Hypoxic-ischemic encephalopathy
Hypoxic-ischemic encephalopathy (HIE) is a medical emergency and serious birth complication caused by impaired cerebral blood flow and oxygen delivery to the brain
- What is HIE?
- HIE & cannabinoids
- Text references, literature discussion
& clinical trials
What is Hypoxic-ischemic encephalopathy ?
Definition & Cause
Hypoxic-ischemic encephalopathy (HIE) is a medical emergency and serious birth complication caused by impaired cerebral blood flow and oxygen delivery to the brain. The complication may be fatal in newborns and/or cause severe disabilities such as developmental delay, cognitive impairments, or cerebral palsy.1
- Cannabinoids
- Cannabinoid receptors
- Endocannabinoids
- CBD
- 5-HT1A
- CB1
- CB2
- PPARγ
- A2A (Adenosine)
- 2AG
- Anandamide
- OEA
- PEA
- Terpenes
- Strains
- Enzymes
- Metabolites
Terpenes
Strains
Synthesizing & Degrading Enzymes
Metabolites
The connection between HIE
& cannabinoids
The endocannabinoid system may be involved in controlling the underlying processes of HIE when it is happening. Therefore, cannabinoids may help improve the symptoms associated with it. Preclinical data proposes that the cannabinoid CBD may be a viable therapeutic in the treatment of HIE.2
Note: If you have any further information relevant to the connection between HIE and cannabinoids, or find any of the information inaccurate, outdated or incomplete please contact us here.
Text references, literature discussion
& clinical trials
- Text references
- Literature discussion
- Clinical trials
Review
The endocannabinoid system is involved in neonatal Hypoxic-ischemic encephalopathy. It was shown that CB1 and CB2 are increased and AEA, 2-AG, OEA, and PEA demonstrate elevated levels after cerebral ischemia (England et al., 2015; Lara-Celador et al., 2013).
Astrocytic reaction, neuronal death, and dendritic loss can be reduced through selective activation of CB1 in a stoke model in adult mice (Caltana et al., 2015).
Neuroinflammation, ischemic injury, and cognitive deficits can be reduced through selective activation of CB2 in different models of stroke (Choi et al., 2013; Ronca et al., 2015; Zarruk et al., 2012).
In hypoxia-ischemic animal models, CBD has been demonstrated to have neuroprotective properties with functional and behavioral recovery (Alvarez et al., 2008; Lafuente et al., 2011).
References
Clinical trials
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