Bell's palsy

Abstract

Bell's palsy is the term given to an idiopathic lower motor neurone facial nerve paresis or paralysis. It is of rapid onset, almost always unilateral, and may be associated with facial or retro-auricular pain or otalgia. It is the most common diagnosis associated with facial nerve palsy; a GP will see a case approximately every 2 years in practice in the United Kingdom. Early diagnosis and steroid treatment increase the likelihood of full recovery, whereas ocular complications can be prevented by lubricants and lid taping. Over 70% of patients recover within a year. Options to improve facial appearance and function, in those who do not experience a complete recovery, include surgery.

Clinical case scenario

Jess, a 40-year-old café manager, attends your morning surgery. She was seen in accident and emergency (A&E) 48 hours ago with a left-sided facial weakness, which appeared over 2 days. She was given a diagnosis of Bell’s palsy, a 10-day tapering course of oral prednisolone and advised to see her GP for follow-up. Jess admits she was relieved when the A&E doctor excluded a stroke, however, she hurriedly left the department thereafter due to embarrassment over what she perceived to be time-wasting. Jess seeks further information regarding the condition, management and prognosis. She denies any additional symptoms other than irritation of the eye on the left side. How would you advise and manage this patient?

Background and epidemiology

Although anatomist Charles Bell gave his name to the condition in 1821, unilateral facial palsy has been described throughout history. ‘Palsy’ describes both paresis (incomplete weakness) and paralysis (total loss of function). Determining the incidence is challenging, as patients may not always seek medical attention and are seen in a mixture of care settings. The peak age group affected is between 15 and 45 years old. The estimated prevalence in the United Kingdom is 20 per 100 000. A GP in the UK will therefore see a case approximately every 2 years (Gilden, 2004; Holland and Weiner, 2004). There is no significant difference in incidence between ethnicities or males and females, although incidence increases in pregnant women (45 per 100 000), those with recent upper respiratory tract infections, the immunocompromised and in diabetes and hypertension (Eviston et al, 2015; Peitersen, 2002).

Anatomy

The facial nerve is composed of motor fibres (innervating the muscles of facial expression, posterior belly of digastric, stylohyoid and stapedius), parasympathetic fibres (innervating the lacrimal, submandibular and sublingual salivary glands), somatic afferents (from the external ear) and afferent taste fibres from the anterior two thirds of the tongue. The facial nerve (motor root) exits the brainstem at the lower aspect of the pons in the cerebellopontine angle and the nervus intermedius (sensory and parasympathetic secretomotor fibres) emerges between the pons and the inferior cerebellar peduncle (Ellis and Mahadevan, 2013; Sinnatamby, 2011).

Both parts of the nerve pass into the internal auditory meatus in the petrous temporal bone, travelling with the VIIIth nerve until they enter the facial canal (see Fig. 1). The genu of the facial nerve describes a sharp bend over the promontory of the middle ear where the secretomotor fibres for the lacrimal gland leave via the greater petrosal nerve, and the facial nerve travels inferiorly, in the medial wall of the middle ear cavity. Within the facial canal, the nerve to stapedius and chorda tympani are also given off before the facial nerve enters the stylomastoid foramen. The chorda tympani runs between incus and malleus in the middle ear, entering the infratemporal fossa to join the lingual nerve, carrying taste fibres from the anterior tongue and secretomotor fibres to the submandibular ganglion, supplying the submandibular and sublingual salivary glands (Ellis and Mahadevan, 2013; Sinnatamby, 2011).

Figure 1.

Facial nerve anatomy.

Stylohyoid and the posterior belly of digastric muscle are supplied by the nerve on its exit from the stylomastoid foramen, before it enters the parotid gland. The five (temporal, zygomatic, buccal, mandibular and cervical) divisions that arise within the parotid gland innervate the muscles of facial expression (Ellis and Mahadevan, 2013; Sinnatamby, 2011).

Aetiology

Bell’s palsy is idiopathic by definition, and is a diagnosis of exclusion, being the term used for peripheral nerve palsy without a defined cause. A clear understanding of the common and serious differentials is, therefore, required to exclude these and reach the diagnosis.

