1.Neurogenic pulmonary edema.
Chinese Journal of Pediatrics 2008;46(7):510-512
2.Neurologic Complications of Human Immunodeficiency Virus-type 1 Infection.
Ho Jin KIM ; Sang Yun KIM ; Kyung Bok LEE ; Kwang Woo LEE ; Myoung Don OH ; Kang Won CHOE
Journal of Korean Medical Science 2003;18(2):149-157
A wide variety of neurologic complications associated with human immunodeficiency virus-type 1 (HIV-1) infection result from HIV-1 itself or secondarily related to immunosuppression. In Korea, the number of HIV-1 seropositive populations is increasing, but little has been known about the neurologic complications of HIV-1 infection. To investigate the neurologic complications in HIV-1 infected Korean patients, we performed a cross-sectional study in consecutive admissions to the Seoul National University Hospital between March 1998 and June 1999. Thirty-four HIV-1 seropositive patients were included. As a result, a total of 26 HIV-1 related neurologic complications were identified from 17 patients. Among them, 10 patients showed cognitive/motor abnormalities: 3 HIV-1-associated dementia and 7 possible HIV-1-associated minor cognitive/motor disorder. Neuromuscular complications were found in 10 patients: 9 distal symmetric polyneuropathy, and 1 possible chronic inflammatory demyelinating polyradiculoneuropathy. In 3 patients with focal brain lesions, 2 were presumptively diagnosed as having primary CNS lymphoma, and 1 as having progressive multifocal leukoencephalopathy in the posterior fossa, based on history, clinical findings, serology, radiological appearances, and response to empirical therapy. Other complications included cryptococcal meningitis and only soft neurologic signs without any neurologic disease. Most of these complications (88%) occurred in the advanced stage of infection.
Adult
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Brain/pathology
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HIV Infections/complications*
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HIV Seropositivity
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HIV-1*
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Human
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Korea
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Male
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Nervous System Diseases/etiology*
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Nervous System Diseases/pathology
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Nervous System Diseases/physiopathology
3.Osmotic demyelination syndrome in patients with hyponatremia caused by neurologic disorders.
Yi JIANG ; Jun-Ji WEI ; Ren-Zhi WANG ; Zu-Yuan REN
Acta Academiae Medicinae Sinicae 2011;33(6):696-700
Hyponatremia is relatively common in patients with neurologic disorders, while its diagnosis and treatment remain controversial. Osmotic demyelination syndrome (ODS) has shown to be closely associated with hyponatremia. ODS patients often present as central pontine myelinolysis, extrapontine myelinolysis, or both. This article reviews the clinical manifestations, pathogenesis, and risk factors of ODS in patients with hyponatremia caused by neurologic disorders.
Demyelinating Diseases
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etiology
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therapy
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Humans
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Hyponatremia
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complications
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etiology
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Nervous System Diseases
;
complications
5.Progress on the mechanism and treatment of Parkinson's disease-related pathological pain.
Lin-Lin TANG ; Hao-Jun YOU ; Jing LEI
Acta Physiologica Sinica 2023;75(4):595-603
Parkinson's disease (PD) is a common neurodegenerative disease characterized by motor symptoms, including bradykinesia, resting tremor, and progressive rigidity. More recently, non-motor symptoms of PD, such as pain, depression and anxiety, and autonomic dysfunction, have attracted increasing attention from scientists and clinicians. As one of non-motor symptoms, pain has high prevalence and early onset feature. Because the mechanism of PD-related pathological pain is unclear, the clinical therapy for treating PD-related pathological pain is very limited, with a focus on relieving the symptoms. This paper reviewed the clinical features, pathogenesis, and therapeutic strategies of PD-related pathological pain and discussed the mechanism of the chronicity of PD-related pathological pain, hoping to provide useful data for the study of drugs and clinical intervention for PD-related pathological pain.
Humans
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Parkinson Disease/therapy*
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Neurodegenerative Diseases
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Autonomic Nervous System Diseases/complications*
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Anxiety
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Pain/etiology*
7.Alcoholic pellagra encephalopathy combined with Wernicke disease.
Seong Ho PARK ; Duk Lyul NA ; Jae Hong LEE ; Byung Joon KIM ; Ho Jin MYUNG ; Mi Kyung KIM ; Je Geun CHI
Journal of Korean Medical Science 1991;6(1):87-93
Clinical and postmortem findings of a case that had combined alcoholic pellagra encephalopathy and Wernicke disease are described. This 51-year-old malnourished and chronic alcoholic man presented with progressive mental deterioration, pellagra dermatitis, hypertonus of the neck and other musculatures, myoclonic jerks with bizarre involuntary movements, in addition to total external ophthalmoplegia and gait disturbance. After administration of multivitamins, including thiamine and nicotinamide, these neurologic abnormalities were dramatically improved in a few days. However, the patient died thereafter because of sepsis associated with pneumonia. Postmortem examination revealed marked abnormalities in CNS, characterized by diffuse atrophy of gray matter and widespread neuronal degeneration and characteristic central chromatolysis in pontine nuclei, dentate nuclei, cranial nerve nuclei in the brain stem, Betz cells of the cerebral cortex, and Clarke's column and anterior horn cells of the spinal cord. There were also atrophy and gliosis of the mammillary bodies, degeneration and vascular proliferation of periaqueductal gray matter, and massive gliosis around the third ventricle. These neuropathological changes were compatible with symptoms of both alcoholic pellagra encephalopathy and Wernicke's disease, but they were also strongly suspected on clinical grounds.
Alcoholism/*complications
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Central Nervous System Diseases/complications/pathology
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Humans
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Male
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Middle Aged
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Pellagra/*complications/pathology
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Wernicke Encephalopathy/*complications/pathology
9.Regulation of axonal regeneration following the central nervous system injury in adult mammalian.
Ran LIU ; Xi-Ping CHEN ; Lu-Yang TAO
Neuroscience Bulletin 2008;24(6):395-400
It has been well established that the recovery ability of central nervous system (CNS) is very poor in adult mammals. As a result, CNS trauma generally leads to severe and persistent functional deficits. Thus, the investigation in this field becomes a "hot spot". Up to date, accumulating evidence supports the hypothesis that the failure of CNS neurons to regenerate is not due to their intrinsic inability to grow new axons, but due to their growth state and due to lack of a permissive growth environment. Therefore, any successful approaches to facilitate the regeneration of injured CNS axons will likely include multiple steps: keeping neurons alive in a certain growth-state, preventing the formation of a glial scar, overcoming inhibitory molecules present in the myelin debris, and giving direction to the growing axons. This brief review focused on the recent progress in the neuron regeneration of CNS in adult mammals.
Animals
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Axons
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physiology
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Central Nervous System Diseases
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complications
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metabolism
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pathology
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Humans
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Mammals
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physiology
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Nerve Regeneration
;
physiology