Bell's palsy is the most common cause of acute unilateral lower motor neuron-type facial nerve paralysis and is generally managed with early administration of corticosteroids, with or without antiviral therapy. Although most patients experience substantial recovery, a clinically meaningful subset-including older adults, individuals with delayed presentation, and those with comorbid medical conditions-may be left with incomplete resolution, with persistent facial weakness, asymmetry, or synkinesis. Electroacupuncture (EA) has been proposed as an adjunctive treatment modality for facial nerve recovery, with hypothesized mechanisms including enhanced neuromuscular activation, improved regional blood flow, modulation of local inflammatory responses, and facilitation of peripheral nerve regeneration. However, robust clinical evidence and detailed case-based documentation remain limited. We report the case of an 81-year-old male patient who presented with acute left-sided lower motor neuron-type facial paralysis. The diagnosis was consistent with Bell's palsy, after a cerebrovascular accident was excluded, and neuroimaging demonstrated no acute intracranial pathology. An integrative treatment approach incorporating acupuncture with low-frequency electrical stimulation was initiated on day 17 post-onset, targeting facial and cranial acupoints. EA treatment was administered twice weekly for seven weeks and was supplemented with conservative home-based interventions. Facial nerve function improved from House-Brackmann Grade IV at presentation to Grade I-II. While this case suggests that EA may have a role as an adjunctive therapy in Bell's palsy, including in patients with delayed presentation and less favorable prognostic features, its interpretation is limited by the single-case design and the known potential for spontaneous recovery. Accordingly, controlled prospective studies are warranted to further evaluate the efficacy, optimal timing, and clinical utility of EA in the management of acute facial nerve paralysis.

This article describes a rare case where a patient developed Adie's pupil after recovering from Bell's palsy. Adie's pupil, caused by parasympathetic involvement, presents as a dilated, poorly reactive pupil with reduced accommodation; Bell's palsy involves facial nerve dysfunction leading to facial paralysis, usually resolving within 6 months. The patient, with a prior history of fully resolved Bell's palsy, presented with right-sided Adie's pupil and absent deep tendon reflexes. Diagnosis was confirmed with 0.125% pilocarpine. While Adie's pupil has been linked to other conditions, its occurrence post-Bell's palsy is unusual, underscoring the importance of long-term follow-up in such patients.

Background and Objectives: Bell's palsy (BP) is the most common cause of acute unilateral peripheral facial nerve paralysis. The aim of this study was to evaluate the time to complete clinical recovery in patients with BP treated with acupuncture and to identify baseline clinical and electrophysiological predictors of recovery outcomes. In addition, electrophysiological characteristics at the time of complete clinical recovery were examined. Materials and Methods: This prospective, observational, uncontrolled cohort study included 1050 patients with clinically confirmed BP who received acupuncture as the only therapeutic intervention between January 2017 and August 2025. Clinical severity was assessed using the House-Brackmann (HB) and Sunnybrook (SB) grading systems. Electrophysiological evaluation included compound muscle action potential (CMAP) analysis and needle electromyography (EMG). Time-to-event analysis was performed using the Kaplan-Meier method and Cox proportional hazards regression analysis. Results: Complete clinical recovery was achieved in 843 patients (80.3%). The median time to recovery was 40 days (IQR 30-60). Patients with milder baseline deficits (HB II-IV) demonstrated significantly faster recovery than those with severe paralysis (HB V-VI) (log-rank p < 0.001). In multivariable Cox regression analysis, higher baseline HB grade, older age, and more severe EMG denervation were independently associated with slower recovery. Residual electrophysiological abnormalities persisted in most patients despite complete clinical recovery. Conclusions: Recovery from BP is a dynamic and heterogeneous process, significantly influenced by initial clinical severity and the degree of electrophysiological impairment. Combined clinical and electrophysiological assessment may contribute to more precise prognostic stratification and follow-up of patients with BP. Persistent electrophysiological abnormalities despite complete clinical recovery suggest that complete clinical recovery may precede complete neurophysiological regeneration of the facial nerve.