Despite its idiopathic status, several theories on the underlying aetiology of Bell’s palsy have been proposed, including viral and ischaemic options. Inflammation of the facial nerve and resultant compression in the facial canal is implicated in many of these theories and is reflected in histopathological review. Polymerase chain reaction analysis has demonstrated herpes simplex virus (HSV) type 1 DNA in endoneurial fluid from affected patients (Murakami et al., 1996). The theory that reactivation of latent herpes viruses (HSV and herpes zoster virus, HZV) underlies most cases is increasingly popular (Eviston et al., 2015; Holland and Weiner, 2004; Peitersen, 2002). Pregnancy increases the risk of Bell's palsy, and there appears to be an association with preeclampsia, suggesting that extracellular oedema may be causative in pregnant women (Katz et al., 2011).

An association between an intranasal vaccination and Bell's palsy has been previously demonstrated, potentially specific to the combination of heat labile toxin-derived molecules administered via the intranasal route (Lewis et al., 2009). The incidence of Bell’s palsy in recipients of some SARS-CoV-2 vaccines has been reported to be higher than the general population (Cirillo and Doan, 2021), although at the time of writing, the Medicines and Healthcare Products Regulatory Agency has not established a difference in rate of Bell’s Palsy between vaccinated individuals and the general population (Medicines and Healthcare Products Regulatory Agency, 2021). Given the evolving nature of this topic, up-to-date pharmacovigilance findings (such as the Yellow Card reporting system) and guidance should be consulted when offering vaccine advice to patients, including those with previous Bell’s palsy.

Diagnosis

History

Misdiagnosis is common in Bell's palsy, and GPs should be aware of important and urgent differentials for exclusion. Patients will present with an (almost always) unilateral facial weakness, developing within 3 days. This can vary from slight weakness to total paralysis of the affected muscles and may be recognisable at rest as drooping of the eyebrow/mouth and loss of the nasolabial fold (Fig. 2). The weakness may be associated with postauricular (52%), facial or ear pain or altered taste (34%), hearing (hyperacusis in up to 14%) or lacrimation (increased or decreased) on the affected side. Occasionally, weakness of orbicularis ori may result in drooling or difficulty articulating, but as with all symptoms, central causes must be excluded before Bell's palsy is considered (Mettias et al., 2019; National Institute for Health and Care Excellence (NICE), 2019; Peitersen, 2002).

Figure 2.

Bell's palsy in a male patient, demonstrating right-sided facial weakness. Note the inability to raise the right eyebrow (LMN lesion). In UMN lesions (i.e. central cause), forehead sparing is seen.

A focused history should include onset and duration of symptoms listed above. A history of other cranial nerve symptoms including pain, hearing loss, tinnitus and vertigo should be elicited along with any neurological symptoms, including weakness, dysphasia and headache. Systemic history should include recent illness or trauma, systemic conditions (especially diabetes mellitus, autoimmune disease and pregnancy), and any conditions affecting suitability for steroid treatment. A history should cover the atypical features listed in Box 1, which should prompt referral for consideration of other diagnoses (see Box 2 for specialty and timing of referral). Previous Bell's palsy (6.8% of cases are recurrent) and family history of the same (familial in 4.1%) should be elicited (Peitersen, 2002).

Box 1.

Atypical features which should prompt referral to exclude other causes.

• Pain or progressive, chronic course (over 12 weeks), including fluctuating weakness – may suggest neoplasm

• History of: stroke, intracranial mass lesion (including tumour), parotid tumour, head or neck cancer (including skin), facial or temporal trauma

• Systemic illness including fever

• Vertigo, altered hearing (excluding hyperacusis), otorrhoea, visual disturbance, dysphagia

• Forehead sparing (suggests upper motor neurone lesion including stroke or mass lesion)

• Bilateral palsies (may indicate systemic disease e.g. sarcoidosis)

• Recurrent episode

• Weakness indicative of only specific facial nerve branches being affected, or other cranial nerve signs

• Parotid mass, skin changes e.g. vesicles or potential neoplasms

Source: NICE (2019)

Box 2.

Referral to secondary care.

Refer urgently to specialty care those with:

• New (or worsened) neurological signs or symptoms

• Suspected central cause, including upper motor neurone signs, other neurological signs including other cranial nerves (including facial paraesthesia), postural imbalance

• Systemic upset due to infection, or severe local infection

• Evidence of otitis media/externa or vesicles (same day via ENT on-call)

• Trauma

Refer to facial nerve specialist (usually an ENT specialist or neurologist) those with:

• Any atypical features placing doubt on diagnosis of Bell’s, as appropriate e.g. parotid mass via 2-week wait pathway, recurrent Bell’s palsy as an outpatient

• No improvement after 3–4 weeks (NICE guidance states 3 weeks; ENT UK 4 weeks, aiming to be seen within 6 weeks).

