Handbook of clinical neurology
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The central autonomic nervous system (CAN) is a multifaceted, richly connected neural network incorporating the hypothalamus, its descending tracts through the brainstem, the insular cortex and down into the spinal cord. All levels of the CAN are susceptible to injury following traumatic brain injury (TBI), whether from focal or diffuse injury. ⋯ Subarachnoid hemorrhage (SAH), a common complication following TBI, also has predictable effects on autonomic control that can be understood with reference to spontaneous SAH literature. Finally, paroxysmal sympathetic hyperactivity (PSH), a syndrome incorporating episodes of heightened sympathetic drive and motor overactivity following minor stimulation, is discussed as an example of what happens when central inhibitory control of spinal cord autonomics is impaired.
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Over the past 20 years or so, functional magnetic resonance imaging (fMRI) has proven to be an influential tool for measuring perceptual and cognitive processing non-invasively in the human brain. This article provides a brief yet comprehensive overview of this dominant method for human auditory neuroscience, providing the reader with knowledge about the practicalities of using this technique to assess central auditory coding. ⋯ The future utility of fMRI and anticipated technical developments is also briefly evaluated. Throughout the review, key concepts are illustrated using specific author examples, with particular emphasis on fMRI findings that address questions pertaining to basic sound coding (such as frequency and pitch).
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In the past, direct physical evidence of mild traumatic brain injury (mTBI) from explosive blast has been difficult to obtain through conventional imaging modalities such as T1- and T2-weighted magnetic resonance imaging (MRI) and computed tomography (CT). Here, we review current progress in detecting evidence of brain injury from explosive blast using advanced imaging, including diffusion tensor imaging (DTI), functional MRI (fMRI), and the metabolic imaging methods such as positron emission tomography (PET) and magnetic resonance spectroscopic imaging (MRSI), where each targets different aspects of the pathology involved in mTBI. ⋯ Additionally, although used less frequently for conventional mTBI, PET has the potential to characterize a variety of neurotransmitter systems using target agents and will undoubtedly play a larger role, once the basic mechanisms of injury are better understood and techniques to identify the injury are more common. Finally, our MRSI imaging studies, although acquired at much lower spatial resolution, have demonstrated selectivity to different metabolic and physiologic processes, uncovering some of the most profound differences on an individual by individual basis, suggesting the potential for utility in the management of individual patients.
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Explosive blast shock waves and blunt impact to the head are two types of loading shown to result in mild traumatic brain injury (mTBI). While mTBI from these two causes shares some common features behaviorally, there are distinct differences in the pathophysiology of the underlying injury mechanisms. Various elucidations have been offered in the literature to explain the organic damage associated with mTBI resulting from both types of loading. ⋯ Explosive blast studies in large animal models show a unique pattern of periventricular injury, which is different from the classic diffuse axonal injury. Both astrocyte and microglial activation are also seen in explosive blast as well as impact trauma, but this may be a general secondary brain injury response, nonspecific to explosive blast or blunt trauma. Additionally, while moderate to severe impact closed head injuries sometimes result in petechial hemorrhages or hematomas, they do not appear to be associated with explosive blast mTBI even with repeated exposure to blasts.
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Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Despite extensive preclinical research supporting the effectiveness of neuroprotective therapies for brain trauma, there have been no successful randomized controlled clinical trials to date. TBI results in delayed secondary tissue injury due to neurochemical, metabolic and cellular changes; modulating such effects has provided the basis for neuroprotective interventions. ⋯ We discuss the concept of utilizing multipotential drugs that target multiple secondary injury pathways, rather than more specific "laser"-targeted strategies that have uniformly failed in clinical trials. Moreover, we assess data supporting use of neuroprotective drugs that are currently being evaluated in human clinical trials for TBI, as well as promising emerging experimental multipotential drug treatment strategies. Finally, we describe key challenges and provide suggestions to improve the likelihood of successful clinical translation.