u/According_Tourist_69

I'm reading about localisation of stroke rn. The mca supplies the parietal lobe, house of cortical sensations. Mca strokes have face + ul loss, motor and sensory. So is the two point discrimination lost only in upper limb or also lower limbs? And is the superior division responsible for cortical sensation or inferior division? I'm aware motor features are exclusively because of superior division, not sure about cortical sensations

Also can mca infarct of cortex be exclusively motor without sensory loss of the same areas?

I want to read something grim, where the narrator is the only person left currently in the present time. I have already decided to get "I am legend", but I want some more suggestions. Do you guys have anything like this in mind?

I'm missing or diagnosing lafb in rbbb patterns where it's not there. The axis calculation rule is getting tricky because the final s wave in lead 1 and the weird avf complex is throwing me off. Any tips to clear out this confusion?

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How long does the neuronal shock last after stroke occurs? My seniors have said that when patient presents in emergency, they can have exaggerated reflexes with positive babinski, but I have seen patients in ward which lack both and have hypotonia after a stroke. So it just seems paradoxical. Could someone help me out by clearing the timeline a bit for me?

Is it seen in 100% patients of stroke? If no what factors decide in what patients is it seen? What factors decide how long it lasts?

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How long does the neuronal shock last after stroke occurs? My seniors have said that when patient presents in emergency, they can have exaggerated reflexes with positive babinski, but I have seen patients in ward which lack both and have hypotonia after a stroke. So it just seems paradoxical. Could someone help me out by clearing the timeline a bit for me?

How long does the neuronal shock last after stroke occurs? My seniors have said that when patient presents in emergency, they can have exaggerated reflexes with positive babinski, but I have seen patients in ward which lack both and have hypotonia after a stroke. So it just seems paradoxical. Could someone help me out by clearing the timeline a bit for me?

I'm in my early 20s, uc since 6 years at this point. I've accepted it,all the lifestyle changes and limitations are a norm to me at this point and life before uc seems to distant of a thing to miss. But I just hope research gives a definitive answer as to how strongly there is a change of my potential children inheriting this shit. I've read about several anecdotal accounts of people having crohn's disease running in their families, some about uc as well- but I just want a definitive yes or no from research, that's the only thing I want an answer for right now.

Hope the personal experience flair covers this.

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I'm trying to understand the natural course of history for nerve lesions- and have been utterly confused by the topic. I just wanted this to be clarified with someone so thought of making a post.

For small fibers:

Initially symptoms are burning sensation, pins and needles sensation, tingling, allodynia. However after complete loss, loss of temperature sensation, inability to feel pain, autonomic symptoms like loss of sweating.

For large fibers:

Cramps, shock like sensations. Later on complete destruction, loss of power, atrophy of muscles, sensory ataxia(wash basin phenomenon= positive romberg, pseudoathetosis), reduced reflexes.

Is it correct?