Lancet neurology
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The high prevalence of obesity is associated with an enormous medical, social, and economic burden. The metabolic dysfunction, dyslipidaemia, and inflammation caused by obesity contribute to the development of a wide variety of disorders and effects on the nervous system. In the CNS, mild cognitive impairment can be attributed to obesity-induced alterations in hippocampal structure and function in some patients. ⋯ In the peripheral nervous system, obesity-driven alterations in the autonomic nervous system prompt imbalances in sympathetic-parasympathetic activity, while alterations in the sensory-somatic nervous system underlie peripheral polyneuropathy, a common complication of diabetes. Pharmacotherapy and bariatric surgery are promising interventions for people with obesity that can improve neurological function. However, lifestyle interventions via dietary changes and exercise are the preferred approach to combat obesity and reduce its associated health risks.
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Severe traumatic brain injury (TBI) is currently managed in the intensive care unit with a combined medical-surgical approach. Treatment aims to prevent additional brain damage and to optimise conditions for brain recovery. ⋯ Targeted treatment is especially relevant for elderly people-who now represent an increasing proportion of patients with TBI-as preinjury comorbidities and their therapies demand tailored management strategies. Progress in monitoring and in understanding pathophysiological mechanisms of TBI could change current management in the intensive care unit, enabling targeted interventions that could ultimately improve outcomes.
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Review
Olfactory dysfunction in neurodegenerative diseases: is there a common pathological substrate?
In patients with neurodegenerative diseases, there is a spectrum of smell dysfunction ranging from severe loss, as seen in Alzheimer's disease and Parkinson's disease, to relatively little loss, as seen in progressive supranuclear palsy. Given the ubiquitous but varying degrees of olfactory dysfunction among such diseases, it is conceivable that differential disruption of a common primordial neuropathological substrate causes these differences in olfactory function. ⋯ Thus, a key question is whether damage to such a substrate is the basis for the perceptual differences in olfaction or whether disease-specific or other entities, such as respiratory infections or pollution, are responsible. In light of the early preclinical onset of smell deficits in many neurodegenerative diseases, the answer to this question might provide crucial insight into the cause of disease pathology at its earliest stages of development.