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It is the pairing diabetes symptoms forum 10 mg glucotrol xl overnight delivery, in time, of a meaningful relationship that produces the result. The internal mechanisms of the process are solidly established and involve several enzymes and genes. The production of the cellular proteins by this process forms the foundation for the results seen in the therapeutic program. Among these, the professions of physical and occupational therapy hold, as a major tenet, the developmental concepts in neurodevelopmental theory. Therefore, it is important that the process of restoration of function should follow the same sequences that occurred in development. The infant Aplysia is first capable of only habituation; then, with maturity, dishabituation occurs and, finally, sensitization. These sequential stages of learning confirm that learning is a process that builds on previously developed mechanisms and is not complete at birth. This understanding seen in the simple snail lends support to the foundation of some long-standing therapies of rehabilitation3,4 that suggest a hierarchy exists in the development of the individual, and successful therapy must be carried out in the same order. It is not so clear in the cognitive area in which we have only begun to investigate the cognitive functions with modern imaging techniques and cellular neurophysiological experiments. The literature on cognition is rich, indeed, and has provided a foundation of strategies that has been successfully incorporated into this synaptic enhancement can take different forms in different parts of the hippocampus. Recent research has shown that the hippocampus is a key component in early memory and in the final distribution of information to the multimodal association areas of the cerebral cortex. The left hippocampus seems to be involved with verbal memory, whereas the right hippocampus seems to be more involved with the representation of the environment and the ability to find our way in it. These memories of a specific task do not require conscious effort to recall or to reestablish. They require concentration and a focus on the task at hand but not the conscious effort of recall. Implicit memory is seen in the training of skilled movements and perceptual skills. In classical conditioning, there are two stimuli presented, which, after a series of associations with each other, begin to produce a new response. Cognitive scientists tell us that we are first able to describe objects using very simple descriptions of color, size, and shape. From this base, we can move to the descriptions of their usefulness and, eventually, to the features of the object, allowing use of the object for other extended purposes. The neural pathway for vision is known to have two parallel pathways that convey different types of information. The other pathway, the M pathway, is concerned with movement and depth perception or where the object is located.
Potential brain neuronal targets for amphetamine- diabetes diet in sri lanka safe glucotrol xl 10 mg, methylphenidate-, and modafinil-induced wakefulness, evidenced by c-fos immunocytochemistry in the cat. A short review of cognitive and functional neuroimaging studies of cholinergic drugs: Implications for therapeutic potentials. Attention and memory dysfunction after traumatic brain injury: Cholinergic mechanisms, sensory gating, and a hypothesis for further investigation. Cholinergic augmentation with donepezil enhances recovery in short-term memory and sustained attention after traumatic brain injury. Anatomical, physiological, and pharmacological characteristics of histidine decarboxylase knock-out mice: Evidence for the role of brain histamine in behavioral and sleep-wake control. Decreased brain histamine content in hypocretin/orexin receptor-2 mutated narcoleptic dogs. Previously, there were only case reports associating pituitary dysfunction with brain injury. He further noted that endocrine dysfunction can occur more than 10 years after the initial injury and that the injury may not have been substantial enough to require hospitalization or even be remembered by the patient. In order to discuss the pathophysiology of the pituitary damage, we briefly point out the functional anatomy of the gland. The pituitary gland is seated at the base of the skull within the sella turcica, being tethered to the hypothalamus by the infundibulum. Both the anterior and the posterior pituitary receive blood supply from the internal carotids. Moreover, the hypothalamicreleasing hormones are carried by this vascular system to the anterior pituitary. The cellular distribution in the pituitary gland supplied by the long hypophyseal veins includes the somatotrophs (located in the lateral wings of the gland) and the gonadotrophs (mostly located in the peripheral parts of the gland). The short hypophyseal portal veins arise from branches of the intracavernous internal carotid artery, the inferior hypophyseal arteries that enter the sella from below the diaphragma sella, and altogether provide less than 30% of its vascular supply, predominantly in the medial portion of the gland. The posterior lobe receives its blood supply through the inferior hypophyseal arterial branches. The most possible mechanisms of injury are 1) the direct brain injury event itself; 2) the indirect injuries, such as hypoxia or hypotension; 3) the transient effect of critical 213 214 Clinical management of pituitary dysfunction after traumatic brain injury illness or the "stress response;" and 4) the effects of different medications given during the initial critical period after injury that may have the inadvertent effect of suppressing normal hypothalamic and pituitary function. Direct mechanisms refer to fractures through the skull base and sella turcica as well as the shearing injuries of the pituitary, infundibulum, and/or hypothalamus.
