Manifestations Of Traumatic Brain Injury Research Articles

Mesenchymal Stem Cell Therapy: A Potential Treatment Targeting Pathological Manifestations of Traumatic Brain Injury

Traumatic brain injury (TBI) makes up a large proportion of acute brain injuries and is a major cause of disability globally. Its complicated etiology and pathogenesis mainly include primary injury and secondary injury over time, which can cause cognitive deficits, physical disabilities, mood changes, and impaired verbal communication. Recently, mesenchymal stromal cell- (MSC-) based therapy has shown significant therapeutic potential to target TBI-induced pathological processes, such as oxidative stress, neuroinflammation, apoptosis, and mitochondrial dysfunction. In this review, we discuss the main pathological processes of TBI and summarize the underlying mechanisms of MSC-based TBI treatment. We also discuss research progress in the field of MSC therapy in TBI as well as major shortcomings and the great potential shown.

Cerebral Microbleeds and Structural White Matter Integrity in Patients With Traumatic Brain Injury-A Diffusion Tensor Imaging Study.

Diffuse axonal injury (DAI) is a common neuropathological manifestation of traumatic brain injury (TBI), presenting as traumatic alterations in the cerebral white matter (WM) microstructure and often leading to long-term neurocognitive impairment. These WM alterations can be assessed using diffusion tensor imaging (DTI). Cerebral microbleeds (CMBs) are a common finding on head imaging in TBI and are often considered a visible sign of DAI, although they represent diffuse vascular injury. It is poorly known how they associate with long-term white matter integrity. This study included 20 patients with TBI and CMBs, 34 patients with TBI without CMBs, and 11 controls with orthopedic injuries. DTI was used to assess microstructural WM alterations. CMBs were detected using susceptibility-weighted imaging (SWI) and graded according to their location in the WM and total lesion load was counted. Patients underwent SWI within 2 months after injury. DTI and clinical outcome assessment were performed at an average of eight months after injury. Outcome was assessed using the extended Glasgow Outcome Scale (GOSe). The Glasgow Coma Scale (GCS) and length of post-traumatic amnesia (PTA) were used to assess clinical severity of the injury. We found that CMB grading and total lesion load were negatively associated with fractional anisotropy (FA) and positively associated with mean diffusivity (MD). Patients with TBI and CMBs had decreased FA and increased MD compared with patients with TBI without CMBs. CMBs were also associated with worse clinical outcome. When adjusting for the clinical severity of the injury, none of the mentioned associations were found. Thus, the difference in FA and MD is explained by patients with TBI and CMBs having more severe injuries. Our results suggest that CMBs are not associated with greater WM alterations when adjusting for the clinical severity of TBI. Thus, CMBs and WM alterations may not be strongly associated pathologies in TBI.

Afferent Visual Manifestations of Traumatic Brain Injury

Traumatic brain injury (TBI) causes structural and functional damage to the central nervous system including the visual pathway. Defects in the afferent visual pathways affect visual function and in severe cases cause complete visual loss. Visual dysfunction is detectable by structural and functional ophthalmic examinations that are routine in the eye clinic, including examination of the pupillary light reflex and optical coherence tomography (OCT). Assessment of pupillary light reflex is a non-invasive assessment combining afferent and efferent visual function. While a assessment using a flashlight is relatively insensitive, automated pupillometry has 95% specificity and 78.1% sensitivity in detecting TBI-related visual and cerebral dysfunction with an area under the curve of 0.69-0.78. OCT may also serve as a noninvasive biomarker of TBI severity, demonstrating changes in the retinal ganglion cell layer and nerve fiber layer throughout the range of TBI severity even in the absence of visual symptoms. This review discusses the impact of TBI on visual structure and function.

What determines a good outcome from traumatic brain injury

Cognitive impairments are the principal clinical manifestations of traumatic brain injury (TBI) from injury onset throughout the early and late post-injury periods. The functional effects of posttraumatic cognitive impairments and associated neuropsychiatric disturbances present substantial challenges to patients and their families and for clinicians providing their rehabilitative care. In this lecture, a neuropsychiatrically-informed approach to the evaluation and management of the cognitive and non-cognitive neuropsychiatric sequelae of TBI is offered, with the aim of improving TBI outcomes for affected individuals and their families. In the service of meeting that aim, the epidemiology and natural history of cognitive recovery after TBI is reviewed. The differential diagnosis of cognitive problems among people with TBI is considered within the context of acute traumatic encephalopathy, and expectations for long-term outcomes associated with mild versus moderate-to-severe TBI are described. The evidence base for pharmacologic and cognitive rehabilitative interventions for persons with persistent posttraumatic cognitive impairments then are considered and recommendations for evidence-informed treatments are offered.

