Mayo Clinic proceedings
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Esophageal motility disorders often manifest with chest pain and dysphagia. Achalasia is a disorder of the lower esophageal sphincter and the smooth musculature of the esophageal body. In achalasia the lower esophageal sphincter typically fails to relax with swallowing, and the esophageal body fails to undergo peristalsis. ⋯ Spastic disorders of the esophagus, such as diffuse esophageal spasm and nutcracker esophagus, and nonspecific esophageal motility disorder are benign and nonprogressive, with similar findings on esophageal manometry. Although the exact cause remains unknown, these disorders may represent a manifestation of gastroesophageal reflux disease. Treatment of spastic disorders includes medical and surgical approaches and is aimed at symptomatic relief.
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Mayo Clinic proceedings · Sep 2000
ReviewManagement of massive hemispheric cerebral infarct: is there a ray of hope?
Catastrophic infarcts of the cerebral hemisphere often involve occlusion of the middle cerebral artery. In approximately 50% of these patients, consciousness declines because of brain swelling. Management includes prevention of further systemic complications, and recent studies have suggested that decompressive hemicraniectomy or moderate hypothermia may improve outcome. Mortality may be decreased, but morbidity should be carefully evaluated in clinical trials before these interventions are accepted as standard.
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Mayo Clinic proceedings · Sep 2000
ReviewPotential neurotoxicity of spinal anesthesia with lidocaine.
Spinal (intrathecal) anesthesia has evolved into a safe, widely accepted method of anesthesia with many advantages. However, the past decade has seen a large number of case reports and incidence studies that implicate the local anesthetic (LA) lidocaine as being more neurotoxic than other commonly used LAs such as bupivacaine and tetracaine, based on patterns of clinical use current at the time of those reports. Available studies suggest a risk of persistent lumbosacral neuropathy after spinal lidocaine by single injection in about 1 in 1300 procedures and a risk as high as about 1 in 200 after continuous spinal anesthesia with lidocaine. ⋯ Although the pain typically resolves within 1 week without lasting sequelae, it can be severe in up to one third of patients with the syndrome. In addition to clinical studies, both whole animal and in vitro studies have shown that lidocaine can be neurotoxic at clinically available concentrations and that lidocaine is more neurotoxic than equipotent concentrations of other commonly used LAs. The mechanism of this neurotoxicity may involve changes in cytoplasmic calcium homeostasis and mitochondrial membrane potential.
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Mayo Clinic proceedings · Aug 2000
ReviewPrevention and treatment of osteoporosis in women with breast cancer.
Women who have had breast cancer may be at higher risk for osteoporosis than other women. First, they are more likely to undergo early menopause, due to chemotherapy-induced ovarian failure or oopherectomy. In addition, chemotherapy may have a direct adverse effect on bone mineral density (BMD), and osteoclastic activity may increase from the breast cancer itself. ⋯ For osteoporosis, treatment with alendronate should be strongly considered. Raloxifene and calcitonin are alternatives when alendronate is contraindicated. Further studies are needed to evaluate the optimal timing of initial bone mineral analysis in premenopausal women after breast cancer diagnosis and to determine the value of preventive treatment in women scheduled to undergo chemotherapy.
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Recently, a single mutation in the 3'-untranslated region of the prothrombin gene was reported, resulting in a G-to-A substitution. This finding added to the growing list of genetic disorders thought to be responsible for familial thrombophilia. Although most studies generally agree about the increased risk of venous thrombosis in individuals carrying this mutation, its role in the first event of venous thromboembolism and in recurrent events is unclear. ⋯ This mutation has important clinical implications since it is a common cause of genetic thrombophilia, second only to the factor V Leiden mutation. However, the mutation by itself may not be enough to trigger disease because thromboembolic disease is now generally accepted as a multifactorial disorder. Careful evaluation of this mutation will augment the clinician's ability to stratify systematically an individual's risk of developing spontaneous thrombosis.