Is this Injury Reasonable? Do Psychological Injury Expectations Affect Mock Jurors' Legal Decisions in a Sexual Harassment Case?

The experiments examined the viability of a proposed decision-making process to explain how jurors' expectations for a sexual harassment complainant's psychological injury affect their legal decisions. Two experiments provided undergraduate mock jurors with a sexual harassment allegation that manipulated their range of expectations for reasonable psychological injuries (mild vs. mild to severe) and the severity of the complainant's alleged psychological injury (from minimal to extreme). Experiment 1 (N = 295) found that participants expecting mild injuries found the complainant's psychological injury allegations to be less reasonable and credible than participants expecting mild to severe injuries. Experiment 2 (N = 202) investigated whether these expectations influenced liability and compensatory damage decisions. As the injury increased from minimal to moderate severity, participants expecting mild injuries found less liability, whereas participants expecting mild to severe injuries found significantly more liability. Both expectations and injury severity independently impacted damage decisions, but not in an interactive fashion. We discuss the applicability of the proposed decision-making process to explain legal decisions in sexual harassment cases.     

Does Glucocorticoid Administration Prevent Late Seizures after Head Injury?

PURPOSE: Preventing posttraumatic epilepsy has been a difficult challenge. In this study we evaluated the association between glucocorticoid administration after traumatic brain injury (TBI) and posttraumatic seizures. METHODS: We examined a seizure-prevention trial database of 404 patients with severe TBI for exposure to glucocorticoids in the early (<1 week) posttraumatic period. After controlling for seizure risk, we compared the odds of developing first and second late posttraumatic seizures between those that received glucocorticoids and those that did not. RESULTS: Patients dosed with glucocorticoids within 1 day of their TBI were more likely to develop first late seizures than were those without [p = 0.04; hazard ratio = 1.74; 95% confidence interval (CI), 1.01-2.98]; whereas those receiving glucocorticoids > or =2 days after their injury had no similar association (p = 0.66; hazard ratio = 0.77; 95% CI, 0.23-2.56; p = 0.10 among the three groups). Receiving glucocorticoids within 1 day, or > or =2 days after TBI was not associated with second late seizure development. CONCLUSIONS: Glucocorticoid treatment after TBI is not associated with decreased late posttraumatic seizures, and early treatment is associated with increased seizure activity.     

Use-Dependent Exaggeration of Brain Injury: Is Glutamate Involved?

Extreme overreliance on the impaired forelimb following unilateral lesions of the forelimb representation area of the rat sensorimotor cortex (FL-SMC) leads to exaggeration of the initial cortical injury. Glutamate has repeatedly been implicated in the secondary processes leading to neuronal death following traumatic insult, chiefly because of the neuroprotective properties of excitatory amino acid antagonists in a variety of animal models of brain injury. The present study investigated the possibility that NMDA receptor-mediated processes are involved in use-dependent exaggeration of neuronal injury. Rats were fitted with one-sleeved casts that immobilized the intact forelimb for the first 7 days following FL-SMC lesion, a procedure previously shown to result in use-dependent exaggeration of injury and more severe and persistent limb-use deficits. In the present investigation, administration of MK-801 (1 mg/kg ip once daily on alternate days) during the casting period spared neural tissue surrounding the lesion and enhanced functional recovery of the impaired forelimb. These results suggest a role for NMDA receptor-mediated processes in use-dependent exaggeration of injury.     

Parenting Behaviors after Moderate – Severe Traumatic Injury in Early Childhood

ABSTRACT

Purpose: Examine the impact of traumatic brain injury (TBI) on parenting behavior over time.

Method: Included 206 children (3–7 years old) with moderate to severe TBI or orthopedic injury, using a prospective longitudinal cohort study design. Assessments completed at baseline, 6-months, 12-months, 18-months, 3.5 years, and 6.8 years after injury. Dependent variables included authoritative, permissive, and authoritarian parenting.

Results: Injury characteristics had limited impact on parenting behaviors over time. Levels of authoritative parenting remained stable over time; however, levels of warmth and involvement declined over time for those with TBI. Levels of permissive and authoritarian parenting declined for all participants by 3.5 years post injury. SES and stressors impacted parenting behaviors.

