Approach to Facial Weakness

Facial nerve palsy can be defined as paralysis of any structure innervated by the facial nerve, thus inhibiting facial expression.

Introduction

  • Facial nerve palsy can be defined as paralysis of any structure innervated by the facial nerve, thus inhibiting facial expression.
  • Deficits in normal social interactions is a major psychosocial effect.
  • Paralysis of facial muscles can also lead to the following clinical effects, besides deficits in facial expression:
    • Eyelid closure deficits
    • Oral incompetence and drooling
    • Deficits in phonation of labial sounds such as /b/ or /p/
    • Obstructed gaze that is progressive with age
    • Exposure and drying of the cornea
    • Lack of protection of the eye from foreign material
    • Nasal obstruction unilateral or bilateral and potential shift of the nasal base toward the nonparalyzed side
    • Pocketing of food in the buccal sulcus
    • Severe dental caries
  • Facial palsy is a broad term encompassing the entire spectrum of facial movement disorders caused by lower motor neuron / axonal injury of the facial nerve, including:
    • Flaccid facial palsy
      • Can be defined as total or near-total absence of facial movement and tone without synkinesis or hyperactivity.
    • Facial paresis
    • Postparalytic facial palsy
      • Can be defined as a facial movement disorder of postparalyic facial nerve syndrome comprising varying degrees of zonal synkinesis, hypoactivity, and hyperactivity.
      • Postparalytic facial nerve syndrome includes symptomatic gustatory epiphora (also known as Bogorad syndrome or crocodile tears) and facial discomfort.
        • The syndrome is thought to result from aberrant axonal regeneration or ephaptic transmission following a facial nerve insult.
  • A thorough investigation must be done to determine the etiology of the FP and to direct management.
  • An insult leading to acquired facial palsy usually leads to acute flaccid facial palsy (FFP).
    • The eventual outcomes range from total and persistent FFP to complete functional recovery.
    • Between these extremes of range, combinations of hypoactivity and hyperactivity and synkinesis exist;
      • Facial synkinesis can be defined as involuntary and abnormal facial muscle activation with volitional or spontaneous expression.
      • Oculo-oral and the oro-ocular are the most common general forms of synkinesis.
      • Oculo-oral synkinesis may coexist with other types of synkinesis.
      • Other types of facial synkinesis include chin-oral synkinesis, platysma synkinesis, ocular-chin synkinesis, ocular-nasal synkinesis and chin-ocular synkinesis.
    • These combinations of facial palsy may also be accompanied by postparalytic facial nerve syndrome

Epidemiology

  • Acquired facial nerve palsy is uncommon overall in the general population; affecting 20 to 32 per 100,000 people per year in the general population.
  • In children the incidence is even lower, estimated at 2.7 per 100,000 per year in children younger 10 years and 10.1 per 100,000 per year in children 10 to 20 years old.
  • There is a bimodal distribution of infectious and traumatic facial nerve palsy;
    • peaks are at 1 to 3 years and at 8 to 12 years old.
  • Males and females are affected equally.
  • Both sides of the face are affected equally.
  • The lifetime risk is 1 in 60
  • It is more common in pregnancy and diabetes mellitus..

