1.
[Back to the past. Case report and review on retrograde memory loss].
Johannsson, M, Karlsdottir, TA, Sigurdsson, E
Laeknabladid. 2011;(3):159-64
Abstract
Retrograde memory loss where many years disappear suddenly from memory is a known but rare form of memory disturbance among young and old subjects. For those whose brain is affected by a known organic damage such as head trauma the time lost from memory is usually not counted in years, but typically hours or sometimes days or weeks. We review in this article current knowledge on retrograde memory loss as we describe the experience of a 31 year old woman who experienced an unusually long form of retrograde amnesia. She developed the memory loss in the wake of disappointment and a life event. At the time she had major depression. Having described the case and presented the results of neuropsychological testing, we associate her story with the state of knowledge on retrograde memory loss.
2.
A patient with stress-related onset and exacerbations of Graves disease.
Vita, R, Lapa, D, Vita, G, Trimarchi, F, Benvenga, S
Nature clinical practice. Endocrinology & metabolism. 2009;(1):55-61
Abstract
BACKGROUND An 18-year-old, nonsmoking woman presented to her general practitioner with a 1-week history of weakness, fatigue, palpitations, nervousness, tremors, insomnia, heat intolerance, and sudden enlargement of a thyroid goiter that had been detected 2 years earlier. The patient's symptoms had started shortly after she experienced emotional stress. Diagnostic work-up disclosed an avid radioactive iodine uptake by the goiter. On ultrasound examination, the thyroid gland was enlarged with a diffusely hypoechogenic structure and intense vascularization. INVESTIGATIONS Thyroid scintigraphy with (131)I; ultrasonography of the thyroid gland; and measurements of serum free T(3), free T(4), TSH levels and thyroid autoantibodies, including autoantibodies against thyroglobulin (TgAb), thyroperoxidase (TPOAb) and TSH receptor (TRAb). DIAGNOSIS Graves disease, with stress-related onset and subsequent stress-related exacerbations. MANAGEMENT The patient was treated with methimazole to normalize levels of thyroid hormone and thyroid autoantibodies, and with bromazepam to help her cope with stress. The daily dose of methimazole was kept low during pregnancy. Over the 4 year period when the patient was taking methimazole, exacerbations of hyperthyroidism occurred twice: during her first pregnancy and 9 months after her first delivery. On all three occasions, symptoms were preceded by stressful life events. Further exacerbations were avoided by starting bromazepam treatment soon after the patient experienced stressful events.
3.
Broken hearts: differentiating stress-induced cardiomyopathy from acute myocardial infarction in the patient presenting with acute coronary syndrome.
Purgason, K
Dimensions of critical care nursing : DCCN. 2006;(6):247-53; quiz 254-5
Abstract
The link between an emotional or physical stresses and an acute cardiac event was first discovered in Japan. Stress-induced cardiomyopathy is defined as transient left ventricular dysfunction associated with apical and mid ventricular contractile abnormalities and sparing of basal segments that mimics acute myocardial infarction. This article presents an overview of this disorder.
4.
Contemporary strategies for the prevention of stress-related mucosal bleeding.
Martindale, RG
American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists. 2005;(10 Suppl 2):S11-7
Abstract
PURPOSE The purpose of this review is to describe the clinical presentation and pathophysiology of stress-related mucosal bleeding and review the strategies to prevent bleeding. SUMMARY The mortality rate associated with clinically significant stress-related mucosal bleeding is high. Respiratory failure requiring mechanical ventilation for more than 48 hours and coagulopathy are two strong, independent risk factors for bleeding. Splanchnic hypoperfusion is the underlying etiology of stress-related mucosal injury and bleeding. Mucosal damage typically manifests as multiple superficial lesions without perforation, and bleeding often originates in superficial capillaries after the patient is admitted to the intensive care unit. Providing adequate visceral perfusion is vital to preventing bleeding. Gastrointestinal function should be taken into consideration before using enteral nutrition, and enteral nutrition should not be the sole stress ulcer prophylactic therapy. Acid-suppression therapy should be used to raise the intragastric pH above 3.5 because it reduces the incidence of stress-related mucosal bleeding. Proton pump inhibitors are at least as effective, and may be more effective than histamine H2-receptor antagonists in achieving this pH goal and preventing bleeding. CONCLUSION The key to reducing mortality from stress-related bleeding in critically ill patients is to prevent mucosal damage. Providing adequate visceral perfusion and acid-suppression therapy can reduce the risk of stress-related mucosal damage and bleeding.