Efficacy and safety of reoperation for residual or recurrent hemifacial spasm after microvascular decompression: a systematic review and meta-analysis.

The efficacy and safety of revision microscopic microvascular decompression (microscopic MVD) for treating residual or recurrent hemifacial spasm (HFS) remain uncertain. We conducted a systematic review and meta-analysis to evaluate the benefits and risks associated with this reoperation, focusing primarily on spasm relief, facial palsy, and hearing impairment. This study adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines. We performed a comprehensive search of PubMed, Embase, Web of Science, and the Cochrane Library for eligible articles from their inception through June 2024. A total of 17 studies involving 719 patients were included in this meta-analysis. Among these patients, 668 experienced overall symptom relief following reoperation, resulting in a relief rate of 94% (95% CI: 92-96%). Complete relief was achieved in 603 patients, corresponding to a rate of 87% (95% CI: 80-93%). Transient facial palsy developed in 4% (95% CI: 1-8%) of patients, while persistent facial palsy was observed in 5% (95% CI: 2-8%) of patients following reoperation. Transient hearing impairment occurred in 1% (95% CI: 0-3%) of patients, while persistent hearing impairment was reported in 4% (95% CI: 1-7%) of patients. Patients with recurrent HFS have significantly lower overall and complete relief rates after reoperation compared to those with residual HFS and are at higher risk of long-term hearing loss. Our study suggests that reoperation for residual or recurrent HFS after microscopic MVD could be considered a safe and effective treatment option. Early reoperation may be indicated in specific cases, and the timing should be tailored to each patient's specific circumstances to optimize outcomes.

Mechanism and future prospect of treatment of facial paralysis caused by herpes zoster virus infection with acupuncture combined with medicine: A review.

Herpes zoster virus infectious facial paralysis is caused by the reactivation and replication of varicella-zoster virus, which leads to herpetic inflammatory lesions, resulting in peripheral facial paralysis associated with herpes rash in the auricle and external ear, and vestibular cochlear dysfunction. It is also known as Ramsey-Hunter syndrome (Hunt syndrome). Facial paralysis caused by herpes zoster is difficult to cure due to its easy loss of treatment and mistreatment. Cause a greater burden on the patient's body and mind. However, the treatment of Western medicine has lagged behind and there are many adverse reactions, which cannot be completely cured, and new alternatives are urgently needed. This article briefly reviews the advantages and disadvantages of modern medical treatment of Hunt syndrome. This paper expounds the unique ideas of traditional Chinese medicine in the treatment of Hunt syndrome from the perspectives of antiviral, antibacterial, improving blood circulation, protecting cardiovascular, cerebrovascular, and nerve. This article discusses the superiority of traditional Chinese medicine in the treatment of Hunt syndrome from 2 aspects of Chinese medicine therapy and acupuncture therapy, and points out the feasibility of combined treatment of acupuncture and traditional Chinese medicine. So as to provide a new treatment for Hunt syndrome.

Temporal bone fracture related facial palsy: efficacy of decompression with and without grafting.

PURPOSE OF REVIEW: This systematic review investigates the recent literature and aims to determine the approach, efficacy, and timing of facial nerve decompression with or without grafting in temporal bone fractures with facial palsy. RECENT FINDINGS: The surgical management of facial palsy is reserved for a small population of cases in which electrophysiologic tests indicate a poor likelihood of spontaneous recovery. The transmastoid (TM), middle cranial fossa (MCF), and translabyrinthine (TL) approaches to the facial nerve provide access to the entire intracranial and intratemporal segments of the facial nerve. In temporal bone (TB) related facial palsy, the peri-geniculate and labyrinthine portions of the facial nerve are most commonly affected by either direct trauma and/or subsequent edema. When hearing is still serviceable, the combined TM/MCF approach provides the best access to these regions. In the presence of severe sensorineural hearing loss (SNHL), the TL approach is the most appropriate for total facial nerve exploration (this can be done in conjunction with simultaneous cochlear implantation if the cochlear nerve has not been avulsed). Grade I to III House-Brackmann (HB) results can be anticipated in timely decompression of facial nerve injury caused by edema or intraneuronal hemorrhage. Grade III outcomes, with slight weakness and synkinesis, is the outcome to be expected from the use of interpositional grafts or primary neurorrhaphy. In addition to good eye care and the use of systemic steroids (if not contraindicated in the acute trauma setting), surgical decompression with or without grafting/neurorrhaphy may be offered to patients with appropriate electrophysiologic testing, physical examination findings, and radiologic localization of injury. SUMMARY: Surgery of the facial nerve remains an option for select patients. Here, we discuss the indications and results of treatment as well as the best surgical approach to facial nerve determined based on patient's hearing status and radiologic data. Controversy remains about whether timing of surgery (e.g., immediate vs. delayed intervention) impacts outcomes. However, no one with facial palsy due to a temporal bone fracture should be left with a complete facial paralysis.

