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In this placebo-controlled trial of patients in a vegetative or minimally conscious state, amantadine accelerated functional recovery. Recovery slowed after amantadine was discontinued, and functional outcomes at 6 weeks were similar in the amantadine and placebo groups. Severe traumatic brain injury is a catastrophic event that frequently has devastating familial, economic, and societal consequences. Traumatic brain injury is the most common cause of death and disability in persons between 15 and 30 years of age. 1 The most severe injuries can result in prolonged disorders of consciousness. Approximately 10 to 15% of patients with severe traumatic brain injury are discharged from acute care in a vegetative state, 2 a condition in which there is wakefulness without behavioral evidence of conscious awareness. 3 The estimated prevalence of a minimally conscious state, 4 which is distinguished from a vegetative state by the presence . . .

Actinic keratosis is a common precursor to squamous-cell carcinoma. Several topical treatments are effective but require weeks of application. In four randomized trials, topical treatment with ingenol mebutate for 2 to 3 days was effective in clearing actinic keratoses. Actinic keratoses are premalignant lesions that are common in light-skinned populations worldwide. 1 In the United States, the most common form of lesion-directed therapy for actinic keratoses is cryosurgery, although other locally ablative therapies are used. 2 In addition to potential scarring, recurrence rates are high with some of these treatment approaches. 3 Other treatments for actinic keratosis are applied to an entire field of sun-damaged skin, and many studies have shown the emergence of clinically visible actinic keratoses after application. These treatments include imiquimod, fluorouracil, diclofenac, and photodynamic therapy. 1 Drawbacks to the self-applied topical field therapies currently available include a long duration . . .

In this phase 3 trial, progesterone had no benefit as a neuroprotective agent in patients with blunt traumatic brain injury. Together with a second negative clinical trial of progesterone for acute TBI (SYNAPSE), the findings provide no support for this therapeutic approach. More than 2.4 million emergency department visits, hospitalizations, or deaths are related to traumatic brain injury (TBI) annually, and approximately 5.3 million Americans are living with disability from TBI. The aggregate annual cost of TBI in the United States now approaches $76.5 billion. 1 Survivors of severe TBI typically require 5 to 10 years of intensive therapy and are often left with substantial disability. 2 Despite decades of research, no pharmacologic agent has been shown to improve outcomes after TBI. Progesterone is a potent neurosteroid synthesized in the central nervous system. Preclinical studies in laboratory animals indicated that the early administration of . . .

Although animal models and early-phase clinical trials suggested that progesterone had beneficial effects in severe traumatic brain injury, this phase 3 clinical trial showed no benefit of progesterone as a neuroprotective agent for this condition. Traumatic brain injury (TBI) is a major cause of death and disability, with large direct and indirect costs to society. In the United States, more than 1.7 million persons have a TBI annually, 1 and the annual burden of TBI has been estimated at more than $76 billion. 2 Globally, the incidence of TBI is increasing, particularly in developing countries. 3 Although in recent years there has been a heightened interest in mild TBI and concussion, the problem of more severe TBI remains substantial, despite improvements in trauma systems and critical care. Mortality rates of approximately 40% have been reported in a review . . .

In this randomized trial involving 324 patients with severe traumatic brain injury in Bolivia and Ecuador, guideline-based management with intracranial pressure monitoring was not superior to management based on imaging and clinical assessments. Although the monitoring of intracranial pressure is widely recognized as standard care for patients with severe traumatic brain injury, its use in guiding therapy has incomplete acceptance, even in high-income countries. 1 – 3 Successive editions of the guidelines for the management of severe traumatic brain injury 4 – 7 have documented the inadequate evidence of efficacy, calling for randomized, controlled trials while also noting the ethical issues that would be posed if the control group consisted of patients who did not undergo monitoring. The identification of a group of intensivists in Latin America who routinely managed severe traumatic brain injury without using available . . .

There is limited regeneration of lost tissue after central nervous system injury, and the lesion is sealed with a scar. The role of the scar, which often is referred to as the glial scar because of its abundance of astrocytes, is complex and has been discussed for more than a century. Here we show that a specific pericyte subtype gives rise to scar-forming stromal cells, which outnumber astrocytes, in the injured spinal cord. Blocking the generation of progeny by this pericyte subtype results in failure to seal the injured tissue. The formation of connective tissue is common to many injuries and pathologies, and here we demonstrate a cellular origin of fibrosis.

