?
https://www.scidev.net/asia-pacific/news/oral-polio-drops-linked-to-paralysis-in-india/
The news articles lists a study that finds that the flaccid paralysis was unusually high when vaccines were being given in india
"A previous study of data from 2000 to 2010 has detailed the NPAFP rate in a state correlated with the pulse polio rounds conducted there, and the strongest correlation with the NPAFP rate was found when the number of doses from the previous 4 years were used."
They however admit that this doesn't prove a causal relationship
"However, a simple association being found with regression analysis does not prove a causal relationship."
However what they found odd was that the paralysis rates went down as the vaccine rounds went down
NPAFP rate correlated with the OPV pulse polio rounds in that year (R = 0.46; p < 0.001), and the NPAFP rate started to decrease from 2012 when the number of pulse polio rounds had decreased. NPAFP rates in the states of Uttar Pradesh (UP) and Bihar were the highest in the country. Looking at the high-NPAFP states of UP and Bihar, we found that the correlation coefficient was strongest when doses used over 5 years was considered (R = 0.76; p < 0.001). The response to the reduction in OPV rounds (de-challenging) adds credence to the assumption that OPV was responsible for the change in the NPAFP rate. Now that India has been polio-free for over 6 years, we propose that we may be able to reduce NPAFP by further reducing pulse polio rounds
My thoughts: I honestly think that there is a possible causation here since vaccine rounds went up, the NFAFP also went up and went down as the rounds went down. However at the same time though, we have to take in account that correlation doesn't equal causation (especially when other factors haven't been ruled out).
I dont get it at all. If the muscle stays depolarized then the calcium is in the cytoplasm. Assuming there is enough ATP why does the muscle stop contracting? Please help I’m a med student and it makes me so annoyed when I cant understand a concept.
Hi all, just ran into a card in Anking: Acetylcholinesterase inhibitor poisoning causes flaccid paralysis due to NMJ nicotinic ACh receptor overactivation
Does someone know why the paralysis is flaccid? I assume with so much Ach activating the skeletal muscles, you would be hypertonic.
Hello everyone, with COVID-19 and lockdown happening a lot of conspiracy theories are now circling. Well I am not here to discuss these but rather to discuss an article from India about the Polio vaccination program. So I was shown a video from an anti-vaxxer (doesn't matter who) who was talking about the polio campaign and mentioning and interesting article from the "International Journal of Environmental Research and Public Health": https://dx.doi.org/10.3390%2Fijerph15081755
(the numbers were wrongfully interpreted during the video but the article itself is quite interesting)
So there seems to be quite a high correlation of the rounds of polio vaccination and acute flaccid paralysis. The article shows that the incidence of acute flaccid paralysis in children who have received the polio vaccination has increased significantly. The risk rises additionally with each round of vaccination received. The numbers used were official numbers from the WHO statistics. So what I am wondering is why there was so little resonance concerning that article even though there seems to be a significant correlation.
DISCLAIMER: I am still a med student and might have yet the full oversight. But I am happy for everyone who is proficient in that topic.
If a patient has a vertebral subluxation after intubation, wouldn't we expect LMN symptoms at the level of the lesion and then UMN (spastic paralysis) below?
Why does compression of the spinal cord cause flaccid paralysis acutely?
I was under the impression that spastic paralysis is when a muscle is getting depolarized too much and flaccid paralysis when depolarization is not occuring. Is this correct?
My logic above doesn't seem to hold up for this card below. My thinking is that because you have more ACh, more depolarization is occuring so it should be spastic paralysis
https://preview.redd.it/dx92mtyc06u31.png?width=1261&format=png&auto=webp&s=0d8cacdc90e0850e16bba29bd01db3152e2db982
I understand that atropine is an anti-muscarinic drug. Is the reason atropine doesn't reverse flaccid paralysis because nicotinic receptors will still be stimulated by Ach? So techincally, atropine mitigates flaccid paralysis?
https://preview.redd.it/5khzh1q08pa31.png?width=747&format=png&auto=webp&s=aa864a88c5f58b9c47c4c8ef79c9798c60d45137
With my limited undergraduate biology courses, I understand how the toxin responsible for tetanus prevents the release of GABA (neurotransmitter that causes relaxation) without GABA the muscles can't relax. While, botulinum toxin prevents the action of snare proteins that are responsible for the release of acetylcholine into the neuromuscular junction to signal muscle contraction (no snare proteins no contraction i.e. flaccid paralysis). My question is what actually happens to the body? Is one more potent than the other? Do they both act differently on different tissue types?
I dont get it at all. If the muscle stays depolarized then the calcium is in the cytoplasm. Assuming there is enough ATP why does the muscle stop contracting? Please help I’m a med student and it makes me so annoyed when I cant understand a concept.
I dont get it at all. If the muscle stays depolarized then the calcium is in the cytoplasm. Assuming there is enough ATP why does the muscle stop contracting? Please help I’m a med student and it makes me so annoyed when I cant understand a concept.
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