Neglect is the one most fascinating neuropsychological syndrome that is both hard to define and very easy to recognize. To clarify some of the points made in the recent literature and reject some myths we discuss the theory, examination, localization and therapy of Neglect.

Here are some take home messages:

  • Extinction and Neglect are different. They often occur together and extinction can but need not be a part of Neglect – i.e. there are cases of one without the other.
  • Extinction and Anosognosia are different. Ditto.
  • Like language on the left the bermuda triangle of Neglect is situated around the Sylvian fissure and comprises some frontal, parietal and temporal regions that are highly interconnected and also project to deeper structures such as the basal ganglia.
  • The more parietal regions are probably responsible for the more externally oriented part of Neglect, the more temporal have to do with interoceptive and auditive functions and the frontal has to do with motor neglect, roughly similar to the respective regions on the left side for language [this is debated, but – what the heck – this is what I concluded].
  • The line bisection tool might not be good for a screening instrument, being neither sensitive nor specific – hemianopia can completely obscur the result. There are also other situations in which line bisection is pathological without neglect. Still this is a much researched subject.

So how do you recognize Neglect? Watch your patient, speak with him, have him perform some basic tasks, describe objects. It is essential that cueing can temporarily remedy Neglect-driven defects – e.g. reminding a patient to look on the left side might help him recognize stimuli on the left for some seconds.


  • Karnath. The anatomy of spatial neglect. Neuropsychologia 2011
  • Vossel. Neurobiology of Neglect: Implications for New Therapeutic Strategies. Fortschr Neurol Psychiatr 2010

Wallenberg syndrome

It is one of the most complex neurovascular syndromes and serves to repeat the basic neuroanatomical structure of the brainstem. A current patient with embolic vertebral artery occlusion helps us to demonstrate the unique features. I won’t go into the details here, but mention a few things:

  • If it is just the brainstem there may or may not be cerebellar signs (depending on how much the spinocerebellar tract is involved)
  • If it is big enough (as in our patient) and reaches to the front, there may be some pyramidal tract signs.
  • There is often (always, really) some facial neuropathic pain or itch
  • It may lead to sneezing or singultus, 2 neurological fascinating signs that are quite hard to treat.

References: any neuro textbook. Also remember the 4m4s-rule of brainstem anatomy.

Metabolic alkalosis

It was a cool case: called to admit to our stroke unit (which serves as an intermediary care unit as well) a patient from the general ward because of global respiratory insufficiency, we got an ABG that read pH 7,48, CO2 67. Her sats were in the 70ies without oxygen and she showed periodic breathing, yet without any dyspnea.

Obviously this is a case of metabolic alkalosis, so we used it to talk about this most common of all acid-base-disorders.

The take home messages are:

  • Metabolic alkalosis (like most of the physiological “excess” states such as hyponatremia – excess water, hyperkalemia and so forth) has 1. a cause and 2. a reason for being maintained – i.e. a kidney problem, usually hyperaldosteronism, hypovolemia, hypokalemia etc.
  • Differentiate the causes by GI, renal and intracellular.

As for procedural aspects,

  • always get an arterial ABG, serum elytes (Na, K, Cl, Mg, Ca) and urine chloride – and measure the anion gap
  • assess the volume status (hypo-, eu-, hypervolemic)

And therapy? If not sure, try pure chloride. You can get that as HCl, which is hard to get, or as KCl, which isn’t. Since potassium immediately goes into the cell (unless no insulin is present), you are left with chloride which removes an HCO3.

References: any textbook on intensive care.

In fact, we also mentioned the Stewart-Fencl-approach to acid-base-disorders, which I love and – as a mathematician – had to learn in my youth (4 years ago). If you find the time, go read Stewart’s original book (available on or this new textbook.

Differential diagnosis of tachycardia (tachyarrhythmia) and hypertension

  • Tachycardia is a very prevalent rhythm disorder in the Stroke Unit, most often as tachyarrhythmia. We introduce a new – albeit german – mnemonic to remind us of frequent causes: SCHNELL & DEFTIG.
  • Stress – usually with hypertension (see below)
  • Cardiac – coronary, valves, pericarditis, endocarditis, …
  • Hypovolemia
  • eNdocrine (TSH)
  • Elytes (K, Mg, Ca, …)
  • Lung (pulmonary embolism)
  • L
  • Delirium
  • Entzug (withdrawal)
  • Fever
  • Toxic (drugs)
  • Ictal (postictal)
  • Gases (pH)

As for hypertension we also have a cute mnemonic: 3H5A

  • Hirndruck (cerebral hypertension
  • Hemodynamics
  • Harndrang (has to pee)
  • Aua (ouch, pain)
  • Angst
  • Atemnot (dyspnea)
  • Alcohol withdrawal
  • Alzheimer’s (delirium)

Prognostic factors in intracerebral haemorrhage

The prognosis of ICH is largely determined by initial haematoma volume and haematoma growth. Here are the most important factors:

  • Age
  • Elevated blood pressure, diabetes
  • Signs of raised intracranial pressure
  • Clinical impairment (NIHSS)
  • Early clinical deterioration
  • Oral anticoagulants
  • Haematoma volume
  • Intraventricular haemorrhage
  • Infratentorial haemorrhage
  • Spot sign in CTA source images

We discuss the last point, inspired by the recent publication of the PREDICT study.

Differential diagnosis of adult leukencephalopathy

We face the following problem: a patient develops aphasia and apraxia suddenly – assumed ischemic. Her CT shows a diffuse leukencephalopathy which is more than your average SAE. What’s the differential?

There are also some new diseases on the horizon, of course acronymized. LTBL is one of them. 

How to differentiate MS from vascular lesions?