Neuro-ophthalmologic Complications and Manifestations of Upper and Lower Motor Neuron Facial Paresis

Bhatti, M. Tariq; Schiffman, Jade S.; Pass, Anastas F.; Tang, Rosa A.

doi:10.1007/s11910-010-0143-1

Cited by 8 publications

(9 citation statements)

References 39 publications

(33 reference statements)

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“…Incomplete closure of the eyelid may lead to deposition of foreign particles in the eye, corneal abrasions, exposure keratitis and/or corneal ulcerations. 26,[81][82][83] Clinicians should be aware of symptoms such as burning, itching, eye irritation, changes in vision, and pain.…”

Section: Supporting Textmentioning

confidence: 99%

“…Bell's palsy is a condition that predisposes the eye to injury due to incomplete closure of the eyelid (lagophthalmos) from upper eyelid retraction or lower lid ectropion, as well as failure of the lacrimal pump mechanism, decreased blink and tear production, and loss of the corneal “squeegee effect” on the side affected by facial palsy. Incomplete closure of the eyelid may lead to deposition of foreign particles in the eye, corneal abrasions, exposure keratitis and/or corneal ulcerations 26,81‐83 . Clinicians should be aware of symptoms such as burning, itching, eye irritation, changes in vision, and pain.…”

Section: Guideline Key Action Statementsmentioning

confidence: 99%

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Clinical Practice Guideline: Bell's Palsy

Baugh

Basura

Ishii

et al. 2013

Otolaryngol.--head neck surg.

373

114

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Objective Bell’s palsy, named after the Scottish anatomist, Sir Charles Bell, is the most common acute mono-neuropathy, or disorder affecting a single nerve, and is the most common diagnosis associated with facial nerve weakness/paralysis. Bell’s palsy is a rapid unilateral facial nerve paresis (weakness) or paralysis (complete loss of movement) of unknown cause. The condition leads to the partial or complete inability to voluntarily move facial muscles on the affected side of the face. Although typically self-limited, the facial paresis/paralysis that occurs in Bell’s palsy may cause significant temporary oral incompetence and an inability to close the eyelid, leading to potential eye injury. Additional long-term poor outcomes do occur and can be devastating to the patient. Treatments are generally designed to improve facial function and facilitate recovery. There are myriad treatment options for Bell’s palsy, and some controversy exists regarding the effectiveness of several of these options, and there are consequent variations in care. In addition, numerous diagnostic tests available are used in the evaluation of patients with Bell’s palsy. Many of these tests are of questionable benefit in Bell’s palsy. Furthermore, while patients with Bell’s palsy enter the health care system with facial paresis/paralysis as a primary complaint, not all patients with facial paresis/paralysis have Bell’s palsy. It is a concern that patients with alternative underlying etiologies may be misdiagnosed or have unnecessary delay in diagnosis. All of these quality concerns provide an important opportunity for improvement in the diagnosis and management of patients with Bell’s palsy. Purpose The primary purpose of this guideline is to improve the accuracy of diagnosis for Bell’s palsy, to improve the quality of care and outcomes for patients with Bell’s palsy, and to decrease harmful variations in the evaluation and management of Bell’s palsy. This guideline addresses these needs by encouraging accurate and efficient diagnosis and treatment and, when applicable, facilitating patient follow-up to address the management of long-term sequelae or evaluation of new or worsening symptoms not indicative of Bell’s palsy. The guideline is intended for all clinicians in any setting who are likely to diagnose and manage patients with Bell’s palsy. The target population is inclusive of both adults and children presenting with Bell’s palsy. Action Statements The development group made a strong recommendation that (a) clinicians should assess the patient using history and physical examination to exclude identifiable causes of facial paresis or paralysis in patients presenting with acute-onset unilateral facial paresis or paralysis, (b) clinicians should prescribe oral steroids within 72 hours of symptom onset for Bell’s palsy patients 16 years and older, (c) clinicians should not prescribe oral antiviral therapy alone for patients with new-onset Bell’s palsy, and (d) clinicians should implement eye protection for Bell’s palsy patients with impaired eye closure. The panel made recommendations that (a) clinicians should not obtain routine laboratory testing in patients with new-onset Bell’s palsy, (b) clinicians should not routinely perform diagnostic imaging for patients with new-onset Bell’s palsy, (c) clinicians should not perform electrodiagnostic testing in Bell’s palsy patients with incomplete facial paralysis, and (d) clinicians should reassess or refer to a facial nerve specialist those Bell’s palsy patients with (1) new or worsening neurologic findings at any point, (2) ocular symptoms developing at any point, or (3) incomplete facial recovery 3 months after initial symptom onset. The development group provided the following options: (a) clinicians may offer oral antiviral therapy in addition to oral steroids within 72 hours of symptom onset for patients with Bell’s palsy, and (b) clinicians may offer electrodiagnostic testing to Bell’s palsy patients with complete facial paralysis. The development group offered the following no recommendations: (a) no recommendation can be made regarding surgical decompression for patients with Bell’s palsy, (b) no recommendation can be made regarding the effect of acupuncture in patients with Bell’s palsy, and (c) no recommendation can be made regarding the effect of physical therapy in patients with Bell’s palsy.

