Validity Testing in Dually Diagnosed Post-Traumatic Stress Disorder and Mild Closed Head Injury

Prospects for the coexistence of post-traumatic stress syndrome (PTSS) and mild traumatic brain injury (mTBI) rely exclusively on subjective evidence, increasing the risk of response bias in a compensatable social context. Using a priori specificities derived from genuine brain disorder groups, we examined validity failure rates in three domains (symptom, cognitive, motor) in 799 persons reporting persistent subjective disability long after mild neurological injury. Validity tests included the Test of Memory Malingering, MMPI-2 Fake Bad Scale, and Infrequency (F) scales, reliable digit span, and Halstead-Reitan finger tapping. Analyses showed invalidity signs in large excess of actuarial expectations, with rising invalidity risk conditional on post-traumatic complexity; the highest failure rates were produced by the 95 persons reporting both neurogenic amnesia and re-experiencing symptoms. We propose an “over-endorsement continuum” hypothesis: The more complex the post-traumatic presentation after mild neurological injury, the stronger the association with response bias. Late-appearing dual diagnosis is a litigation phenomenon so intertwined with secondary gain as to be a byproduct of it.     

PTSD and Cognitive Functioning: Importance of Including Performance Validity Testing

Many studies have observed an association between post-traumatic stress disorder (PTSD) and cognitive deficits across several domains including memory, attention, and executive functioning. The inclusion of response bias measures in these studies, however, remains largely unaddressed. The purpose of this study was to identify possible cognitive impairments correlated with PTSD in returning OEF/OIF/OND veterans after excluding individuals failing a well-validated performance validity test. Participants included 126 men and 8 women with a history of mild traumatic brain injury (TBI) referred for a comprehensive neuropsychological evaluation as part of a consortium of five Veterans Affairs hospitals. The PTSD CheckList (PCL) and Word Memory Test (WMT) were used to establish symptoms of PTSD and invalid performance, respectively. Groups were categorized as follows: Control (PCL < 50, pass WMT), PTSD-pass (PCL ≥ 50, pass WMT), and PTSD-fail (PCL ≥ 50, fail WMT). As hypothesized, failure on the WMT was associated with significantly poorer performance on almost all cognitive tests administered; however, no significant differences were detected between individuals with and without PTSD symptoms after separating out veterans failing the WMT. These findings highlight the importance of assessing respondent validity in future research examining cognitive functioning in psychiatric illness and warrant further consideration of prior studies reporting PTSD-associated cognitive deficits.     

“Good-old-days” bias: A prospective follow-up study to examine the preinjury supernormal status in patients with mild traumatic brain injury

Primary objective: Postconcussion symptoms (PCS) are common following mild traumatic brain injury (mTBI). A psychological misperception, the “good-old-days” bias, has been indicated as one of the influencing factors on symptom reporting after injury. To date, this response bias has only been examined in a small number of cross-sectional studies. This study thus prospectively evaluated the “good-old-days” bias in patients with mTBI. Research design: A prospective follow-up study. Method and procedures: Fifty-three patients with mTBI were recruited in this study. The PCS was evaluated by the modified Checklist of Postconcussion Symptoms (mCPCS) at 1 month post injury. Twenty-five patients were evaluated again at 3 months after injuries. In addition, 53 healthy participants were also evaluated for the PCS, and 23 of them underwent a second evaluation at 2 months after the first one. Main outcomes and results: Patients with mTBI showed significantly higher PCS reporting at 1 month post injury than healthy participants did, but not at 3 months post injury. Consistent with the “good-old-days” bias, patients remarkably underestimated their preinjury PCS at 1 month post injury. Interestingly, our results further revealed that this response bias diminished more at 3 months than at 1 month after mTBI. Conclusions: This study thus might be the first one to prospectively reveal the progression of the “good-old-days” bias in patients with mTBI.     

