Introduction
The facial nerve (CN VII) is one of the most clinically recognisable cranial nerves. Its mixed motor, sensory, and parasympathetic functions create a distinct pattern of deficits when it is damaged. Because the nerve runs a long and complex course through the posterior cranial fossa, temporal bone, and parotid region, accurate localisation depends on recognising which functions are lost and which are preserved.
This article organises the most exam-relevant facial nerve lesions into clear clinical pearls. The aim is to help you rapidly distinguish upper motor neuron from lower motor neuron lesions, identify key associated features, and localise pathology along the course of the nerve.
Functional Overview of the Facial Nerve
To interpret lesions correctly, you must first understand the functional components of the facial nerve:
- Motor (branchial efferent) fibres to the muscles of facial expression, stapedius, stylohyoid, and posterior belly of digastric.
- Parasympathetic (visceral efferent) fibres to the lacrimal, submandibular, and sublingual glands.
- Taste (special visceral afferent) from the anterior two-thirds of the tongue via chorda tympani.
- General sensory fibres to a small region of the external ear.
The relationship between these functions and the nerve's anatomical segments (intracranial, intrapetrous, and extracranial) is described under the course of the facial nerve. Clinical localisation is essentially the reverse process: you infer the site of the lesion by analysing which functions are affected.
Pearl 1: Forehead Involvement Separates UMN from LMN Lesions
The first and most important step is to distinguish an upper motor neuron (UMN) lesion from a lower motor neuron (LMN) lesion.
Upper Motor Neuron Lesions
- Commonly due to stroke, brain tumour, or demyelinating disease.
- Classically affect the contralateral lower face.
- The patient can still wrinkle the forehead and close both eyes because the upper facial muscles receive bilateral cortical innervation.
Lower Motor Neuron Lesions
- Include Bell palsy, temporal bone fractures, middle ear disease, and parotid pathology.
- Affect the entire ipsilateral face, including the forehead.
- The patient cannot wrinkle the forehead, close the eye tightly, or move the corner of the mouth symmetrically on the affected side.
Clinical pearl: If the forehead is weak, the lesion is almost certainly lower motor neuron. If the forehead is spared and only the lower face is weak, suspect an upper motor neuron lesion (e.g. stroke) and expand your cranial nerve and central nervous system examination.
Pearl 2: Hyperacusis Indicates a Lesion Proximal to the Stapedius Branch
Within the temporal bone, the facial nerve gives a branch to stapedius in the middle ear. Paralysis of stapedius causes hyperacusis (sound sensitivity), because the muscle can no longer dampen movements of the stapes.
Patients describe normal environmental sounds as uncomfortably loud or distorted. This complaint is easy to miss if you do not ask about it specifically.
Clinical pearl: Hyperacusis localises the lesion proximal to the stapedius branch, within the facial canal. It effectively rules out pure extracranial causes, such as isolated parotid gland branch injuries.
Pearl 3: Loss of Taste in the Anterior Two-Thirds of the Tongue
Taste fibres from the anterior two-thirds of the tongue travel with chorda tympani, which joins the lingual nerve and eventually reaches the submandibular gland region. Loss of taste in this distribution suggests that the lesion is proximal to the origin of chorda tympani.
In practice, many patients notice altered taste or a metallic flavour rather than complete loss. Exam scenarios may simply state "loss of taste on anterior two-thirds of tongue" on the affected side.
Clinical pearl: If taste is impaired but basic facial movements are also affected, think of a lesion within the petrous temporal bone, rather than a lesion after the nerve exits the stylomastoid foramen.
Pearl 4: Dry Eye Localises to Greater Petrosal / Geniculate Ganglion Region
Parasympathetic fibres to the lacrimal gland branch via the greater petrosal nerve near the geniculate ganglion, reaching the lacrimal apparatus through a complex pathway. Damage in this region can significantly reduce tear production.
Patients may present with dry, irritated eyes or a desire to blink frequently. In the context of a facial palsy, this suggests a lesion proximal to the geniculate ganglion.
Clinical pearl: Dry eye plus facial weakness points to a lesion proximal to the geniculate ganglion and greater petrosal origin. Typical Bell palsy, by contrast, often spares lacrimation.
Pearl 5: Bell Palsy Is an Isolated LMN Facial Weakness
Bell palsy is an acute idiopathic LMN facial palsy, usually attributed to inflammation and swelling of the nerve in the facial canal.
