Traumatic head injury

Aspirin allergy, nasal polyps, and Traumatic head injury... 

Naredi S, Olivecrona M, Lindgren C, Ostlund AL, Grande PO, et al. 2001. An outcome study of severe traumatic head injury using the lund therapy with low-dose prostacyclin. Acta Anaesthesiol Scand 45(4) 402-406. 

Like spinal cord trauma, traumatic head injury consists of a primary injury, attributable to the mechanical insult itself, and a secondary injury, attributable to the series of systemic and local neurochemical changes that occur in brain after the initial traumatic insult (Klussmann and Martin-Villalba, 2005). The primary injury causes a rapid deformation of brain tissues, leading to rupture of neural cell membranes, release of intracellular contents, and disruption of blood flow and breakdown of the blood-brain barrier. In contrast, secondary injury to the brain tissue includes many neurochemical alterations such as release of cytokines, glial cell reactions involving both activated microglia and astroglia, and demyelination... 

Ikonomidou and Turski, 2002 Yi and Hazell, 2006). This suggests a cocktail of glutamate receptor antagonists, glutamate transporter inhibitors, antioxidants, and anti-inflammatory drugs may have beneficial effects in traumatic head injury. 

This case of herbs complementing technology is not an isolated incidenti have had similar experiences with other conditions. For example, although best treated initially by Western medicine, traumatic head injuries have responded well to adjunctive herbal therapies, as have various cancers, heart disease, and autoimmune disorders such as lupus, ankylosing spondylitis, and scleroderma. 

A number of environmental factors have been associated with an increased risk of AD, including stroke, alcohol abuse, small head circumference, repeated or severe head trauma, Down syndrome, and lower levels of education. ° In particular, traumatic head injury in combination with the apo E4 genotype has been associated with an increased risk of AD. ... 

Apoptosis has been implicated in delayed neuronal death associated with many neurodegenerative disorders such as Parkinson s disease, stroke, Huntington s disease, traumatic head injury, Alzheimer s disease, motor neuron degeneration, spinal cord injury, and multiple sclerosis. Since an extensive description of the role of apoptosis in each of these disorders is beyond the scope of the present text, we shall focus on anti-apoptotic strategies for stroke, Parkinson s disease, and multiple sclerosis. 

Sydenham, E., Roberts, L, Alderson, R, 2009. Hypothermia for traumatic head injury. Cochrane Database Syst. Rev., CD001048. 

Traumatic Dementias. Traumatic brain injury can also result in dementia. This can result from a single massive head injury such as in a motorcycle accident or a gunshot wound. Repeated small head injuries can also cause dementia. The best example is dementia pugilistica, the dementia observed in professional boxers after many years and many prizefights. 

By definition, most patients who suffer a serious TBI present to an emergency room in the immediate aftermath of the traumatic event. However, patients may also be brought to medical attention days or even weeks after an apparently mild head injury when the symptoms are delayed or so subtle that they initially escaped detection. In some instances, patients may even visit a clinic unaware that their psychiatric symptoms are attributable to a remote head injury. One extreme example is so-called dementia pugilistica that occurs after years of repeated minor TBIs over the course of a boxer s career. 

Glenn MB. A differential diagnostic approach to the pharmacological treatment of cognitive, behavioral, and affective disorders after traumatic brain injury. J Head Trauma Rehabil 2002 17(4) 273-283. 

Pema, R.B., Rouselle, A., Brennan, P. (2003) Traumatic brain injury depression, neurogenesis, and medication management. J Head Trauma Rehabil 18, 201-3. 

Morphine releases histamine and may cause peripheral vasodilation and orthostatic hypotension (Figure 47.7). The cutaneous blood vessels dilate around the blush areas such as the face, neck, and upper thorax. Morphine causes cerebral vasodilation (due to increased carbon dioxide retention secondary to respiratory depression), and hence, it increases the cerebrospinal fluid pressure. Therefore, morphine should be used cautiously in patients with either meningitis or a recent head injury. When given subcutaneously, morphine is absorbed poorly whenever there is either traumatic or hemorrhagic shock. 

Numerous studies have been carried out using a cat fluid percussion head injury model to investigate the biochemical and physiological mechanisms of post-traumatic brain microvascular damage [48], Following moderately severe injury, there is a secondary cerebral (pial) arteriolar dilation, together with a loss of... 

Coincident with the reduction in brain level of hydroxyl radicals, U-74006F administered at 5 minutes post-injury also acts to reduce post-traumatic opening of the blood-brain barrier (i.e. decreased brain uptake of 14C-albumin) [56]. This effect of U-74006F to close the barrier may be related to the attenuation of hydroxyl-radical levels or an antagonism of the effects of free radicals on the barrier endothelium (i.e. decreased membrane-lipid peroxidation). Indeed, free radicals are known to increase barrier permeability [57]. Consistent with this reduction in post-traumatic opening of the blood-brain barrier which would lead to vasogenic brain edema, U-74006F has been shown to attenuate post-traumatic brain edema in a rat model of fluid percussion head injury [58]. 

Diffuse axonal injury is one of the most common and devastating types of traumatic brain injury it refers to the extensive lesions in white-matter tracts and is one of the major causes of unconsciousness and persistent vegetative state after head trauma. 

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