Post-traumatic syndrome after minor head injury cannot be predicted by neurological investigations

The aim of this study is to investigate predictive factors of post-traumatic syndrome in children with minor head injury. Prospective neurological, electroencephalographic and psychological investigations were performed in 98 children aged 3-13 years within 24 h after the trauma and 4-6 weeks later. Inclusion criteria for mild head injury were unconsciousness <10 min or none at all, lack of overt neurological symptoms and other complications requiring intensive care. Twenty-six of the children had been unconscious for a short period. Ten had suffered a skull fracture. Within the first 24 h, nearly all children reported acute symptoms of concussion and 64 of 98 showed abnormal EEG findings. After 4-6 weeks, 23 of 98 still exhibited post-traumatic complaints with headache, fatigue, sleep disturbances, anxiety and affect instability. Such post-traumatic symptoms did not correlate with somatic, neurological or electroencephalographic findings observed immediately after the injury or at the follow-up investigation. As opposed to the situation in more severe head trauma, post-traumatic syndrome after minor head injury in children is apparently not due to central nervous injury detectable by neurological examination or electroencephalography. Irrespective of the necessity of neuroradiological investigations and repeated EEGs in more severe and complicated head trauma, we discourage the routine EEG examination in very slight head injury and instead rather recommend parent and patient counselling.     

Assessment of response bias in mild head injury: beyond malingering tests

The evaluation of response bias and malingering in the cases of mild head injury should not rely on a single test. Initial injury severity, typical neuropsychological test performance patterns, preexisting emotional stress or chronic social difficulties, history of previous neurological or psychiatric disorder, other system injuries sustained in the accident, preinjury alcohol abuse, and a propensity to attribute benign cognitive and somatic symptoms to a brain injury must be considered along with performances on specific measures of response bias. This article reviews empirically-supported tests and indices. Use of the likelihood ratio and other statistical indicators of diagnostic efficiency are demonstrated. Bayesian model averaging as a statistical technique to derive optimal prediction models is performed with a clinical data set.     

Assessment of Response Bias in Mild Head Injury: Beyond Malingering Tests

The evaluation of response bias and malingering in the cases of mild head injury should not rely on a single test. Initial injury severity, typical neuropsychological test performance patterns, preexisting emotional stress or chronic social difficulties, history of previous neurological or psychiatric disorder, other system injuries sustained in the accident, preinjury alcohol abuse, and a propensity to attribute benign cognitive and somatic symptoms to a brain injury must be considered along with performances on specific measures of response bias. This article reviews empirically-supported tests and indices. Use of the likelihood ratio and other statistical indicators of diagnostic efficiency are demonstrated. Bayesian model averaging as a statistical technique to derive optimal prediction models is performed with a clinical data set.     

Neuropsychological testing following head injuries: prosopagnosia without visual field defect.

Assessment of residual cerebral dysfunction in the post-traumatic patient poses considerable problems particularly when the neurological examination yields minimal or equivocal findings. The clinical picture is frequently complicated by emotional disturbance not easily differentiated from "post-traumatic neurosis." This report describes such a patient whose disorder was elicidated by neuropsychological testing. Numerous studies have established the validity of neuropsychological tests particularly when they are interpreted by psychologists specifically trained in their use. These procedures are also useful in differentiating patients with neurologic complaints of a nonorganic etiology from patients with similar complaints secondary to confirmed brain lesions. Although the findings reported here pertain to a patient exhibiting a rare neurologic consequence of closed head injury, the methods employed are applicable to subtle behavioral manifestations of diverse etiologies. Neurophyshological findings in a patient unable to recognize faces of familiar persons (prosopagnosia) disclosed a severe impairment of visual perception despite intact visual acuity and fields. The prosopagnosia was also associated with a pervasive memory deficit without dementia. Our results challenge current concepts of prosopagnosia and support the need for neuropsychological evaluation of post-traumatic patients.     

