• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.14 no.1
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• pp.54-56
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• 2003

Spasmodic dysphonia is a task-specific dystonia affecting the laryngeal muscles, resulting forced, strained voice. The pathophysiologic mechanism is not fully understood. We experienced a patient with epilepsy developed transient spasmodic dysphonia during valproic acid monotherapy. The spasmodic dysphonia resolved with dose reduction of valproic acid. Change of neurotransmitters, such as GABA in basal ganglia or blockade of sodium channel is possible mechanism in our case of drug-related spasmodic dysphonia.

• Korean Journal of Biological Psychiatry
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• v.4 no.1
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• pp.29-35
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• 1997

Many disorders in neuropsychiatric field demonstrate variable motor disturbances as their clinical feature or in their courses of illness and also due to psychopharmacological treatment. Although association of such motor disturbances with the pathophysiological aspect of various neuropsychiatric illness are still lacking, some form of motor disturbance offer a window through which pathophysiologic mechanism of such illnesses can be viewed. Cognitive control of motor functions are briefly reviewed in this article and the importance and method of motor function assessment in major neuropsychiatric disorders are also discussed. Motor dysfunction of major neuropsychiatric illness such as schizophrenia and mood disorders may offer a chance of a deeper understanding on the pathophysiologic aspect of their clinical presentation.

• Journal of Chest Surgery
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• v.27 no.4
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• pp.335-338
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• 1994

Traumatic asphyxia is a distinctive clinical syndrome characterized by cervicofacial cyanosis and edema, bilateral subconjuctival hemorrhage, and multiple petechiae of the face, neck, and upper part of the chest after a severe compressive crush injury of the thorax or of the upper part of the abdomen.The pathophysiologic mechanism of traumatic asphyxia is reflux of blood from the heart retrograde through the valveless superior vena cava and the great veins of the head and neck by severe compression of the thorax or the abdomen.We experienced one case of the traumatic asphyxia, and its clinical features are discussed.

• Annals of Clinical Neurophysiology
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• v.20 no.1
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• pp.3-11
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• 2018

Skin biopsy and staining the specimens with immuno-reactive markers has been proven to be a useful method to demonstrate the pathologic status of small nerve fibers. Quantification of intraepidermal nerve fiber density using anti-protein gene product 9.5 antibody is a standard method to diagnose small fiber neuropathy. Skin biopsy also makes it possible to differentiate the nerve fibers according to their function by using different markers. Quantification of dermal structures with different types of nerve fibers could reveal the pathophysiologic mechanism of the disease state.

• Sleep Medicine and Psychophysiology
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• v.24 no.1
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• pp.12-18
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• 2017

Adequate amount and quality of sleep are important for metabolic control in patients with type 2 diabetes. Too short or too long sleep time disrupts glycemic control in both prediabetes and type 2 diabetic patients. Circadian misalignment such as shift work is also associated with an increased risk of developing type 2 diabetes. Clinicians should pay attention to the sleep problems and circadian patterns of patients. However, the pathophysiologic mechanism of the association between sleep and diabetes is likely to be complex and bidirectional. The underlying mechanism remains poorly understood, and further research is warranted.

• Tuberculosis and Respiratory Diseases
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• v.41 no.2
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• pp.73-86
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• 1994

In addition to classic cholinergic and adrenergic pathways, the existence of a third division of autonomic control in the human airways has been proved. It is called a nonadrenergic noncholinergic(NANC) nervous system, and difficult to study in the absence of specific blockers. Neuropeptides are certainly suggested to be transmitters of this NANC nervous system. It is very frustrating to understand the pathophysiologic role of these peptides in the absence of any specific antagonists. However, further studies of neuropeptides might eventually lead to novel forms of treatment for bronchial asthma. Another study of the interaction between different components of the autonomic nervous system, either in ganglionic neurotransmission or by presynaptic modulation of neurotransmitters at the end-organ will elute neural control in airway disease, particularly in asthma. Studies of how autonomic control may be disordered in airway disease should lead to improvements in clinical management. Epithelial damage due to airway inflammation in asthma may induce bronchial hyperresponsiveness. Axon reflex mechanism is one of possible mechanisms in bronchial hyperresponsiveness. Epithelial damage may expose sensory nerve terminals and C-fiber nrve endings are stimulated by inflammatory mediators. Bi-directional communication between the nerves and mast cells may have important roles in allergic process. The psychological factors and conditioning of allergic reactions is suggested that mast cell activation might be partly regulated by the central nervous system via the peripheral nerves. Studies in animal models, in huamn airways in vitro and in patients with airway disease will uncover the interaction between allergic disease processes and psychologic factors or neural mechainsms.

• 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.

• Annals of Clinical Neurophysiology
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• v.8 no.2
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• pp.107-124
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• 2006

The basal ganglia are a group of nuclei located in the deep portion of the brain. Along with the cerebellum, the basal ganglia have a major role in controlling human voluntary movements, and their dysfunction is apparently responsible for various involuntary movements. Although the exact mechanism of how the basal ganglia control movements has yet to be clarified, the model of focused selection (through the direct pathway) and tonic inhibition (via the indirect pathway) is proposed to be a principal functional model of the basal ganglia. Parkinson's disease (PD) is classically characterized by bradykinesia, rigidity and tremor-at-rest. All features seem to be associated with dopamine depletion resulting from the degeneration of the nigrostriatal pathway, which produces reduced activity of the direct pathway and a concurrent enhancement of excitatory output from STN. This change may result in increased tonic background inhibition and reduced focused selection via the direct pathway, causing difficulties in performing voluntary movements selectively. However, it has not been possible to define a single underlying pathophysiologic mechanism that explains all parkinsonian symptoms. Here the data that give separate understanding to each of the three classic features are discussed.

• Annals of Clinical Neurophysiology
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• v.13 no.1
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• pp.26-30
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• 2011

Although the pathophysiologic mechanism is unknown, there has been long-running debate on whether periodic discharges such as periodic lateralized epileptiform discharges (PLEDs) and generalized periodic epileptiform discharges are an ictal or interictal EEG pattern. The goal of this review is to give evidence that such periodic discharges on EEG are not ictal phenomenon and just represent underlying acute brain damage. This review includes coma with epileptiform EEG pattern and its prognostic and therapeutic implications. Based on previous reports, rather than taking the view PLEDs represent either an underlying ictal process or an electrographic correlate of neuronal injury, it would be more reasonable that PLEDs are considered as a dynamic pathophysiological state in which unstable neurobiological processes create an ictal-interictal continuum.

• Korean Journal of Biological Psychiatry
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• v.18 no.2
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• pp.72-79
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• 2011

Recent advances in brain imaging research are remarkable. Among them, many results from a variety of neuroimaging modalities in Alzheimer's dementia accompanied by the development and growing of imaging techniques have been presented in the research field. In this review we are focused on the imaging biomarkers for the Alzheimer's dementia to investigate the pathophysiologic mechanism. Future research on biomarkers for Alzheimer's dementia will provide more diverse and complex mechanisms or hypotheses than have been proposed in the current hypothesis about the pathogenesis of Alzheimer's dementia.