Medullary infarction with central facial paralysis as the only symptom: a case report.

The anatomical structure of the medulla oblongata is complex, its nerve fibers are dense, and its blood vessels are complex. Clinical manifestations of ischemic damage to the medulla oblongata are therefore relatively diverse, and include vertigo, dysphagia, and dysarthria. Although facial paralysis may also occur, medullary infarction with facial paralysis as the first and only symptom is rare. Herein, we report a case of medullary infarction with ipsilateral central facial paralysis as the only symptom.

Facial Nerve Paresis After Combined Intraoral and Preauricular Approach to High Condylar Fractures: A Case Report.

Condylar fractures are the most common mandibular fractures, and a variety of open and closed approaches are used for repair, each with its own inherent risks and benefits. A 27-year-old man had a severely displaced and angulated high subcondylar fracture with anterior open bite deformity. The patient underwent open reduction and internal fixation of the condyle via a combined preauricular and intraoral approach as well as maxillomandibular fixation to repair his fracture. This combined approach allows the surgeon to maximize exposure while limiting risks of permanent injury from surgery.

Facial Paralysis in Otitis Media Due to Granulomatosis with Polyangiitis.

Granulomatosis with polyangiitis (GPA), formerly Wegener's granulomatosis, commonly presents primarily with otitis media and hearing loss, as well as upper and lower respiratory symptoms. However, facial nerve paralysis is a rare manifestation of this uncommon necrotizing vasculitis. We report a patient with facial paralysis accompanied by otitis media. In further studies, our patient was diagnosed with GPA, which was neglected before. In such a presentation, acute suppurative otitis media is the most likely cause of the facial paralysis, but GPA must also be considered, especially in cases with new-onset, painful serous otitis, acute otitis media, or pale granulation tissue in the middle ear, in adults with no previous history of Eustachian tube dysfunction.

A case report of fifteen-and-a-half syndrome.

BACKGROUND: Fifteen-and-a-Half Syndrome is an uncommon clinical presentation characterized by the coexistence of one-and-a-half syndrome and bilateral facial palsy. In this study, we provide a comprehensive description of symptom evolution and imaging changes in a patient with Fifteen-and-a-Half Syndrome. CASE PRESENTATION: A 54-year-old male presented with sudden onset of one-and-a-half syndrome, which gradually progressed to fifteen-and-a-half syndrome. The final diagnosis was confirmed to be pontine infarction which occurred at the midline of the pontine tegmentum. CONCLUSION: This case highlights the diverse and progressive early clinical manifestations associated with Fifteen-and-a-half Syndrome. Currently, all reported cases of this syndrome are linked to brainstem infarction; however, early differential diagnosis is crucial to ensure prompt initiation of appropriate treatment for affected patients.

Bilateral facial nerve palsy complicating Kawasaki disease: A case report and literature review.

RATIONALE: Kawasaki disease (KD) manifests as an acute, self-limited vasculitis disease that constitutes the primary cause of acquired heart disease in children under 5 years of age. Facial nerve palsy (FNP) is a rare complication associated with coronary artery lesions (CALs) in patients with KD. Patients with KD and FNP usually present atypically, leading to a delayed diagnosis and treatment of KD. PATIENT CONCERNS: A 4-month-old boy with fever, left FNP and bilateral conjunctival injection with spontaneous resolution, was admitted to the hospital, received a short course of intravenous dexamethasone, and experienced rapid FNP recovery on the first admission. The patient experienced a resurgence of fever, bilateral conjunctival injection, and right FNP, which led to readmission. Physical examination revealed redness at the site of Bacillus Calmette-Guérin inoculation, reddening of lips, and desquamation of the distal extremities. Echocardiography revealed right-sided CALs. DIAGNOSES: The patient initially missed KD on the first admission, and was later diagnosed with complete KD with FNP on the second admission. INTERVENTIONS AND OUTCOMES: After a short course of intravenous dexamethasone, the left FNP resolved quickly. However, right FNP recurred after corticosteroids withdrawal. Meanwhile, more typical symptoms were observed, and KD was diagnosed. Treatment ensued with intravenous immunoglobulin (IVIG), aspirin, and dexamethasone. The patient achieved rapid remission, without recurrence. Echocardiography continued to show normal findings during 1-year follow-up after discharge. LESSONS: The clinical symptoms of FNP complicating KD in children are atypical and can easily lead to delayed diagnosis and treatment. FNP in patients with KD may serve as a risk factor for CALs, which are more challenging to resolve than the FNP itself. Adding corticosteroids to IVIG may be recommended to reduce IVIG resistance, decrease the risk of developing CALs, and alleviate CALs.

