Types of syncope

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types of syncope classification diagram

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Types of Syncope

Syncope is a transient loss of consciousness due to temporary global cerebral hypoperfusion, with spontaneous complete recovery. The common final pathway is always inadequate cerebral blood flow. Causes are classified by pathophysiological mechanism.

Classification (BOX 2.1 - Bradley and Daroff's Neurology in Clinical Practice)

1. Neurally-Mediated (Reflex) Syncope

The most common category overall. A reflex arc causes inappropriate vasodilation, bradycardia, or both, leading to a sudden drop in blood pressure.

a. Vasovagal (Vasodepressor) Syncope

The classic "simple faint." Triggered by emotional stress, pain, fear, unpleasant visual stimuli, venipuncture, prolonged standing, or heat. The mechanism involves a paradoxical withdrawal of sympathetic tone and surge in parasympathetic activity. Features include:

Prodrome of lightheadedness, nausea, pallor, diaphoresis, visual blurring, tinnitus
Gradual onset allowing the patient time to fall safely
Weak, slow pulse during the episode (transient bradycardia + vasodilation)
Rapid recovery once supine; no postictal confusion
Minor myoclonic jerks may occur but no tonic-clonic activity

b. Situational Syncope

Vasovagal mechanism triggered by specific activities:

Cough syncope - forceful coughing raises intrathoracic pressure, reduces venous return
Micturition syncope - sudden release of bladder pressure + vagal response; common in men at night
Defecation syncope - Valsalva effect during straining
Swallowing syncope - reflex bradycardia triggered by esophageal stimulation
Diving/Valsalva syncope - breath-holding with increased intrathoracic pressure

c. Carotid Sinus Hypersensitivity (CSH)

Exaggerated reflex response to carotid sinus stimulation (e.g., tight collar, head turning). Particularly common in older men. Can produce sinus arrest > 3 seconds or a >50 mmHg drop in systolic BP. Often asymptomatic but may cause syncope or unexplained falls.

2. Orthostatic (Postural) Syncope

Loss of consciousness upon standing due to a failure of compensatory vasoconstriction, causing blood to pool in the lower extremities.

a. Primary Dysautonomia

Pure autonomic failure, Parkinson disease, multiple system atrophy (Shy-Drager syndrome)
Impaired baroreceptor reflex arc

b. Secondary Dysautonomia

Diabetes mellitus (autonomic neuropathy), amyloidosis, spinal cord injury
A drop in systolic BP >20 mmHg (or diastolic >10 mmHg) within 3 minutes of standing is diagnostic

c. Drug-Induced Orthostatic Hypotension

Antihypertensives (alpha-blockers, diuretics), nitrates, antidepressants, antipsychotics, alcohol

d. Volume Depletion

Dehydration, hemorrhage, prolonged bedrest, Addison's disease

e. Postprandial Hypotension

Blood pools in splanchnic circulation after eating; especially in the elderly

3. Cardiac (Cardiovascular) Syncope

Often abrupt onset without prodrome; may occur in any position. Associated with higher short-term mortality risk. Key causes:

a. Arrhythmias (most common cardiac cause)

Bradyarrhythmias: Sick sinus syndrome (sinoatrial disorder), complete AV block (Stokes-Adams attacks), prolonged sinus pause, medication-induced
Tachyarrhythmias: Ventricular tachycardia/fibrillation, supraventricular tachycardia (SVT), atrial fibrillation with rapid ventricular rate
Reflex arrhythmias: Transient sinus pause from neural reflexes
Long QT syndrome (hereditary or drug-induced) - especially consider in females with family history of sudden cardiac death

b. Structural/Obstructive Cardiac Causes

Outflow obstruction: Aortic stenosis (syncope occurs with exertion due to inability to increase cardiac output + vasodepressor reflex), hypertrophic obstructive cardiomyopathy (HOCM), pulmonary stenosis, pulmonary hypertension
Inflow obstruction: Left atrial myxoma/thrombus, mitral stenosis, cardiac tamponade, tension pneumothorax
Cardiomyopathies: Dilated cardiomyopathy, amyloid cardiomyopathy

4. Cerebrovascular Syncope

Less common; caused by focal brain ischemia affecting the reticular activating system. True syncope from cerebrovascular disease requires bilateral hemisphere or brainstem involvement.