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Section: Supporting Textmentioning

confidence: 99%

Section: Guideline Key Action Statementsmentioning

confidence: 99%

Clinical Practice Guideline: Bell's Palsy

Baugh

Basura

Ishii

et al. 2013

Otolaryngol.--head neck surg.

373

114

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“…Consequently, a crucial clinical sign distinguishing a central from a peripheral FNP etiology is that a supranuclear or upper motor neuron lesion should present with weakness in the contralateral lower face with a normal tone and movement of both sides of the forehead. Conversely, an infranulcear or a peripheral nuclear lower motor neuron lesion should present with an ipsilateral abnormal movement of the entire half of the face including the forehead 6,14 . Furthermore, because the facial nerve has the longest intraosseous route of any cranial nerve, it is particularly vulnerable to trauma or infections along this remarkably long and tortuous course 6,7,10,11 …”

Section: Anatomic Considerationsmentioning

confidence: 99%

“…2). 41 This should be differentiated from the synkinetic narrowing of the palpebral fissure on attempted smiling 14,41 …”

Section: Clinical Presentationmentioning

confidence: 99%

Facial Nerve Palsy and the Eye: Etiology, Diagnosis, and Management

Tawfik¹,

Dutton²

2023

International Ophthalmology Clinics

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“…The disorder is typically unilateral and affects mainly voluntary facial muscle contraction [ 2 ]. Motor dysfunction may lead to incomplete eyelid closure, predisposing to corneal abrasion, exposure keratitis or corneal ulcerations [ 3 ]. Patients with Bell’s palsy may also complain of xerostomia, dysgeusia and aural pain.…”

Section: Introductionmentioning

confidence: 99%

Delayed facial nerve decompression for severe refractory cases of Bell's palsy: A 25-year experience

Berania

Awad

Saliba

et al. 2018

Journal of Otolaryngology - Head & Neck Surgery

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BackgroundThis study aims to assess the effectiveness of delayed facial nerve decompression for Bell’s palsy (BP).MethodsWe performed a retrospective case review of all patients having undergone facial nerve decompression for severe refractory BP between 1984 and 2009 at our tertiary referral center. Demographics, timing between onset of symptoms and surgical decompression, degree of facial nerve dysfunction pre- and post-operatively, follow-up length after surgery and postoperative complications were recorded. Facial nerve dysfunction was assessed using the House-Brackmann (HB) scale. Electroneuronography, electromyography and imaging results were assessed when available.ResultsEighteen patients had surgery between 21 and 60 days after onset of BP (group I), and 18 patients had surgery more than 60 days after onset of symptoms (group II). In group II, 11 patients had surgery between 61 and 89 days and 7 patients after 90 days. Groups I and II showed similar functional gain and rates of improvement to HB 3 or better (11/18 vs. 11/18, p > 0.05). In group II, patients operated 60 to 89 days after onset of BP showed a significantly higher rate of improvement to HB 3 or better (9/11 vs. 2/6, p = 0.049) with higher functional gain compared to those operated after 90 days (p = 0.0293).ConclusionsWhen indicated, facial nerve decompression for BP is usually recommended within the first 2 weeks of onset of facial paralysis. Nonetheless, our results suggest that patients with severe BP could benefit from decompression surgery within 90 days after onset of symptoms in the absence of an opportunity to proceed earlier to surgery. Further investigation is still required to confirm our findings.Trial registrationRetrospective registered. IRB# 2016–6154, CE 15.154 – CA

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Neuro-ophthalmologic Complications and Manifestations of Upper and Lower Motor Neuron Facial Paresis

Cited by 8 publications

References 39 publications

Clinical Practice Guideline: Bell's Palsy

Clinical Practice Guideline: Bell's Palsy

Facial Nerve Palsy and the Eye: Etiology, Diagnosis, and Management

Delayed facial nerve decompression for severe refractory cases of Bell's palsy: A 25-year experience

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