Prospective validation of a proposal for diagnosis and management of patients attending the emergency department for mild head injury

BACKGROUND: In mild head injury, predictors to select patients for computed tomography (CT) and/or to plan proper management are needed. The strength of evidence of published recommendations is insufficient for current use. We assessed the diagnostic accuracy and the clinical validity of the proposal of the Neurotraumatology Committee of the World Federation of Neurosurgical Societies on mild head injury from an emergency department perspective. METHODS: In a three year period, 5578 adolescent and adult subjects were prospectively recruited and managed according to the proposed protocol. Outcome measures were: (a) any post-traumatic lesion; (b) need for neurosurgical intervention; (c) unfavourable outcome (death, permanent vegetative state or severe disability) after six months. The predictive value of a model based on five variables (Glasgow coma score, clinical findings, risk factors, neurological deficits, and skull fracture) was tested by logistic regression analysis. FINDINGS: At first CT evaluation 327 patients (5.9%) had intracranial post-traumatic lesions. In 16 cases (0.3%) previously undiagnosed lesions were detected after re-evaluation within seven days. Neurosurgical intervention was needed in 71 patients (1.3%) and an unfavourable outcome occurred in 39 cases (0.7%). The area under the ROC curve of the variables in predicting post-traumatic lesions was 0.906 (0.009) (sensitivity 70.0%, specificity 94.1% at best cut off), neurosurgical intervention was 0.926 (0.016) (sensitivity 81.7%, specificity 94.1%), and unfavourable outcome was 0.953 (0.014) (sensitivity 88.1%, specificity 95.1%). INTERPRETATION: The variables prove highly accurate in the prediction of clinically meaningful outcomes, when applied to a consecutive set of patients with mild head injury in the clinical setting of a 1st level emergency department.     

The role of mitochondrial transition pore, and its modulation, in traumatic brain injury and delayed neurodegeneration after TBI

Following severe traumatic brain injury (TBI), a complex interplay of pathomechanism, such as exitotoxicity, oxidative stress, inflammatory events, and mitochondrial dysfunction occurs. This leads to a cascade of neuronal and axonal pathologies, which ultimately lead to axonal failure, neuronal energy metabolic failure, and neuronal death, which in turn determine patient outcome. For mild and moderate TBI, the pathomechanism is similar but much less frequent and ischemic cell death is unusual, except with mass lesions. Involvement of mitochondria in acute post-traumatic neurodegeneration has been extensively studied during the last decade, and there are a number of investigations implicating the activation of the mitochondrial permeability transition pore (mPTP) as a “critical switch” which determines cell survival after TBI. Opening of the mPTP is modulated by several factors occurring after a severe brain injury. Modern neuroprotective strategies for prevention of the neuropathological squeal of traumatic brain injury have now begun to address the issue of mitochondrial dysfunction, and drugs that protect mitochondrial viability and prevent apoptotic cascade induced by mPTP opening are about to begin phase II and III clinical trials. Cyclosporin A, which has been reported to block the opening of mPTP, showed a significant decrease in mitochondrial damage and intra-axonal cytoskeletal destruction thereby protecting the axonal shaft and blunting axotomy. This review addresses an important issue of mPT activation after severe head injury, its role in acute post-traumatic neurodegeneration, and the rationale for targeting the mPTP in experimental and clinical TBI studies.     

The management of immediate post-traumatic seizures in children following minor head injury – time for a multicentre study?

BACKGROUND: Children have a much lower threshold for seizure activity than adults. Consequently, an immediate post-traumatic seizure in a child following a minor head injury does not have the same potentially serious implications as one in an adult. METHODS: The records of children admitted with a post-traumatic fit occurring within 24 h of a minor head injury and with a normal CT scan of the brain on admission were critically reviewed. Those with previous neurological disorders, especially fits (excepting febrile convulsions), or systemic injuries requiring admission to an intensive care unit were excluded. RESULTS: There were 13 children who were not intubated and ventilated, forming the control group, and 13 children who were intubated and ventilated and formed the study group. All the children in both these groups made a good recovery, and none of them had any neurological deficit either at discharge or at follow-up. CONCLUSION: The clinical data suggest that children with immediate post-traumatic seizures following a minor head injury whose CT scan shows no major intracranial abnormalities and who have no prior history of neurological disease are at low risk of developing recurrent seizures or neurological complications and can be safely managed without recourse to intubation and ventilation.     

