we had another firm of students join the acute admissions unit today
as usual we introduced ourselves, briefly mentioning our genetic inheritances
this time the group's knowledge of what a SNP is was good, thanks to the presence of a geneticist
i have written about SNPs before - it is an area of such growing importance that i would strongly recommend you find out something about them
_ _ _
our case discussion, truncated because of time was again centred around 'dizziness'
while we did not go through things in great detail, the importance of disentangling the terminology was highlighted (see previous post)
the other thing that struck me was the need for detail when it comes to the history in this presenting problem
you really do need to find out everything you can about the circumstances of what happened
eg, where: which shop? which department? having just done what? carrying what? wearing what?
all these details will help you to build up a picture of 1) what this lady's cognitive function is like and 2) clues that point to a specific diagnosis (eg fast onset-fast offset for arrhythmia)
_ _ _
we also mentioned how to start a case presentation well (content - the right amount of data & process - a positive, professional dialogue)
'framing' the problem is key, because without asking the right question, you cannot hope to find the right answer
i would encourage you to watch how real doctors present cases
how many of them need the notes to present? not many i suspect
could you present without your notes?
Salaam
sabih
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As proof of our unrivalled dedication to the new AAU firm, we thought we'd say hi from AAU take at 3:05am!
ReplyDeletePutting earlier neuro exam recap into practice.
Yours as always,
Lyndon and Kirstin
On causes of 'dizziness'/LOC:
ReplyDeleteReading one of your earlier posts '2 elderly women with falls' (Nov 09) you list stroke as a possible cause of LOC, but I thought we said on monday that it was quite unlikely?
The brain structures underlying consciousness are not completely delineated (and some would argue they never will be: see ray tallis in the new scientist, helpfully reposted here for those without a NS subscription: http://www.brainwaving.com/2010/02/23/can-you-find-consciousness-in-the-brain/) but if we stick to basic arousal then we're generally talking about the reticular formation (as we talked about on monday) and the thalamus (see http://www.jneurosci.org/cgi/content/full/19/13/5506 for an interesting paper on the mechanism of propofol-induced LOC, the introduction has a brief discussion of the regions involved).
Obviously, for a stroke to damage these areas the arteries that supply them have to be the ones that have been affected. We discussed the reticular formation and its blood supply on monday - from the vertebrobasilar system. The thalamus has a relatively complex blood supply: 3 arteries from the veretebrobasilar system and one from the Posterior communicating artery (see http://stroke.ahajournals.org/cgi/content/full/34/9/2264/FIG1 for a good diagram - NB many of the 'four' arteries are actually made of up several smaller arteries e.g .the 'choroidal artery' which is shown in all it's proper (slightly confusing) glory on this diagram).
As far as I can see - and my interpretation of the circle of willis may be dodgy - if an infarct/haemorrage occured proximal enough and was large enough to affect the reticular formation the patient is likely to be dead. A thalamic infarct would be caused by a problem further out. Indeed, paramedian thalamic infarct is one of the possible presentations of a posterior cerebral artery stroke (http://emedicine.medscape.com/article/1160677-overview). However, the effect on consciousness seems to present quite differently from the sort of transient LOC that might cause a fall or a patient complaining of dizziness: it can range from lethargy to coma and generally takes at least days to resolve (which makes sense, considering the pathophysiology).
On that basis, then, I can't see how stroke should cause LOC - which is the conclusion we came to on monday - but is there another reason you included it in your list in November?
charis kai eirene,
Kirstin
Hello!
ReplyDeleteDespite not staying all night, we still managed to have a really interesting AAU on take, esp. as we were there from 5 pm!
We saw a really interesting pt who is now on the ward. His range of symptoms make for a good history but we dont want to give too much away (as we would like to present him at JCCP)!
We hope you all enjoy your on takes as much as we enjoyed ours! :))
Christiana and Hend
I tried to post this yesterday but it didn’t seem to work and I ended up deleting it accidentally! To try again:
ReplyDeleteA thought that occurred to me while reading some of the other posts on here: in '2 women with falls' (nov 09) you list stroke as a possible cause of LOC, but on monday I thought we'd said that it wasn't…
To think it through, the areas involved in consciousness aren’t wonderfully well demarcated (and some people think they never will be: see Ray Tallis in the New Scientist, helpfully re-posted here for those without a NS subscription: http://www.brainwaving.com/2010/02/23/can-you-find-consciousness-in-the-brain/ ) but if we stick to basic arousal we’re talking about the reticular formation (as we discussed on Monday) and the thalamus (see: http://www.jneurosci.org/cgi/content/full/19/13/5506 for an interesting paper on the mechanism of propofol-induced LOC, the introduction has a brief discussion of the areas and mechanisms involved).
In strokes we’re dealing with the vascular supply to the affected area. The RF is supplied by the vertebrobasilar system and the thalamus has a relatively complex blood supply via 3 arteries from the vertebrobasilar system and one from the posterior communicating artery (see: http://stroke.ahajournals.org/cgi/content/full/34/9/2264/FIG1 for a beautiful diagram of this, though NB that many of the ‘arteries’ are actually made up of lots of little arteries which this diagram shows in their full, but slightly confusing, glory).
