Presenting complaint

Mrs Johnson is a 42-year-old games developer who has just arrived in A&E. Today whilst working she suddenly collapsed onto her desk. A colleague witnessed the collapse, describing the lady holding her head briefly, then losing consciousness, hitting the front of her face against the desk.  The colleague explains that her whole body began jerking and he was unable to rouse her. The jerking stopped after a few minutes and she remained very drowsy, localizing to pain, making incomprehensible sounds and not opening her eyes.

On arrival of the paramedics, Mrs Johnson’s conscious level had improved, with her following commands, opening her eyes spontaneously, but remaining disorientated in place and time.

As you enter Mrs Johnson’s hospital room, she appears alert, with eyes opening spontaneously.  She is orientated in time, place, person and is able to follow commands.





Memory of the event / preceding the event? – useful for determining if the patient lost consciousness

Any prodromal symptoms? – headache / nausea & vomiting / visual disturbance / confusion

Any weakness / sensory disturbance? 

Bowel/bladder incontinence? – loss of consciousness & incontinence is common with seizures

History of seizures/epilepsy?

Palpitations? / Chest pain? – could suggest an arrhythmia causing syncope

History of preceding trauma? – useful if considering the possibility of intracranial haemorrhage

Patient answer

Mrs Johnson has very little recollection of the events surrounding the collapse, indicating she did indeed lose consciousness.  The only thing she remembers is what she describes as “the worst headache I’ve ever had” “It felt like I’d imagine getting a bullet in the head would feel!“. The headache was localised to her forehead. She does not recall any chest pain/palpitations/weakness / sensory disturbance.  She did have evidence of urinary incontinence after the episode.  She has never had a seizure before. She denies any history of trauma, she woke up as normal that morning and biked to work, with no issues on the way. 

Is the headache still present? – worsening or improving? / ask SOCRATES questions


Visual disturbance? – diplopia / decreased acuity / tunnel vision

Any weakness / sensory disturbance?

Further episodes of bladder/bowel incontinence?

Any residual confusion?

Neck stiffness / photophobia?

Fever/rigors ?

Patient answer

Mrs Johnson has a mild headache still, which is located as before in the front of her head. She feels quite nauseated and has vomited twice, requiring IV antiemetics from the paramedics. Her neck doesn’t feel too bad, “maybe a little stiff, but that might be because I’ve been laid down” she states.  Her vision is normal, she denies photophobia. She has not felt feverish and has no weakness or sensory disturbance. She has managed to pass urine and open her bowels on arrival to the hospital as normal. She no longer feels confused and her MMSE score is normal.


Past medical history
Pre-syncope/syncope – has the patient has previous symptoms of dizziness or loss of consciousness?

Seizures – is the patient known to have epilepsy?

Cardiac history – arrhythmias / myocardial infarction 

Intracranial haemorrhage – e.g. trauma-related / spontaneous / aneurysms 

Malignancy – loss of consciousness/seizures can be the presenting symptom of primary brain malignancy or secondary intracerebral metastases



Regular medications?

  • Pay attention to any that might cause syncope e.g. antihypertensives
  • Anticonvulsant medication – has the patient been taking this reliably or missing doses?
  • Antiplatelets / Anticoagulants – important when considering intracranial haemorrhage 

Recreational drug use? – Cocaine/amphetamines can cause loss of consciousness, seizures and intracranial haemorrhage 


Family history

Seizures / Syncope / Intracranial bleeding 


Social history

  • Living situation – where does she live and who with?
  • Alcohol intake 
  • Smoking status
  • Occupation


Systemic enquiry

  • Any other symptoms in other body systems? – weight loss etc

Patient answer

Mrs Johnson has no past medical history and takes no regular medication. She is not aware of any family history of disease. She smokes 10 cigarettes a day and has done for the last 20 years. She doesn’t drink alcohol. She lives with her husband in a house and can carry out all her activities of daily living independently.”


  • Cardiovascular – cardiogenic syncope? 
  • Respiratory – hypoxic cause for collapse?
  • Upper / lower limb neurology and cranial nerves – neurogenic cause for collapse?
  • General examination – soft tissue injury/fractures

On examination

General examination

  • Bruising is noted on this ladies forehead
  • There is dried blood in her nostrils
  • A small laceration is present on her left cheek
  • Some neck stiffness is noted, with the patient struggling to touch her chin to her chest due to pain.
  • Otherwise, there appear to be no other significant injuries


Cardiovascular examination

  • CRT <2
  • Regular pulse –  76 bpm
  • BP – 130/80
  • Normal heart sounds with no added sounds.


Respiratory examination

  • Respiratory rate 16
  • O2 saturations of 99% on air
  • Good air entry in both lungs with no added sounds


Neurological examination

  • Upper / lower limbs:
    • Tone – normal in all 4 limbs
    • Power – 5/5 power in all 4 limbs
    • Reflexes – normal in all 4 limbs
    • Coordination – normal
    • Sensation – normal
    • No pronator drift
  • Cranial nerves:
    • Pupils equal and reactive to light
    • No other deficits noted


Bedside investigations


BP – hypotension may have caused collapse/hypertension may have caused intracranial bleed

Pulse – arrhythmia? / bradycardia?

