Short-term loss of consciousness - syncopy and other causes

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Introduction

Short-term loss of consciousness (tLOC) is a sudden or gradual, transient interruption of awareness, followed by either fast or slow regaining of consciousness. It results from a temporary disturbance in cerebral function, most commonly due to reversible cerebral hypoperfusion, metabolic disturbances, or transient neurological dysfunction.

tLOC may present with:

• Instant onset – the patient collapses suddenly. Recovery may be:
  • Fast → think syncope
  • Slow → think epileptic seizure (generalised) or TIA of the brainstem
• Gradual onset – usually metabolic or toxic causes (e.g. hypoglycaemia, intoxication)

Instant onset with fast, complete recovery is characteristic of syncope.

Pathophysiology of Syncope

Syncope is a transient, reversible loss of consciousness caused by acute global cerebral hypoperfusion. When cerebral perfusion falls below a critical threshold, consciousness is lost. When blood flow returns, the patient rapidly regains full awareness.

Basic mechanism:

• Sudden ↓ venous return or ↓ cardiac output
• ↓ Systemic arterial pressure
• ↓ Cerebral blood flow → transient cerebral hypoxia
• Restoration of perfusion → rapid recovery

If perfusion does not return, LOC may progress from syncope → vegetative state → coma → brain death. Syncope itself can occasionally trigger secondary seizures due to cerebral hypoxia.

Causes of Syncope

Cardiac Causes (≈25%)

Abrupt reduction in cardiac output:

• Ventricular arrhythmias (ventricular tachycardia, ventricular fibrillation)
• Bradyarrhythmias:
  • Sick sinus syndrome
  • 2nd-degree AV block (Mobitz II)
  • 3rd-degree AV block

Non-cardiac Causes (30–50% idiopathic)

Reflex (Neurally Mediated) Syncope

Due to exaggerated autonomic reflex causing vasodilation ± bradycardia.

• Vasovagal syncope – emotional stress, fear, pain, heat
• Situational syncope – micturition, defecation, cough, Valsalva manoeuvre
• Carotid sinus syndrome – carotid sinus hypersensitivity (tight collars, shaving, seatbelt)

Mechanism: ↑ parasympathetic and ↓ sympathetic activity → vasodilation and/or bradycardia → hypotension → cerebral hypoperfusion.

Orthostatic Syncope

Occurs on standing quickly after prolonged sitting or lying.

• Failure of autonomic reflexes
• Inadequate vasoconstriction
• Hypovolaemia (dehydration, blood loss)
• Drugs (antihypertensives, vasodilators)

Vertebrobasilar Syncope (Drop Attacks)

• Transient compromise of vertebral or basilar artery flow (e.g. with neck rotation)
• Sudden fall with rapid recovery of consciousness

Differential Diagnosis of tLOC

Syncope vs Epileptic Seizure

Feature	Syncope	Epileptic seizure
Onset	Sudden collapse	Sudden collapse
Recovery	Immediate full lucidity	Slow – postictal confusion, fatigue
Tongue bite	Rare	Common
Sphincter control	Usually preserved	Often lost (incontinence)
Muscle pain afterwards	Absent	Common (myalgia, headache)
Movements	Brief myoclonic jerks possible (hypoxia)	Tonic–clonic movements typical
Trigger	Standing, pain, emotion, heat	Often none

Other Non-syncope Causes of tLOC

Epileptic Seizures

• Excessive synchronous neuronal discharge
• Slow return of consciousness
• Postictal confusion, headache, muscle soreness
• Tongue biting, urinary incontinence common

Transient Ischaemic Attack (Brainstem)

• Focal neurological cause of LOC
• Possible associated signs: diplopia, dysarthria, limb weakness
• No typical postictal phase

Metabolic and Toxic Causes

Usually cause more gradual onset of LOC.

• Hypoglycaemia
• Hypoxia
• Electrolyte disturbances
• Drug or alcohol intoxication
• Severe systemic infection or organ failure

Illustrations

1. Pathophysiology of Syncope

Reduced cardiac output causing decreased cerebral blood flow and syncope.

2. Cardiac Arrhythmia Causing Syncope

Ventricular tachycardia causing sudden loss of consciousness.

3. Orthostatic Syncope

Failure of compensatory vasoconstriction on standing.

4. Syncope vs Seizure

Key differences between syncope and epileptic seizure.

Summary

Short-term loss of consciousness is a common clinical problem. Syncope is defined as a sudden, transient loss of consciousness with rapid, complete recovery due to reversible global cerebral hypoperfusion. Major causes include cardiac arrhythmias, neurally mediated (vasovagal) mechanisms, orthostatic hypotension, and vertebrobasilar insufficiency.

Syncope must be distinguished from epileptic seizures, TIAs, and metabolic or toxic disturbances. Accurate evaluation of the circumstances, associated signs, and recovery pattern is essential for correct diagnosis and risk stratification.

Sources

• Adams and Victor’s Principles of Neurology, 11th Edition – Chapter: Syncope and Transient Loss of Consciousness.
• Harrison’s Principles of Internal Medicine, 21st Edition – Sections on Syncope and Seizure Disorders.
• Braunwald’s Heart Disease, 12th Edition – Chapters on Arrhythmias Causing Syncope.
• 2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope.
• Guyton & Hall, Textbook of Medical Physiology, 14th Edition – Cerebral blood flow and its regulation.