Handbook of clinical neurology
-
Mild traumatic brain injury (TBI) is common but accurate diagnosis and defining criteria for mild TBI and its clinical consequences have been problematic. Mild TBI causes transient neurophysiologic brain dysfunction, sometimes with structural axonal and neuronal damage. Biomarkers, such as newer imaging technologies and protein markers, are promising indicators of brain injury but are not ready for clinical use. ⋯ Effective early phase management may prevent or limit the later phase disorder and should include education about symptoms and expectations for recovery, as well as recommendations for activity modifications. Later phase treatment should be informed by thoughtful differential diagnosis and the multiplicity of premorbid and comorbid conditions that may influence symptoms. Treatment should incorporate a hierarchical, sequential approach to symptom management, prioritizing problems with significant functional impact and effective, available interventions (e.g., headache, depression, anxiety, insomnia, vertigo).
-
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.
-
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. ⋯ 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.
-
Traumatic brain injury (TBI) is an important cause of death and disability, particularly in younger populations. The prehospital evaluation and management of TBI is a vital link between insult and definitive care and can have dramatic implications for subsequent morbidity. Following a TBI the brain is at high risk for further ischemic injury, with prehospital interventions targeted at reducing this secondary injury while optimizing cerebral physiology. ⋯ We evaluate patient management strategies including indications for advanced airway management, oxygenation, ventilation, and fluid resuscitation, as well as prehospital strategies for the management of suspected or impending cerebral herniation including hyperventilation and brain-directed hyperosmolar therapy. Transport decisions including the role of triage models and trauma centers are discussed. Finally, future directions in the prehospital management of traumatic brain injury are explored.
-
Carbon monoxide (CO) is a colorless, odorless, nonirritant gas that accounts for numerous cases of CO poisoning every year from a variety of sources of incomplete combustion of hydrocarbons. These include poorly functioning heating systems, indoor propane-powered forklifts, indoor burning of charcoal burning briquettes, riding in the back of pick-up trucks, ice skating rinks using propane-powered resurfacing machines, and gasoline-powered generators that are not in correct locations. Once CO is inhaled it binds with hemoglobin to form carboxyhemoglobin (COHb) with an affinity 200 times greater than oxygen that leads to decreased oxygen-carrying capacity and decreased release of oxygen to tissues leading to tissue hypoxia. ⋯ Though not as common, toxic or ischemic peripheral neuropathies are associated with CO exposure in humans and animals. The cornerstone for treatment for CO poisoning is 100% oxygen using a tight-fitting mask for greater than 6 hours. The indications for treatment with hyperbaric oxygen to decrease the half-life of COHb remain controversial.