Diseases
The interdependence concept suggests that there must be an interconnection or interrelationship among two or more entities diabetes medications made easy purchase glucotrol xl 10 mg without a prescription. In our case, medical, family, educational, and community entities should be responsible to interprofessionally team with one another as points of contact on the circle. In this concept, the injury or illness begins in the community where the child or adolescent is a living, contributing member. As this concept is based on a circle, any point on the circle may be the beginning point of care. Endocrine system abnormalities that result in short stature, premature development of breasts and menstrual cycle in females, aggressiveness, weight gain and hypothyroidism, and pituitary gland dysfunction 2. Treatment is provided with consideration of the eventual return of this child to the community, and providers in the educational and life-long living community receive the child or adolescent with an appreciation of the complex and unique medical aspects that will affect learning by this child. Using this thought process, we are better able to focus on the total needs of the child or adolescent to function within the community. When this interprofessional concept is employed by all those seeking to assist the child or adolescent, arguments for obtaining financial, social supports, and agency services can be justified. In this article, we operate from two concepts-that the majority of rehabilitation for children and adolescents occurs at school and in the community and that there is a circle of community care that should guide interventions- and one concern: that the link between cognitive communication and learning is often ignored when planning for these children. If these perspectives are accepted, we can begin to plan, interactively and proactively, for this population. The processes of attention, processing speed, short- and long-term memory, organization, and problem solving are often challenged. In addition, impulsive behaviors and receptive, expressive, and social pragmatic language skills are potentially problematic. Unfortunately, many teachers attempt to alter the behaviors without considering the underlying processes that are affecting the behaviors. If these underlying processes are considered in the educational process, classroom behaviors and learning can be modified. The behaviors are simply examples of what can occur in the classroom and should serve to stimulate discussion about processes that may be affecting the capacity for learning in a specific student and what behaviors might occur in a particular classroom. Additional information should be provided in the report about what the behaviors that reflect the problem areas might look like in the classroom.
Ultimately diabetes symptoms nhs glucotrol xl 10 mg order on-line, we will return to the common problem mentioned in the opening of this section of the chapter above in tying the use of the skill sets used in the cognition module to problem solving in everyday life. However, to begin, we envision an individual beginning the cognition module at Level I with the object stimulus presented being a No. One set of the many appropriate responses for the individual to give would be that the pencil is yellow, cylindrical, composed of wood and graphite, 8 inches long with a diameter of 1/4 of an inch, a few ounces in weight, smoothly textured, possessed of an eraser, and used for writing. The question relevant to this discussion is what cognitive processes are required in order to generate these responses and what are the neuroanatomical underpinnings of those processes. One of the most basic cognitive processes requisite to success in completing the cognition module is attention. In order to adequately perceive and identify features of an object, it is first necessary to attend to that object in a selective fashion. Specifically, in our therapy task, the individual would be required to selectively attend to the stimulus presented (the pencil) to the exclusion of various other stimuli that might be present. In addressing each specific feature identification task, the individual must selectively attend only to those stimuli that appear relevant to this task. This type of selective attention has been described as being determined by the processes of competitive selection and top-down sensitivity control. The results of these studies have indicated that attention is a process that is mediated by widely distributed neural structures. Attention is dependent upon arousal/vigilance, which is subserved by the ascending reticular activating system. The influence of the pulvinar has been most explored in relation to the visual and spatial attentional systems. However, the manner in which the pulvinar complex becomes tuned to a particular task demand remains unresolved. In addition to the pulvinar complex, the posterior parietal cortex also appears to be implicated in the process of competitive selection and is another area likely involved in top-down influences on attention. Encoding of the relative salience of visual field stimuli, for example, appears to be located in the lateral intraparietal area. Specifically, the catecholaminergic neurotransmitters, dopamine and norepinephrine, are thought to modulate processes of attention. Bringing the discussion back to the example above, the individual would be charged with the task of attending to the pencil in very particular ways in order to discriminate its perceptual features. In this case, because the information refers to shape, the occipitotemporal cortex is likely to be involved in attending to this specific type of information. Based upon the bias criteria imposed, specific cells programmed to respond ideally to the form presented by the pencil would be preferentially selected for firing, thus making them more effective in competitive selection, and more likely to enter working memory as salient information to the task of determining the perceptual feature of shape for this object.