Temperature – fever may suggest an infection/fever can also cause seizures

Respiratory rate / O2 saturations – hypoxia may have preceded a collapse or seizure



FBC – anaemia / raised WCC may suggest infection

U&E (inc Mg & Phosphate) – To rule out any electrolyte imbalance that may have caused seizure

CRP – again useful to help rule out infection / inflammatory trigger for headache/seizure



If considering infective cause this could potentially be a source.

A urine dipstick would provide immediate information as to the likelihood of infection.

Sending an MSU (mid-stream specimen of urine) may allow identification of a particular organism.



  • Observations are all within the normal physiological range
  • Blood tests reveal no abnormalities
  • Urine dipstick is negative


CT head

Given the history of headache + collapse + nausea/vomiting 


CT Head

CT Head


  • No signs of bleeding
  • No space occupying lesions
  • No evidence of ischaemia

Further investigations

Lumbar puncture

Lumbar puncture, in which cerebrospinal fluid (CSF) is removed with a needle from the lumbar sac, will show evidence of haemorrhage in 3 percent of people in whom CT was found normal; lumbar puncture is therefore regarded as mandatory in people with suspected subarachnoid haemorrhage (SAH) if imaging is negative.3

  • Multiple tubes of CSF are taken and labelled in order of removal.
  • Red cell count (RCC) is assessed in each.
  • A consistently raised RCC in all bottles is suggestive of SAH


Xanthochromia is also assessed

The CSF sample is also examined for xanthochromia—the yellow appearance of centrifuged fluid. This can be determined by spectrophotometry (measuring the absorption of particular wavelengths of light) or visual examination.

  • Xanthochromia remains a reliable ways to detect SAH several days after the onset of headache.
  • An interval of at least 12 hours between the onset of the headache and lumbar puncture is required, as it takes several hours for the haemoglobin from the red blood cells to be metabolized into bilirubin.


Tube 1 – RCC 400
Tube 2 – RCC 412
Tube 3 – RCC 409

(The RCC is consistently raised in keeping with blood being present in the CSF.)

Xanthochromia – positive


Subarachnoid haemorrhage

Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space — the area between the arachnoid membrane and the pia mater surrounding the brain. Symptoms of SAH include a severe headache with a rapid onset (“thunderclap headache”), vomiting, confusion or a lowered level of consciousness, and sometimes seizures. Neck stiffness or neck pain area also relatively common.[3]

Further investigations

CT head angiogram

After a subarachnoid haemorrhage is confirmed, its origin needs to be determined. If the bleeding is likely to have originated from an aneurysm (as in this case given the absence of any trauma), the choice is between cerebral angiography (injecting radiocontrast through a catheter to the brain arteries) and CT angiography (visualizing blood vessels with radiocontrast on a CT scan) to identify aneurysms. Catheter angiography also offers the possibility of coiling an aneurysm 3

The CT angiogram (CTA) reveals a small berry aneurysm in the anterior communicating artery (Acom).


Cerebral angiography

This confirms the CTA result of an anterior communicating artery aneurysm.

GDCcoilAneurysm - no coil


The anterior communicating artery connects the left and right anterior cerebral arteries.

The anterior communicating artery is the most common location for aneurysms within the circle of Willis.

These aneurysms can sometimes present pre-rupture with visual field defects due to compression of the optic chiasm

Circle of willis

Circle of Willis


Coiling vs Clipping


  • This involves inserting a catheter into the femoral artery under x-ray guidance.
  • This is then taken up through the aorta, into the carotid vessels and into the cerebral circulation.
  • Once the aneurysm is reached, platinum coils are released into it.
  • This causes coagulation within the aneurysm, obliterating it.



  • This procedure is more invasive, requiring a craniotomy to access the aneurysm.
  • It is often used for aneurysms that have a wide neck and are therefore unsuitable for coiling.
  • The aneurysm is located visually and a clip is placed around the neck of the aneurysm.
  • This method is often not possible for aneurysms of vessels that are difficult to access surgically (e.g. posterior circulation).

The interventional neuroradiologists felt that coiling of this aneurysm was possible.

They performed this at the same time as they were performing the cerebral angiography. 

It was successful and the patient was left with no residual neurological deficit. 


Anterior communicating aneurysm (Before/After coiling)

Anterior communicating aneurysm (Before/After coiling)


1. CT Head image – courtesy of Dr Aaron G. Filler, MD, PhD, FRCS –

2. Anterior communicating artery coiling image –

3. Van Gijn J, Kerr RS, Rinkel GJ (2007). “Subarachnoid haemorrhage”. Lancet. 369 (9558): 306–18. doi:10.1016/S0140-6736(07)60153-6. PMID 17258671.


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