When we said that ‘posterior’ strokes are quite rare, what did we mean by ‘posterior’? Does this term only cover arteries derived from the posterior cerebral, or also from the vertebral/basilar/posterior communicating? As far as I can see, complete occlusion of the vertebral artery would kill the patient, but are occlusions of more minor vessels possible/common, and would they produce a functional effect?
Leaving the reticular formation aside, as it seems too diffuse a structure to be severely affected by anything but a pretty massive infarct, thalamic infarct can cause LOC. http://emedicine.medscape.com/article/1160677-overview describes paramedian thalamic infarct as one of the possible types of posterior artery stroke. However, the presentation of the effect on consciousness doesn’t really seem consistent with the sort of transient LOC that would cause a fall: severity ranges from lethargy through to coma, and it resolves in days or longer (which makes sense considering the pathophysiology).
Considering all that, I guess I’d agree with our conclusion on Monday, but was there another reason you listed stroke as one of your LOC differentials previously?
So here's a try at reposting that stroke comment in two halves:
ReplyDeleteA thought that occurred to me while reading some of the other posts on here: in '2 women with falls' (nov 09) you list stroke as a possible cause of LOC, but on monday I thought we'd said that it wasn't…
To think it through, the areas involved in consciousness aren’t wonderfully well demarcated (and some people think they never will be: see Ray Tallis in the New Scientist, helpfully re-posted here for those without a NS subscription: http://www.brainwaving.com/2010/02/23/can-you-find-consciousness-in-the-brain/ ) but if we stick to basic arousal we’re talking about the reticular formation (as we discussed on Monday) and the thalamus (see: http://www.jneurosci.org/cgi/content/full/19/13/5506 for an interesting paper on the mechanism of propofol-induced LOC, the introduction has a brief discussion of the areas and mechanisms involved).
In strokes we’re dealing with the vascular supply to the affected area. The RF is supplied by the vertebrobasilar system and the thalamus has a relatively complex blood supply via 3 arteries from the vertebrobasilar system and one from the posterior communicating artery (see: http://stroke.ahajournals.org/cgi/content/full/34/9/2264/FIG1 for a beautiful diagram of this, though NB that many of the ‘arteries’ are actually made up of lots of little arteries which this diagram shows in their full, but slightly confusing, glory).
And part 2:
ReplyDeleteWhen we said that ‘posterior’ strokes are quite rare, what did we mean by ‘posterior’? Does this term only cover arteries derived from the posterior cerebral, or also from the vertebral/basilar/posterior communicating? As far as I can see, complete occlusion of the vertebral artery would kill the patient, but are occlusions of more minor vessels possible/common, and would they produce a functional effect?
Leaving the reticular formation aside, as it seems too diffuse a structure to be severely affected by anything but a pretty massive infarct, thalamic infarct can cause LOC. http://emedicine.medscape.com/article/1160677-overview describes paramedian thalamic infarct as one of the possible types of posterior artery stroke. However, the presentation of the effect on consciousness doesn’t really seem consistent with the sort of transient LOC that would cause a fall: severity ranges from lethargy through to coma, and it resolves in days or longer (which makes sense considering the pathophysiology).
Considering all that, I guess I’d agree with our conclusion on Monday, but was there another reason you listed stroke as one of your LOC differentials previously?
And part 2 (the third attempt at posting this - I don't know why it doesn't like me!)
ReplyDeleteWhen we said that ‘posterior’ strokes are quite rare, what did we mean by ‘posterior’? Does this term only cover arteries derived from the posterior cerebral, or also from the vertebral/basilar/posterior communicating? As far as I can see, complete occlusion of the vertebral artery would kill the patient, but are occlusions of more minor vessels possible/common, and would they produce a functional effect?
Leaving the reticular formation aside, as it seems too diffuse a structure to be severely affected by anything but a pretty massive infarct, thalamic infarct can cause LOC. http://emedicine.medscape.com/article/1160677-overview describes paramedian thalamic infarct as one of the possible types of posterior artery stroke. However, the presentation of the effect on consciousness doesn’t really seem consistent with the sort of transient LOC that would cause a fall: severity ranges from lethargy through to coma, and it resolves in days or longer (which makes sense considering the pathophysiology).
Considering all that, I guess I’d agree with our conclusion on Monday, but was there another reason you listed stroke as one of your LOC differentials previously?
thanks kirsten for your thoughtful and useful post
ReplyDeletei agree with you stroke is an uncommon cause of loss of consciousness
it can happen with a posterior territory event, however these do not occur that often
it can also happen with a very large anterior circulation event if there is oedema and possible brainstem compression
thank you also to lyndon, hend & christiana
ReplyDeletei would strongly echo your sentiments about how much you can learn when on call
we are currently doing some work on making the experience easier for third year students
if anyone wants to help with this, please email me: 786smh@clin-pharm.net