History

  • Arriving at a diagnosis for the underlying cause of the facial movement disorder is paramount.
  • A complete and careful history is valuable in establishing the diagnosis.
  • Bell’s Palsy is the most common cause of facial paralysis followed by trauma to the facial nerve.
  • Timely recognition of facial weakness is important to detect causes that require early intervention, such as stroke.
  • Causes of Acute Facial Palsy (FP) include:
    • Bell’s palsy
      • Thought to be mostly caused by Herpes Simplex Virus infection
    • Trauma, including:
      • Temporal bone fractures (most common)
      • Soft tissue injuries
      • Birth trauma
      • Iatrogenic injuries
    • Ramsay-Hunt syndrome (Varicella zoster virus)
    • Lyme disease
    • Otic infections and cholesteatomas
    • Postsurgical insult, for example:
      • Following vestibular schwannoma extirpation
    • Adjuvant treatments for disease adjacent to or involving the facial nerve, for example:
      • Radiation
      • Chemotherapy
    • Benign tumors, for example:
      • Facial nerve schwannomas
      • Venous vascular malformations of the facial nerve
      • Geniculate ganglion hemangiomas
    • Malignant tumors, for example:
      • Parotid or hematogenous primaries
      • Facial nerve squamous cell carcinomas
      • Regional spread of cutaneous malignancies
      • Solid tumor metastases
      • Sarcomas
    • Congenital malformations
    • Systemic infections, for example:
      • Human immunodeficiency virus
      • Syphillis
      • Poliomyelitis
    • Autoimmune conditions, for example:
      • Guillain-Barre syndrome
      • Antiphospholid antibody syndrome
      • Sarcoidosis
      • Systemic lupus erythematosus
      • Sjogen’s
    • Sarcoidosis
    • Genetic syndromes
      • Melkersson-Rosenthal Syndrome
      • Albers-Schönberg Disease (Osteopetrosis)
      • Möbius Syndrome
      • Goldenhar Syndrome (Oculoauriculovertebral Dysplasia)
    • Hypertension
      • Believed to be due to hemorrhage into the facial nerve canal
    • Pontine infarcts or hemorrhages may present with isolated FP, although rare.
  • Factors of the history that have a significant effect on facial function and quality of life and are well documented include:
    • Time course of onset of palsy
    • Progression
    • Previous therapies
    • Resultant symptoms
  • The presence of the following symptoms in the history may help narrow down the diagnosis:
    • Otovestibular symptoms
      • Hearing loss
      • Hyperacusis
      • Vertigo
      • Imbalance
      • Otorrhea
      • Otalgia
    • Other focal neurologic deficits
      • Diplopia
      • Facial anesthesia
    • Constitutional symptoms
      • Fever
      • Chills
      • Fatigue
      • Malaise
      • Sweats
      • Weight loss
    • Meningitic
      • Headache
      • Nuchal rigidity
    • Lyme-specific symptoms
      • Recent tick bite or exposure
      • Erythema migrans rash,
      • Arthralgias
      • Myalgias
      • Low back pain
    • Inflammatory symptoms
      • Orofacial swelling or parotitis
      • Uveitis
      • Known autoimmune conditions
    • In the case of palsy at or shortly following birth:
      • Prolonged labor
      • Forceps use
      • Facial and periauricular ecchymoses (at delivery or shortly thereafter)
  • In the case of acute idiopathic FP, certain ‘red flag’ features point to an alternate diagnosis to Bell’s palsy, including:
    • Bilateral paralysis
    • Slow onset of facial weakness;
      • Weakness in Bell’s palsy fully progresses over 24–72 hours
    • Asymmetric weakness across facial zones at onset
    • Constitutional symptoms;
      • Fever, lethargy, malaise, myalgias
    • Headache;
      • Other than retroauricular pain and otalgia, which occur frequently in Bell palsy
    • Presence of other focal neurologic deficits;
      • Diplopia, hearing loss, vertigo
    • Absence of recovery of facial tone within 4 months of palsy onset
  • Variations in facial symptoms exist with respect to the timing of presentation and degree of recovery.
  • Newly acquired deficits from neurapraxic or axonotmetic injuries may continue to resolve for 12 months or longer without surgical intervention.
    • Successful muscle recovery is highly correlated with denervation time
  • FFP results in:
    • Paralytic lagophthalmos and ocular irritation
    • Loss of facial symmetry at rest
    • Collapse of the external nasal valve
    • Oral incompetence
  • Postparalytic facial palsy (PFP) presents with:
    • Facial synkinesis
    • Muscle hyperactivity
    • Contracture
    • Epiphora
  • Platysmal synkinesis results in:
    • Neck discomfort
    • Facial fatigue
  • Periocular synkinesis results in:
    • A narrowed palpebral fissure width
  • Lack of meaningful smile occurs in severe cases
  • Although facial sensation is preserved, some patients may complain of a sensation of numbness
  • One important difference between FP of HSV origin and that of VZV origin is that the former may recur whereas recurrence of zoster is very rare in immuocompetent individuals
  • Family history is of particular importance in diagnosing autoimmune causes, along with a personal history of:
    • Other autoimmune conditions
    • Rashes
    • Orofacial edema
    • Nasal septal perforation
    • Multiple miscarriages