Facial nerve palsy after middle meningeal artery embolization for chronic subdural hematoma: a case report.

Middle meningeal artery embolization (MMAE) has emerged as a safe and efficacious alternative to surgery for the treatment of new or recurrent chronic subdural hematoma (CSDH). Several complications such as facial palsy may suddenly occur even in the absence of evident dangerous anastomoses in the angiogram. We herein present a case-report of left facial nerve palsy after MMAE.

A Rare Multinuclear Lesion Secondary to Multifactorial Ischemic Stroke: A Case Report on Eight-and-a-Half Syndrome.

Internuclear ophthalmoparesis (INO) is a horizontal eye movement disorder that is associated with a lesion at the medial longitudinal fasciculus (MLF). One-and-a-half syndrome occurs when the lesion involves the MLF and the ipsilateral abducens nuclei or the paramedian pontine reticular formation (PPRF) in the dorsomedial tegmentum of the pons. When the lesion is large enough, the fascicles of the facial nerve (CNVII) can also be involved, resulting in an ipsilateral facial nerve palsy. In combination with one-and-a-half syndrome, this condition becomes eightand- a- half syndrome (EHS). Here, we describe a unique case of EHS in a 72-year-old male with multiple ischemic stroke risk factors who presented with INO, conjugate gaze palsy, ipsilateral facial palsy, and a transient contralateral hemiparesis. Recognizing this pattern of neurologic deficits improves localization of the lesion, prevents misdiagnosis of Bell's Palsy, and expedites proper treatment.

Facial nerve palsy after ethylene vinyl alcohol arterial embolization of glomus tympanicum.

BACKGROUND & OBJECTIVE: Glomus tympanicum and jugulare tumors are highly vascular and are therefore commonly embolized before surgical resection to prevent intra-operative bleeding. We report a case of facial nerve paralysis after pre-operative embolization for a glomus tympanicum tumor with ethylene vinyl alcohol (EVOH also known as Onyx) embolic agent. We discuss the choice of embolic agent in relation to the risk of this complication and potential management strategies. METHODS: A 57F with right glomus tympanicum developed right facial nerve palsy immediately after embolization. She received 24 mg of dexamethasone over the course of 24 h immediately following her embolization, surgical facial nerve decompression concurrent with tumor resection, and a 10-day prednisone taper. Our main outcome measure was facial nerve function on follow-up physical examinations. RESULTS: The patient developed right facial paralysis (HB 6/6) after Onyx embolization of branches of the external carotid artery system, likely due to translocation of embolic agent into facial nerve vasa nervosa as seen on post-embolization CT. No immediate improvement was observed with high dose steroids and decompression, however over the next 6 months her facial nerve function began to improve (HB 3/6). CONCLUSIONS: Surgical excision is the standard of care for glomus jugulare and glomus tympanicum tumors. Due to their propensity to bleed, their arterial feeders (branches of the external carotid) are often embolized prior to surgery, however, facial nerve paralysis is a rare but serious complication. There is a possible relationship between the choice of embolic agent and this complication. Though facial palsy is of sufficient rarity that no standard treatment pathway exists, due to the impact on a patient's quality of life, we recommend aggressive therapy to salvage nerve function.

Risk factors for nonidiopathic and idiopathic facial nerve palsies: findings of a retrospective study.

