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[Neuropathic pain is a chronic pain disorder due to a primary lesion and/or dysfunction of the peripheral or central nervous system. This tormenting condition causes a lot of distress to the patients, impairs their quality of life, and demands significant expenses. Chronic neuropathic pain is frequently under-diagnosed and mistreated. Explanations for these problems are the complex underlying pathomechanism, variability of symptoms, difficulties in diagnosis, and the differences between the treatment of this and other painful disorders. In addition, comorbid conditions such as anxiety, depression, and sleep disorders are often overlooked. Apart from the diagnostic difficulties, also treatment is usually unsatisfactory. Frequently NSAIDs are used, but they are usually not effective. Undoubtedly, even with the use of evidence-based treatment - such as duloxetine and pregabalin - complete pain relief is not always possible. Lack of proper medical education also contributes to problems in diagnosis and treatment. In western countries, diabetes is the most common cause of polyneuropathy. Painful diabetic neuropathy is the most intensely studied neuropathic pain condition; a lot of evidence comes from randomized controlled trials of this type of neuropathy. The same drugs as in the case of other neuropathic pain conditions are used for the symptomatic treatment of painful diabetic neuropathy. Etiological therapy is based on the best achievable glycemic control. A combination of etiological and symptomatic therapy can be a future treatment, but proving this will require further studies.]
[INTRODUCTION - A number of diseases can cause hyperreninaemia and secondary hyperaldosteronism due to the stimulation of the renin-angiotensin system (RAS). The authors present a case of a patient suffering from a feeding disorder, whose secondary hyperaldosteronism verified by hormone examinations recovered after resolution of the feeding disorder. CASE REPORT - The authors found that the patient, who had been on an extreme vegetarian diet and avioded all forms of common salt as well as natural sodium intake for 8 years, had consistently normal electrolite levels, normal blood pressure, elevated plasma renin activity (PRA) and plasma aldosterone levels. Salt loading and postural tests verified secondary hyperaldosteronism. All known diseases that might lead to elevated RAS activity were excluded. After cessation of the salt-restricted diet, the patient’s PRA and plasma aldosteron levels returned to the normal range, which confirmed the possibility that the secondary hyperaldosteronism developed because of the feeding disorder. CONCLUSION - The authors have not found similar hormon alterations due to alimentary causes in humans in the literature. According to their hypothesis, the feeding disorder might lead to secondary hyperaldosteronism via affecting the system or systems that regulate RAS activity.]
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Clinical Neuroscience
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Is there any difference in mortality rates of atrial fibrillation detected before or after ischemic stroke?4.
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[The effects of demographic and clinical factors on the severity of poststroke aphasia]1.
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