Loss of Consciousness History Taking – OSCE guide

Loss of consciousness occurs when the function of both cerebral hemispheres or the brainstem reticular activating system is compromised. The two major causes of transient loss of consciousness, syncope and seizures, can be easily confused. When taking a history for an episode of transient loss of consciousness, it is important to keep in mind the different possible causes. Throughout the interview with the patient, narrow the differential diagnosis by asking targeted questions. Check out the loss of consciousness history taking mark scheme here.

Causes of transient loss of consciousness

Syncope (caused by global cerebral hypoperfusion)

Reflex syncope (a.k.a. neurally mediated syncope)

Syncope associated with a sudden decrease in blood pressure and heart rate in response to a trigger.

Vasovagal syncope:

  • Emotional distress: fear, pain, instrumentation, blood phobia, enclosed space
  • Orthostatic stress: prolonged standing

Situational syncope: cough, sneeze, defecation, post-micturition, post-exercise, post-prandial

Carotid sinus hypersensitivity: triggered by sudden head turning, tight collar, shaving


Cardiovascular syncope

Loss of consciousness associated with decreased cardiac output.

Causes include:

  • Arrhythmia
  • Structural cardiovascular disease: coronary artery disease, valve disease, cardiac tamponade, hypertrophic cardiomyopathy, aortic dissection
  • Structural pulmonary disease: pulmonary embolism


Orthostatic hypotension

Syncope associated with a sudden drop in blood pressure after standing up.

Causes include:

  • Hypovolaemia: haemorrhage, diarrhoea, vomiting
  • Iatrogenic: beta-blockers, diuretics, alcohol, vasodilators, antidepressants, phenothiazines
  • Autonomic failure: diabetic neuropathy, Parkinson’s disease, spinal cord injury 



Seizures are caused by abnormal excessive neuronal activity in the brain, leading to impairment of normal cognitive function.

Seizures that involve a complete loss of consciousness are known as generalised seizures (either convulsive or non-convulsive).


Metabolic disturbances hypoglycaemia, electrolyte abnormalities, drug or alcohol intoxication, adrenal insufficiency

Space-occupying lesions

Head trauma


Medication – some medications lower the seizure threshold (e.g. Nefopam)

Epilepsy  spontaneous abnormal excessive neuronal activity in the brain

Opening the consultation

Introduce yourself – name/role

Confirm patient details – name/DOB

Ensure the patient is comfortable

Explain the need to take a history

Gain consent

Presenting complaint

It’s important to use open questioning to elicit the patient’s presenting complaint.

“So what’s brought you in today?”  or “Tell me about your symptoms.”


Allow the patient time to answer, trying not to interrupt or direct the conversation.


Facilitate the patient to expand on their presenting complaint if required.

“Ok, so tell me more about that.” or “Can you explain what that pain was like?”

History of presenting complaint

Effective history taking is key to narrowing the differential diagnosis when the presenting complaint is loss of consciousness. A collateral history provided by someone who witnessed the episode is often required to gain accurate details about what happened during and after the loss of consciousness.

Before the loss of consciousness

Was there a trigger?

Reflex syncope is often associated with a trigger:

  • Vasovagal syncope – emotional distress (fear, pain, instrumentation, blood phobia) // orthostatic stress (prolonged standing)
  • Situational syncope – cough, sneeze, defecation, post-micturition, post-exercise, post-prandial
  • Carotid sinus hypersensitivity – shaving, tight-fitting collar, sudden head-turning


Physical exertion: cardiovascular syncope (e.g. aortic stenosis/arrhythmia)

Standing from sitting: orthostatic hypotension (e.g. hypovolaemia/autonomic failure)

Working with arms elevated above head: subclavian steal syndrome

Exposure to rapid flickering lighting: photosensitive epilepsy


Were there prodromal symptoms or an aura?

Vasovagal syncope is often preceded by prodromal symptoms:

  • Progressive light-headedness
  • Visual disturbances (dimming of vision or loss of vision)
  • Weakness of the extremities
  • Sweating
  • Nausea
  • Tinnitus


Seizures can also begin with subjective symptoms (called “epileptic auras”):

  • Olfactory or gustatory hallucinations (specific smell/taste)
  • Visual hallucinations (e.g. flashing lights/blurring of vision)
  • Déjà-vu feeling
  • Sensory disturbances (numbness/tingling/burning)


Cardiovascular syncope often lacks any prodromal symptoms, with the patient feeling ok and then losing consciousness suddenly with no warning. You should, therefore, consider underlying arrhythmia or structural heart disease if there is an absence of prodromal symptoms.


Were there any other symptoms occurring before the loss of consciousness?

