저산소성허혈성뇌병증의 합병증
Common Complications after Hypoxic-ischemic Encephalopathy
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Hypoxic-ischemic encephalopathy (HIE) is one of the major disease for neuro-rehabilitation, as well asone of the important impairment. HIE typically shows global deterioration of brain function with relativepreservation of brain stem reflexes, and topographic pattern of damage; the CA1 hippocampal cells,cerebellar Purkinje cells, neocortical neurons in layers 3, 5, 6 and basal ganglia. The characteristics ofpatho-mechanism including persistent vegetative state, seizure, autonomic dysfunction and secondaryParkinsonism are causative factors of several complications. Management of these complications sometimescurative, but more often re-adaptive and palliative. Understanding and proper rehabilitation of complicationswill be one of the most important therapeutic strategies for patients with HIE.
Abstract
Hypoxic-ischemic encephalopathy (HIE) is one of the major disease for neuro-rehabilitation, as well asone of the important impairment. HIE typically shows global deterioration of brain function with relativepreservation of brain stem reflexes, and topographic pattern of damage; the CA1 hippocampal cells,cerebellar Purkinje cells, neocortical neurons in layers 3, 5, 6 and basal ganglia. The characteristics ofpatho-mechanism including persistent vegetative state, seizure, autonomic dysfunction and secondaryParkinsonism are causative factors of several complications. Management of these complications sometimescurative, but more often re-adaptive and palliative. Understanding and proper rehabilitation of complicationswill be one of the most important therapeutic strategies for patients with HIE.
참고문헌 (33)
- Kaplan PW, "Electrophysiological prognostication and brain injury from cardiac arrest", Seminars in neurology, 26, pp.403~412 (2006)
- Khot S, "Long-term neurological complications after hypoxic-ischemic encephalopathy", Semin Neurol, 26, pp.422~431 (2006)
- Greer DM, "Mechanisms of injury in hypoxic-ischemic encephalopathy:implications to therapy", Seminars in neurology, 26, pp.373~379 (2006)
- Plum F, "Delayed neurological deterioration after anoxia", Arch Intern Med, 110, pp.18~25 (1962)
- Petito CK, "Delayed hippocampal damage in humans following cardiorespiratory arrest", Neurology, 37, pp.1281~1286 (1987)
- Foreman B, "Epilepsy emergencies: diagnosis and management", Neurol Clin, 30, pp.11~41 (2012)
- Lu-Emerson C, "Neurological sequelae of hypoxicischemic brain injury", NeuroRehabilitation, 26, pp.35~45 (2010)
- PVS TM-STFo, "Medical aspects of the persistent vegetative state (2)", N Engl J Med, 330, pp.1572~1579 (1994)
- Dougherty JH, Jr, "Hypoxic-ischemic brain injury and the vegetative state: clinical and neuropathologic correlation", Neurology, 31, pp.991~997 (1981)
- Physicians AroawpotRCo, "The vegetative state: guidance on diagnosis and management", Clin Med, 3, pp.249~254 (2003)
- Levy DE, "Predicting outcome from hypoxic-ischemic coma", JAMA, 253, pp.1420~1426 (1985)
- Group BRCTIS, "Randomized clinical study of thiopental loading in comatose survivors of cardiac arrest", N Engl J Med, 314, pp.397~403 (1986)
- Krumholz A, "Outcome from coma after cardiopulmonary resuscitation: relation to seizures and myoclonus", Neurology, 38, pp.401~405 (1988)
- DeLorenzo RJ, "Epidemiology of status epilepticus", J Clin Neurophysiol, 12, pp.316~325 (1995)
- Hirsch LJ, "Status epilepticus", Continuum (Minneap Minn), 19, pp.767~794 (2013)
- Jumao-as A, "Myoclonic status epilepticus: a clinical and electroencephalographic study", Neurology, 40, pp.1199~1202 (1990)
- Baguley IJ, "Autonomic complications following central nervous system injury", Semin Neurol, 28, pp.716~725 (2008)
- Fernandez-Ortega JF, "Paroxysmal sympathetic hyperactivity after traumatic brain injury : clinical and prognostic implications", Journal of neurotrauma, 29, pp.1364~1370 (2012)
- Perkes I, "A review of paroxysmal sympathetic hyperactivity after acquired brain injury", Annals of neurology, 68, pp.126~135 (2010)
- Baguley IJ, "A critical review of the pathophysiology of dysautonomia following traumatic brain injury", Neurocrit Care, 8, pp.293~300 (2008)
- Baguley IJ, "The excitatory:inhibitory ratio model (EIR model):An integrative explanation of acute autonomic overactivity syndromes", Med Hypotheses, 70, pp.26~35 (2008)
- Do D, "Treatment of paroxysmal sympathetic storm with labetalol", J Neurol Neurosurg Psychiatry, 69, pp.832~833 (2000)
- Levy ER, "Paroxysmal sympathetic hyperactivity (sympathetic storm) in a patient with permanent vegetative state", J Palliat Med, 14, pp.1355~1357 (2011)
- Venkatesan A, "Movement disorders after resuscitation from cardiac arrest", Neurologic clinics, 24, pp.123~132 (2006)
- Eltahawy HA, "Primary dystonia is more responsive than secondary dystonia to pallidal interventions: outcome after pallidotomy or pallidal deep brain stimulation", Neurosurgery, 54, pp.613~619 (2004)
- Ghika J, "Postanoxic generalized dystonia improved by bilateral Voa thalamic deep brain stimulation", Neurology, 58, pp.311~313 (2002)
- Sage JI, "Man-in-the-barrel syndrome", Neurology, 36, pp.1102~1103 (1986)
- Duggal N, "Selective vulnerability of the lumbosacral spinal cord after cardiac arrest and hypotension", Stroke, 33, pp.116~121 (2002)
- Montero J, "Report of four cases with watershed parieto-occipital lesions from vertebrobasilar ischemia or systemic hypotension", Acta Neurol Belg, 82, pp.270~280 (1982)
- Gottfried JA, "Association with arylsulfatase A deficiency and lactic acidosis on proton MR spectroscopy", Neurology, 49, pp.1400~1404 (1997)
- Custodio CM, "Delayed postanoxic encephalopathy : a case report and literature review", Arch Phys Med Rehabil, 85, pp.502~505 (2004)
- Khot S, "An unsuccessful trial of immunomodulatory therapy in delayed posthypoxic demyelination", Neurocrit Care, 7, pp.253~256 (2007)
- Thacker AK, "Delayed post-anoxic encephalopathy", Postgrad Med J, 71, pp.373~374 (1995)
