3 ms·
My outsider's opinion is that I think that a lot of cited articles are not always thoroughly examined, or of they are examined they are used to confirm the bias
by finton 16y ago
My outsider's opinion is that I think that a lot of cited articles are not always thoroughly examined, or of they are examined they are used to confirm the biases of a particular researcher.
I recently became interested in the idea of possible anesthetic neurotoxicity in infants and looked at a number of papers. The basic research seems solid, but the conclusions drawn are strangely inconsistent.
Neonatal rat, mouse and pregnant guinea pig models are used, and recent studies have been done on monkeys. It appears that there is a high incidence of cell death after exposure to anesthesia, but there is a relatively narrow window of vulnerability, which apparently peaks at 7 days postnatal in rats and rapidly diminishes. 5 day old monkeys were affected by prolonged exposure to ketamine, and 35 day old monkeys were not. Similar results were seen in guinea pigs.
What strikes me, is that this window of vulnerability is differently equated to human development by researchers, despite years of research into ethanol neurotoxicity (anesthetic studies seem to be more recent). Estimates for 7 to 14 day old rat-human equivalents range from pre-term infants to full-term newborns, to mid-gestation human fetuses and to children up to 3 years old. Two monkey papers, one using ketamine, and another using isoflurane also came up with different vulnerability periods based on similar data by using different sources of information on neurodevelopment, one published in the 1970's and one more recent.
I cannot understand how so many studies could have statements about possible windows of human neurotoxicity, without any certainty about what phase in neurodevelopment they were dealing with. And, oddly enough, the paper describing the model that is used to claim a mid-gestation vulnerability (based on a "bioinformatics approach") clearly states that it cannot be used to predict the "coordinated surge in synaptogenesis just prior to birth in primates", which is hypothesized to be the peak period of vulnerability to anesthetic-induced cell death. So why is it used as a source?
- finton 16y agoTo extend my comment, there are dozens of citations for the 1970's era paper that assert that the "brain growth spurt" extends from the third trimester to the first few years of life. It is then equated with synaptogenesis or "peak synaptogenesis", even though this association may be unclear. The papers then further equate peak synaptogenesis with the period of vulnerability to anesthesia. Many then postulate mechanisms for anesthesia-related neurotoxicity in infants related to mechanisms of synaptogenesis. Not being an expert in the field, I can't refute this argument, but I do find the links between these phenomena to be rather shaky, especially when based on a throwaway reference to a decades old paper.