![]() ![]() The present study aims to investigate the expression of ORXA, that is more stable neurotransmitter, using immunohistochemical techniques in human hypothalamus after TBI. Īlthough the orexins A and B are neurotransmitters that have different functions, it was demonstrated that the orexin-B have lower stability in the CFS compared with orexin-A preferentially mediates shorter-durable effects. It is currently the gold standard in detecting traumatic axonal injury, as it is very sensitive, and a positive reaction is identifiable less than 2 h after traumatic brain injury,. Its functions include cell adhesion, growth, neuroprotection, and response to injury (promotion of axonal sprouting, synaptogenesis, neurite outgrowth). It is processed by the Golgi apparatus and carried along the axon by fast anterograde transport. Injury of the hypothalamus is common in patients with TBI and damage in the hypothalamic neurons may contribute to the coma, chronic sleepiness, and other disorders of arousal frequently seen after TBI.īeta-amyloid precursor protein (β-APP) is a transmembrane glycoprotein and a normal constituent of neuronal cells. Circadian oscillations in orexin-A within cerebrospinal fluid (CSF) correlate with arousal cycles and exogenous administration of orexin promotes wakefulness. Orexin-A is a neuropeptide expressed by neurons in the lateral hypothalamus that have extensive projections to other hypothalamic nuclei, the limbic system, thalamus, cortex, and spinal cord, exciting several monoaminergic and cholinergic woke-promoting systems. In addition, orexin neurons provide a link between energy homeostasis and vigilance states. Orexin neurons receive abundant input from limbic system and enhance arousal signal in this area. Hypocretin or orexin selectively increases dopaminerge neurotransmission within the prefrontal cortex and the shell subregion of the nucleus accumbens, which is also important in cognitive and affective process. They are synthesized by neurons situated within the caudal hypothalamus, which projects to the locus coeruleus and other nuclei involved in the regulation of sleep and wakefulness. Orexins, including orexin-A and orexin-B are two excitatory hypothalamic neuropeptides, which are implicated in narcolepsy. Previous evidence has indicated that the central orexinergic/ hypocretinergic system exhibit prominent arousal promoting actions. There are grown concerns about prevalence of sleep-woke disturbances among survivors of TBI that exacerbate the resulting long-term behavioral dysfunction. ![]() The arousal of a patient from coma is a priority in improving the functional outcome of the patient, reducing disability, and increasing quality of life. Ĭoma is a serious complication which can occur following TBI. ![]() It is characterized by two distinct types of axonal pathology: swelling or varicosities along the length of axons, and the presence of large terminal bulbs. DAI is a clinicopathological entity, clinically characterized by the immediate and prolonged unconsciousness after the mechanical impact to the head, typically without any lucid interval, leading to severe brain failure, vegetative state, and death and pathologically defined by the feature of the widespread and disseminated damage of axonal fibers inside the white brain matter, including the fiber tracts and the brainstem. Diffuse axonal injury (DAI), regarded as an integral process in all grades of traumatic brain injury, results typically from head rotational acceleration/deceleration, as well as the propagation of force through the brain following impact. Amongst the key component of TBI pathophysiology is traumatic axonal injury (TAI), commonly referred to as diffuse axonal injury (DAI). TBI is a common clinical condition with multiple causes that include traffic accidents, falls, gunshot wounds, sports, and combat-related events. TBI is defined as an alteration in brain function caused by an external force. Traumatic brain injury (TBI) is one of the major causes of death and disability for young people in the develop world. ![]()
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