Physical Examination

  • An exhaustive head and neck examination is indicated along with otoscopy and a complete cranial nerve examination.
  • Assessment of the zones of facial function is essential, both at rest and with movement.
  • The following aspects of the facial structures should be evaluated:
    • The postion of the brow
      • The effect of the brow position on the periocular complex
    • The degree of paralytic lagophthalmos
    • Whether or not Bell’s phenomenon is present
    • Palpebral fissure width
    • Lower lid position
    • Laxity using methods such as:
      • Distraction
      • Snap-back test
    • Depth and Orientation of the Nasiolabial Fold (NLF)
    • Oral commisure position
    • The degree and presence of synkinesis of the following muscle groups:
      • Brow
      • Ocular
      • Midface
      • Depressor
      • Mentalis
      • Platysma
    • The contralateral hemi-face is assessed to look for weakening of paired muscle groups;
      • If present, it is likely to produce improved symmetry
    • Spontaneous smile may be assessed;
      • Humorous video clips may be used for this purpose, for example
    • The appearance of the face is documented in the following 9 movements, using photography and videography:
      • Face at rest
      • Pucker
      • Complete eye closure
      • Brow elevation
      • Grin
      • Nose wrinkling
      • Whistling
      • Pouting and lower lip depression
      • Profile view for the assessment of the platysma action
      •  

        Figure 1: The nine standard frontal views, as described above, beginning at top row, on the far left, respectively.

        notion image
      Figure 3: de Sanctis Pecora C, Shitara D. Botulinum Toxin Type A to Improve Facial Symmetry in Facial Palsy: A Practical Guideline and Clinical Experience. Toxins (Basel). 2021 Feb 18;13(2):159. doi: 10.3390/toxins13020159. PMID: 33670477; PMCID: PMC7923088.
       
  • Functional integrity of the muscles of the forehead is helpful to differentiate a central from a peripheral lesion of the facial nerve;
    • A central nervous system lesion will show normal tone and movement of both sides of the forehead
    • A peripheral facial nerve lesion will show abnormal motor tone and movement on the affected side of the forehead
  • Systems for identifying and quantifying facial weakness in relation to stroke from static frames or video data have emerged over the course of the previous decade.
  • However, video or in-person examination by a neurologist remains the gold standard.
  • These systems rely on varied techniques to extract relevant features from static frame pixel data;
    • In general they can be categorized into landmark-based features and intensity-based features
    • Landmark-based features encode information generally associated with position of key facial features such as shape
    • Intensity-based features focus on information such as skin color, creases, texture, etc

