Tarsal tunnel syndrome

We start with a differential of burning feet (the Burning Feet Syndrome – in my view a somewhat aloof entity about as specific as headache) and come to the neurological possibilities of aquiring foot pain, then on to the symptoms of tarsal tunnel syndrome and why it is definitely completely unalike the carpal tunnel syndrome:

  • rare in the Neurologist’s hand (foot?), but a very prevalent working diagnosis both of podiatrists and orthopedists
  • hard to identify clinically
  • probably not caused (albeit possibly triggered) by exercise / marathon running / high heels
  • often misdiagnosed in PNP, radicular syndromes
  • electrophysiologically even more elusive than CTS
  • definitely not as treatable.

My favorite diagnostics is lidocaine injection, although I do ephys to rule out PNP and S1, if not clinically evident. My experience with the various ways to investigate the tarsal tunnel itself is limited and anyone has a different favorite, but I’d forgo EMG, do motor NCS over the tibial nerve to the medial and lateral plantar nerve as well as antidromic sensory NCS, possibly below and above the tunnel, always comparing left to right.

As for reference, I recommend my favorite book on electrophysiology, namely Preston/Shapiro – electromyography and neuromuscular disorders. In our house, the Mumenthaler/Stöhr is (of course) a similarly helpful source.

Ocular bobbing and dipping

Ocular bobbing, dipping and floating are not too rare, if you keep examining your comatose and brainstem patients repeatedly. We discuss the few things that are known about these eye movement disorders and relish the wonderful poem of Ross 1992:

You’re called to the bedside, the eye movements are strange.
There must be a reason, can you give it a name?
You’ve seen this before, but can you recall?
You’re the Neurologist, you’re supposed to know all!

In bobbing and dipping, the eyes go down.
“How is that?” you ask with a frown.
The first is brisk, the second is slow.
The meaning differs; you must know.

Bobbing suggest pons; dipping an anoxic brain.
As always, there are some exceptions to name.
Metabolic encephalopathy can make the eyes bob.
Cerebellar hemorrhage and trauma complete the log.

To remember all this, you need something terse.
But wait, don’t forget, it could be reverse!
In each of these cases, it’s up the eyes go.
Bobbing is fast and dipping is slow.

Reverse bobbing may be something you see,
again, with metabolic encephalopathy.
Reverse dipping, a rare clinical nidus,
is reported in AIDS with cryptococcal meningitis.

Despite the confusion, one thing is plain.
The eyes don’t work right, whatever the name.
Wheter bobbing or dipping or reversing is true,
it can’t be good; just be glad it’s not you!

I would add that in Bobbing usually the horizontal VOR fails (with calorics or doll’s head maneuver). Here is a link to an article about the stuff (although I got my facts from Frank Thömke’s great book on Augenbewegungsstörungen):

N-of-1 studies: individual trials

A patient asks you to prescribe Lacosamid for prevention of his migraine. She seems to have discovered by chance (when she was given Lacosamid for presumed seizures which then turned out to be syncopes) that her migraines – gravely discomforting her for up to 2 days a week – improved on Lacosamid, getting milder if not disappearing totally.

How do you substantiate her claim of benefit? How do you convince her HMO to pay for it?

The answer – as usual – lies in EBM. We discuss the n-of-1 trial, the statistics and the ethical dimensions, using the following resources:

By the way: The JAMA evidence home page is restricted to registered (paying) users. But the former version of the book above is still online and available under usersguides.org!

Basics of DWI

We use current DWIs from pts on our stroke unit to discuss the unterpretation of DWI. We also aim to mention the physics of diffusion imaging in general, including DTI and DSI, perhaps with some fiber tracking.

  • For the physics part, we use the following article: http://radiographics.rsna.org/content/26/suppl_1/S205.full.pdf
  • Some animations on this page can help explaining.
  • This recent article in stroke clarifies which part of the DWI lesion actually will become stroke core, using PWI-MTT

Here is the differential for DWI bright lesions:

  • Stroke (ADC low, DWI high, T2 high if > 2-3h; ADC/DWI normalizes in 10-14d, might become bright than with elevated ADC)
  • The core of edematous lesions (venous thrombosis, PRES, …): ADC decreased in some areas, mostly high
  • T2 shine through (ADC high, DWI high, T2 high): old lesion
  • Abscess
  • Tumors with central necrosis or low cytoplasma/nuclear ratio
  • Encephalitis
  • CJD
  • Metbolic lesions (Wernicke, CPM, Leukodystrophies)
  • Proteinaceous fluid (aka pus) or subacute blood
  • Acute demyelination
  • Trauma

Physical examination of the chest

Since stroke care overlaps a lot with internal medicine we ran through the basics of the physical examination of the chest today, using a case of a patient with deteriorating oxygen saturation and the differential of pleural effusion vs. aspiration pneumonia.

The aim was not so much to repeat all the fascinating details of the chest exam, but to stress the importance of

  • doing regular exams on your stroke patients daily (at least if they are sick or bedridden)
  • of inspection and palpation to judge unilateral chest disease as compared to auscultation (which often yields results that require percussion, fremitus, egophony or bronchophony to intrepret)

With regard to chest x ray: They are important, but much less than the PE. In particular in bedridden patients with dyspnea.

So here is the final question: How do you distinguish the two entities (effusion vs. infiltrate) if it is lobar or bronchopneumonia.

Deep cerebral vein thrombosis

We have a great case on my Stroke Unit: A young pediatric intensive care unit nurse, non-smoker, taking the pill that developed headache over a few days, then over the course of a morning (some hours) became somnolent, slow in thinking, slightly confused. CT being “normal”, we got an LP, showing 9 neutrophilic cells and a high protein of 1,7 g/l – unfortunately, no pressure was measured. Ceftriaxone, Ampicilline and Aciclovir iv were initiated and she was admitted to our Stroke Unit, since this is the nearest thing to an intermediate care neurology ward that we have.

The next day she complained about persistent headache, slightly nebulous thinking. Psychopathologically she was slow, somewhat distanced, hard to get information from. An MRI showed dramatic T2 changes bilaterally in the basal ganglia and the thalami with not so extensive DWI lesions (ADC down), yet no involvement of white matter. Additionally a single DWI lesion flared up behind the right lateral ventricle (again, ADC down). The veins were identifiable.

We discussed the differential of this image extensively, until we had to conclude it was internal vein thrombosis. In retrospect, you could discover all the relevant imaging findings in the first CT.

So before you start reading up on cerebral venous thrombosis (vide infra), remember the anatomy of the cerebral veins. The best source for this (at least for me) is this wonderful page from the neuroangio site.

Next I list a few things on imaging and deep venous thrombosis…