Vertebrobasilar insufficiency - drop attacks, diplopia, dysarthria, ataxia
Subclavian steal syndrome - exercise of the arm on the side of subclavian stenosis diverts blood away from vertebral artery
Takayasu arteritis (pulseless disease) - vasculitis causing stenosis of great vessels
Carotid disease - unilateral carotid stenosis rarely causes syncope alone
Cerebral vasospasm - e.g., in migraine (basilar-type migraine, more common in young females)

5. Metabolic Syncope

Not true syncope in the strict hemodynamic sense, but produces loss of consciousness through inadequate substrate delivery:

Hypoglycemia - impaired glucose delivery to neurons; gradual onset, prolonged
Hypoxia/Anoxia - respiratory failure, severe anemia (reduced oxygen-carrying capacity)
Hypoventilation - hypocapnia from hyperventilation causes cerebral vasoconstriction (common in anxiety-related episodes)

6. Multifactorial Syncope

Particularly common in older adults, where multiple contributing factors interact:

Age-related reductions in baroreceptor responsiveness, cardiac compliance, and vestibulosympathetic reflexes
Polypharmacy
Multimorbidity (diabetes, Parkinson disease, heart disease)
In elderly patients, syncope may present as an unexplained fall without a recognized prodrome

Key Distinguishing Features

Feature	Vasovagal	Cardiac	Orthostatic
Onset	Gradual	Abrupt	On standing
Prodrome	Yes (nausea, pallor)	Often none	Brief presyncope
Position	Usually standing	Any position	Standing
Precipitants	Pain, heat, emotion	Exertion, palpitations	Posture change
Recovery	Prompt, no confusion	Prompt	Prompt if supine

Syncope vs. Seizure (Key Differential)

Syncope is frequently misdiagnosed as epilepsy. Important distinguishing features from Bradley and Daroff's Neurology:

Syncope: pallor, diaphoresis, gradual or positional onset, minor irregular twitching only, no postictal confusion, no tongue biting, no urinary incontinence (rarely)
Seizure: cyanosis, rhythmic jerking, tongue biting, urinary incontinence common, postictal confusion lasting minutes to hours

Sources:

Bradley and Daroff's Neurology in Clinical Practice, Box 2.1, Table 2.1
Braunwald's Heart Disease - A Textbook of Cardiovascular Medicine
Goldman-Cecil Medicine
ROSEN's Emergency Medicine - Concepts and Clinical Practice

Innervation of facial nerve on the face, ipsilateral and bilateral lesion

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facial nerve innervation upper and lower motor neuron lesion

This clinical photograph displays a close-up view of the upper facial region of a patient, demonstrating clinical signs of delayed-onset left peripheral facial nerve palsy. The primary educational focus is the visual differentiation between preserved and lost frontalis muscle function. The patient's right side (anatomical right) shows prominent, deep transverse forehead wrinkles, indicating normal motor innervation and active contraction of the right frontalis muscle. In contrast, the left side of the forehead appears strikingly smooth and flattened, with a complete absence of wrinkling or furrows, representing paralysis of the left facial nerve (Cranial Nerve VII). The anatomical region includes the forehead, eyebrows, and the superior orbital area, with the eyes partially obscured for privacy. This visual finding is characteristic of a lower motor neuron lesion, such as House-Brackmann grade III palsy, where the entire ipsilateral side of the face is involved, including the forehead, distinguishing it from an upper motor neuron lesion (stroke) where forehead movement is typically spared due to bilateral cortical innervation. The image is a critical diagnostic reference for neurology and neurosurgery regarding postoperative complications following microvascular decompression.

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facial nerve branches temporal zygomatic buccal marginal mandibular cervical

This composite of four clinical photographs illustrates intraoperative findings and gross pathology from a right parotidectomy for a deep-lobe tumor. Panel A shows the surgical field with a white arrow indicating a communicating nerve branch between the marginal mandibular and buccal branches of the facial nerve. Panel B demonstrates the tumor's location within the deep lobe of the parotid gland, adjacent to the masseter muscle. Panel C provides a comprehensive view of the preserved facial nerve branches following dissection, labeled as temporal (T), zygomatic (Z), buccal (B), marginal mandibular (M), and cervical (C). Panel D presents the gross surgical specimens against a green background with a metric scale; it differentiates the irregular superficial lobe parotid tissue ('Supf.') from the main, well-demarcated, multi-lobulated tumor mass ('Main (Deep)'). These images serve as educational material for head and neck surgery, specifically illustrating parotid gland anatomy, facial nerve preservation techniques, and surgical management of parotid neoplasms.

