Facial palsy — Diagnosis, causes and the clock that starts ticking
How to separate a central from a peripheral palsy in thirty seconds, the real distribution of causes with figures, Bell’s palsy and what the evidence says about its treatment, the red flags that force reconsideration, and the time window that decides which surgery is possible.
Content intended for healthcare professionals. It does not replace clinical assessment and is not written as patient information.
Key points
- The first question is not the cause but the level: does the forehead move? If it does, the lesion is central; if not, peripheral. The bilateral cortical representation of the upper third explains everything.
- Bell’s palsy accounts for around 54 % of peripheral palsies, but the remaining 46 % includes tumours. A diagnosis of Bell’s is one of exclusion and with an expiry date.
- Oral corticosteroid started within the first 72 hours improves complete recovery; antiviral therapy alone is no better than placebo. It is the only medical treatment with Class I evidence behind it.
- The eye does not wait. Corneal protection starts the day of diagnosis, not when ocular symptoms appear.
- What decides which surgery is possible is not the diagnosis but the elapsed time: while the mimetic muscle remains reinnervable, a nerve can be given back to it; afterwards, a new muscle must be brought in.
Central or peripheral: the forehead decides
At the initial examination the first task is to establish the level of the lesion, and the upper third resolves it. A central lesion — thrombosis, haemorrhage, tumour or trauma affecting the voluntary corticofacial projections — produces weakness of the contralateral lower face with an effaced nasolabial fold and a dropped oral commissure, but the forehead wrinkle and eye closure remain intact because the upper face has bilateral cortical representation. Two nuances are worth knowing. First: in a central lesion involuntary emotional expression is unaffected, and if it is affected, the lesion involves the cingulate corticofacial projections. Second: acute ischaemic stroke from arterial obstruction has an immediate onset, unlike the progressive onset over hours of peripheral palsy.
What peripheral palsies are due to
| Cause | Approximate frequency | What it includes and implies |
|---|---|---|
| Idiopathic (Bell’s) | 54 % | By far the commonest, but it is a diagnosis of exclusion: the proportion varies between series from 38 % to 66 % depending on the referral centre |
| Neoplastic | 10 % | Vestibular schwannoma, head and neck cancer, facial nerve tumour, benign and malignant parotid lesions, cholesteatoma, metastases. This is why a palsy that does not improve gets imaged |
| Infectious | 7 % | Herpes zoster — Ramsay Hunt syndrome — Lyme neuroborreliosis, acute and chronic otitis and mastoiditis, HIV, mononucleosis, meningitis |
| Congenital and neonatal | 6 % | Non-syndromic forms, congenital unilateral lower lip palsy, Möbius syndrome, forceps delivery, myotonic dystrophy |
| Traumatic | 5 % | Skull base fracture, facial soft tissue and bone injury, middle ear injury. The proportion varies hugely between series, from 4 % to 23 % |
| Genetic and metabolic | 4 % | Diabetes, pregnancy, thyroid disorders, hypertension, alcoholic neuropathy |
| Autoimmune and neurological | 3 % | Melkersson-Rosenthal, sarcoidosis, multiple sclerosis, Guillain-Barré, myasthenia gravis, Charcot-Marie-Tooth |
| Iatrogenic | 3 % | Oral, head and neck, otological, neurosurgical and cosmetic surgery. Also temporal artery biopsy, mandibular block anaesthesia and sagittal split osteotomy |
Bell’s palsy, in figures
It is defined as rapid-onset unilateral weakness or paralysis — maximal within 48 hours — from acute peripheral facial nerve dysfunction, with no identifiable cause, and with some recovery within 3 to 6 months. It accounts for 50-70 % of peripheral palsies, with an annual incidence of around 30 per 100,000. There is no difference by sex or side, no seasonal clustering, and the peak is between ages 30 and 60. Diabetes, hypertension and pregnancy — third trimester and the two weeks postpartum — are considered risk factors. Accompanying symptoms are informative and worth seeking actively: ipsilateral periauricular or neck pain in 50-60 %, taste disturbance in 35 % and hyperacusis in 30 %. That triad also has topographic value: reduced lacrimation places the lesion proximal to the greater superficial petrosal nerve, and hyperacusis and taste loss proximal to the stapedial and chorda tympani branches respectively.
The red flags that force a rethink
A wrongly made diagnosis of Bell’s delays the diagnosis of a tumour, and that delay does have consequences. It must be reconsidered whenever there is: gradual rather than abrupt onset; absence of any improvement at 3-4 months; selective involvement of a single branch rather than the whole hemiface; recurrent palsy on the same side; associated signs or symptoms of other cranial neuropathies — hearing loss, tinnitus, vertigo, altered facial sensation; and a palpable parotid or neck mass. The mental rule is simple: Bell’s palsy improves. A palsy that has not begun to improve at four months is not Bell’s palsy until imaging says otherwise.