Learning can occur at any point postinjury 398 Neuropsychological interventions following traumatic brain injury and learning has no end point diabetes insipidus pathophysiology and treatment glucotrol xl 10 mg order line. It follows that intervention can begin at any point postinjury and with no time-dependent limit on the degree to which an individual can benefit from treatment. In addition to those studies referenced, the reader is directed to the Cognitive Rehabilitation Manual authored by the Brain InjuryInterdisciplinary Special Interest Group of the American Congress of Rehabilitation,68 which describes in detail neuropsychological interventions shown to result in positive functional gains in methodologically rigorous outcome studies. Treatment is typically conducted in individual sessions with feedback on performance provided to the patient consistently throughout the session. For example, several interventions have been developed to improve working memory and range from simple tasks, such as using flash cards to improve orientation,69 to more complex tasks, such as mental arithmetic, anagram solutions, and n-back procedures and other serial logic verbal tasks. Improvements in other cognitive domains may be further hampered because of difficulties in learning and recalling new material, difficulties remembering when and how to use rehabilitation tools and strategies, and difficulty maintaining motivation in both the patient and the clinician due to the extensive time and effort required to notice improvements. This illustrates the point that some cognitive abilities, particularly attention, are foundational in that they support more complex cognitive abilities, such as learning. Treatment must first focus on the most foundational skills that have been impaired in order to improve more complex skills as training more complex skills when foundational skills are impaired will yield little improvement in more complex skills. Restorative approaches have included word-list learning, paragraph listening, visual imagery, and use of mnemonic strategies,32,68,75 all of which are especially useful for mild memory deficits. Sohlberg and Mateer75 presented a method of training individuals to develop and use a Neuropsychological interventions: Some highlights 399 structured memory book that is personally relevant to the individual. The memory book can include sections for orientation, a memory log, a calendar, "things to do," transportation, a "feelings log," and "important information. Using the pioneering work of Sohlberg and Mateer75 as a springboard, Donaghy and Williams73 developed a protocol for memory book training to assist clinicians working with individuals with memory deficits to increase the effective use of the memory book by their clients. Effective use of a memory notebook should include the ability to schedule future events (prospective memory) and track past events, a note-keeping system that makes retrieval effortless, and ease of use that fosters independence. These factors illustrate the need for psychotherapeutic and/or family interventions as complements to memory book training. Finally, evidence suggests that patients often require extensive training and reinforcement to use external memory aids effectively and consistently,88 highlighting the need for clinicians to remain undeterred in their efforts to teach and reinforce the use of external memory aids despite resistance, reluctance, and/or confusion from patients who are otherwise good candidates for training. Einstein and McDaniel90 identify two components to prospective memory: 1) remembering what actions are to be carried out and the cue for implementing the action and 2) recall and initiation of the action at a given time following the cue. Prospective memory has been enhanced significantly with the use of technology-based tools, such as smartphones, which can be programmed to provide portable cues and reminders that are visual and/or audible, but challenges, such as training individuals to use the technology and ensuring consistent use, remain. Interventions have been based on explicit theoretical models of executive function. The key to improving executive functioning by mastering metacognitive skills is increasing self-awareness. Similarly, Cicerone and colleagues have identified metacognitive strategy training as a practice standard in their most recent systematic review on the cognitive rehabilitation literature. The problem-solving intervention entails learning a step-by-step procedure that facilitates identification of problems, reduction of the problem to more elemental components, generation of possible solutions, carrying out one or more possible solutions, and self-monitoring the result.
