or escape foot shock nor motivation to acquire sucrose was modified by mTBI. Our results suggest that individuals experiencing mTBI may experience more stress because of poor proactive control of stress resulting from reduced hedonic value of avoiding aversive events.

2020 ◽  
Vol 35 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Nancy Greer ◽  
Nina A. Sayer ◽  
Michele Spoont ◽  
Brent C. Taylor ◽  
Princess E. Ackland ◽  
...  

Author(s):  
Vani Rao

Traumatic brain injury (TBI) is a significant cause of disability in the United States, with an incidence of about 1.5 million cases per year (National Institutes of Health Consensus Development Panel, 1999). It is associated with both neurologic and psychiatric consequences. Although the neurologic problems usually stabilize with time, the psychiatric disorders often continue to remit and relapse. Factors associated with the development of psychiatric disorders include older age, arteriosclerosis, and chronic alcoholism, all of which interfere with the reparative process within the central nervous system. Other contributors to psychiatric disability include a pre-TBI history of psychiatric illness, illicit drug abuse, and lack of social support. Because post-TBI psychiatric disturbances interfere with rehabilitation and cause emotional and financial burden for patients and caregivers, early diagnosis and treatment are important. Post-TBI psychiatric disturbances are best classified according to their clinical presentation. These disturbances are discussed below and their pharmacologic and nonpharmacologic treatment strategies are recommended. The mood disturbances most commonly associated with TBI are major depression, mania, anxiety, and apathy. Major depression is seen in about 25% of people with TBI. Symptoms of major depression include persistent sadness; guilt; feelings of worthlessness; hopelessness; suicidal thoughts; anhedonia; and changes in patterns of sleep, appetite, and energy. Sometimes these symptoms may be associated with psychotic features such as delusions and hallucinations. It is important to remember that changes in sleep, appetite, or energy are not specific to the syndrome of major depression and may be due to the brain injury itself, or to the noise, stimulation, or deconditioning associated with hospitalization. If due to the latter conditions, gradual improvement occurs with time in most patients. Sadness in excess of the severity of injury and poor participation in rehabilitation are strong indicators of the presence of major depression. The presence of poor social functioning pre-TBI and left dorsolateral frontal and/or left basal ganglia lesion have been associated with an increased probability of developing major depression following brain injury ( Jorge et al., 1993a; Jorge et al., 2004). Major depression should be differentiated from demoralization, primary apathy syndrome, and pathologic crying.


2006 ◽  
Vol 146 (3) ◽  
pp. 263-270 ◽  
Author(s):  
Salla Koponen ◽  
Tero Taiminen ◽  
Timo Kurki ◽  
Raija Portin ◽  
Heli Isoniemi ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Laura B. Ngwenya ◽  
Sarmistha Mazumder ◽  
Zachary R. Porter ◽  
Amy Minnema ◽  
Duane J. Oswald ◽  
...  

Cognitive deficits after traumatic brain injury (TBI) are debilitating and contribute to the morbidity and loss of productivity of over 10 million people worldwide. Cell transplantation has been linked to enhanced cognitive function after experimental traumatic brain injury, yet the mechanism of recovery is poorly understood. Since the hippocampus is a critical structure for learning and memory, supports adult neurogenesis, and is particularly vulnerable after TBI, we hypothesized that stem cell transplantation after TBI enhances cognitive recovery by modulation of endogenous hippocampal neurogenesis. We performed lateral fluid percussion injury (LFPI) in adult mice and transplanted embryonic stem cell-derived neural progenitor cells (NPC). Our data confirm an injury-induced cognitive deficit in novel object recognition, a hippocampal-dependent learning task, which is reversed one week after NPC transplantation. While LFPI alone promotes hippocampal neurogenesis, as revealed by doublecortin immunolabeling of immature neurons, subsequent NPC transplantation prevents increased neurogenesis and is not associated with morphological maturation of endogenous injury-induced immature neurons. Thus, NPC transplantation enhances cognitive recovery early after LFPI without a concomitant increase in neuron numbers or maturation.


2016 ◽  
Vol 46 (6) ◽  
pp. 1331-1341 ◽  
Author(s):  
Y. Alway ◽  
K. R. Gould ◽  
L. Johnston ◽  
D. McKenzie ◽  
J. Ponsford

BackgroundPsychiatric disorders commonly emerge during the first year following traumatic brain injury (TBI). However, it is not clear whether these disorders soon remit or persist for long periods post-injury. This study aimed to examine, prospectively: (1) the frequency, (2) patterns of co-morbidity, (3) trajectory, and (4) risk factors for psychiatric disorders during the first 5 years following TBI.MethodParticipants were 161 individuals (78.3% male) with moderate (31.2%) or severe (68.8%) TBI. Psychiatric disorders were diagnosed using the Structured Clinical Interview for DSM-IV, administered soon after injury and 3, 6 and 12 months, and 2, 3, 4 and 5 years post-injury. Disorder frequencies and generalized estimating equations were used to identify temporal relationships and risk factors.ResultsIn the first 5 years post-injury, 75.2% received a psychiatric diagnosis, commonly emerging within the first year (77.7%). Anxiety, mood and substance-use disorders were the most common diagnostic classes, often presenting co-morbidly. Many (56.5%) experienced a novel diagnostic class not present prior to injury. Disorder frequency ranged between 61.8 and 35.6% over time, decreasing by 27% [odds ratio (OR) 0.73, 95% confidence interval (CI) 0.65–0.83] with each year post-injury. Anxiety disorders declined significantly over time (OR 0.73, 95% CI 0.63–0.84), whilst mood and substance-use disorder rates remained stable. The strongest predictors of post-injury disorder were pre-injury disorder (OR 2.44, 95% CI 1.41–4.25) and accident-related limb injury (OR 1.78, 95% CI 1.03–3.07).ConclusionsFindings suggest the first year post-injury is a critical period for the emergence of psychiatric disorders. Disorder frequency declines thereafter, with anxiety disorders showing greater resolution than mood and substance-use disorders.


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