• Evidence of aberrant reinnervation (e.g. gustatory sweating), in adults diagnosed over 5 months ago (consider referral to neurology)

Discuss with ophthalmology patients with:

• Ocular symptoms e.g. pain, redness, irritation

• Significant lagophthalmos and a poor Bell’s reflex (meaning corneal exposure on attempted eye closure)

Offer referral for psychological support to:

• Patients with ongoing symptoms

Adapted from Mettias et al., (2019) and NICE (2019)

Examination

The first step in making the diagnosis is to establish lower motor neurone (LMN) facial weakness. Ask the patient to close their eyes, raise their eyebrows, bare their teeth, pucker their lips and tense platysma – this can be achieved with an attempted grimace. Documenting the degree of weakness according to a recognised scale, such as the House– Brackmann scale (Table 1), allows the course of the weakness to be followed accurately by different clinicians, should the need arise.

Table 1.

House– Brackmann scale of facial weakness. Many methods of measuring facial weakness have been described, but the aim is providing an objective measure which can be used by different clinicians. Of note, grade IV represents loss of eye closure.

Grade	Degree of weakness	Findings at rest	Findings when movement attempted
I	Normal	Normal for patient	Normal function throughout
II	Slight dysfunction	At rest – normal symmetry and tone +/− slight synkinesis	Slight weakness of forehead. Strong resistance to eye opening/complete closure with minimum effort. Slight asymmetry of mouth
III	Moderate dysfunction	Noticeable asymmetry Synkinesis.	Obvious weakness. Eye closure but weak resistance to opening.
IV	Moderate severe dysfunction	Obvious weakness and asymmetry	Incomplete eye closure. Unable to raise brow, limited mouth movement with maximal effort
V	Severe dysfunction		Flicker of movement only
VI	Total paralysis		No movement

Adapted from Mettias et al., (2019) and House and Brackmann (1985).

When assessing facial weakness, it is important to differentiate upper motor neurone (UMN) lesions from lower ones. LMN pathologies, affecting the facial nerve itself, such as Bell's palsy – will exhibit frontalis weakness, and thus, do not have forehead sparing (Fig. 2). Forehead sparing describes the intact ability to raise both brows in the context of facial weakness. It occurs in UMN lesions because the frontalis receives supply from both cortices, meaning it has a maintained supply in the event of UMN neurone lesions, such as those listed in Table 2.

Table 2.

Differential diagnoses for facial weakness.

Diagnosis	Key features
Central cause – stroke, transient ischaemic attack	Forehead sparing, other neurology, risk factors
Brain tumour, including metastases	History of (or in keeping with) another primary cancer, gradual onset, altered mental state, headache
Trauma	Surgery, basal skull fracture, facial trauma – assess for scars, bruising, blood
Head/neck tumours – benign or malignant	Parotid, skin cancer, tumour of facial nerve or nearby structures (e.g. acoustic neuroma). May be insidious or painful, affects only certain branches or other cranial nerves.
Cholesteatoma	May have otorrhoea, hearing loss, visible lesion on otoscopy
Infective	Herpes simplex: Malaise, fever Lyme disease: May be bilateral. Previous history of tick exposure, rash, joint pain Otitis media: Conductive hearing loss, pain Mastoiditis: Asess mastoid and tympanic membrane Necrotising otitis externa: Chronic otitis externa, pain, typically older diabetic patients Ramsay Hunt syndrome: Pain, vesicular rash, sensorineural hearing loss/vestibular symptoms Encephalitis/meningitis: Headache, neck stiffness HIV: Fever, malaise, known infection Syphilis: Usually with other neurological or skin changes Glandular fever: Malaise, lymphadenopathy, known infection
Diabetes	Known diagnosis or features suggestive of diabetes
Multiple sclerosis	Intermittent symptoms, other neurology.
Guillain-Barre syndrome	Ascending paralysis (facial weakness – often bilateral – is rarely seen without other features)
Sarcoidosis	May be bilateral, other symptoms
Arteriovenous malformation	May be known

Adapted from NICE (2019)

Particular note should be made of the patient’s ability to close their eyes, including unresisted at minimal effort and against resistance. This helps to adequately assess the risk to the eye – a patient who must use conscious effort to close the eye in the absence of resistance will not achieve full eye closure when blinking or asleep. Bell’s phenomenon (the upward movement of the eye when attempting to close it, see Fig. 3) is a reflex to protect the cornea, it is found in most people (Jones, 2001). This reflex is not pathognomonic of Bell's palsy, although it may be more easily noticed when eye closure is lost. In these cases, it has a defensive role, but eye care is still required.