However diabetes symptoms muscle weakness order 10 mg glucotrol xl overnight delivery, there was a trend toward a greater rate of improvement in global cognitive functioning if patients were started on donepezil early during their inpatient rehabilitation program. The authors suggested that perhaps the measurement tools used in this pilot study might have been too crude to detect subtle improvements in cognition. As with the other medications reviewed in this chapter, the use of this drug is considered off-label when prescribed for disorders of consciousness. Cholinesterase inhibitors should be used with caution in patients with bradycardia or cardiac conduction abnormalities and in patients with asthma or obstructive pulmonary disease. Common side effects include nausea, vomiting, diarrhea, fatigue, insomnia, muscle cramping, and anorexia. Supporting this contention are recent animal studies that demonstrate that histidine decarboxylase knockout mice are unable to remain awake when high task vigilance is required. How chronic neurotransmitter dysfunction affects receptor sensitivity or produces adaptive changes in other neuronal systems is largely unknown. Augmentation of a single neurotransmitter system may have far-reaching effects on other neurochemical networks. Patients with disorders of consciousness may have a range of underlying neuroanatomical and neurochemical alterations. Currently, we are closer to identifying the neurotransmitter systems and the structural and functional neural networks that are important in maintaining consciousness. As our ability to detect these unique differences among patients improves, the term disorders of consciousness will likely be replaced with more exact diagnoses that reflect the distinct anatomic and neurochemical networks involved. These advances will hopefully allow new and effective therapeutic agents to be developed to improve the lives of brain injury survivors. Diagnostic accuracy of the vegetative and minimally conscious state: Clinical consensus versus standardized neurobehavioral assessment. Residual cerebral activity and behavioural fragments can remain in the persistently vegetative brain. Cortical processing of noxious somatosensory stimuli in the persistent vegetative state. Default network connectivity reflects the level of consciousness in non-communicative braindamaged patients. Resting brain activity in disorders of consciousness: A systematic review and metaanalysis. Disruptions of functional connectivity in the default mode network of comatose patients. Restoration of thalamocortical connectivity after recovery from persistent vegetative state. The Quality Standards Subcommittee of the American Academy of Neurology, Practice parameters: Assessment and management of patients in the persistent vegetative state (summary statement).
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The anatomical distribution of glycinergic neurons has not been extensively mapped metabolic disease you can get from dogs discount glucotrol xl 10 mg overnight delivery. Neuronal pathways suggested to be glycinergic include spinal interneurons, a corticohypothalamic pathway, reticulospinal projections from the raphe and reticular formation, brain stem afferents to the substantia nigra, cerebellar golgi cells, and retinal amacrine cells. Radioactive tracer studies show that most of the glycine in the brain is made from serine. Moreover, it is not clear whether neurons utilizing glycine as a neurotransmitter must synthesize it de novo or whether they accumulate existing glycine. Enzymatic degradation of glycine can occur via a glycine cleavage system, which is also located in the mitochondria, mainly of astrocytes. After its release into the synaptic cleft, glycine is primarily inactivated by reuptake into the terminal of the releasing neuron or by uptake into glial cells. The Na+ and Cl- electrochemical gradients assist in the movement of glycine against its concentration gradient. Three alpha and two beta subunits are often responsible for forming the ion channel. Gephyrin is believed to function as an anchoring protein that connects the membrane receptor protein with the protein tubulin in the cytoplasm. The strychnine binding site is on the 48-kDa subunit, which is where glycine also binds. However, 7-cholorkynurenic acid is a more selective and more potent antagonist and is now being widely used to study this glycine receptor. At the present time, there is considerable interest among drug companies to explore the use of strychnine-insensitive glycine antagonists. The antagonist at the strychnine-insensitive glycine receptor (7-chlorokynurenic acid) may prove to be useful in the future. Aspartate is also plentiful and was once thought to function as an excitatory amino acid neurotransmitter, but it is not concentrated in synaptic vesicles and therefore is unlikely to function as a neurotransmitter. There are, however, some specific pathways that have been mapped using lesion and biochemical analyses. These include the well-known corticostriate pathway from the cerebral cortex to the striatum as well as many other corticofugal pathways. However, there is an experimental drug called milacemide that is believed to increase glycine levels in the brain and has been shown to have anticonvulsant effects in experimental animals. Glycinergic neurons in the brain stem and spinal cord have been shown to play a role in suppressing pain, and there is now much interest in developing inhibitors of the glycine transporter-2 (GlyT2) to treat chronic pain. The glutamate formed from glucose, however, occurs in all brain cells (neurons and glia) and has many roles in the brain.
