• Title/Summary/Keyword: 병태 생리

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The Pathophysiology of Restless Legs Syndrome/Willis-Ekbom Disease (하지불안증후군/윌리스-엑봄병의 병태생리)

  • Cyn, Jaegong
    • Sleep Medicine and Psychophysiology
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    • v.28 no.2
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    • pp.43-52
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    • 2021
  • Restless Legs Syndrome/Willis-Ekbom Disease (RLS/WED) is a sleep disorder characterized by sensorimotor symptoms such as unpleasant sensations before sleep, akathisia, and periodic limb movements during sleep. It is also closely related to hyperarousal and is often accompanied by insomnia. Although the mechanism is not clear, the understanding of etiology and pathophysiology has greatly expanded through recent advances in genetic and neurobiological research. The most important pathophysiology of RLS/WED is brain iron deficiency. Such iron deficiency in the brain is caused by complex interactions between several genetic factors and various environmental factors, including comorbidities. Iron deficiency in the brain results in dysfunction of several neurotransmitters. A decrease in adenosine activity appears first, followed by an increase in the activity of glutamate and dopamine. A decrease in adenosine activity and an increase in glutamate activity stimulate the brain arousal system, resulting in hyperarousal. In addition, overproduction of dopamine and glutamate leads to dysfunction of the cortical-striatal-thalamic circuit, resulting in symptoms such as akathisia and periodic limb movements during sleep.

Depression and Coronary Artery Disease(I) : Pathophysiologic Mechanisms (우울증과 관상동맥 질환(I) : 병태생리적 기전)

  • Bae, Kyung-Yeol;Kim, Jae-Min;Yoon, Jin-Sang
    • Korean Journal of Biological Psychiatry
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    • v.15 no.4
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    • pp.275-287
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    • 2008
  • Depression and coronary artery disease are both highly prevalent diseases. Many previous studies suggest that depression is a common comorbid condition in patients with coronary artery disease and has a significant negative impact on the onset, course, and prognosis of coronary artery disease. However, the exact mechanisms that underlie the association between these two diseases remain unclear. Pathophysiologic mechanisms that may explain the effect of depression on coronary artery disease include hypercoagulability, hypothalamus-pituitary-adrenal axis and autonomic nervous system dysregulation, altered inflammatory response. On the contrary, pathophysiologic mechanisms in coronary artery disease that affect depression are less well known. It is also suggested that both diseases may share a common genetic vulnerability. The authors reviewed the literature on the pathophysiologic relationships of depression and coronary heart disease.

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