Figure 3.

Bell’s phenomenon, seen on the left eye in a patient with left-sided facial weakness, demonstrating that the cornea may be exposed despite this protective reflex.

A full neurological examination to exclude a central cause must be undertaken for all cases. Once an UMN palsy, other neurological symptoms or signs, and bilateral weakness, have been excluded, examination to assess for other causes of LMN facial palsy should be undertaken. Perform an ear, nose and throat (ENT) examination, including the scalp and skin, mastoid region, parotid gland (for masses) and tympanic membranes. Visualise the attic when examining the tympanic membrane in order to help assess for cholesteatoma (see Fig. 4). A thorough examination of the oral cavity/pharyngeal mucosa, skin and external auditory canal should be undertaken to assess for scabbing or vesicles, in keeping with zoster infection. Ramsay Hunt syndrome typically presents with pain, sensorineural hearing loss and a vesicular rash on the ear or oropharynx.

Figure 4.

Attic cholesteatoma with retraction pocket, seen as a crusty mass on otoscopy, although it may appear white or wax-like.

Atypical features, not in keeping with Bell's palsy, are found in Box 1. In a unilateral LMN weakness with no atypical features, no other neurology and no other cause found (see Table 2), a diagnosis of Bell's palsy may be made in primary care without the need for laboratory tests or diagnostic imaging (NICE, 2019).

Management

Management of Bell's palsy should take into account severity of the palsy, including eye closure, timing of presentation and the patient’s suitability for corticosteroid treatment. Clear information should be provided to patients to help them manage their symptoms.

Medication

The evidence for medical therapy in reducing permanent weakness in Bell's palsy is mixed, and guidelines vary. If the diagnosis of Bell's palsy has been made within 72 hours of symptom onset, prednisolone should be prescribed if not contraindicated (NICE, 2019). Mettias et al., (2019) extends this window to 5 days, with advice to discuss the likelihood of benefits with patients who present at 5–10 days. An example regime of prednisolone is 60 mg for 5 days, reduced by 10 mg per day, for a total course of 10 days. Consider adjunct antacid therapy if appropriate (Mettias et al., 2019; NICE, 2019).

Antiviral therapy without corticosteroids is not recommended. The addition of antiviral therapy to corticosteroid treatment remains an area of debate, although a number of guidelines recommend consideration. A 2019 Cochrane review found that combined corticosteroid and antiviral therapy was probably beneficial in reducing late sequelae (e.g. crocodile tears, motor synkinesis). Evidence of a beneficial effect on incomplete recovery is limited (Gagyor, 2019). Mettias et al., (2019) recommends combined corticosteroid and antiviral therapy in palsies of grade V and above. An example antiviral regime, to be given in addition to a corticosteroid, includes treatment for 7 days with valaciclovir 1000 mg three-times per day (Jeffrey and Khatkhate, 2007). NICE (2019) advises discussion with a specialist if this is being considered.

The scope of this article is limited to treatment of Bell’s palsy (where clinical assessment identifies no cause of facial palsy). Clinical evidence of a viral process (e.g. vesicular rash) in the presence of facial weakness excludes a diagnosis of Bell’s palsy, but should instead prompt investigation and management for the appropriate suspected condition. For instance, early aciclovir and prednisolone have been shown to improve outcomes in Ramsay Hunt syndrome (Primary Care Dermatology Society, 2021).

Eye protection

Facial nerve weakness can impact on the action of orbicularis oculi, impacting eye closure, thus leaving the cornea exposed. Prophylactic eye care can prevent potential sight-threatening infection. All patients should use eye lubricants in the form of drops administered frequently during the day (e.g. Viscotears, Celluvisc) and a thicker ointment for nocturnal use (e.g. Lacrilube) (Mettias et al., 2019). General protective measures include taping at night.