However blood sugar goes up after exercise discount glucotrol xl 10 mg otc, it appears that the displacement of the brain tissue and strain rate, relative to the skull, lead to more devastating results than the acceleration per se-that is, a particular group of axons will suffer more damage if strained (or displaced) with more intensity and longer duration than if the same axons were strained at a lower rate of intensity and shorter amount of time. These lesions include contusions resulting from hemorrhagic lesions that can lead to cell death. The mechanism of diffuse neuronal cell loss involves both necrotic and apoptotic neurocascades. Necrotic death is attributed to ischemia (secondary to cell membrane failure), whereas apoptotic cell death evolves more slowly and is not clearly understood. In less severe injuries, focal alterations of axolemma can lead to progressive changes and a cascade of electrochemical events interfering with axonal transport (anterograde and retrograde), focal axonal swelling, and detachment from the distal axonal segment. The exact nature of the reactive axonal changes is unknown, but because the effects are delayed, future research might determine how to prevent certain axonal changes. In an experimental mildto-moderate brain injury with cats, some of the swellings showed numerous reactive neuritic sprouts in the brain stem area. Some of these neuritic outgrowths were reorganized to course into the parenchyma (where myelin was absent) or course parallel to the distended myelin sheath. In the second and third month postinjury, there is great variability in the regenerative responses of animals. The more mature sprouting shows further maturation and seems to gain easy access to the rest of the brain. Metabolic dysfunction the mechanical and cellular changes, described previously, can lead to a wide array of metabolic changes. Similar to the aforementioned changes, the metabolic cascade can also be focal, multifocal, and/or diffuse. It appears that this metabolic imbalance is heterogeneous and affects brain areas differently. A massive release of the excitatory neurotransmitter glutamate leading to excitotoxicity and also to an increase in glucose metabolism (hyperglycolysis)-the temporal lobe and hippocampal areas are particularly vulnerable to the glutamate surges. Production of reactive forms of oxygen species that cause damage via the induction of lipid and oxygen oxidation. The acute period of hyperglycolysis is followed by a period of metabolic depression and reduction in glucose utilization. If the postsynaptic cell survives, its soma and/or dendrites will have vacant locations where presynaptic degeneration has occurred. At this point, a number of possible events can occur that can result in recovery of function. The damaged axons can regenerate and form new terminals on the cells they previously innervated, or axons from other neurons can sprout new terminals that form synapses at the vacant locations on the postsynaptic neuron. This sprouting constitutes a reorganization of the connections among the surviving brain structures and can serve as a major impetus for recovery of function. As mentioned previously in this chapter, it is possible for the newly sprouted connections to result in maladaptive behaviors.
These primary sensory areas project their specific modality to the surrounding association cortex for more complex processing diabetic diet guide pdf buy 10 mg glucotrol xl. These different sensory-specific association cortices then communicate with each other via bidirectional, divergent, and convergent fibers to form the posterior multimodal association area. There are three multimodal association cortices: the posterior, anterior, and limbic association areas. It should be noted that approximately 90% of the lateral surface of the cerebral hemisphere is covered with association areas. The posterior multimodal association area allows for spatial and temporal integration of all sensory modalities and is located in the posterior parietal lobe predominately in the angular gyrus. The anterior association area is located in the prefrontal area and allows for visual percepts to be incorporated into higher cortical function by determining which of the unimodal and multimodal inputs from other parts of the brain should be attended to at any specific time. The limbic association cortex, the allocortex, serves as a supervisor that processes feelings and emotion that interface between the external world and the internal self in addition to mediating memory. These supramodal areas, the anterior and limbic association areas, help bring our personal past and the present into the future. They bring explicit and implicit knowledge gained through past experience to bear on information processed in the here and now. The supramodal system can give rise to de novo creativity, ideas, thought, memory, motivation, and free will in the absence of sensory stimulation or action in the immediate present. In addition to the cortical areas, subcortical structures are involved in sensory, motor, and complex behaviors in a manner determined by both their intrinsic anatomical organization as well as their connectivity to the cerebral cortex. These linkages are carried out by numerous axonal pathways located both in the cortex and subcortical white matter. These pathways consist of large groups of axons covered with a myelin coat and are identified as fasciculi, tracts, or bundles. Vision is created by the simultaneous integration of neural networks modulated by attention. They can converge or diverge from lower to higher centers, higher to lower centers, or can be collateral or spread out at the same level. Neurons within a specific cortical area give rise to three distinct categories of fiber systems that can be distinguished within the white matter beneath the gyrus. The local association fiber system, or the U system, leaves a given area of the cortex and travels to an adjacent gyrus running in a thin identifiable band beneath the sixth layer of the neocortex. The neighborhood association fiber system arises from a given cortical area and is directed to nearby regions but is distinguished from the U fiber system that runs immediately beneath the cortex. The long association fiber system emanates from a given cortical point and travels in a distinct bundle leading to other cortical areas in the same hemisphere.
