Mild hypothermia in neurologic emergency: An update

Inamasu, Joji; Ichikizaki, Kiyoshi

doi:10.1067/mem.2002.123697

Cited by 60 publications

(35 citation statements)

References 100 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Mild cooling may result in a reduction of the delivery of ammonia to the brain (Inamasu and Ichikizaki 2002;Polderman 2004;Vaquero and Blei 2005;. In patients with severe hyperammonaemia due to hepatic encephalopathy without elevations of intracranial pressure (ICP), mild hypothermia appeared to reduce the risks of developing elevated ICP (BelangerQuintana et al 2003;Jalan et al 2004;Zwingmann et al 2004).…”

Section: Hypothermiamentioning

confidence: 99%

Neurological implications of urea cycle disorders

Gropman

Summar

Leonard³

2007

J of Inher Metab Disea

191

152

View full text Add to dashboard Cite

SummaryThe urea cycle disorders constitute a group of rare congenital disorders caused by a deficiency of the enzymes or transport proteins required to remove ammonia from the body. Via a series of biochemical steps, nitrogen, the waste product of protein metabolism, is removed from the blood and converted into urea. A consequence of these disorders is hyperammonaemia, resulting in central nervous system dysfunction with mental status changes, brain oedema, seizures, coma, and potentially death. Both acute and chronic hyperammonaemia result in alterations of neurotransmitter systems. In acute hyperammonaemia, activation of the NMDA receptor leads to excitotoxic cell death, changes in energy metabolism and alterations in protein expression of the astrocyte that affect volume regulation and contribute to oedema. Neuropathological evaluation demonstrates alterations in the astrocyte morphology. Imaging studies, in particular 1 H MRS, can reveal markers of impaired metabolism such as elevations of glutamine and reduction of myoinositol. In contrast, chronic hyperammonaemia leads to adaptive responses in the NMDA receptor and impairments in the glutamate-nitric oxide-cGMP pathway, leading to alterations in cognition and learning. Therapy of acute hyperammonaemia has relied on ammonia-lowering agents but in recent years there has been considerable interest in neuroprotective strategies. Recent studies have suggested restoration of learning abilities by pharmacological manipulation of brain cGMP with phosphodiesterase inhibitors. Thus, both strategies are intriguing areas for potential investigation in human urea cycle disorders.

show abstract

Section: Hypothermiamentioning

confidence: 99%

Neurological implications of urea cycle disorders

Gropman

Summar

Leonard³

2007

J of Inher Metab Disea

191

152

View full text Add to dashboard Cite

show abstract

“…Man etterspør mer forskning som kan dokumentere at indusert hypotermi gir bedre utkomme og er en sikker behandling også for denne aldersgruppen. Inamasu og Ichikizaki (26) forfekter dette synet etter en litteraturgjennomgang i 2002. Dette blir også støttet av en undersøkelse fra 2006 gjort blant leger, hovedsakelig amerikanske, som jobbet med akutt og kritisk syke barn.…”

Section: Diskusjonunclassified

Kjøler ned barn etter hjertestans

Flydal¹,

Grevstad²

2011

Sykepleien

View full text Add to dashboard Cite

“…Although agreement on terminology is lacking, it is generally accepted that, depending on the core temperature, hypothermia is classified as mild (33–36°C), moderate (28–32°C), deep (10–28°C), profound (5–10°C), and ultraprofound (0–5°C) [13]. Despite this widely used classification, the use of term ‘moderate hypothermia’ varies widely in neurocritical care [14] and, surprisingly, in this classification, the 32–33°C range, which is the most widely used range in neuro-ICUs, has simply been forgotten. For the sake of consistency, we will consider the usual lower core temperature used in the management of stroke and head injury (32–33°C) as moderate hypothermia.…”

Section: Induced Hypothermia: Basic Conceptsmentioning

confidence: 99%

Neuroprotection in Malignant MCA Infarction

Delgado

Sahuquillo²,

Poca³

et al. 2006

Cerebrovasc Dis

View full text Add to dashboard Cite

Massive unilateral hemispheric infarction often develops progressive postischemic edema that leads to a malignant course of stroke with mortality of up to 80% with conventional medical therapies. Hypothermia and decompressive hemicraniectomy have shown neuroprotective effects in several animal models of focal transient and permanent MCA occlusion by reducing infarct size and improving neurological outcome. Our aim in this paper was to review the possible mechanisms of both therapies as well as the optimal time window and duration of application of each treatment in animal model and in human malignant MCA infarction reported in the literature.

show abstract

Mild hypothermia in neurologic emergency: An update

Cited by 60 publications

References 100 publications

Neurological implications of urea cycle disorders

Neurological implications of urea cycle disorders

Kjøler ned barn etter hjertestans

Neuroprotection in Malignant MCA Infarction

Contact Info

Product

Resources

About