Other treatments

There is minimal guidance around the role of physical therapy in improving weakness or reducing long-term sequelae. The term ‘physical therapy’ in the context of Bell's palsy is used to describe several treatments including massage, neuromuscular exercises, electrical stimulation, thermal treatment and, in some trials, acupuncture, making trial data interpretation difficult. Trial designs have been deemed insufficient to form recommendations on whether it improves the condition. There is low quality evidence that facial exercises may be beneficial and that engagement with therapy may benefit patients psychologically (Baugh, 2013; Mettias et al., 2019; NICE, 2019).

A meta-analysis of 11 randomised control trials (RCTs) (1258 patients) concluded that more work is required to prove adequate safety and effectiveness of acupuncture, as current evidence comes from a dataset with high heterogeneity and low-quality study design (Zhang, 2019).

Referral

Patients with other neurological signs or symptoms, UMN weakness or bilateral palsies should be referred to stroke or neurology. Suspected acute stroke is an emergency. ENT referral is warranted in the case of observed palpable parotid mass, visible vesicles, otorrhoea or other evidence of otitis media/externa. Refer to an ENT outpatient clinic if the Bell's palsy is recurrent or shows no signs of recovery within a month. Ophthalmology referral is warranted urgently if ocular complications are suspected. Box 2 summarises referral timings and specialties.

Advice

Bell's palsy can be alarming for patients – in one study, half thought they were having a stroke and a quarter believed symptoms represented a brain tumour (Peitersen, 2002). Reassurance and clear advice are essential once a diagnosis has been made.

Advice on ocular and oral care

Advise the patient on proper use of eye lubricants, and to seek urgent review in the event of visual deterioration, eye pain or irritation. Atraumatic (microporous, or silicone) tape should be used at night to keep the eye closed, and it is important that the patient is shown how to do this (Fig. 5). Dusty, windy or irritant environments should be avoided (NICE, 2019).

Figure 5.

Atraumatic tape should be applied horizontally (not vertically) covering the upper and lower lid, to prevent the eye opening (shown here on the left eye), after instilling drops.

Mouth closure can be affected, which can make talking and eating difficult, and may be embarrassing for patients. The buccal mucosa may also be at risk of trauma from the teeth when chewing. If eating or drinking is affected, a softer diet and use of straws may be helpful (Eviston et al., 2015; NICE, 2019).

Resources

There is a wealth of resources available to help guide patients experiencing Bell's palsy. Patient UK provides a thorough introductory explanation for the newly diagnosed. Bell's palsy UK has an informative FAQ section. Facial Palsy UK provides information for a range of patients from acute sufferers to those with an established palsy, including treatment explanations and informative videos, for example on taping for eye closure. See Box 3.

Box 3.

Patient resources.

Bell's Palsy UK: https://bellspalsy.org.uk/frequently-asked-questions

Facial Palsy UK: www.facialpalsy.org.uk/causesanddiagnoses/bells-palsy

Patient: https://patient.info/brain-nerves/bells-palsy

Prognosis

More than two thirds of patients will recover fully within a year, even without corticosteroids, and patients should be advised of this outcome. In explaining the potential benefit of steroid therapy to patients, it is of note that an RCT of corticosteroid vs placebo in 551 patients demonstrated complete recovery rates of 83% (steroid) vs 64.7% (placebo) at 3 months. This increased to 94.4% (steroid) vs 85.2% (placebo) by 9 months (Sullivan et al., 2007). Full recovery is less likely in certain groups (Box 4).

Box 4.

Poor prognostic indicators.

• Associated conditions e.g. pregnancy, hypertension, diabetes

• Complete paralysis

• Age over 60 years

• No evidence of early recovery

• Pain as a significant feature

The literature definition of ‘early’ recovery, in this instance, ranges from 2 weeks to 3–4 months. Those who show some improvement within weeks have an improved chance of full recovery (likely within months). Those who show signs of improvement after 3–4 months are thought to be those who undergo nerve regrowth and reinnervation. This group is less likely to experience a return to entirely normal function: findings at 6 months are a good indicator of long-term prognosis. In around 7% of sufferers, palsy is a recurrent event, usually with years between episodes (Holland and Weiner, 2004; Eviston et al., 2015; NICE, 2019; Peitersen, 2002).