Conclusions: While there was limited effect of TBI on parenting behavior over time, it remains unclear how individuals respond to these parenting behaviors years after injury. Clinicians should monitor family and parenting behaviors to foster an environment to promote positive recovery.     

Traumatic Brain Injury and Psychosis: What Is the Connection?

Psychotic syndromes occur more frequently in individuals who have had a traumatic brain injury (TBI) than in the general population. Psychotic syndromes following a TBI can present in the period of post-traumatic anmesia, in association with post-traumatic epilepsy, in association with TBI-related mood disorders, and as a chronic, schizophrenia-like syndrome. Individuals with schizophrenia (a chronic psychotic disorder) have a higher frequency of prior TBI than individuals with other psychiatric disorders. These observations suggest an intriguing link between psychosis and TBI. The study of the neuroanatomical and neuropathological substrate of schizophrenia, and of the core symptoms of the disorder ("negative" symptoms, hallucinations, delusions), suggests that abnormalities in the structure and function of certain brain regions play a role in the genesis and maintenance of these core symptoms. The key brain regions include the dorsolateral prefrontal cortex, temporal lobe structures, basal ganglia, thalamus, and cingulate gyrus. These brain regions are commonly injured in many patients with TBI, suggesting a possible mechanism underlying the observed link between TBI and psychosis. This article reviews the literature on TBI and psychosis, and suggests an approach to the evaluation and treatment of individuals with TBI and psychosis.     

“Good Old Days” Bias Following Mild Traumatic Brain Injury

A small percentage of people with a mild traumatic brain injury (MTBI) report persistent symptoms and problems many months or even years following injury. Preliminary research suggests that people who sustain an injury often underestimate past problems (i.e., “good old days” bias), which can impact their perceived level of current problems and recovery. The purpose of this study was to examine the influence of the good old bays bias on symptom reporting following MTBI. The MTBI sample consisted of 90 referrals to a concussion clinic (mean time from injury to evaluation = 2.1 months, SD = 1.5, range = 0.8–8.1). All were considered temporarily fully disabled from an MTBI and they were receiving financial compensation through the Worker's Compensation system. Patients provided post-injury and pre-injury retrospective ratings on the 16-item British Columbia Post-concussion Symptom Inventory (BC-PSI). Ratings were compared to 177 healthy controls recruited from the community and a local university. Consistent with the good old bays bias, MTBI patients retrospectively endorsed the presence of fewer pre-injury symptoms compared to the control group. Individuals who failed effort testing tended to retrospectively report fewer symptoms pre-injury compared to those patients who passed effort testing. Many MTBI patients report their pre-injury functioning as better than the average person. This can negatively impact their perception of current problems, recovery from injury, and return to work.     

Differential Disruption of Blood–Brain Barrier in Severe Traumatic Brain Injury

Background

Traumatic brain injury (TBI) is a significant cause of death and disability in young adults, but not much is known about the incidence and characteristics of blood–brain barrier (BBB) dysfunction in this group. In this proof of concept study, we sought to quantify the incidence of BBB dysfunction (defined as a cerebrospinal fluid (CSF)–plasma albumin quotient of ≥0.007) and examine the relationship between plasma and CSF levels of proteins and electrolytes, in patients with severe TBI.

Methods

We recruited 30 patients, all of whom were receiving hypertonic 20 % saline infusion for intracranial hypertension and had external ventricular drains in situ. Simultaneous CSF and blood samples were obtained. Biochemical testing was performed for sodium, osmolality, potassium, glucose, albumin, immunoglobulin-G, and total protein.

Results

Eleven patients (37 %) showed evidence of impairment of passive BBB function, with a CSF–plasma albumin quotient of ≥0.007. There were strong positive correlations seen among CSF–plasma albumin quotient and CSF–plasma immunoglobulin-G quotient and CSF–plasma total protein quotient (r = 0.967, P < 0.001 and r = 0.995, P < 0.001, respectively). We also found a higher maximum intracranial pressure (24 vs. 21 mmHg, P = 0.029) and a trend toward increased mortality (27 vs. 11 %, P = 0.33) in patients with BBB disruption.