Typical Features
- Sudden onset over hours to a day.
- Complete ipsilateral LMN facial weakness (forehead and lower face).
- Absence of vesicular rash around the ear.
- No other cranial nerves involved.
- No major abnormalities in hearing, taste, or tearing in simple exam scenarios.
Clinical pearl: Bell palsy should be diagnosed only when you have excluded more specific causes. A "pure" LMN facial weakness without additional signs is most consistent with Bell palsy.
Pearl 6: Ramsay Hunt Syndrome Combines Paralysis with Ear Vesicles
Ramsay Hunt syndrome (herpes zoster oticus) is caused by reactivation of varicella-zoster virus in the geniculate ganglion. It is a critical diagnosis not to miss.
Key Features
- Severe ear pain.
- LMN facial paralysis.
- Vesicular eruption in the external ear, concha, or auditory canal.
- May be associated with taste loss, hyperacusis, or dry eye.
Clinical pearl: The combination of ear vesicles + LMN facial weakness should immediately suggest Ramsay Hunt syndrome rather than Bell palsy. This distinction affects both prognosis and treatment decisions.
Pearl 7: Extracranial Lesions Spare Taste, Hearing, and Lacrimation
Once the facial nerve exits the stylomastoid foramen, it gives branches to the posterior belly of digastric, stylohyoid, and then enters the parotid gland. Within the gland, it forms the parotid plexus that supplies motor fibres to the muscles of facial expression.
Lesions in this extracranial segment, such as from parotid tumours or parotidectomy, typically cause:
- Weakness of specific groups of facial muscles, depending on which terminal branches are involved.
- No disturbance of taste, lacrimation, or stapedius function.
Clinical pearl: If facial expression is weak but taste, hearing, and tearing are unaffected, the lesion is almost certainly extracranial, distal to the stylomastoid foramen, usually related to parotid gland pathology.
Pearl 8: Branch-Specific Weakness Suggests Parotid-Level Pathology
The facial nerve divides within the parotid gland into five main terminal branches. Selective involvement of these branches can produce subtle but localised weakness.
- Temporal branch: Difficulty raising the eyebrow or closing the eye tightly.
- Zygomatic branch: Impaired eye closure and lower lid movement.
- Buccal branch: Inability to blow out the cheeks or smile symmetrically.
- Marginal mandibular branch: Asymmetric depression of the lower lip.
- Cervical branch: Reduced platysma contraction.
Clinical pearl: Regional facial weakness confined to one or two territories strongly suggests a lesion within the parotid gland rather than a proximal lesion in the temporal bone or brainstem. Always correlate with parotid swelling, pain, or postoperative status.
Pearl 9: Eye Closure and Corneal Protection Are Critical in LMN Lesions
In LMN facial palsy, orbicularis oculi is weak, leading to incomplete eyelid closure. Poor blink reflex and lagophthalmos may expose the cornea to drying and trauma. This risk is heightened when tearing is also reduced due to proximal involvement of fibres to the lacrimal apparatus.
On examination, ask the patient to close their eyes tightly. In LMN palsy, you can often gently overcome the lid closure with your fingers, and the sclera remains visible.
Clinical pearl: In any LMN facial palsy, eye protection is a management priority. Document eyelid closure carefully and consider lubricants or taping to protect the cornea.
Pearl 10: Facial Synkinesis Indicates Aberrant Regeneration
After a severe LMN facial nerve lesion, regenerating fibres may reinnervate inappropriate muscle groups. This leads to facial synkinesis, where voluntary movement in one region triggers involuntary movement in another.
- Eye closure may cause the corner of the mouth to twitch.
- Smiling may cause involuntary eye narrowing.
- Cheek puffing may produce unwanted neck muscle contraction.
Clinical pearl: Facial synkinesis is a late sign of incomplete recovery and aberrant reinnervation. It confirms a previous LMN lesion but does not indicate current site of damage.
Summary
Facial nerve lesions can be approached systematically by analysing forehead involvement, hearing changes, taste, lacrimation, and the pattern of facial muscle weakness. By combining knowledge of the functional components and anatomical course of the nerve with focused examination of the muscles of facial expression, you can reliably localise the lesion as UMN or LMN and then more precisely along its path from brainstem to parotid branches. These clinical pearls form the core framework for OSCE stations, viva questions, and real-world neurological assessment.