In a study of 37 amateur soccer players diabetes mellitus type 2 medscape glucotrol xl 10 mg amex, the number of estimated headers was associated with white matter abnormalities and neurocognitive deficits after 1 year. Linear and rotational, acceleration-deceleration forces cause the gelatinous brain to elongate and stretch; this distortion is greatest at the depths of the cerebral sulci of the brain and around the microvasculature. Traumatic axonal injury also results in alterations in axonal membrane permeability; ionic shifts, including massive influx of calcium; release of caspaces and calpains; hyperphosphorylation and mislocalization of the microtubule-associated protein tau. Under normal physiological conditions, tau is phosphorylated at a small number of sites and is localized to the axon where it binds to microtubules and stabilizes the cytoskeleton. Cumulative accumulation of p-tau eventually builds to a critical threshold that overwhelms recovery mechanisms and triggers a widespread neurodegenerative process. The progressive neurodegeneration results in widespread p-tau accumulation in the cortex, medial temporal lobe (hippocampus, amygdala, and entorhinal cortex), and deep nuclei (including the nucleus basalis of Meynert, substantia nigra, locus ceruleus, and others). When the individual first becomes symptomatic may depend on individual resistance and susceptibility factors that modulate compensatory responses to the pathology; however, with progressive accumulation and neurodegeneration, most individuals eventually develop symptoms. In response, the brain elicits a neuroprotective inflammatory response characterized by meningeal neutrophil swarming and microglial reconstitution of the damaged glial limitans. This initial inflammatory reaction to brain injury appears to limit the extent of the injury;142 however, chronic activation of this pathway might enhance neurodegeneration. It is hypothesized that if a critical level of p-tau accumulates, it may trigger a feed-forward process of continued accumulation and toxic spread throughout the nervous system even in the absence of further exposure to trauma. Neuroinflammation associated with the initial trauma and aggravated by the accumulation of toxic p-tau fragments might exacerbate the neurodegeneration. Positron emission tomography using p-tau ligands and blood biomarkers look encouraging as methods for early in vivo detection. Finally, there is great hope for the development of therapies that would limit p-tau accumulation and spread and thus interfere with further decline in subjects already exposed to traumas and at high risk for chronic neurodegeneration. Neuropathological observations in a case of autism presenting with self-injury behavior. Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model. Diagnosis of chronic cerebral symptoms in boxers (dementia pugilistica & traumatic encephalopathy of boxers). Editorial on consensus recommendations for the postmortem diagnosis of Alzheimer disease from the National Institute on Aging and the Reagan Institute Working Group on diagnostic criteria for the neuropathological assessment of Alzheimer disease. Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: Consensus of the Consortium for Frontotemporal Lobar Degeneration. Chronic traumatic encephalopathy pathology in a neurodegenerative disorders brain bank. Histological evidence of chronic traumatic encephalopathy in a large series of neurodegenerative diseases.
Denpok, 45 years: Screening of oculomotor function can be conducted by an experienced occupational therapist along with detailed objective testing of visual perceptual functions. The percepts of our visual world that we construct during reception and perception are used to guide further motor activity, both within the visual system and in visually guided motor activity, such as mobility or eyehand coordination.
Karrypto, 63 years: This seems to be a good rule for visual perceptual and visual memory rehabilitation with the modification that some compensatory strategies are often applied immediately to help the patient function while pursuing therapy. Anatomical, physiological, and pharmacological characteristics of histidine decarboxylase knock-out mice: Evidence for the role of brain histamine in behavioral and sleep-wake control.
Knut, 40 years: Because the eyes are fluid-filled organs, they are vulnerable to damage secondary to the primary overpressurization wave (both positive and negative phases of the blast wind cycle) and to fragment injuries that result from the explosive device and secondary damage. Glucose administration after traumatic brain injury exerts some benefits and no adverse effects on behavioral and histological outcomes.
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