BACKGROUND: Idiopathic (IF) and nonidiopathic facial (NIF) nerve palsies are the most common forms of peripheral facial nerve palsies. Various risk factors for IF palsies, such as weather, have been explored, but such associations are sparse for NIF palsies, and it remains unclear whether certain diagnostic procedures, such as contrast agent-enhanced cerebral magnetic resonance imaging (cMRI), are helpful in the differential diagnosis of NIF vs. IF. METHODS: In this retrospective, monocentric study over a five-year period, the medical reports of 343 patients with peripheral facial nerve palsy were analysed based on aetiology, sociodemographic factors, cardiovascular risk factors, consultation time, diagnostic procedures such as cMRI, and laboratory results. We also investigated whether weather conditions and German Google Trends data were associated with the occurrence of NIF. To assess the importance of doctors' clinical opinions, the documented anamneses and clinical examination reports were presented and rated in a blinded fashion by five neurology residents to assess the likelihood of NIF. RESULTS: A total of 254 patients (74%) had IF, and 89 patients (26%) had NIF. The most common aetiology among the NIF patients was the varicella zoster virus (VZV, 45%). Among the factors analysed, efflorescence (odds ratio (OR) 17.3) and rater agreement (OR 5.3) had the highest associations with NIF. The day of consultation (Friday, OR 3.6) and the cMRI findings of contrast enhancement of the facial nerve (OR 2.3) were also risk factors associated with NIF. In contrast, the local weather, Google Trends data, and cardiovascular risk factors were not associated with NIF. CONCLUSION: The findings of this retrospective study highlight the importance of patient history and careful inspections to identify skin lesions for the differential diagnosis of acute facial nerve palsy. Special caution is advised for hospital physicians during the tick season, as a surge in NIF cases can lead to a concomitant increase in IF cases, making it challenging to choose adequate diagnostic methods.

[Bilateral facial palsy: an atypical presentation of Lyme disease (a case report)]. / Paralysie faciale bilatérale : une présentation atypique d'une maladie de Lyme (cas clinique).

Lyme neuroborreliosis is a rare zoonosis which can be difficult to diagnose, in particular in low endemic areas. We here report the case of a 35-year-old man presenting with disabling back pain preceded by facial monoplegia, which was wrongly treated as Bell's palsy (paralysis a frigore) and then as post-traumatic lumbosciatica. The onset of facial diplegia allowed for a definitive diagnosis. The patient was treated with ceftriaxone and symptoms gradually improved.

A Rare Case of Hyperglycemia, Ketoacidosis, and Central Facial Paralysis in a Newly-Diagnosed Diabetic Woman.

BACKGROUND Diabetes mellitus is a chronic disease that occurs when the pancreas does not produce enough insulin or when the body is unable to effectively use the insulin it produces. Uncontrolled diabetes mellitus is usually associated with neurological manifestations, such as hemichorea, focal epileptic seizures, peripheral neuropathy, and peripheral facial paralysis. This report describes a 59-year-old woman presenting with hyperglycemia and ketoacidosis due to newly diagnosed diabetes mellitus, as well as a temporary episode of central facial paralysis, which regressed within a few days after medical treatment and metabolic correction. CASE REPORT A 59-year-old patient with hypertension and a family history of diabetes mellitus presented with polyuro-polydipsic syndrome and signs of metabolic ketoacidosis, with an elevated anion gap, compatible with newly discovered type 1 diabetes mellitus. Six hours after admission, we noted the abrupt onset of left central facial paralysis, with no brain damage shown on magnetic resonance imaging. Initially, the diagnosis was transient ischemic attack. After a second, normal cerebral magnetic resonance image on the fourth day, and clinical improvement on the fifth day after metabolic correction by insulin therapy and rehydration, the diagnosis of a regressive central facial paralysis was retained. CONCLUSIONS Central facial paralysis in diabetic ketoacidosis is a rare neuroendocrine entity. The pathophysiological mechanisms that can explain the occurrence of central facial paralysis are not yet described and require further investigation. This report highlights the importance of diagnosis, early management of hyperglycemia and diabetic ketoacidosis, and reversibility of central facial paralysis after treatment.

Masseteric Atrophy Following Masseteric Nerve Transfer: Radiographic Findings of Asymmetry in the Paralyzed Face?

