Long-term neurological complications after hypoxic-ischemic encephalopathy
- PMID: 16969743
- DOI: 10.1055/s-2006-948323
Long-term neurological complications after hypoxic-ischemic encephalopathy
Abstract
Hypoxic-ischemic encephalopathy accompanying cardiac arrest is a common cause of long-term neurological dysfunction. With the improvement in prehospital emergency systems, larger numbers of people are resuscitated from cardiac arrests, although with the increased prospect of neurological sequelae. Neurological impairment after cardiac arrest is dependent on the degree of brain damage suffered during the arrest. Although the duration and severity of brain ischemia is often difficult to determine, clinicians are often faced with difficult issues related to predicting outcome related to awakening and long-term neurological deficits after the arrest. Neurological impairments range from mild cognitive deficits to severe motor and cognitive deficits that preclude independence in many activities of daily living. Several neurological syndromes have been described in patients who awaken from hypoxic-ischemic coma with lasting motor and cognitive deficits. This review will address many of the common syndromes after hypoxic-ischemic encephalopathy, including persistent vegetative states, seizures, myoclonus, movement disorders, cognitive dysfunction, and other neurological abnormalities.
Similar articles
-
Neurological sequelae of hypoxic-ischemic brain injury.NeuroRehabilitation. 2010;26(1):35-45. doi: 10.3233/NRE-2010-0534. NeuroRehabilitation. 2010. PMID: 20130354 Review.
-
Adult neurological function following neonatal hypoxia-ischemia in a mouse model of the term neonate: water maze performance is dependent on separable cognitive and motor components.Brain Res. 2006 Nov 6;1118(1):208-21. doi: 10.1016/j.brainres.2006.08.030. Epub 2006 Sep 25. Brain Res. 2006. PMID: 16997287
-
Prognostic role of somatosensory and auditory evoked potentials in paediatric hypoxic-ischemic encephalopathy managed with hypothermia: an illustrative case.Neurophysiol Clin. 2009 Apr;39(2):101-5. doi: 10.1016/j.neucli.2009.02.003. Epub 2009 Mar 17. Neurophysiol Clin. 2009. PMID: 19467440
-
Brain injury from cardiac bypass procedures.Semin Neurol. 2006 Sep;26(4):432-9. doi: 10.1055/s-2006-948324. Semin Neurol. 2006. PMID: 16969744 Review.
-
Movement disorders after resuscitation from cardiac arrest.Neurol Clin. 2006 Feb;24(1):123-32. doi: 10.1016/j.ncl.2005.11.001. Neurol Clin. 2006. PMID: 16443134 Review.
Cited by
-
Long-term depression in Purkinje neurons is persistently impaired following cardiac arrest and cardiopulmonary resuscitation in mice.J Cereb Blood Flow Metab. 2017 Aug;37(8):3053-3064. doi: 10.1177/0271678X16683691. Epub 2016 Dec 19. J Cereb Blood Flow Metab. 2017. PMID: 28168893 Free PMC article.
-
Factors Associated with Newly Developed Postoperative Neurological Complications in Patients with Emergency Surgery for Acute Type A Aortic Dissection.Medicina (Kaunas). 2023 Dec 23;60(1):27. doi: 10.3390/medicina60010027. Medicina (Kaunas). 2023. PMID: 38256288 Free PMC article.
-
Ammonia-induced stress response in liver disease progression and hepatic encephalopathy.Nat Rev Gastroenterol Hepatol. 2024 Nov;21(11):774-791. doi: 10.1038/s41575-024-00970-9. Epub 2024 Sep 9. Nat Rev Gastroenterol Hepatol. 2024. PMID: 39251708 Review.
-
Calcium/Calmodulin-Dependent Kinase (CaMKII) Inhibition Protects Against Purkinje Cell Damage Following CA/CPR in Mice.Mol Neurobiol. 2020 Jan;57(1):150-158. doi: 10.1007/s12035-019-01765-9. Epub 2019 Sep 13. Mol Neurobiol. 2020. PMID: 31520314 Free PMC article.
-
Increasing small conductance Ca2+-activated potassium channel activity reverses ischemia-induced impairment of long-term potentiation.Eur J Neurosci. 2014 Oct;40(8):3179-88. doi: 10.1111/ejn.12683. Epub 2014 Jul 31. Eur J Neurosci. 2014. PMID: 25080203 Free PMC article.
Publication types
MeSH terms
LinkOut - more resources
Full Text Sources
Medical