Brain no functioning

Based on Year 3 Imperial, Week One teaching at Hillingdon

A 29 year old man (Mo Tourist) is BIBA (brought in by ambulance) following a motor cycle accident. His helmet has flown off. There is extensive bruising around the head.

On arrival, he appears unconscious.

You start with an ABCDE approach. You pay particular attention to A because you know that in patients with reduced consciousness, the airway can be at risk (because of the loss of muscle tone leading to a floppy airway, as well as the tongue falling backwards). Think of a very drunk person (i.e. someone with reduced consciousness) deeply snoring. Think of the folds of fat and soft tissue vibrating in that floppy airway. Now imagine that airway getting even more floppy to the point where it occludes. A GCS of around 8 or lower is traditionally taught as when you would get support for the airway.

B and C are fine, so you move on to ‘D’. This stands for disability.

Why are we assessing the patient’s disability/handicap at this stage? 

Although the word ‘disability’ is used, I prefer to think of it as neurological ‘deficit’. When someone has reduced consciousness, the challenge is to work out if this is because of a focal problem (i.e. in the brain), or a system problem (i.e. in the body).


Arousal comes from the ascending reticular activating system in the brainstem. To cause reduced consciousness, there must either be extensive bilateral cortical damage (as if one hemisphere is working normally, this will still project to the reticular activating system as normal, so consciousness will be maintained), or damage in the brainstem. Alternatively, there may be a systemic problem with the blood supply to the brain e.g. hypoglycemia or a toxin.

Focal problems

Anything that raises intracranial pressure can cause a reduced consciousness. The commonest problems are haemorrhage and space occupying lesions such as tumours/abscesses. Reduced consciousness can also occur after brain injury without a specific space occupying haemorrhage e.g. multiple brain contusions.

The patient could also be post ictal after a seizure. This seizure could have been focal or generalised to begin with, but would have had to been focal with secondary generalisation or primarily generalised to cause reduced consciousness.

Raised intracranial pressure…?

Think persistent headache that worsens with lying flat, bending over or coughing, vomiting (especially effortless), focal neurology and seizures. Late on, you get Cushing’s reflex and papilloedema (can you make out the optic disc margin below? Me neither. That’s a big clue for papilloedema).

By Jonathan Trobe, M.D. - University of Michigan Kellogg Eye Center - The Eyes Have It, CC BY 3.0,
By Jonathan Trobe, M.D. – University of Michigan Kellogg Eye Center – The Eyes Have It, CC BY 3.0,

Ischaemic strokes cause sudden onset, focal, negative neurological symptoms. These almost always occur without impaired consciousness.


Now we’re talking (unless your GCS – V is less than 3). These can be split into exogenous problems (drugs) and endogenous (toxins and metabolic abnormalities):


  • Hypoglycemia (and sometimes hyperglycemia, if HHS has developed for example)

  • Hyponatremia

  • Hypo/ernatremia

  • Hyper/pocalcemia

  • Severe hypothyroidism (“myxodema coma”)

  • Acute panhypopituitarism

  • Acute uremia (renal failure)

  • Hyperbilirubinemia (liver failure usually. High levels of ammonia can also occur in liver failure leading to hepatic encephalopathy)

  • Hypercapnia

A fall in cardiac output leading to reduced cerebral perfusion causes either a transient loss of consciousness until cardiac output improves, or death.

Exogenous (drugs)

Many drugs in overdose can cause reduced consciousness, but the main ones to bear in mind are alcohol, benzodiazepines and opiods.

Assessment of reduced consciousness

There are three main parts:

a) Assess the level of consciousness

b) Assess the pupils

c) Look for focal neurology using signs that do not rely on consciousness

Assessing the level of consciousness 

This is done with the Glasgow Coma Scale. You can’t get better than this video, made under the direction of one of the authors (Teasdale) of the original 1974 paper on the GCS:

Points to remember:

  • Motor is the most predictive component for prognosis
  • You can’t score less than 3/15
  • The best response is recorded
  • Decorticate posturing links with abnormal flexion, and decerebrate links with extension (which is always seriously abnormal). This reflects if damage has occured above (decorticate) or below (decerebrate) the red nucleus.
  • In other words, don’t get too hung up on decerebrate vs decorticate posturing. By the time we need to be working those sorts of things out, the patient is probably in ITU or for DNAR.


Assess the pupils 

Have a look at his face. Did you notice anything?

One pupil is bigger than the other. This is anisocoria.

It can be difficult to work out which pupil is abnormal. The trick is to remember that whichever one is abnormal is either struggling to dilate or constrict. If the patient is in a bright room and one pupils fails to dilate, this is the abnormal pupil. If the patient is in a dark room and one pupil fails to constrict, this is the abnormal pupil.

Eye see
Eye see

You would then check the pupils for reactivity and the direct/consensual reflex.

This patient had a larger left pupil than right. The left pupil failed to constrict in dark light.

The patient most likely had an uncal herniation leading to compression of the 3rd cranial nerve. The main types of brain herniation are wonderfully summarised in this link.

Look for focal neurology using signs that do not rely on consciousness

Your next step of the assessment is to look for focal neurology. We can’t ask an unconscious patient to raise his arms or if he can feel everything as normal, so we rely on signs that do not requires consciousness.

In the limbs, this means signs like tone, spasticity and reflexes.

For the cranial nerves, this can include the doll’s eye reflex, vestibulocular reflex and corneal reflexes.

Remember that the location of cranial nerve lesions can hint at where there may be brainstem damage. The cranial nerve nuclei (apart from I and II) all live in the brainstem. A lesion in a cranial nerve means either a problem in the nuclei, or somewhere along the path from the brainstem to where the nerve has its motor/ sensory action.

In summary, the three main parts of assessment are:

a) Assess the level of consciousness

b) Assess the pupils

c) Look for focal neurology using signs that do not rely on consciousness


You would generally work up the patient for both metabolic/systemic causes (with the appropriate tests, which often includes a VBG in the acute setting to get a snapshot of any metabolic/electrolyte/glucose derangements) and if this proves fruitless or if there is clearly evidence of a focal intracranial problem then intracranial imaging is done. CT Head is more often used acutely than MRI Head as it is more easily available, and in very acute bleeds actually can perform better than MRI Head.

Delirium handout