“Broken Heart Syndrome” Cardiovascular Manifestations of Traumatic Brain Injury

Cardiovascular dysfunction frequently complicates outcomes of traumatic brain injury (TBI), resulting in higher morbidity and mortality. TBI results in dysfunctions of the autonomic nervous system (mediated by catecholamines), altered systemic circulation homeostasis medicated by neurogenic stimuli, electrocardiographic, echocardiographic abnormities, and change in serum cardiac enzyme levels (not attributed to primary cardiac pathology). The present review attempts to find cardiovascular alterations following TBI, management to these patients, and their outcome.

Assessing connectivity related injury burden in diffuse traumatic brain injury.

Many of the clinical and behavioral manifestations of traumatic brain injury (TBI) are thought to arise from disruption to the structural network of the brain due to diffuse axonal injury (DAI). However, a principled way of summarizing diffuse connectivity alterations to quantify injury burden is lacking. In this study, we developed a connectome injury score, Disruption Index of the Structural Connectome (DISC), which summarizes the cumulative effects of TBI-induced connectivity abnormalities across the entire brain. Forty patients with moderate-to-severe TBI examined at 3months postinjury and 35 uninjured healthy controls underwent magnetic resonance imaging with diffusion tensor imaging, and completed behavioral assessment including global clinical outcome measures and neuropsychological tests. TBI patients were selected to maximize the likelihood of DAI in the absence of large focal brain lesions. We found that hub-like regions, with high betweenness centrality, were most likely to be impaired as a result of diffuse TBI. Clustering of participants revealed a subgroup of TBI patients with similar connectivity abnormality profiles who exhibited relatively poor cognitive performance. Among TBI patients, DISC was significantly correlated with post-traumatic amnesia, verbal learning, executive function, and processing speed. Our experiments jointly demonstrated that assessing structural connectivity alterations may be useful in development of patient-oriented diagnostic and prognostic tools. Hum Brain Mapp 38:2913-2922, 2017. © 2017 Wiley Periodicals, Inc.

Role of bromocriptine in multi-spectral manifestations of traumatic brain injury

PurposeDespite the prevalence and cost of traumatic brain injury related disabilities, there is paucity in the literature on modern approaches to pharmacotherapy. Medications may promote recovery by enhancing some neurological functions without impacting others. Herein we discussed the role of bromocriptine in neurorehabilitation for patients with traumatic brain injury. MethodsA cohort comprising of 36 selective nonsurgical cases of traumatic brain injury in minimally conscious state were enrolled in the study. After hemodynamic stability, bromocriptine was given at paediatric dose of 3.75 mg/d and adult dose of 7.5 mg/d. It was administered through a naso-gastric (NG) feeding tube in the patients with minimally conscious state, then changed to oral route after proper swallowing and good gag reflex were ensured in the patient. The drug was slowly reduced over three weeks after neurological improvement in the patients. Positive result was determined by improved GCS score of 2 and motor power by at least 1 British Medical Council (BMC) motor score. Improvement of deficits was evaluated in terms of fluency of speech for aphasia, task switching, digit span double tasking and trail-making test for cognition and attention, and functional independence measure score for motor functioning and self-independence. ResultsAccelerated arousal was seen in 47.0% of cases (8/17) in 4–40 days. In 41.2% of cases (7/17), Glasgow outcome score (GOS) was improved to 4/5 in 90 days. Improvement in hemiparesis by at least 1 BMC score was seen in 55.6% of cases (5/9) in 40 days. Aphasia was improved in 80% of cases (4/5) in 7–30 days. Moderate improvement in cognitive impairment was seen in 66.7% of cases (2/3) in 14–20 days. Improvement in memory was observed in 50% of cases (1/2) in over 30 days. No cases were withdrawn from the study because of adverse reactions of the drug. There was no mortality in the study group. ConclusionBromocriptine improves neurological sequelae of traumatic brain injury as well as the overall outcome in the patients. If medication is given to promote recovery and treat its associated disabilities, clinicians should thoroughly outline the goals and closely monitor adverse effects.

Time of admission and outcome in traumatic brain injury patients

Introduction: In spite of heterogeneous manifestation of traumatic brain injury (TBI), it is affected by multiple factors at the time of admission. This pilot study aims to detect the effect of admission time, day, and month with outcome at discharge, among patients with TBI. Materials and Methods: It is a prospective study conducted in the Department of Neurosurgery at Narayana Medical Health Hospital, Nellore. The head injury patient data were documented on a standard proforma. FileMaker Pro Advanced 13 was used for electronic data entry interface. The analysis was done using Stats Direct version 3.0.150. The variables in categories and continuous were evaluated with descriptive and frequencies, respectively. Results: In the study, 337 head injury patients were reported with 7.12% (n = 24) mortality. The hospital discharge outcome was significant with age, gender, severity of injury, and seasons. More number of patients were admitted during 9 pm to 7 am, but was not significant. During all the seasons of a year, there was significance with admittance of head injury patients in working days of a week and patients' undergoing intracranial surgery. Conclusion: The pilot study reports that the outcome at discharge of a head injury patient has significance with admission at week, day, and season.