Investigations

  • In cases where the signs and symptoms are indicative of Bell’s Palsy, no further investigations are required.
    • Exceptions include titers to confirm specific diagnoses that have specific therapies such as Lyme-disease.
  • Imaging studies are indicated in cases where there is suspicion of benign/malignant tumors or signs of infection.
    • Examples of such studies include:
      • Fine-cut CT of the temporal bone without contrast
      • Gadolinium-enhanced MRI of the temporal bones and parotid glands
    • Imaging of the facial nerve must be accompanied by images of:
      • The brain and pons
      • The cerebellopontine angle
      • The internal auditory canal
      • All 3 portions of the facial canal
      • The geniculate ganglion
      • The stylomastoid foramen
      • The parotid gland
    • Indications in such cases include:
      • Abnormal otoscopy or tuning fork findings
      • Palpable parotid or neck mass
      • Slow- or asymmetric-onset of FP
      • Slowly progressive FP
      • Unilateral recurrent FP
      • Recent FP with absence of recovery at 4 months
    • Not recommended as part of the initial evaluation for patients whose history is otherwise consistent with BP as it is relatively rare for masses to present with acute FP.
    • Abnormalities in addition to facial palsy should also lead to imaging studies of the brain.
  • Blood studies are used in cases that are recurrent or are suspected to be autoimmune in nature; examples are:
    • Complete blood count
    • Erythrocyte sedimentation rate
    • C-reactive protein
    • Rheumatoid factor
    • Antinuclear antibody
    • Antineutrophil cytoplasmic antibody
    • Antiphospholipid antibodies
    • Angiotensin converting enzyme
  • Electrophysiologic testing can be helpful in predicting functional recovery in acquired deficits.
    • For example; following acoustic neuroma resection with a facial nerve thought to be in-continuity.
    • In such cases, serial electrophysiologic examinations may show early electrical recovery before clinical recovery
    • Electrophysiologic testing of multiple facial muscle patterns, in patients with Bell palsy, can provide clinically undetectable evidence of neural recovery;
      • It is useful for mapping available muscle motors before contiguous muscle transfer
    • Electroneuronography (ENoG) is indicated in cases with delayed traumatic or cases of idiopathic FFP with complete absence of hemi-facial movement on examination.
      • It is done to ascertain acute facial nerve decompression use for treatment
      • It is indicated between 3 and 14 days of onset of symptoms

Treatment and Management

  • Management of FP includes
    • Diagnosis
    • Forming a therapeutic plan according to:
      • The timing of presentation in flaccid cases
      • Specific pattern of facial dysfunction in patients presenting with aberrant neural regeneration
    • A wide range of therapeutic options available which can be classified into the following therapeutic strategies:
      • Pharmaceutical agents
      • Corneal protective measures
      • Physical therapy (PT)
      • Chemo-denervation agents
      • Fillers
      • Surgical procedures
  • In the multidisciplinary management of facial paralysis, every patient should be aware of the potential problems he or she may encounter
  • Outpatient referrals to neurology, audiology, otolaryngology, and/or ophthalmology and further testing by consultants may be warranted
    • More urgent consultations may be necessary if:
      • The FP does not appear peripheral
      • Other neurological signs or symptoms are present
  • In case of an anatomically intact nerve or a nerve injury limited to the medial portion of a peripheral branch:
    • Medical treatment with close observation
    • Possible electrophysiologic testing for monitoring of progression
  • In case of a transected nerve, immediate exploration with direct anastamosis provides the best chance of recovery.
  • In case of an injury to a large segment of the nerve, an interposition graft should be placed immediately.
  • If the injured segment is not easily accessible for repair, nerve transposition is the treatment of choice.
  • For facial muscles with irreparable damaged or extensive disuse atrophy, muscle transfer procedures are the best option for dynamic facial reanimation.
  • Corneal protection should be a primary concern and initiated in all causes of FP.
  • If the cause cannot be determined:
    • Therapy with prednisone, with or without an antiviral medication can be considered
    • The above therapy can begin as early as possible after onset of symptoms
  • It is useful to classify FP cases into 1 of 5 categories for the purpose of narrowing range of therapeutic options.
    • The categories are based on timing of presentation and status of the facial nerve and musculature.
    • The categories include:
      • Acute FFP
      • FFP with potential for spontaneous recovery
      • FFP with viable facial musculature with low potential for spontaneous recovery
      • FFP without viable facial musculature
      • Paralytic FP (PFP)
    • It is also useful to group potential interventions by type and side of FP and facial zone to develop a plan for management
    • Further details on management according to the category of FP are given below