Peripheral facial palsy is often attributed to idiopathic Bell's palsy, but secondary structural causes should be considered when local red flags are present. A 61-year-old man with a 40-pack-year smoking history and former betel quid chewing presented with a verrucous-appearing mass involving the left oral commissure and buccal mucosa, intermittent purulent discharge from the lesion, progressive left facial swelling, and ipsilateral lower-motor-neuron facial palsy with lagophthalmos. Magnetic resonance imaging demonstrated a left buccal/oral-cavity lesion with ipsilateral parotid duct obstruction. He underwent tracheostomy, wide excision, left supraomohyoid neck dissection, and radial forearm free-flap reconstruction. Pathology confirmed squamous cell carcinoma, pT2N0, cM0 (stage II), with perineural invasion; surgical margins were negative, and lymphovascular invasion was not identified. At follow-up, wound healing was satisfactory and purulent discharge had resolved, but lower-motor-neuron facial palsy persisted; adjuvant radiotherapy was recommended. This case emphasizes that lower-motor-neuron facial palsy with an oral mass, purulent discharge, facial swelling, or salivary-duct obstruction should prompt careful oral examination and head-and-neck imaging.

We report a rare case of delayed peripheral facial paralysis following left anterior temporal lobectomy (ATL) for mesial temporal sclerosis in a 58-year-old woman with a long-standing history of seizures. Preoperative evaluation confirmed left temporal sclerosis as the epileptogenic focus. Surgery with neurophysiologic monitoring was performed, and initial postoperative assessment revealed no facial deficits. However, 4 days later, the patient developed left-sided peripheral facial paralysis (House-Brackmann grade 4), which improved after a 10-day course of oral corticosteroids. This case underscores that delayed facial paralysis, although uncommon, can occur after ATL, potentially due to mechanical or thermal injury near the geniculate ganglion or viral reactivation induced by direct manipulation or surgical stress. Awareness and timely follow-up are essential for early detection and management of such complications.

The use of chimeric antigen receptor T-cell (CAR-T) therapy has become more widespread in recent years, most commonly for hematologic malignancies. This therapy can be potentially associated with neurotoxic side effects. We present a patient with refractory multiple myeloma who developed diplopia, bilateral upward gaze limitation, abducens palsy, bilateral facial nerve palsy, and thoracic sensory radiculopathy following a course of CAR-T therapy, which were suspected to represent delayed immune effector cell-associated nerve palsies (IEC-NPs). His symptoms progressed despite oral and intravenous steroids. Subsequent intrathecal methotrexate and systemic cyclophosphamide resulted in acute symptomatic improvement and eventual resolution of diplopia and gradual recovery of extraocular movements and facial nerve palsies.

Acute peripheral facial palsy (APFP) sometimes known as Bell's palsy is a common neurological condition and is marked by the acute onset of lower motor weakness on one side of the face. Whereas spontaneous recovery is widespread, there is a significant rate of incomplete recovery, synkinesis, or enduring functional and psychosocial disability of patients. The past decades witnessed the improvement of the diagnostic and therapeutic plans, particularly the pharmacological and adjunctive ones, due to the developments in pathophysiological and clinical trials and the creation of guidelines. This narrative review summarizes the existing evidence on the classification, diagnosis, and treatment of APFP, particularly corticosteroid disease treatment, antiviral medication, combination therapy, adjunct, and rehabilitative therapies, and the future of precision medicine. Randomised controlled trials and high-quality systematic reviews have shown evidence in support of the early initiation of systemic corticosteroids within 72 h of symptom onset as the foundation of treatment practice, improving the likelihood of achieving full facial nerve recovery and less morbidity in the long run. Conversely, antiviral monotherapy has not demonstrated significant clinical benefit with combination therapy with antivirals potentially presenting some benefit to older patients and with severe cases of paralysis. New data highlight the significance of risk stratification, electrophysiological testing, and focal rehabilitation to maximize the results and reduce the sequelae. The developments in artificial intelligence, the work on biomarkers and adaptive clinical trial designs will likely enable more personalized prognostication and treatment choice. In general, a shift towards precision risk-based approaches to the management of acute peripheral facial palsy is also being considered and emerging diagnostic strategies, promotion of the use of corticosteroids as early as possible and focused adjunctive operations that are tailored to a child are becoming the key to improving functional outcomes in the long term.