An anatomical dissection photograph illustrating the terminal branching patterns of the human facial nerve (CN VII) and its cervical connections. The image displays a 'Type I' branching variant characterized by a fan-like distribution over the facial musculature. Key structures labeled include the temporal branches (1) extending superiorly, zygomatic branches (2) coursing toward the midface, and buccal branches (3) distributed across the cheek area. Inferiorly, the marginal mandibular branch (4) follows the lower border of the mandible, while the cervical branch (5) descends toward the neck. The dissection also highlights the greater auricular nerve (6) and the lesser occipital nerve (8). Of clinical and surgical significance is the depicted connection (7) between the cervical branch of the facial nerve and the transverse cervical nerve of the cervical plexus. This anatomical resource serves to educate on neuroanatomical variations relevant to parotid surgery, facial reconstruction, and local anesthesia.

A clinical intraoperative photograph showing the anatomical arrangement of the facial nerve branches in a surgical dissection, following parotidectomy. The image provides a lateral view of the cervicofacial region where the parotid gland has been removed to expose the extratemporal facial nerve plexus. Labeled branches include the temporal branch extending superiorly, the zygomatic and buccal branches traveling toward the mid-face, and the marginal mandibular and cervical branches descending inferiorly. The cervical branch is depicted in close proximity to the jugular vein, which is visible in the lower surgical field. Surgical instruments (retractors) are positioned to maintain exposure of the deep tissues. A 5mm grid scale is included for anatomical measurement. This visual serves as an educational guide for surgical anatomy, identifying key landmarks for nerve preservation during parotid gland surgery or facial nerve decompression.

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Facial Nerve (CN VII) - Innervation of the Face, and Lesion Patterns

1. Overview: Peripheral Distribution on the Face

The facial nerve exits the skull through the stylomastoid foramen, enters the parotid gland, and divides into upper and lower trunks. Through the substance of the parotid gland, it forms the parotid plexus and gives off five terminal branches that emerge from the borders of the parotid gland:

Branch	Region Supplied
Temporal	Frontalis (forehead wrinkling), orbicularis oculi (upper), corrugator supercilii
Zygomatic	Orbicularis oculi (lower), lower eyelid closure
Buccal	Buccinator, orbicularis oris, muscles of the upper lip and cheek
Marginal mandibular	Muscles of the lower lip and chin (depressor labii, mentalis)
Cervical	Platysma

Facial nerve branches - temporal (T), zygomatic (Z), buccal (B), marginal mandibular (M), cervical (C) exposed after parotidectomy

2. Central (Cortical/Supranuclear) Innervation - The Key Concept

The facial nerve nucleus in the pons is divided functionally into two parts:

Upper facial nucleus (forehead/eye division)

Receives bilateral corticobulbar input - from BOTH ipsilateral and contralateral motor cortex
Controls: frontalis (forehead wrinkling), orbicularis oculi (eye closure), corrugator

Lower facial nucleus (mouth/cheek division)

Receives predominantly contralateral corticobulbar input
Controls: buccinator, orbicularis oris, depressor muscles, platysma

This bilateral vs. unilateral cortical representation is the anatomical basis for the classic UMN vs. LMN facial palsy distinction.

3. Upper Motor Neuron (UMN) Lesion - Central Facial Palsy

Location: Lesion is above the facial nucleus - in the motor cortex, internal capsule (genu/posterior limb), corona radiata, or cerebral peduncle. Typically caused by stroke, tumor, or demyelination.