Conclusions

In summary, passive BBB dysfunction is common in patients with severe TBI, and may have important implications for effectiveness of osmotherapy and long-term outcomes. Also, our results suggest that the CSF–plasma total protein quotient, a measurement which is readily available, can be used instead of the CSF–plasma albumin quotient for evaluating BBB dysfunction.     

Is Routine Repeated Head CT Necessary for All Pediatric Traumatic Brain Injury?

Objective

Repeated computed tomography (CT) follow up for traumatic brain injury (TBI) patients is often performed. But there is debate the indication for repeated CT scans, especially in pediatric patients. Purpose of our study is to find risk factors of progression on repeated CT and delayed surgical intervention based on the repeated head CT.

Methods

Between March, 2007 and December, 2013, 269 pediatric patients (age 0-18 years) had admitted to our hospital for head trauma. Patients were classified into 8 subgroups according to mechanisms of injury. Types, amount of hemorrhage and amount changes on repeated CT were analyzed as well as initial Glasgow Coma Scale (GCS) scores.

Results

Within our cohort of 269 patients, 174 patients received repeat CT. There were progression in the amount of hemorrhage in 48 (27.6%) patients. Among various hemorrhage types, epidural hemorrhage (EDH) more than 10 cc measured in initial CT was found to be at risk of delayed surgical intervention significantly after routine repeated CT with or without neurological deterioration than other types of hemorrhage. Based on initial GCS, severe head trauma group (GCS 3-8) was at risk of delayed surgical intervention after routine repeated CT without change of clinical neurologic status.

Conclusion

We suggest that the patients with EDH more than 10 cc or GCS below 9 should receive repeated head CT even though absence of significant clinical deterioration.     

Functional and Molecular Characterization of a Novel Traumatic Peripheral Nerve–Muscle Injury Model

Traumatic injuries to human peripheral nerves are frequently associated with damage to nerve surrounding tissues including muscles and blood vessels. Currently, most rodent models of peripheral nerve injuries (e.g., facial or sciatic nerve) employ surgical nerve transection with scissors or scalpels. However, such an isolated surgical nerve injury only mildly damages neighboring tissues and weakly activates an immune response. In order to provide a rodent nerve injury model accounting for such nerve-associated tissue damage and immune cell activation, we developed a drop tower-based facial nerve trauma model in mice. We compare nerve regeneration in this novel peripheral nerve trauma model with the established surgical nerve injury along several parameters. These include gene expression, histological and functional facial motoneuron (FMN) regeneration, facial nerve degeneration, immune cell activation and muscle damage. Regeneration-associated genes (RAGs; e.g., Atf3) were strongly induced in FMNs subjected to traumatic and surgical injury. Regeneration of FMNs and functional recovery of whisker movement were faster in traumatic versus complete surgical injury, thus cutting down experimentation time. Wallerian degeneration of distal nerve stumps was readily observed in this novel trauma injury model. Importantly, drop tower-inflicted facial nerve injury resulted in muscle damage, activation of muscle satellite cell markers (PAX7) and pronounced infiltration of immune cells to the injury site only in this model but not upon surgical nerve transection. Thus, we provide a novel rodent PNS trauma model that can be easily adopted to other PNS nerves such as the sciatic nerve. Since this nerve trauma model replicates multiple tissue damage frequently encountered in clinical routine, it will be well suited to identify molecular and cellular mechanisms of PNS nerve repair in wild-type and genetically modified rodents.     

The Expression Changes of Cystathionine-β-synthase in Brain Cortex After Traumatic Brain Injury

Cystathionine-β-synthase (CBS) catalyzes the condensation of serine with homocysteine to form cystathionine and occupies a crucial regulatory position between the methionine cycle and the biosynthesis of cysteine by transsulfuration. It was reported that CBS was a novel marker of both differentiation and proliferation for certain cell types, suggesting that CBS represents a survival-promoting protein. However, its expression and function in the central nervous system lesion are not well understood. To investigate changes of CBS after traumatic brain injury (TBI) and its possible role, mice TBI model was established by controlled cortical impact system, and the expression and cellular localization of CBS after TBI was investigated in the present study. Western blot analysis revealed that CBS was present in normal mice brain cortex. It gradually decreased, reached a valley at the third day after TBI, and then restored to basal level. Importantly, more CBS was colocalized with neuron. In addition, Western blot detection showed that the third day postinjury was also the apoptosis peak indicated by the elevated expression of caspase-3. Importantly, immunohistochemistry analysis revealed that injury-induced expression of CBS was colabeled by Bcl-2 and had no co-localization with caspase-3. These data suggested that CBS may be implicated in the apoptosis of neuron and involved in the pathophysiology of brain after TBI.     

