Medical hypotheses
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The common physiological rationale for migraine, anger, and epileptic attacks is discussed. The potential importance of homeostatic reactions in brain blood perfusion is described. The author speculates that these attacks are induced to meet some urgent biological needs. ⋯ Migraine attack is a subacute local vasomotor response. In contrast, anger and epileptic attacks are different manifestations of acute solemn general neuropsychiatric vasomotor reflexes. The newer paradigm of the etiological integration of these three kinds of attacks based on cerebral hemodynamic change does not only explain the mechanism of seizure-producing treatments such as electroconvulsive therapy, but also indicates the significance of cerebral vasodilative demands for the particular treatment of migraine, aggressive behavior, and epileptic seizures.
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There is growing dissatisfaction regarding the available diagnostic systems for psychiatric disorders (DSM, ICD). Psychiatrists acknowledge that though mental disease reflects brain disorders, the descriptive and symptom based nature of psychiatric diagnosis bears no relation to brain functions. According to Helmut's article published in the October 2003 issue of Science, in the coming decade researchers and psychiatrists will be called upon to propose a basis for the psychiatric diagnostic system of the future. ⋯ Depression and anxiety have been recently linked to alterations of adaptive neuronal plasticity thus reconceptualized as disorders of matching complexity. Finally, psychoses, including schizophrenia spectrum disorders, are reconceptualized as disturbances of neural complexity resulting in altered fast stabilizing plasticity. The new diagnostic system generates testable predictions regarding diagnosis and treatments of mental disorders which may be the future of psychiatry.
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Congenital long QT syndrome (LQTS) is a cardiac electrophysiological disorder due to genetic mutations. Patients with LQTS, if untreated, have a high incidence of ventricular tachycardia and cardiac arrest. Adrenergic activities are believed to play a major role in triggering the onset of cardiac events. ⋯ Its clinical use, however, has been hindered by the complexity of the procedure and complications after the surgery. Video-assisted thoracoscopic sympathectomy has been used to treat patients with palmar and axillary hyperhidrosis. We suggest that the use of the microinvasice thoracoscopic technique may greatly simplify the LSCD procedure, making it the first-line therapy for LQTS.
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Bone metastasis are a frequent complication of cancer, occurring in up to 70% of patients with advanced breast or prostate cancer. The consequences of bone metastasis are often devastating. Osteolytic metastasis can cause different kinds of skeletal related events including severe pain, pathologic fractures, life-threatening hypercalcemia, spinal cord compression, and other nerve-compression syndromes. ⋯ Local calcium also promotes tumor growth and the production of parathyroid hormone-related peptide which in turn stimulates bone resorption. Vitamin D and calcium supplementation during bisphosphonate administration for the purpose of elimination of the side effects related to hypocalcemia in patients with bone metastasis may increase the bone resorption and decrease the efficacy of bisphosphonates. Therefore, vitamin D and calcium supplementation must not be routinely recommended during bisphosphonate administration.
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Alzheimer's disease (AD) includes etiologically heterogeneous disorders characterized by senile or presenile dementia, extracellular amyloid protein aggregations containing an insoluble amyloid precursor protein derivative, and intracytoplasmic tau protein aggregations. Recent studies also show excess neuronal aneuploidy, programmed cell death (PCD), and mitochondrial dysfunction. The leading AD molecular paradigm, the "amyloid cascade hypothesis", is based on studies of rare autosomal dominant variants and does not specify what initiates the common late-onset, sporadic form. ⋯ In our model, the inherited, gene-determined make-up of an individual's electron transport chain sets basal rates of reactive oxygen species (ROS) production, which determines the pace at which acquired mitochondrial damage accumulates. Oxidative mitochondrial DNA, RNA, lipid, and protein damage amplifies ROS production and triggers three events: (1) a reset response in which cells respond to elevated ROS by generating the beta-sheet protein, beta amyloid, which further perturbs mitochondrial function, (2) a removal response in which compromised cells are purged via PCD mechanisms, and (3) a replace response in which neuronal progenitors unsuccessfully attempt to re-enter the cell cycle, with resultant aneuploidy, tau phosphorylation, and neurofibrillary tangle formation. In addition to defining a role for aging in AD pathogenesis, the mitochondrial cascade hypothesis also allows and accounts for histopathologic overlap between the sporadic, late-onset and autosomal dominant, early onset forms of the disease.