Medical treatment of Bell’s palsy
- Oral corticosteroidStarted within the first 72 hours. Two Class I regimens: prednisolone 50 mg for 10 days, or 60 mg for 5 days with a 5-day taper. It improves complete recovery at 3 and 9 months and shortens the time to it
- If they present lateClass I data beyond 72 hours are lacking. The usual reasoning is that in complete palsy the prognosis is far worse and treatment is worth giving even if presentation is delayed a week; beyond two weeks it is unlikely any treatment alters the course
- AntiviralAlone, no better than placebo. That is the concordant conclusion of the large trials and systematic reviews. Its role is limited to combination with corticosteroid in selected cases
- The eye, from day oneArtificial tears 6-8 times daily, manual lid closure by the patient, close-fitting glasses by day, ointment at night, lateral cross-taping and, in severe cases, a moisture chamber. Pain, irritation or itching mandate same-day ophthalmology referral
- Surgical decompressionContested ground. Transmastoid decompression is insufficient because the initial lesion lies in the meatal or labyrinthine segment. The middle fossa approach in severe palsies operated within two weeks improved outcomes in a case-control study, but randomised evidence is of very low quality
How it is graded, and what each scale is for
| Instrument | How it works | What it is for |
|---|---|---|
| House-Brackmann | A global six-grade scale, from I — normal — to VI — total paralysis — assessing the face as a whole | It is the lingua franca: quick, universal and comparable across publications. In exchange it is insensitive to small change and does not discriminate by region |
| Sunnybrook | A regionally weighted system scoring resting symmetry, symmetry of voluntary movement and synkinesis separately | Far more sensitive to change and the only one of the two that quantifies synkinesis, which is what bothers patients most in the sequela phase |
| Smile excursion scale | Measures commissure excursion in millimetres relative to the healthy side | It is the natural outcome measure for smile reanimation surgery, where the goal is one specific movement rather than global function |
| Patient-reported outcome measures | They capture the patient’s own assessment of function, appearance and social impact | They add what no clinical scale measures: how much it weighs on the patient. They correlate poorly with clinician grading, and that discrepancy is information, not noise |
The clock: what recent palsy means
The distinction that organises all reanimation surgery is neither the cause nor the grade, but whether the mimetic musculature is still reinnervable. Recent palsies are those in which electromyography still detects fibrillations in the mimetic muscles: the sign that the muscle is denervated but alive and waiting. Those fibrillations usually disappear between 18 and 24 months after onset. While they last, surgery can be limited to giving nerve input back to the muscle that is already there, always the more elegant option and the one giving the best quality of movement. Once they vanish, the muscle no longer responds to any nerve and new muscle must be brought in: free muscle transfer or temporalis transposition. That boundary is why early referral matters so much in facial palsy, and why a patient arriving at two years has lost options nobody will give back.
Terminology, which here is used loosely
- Paresis means some muscle function remains; paralysis, complete loss with a flaccid face. In the literature the two are used interchangeably far too often.
- The terms incomplete and complete are used both in the early and the recovery phase, and there they create confusion: in the recovery phase the correct wording is complete or incomplete recovery, not palsy.
- Bilateral palsy is rare but real, and when it appears it changes the differential entirely: it demands thinking of Guillain-Barré, sarcoidosis, Lyme or Möbius before Bell’s.
- Post-paralytic synkinesis is not residual palsy but its opposite: aberrant reinnervation producing coupled involuntary movements. It is an entity with its own treatment and deserves its own section in the examination.
The patient who arrives with a drooping face
Does the forehead move and the eye close?
Abrupt onset, whole hemiface, no other signs and no palpable mass?
Months later: has recovery started?
References
- 1.House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg. 1985;93(2):146-147.
- 2.Ross BG, Fradet G, Nedzelski JM. Development of a sensitive clinical facial grading system. Otolaryngol Head Neck Surg. 1996;114(3):380-386.
- 3.Sullivan FM, Swan IRC, Donnan PT, Morrison JM, Smith BH, McKinstry B, et al. Early treatment with prednisolone or acyclovir in Bell’s palsy. N Engl J Med. 2007;357(16):1598-1607.
- 4.Peitersen E. Bell’s palsy: the spontaneous course of 2500 peripheral facial nerve palsies of different etiologies. Acta Otolaryngol. 2002;122(7):4-30.
- 5.Hohman MH, Hadlock TA. Etiology, diagnosis, and management of facial palsy: 2000 patients at a facial nerve center. Laryngoscope. 2014;124(7):E283-E293.
- 6.Biglioli F. Facial reanimations: part I—recent paralyses. Br J Oral Maxillofac Surg. 2015;53(10):901-906.
- 7.Biglioli F. Facial reanimations: part II—long-standing paralyses. Br J Oral Maxillofac Surg. 2015;53(10):907-912.
- 8.Tzou CHJ, Rodríguez-Lorenzo A, eds. Facial Palsy: Techniques for Reanimation of the Paralyzed Face. Cham: Springer; 2021.
Related specialty: Facial Paralysis