  • Focal motor or sensory deficits: suggestive of focal seizures that may have then progressed to a generalised seizure (causing loss of consciousness)
  • Palpitations: arrhythmia
  • Chest pain: myocardial infarction / pulmonary embolism / aortic dissection
  • Slow controlled collapse towards the ground is typical of vasovagal syncope


Whilst the patient was unconscious


Flaccidity: cerebral hypoperfusion

Initial tonic stiffening, followed by clonic (jerking) movements of the extremities: generalized tonic-clonic seizures

Cerebral hypoperfusion can also result in stiffening or jerking movements.



Syncope: <20 seconds typically

Seizure: often longer than 20 seconds



Tongue biting (lateral aspect): generalized tonic-clonic seizure

Urinary or faecal incontinence: more common in seizure than syncope

Cyanosis (caused by cardiorespiratory arrest): arrhythmia/structural cardiac disease/pulmonary embolism

Cyanosis can also occur in a prolonged seizure, but tonic-clonic movements precede cyanosis.


After the loss of consciousness

How long did it take for full recovery?

Syncope: rapidly regains full lucidity (within 20-30 seconds)

Seizure: post-ictal period of confusion and/or agitation lasting several minutes to hours (often not recalled by the patient)

Were there any relieving factors?

Seated or supine position: orthostatic hypotension

Other questions

Ask about any secondary injuries as a result of the loss of consciousness

Past medical history

Syncope – clarify type of syncope, triggers, frequency and last event

Epilepsy/febrile seizures – clarify frequency, treatment and last event

Hypertension, hypercholesterolemia, coronary artery disease, arrhythmia (all relevant to cardiovascular syncope)

Parkinson’s disease/diabetes (orthostatic hypotension)

Head trauma (increased risk of seizures)

Pacemaker (cardiovascular syncope) – also useful to know, as this can be interrogated to look for arrhythmias at the time of the event

Recent surgery (increased risk of pulmonary embolism)

Patients with syncope and heart disease are at a markedly increased risk for ventricular tachycardia and sudden death.

Drug history

Oral/subcutaneous hypoglycaemic agents (hypoglycaemia)

Anticonvulsants (check if patient has been taking these as prescribed)

Beta-blockers (bradycardia/hypotension)

Diuretics and antihypertensive agents (orthostatic hypotension)

Tricyclic amines (orthostatic hypotension and seizures)

Short-acting benzodiazepines (seizures upon withdrawal)

Anti-inflammatory agents (syncope secondary to gastrointestinal haemorrhage)

Oral contraceptives (pulmonary embolism) 

Recent changes (e.g. cessation of corticosteroid therapy potentially leading to adrenal insufficiency)

Compliance (e.g. inadequate administration of insulin in diabetes could lead to hypoglycemia)

Family history 

Cardiovascular disease (structural cardiac disease/arrhythmias/channelopathies)



Social history

Smoking – How many cigarettes a day? How many years have they smoked for?

Alcohol – How many units a week? – be specific about type/volume/strength of alcohol (seizures caused by withdrawal/intoxication)


Level of functional independence:

  • It’s important to understand the patient’s care needs, as this will influence how you manage them
  • Understanding the patient’s daily activities also allows you to consider the risk posed by further episodes of loss of consciousness



  • Check what their job involves, as they may need to be advised to take time off work until a diagnosis is established (e.g. someone working at heights)



  • Depending on the suspected diagnosis there may be restrictions that result in temporary driving suspension (e.g. seizure)
  • You should also check the kind of vehicle operated, as heavy goods vehicles often have different rules


Systemic enquiry

Systemic enquiry involves performing a brief screen for symptoms in other body systems, that are not directly linked to the patient’s presenting complaint, but may, however, be relevant to the diagnosis.

Choosing which symptoms to ask about varies depending on the patient characteristics and his presenting complaint.

Cardiovascular Chest pain (myocardial ischemia) / Back pain (aortic dissection) / Palpitations (arrhythmias)

Respiratory Dyspnoea (pulmonary embolism)

Gastrointestinal   Sudden abdominal pain (aortic aneurysm rupture/pancreatitis)

Neurological – Weakness / Sensory disturbance / Visual disturbance

Musculoskeletal Joint/bone pain (fractures secondary to fall)

Closing the consultation

Address any patient concerns

Summarise the history

Suggest an appropriate differential diagnosis

Explain the need for further investigations

Thank the patient


  • Developed in collaboration with, European Heart Rhythm Association (EHRA), Heart Failure Association (HFA), et al. Guidelines for the diagnosis and management of syncope (version 2009): The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC). European Heart Journal. 2009;30(21):2631-2671. doi:10.1093/eurheartj/ehp298.
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