Inhibition of endoplasmic reticulum stress alleviates secondary injury after traumatic brain injury

Apoptosis after traumatic brain injury has been shown to be a major factor influencing prognosis and outcome. Endoplasmic reticulum stress may be involved in mitochondrial mediated neuronal apoptosis. Therefore, endoplasmic reticulum stress has become an important mechanism of secondary injury after traumatic brain injury. In this study, a rat model of traumatic brain injury was established by lateral fluid percussion injury. Fluorescence assays were used to measure reactive oxygen species content in the cerebral cortex. Western blot assays were used to determine expression of endoplasmic reticulum stress-related proteins. Hematoxylin-eosin staining was used to detect pathological changes in the cerebral cortex. Transmission electron microscopy was used to measure ultrastructural changes in the endoplasmic reticulum and mitochondria. Our results showed activation of the endoplasmic reticulum stress-related unfolded protein response. Meanwhile, both the endoplasmic reticulum stress response and mitochondrial apoptotic pathway were activated at different stages post-traumatic brain injury. Furthermore, pretreatment with the endoplasmic reticulum stress inhibitor, salubrinal(1 mg/kg), by intraperitoneal injection 30 minutes before injury significantly inhibited the endoplasmic reticulum stress response and reduced apoptosis. Moreover, salubrinal promoted recovery of mitochondrial function and inhibited activation of the mitochondrial apoptotic pathway post-traumatic brain injury. These results suggest that endoplasmic reticulum stress might be a key factor for secondary brain injury post-traumatic brain injury.     

The use of mild hypothermia for patients with severe vasospasm: a preliminary report.

The purpose of this study was to determine the effect of mild hypothermia on cerebral ischaemia due to severe vasospasm, which was refractory to medical and intravascular treatments and to assess the brain protection of this treatment in patients who underwent delayed aneurysm clipping after presenting with ischaemic neurological deficits. Mild hypothermia (32-34 degrees C of brain temperature) was employed in two groups: (1) Patients (Hunt and Kosnik grades I to II) who showed progressive neurological deficits due to vasospasm and did not respond to conventional therapy (Group 1) and (2) Patients who received delayed aneurysm clipping after presenting with ischaemic neurological deficits due to vasospasm (Group 2). Seven of 8 patients in both Groups showed a favorable outcome with mild hypothermia (good recovery in 5 and moderate disability in two patients). Mild hypothermia is considered to be effective on critical cerebral ischaemia due to vasospasm even after failure to response the conventional therapies and to provide brain protection in delayed aneurysm clipping.     

Workers' risk of unemployment after traumatic brain injury: a normed comparison.

We examined, among those persons working preinjury, the risk of unemployment 1 year after traumatic brain injury (TBI) relative to expected risk of unemployment for the sample under a validated risk-adjusted econometric model of employment in the U.S. population. Results indicate that 42% of TBI cases were unemployed versus 9% expected, relative risk (RR) = 4.5, 95% confidence interval (CI) (4.12, 4.95). The relative risk for unemployment was higher among males, those with higher education, persons with more severe injuries, and more impaired early neuropsychological or functional status. Difference in unemployment rates gave similar results for gender, severity of injury, and early neuropsychological and functional status. However, for education, the excess was smaller among those more highly educated, but the unemployment rate in the more highly educated in the general population was sufficiently small to yield a larger relative risk. In conclusion, after accounting for underlying risk of unemployment in the general population, unemployment is substantially higher after TBI for people who were employed when they were injured. The differential employment status varies depending on demographics, severity of brain injury, early functional outcome, and neurobehavioral indicators. For characteristics such as education, associated with rates of unemployment in the general population, different methods used to compare the rates may yield different results.     

颅脑损伤患者术后创伤后成长与创伤后应激障碍的相关性

目的观察颅脑损伤患者术后创伤后成长水平及创伤后应激障碍(PTSD)情况,分析创伤后成长水平与PTSD的关系。方法选取2017-02—2019-02郑州市第九人民医院手术治疗的63例颅脑损伤患者,所有患者术后1个月接受创伤后成长评定量表(PTGI)评估,依据评估结果分为高水平组与低水平组,调查2组一般资料并评估患者术后PTSD评分,分析颅脑损伤患者术后PTSD与创伤后成长水平较低的关系。结果63例颅脑损伤患者经外科手术治疗后,创伤后成长低水平患者43例(68.25%)。不同创伤后成长水平的颅脑损伤患者年龄、性别、婚姻、职业、家庭月收入、发病原因、疾病类型、居住环境情况比较差异无统计学意义(P>0.05);低水平患者受教育年限(<12 a)、PTSD评分高于高水平患者,差异有统计学意义(P<0.05)。相关性分析显示,颅脑损伤患者术后创伤后成长与PTSD间呈负相关(r<0,P<0.05)。经单项Logistic回归分析,建立多元回归模型,在在校正各基线资料带来的影响后,结果显示受教育年限(<12 a)、PTSD可能是颅脑损伤患者术后创伤后成长水平低下的影响因素(OR>1,P<0.05)。结论颅脑损伤患者术后创伤后应激水平偏低,可能与PTSD有关,未来可考虑通过颅脑损伤术后早期评估患者是否伴有PTSD指导干预,可能对提高患者创伤后成长水平有积极意义。     