Acute Hypothalamic–pituitary–adrenal Response in Traumatic Brain Injury with and Without Extracerebral Trauma

Objective  Endocrine disturbances are common after traumatic brain injury (TBI). Hypothalamic–pituitary–adrenal (HPA) axis response in TBI patients may be related with hemodynamic status. However, its relationship with outcome is unclear. Our objective was to evaluate HPA axis response in the acute phase after TBI in patients with or without extracerebral trauma (ECT), and to investigate the impact of systemic injury and the mechanisms underlying HPA response. Methods  We prospectively studied 165 patients with moderate to severe TBI. Between 24 and 48 h after TBI, blood samples were taken for plasma adrenocorticotrophin hormone (ACTH) and baseline cortisol measurements. Afterwards, a short corticotrophin hormone test (250 μg Synacthen) was performed and samples were obtained at 30 and 60 min. We compared HPA response in TBI patients presenting with and without ECT and investigate potential mechanisms underlying this response. Results  One hundred and eight patients presented with isolated TBI, whereas 57 patients presented associated ECT. Both groups were comparable. Overall, 23.6% of patients fulfilled adrenal insufficiency (AI) criteria. Patients with plasma ACTH <9 pg/ml and patients presenting with hemorrhagic shock were more likely to present adrenal impairment. Variables associated with mortality were Injury Severity Score, Glasgow Coma Scale, Traumatic Coma Data Bank classification different than type II, need of second level measures to control intracranial pressure and plasma ACTH >9 pg/ml. Conclusion  Patients with TBI presenting with or without associated ECT present similar acute HPA response. AI is present in 23.6% of patients. Risk is increased in patients with low plasma ACTH levels and in patients with hemorrhagic shock. Both primary and secondary mechanisms of HPA failure were found. However, AI did not affect outcome.     

Do Survivors of Acute Neurologic Injury Remember Their Stay in the Neuroscience Intensive Care Unit?

Background

Patients in medical, surgical, and trauma intensive care units (ICUs) are at risk for later development of symptoms of post-traumatic stress disorder (PTSD). Because acute brain injury can impair recall; we sought to show that neuroscience patients undergoing prolonged neuroscience ICU admission have limited memory of their ICU stay and thus are less likely to develop symptoms of PTSD.

Methods

We surveyed patients >18 years admitted for 10 days or more to our neuroscience ICU over a 10-year period.

Results

The survey response rate was 50.5 % (47/93). Forty percent (19/47) of respondents presented with coma. Recall of details of the ICU admission was limited. Fewer than 10 % of patients who required mechanical ventilation recalled being on a ventilator. Only five patients (11 %) had responses suggestive of possible post-traumatic stress syndrome. The most commonly experienced symptoms following discharge were difficulty sleeping, difficulty with concentration, and memory loss.

Conclusion

Patients requiring prolonged neuroscience ICU admission do not appear to be traumatized by their ICU stay.     

Is Traumatic Brain Injury A Risk Factor for Schizophrenia? A Meta-Analysis of Case-Controlled Population-Based Studies

Traumatic brain injury (TBI) is known to lead to a range of adverse psychiatric sequelae but the question of whether TBI is a risk factor for psychosis and, in particular, schizophrenia remains unclear. Studies examining this issue have yielded conflicting results. We carried out a systematic review of the literature on TBI and psychosis in order to identify all population-based controlled studies which provide estimates of risk for schizophrenia following TBI. Odds ratios (ORs) were combined using random effects meta-analysis. Our literature search yielded 172 studies which were considered to be potentially relevant. From these, we identified 9 studies that could provide estimates of risk in the form of ORs. The pooled analysis revealed a significant association between TBI and schizophrenia (OR = 1.65; 95% CI = 1.17-2.32), with significant heterogeneity between the studies. Estimates from the family studies (OR = 2.8: 95% CI =1.76-4.47) were higher than those from the cohort/nested case-control studies (OR = 1.42: 95% CI = 1.02-1.97) by a factor of almost 2. There did not appear to be a dose-response relationship between severity of head injury and subsequent risk of schizophrenia. This meta-analysis supports an increased risk of schizophrenia following TBI, with a larger effect in those with a genetic predisposition to psychosis. Further epidemiological and neuroscientific studies to elucidate the mechanisms underlying this association are warranted.     

