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Recent studies have demonstrated that hypopituitarism, and in particular growth hormone (GH) deficiency, is common among survivors of traumatic brain injury (TBI) tested several months or years following head trauma. In addition, it has been shown that post-traumatic neuroendocrine abnormalities occur early and with high frequency. These findings may have significant implications for the recovery and rehabilitation of patients with TBI. Although data emerging after 2000 demonstrate the relevance of the problem, in general there is a lack of awareness in the medical community about the incidence and clinical repercussions of the pathology. Most, but not all, head trauma associated with hypopituitarism is the result of motor accidents. The subjects at risk are those who have suffered moderate-to severe head trauma although mild intensity trauma may precede hypopituitarism also. Particular attention should be paid to this problem in children and adolescents. Onset of pituitary deficits can evolve over years following injury. For the assessment of the GH-IGF axis in TBI patients, plasma IGF-I concentrations, plus dynamic GH testing is indicated. Some degree of hypopituitarism is found in 35-40% of TBI patients. Among multiple pituitary deficits, the most common ones were GHD and gonadotrophin deficiency. In most series 10-15% presented with severe GHD and 15% with partial GHD after stimulating GH secretion confirming that the most common isolated deficit is GHD. Psychometric evaluation together with neurocognitive testing shows variability of disability and the possibility that untreated TBI induced hypopituitarism contributes to the chronic neurobehavioral problems seen in many head-injured patients warrants consideration. Preliminary data, from small pilot, open-label studies show that subjects treated with GH experience significant improvements in concentration, memory, depression, anxiety and fatigue. In conclusion, pituitary failure can occur even in minor head injuries and is poorly recognized.
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PMID:Hypopituitarism following traumatic brain injury. 1593 80

Multiple sclerosis (MS) is the most common nontraumatic neurological condition of early and middle adulthood. Cognitive and neurobehavioral problems associated with this disorder are common. Approximately 50% of MS patients experience lifetime clinical depression, and at least 50% will experience significant cognitive difficulties. Fatigue is also extremely common and disabling in MS and appears to be associated with sleep problems and primary neurological features, in addition to secondary factors, including depression and pain. Quality of life is affected in MS by all of these factors and is an especially salient issue given that patients often live for many years following diagnosis. In this article, we explore the literature on cognitive and neurobehavioral features in MS, provide a commentary on the state of the literature and make suggestions for research directions over the next 5 years that would move the field forward significantly.
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PMID:Cognitive and neurobehavioral features in multiple sclerosis. 2137 46

Outcome of 295 rehabilitation patients with mild, moderate, and severe brain injury was investigated prospectively at five regional medical centers using the Neurobehavioral Rating Scale. Mean factor scale scores were generally low. with the cognition mean highest and the excitement mean lowest. Regardless of scale, the most significant neurobehavioral difficulties were related to memory, insight, attention, alertness, fatigue, and blunted affect. Conversely, problems rated as least severe included hallucinations, guilt, excitement and lability of mood. Approximately 9% of the sample had at least a moderate problem with agitation, an item on the excitement scale. The general pattern of mean factor scale elevations was consistent with other studies. No relationship was found between injury severity and neurobehavioral characteristics. The relatively low incidence of neurobehavioral problems may reflect recovery and effective interdisciplinary management.
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PMID:A multi-center investigation of neurobehavioral outcome after traumatic brain injury. 2452 40

Neuropsychiatric symptoms following traumatic brain injury (TBI) are common and contribute negatively to TBI outcomes by reducing overall quality of life. The development of neurobehavioral sequelae, such as concentration deficits, depression, anxiety, fatigue, and loss of emotional well-being has historically been attributed to an ambiguous "post-concussive syndrome," considered secondary to frank structural injury and axonal damage. However, recent research suggests that neuroendocrine dysfunction, specifically hypopituitarism, plays an important role in the etiology of these symptoms. This post-head trauma hypopituitarism (PHTH) has been shown in the past two decades to be a clinically prevalent phenomenon, and given the parallels between neuropsychiatric symptoms associated with non-TBI-induced hypopituitarism and those following TBI, it is now acknowledged that PHTH is likely a substantial contributor to these impairments. The current paper seeks to provide an overview of hypothesized pathophysiological mechanisms underlying neuroendocrine abnormalities after TBI, and to emphasize the significance of this phenomenon in the development of the neurobehavioral problems frequently seen after head trauma.
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PMID:Neuroendocrine Abnormalities Following Traumatic Brain Injury: An Important Contributor to Neuropsychiatric Sequelae. 2992 24