|The inventor of the modern reductionist approach to brain function has led a fascinating life from 1758-1828 in a time where much happened in this world. Read this article, if you want to know more about the man and his enemies. If that is too long, try this very short article in the Wiener Medizinische Wochenschrift (they ought to know about Gall, since he started his career in Wien).
By the way: phrenology is a word coined by Gall’s successors – he called his teaching “Schädellehre”.
How do you come by such a topic? You bump into bumpology whenever you discuss with critics of fMRI studies…
I used to grow up with Macrodex and Promit on our ambulances. Then HAES came about and some albumin. In the first decade of this century, HAES fell into the abyss of the VISEP study, leaving gelatine for colloids. Now there is again evidence against that, so that we are left with albumin (some evidence for sepsis – see the SAFE study) and cristalloids and maybe some obscure stuff.
This course of modern volume therapy, in particular for sepsis, is beautifully illustrated by this ingeniously crafted study, which correlates acute kidney injury with the current volume replacement fluid of choice.
I am happy to say after at least 30 years of bitter debate that colloids have no place in volume replacement anymore, perhaps with the exception of Albumin and Macrodex (for which no proper data on harm exists). At least that is what the recent recommendations of ESCIM and Cochrane’s say (though with slightly more paragraphs). There might be some instances (cirrhosis, say) where albumin is particularly good, but that still has to be determined.
We used to measure it for every neurovascular patient, but then reduced our routine to judging intensity of atherosclerosis in the common carotid artery as a vague hint of predicting coronary or general atherosclerosis.
Reasons for this are manifold:
- The interrater reliability is bad – even if the location (say 1 cm below the bifurcation) or the insonation angle is fixed (which is hard to standardize – thing of thick necks)
- The reliability is bad from systole to diastole, from hour to hour and due to circadian changes in vessel diameter
- The prognostic validity is bad. It used to be better when studies were done monocentrically, often with one ultrasound specialist. But nowadays 20.000 pts are included in therapeutic studies… More recent metanalyses such as this and this lead one to doubt the method.
- Insonate any CCA longitudinally where it runs absolutely parallel to the skin.
- Choose the medial wall where the IMT seems largest without being elevated to a plaque
- Identify the angle where the vessel diameter is biggest, trying not to hit the carotid tangentially
- Stop the picture during diastole (the least diameter of the vessel, the biggest IMT)
- Zoom in until the two lines fill the screen at least to one third
- Mark the exact lines where the grey changes to white and measure the distance
Don’t bother with measuring multiple times or from multiple angles or at varying locations – the validity of the measurement is not good enough to justify the effort.
If you want to know whether someone has atherosclerosis, look for plaques and stenoses. If you find nothing and the patient has few risk factors then the IMT makes sense – this is primary care and prophylaxis more than hospitalists’ problems.
Spasticity is not automatically an upper motor neuron syndrome. Is this true? What about the converse? Where is the pathophysiology localized. What about the phenomena related to spasticity such as spasms, spastic dystonia, spastic cocontractions, pathological reflexes and so forth?
You find the answers to most (if not all) of these questions in a current Practical Neurology review that I highly recomend.
Latent late Syphilis is something we rarely encounter, because we only treat neurological patients and every neuro patient has a problem, which in turn can be attributed to some form of Syphilis, so that when we test him for Syphilis he has an active Neurosyphilis (this is regardless of his CSF status).
This is why we know practically nothing about the form of Syphilis that was covered by the infamous Tuskeegee study. We discuss the relevant core facts, why it raised a huge anti-racialists hype. We try to understand what happened and use the information of this excellent article to excuse the Syphilologists of the time.
We investigate the differential etiology of cSAH, which is completely different than that of your average SAH. A good exposition of this topic can be found in this neuroradiologic article of 2010. As our patient has a central cSAH we also discuss the peculiarities of cerebral amyloid angiopathy, it’s relation to Alzheimer’s, how it can lead to some inflammation (inflammatory CAA) and how it can lead to the fulminant picture of Amyloid beta related angiitis (ABRA).
Due to our wonderful investigative reporters at Frontal we have a small PR catastrophe here. Lamentably a patient died after a flow diverter was used to treat a giant aneurysm of the distal ICA. Now the TV show couldn’t possibly get the details right, but we covered the topic of flow diverters nevertheless, since they are often the only option to treat inoperable and potentially lethal aneurysms (which are rare). In fact, they might become a tool to treat aneurysms more effectively endovascularly since they could break through the pathophysiological cycle that leads to regrowth of the aneurysm – but this is still controversial.
As for references
- here is the latest series on FDs
- here is a recent collection of complications in a postmarket study
- here is a review article in Stroke from 2011
- and here a review article in J Clin Sci of 2011
When evaluating papers about these technical gadgets, consider
- how many acutely bleeding patients were treated (this is problematic since the theory implies that the aneurysm is only slowly shrinking after FD deployment)?
- how many potentially operable aneurysms were treated (there is an ethic controversy)?
- the usual EBM facts (length and completeness of follow-up).