Complications

Some complications can be prevented (e.g. corneal ulceration, with good eye care). Others may not be volunteered and should be asked about at review (see Box 5) so that ongoing management may be considered.

Box 5.

Complications of Bell's palsy.

• Corneal ulceration, resultant loss of vision

• Dry mouth (effect on parasympathetic innervation to salivary glands)

• Damage to buccal mucosa (from buccinator weakness)

• Gustatory lacrimation (production of tears on eating, due to erroneous nerve regeneration)

• Hyperacusis (effect on nerve to stapedius)

• Facial pain/paraesthesia

• Synkinesis (facial spasms, other involuntary movements such as uncoordinated eye closure)

• Psychological and social impact of symptoms

Source: Eviston et al. (2015) and Glass and Tzafetta (2014)

Review patients within a month and refer those without improvement at 3–4 weeks (Mettias et al., 2019; NICE, 2019). For patients with longstanding symptoms, a number of treatment options exist, under the care of a multidisciplinary team. Examples include botulinum injections, which can restore a more symmetrical appearance or reduce synkinesis, and surgical options for facial reanimation, which can offer functional and aesthetic improvements. Nerve conduction studies may be undertaken to assess suitability for surgery. Facial rehabilitation may help in managing symptoms such as synkinesis and in achieving more symmetrical expressions. Speech and language therapy can benefit those with ongoing difficulty in phonation or mastication. NHS provision of treatments such as botulinum toxin injection can demonstrate regional variation (Facial Palsy UK, 2019; Wessex Facial Nerve Centre, 2019).

Bell's palsy in special groups

Children

Bell's palsy is a less common cause of facial weakness in children than in adults, so careful consideration of other causes is required before making the diagnosis. A full physical and neurological examination should be undertaken, including blood pressure to exclude hypertension. Ear infections are common in children and must be excluded. Red flags must also be considered including those for malignancy, infection or undeclared trauma. Lyme disease may underlie half of paediatric cases of facial weakness in endemic areas, including in the UK (Holland and Weiner, 2004; Wessex Neurosciences Clinical Network, 2020).

Regional guidance varies in the UK, but assessment of facial palsy is generally assumed to be undertaken in the acute paediatric setting, rather than in general practice. Some regions stipulate full blood count, blood film, Lyme serology and/or ENT review as part of paediatric facial palsy assessment, as well specific pharmacological approaches in cases of Bell’s palsy (El-Hawrani et al,, 2005; Norfolk and Norwich University Hospitals, 2020; Wessex Neurosciences Clinical Network, 2020). Always consult guidance local to your practice. NICE does not offer guidance on the treatment of Bell's palsy in children under 16 years in age, and there is no clear agreement from the limited evidence base on pharmacological treatment in children (Karatoprak and Yilmaz, 2019; Yoo et al., 2018). North American guidance states that early oral steroids may be considered in children with Bell's palsy (Baugh et al., 2013). Prognosis is better than in adults even without steroids. Other advice, such as eye care, remains important, and should be ensured wherever the child goes, for example at school, and at night-time.

Pregnant women

Pregnant women are more likely to suffer from Bell's palsy than the general population and may have a worse prognosis in complete paralysis. It can be associated with other conditions such as hypertension, diabetes and preeclampsia, so these should be considered and monitored for. Corticosteroids are used in the treatment of other conditions in pregnancy and should be considered. An individualised approach is recommended, so discussion of risk/benefit ratio with the patient is paramount. Specific cases may warrant specialist discussion (Baugh et al., 2013; Hussain et al., 2017).

KEY POINTS

Bell’s palsy is an idiopathic unilateral LMN paresis/paralysis of cranial nerve VII and is always a diagnosis of exclusion

Maintain a high index of suspicion for alternative serious aetiology such as acute stroke, systemic or neurological conditions, intracranial malignancy, head and neck cancer, trauma and infection

Prompt diagnosis and treatment of Bell’s palsy with corticosteroid therapy improves the chance of full recovery

In adults, antivirals with corticosteroids may be considered in severe palsies, but antivirals should never be prescribed without steroids

Advise lubricant drops and horizontal lid taping to prevent serious complications such as corneal ulcers and subsequent visual loss

Failure to improve within 3–4 weeks, despite appropriate treatment, should prompt urgent referral to ENT

ORCID iD

Miss Frith Cull https://orcid.org/0000-0002-4683-1227

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