Levo-tetrahydropalmatine Attenuates Neuron Apoptosis Induced by Cerebral Ischemia–Reperfusion Injury: Involvement of c-Abl Activation

Ischemic stroke is one of the most dangerous acute diseases which causes death or deformity. Apoptosis has been shown to play an important role in the development and pathogenesis of cerebral ischemia–reperfusion injury (I/R injury), but the related mechanism is unclear. Levo-tetrahydropalmatine (l-THP), a bioactive ingredient extracted from the Chinese herb Corydalis, can penetrate the blood–brain barrier and exert various pharmacological effects on neural tissues. The present study examined the neuroprotective effect of l-THP on neuronal apoptosis induced by cerebral I/R injury. Results showed that pretreatment with l-THP (12.5, 25, and 50 mg/kg) improved neurological outcomes and reduced infarct volume and cerebral edema in comparison with the brains of the middle cerebral artery occlusion (MCAO) group. These findings provided evidence for the neuroprotective effects of l-THP against cerebral I/R injury. Furthermore, administration of l-THP enhanced the expression of Bcl-2 and attenuated the content of Bax, cleaved caspase-3, and PARP. l-THP could improve the reduction of NeuN-positive cells induced by I/R injury. These results suggested that l-THP could inhibit neuroapoptosis in cerebral ischemic rats. c-Abl was discovered as the critical protein responsible for neurocyte apoptosis; however, few data have been published on the relation between ischemic stroke and the expression of c-Abl. We found that both c-Abl expression and neuronal apoptosis were significantly increased in the MCAO group, while pretreatment with l-THP could ameliorate this effect. Therefore, we deduced that reduced c-Abl overexpression may play a role in the anti-apoptosis effect of l-THP after cerebral I/R injury. Thus, l-THP may provide a potential therapeutic approach for the treatment of ischemic stroke.

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Graphical Abstract ?

     

The Effect of Therapeutic Mild Hypothermia on Brain Microvascular Endothelial Cells During Ischemia–Reperfusion Injury

Background

To determine the cerebral protective effects of mild hypothermia (MH) on cerebral microcirculation.

Methods

We established ischemia–reperfusion (I/R) injury and MH treatment models with rat brain microvascular endothelial cells (RBMECs) in vitro and examined the apoptotic changes. The cultured RBMECs were randomly divided into the control group, I/R group, and MH group, which was further divided into two subgroups: intra-ischemia hypothermia (IIH) and post-ischemia hypothermia (PIH). Cell morphological changes were assessed using fluorescence microscopy. Apoptotic rates were obtained by flow cytometry. Expressions of caspase-3, Bax, and Bcl-2 were analyzed by Western blot.

Results

I/R injury in vitro induced apoptosis of RBMECs. The apoptotic rates in the control group, I/R group, and MH group were 0.13, 19.04, and 13.13%, respectively (P < 0.01). Compared with the I/R group, the MH group showed a significant decrease in the number of apoptotic cells, mainly in stage I apoptotic cells (P < 0.0083). The caspase-3 and Bax expressions were significantly enhanced (P < 0.05) in RBMECs after I/R injury, while substantial decreases in Bcl-2 expression were noted (P < 0.05). Following MH intervention, the increase in caspase-3 and Bax expression was suppressed (P < 0.05), while Bcl-2 expression significantly increased. The apoptotic rates or protein expressions between the two subgroups were not different significantly (P > 0.05).

Conclusions

These results indicate that MH could inhibit RBMEC apoptosis by preventing pro-apoptotic cells and early apoptotic cells from progressing to intermediate and advanced stages. This may be due to the effect of MH on I/R-induced apoptotic gene expression changes.