Vomiting in children following head injury

The criteria for hospital admission of children who have suffered a minor head injury are highly subjective. Often the presence of post-traumatic emesis becomes an influential factor, but the mechanisms that trigger emesis following minor head injuries are not known. From a prospective study of 96 consecutive children with their first mild head injury (GCS 13–15) and a retrospective study of 29 consecutive more seriously injured children (GCS 8–12), we conclude that post-traumatic emesis is more common: (1) following minor head injuries than following more severe head injuries (P<0.05); (2) in children over 2 years old; (P<0.001); (3) in children injured within an hour of a meal or snack (p<0.001). The presence of a skull fracture or the site of the impact does not influence the incidence or duration of post-traumatic emesis. Retching and vomiting generally subside within 3 h in children injured within an hour of a meal or snack. When vomiting appears in children injured more than an hour after a meal or a snack, it may be quite protracted (mean=7.5 h). Children over 2 years of age with post-traumatic emesis who are neurologically stable following a mild head injury that occurred within an hour of a meal or snack can be expected to improve quickly. Their counterparts injured more than an hour after a meal or snack are likely to remain distressed much longer and are best admitted to hospital.     

Release of biochemical markers of damage to neuronal and glial brain tissue is associated with short and long term neuropsychological outcome after traumatic brain injury

OBJECTIVES: The present study aimed at the analysis of release patterns of neurobiochemical markers of brain damage (neuron specific enolase (NSE) and protein S-100B) in patients with traumatic brain injury and their predictive value with respect to the short and long term neuropsychological outcome. METHODS: Serial NSE and S-100B concentrations were analysed in blood samples taken at the first, second, and third day after traumatic brain injury. In 69 patients who fulfilled the inclusion criteria (no history of neurological or psychiatric disorder or alcohol or drug dependency, blood sampling according to the scheduled time scale, aged between 16 and 65 years) standardised neurological examinations and qualitative and quantitative evaluation of CT were performed. Comprehensive neuropsychological assessment was performed in 39 subjects 2 weeks after admission and in 29 subjects at a 6 month follow up examination. RESULTS: Most patients presented with minor head injuries (GCS>/=13) at the time of admission. Six months later most patients were fully independent in activities of daily living. Two thirds of the patients, however, still had neuropsychological dysfunction. Patients with short and long term neuropsychological disorders had significantly higher NSE and S-100B serum concentrations and a significantly longer lasting release of both markers. A comparative analysis of the predictive value of clinical, neuroradiological, and biochemical data showed initial S-100B values above 140 ng/l to have the highest predictive power. CONCLUSIONS: The analysis of post-traumatic release patterns of neurobiochemical markers of brain damage might help to identify patients with traumatic brain injury who run a risk of long term neuropsychological dysfunction.     

Concussive convulsions: seizure or no seizure?

Convulsions following traumatic brain injury (TBI) represent a diagnostic and therapeutic challenge. They can be differentiated into late (> 7 days after TBI), early (1 - 7 days after TBI), immediate (within the first 24 h after TBI), and impact seizures (within seconds after TBI). Some authors suggest that most impact seizures are non-epileptic in origin and hence coined the term "concussive convulsions" for benign impact seizures. Early and late post-traumatic seizures frequently indicate structural brain damage and transition to chronic, post-traumatic epilepsy. The data for impact seizures or concussive convulsions is less clear: only a small percentage of impact seizures is associated with structural brain damage and the development of post-traumatic epilepsy, rather the majority of cases are benign and associated with an excellent prognosis. Here, we present a case report as a starting point for pathophysiological and clinical considerations regarding convulsions that start within seconds after TBI.     