Simultaneous Multiple Extradural Hematomas

Objective Simultaneous multiple epidural hematomas (EDHs) are very rare and are associated with high mortality. The purpose of this study is to identify the clinical features, varying mechanisms that may be responsible for production of these hematomas, location of hematomas, and outcome of simultaneous multiple EDHs. Methods Our study consisted of 528 patients who were admitted in our emergency department with diagnosis of traumatic brain injury (TBI) over a period of 14 months from September 2012 to October 2013 and retrospective analysis of all cases with EDH, particularly those with simultaneous multiple EDHs was done. All the patients were carefully examined clinically, Glasgow Coma Scale (GCS) was noted, plain computed tomographic scan (CT scan) was done and managed accordingly. Results We came across six cases of multiple EDHs which accounted to 1.13% of all TBI. All of the cases except one were diagnosed within the first 6 hours. The GCS was used for neurological evaluations on admission and during hospital stay. A CT scan was done in all cases. Five patients underwent surgical intervention and one was managed conservatively. Two patients expired due to pre- and postoperative complications. Conclusion EDHs are serious manifestation of TBI, of which multiple EDHs are even worse. These are life-threatening conditions. Early recognition and treatment can save a precious life. Widespread use of CT scan leads to early diagnosis before deterioration of the neurological status and affects the outcome of surgery.

Chapter 14 - Systemic manifestations of traumatic brain injury

Traumatic brain injury (TBI) affects functioning of various organ systems in the absence of concomitant non-neurologic organ injury or systemic infection. The systemic manifestations of TBI can be mild or severe and can present in the acute phase or during the recovery phase. Non-neurologic organ dysfunction can manifest following mild TBI or severe TBI. The pathophysiology of systemic manifestations following TBI is multifactorial and involves an effect on the autonomic nervous system, involvement of the hypothalamic-pituitary axis, release of inflammatory mediators, and treatment modalities used for TBI. Endocrine dysfunction, electrolyte imbalance, and respiratory manifestations are common following TBI. The influence of TBI on systemic immune response, coagulation cascade, cardiovascular system, gastrointestinal system, and other systems is becoming more evident through animal studies and clinical trials. Systemic manifestations can independently act as risk factors for mortality and morbidity following TBI. Some conditions like neurogenic pulmonary edema and disseminated intravascular coagulation can adversely affect the outcome. Early recognition and treatment of systemic manifestations may improve the clinical outcome following TBI. Further studies are required especially in the field of neuroimmunology to establish the role of various biochemical cascades, not only in the pathophysiology of TBI but also in its systemic manifestations and outcome.

Magnetic resonance imaging of traumatic brain injury: a pictorial review.

Traumatic brain injury (TBI) is a significant source of major morbidity and mortality in blunt trauma patients. Computed tomography (CT) is the primary imaging modality of choice for patients with potential brain injury in the acute setting, with magnetic resonance imaging (MRI) playing a role in evaluating equivocal CT findings and may help with determining long-term prognosis and recovery. MRI is being utilized more commonly in the acute and subacute setting of TBI; therefore, radiologists should be familiar with the MRI appearance of the various manifestations of TBI. Here, we review the imaging of common intracranial injuries with illustrative cases comparing CT and MRI.

Head orientation affects the intracranial pressure response resulting from shock wave loading in the rat

Since an increasing number of returning military personnel are presenting with neurological manifestations of traumatic brain injury (TBI), there has been a great focus on the effects resulting from blast exposure. It is paramount to resolve the physical mechanism by which the critical stress is being inflicted on brain tissue from blast wave encounters with the head. This study quantitatively measured the effect of head orientation on intracranial pressure (ICP) of rats exposed to a shock wave. Furthermore, the study examined how skull maturity affects ICP response of animals exposed to shock waves at various orientations. Results showed a significant increase in ICP values in larger rats at any orientation. Furthermore, when side-ICP values were compared to the other orientations, the peak pressures were significantly lower suggesting a relation between ICP and orientation of the head due to geometry of the skull and location of sutures. This finding accentuates the importance of skull dynamics in explaining possible injury mechanisms during blast. Also, the rate of pressure change was measured and indicated that the rate was significantly higher when the top of the head was facing the shock front. The results confirm that the biomechanical response of the superior rat skull is distinctive compared to other areas of the skull, suggesting a skull flexure mechanism. These results not only present insights into the mechanism of brain injury, but also provide information which can be used for designing more effective protective head gear.

