Which brainstem pathologies most commonly produce isolated facial palsy and how often are they misdiagnosed?

1. Brainstem ischemia: the stealth pontine infarct that looks like Bell’s palsy

Small ischemic strokes in the pons or pontomedullary junction can produce a lower motor–pattern hemifacial weakness that includes the forehead, thereby imitating peripheral Bell’s palsy; case reports emphasize that these infarcts are uncommon presentations and that diffusion‑weighted MRI can be falsely negative early on, which contributes to misclassification as benign facial palsy ^{[1] [8] [9]}. While brainstem strokes more typically present with additional cranial nerve dysfunction, vertigo, or long‑tract signs, the literature documents isolated facial presentations as rare but real and diagnostically treacherous ^{[8] [9]}.

2. Multiple sclerosis: demyelinating plaques masquerading as “idiopathic” palsy

Multiple sclerosis can produce peripheral‑appearing facial palsy when demyelinating plaques involve the facial nucleus or intrapontine fibers; studies report that roughly 60% of MS patients with facial palsy have pontine plaques on imaging, yet the overall incidence of peripheral facial nerve palsy in MS is low (estimated ~0.2%) and isolated cranial neuropathies in MS occur in about 1.6% of patients — facts that explain why MS occasionally presents as apparent Bell’s palsy and why steroid treatment can mask the underlying diagnosis if MRI is not obtained ^{[2] [3]}.

3. Tumors and compressive lesions: slow growers that start fast on the wrong diagnosis

Tumors along the facial nerve or in the cerebellopontine angle — vestibular schwannomas and intratemporal facial nerve schwannomas — can present initially with isolated facial weakness and be mislabelled as Bell’s palsy; systematic reviews show that an appreciable minority of intratemporal facial nerve schwannomas were initially misdiagnosed as Bell’s palsy (about 8.14% in pooled series), and case reports document delays in imaging that allowed progressive disease to go unrecognized ^{[5] [4] [10]}.

4. How often are central or structural causes missed — the numbers and the caveats

Published estimates of misdiagnosis vary by study design: an emergency‑department study found an overall Bell’s palsy misdiagnosis rate of ~0.8% with most errors being stroke or infectious mimics, whereas prior literature reviews cited misdiagnosis rates up to 20% and noted that roughly 5% of lower motor–unit facial palsies ultimately reflected tumor ^{[6] [7]}. Those ranges reflect heterogeneity in case mix, referral bias toward tertiary centers, reliance on case reports, and differing thresholds for imaging; specific pathologies have clearer signals (e.g., schwannoma series with ~8% initial misdiagnosis), whereas sporadic pontine infarcts and MS presentations are rarer and therefore less precisely quantified in population studies ^{[5] [1] [2] [7]}.

5. Practical import: when to suspect a brainstem cause and avoid diagnostic error

Clinical red flags that should prompt neuroimaging and neurology consultation include accompanying cranial neuropathies, sensory or cerebellar signs, dysarthria or dysphagia, atypical progression, absence of classic Bell’s palsy prodrome, or lack of forehead sparing patterns that don’t fit UMN versus LMN paradigms; authoritative reviews and textbooks advise MRI when features are atypical because early imaging can still miss tiny brainstem infarcts and because steroid treatment alone can mask MS or tumor ^{[9] [8] [2] [7]}. The literature therefore supports a low threshold for targeted imaging and follow‑up in atypical cases to reduce the documented — and variable — risk of missed central or structural etiologies ^{[6] [5]}.