What nerves are involved in Horner's syndrome vs Bell's palsy?

Nerves Involved in Horner's Syndrome vs Bell's Palsy

Bell's palsy affects the facial nerve (CN VII), causing ipsilateral facial muscle weakness including the forehead, while Horner's syndrome results from disruption of the oculosympathetic pathway (a 3-neuron sympathetic chain from hypothalamus to eye), causing miosis, ptosis, and anhidrosis without facial weakness. 1, 2, 3

Bell's Palsy: Facial Nerve (CN VII)

Anatomical pathway and clinical presentation:

• The facial nerve (CN VII) is one of the most complex cranial nerves, containing branchial motor fibers (innervating muscles of facial expression), visceral motor fibers (parasympathetic innervation to head glands), general sensory fibers (external ear and tympanic membrane), and special sensory fibers (taste to anterior two-thirds of tongue) 1

• The nerve courses from the pons through the cerebellopontine angle, enters the internal auditory canal, traverses the temporal bone (including labyrinthine, tympanic, and mastoid segments), exits at the stylomastoid foramen, and courses through the parotid gland 1

• Bell's palsy affects the entire ipsilateral side of the face because CN VII innervates all facial muscles on one side after exiting the brainstem, producing characteristic complete hemifacial weakness including forehead involvement 2

Key distinguishing features:

• Rapid onset within 72 hours of unilateral facial weakness involving the forehead 2
• Additional features may include taste disturbance, hyperacusis, dry eye, and sagging of the mouth corner 2
• The peripheral location of the lesion (typically within the narrow temporal bone canal where inflammation causes compression) means all ipsilateral facial muscles lose innervation 2

Horner's Syndrome: Oculosympathetic Pathway

Anatomical pathway (3-neuron chain):

• First-order (central) neuron: Originates in the hypothalamus and descends through the brainstem to the intermediolateral gray substance of the spinal cord at C8-T2 levels 4, 3

• Second-order (preganglionic) neuron: Arises from the first 3 thoracic spinal cord segments (T1-T3), travels through the thorax and cervical region, and synapses at the cranial cervical ganglion 5, 3

• Third-order (postganglionic) neuron: Travels from the cranial cervical ganglion along the internal carotid artery to the orbit 5, 3

Clinical presentation:

• Classic triad: miosis (pupillary constriction), ptosis (slight drooping of upper lid), and anhidrosis (decreased sweating on affected side of face) 5, 6, 3
• May also present with enophthalmos and protrusion of the third eyelid 5
• Does NOT cause facial muscle weakness or affect facial expression 3

Critical Clinical Distinctions

Forehead involvement is the key differentiator:

• Bell's palsy: Forehead IS affected (peripheral CN VII lesion) - patient cannot wrinkle forehead on affected side 2
• Stroke (central facial palsy): Forehead is SPARED due to bilateral cortical innervation - this distinguishes stroke from Bell's palsy 2, 7
• Horner's syndrome: No facial weakness at all; only autonomic signs (pupil, eyelid, sweating) 3

Anatomical vulnerability:

• Bell's palsy results from inflammation and edema within the narrow temporal bone canal compressing CN VII 2, 7
• Horner's syndrome can result from lesions anywhere along the long sympathetic pathway from hypothalamus through chest and neck to orbit, making it a warning sign of potentially serious pathology (including carotid dissection, lung malignancy, or thoracic disk herniation) 4, 6, 3

Common pitfall to avoid:

• Do not confuse incomplete Horner's syndrome (which may lack anhidrosis) with other causes of isolated ptosis or miosis 8
• Always document function of all other cranial nerves when evaluating facial weakness to exclude stroke and other central causes 2