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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2013.1
- 수록면
- 65 - 74 (10page)
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초록· 키워드
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The development of hyperexcitability in amyotrophic lateral sclerosis (ALS) is a well-known phenomenon. Despite controversy as to the underlying mechanisms, cortical hyperexcitability appears to be closely related to the interplay between excitatory corticomotoneurons and inhibitory interneurons. Hyperexcitability is not a static phenomenon but rather shows a pattern of progression in a spatiotemporal aspect. Cortical hyperexcitability may serve as a trigger to the development of anterior horn cell degeneration through a ‘dying forward’process. Hyperexcitability appears to develop during the early disease stages and gradually disappears in the advanced stages of the disease, linked to the destruction of corticomotorneuronal pathways. As such, a more precise interpretation of these unique processes may provide new insight regarding the pathophysiology of ALS and its clinical features. Recently developed technologies such as threshold tracking transcranial magnetic stimulation and automated nerve excitability tests have provided some clues about underlying pathophysiological processes linked to hyperexcitability. Additionally, these novel techniques have enabled clinicians to use the specific finding of hyperexcitability as a useful diagnostic biomarker, enabling clarification of various ALS-mimic syndromes, and the prediction of disease development in pre-symptomatic carriers of familial ALS. In terms of nerve excitability tests for peripheral nerves, an increase in persistent Na+ conductances has been identified as a major determinant of peripheral hyperexcitability in ALS, inversely correlated with the survival in ALS. As such, the present Review will focus primarily on the puzzling theory of hyperexcitability in ALS and summarize clinical and pathophysiological implications for current and future ALS research.
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참고문헌 (26)
참고문헌 신청
/ 2001 / Section I: Alphabetic list of terms with definitions / Muscle & Nerve 24 : S5 ~ S28
Bostock H / 1998 / Threshold tracking techniques in the study of human peripheral nerve / Muscle & Nerve 21 : 137 ~ 158
Chou SM / 1993 / Amyotrophic lateral sclerosis: lower motor neuron disease spreading to upper motor neurons / Muscle & Nerve 16 : 864 ~ 869
Eisen A / 1992 / Amyotrophic lateral sclerosis (ALS): a phylogenetic disease of the corticomotoneuron? / Muscle & Nerve 15 : 219 ~ 224
Eisen A / 2009 / Amyotrophic lateral sclerosis-Evolutionary and other perspectives / Muscle & Nerve 40 : 297 ~ 304
Bostock H / 1998 / Threshold tracking techniques in the study of human peripheral nerve / Muscle & Nerve 21 : 137 ~ 158
Chou SM / 1993 / Amyotrophic lateral sclerosis: lower motor neuron disease spreading to upper motor neurons / Muscle & Nerve 16 : 864 ~ 869
Eisen A / 1992 / Amyotrophic lateral sclerosis (ALS): a phylogenetic disease of the corticomotoneuron? / Muscle & Nerve 15 : 219 ~ 224
Eisen A / 2009 / Amyotrophic lateral sclerosis-Evolutionary and other perspectives / Muscle & Nerve 40 : 297 ~ 304
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