Pattern: Contralateral lower face weakness only

Forehead is SPARED - because the upper facial nucleus receives bilateral cortical input; the intact contralateral (now ipsilateral to the lesion) hemisphere still drives the upper face
Lower face (mouth/cheek) is WEAK contralateral to the lesion - because this nucleus receives predominantly crossed input, which is now lost
Voluntary movement is more impaired than emotional/spontaneous movement (e.g., patient cannot voluntarily retract the corner of the mouth, but may still smile asymmetrically during genuine emotion - because emotional facial pathways run separately through the thalamus/limbic system)
No taste loss, no hyperacusis, no loss of lacrimation

Clinical mnemonic: UMN facial palsy = "forehead spared" = central = opposite side of face

4. Lower Motor Neuron (LMN) Lesion - Peripheral Facial Palsy

Location: Lesion is at or below the facial nucleus - in the pons, cerebellopontine angle, internal auditory canal, facial canal (petrous bone), stylomastoid foramen, parotid gland, or peripheral branches.

Pattern: Complete ipsilateral facial weakness (ENTIRE side of face)

Forehead IS affected - because both upper and lower facial nuclei are damaged or their axons are cut; the bilateral cortical input is irrelevant once the final common pathway is lost
All ipsilateral muscles weak: frontalis (no forehead wrinkling), orbicularis oculi (cannot close eye - leading to corneal exposure/lagophthalmos), buccinator, orbicularis oris, platysma
Eye closure failure is a key sign and risk - exposure keratitis can develop
Depending on the level of the lesion, additional features may appear:

Level of LMN Lesion	Extra Features
Pontine nucleus (e.g., Millard-Gubler syndrome)	Ipsilateral VI palsy (lateral gaze palsy) + contralateral hemiplegia (long tract signs)
Cerebellopontine angle (e.g., vestibular schwannoma)	Ipsilateral VIII palsy (hearing loss, tinnitus, vertigo)
Internal auditory canal	VIII involvement
Above stapedius branch (within petrous bone)	Hyperacusis (stapedius paralysis), taste loss (chorda tympani), dry eye (GSPN)
Above chorda tympani	Taste loss (anterior 2/3 tongue) + dry mouth
Below chorda tympani / at stylomastoid foramen	Pure motor facial palsy (Bell's palsy typical site)
Parotid gland (tumor, surgery)	Selective branch palsies

Left peripheral facial nerve palsy - note smooth forehead on left (ipsilateral), prominent wrinkles on right (normal), characteristic of lower motor neuron lesion

5. Bilateral Lesion (Pseudobulbar Palsy / Bilateral LMN)

Bilateral UMN Lesion - Pseudobulbar Palsy

Requires damage to corticobulbar fibers from both hemispheres (e.g., bilateral capsular strokes, MND, Steele-Richardson syndrome)
After the first capsular stroke, residual 50% supranuclear innervation from the intact side maintains some function
After a second contralateral stroke, both lower cranial nerve nuclei lose all supranuclear input
Result: bilateral lower face weakness + dysarthria + dysphagia + emotional lability (pathological laughing/crying)
The forehead may remain relatively spared (bilateral cortical input), but emotional expression is lost

Bilateral LMN Lesion

Both peripheral facial nerves affected (e.g., Lyme disease, Guillain-Barré syndrome, sarcoidosis, bilateral Bell's palsy)
Complete bilateral facial diplegia - expressionless "mask-like" face
Both foreheads smooth, bilateral lagophthalmos, bilateral loss of taste

Summary Table

Feature	UMN Lesion (Central)	LMN Lesion (Peripheral)
Side of weakness	Contralateral	Ipsilateral
Forehead	Spared	Affected
Eye closure	Intact	Weak/lost (lagophthalmos)
Taste	Preserved	Lost (if above chorda tympani)
Hyperacusis	No	Yes (if above stapedius branch)
Lacrimation	Preserved	Reduced (if above GSPN)
Voluntary vs. emotional	Voluntary worse	Both equally affected
Associated signs	Hemiplegia, UMN signs	CN VI palsy, hearing loss (by level)

Sources:

Localization in Clinical Neurology, 8th Ed. - Anatomy of the Motor System
Scott-Brown's Otorhinolaryngology Head & Neck Surgery Vol. 2 - Clinical Disorders of CN VII, Pseudobulbar Palsy
Cummings Otolaryngology Head and Neck Surgery - Facial Nerve chapter
Tintinalli's Emergency Medicine - CN VII lesion patterns
Gray's Anatomy for Students - Facial nerve terminal branches

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