OBJECTIVES: To characterize the effect of facial reanimation using masseteric nerve transfer on the masseter muscle itself, examining whether there is any demonstrable atrophy postoperatively. METHODS: Electronic medical records of adult patients who underwent facial reanimation using masseteric nerve transfer at our institution over a 15-year period were reviewed. To account for the impact of postoperative radiation, randomly selected patients who underwent radical parotidectomy without nerve transfer and received postoperative radiation served as controls in a 1:1 fashion against those who underwent masseteric nerve transfer with postoperative radiation. RESULTS: Twenty patients were identified who underwent masseteric nerve transfer and had sufficient pre- and postoperative imaging to assess masseter volume (mean age 58.2, 60% female). Of the four patients who did not receive postoperative radiation, each demonstrated masseteric atrophy on the side of their nerve transfer, with a mean reduction in masseter volume of 20.6%. The remaining 16 patients were included in the case-control analysis accounting for radiation. When compared with controls, those in the study group were found to have a statistically significant difference in atrophy (p = 0.0047) and total volume loss (p = 0.0002). The overall reduction in masseter volume in the study group was significantly higher compared with the control group, at 41.7% and 16.6%, respectively (p = 0.0001). CONCLUSION: Facial reanimation utilizing masseteric nerve transfer appears to result in atrophy of the denervated masseter when compared with the contralateral muscle. This volume deficit may lead to further facial asymmetry for patients undergoing comprehensive reanimation surgery. LEVEL OF EVIDENCE: 3 Laryngoscope, 134:4514-4520, 2024.

A case of lenticulostriate artery infarction presenting with peripheral type facial palsy.

An 82-year-old woman developed a droopy right eyelid with ipsilateral hemiparesis. Her ocular symptom was caused by weakness of the right frontalis, which is usually seen in patients with peripheral facial nerve palsy. However, head MRI showed acute cerebral infarction of the left lenticulostriate artery, and electroneurography did not detect damage to the right facial nerve. To explain the pathophysiology in this patient, asymmetrical bilateral cortex innervation to the right upper face was hypothesized. This case suggested that patients with some hemispheric strokes could develop upper facial weakness mimicking facial nerve palsy, and clinicians should pay attention to this potential pitfall in the differential diagnosis of facial nerve palsy.

Case report: Bilateral facial palsy with paresthesias and positive anti-GT1a antibodies.

Bilateral facial palsy with paresthesia (FDP) is a rare variant of GBS, characterized by simultaneous bilateral facial palsy and paresthesia of the distal limbs. Mounting evidence indicates that the presence of anti-GT1a IgG has a pathogenic role as an effector molecule in the development of cranial nerve palsies in certain patients with GBS, whereas anti-GT1a antibody is rarely presented positive in FDP. Here, we report the case of a 33-year-old male diagnosed with FDP presented with acute onset of bilateral facial palsy and slight paresthesias at the feet as the only neurological manifestation. An antecedent infection with no identifiable reason for the fever or skin eruptions was noted in the patient. He also exhibited cerebrospinal fluid albuminocytologic dissociation and abnormal nerve conduction studies. Notably, the testing of specific serum anti-gangliosides showed positive anti-GT1a IgG/IgM Ab. The patient responded well to intravenous immunoglobulin therapy. This case brings awareness to a rare variant of GBS, and provides the first indication that anti-GT1a antibodies play a causative role in the development of FDP. The case also suggests that prompt management with IVIG should be implemented if FDP is diagnosed.

Immediate Facial Nerve Palsy Secondary to Otological Surgery: A Systematic Review and Narrative Synthesis.

OBJECTIVES: Iatrogenic facial nerve palsy following otological surgery is a devastating complication that results in adverse aesthetic and functional outcomes. This study aims to review studies that have reported cases of immediate facial nerve palsy to learn why and where injuries occurred and to assess outcomes following management. DATABASES REVIEWED: MEDLINE, Embase, Cochrane CENTRAL, and Pubmed up to June 20, 2023. METHODS: Clinical studies of immediate facial nerve palsies following middle ear and cochlear implantation surgery were included. Risk of bias was examined using the Brazzelli risk of bias tool. Due to the inconsistency in reporting of outcomes, we were unable to perform a meta-analysis. RESULTS: Of 234 studies identified, 11 met the inclusion criteria. The most common causes of injury were excessive drilling, use of sharp hooks to remove disease, or disorientation of the surgeon secondary to bleeding or inflammation. Variable usage of preoperative computed tomography (CT) imaging and intraoperative facial nerve monitoring was reported. The tympanic segment was the most common site of injury. A variety of surgical techniques were employed to approach the facial nerve injury including facial nerve decompression, direct closure, and repair using an autologous nerve graft. CONCLUSIONS: Otological surgeons should consider utilizing preoperative CT imaging to establish a three-dimensional mental image of key landmarks and anatomical variations before embarking on surgery. Intraoperative FN monitoring enables safe practice. Despite these measures, complex disease processes and hostile intraoperative conditions can present difficulty. Multiple treatment options are available to treat the underlying injury.