Addressing neuropsychiatric disturbances during rehabilitation after traumatic brain injury: current and future methods

Cognitive, emotional, behavioral, and sensorimotor disturbances are the principal clinical manifestations of traumatic brain injury (TBI) throughout the early postinjury period. These post-traumatic neuropsychiatric disturbances present substantial challenges to patients, their families, and clinicians providing their rehabilitative care, the optimal approaches to which remain incompletely developed. In this article, a neuropsychiatrically informed, neurobiologically anchored approach to understanding and meeting challenges is described. The foundation for that approach is laid, with a review of clinical case definitions of TBI and clarification of their intended referents. The differential diagnosis of event-related neuropsychiatric disturbances is considered next, after which the clinical and neurobiological heterogeneity within the diagnostic category of TBI are discussed. The clinical manifestations of biomechanical force-induced brain dysfunction are described as a state of post-traumatic encephalopathy (PTE) comprising several phenomenologically distinct stages. PTE is then used as a framework for understanding and clinically evaluating the neuropsychiatric sequelae of TBI encountered commonly during the early post-injury rehabilitation period, and for considering the types and timings of neurorehabilitative interventions. Finally, directions for future research that may address productively the challenges to TBI rehabilitation presented by neuropsychiatric disturbances are considered.

Simultaneous Measurement of Perceptual and Motor Cortical Potentials

Psychomotor slowing is a common manifestation of traumatic brain injury. Previous electrophysiological studies of traumatic brain injury have focused on abnormal attentional and perceptual responses to incoming stimuli. We hypothesize that traumatic brain injury is also associated with abnormal cortical components of motor execution. To test this hypothesis, we analyzed event-related potentials of 22 subjects (11 with a history of severe traumatic brain injury and 11 age-matched healthy subjects) during oddball discrimination tasks. In addition to the usual stimulus-locked averaging of electrophysiological data to reveal cognitive components, such as the P300, we also analyzed subjects' response-locked data to reveal motor potential waveforms. To focus on generalized effects across modality, analyses were performed on composite measures from both auditory and visual event-related potentials. (1) Traumatic brain injury subjects had abnormal P300 responses (with reduced amplitude and prolonged latency) in both sensory modalities. (2) Traumatic brain injury subjects' motor potential waveforms showed significantly reduced amplitude in both sensory modalities. (3) Abnormalities in P300 latency, amplitude, and motor potential amplitude (effect sizes = 1.2-1.5 SD) were greater than behavioral slowing, as measured by reaction times (0.7 SD). (4) P300 latency and motor potential amplitude together accounted for much of the reaction time prolongation (r = 0.73). This study demonstrates the value of concurrently analyzing stimulus-locked and response-locked event-related potential data to evaluate cortical components of perceptual and motor processing. The present findings indicate that patients with traumatic brain injury have impairments in both the perceptual interpretation of incoming stimuli and the execution of motor responses and that both abnormalities contribute to psychomotor slowing in patients with traumatic brain injury.

Partial Kluver-Bucy syndrome as a delayed manifestation of head injury

After traumatic brain injury (TBI), the most disabling problems are generally related to neuropsychiatric sequelae, including personality change and cognitive impairment, rather than neurophysical sequelae. Kluver-Bucy syndrome (KBS) is a rare neurobehavioral condition, first described in 1937 as an experimental neurobehavioral syndrome in monkeys with bitemporal brain lesions. The syndrome in man was subsequently observed to be transient or permanent in a variety of neurodegenerative disorders and after traumatic, nontraumatic and infectious brain injury. However, partial KBS may occur in the absence of the classic bilateral temporal lesion, though rare. Pharmacological treatment of post-TBI neuropsychiatric sequelae consists of symptomatic, functional and hypothetical approaches. Specific pharmacological treatment consists of antipsychotics, anti-kindling anticonvulsants or a combination thereof. A case of partial KBS presenting as delayed manifestation of traumatic brain injury that improved with carbamazapine and antipsychotics is presented.

Cross-Cultural Neuropsychological Assessment: Theory and Practice

Book ReviewsCross-Cultural Neuropsychological Assessment: Theory and PracticeEliane Miotto DrEliane Miotto DrSearch for more papers by this authorPublished OnlineNovember 17, 2006https://doi.org/10.1027//0269-8803.15.2.128PDFView Full Text ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinkedInReddit SectionsMoreFiguresReferencesRelatedDetailsCited byModelling difficulties in abstract thinking in psychosis: the importance of socio-developmental background22 December 2016 | Cognitive Neuropsychiatry, Vol. 22, No. 1 Volume 15Issue 2April 2001ISSN: 0269-8803eISSN: 2151-2124 tabs.informationJournal of Psychophysiology (2001), 15, pp. 128-129 https://doi.org/10.1027//0269-8803.15.2.128.© 2001The Federation of European Psychophysiology SocietiesPDF download