Acute Flaccid Facial Palsy (Intact Facial Nerve)

  • First 72 hours to 2 weeks following onset of acute facial nerve injury.
  • Most cases are viral in origin.
  • Clinician’s role:
    • Diagnosis
    • Begin proper medical therapy, for example:
      • immunosuppressants
      • antivirals
      • antibiotics
    • mitigate risk of exposure keratopathy
    • determine candidacy for acute surgical intervention
  • For cases of Bell’s palsy; high-dose corticosteroids, within 72 hours of onset of symptoms, shortens time to recovery
    • Combination of antivirals and corticosteroids may have further clinical benefit
      • Particularly in cases with severe to complete paralysis
      • Significant evidence supports the use of combination therapy in VZV
  • In cases of Facial Nerve trauma:
    • Corticosteroids and observation are indicated, in cases of delayed onset or incomplete FP following trauma or iatrogenic insult
    • Iatrogenic injury resulting in immediate and complete paralysis of one or more FN branches warrants urgent surgical exploration
    • Patients are referred for neuro-otology consultation for consideration of surgical decompression within 14 days of symptom onset, if there is both of the following:
      • Total idiopathic or post-traumatic paralysis with an ENoG response demonstrating greater than 90% degeneration
      • absent voluntary motor units on electromyography (EMG)
  • FP associated with Lyme disease is treated with
    • Prolonged course of oral doxycycline or intravenous ceftriaxone
    • The role of accessory corticosteroid therapy is unclear
  • FP assoicated with otitis media is treated with:
    • Wide myringotomy
      • with or without mastoidectomy
    • Corticosteroids
    • Topical and parenteral antibiotics
  • Autoimmune causes may be a cause but are a diagnostic challenge
  • Eye lubrication with taping the eye shut at night is done to prevent exposure keratopathy
  • PT can be done to teach patients upper eyelid stretching
    • This assists in passive closure of the eye
  • Correction of paralytic lagophthalmos may be achieved by
    • Temporary tarsorrhaphy
    • Upper eyelid weighting
    • Indications include:
      • Poor prognosis for rapid recovery
      • Ocular symptoms with functional interference
      • Insufficient Bell phenomenon
      • Absence of recovery at 4 months
  • Other therapies include mirror therapy

Flaccid Facial Palsy with Potential for Spontaneous Recovery

  • These are cases in which nerve continuity is thought intact in the setting of FFP
    • For example, following resection of a vestibular schwannoma where FN stimulation was noted before closure
  • There is potential for spontaneous recovery in these cases
  • Return of facial tone and movement are expected within 6 to 12 months
  • Patients may benefit from therapeutics such as:
    • PT
    • Corneal protective measures
    • Static periocular reanimation
    • Temporary chemodenervation of the healthy-side depressor labii inferioris muscle
      • To improve oral competence and articulation during this period
      • Botulinum Toxin Type A may be used as a chemodenernation agent
  • Close follow-up (every 3 months) is warranted to ensure recovery of function

Flaccid Facial Palsy with Viable Facial Musculature and Low Potential for Spontaneous Recovery

