Essay Example on Traumatic brain injury affects more than 10 million People









Traumatic brain injury affects more than 10 million people worldwide annually and continues to be a major global cause of mortality and long term morbidity in young adults Hyder et al 2007 Therefore it is a major drain on health care funding throughout the world Despite being one of the leading causes of preventable death the first study to test the presence of SD in the human cortex was only published in 1996 Mayevsky et al 1996 Of a total of 15 patients with severe TBI only one brain was recorded with depolarization But in 2002 Strong verified by using EcoG the presence of more depolarizations in TBI Anthony J Strong et al 2002 These findings have been confirmed later in a study published by Fabricius in 2006 Fabricius et al 2006a In 2009 Hartings et al also investigated the incidence of SDs after TBI and its relationship with physiological values Hartings et al 2009 They recorded a total of 280 SDs in 53 of 32 patients with TBI They also found that the presence of SDs increased the lower the mean blood pressure and cerebral perfusion pressure and the higher the body temperature 

Also intracranial pressure was higher in patients with SDs In a subsequent study Hartings studied the presence and effect of SDs in the penumbral in 53 patients with TBI Hartings Watanabe et al 2011 57 of the patients were observed with depolarizations and all patients with isoelectric SD 19 had a poor prognosis at 6 months In another prospective study Hartings et al again confirmed the association between depolarizations and clinical outcome in 103 patients with TBI 56 of patients suffered 1 328 depolarizations and were associated with poor outcome Hartings Bullock et al 2011 Taking all evidence into account it can be concluded with high level of certainty that SDs are associated with an increased risk of unfavorable outcome in patients with TBI Therefore the control and management of SDs in TBI could and should be used to guide future therapy decisions 1 1 2 5 Migraine with aura About 18 of women in middle age and 6 of male population are affected by migraine L J Stovner and Hagen 2006 Lipton et al 2007 Bigal and Lipton 2009 and around 20 of them have aura symptoms He Li and Nie 2015 Migraine is a severely disabling intermittent headache disorder associate with a 2 fold increased risk of ischemic stroke and this association is even stronger in migraine with aura Schürks et al 2011 Spector et al 2010 Santos et al 2012 MA carries a tremendous individual social and economic burden Stewart et al 2003 L Stovner et al 2007 According to the International Headache Society it is characterized by the presence of neurological symptoms that usually develop gradually and do not last no more than 60 min 

Headache Classification Committee of the International Headache Society IHS 2013 with the appearance of visual 90 auditory motor somatosensory and even gastrointestinal symptoms He Li and Nie 2015 The neuropathophysiology of MA is defined as a neurovascular disorder with blood vessel constriction followed by decreased cerebral blood flow as the consequence of neuronal activity changes during aura M Lauritzen 1994 MA was the first neurological disorder suspected to have a possible association with SDs In 1958 Milner noticed a similarity between the waves of depolarization from Leão and scotomas of migraine Milner 1958 This hypothesis did not have much relevance until the 80 s 90 s when with the help of new imaging techniques waves with the characteristics of SDs were detected in brains with MA Since then many clinical and neuroimaging reports support the idea that SD is an etiological factor of the neurological symptoms in MA Diener 1997 Tfelt Hansen 2010 Sánchez del Rio and Alvarez Linera 2004 Using magnetoencephalography it was possible to obtain even stronger evidence that depolarization can occur spontaneously during MA or be visually triggered in regions of hyperexcitable occipital cortex Bowyer et al 2001 Furthermore different experimental studies have improved our understanding of the underlying neuronal mechanisms and cerebral blood flow changes of SD in MA Smith et al 2006 2008 Recently it was shown that meningeal nociceptors can be activated by SDs crossing the visual area of rats being capable of activate trigeminovascular neurons responsible for headache Zhang et al 2011 Even though SD seems to influence both MA and ischemic stroke the relationship between MA and ischemic stroke itself is not entirely clarified 

Several hypothesis have been proposed that assume a comorbidity association between migraine and cerebral ischemia Lipton and Silberstein 1994 where SD would be the underlying factor that explains this association Del Zotto et al support this idea and suggest that ischemic stroke can occur during migraine attacks with aura They explain that SD may induce due to vasoconstriction an extended ischemia so intense as to generate a significant ischemic damage Del Zotto et al 2008 Also supporting this association Santos et al recently described the case of a patient who presented migraine attacks preceded by scotomas nauseas and photophobia a month before suffering an ischemic stroke it was recorded that 60 of 20 SDs coincided with increased concentrations of glutamate and lactate pyruvate ratio These findings thereby demonstrate that the symptoms of MA can be generated by SDs induced in hypoperfusion areas Santos et al 2012 Future research on the occurrence of SD should further investigate and supply meaningful information with regard to the role of SD in MA as well as the potential comorbidity with other neurological disorders such as ischemic stroke

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