Long-term outcome of head injuries: a 23 year follow up study of children with head injuries.

The purpose of the 23 year follow up study was to determine the relationship between trauma variables including measures of head injury and very long-term sequelae. The study included 159 individuals with a mean age 31.40 years, of whom approximately 90% were admitted to hospital with a mild head injury during childhood (mean age 7.96). Extent of head injury was determined by unconsciousness, neurological status, skull fracture, EEG, post-traumatic seizures and a composite measure. The composite measure of neurological variables was the best predictor of long-term outcome. In addition, IQ recorded in the post-acute phase was a reliable predictor of long-term outcome. Of the sample, 32.7% reported physical complaints and 17.6% reported current psychological/psychiatric problems unrelated to the head injury. Subjective sequelae (physical, intellectual and emotional) specified as due to the head injury were reported by 31% of the sample, and the sequelae were found to be related to the extent of the head injury and initial IQ. There were no discernible relationships between attribute variables including premorbid status and age with subjective sequelae. There were, however, significant relationships between subjective sequelae and objective, psychosocial measures of adaptation including educational lag, unemployment, current psychological/psychiatric problems and relationships with family members. Finally, there appeared to be continuity of complaints elicited during the five year follow up of the original project and current sequelae. The severity of the head injury was identified as the primary contributory factor in the reconstitution process and in the prediction of long term outcomes.     

The risks of epilepsy after traumatic brain injury.

The aim of this study is to present the incidence of traumatic brain injury (TBI) and identify those characteristics of brain injuries that are associated with the development of seizures. We identified 5984 episodes of TBI (loss of consciousness, post-traumatic amnesia, or skull fracture) in Olmsted County, Minnesota, from 1935 to 1984. Of these, 4541 were followed for seizure. Injuries were classified as mild (loss of consciousness or amnesia less than 30 minutes), moderate (loss of consciousness 30 minutes to 1 day or a skull fracture), or severe (loss of consciousness of more than 1 day, subdural hematoma, or brain contusion). The incidence of TBI in the period from 1975 to 84 peaked at 800 per 100 000 in males aged 15-24. The relative risk of seizures was 1.5 (95 percent confidence interval 1.0-2.2) after mild injuries, but with no increase after 5 years; 2.9 (95 percent confidence interval 1.9-4.1) after moderate injuries; and 17.2 (95 percent confidence interval 12.3-23.6) after severe injuries. Significant risk factors were brain contusion with subdural hematoma, skull fracture, loss of consciousness or amnesia of 1 day or more, and age over 65 years. We conclude that TBI is a major public health problem and contributes to the occurrence of seizures and epilepsy.     

Erythropoietin protects from post-traumatic edema in the rat brain.

Erythropoietin (Epo) is gaining interest in various neurological insults as a possible neuroprotective agent. We determined the effects of recombinant human Epo (rhEpo, 5000 IU per kg bw) on brain edema induced in rats by traumatic brain injury (TBI; impact-acceleration model; rhEpo administration 30 mins after injury). Magnetic resonance imaging (MRI) and a gravimetric technique were applied. In the MRI experiments, the apparent diffusion coefficient (ADC) and the tissue T(1) relaxation time were measured hourly in the neocortex and caudoputamen, during a 6 h time span after TBI. In the gravimetric experiments, brain water content (BWC) was determined in these two regions, 6 h after TBI. Apparent diffusion coefficient measurements showed that rhEpo decreased brain edema early and durably. Gravimetric measurements showed that rhEpo decreased BWC at H(6) in the neocortex as well as in the caudoputamen. No significant differences in ADC, in T(1), or in BWC were found between rhEpo treated-TBI rats and sham-operated rats. Our findings show that post-traumatic administration of rhEpo can significantly reduce the development of brain edema in a model of diffuse TBI. Further studies should be conducted to identify the biochemical mechanisms involved in these immediate effects and to assess the use of rhEpo as a possible therapy for post-traumatic brain edema.