The zebrafish regenerates its brain after injury and hence is a useful model organism to study the mechanisms enabling regenerative neurogenesis, which is poorly manifested in mammals. Yet the signaling mechanisms initiating such a regenerative response in fish are unknown. Using cerebroventricular microinjection of immunogenic particles and immunosuppression assays, we showed that inflammation is required and sufficient for enhancing the proliferation of neural progenitors and subsequent neurogenesis by activating injury-induced molecular programs that can be observed after traumatic brain injury. We also identified cysteinyl leukotriene signaling as an essential component of inflammation in the regenerative process of the adult zebrafish brain. Thus, our results demonstrate that in zebrafish, in contrast to mammals, inflammation is a positive regulator of neuronal regeneration in the central nervous system.

Patients with severe traumatic brain injury and refractory intracranial hypertension were randomly assigned to either decompressive craniectomy or standard care. Craniectomy was associated with a significant reduction in intracranial pressure but worse outcomes. Among patients who are hospitalized with severe traumatic brain injury, 60% either die or survive with severe disability. 1 – 3 Of Australia's population of 22 million, 4 approximately 1000 patients annually sustain a severe traumatic brain injury, with associated lifetime costs estimated at $1 billion. 5 In the United States, the annual burden of traumatic brain injury is more than $60 billion. 6 After severe traumatic brain injury, medical and surgical therapies are performed to minimize secondary brain injury. 7 – 9 Increased intracranial pressure, which is typically caused by cerebral edema, is an important secondary insult. 7 , 9 , 10 Although few data regarding the monitoring of . . .

Motion sickness is a complex syndrome that includes many features besides nausea and vomiting. This review describes some of these factors and points out that under normal circumstances, many cases of motion sickness go unrecognized. Motion sickness can occur during exposure to physical motion, visual motion, and virtual motion, and only those without a functioning vestibular system are fully immune. The range of vulnerability in the normal population varies about 10,000 to 1. Sleep deprivation can also enhance susceptibility. Systematic studies conducted in parabolic flight have identified velocity storage of semicircular canal signals—velocity integration—as being a key factor in both space motion sickness and terrestrial motion sickness. Adaptation procedures that have been developed to increase resistance to motion sickness reduce this time constant. A fully adequate theory of motion sickness is not presently available. Limitations of two popular theories, the evolutionary and the ecological, are described. A sensory conflict theory can explain many but not all aspects of motion sickness elicitation. However, extending the theory to include conflicts related to visceral afferent feedback elicited by voluntary and passive body motion greatly expands its explanatory range. Future goals should include determining why some conflicts are provocative and others are not but instead lead to perceptual reinterpretations of ongoing body motion. The contribution of visceral afferents in relation to vestibular and cerebellar signals in evoking sickness also deserves further exploration. Substantial progress is being made in identifying the physiological mechanisms underlying the evocation of nausea, vomiting, and anxiety, and a comprehensive understanding of motion sickness may soon be attainable. Adequate anti-motion sickness drugs without adverse side effects are not yet available.

Disruption of the blood–brain barrier (BBB) has an important part in cellular damage in neurological diseases, including acute and chronic cerebral ischemia, brain trauma, multiple sclerosis, brain tumors, and brain infections. The neurovascular unit (NVU) forms the interface between the blood and brain tissues. During an injury, the cascade of molecular events ends in the final common pathway for BBB disruption by free radicals and proteases, which attack membranes and degrade the tight junction proteins in endothelial cells. Free radicals of oxygen and nitrogen and the proteases, matrix metalloproteinases and cyclooxgyenases, are important in the early and delayed BBB disruption as the neuroinflammatory response progresses. Opening of the BBB occurs in neurodegenerative diseases and contributes to the cognitive changes. In addition to the importance of the NVU in acute injury, angiogenesis contributes to the recovery process. The challenges to treatment of the brain diseases involve not only facilitating drug entry into the brain, but also understanding the timing of the molecular cascades to block the early NVU injury without interfering with recovery. This review will describe the molecular and cellular events associated with NVU disruption and potential strategies directed toward restoring its integrity.