Caudate strokes

We run through the case of a patient with bilateral caudate head lesions (one old, one new) and mention the famous neuropsychological and behavioural abnormalities, arising from caudate strokes.

I particularly like Mendez’ classification of caudate behavioural abnormalities:

  • apathetic with decreased spontaneous verbal and motor activities (mainly dorsolateral caudate involvement)
  • disinhibited, inappropriate and implusive (small ventromedial lesions)
  • affective symptoms with psychotic features (dorsolateral caudate involvement, usually bigger infarcts)

En passant we talk about the localization of stroke-induced agitation (caudate, temporal lobe, parietooccipital).

Here are some of the clinical specialties in caudate strokes (taken from Kumral):

  • Agitation
  • Abulia
  • Neglect (right sided lesions, 25%)
  • Mood changes (1/3)
  • Memory disturbance (1/3, bilateral: dementia)
  • Dysarthria
  • Aphasia (left sided lesions, 50%)
  • Movement disorders (ballistic, choreatiform)
  • Motor weakness

We discuss the vascular anatomy of the caudate nucleus, mention Heubner’s recurrent artery/arteries.




Tirofiban and SATIS

In August, the SATIS trial was finally published. After the disturbing results of AbESTT (or however it was spelled) this reintroduces GP IIb/IIIa antagonists into the stroke arsenal. Although the data look fine to me and I really use Tirofiban a lot, I wonder

  • The trial stopped enrolling 2008, since then the manuscript is “pending” according to
  • The manuscript was received in August 2010.

So what happened during all those years?

We discuss the publication and the pharmacology of Tirofiban.

What are the indications? The following is my personal opinion:

  • Lacunar stroke with fluctuating course
  • After thrombolysis AND recanalization
  • In high grade stenoses before intervention (say basilar artery stenosis)

Autoimmune encephalopathy

On the general ward there is a 49 yo female patient with rapidly progressive encephalopathy, starting with vertigo and predominant ataxia, developing bilateral Babinski’s and cognitive decline over three weeks. There are slight FLAIR hyperintensities in the mesial temporal lobe on the left, diffuse slowing, triphasic waves and later epileptiform discharges in the EEG, lymphocytic pleocytosis and a 3-class-reaction with bands in the CSF. Blood works show some antibodies (ANA 1:400, TPO, PCA) and nothing fancy otherwise. Malignancy search (FDG-PET, CT trunk) is more or less normal. Finally, there is no improvement on steroids 1g x now 3 days. Quite remarkably, she has the skin changes of Neurofibromatosis (cafe au lait, neurofibromas) and a huge DVA in the right frontal lobe – all things we could not yet connect to the current disease.

We discuss the differential, using the wonderful article

Subtle central motor weakness

In a screening neurological examination, you need efficient sensitive examinations to detect subtle motor deficits, e.g. in your basic r/o MS or stroke patient. We usually do pronator drift, but there are some simple additional tests that could be included in your (and my) routine, especially the forearm rolling test and – even better – the finger rolling test.

We use these tests in a few patients to illustrate their practical application and also discuss the relevant data, using 2 of Anderson’s articles, namely

Finally, there is yet another of these tests, which seems even simpler to me: The thumb rolling tests. If you believe the Canadians, then it is the best.

Herniation syndromes

This most classical of all Neurointensive-care-topic is – in my eyes – not only very important, but also quite hard to understand. If you belive Plum/Posner, it alls seems quite simple, but the details are often wrong. This starts with the reason for pupil dilatation in tentorial herniation (there are at least 3 different ways to achieve it and sometimes more than one applies), it goes on with the role of midline shift, the horizontal and vertical displacement and so on.

Here are my core teaching messages:

  • The third nerve runs between the SCA and PCA.
  • Inspect your CT completely, thinking about pressure and tissue shifts. Look at the midline, the mesencephalon, the third nerve, the pyramidal tract, the ARAS, the thalami, the uncus, the falx etc. Look everywhere.
  • Midline shift is (in stroke and ICH) irrelevant, if nothing else happens.
  • Pupils and drowsiness need not happen together.
  • Think about why the pupils dilate, the pt is drowsy, he vomits in each patient. The mechanism can be different each time.
  • Operation only helps if it heals the pathological mechanism.


Breaking bad news

Starting with a semi-bad news – the diagnosis of MS – we’ll roleplay through the standard situation of telling and explaining the diagnosis to the patient on the ward.

I am a happy user of the Cambridge-Calgary-Guide for Communication Skills and use the chapter on Breaking Bad News from the book “Skills for Communicating with patients” as a guide, although there is certainly plenty of literature on the subject.

There is one specific point that leaves much room for individual style – namely “Gauge how much the patient wishes to know”. We discuss the most prevalent approaches, including

  • Stepwise: Offer euphemisms of increasing clarity
  • Once and for all: Start with the diagnosis and see what the patient makes of it
  • Introduce the news with a sentence such as “If the diagnosis turns out to be serious how much detail do you want to know?”

There is even a recent article on Bad News in Neurology: Communication and neurology – bad news and how to break them

Stroke associated infections

Yesterday, we discussed the situation of an elderly patient with dysphagia and right hemiparesis due to a third media stroke developing fever. We stressed that

  • Not every elevated temperature is fever
  • Not every fever means infection
  • Not every infection in stroke is aspiration or UTI

We mentioned the peculiarities of stroke-induced immunosuppression with highly reagible yet insufficient nonspecific immune reactions. Then we came to the core of the topic, namely the difference between stroke-associated pulmonary disease and aspiration pneumonia, developing criteria to be used in our local “Weissbuch” – the stroke manual of the Zentralklinikum Augsburg.