We present a rare case of recurrent glomus jugulare tumour, manifesting as an isolated facial nerve palsy. Glomus jugulare tumours are slow-growing paragangliomas of the jugular bulb adventitia. We report the case of a 73-year-old female referred for oculoplastic management of a facial nerve palsy, with a history of a right-sided glomus jugulare tumour treated surgically 40 years prior. Her 6-month history of facial palsy had initially been attributed towards Bell's palsy, particularly in the context of communication challenges related to residual dysphonia and hearing loss following her prior skull-base surgery. This case underscores the importance of maintaining a high index of suspicion in patients with atypical or high-risk clinical features and highlights the necessity of timely neuroimaging to exclude underlying structural pathology.

Bell's palsy, an idiopathic facial nerve paralysis (FNP), causes one-sided facial muscle weakness. Although this is a common clinical diagnosis in the pediatric population, further workup is warranted if FNP is accompanied by atypical symptoms or recurrence as this could be indicative of an alternative diagnosis. We report a 12-year-old female patient who experienced two right-sided episodes of lower motor neuron FNP occurring 10 months apart with atypical sensory nerve involvement. Both episodes resolved with oral corticosteroid therapy, and the patient did not follow up with pediatric neurology for further workup. This case is notable for its recurrent ipsilateral presentation in a child with otherwise normal systemic workup, contributing to the limited literature on pediatric recurrence patterns. It underscores the diagnostic challenge of distinguishing idiopathic from secondary causes, reinforces the role of corticosteroids in management, and highlights the importance of clinical follow-up despite spontaneous recovery.

In this report, we describe a case of idiopathic bilateral facial nerve palsy in a previously healthy male in his 30s, with recent unprotected sexual activity and a possible genetic predisposition as the only identifiable risk factors. The case highlights both the diagnostic complexity of bilateral facial palsy and the importance of methodical exclusion of systemic causes and early initiation of corticosteroid therapy, which led to complete recovery.

Background Facial synkinesis describes a sequela of transient facial nerve injury that can occur following viral reactivation syndromes such Bell's palsy or following traumatic facial nerve injury. Facial synkinesis is frequently characterized by muscle hypertonicity, involuntary co-contraction of facial muscles, and spasm, and can have severe functional and aesthetic consequences. Although this condition is not curable, several treatment options exist; however, there is currently a lack of consensus regarding the appropriate timeline and sequence of synkinesis treatment strategies. Summary Treatment for facial synkinesis is nuanced and constantly evolving. A range of both noninvasive and invasive treatment options exist, including physical therapy, chemodenervation with botulinum toxin, and various surgical interventions such as selective myectomy and selective neurectomy. The optimal treatment strategy is often dependent on patient preference, clinical presentation, and provider comfort, and can be further complicated by confusion regarding the appropriate timeline for escalation of care. This review summarizes the current treatment trends and proposes a nuanced algorithm that integrates current practice and individualized decision-making to provide a framework to care for this patient population. Key Messages Management of facial synkinesis is complicated by the wide range of treatment options in addition to the lack of clear consensus on how to integrate these modalities into a cohesive treatment plan. The algorithmic approach outlined here represents one of several possible frameworks for evaluating and managing patients with this challenging condition.

Facial nerve palsy, including Bell's palsy, can occur as a post-dental complication, leading to sudden facial muscle weakness or paralysis. This study reviewed 2543 subjects with idiopathic facial palsy over 10 years, identifying 18 cases (0.70%) of facial paralysis post-dental treatment. All cases involved ipsilateral paralysis, with a mean onset of 3.82 days after treatment. Early diagnosis and management significantly improve prognosis, highlighting the importance of preventive measures and awareness. The identification of facial paralysis as a rare post-dental complication and the finding that early diagnosis and management significantly improve the prognosis of the condition.

Most cases of unilateral facial paralysis are caused by Bell's palsy, which is usually an idiopathic lower motor neuron facial nerve palsy. However, some cases result from an infarction of the ipsilateral facial nerve region in the pons, which mimics Bell's palsy and is referred to as a pontine stroke. This study reports a case of a 63-year-old male who presented with complaints of dizziness, giddiness, nausea, vomiting, and headache for 12 hours. He developed facial deviation to the right and slurred speech seven hours before presentation. Additionally, he had a history of hypertension and diabetes. No signs of meningeal irritation were noted. Cranial nerve examination and MRI were suggestive of a left lacunar pontine infarct. The patient was given aspirin, clopidogrel, and atorvastatin along with antihypertensive medications and other symptomatic treatments. He was discharged after seven days in a stable condition. This report highlights the importance of clinicians being aware of the need to investigate for stroke when a patient presents with peripheral facial nerve palsy.

Facial nerve palsies are a common and significant presentation specifically to ear, nose, and throat (ENT) surgeons but also in general medical practice. The facial nerve is a fundamental structure both for communication and emotion, and as such, functional impairment can lead to a significant deterioration in the quality of life.[1] A key element in the initial assessment of a patient presenting with facial weakness is distinguishing between a lower motor neuron (LMN) versus an upper motor neuron (UMN) palsy, as the likely causes and, therefore, treatment for these vary significantly. Applying anatomy to clinical history and examination, a clinician can identify the probable cause of facial nerve palsy and subsequently direct management appropriately.

The nerve supply of the face has an intricate branching pattern that is often difficult to differentiate. The present study was undertaken to highlight the historical discoveries that helped understand the distribution of peripheral nerves in the face, identify the difficulty in comprehending the relevant anatomy due to complex details, and explore the relevance of historical details in addressing how the facial nerve is currently taught. Historically, Galen (third century AD) described the trigeminal nerve as dominant in regulating the motor and sensory supply of the face; however, he saw the facial nerve as being limited to a minor role in motor innervation, with a common origin alongside the vestibulocochlear nerve. This inaccurate concept persisted throughout the Middle Ages until the Early Renaissance in Europe. Thereafter, scientific studies by Fallopio and Eustachio (sixteenth century) and Sömmerring (eighteenth century) established the autonomous origin and extensive motor distribution of facial nerves. Despite considerable differences, Bell and Mayo (nineteenth century) agreed that the facial nerve is the nerve of facial expression. The discovery of facial nerve nuclei within the brainstem (early twentieth century) has allowed us to understand the motor, sensory, and autonomic components of the facial nerve. Advances in neurophysiology (twentieth century) have identified sensory fibers from the trigeminal nerve to the facial muscles (key to facial proprioception), in addition to motor innervation from branches of the facial nerve. This finding solved the puzzle regarding dual nerve supply of the facial muscles, often presenting as intricate connections. Similarly, the discovery of the upper motor neuron and lower motor neuron (late nineteenth and early twentieth centuries) solved the conundrum of facial palsy and the location of lesions in relation to the facial nerve nuclei. Comprehensive three-dimensional models elucidating the intricate details of the nerve supply to the face and facial nerve are effective in mapping, retaining, and reproducing relevant knowledge in academic and clinical practice. This methodology is currently used in anatomical sciences to teach the anatomy of the facial nerve.