  • In such cases, there is discontinuity of the FN or the absence of recovery of facial function is within 6 to 12 months of FP onset
  • Facial musculature is intact and likely receptive to re-innervation
  • Common clinical scenarios involve patients presenting with dense FFP resulting from:
    • Necessary facial nerve resection during surgery for advanced parotid and cutaneous malignancies
    • Temporal bone tumors such as:
      • Facial nerve schwannomas
      • Venous vascular malformations
      • Cholesteatomas
    • Cerebellopontine angle tumor extirpations
    • Pontine hemorrhage
  • There is evidence that facial musculature remains responsive to re-innervation for periods up to;
    • 24 months following denervation in adults
    • Possibly for longer periods in children
  • Options regarding rehabilitation of facial paralysis following nerve transection include:
    • Grafting procedures
    • Static suspension
    • Regional muscle transfer
    • Free tissue transfer
  • Nerve grafting is the best option for long-term recovery of tone and function;
    • However, the effects of nerve grafting may not be noticeable for up to 12 months
    • This may be significant in the setting of potential tumor recurrence or progression
    • Combined methods which both mitigate immediate functional deficits and allow for optimal long-term outcomes are ideal.
  • Interposition graft repair should be considered in the setting of neural discontinuity;
    • Split-hypoglossal nerve transfer to the main trunk of the facial nerve is an alternative option in cases where:
      • Interposition graft repair is unfeasible
      • No recovery is noted within 12 months.
  • The objective of main trunk repairs and transfers is to:
    • Restore facial tone
    • Restore some form of blink
    • Meaningful reanimation of expression is rare
  • Voluntary expressions may be restored through targeted nerve transfers during this period, such as:
    • Nerve-to-masseter transfer to lower zygomatic branches of the facial nerve for smile reanimation
    • Cross-face nerve grafting to upper zygomatic branches for blink restoration
    • Considered in patients demonstrating minimal to no improvement in facial function 7 months following vestibular schwannoma resection with facial nerve preservation
      • As the probability of ultimate recovery of meaningful expression is less than 10%
  • Static periocular reanimation is offered early in the course of palsy onset where recovery is likely to take several months.
    • Examples are upper lid weighting and lateral tarsal strip procedure
  • Methods to improve facial symmetry may be of benefit in patients awaiting facial nerve recovery, including:
    • Brow lifts
    • Autologous fat augmentation
    • Selective and directed chemodenervation
      • Platysmectomy can be considered in patients with good response to chemodenervation of platysmal banding and spasm, for a more permanent form of treatment

Flaccid Facial Palsy Without Viable Facial Musculature

  • Facial musculature may be absent;
    • For example, following resection or congenital absence
  • Facial musculature may be unlikely to be responsive to re-innervation;
    • For example, long denervation period or marked distal perineural spread of a malignant tumor
  • Nerve repair or transfers are NOT indicated in such cases
  • PT is indicated
  • Targeted chemodenervation of the healthy side lip depression can be done
  • Brow elevation can be done
  • Surgical interventions such as the following are indicated:
    • Static facial suspensions
    • Static peri-ocular reanimation
    • Muscle transfers
  • Targeted suspensions may be achieved .
    • Following may be used:
      • Sutures
      • Fascia lata
      • Bioabsorbable or permanent implants.
    • Areas of the face that may be targeted include:
      • Brow
      • Lower eyelid
      • Midface
      • Nasal valve
      • NLF
      • Oral commissure
  • Tightening of the lower lid may be achieved by the lateral tarsal strip procedure
    • With or without medical canthal tendon plication
  • Dynamic smile reanimation may be achieved through:
    • Antidromic or orthodromic temporalis muscle transfer
    • Free muscle transfer with motor innervation provided through cranial nerve transfer
  • Options for dynamic reanimation of the lower lip include
    • Anterior digastric muscle transfer
    • Inlay of a T-shaped fascia graft

Postparalytic Facial Palsy

  • Develops 6 to 18 months following severe facial nerve insult;
    • With spontaneous, yet aberrant, regeneration
    • Or following main trunk nerve grafting
  • It is permanent
  • Lagophthalmos is rare
  • PT is first-line treatment
  • A comprehensive management program includes
    • Patient education
    • Soft tissue mobilization
    • Mirror and EMG biofeedback
    • Neuromuscular retraining
  • Blunting of hyperactivity is indicated through filler injection and weakening of hyperactive muscles through:
    • Targeted chemodenervation
    • Neurectomy
    • Resection in advanced disease
  • Targeted chemodenervation of diseased side muscles may offer improvement in certain patients.
    • Examples of the muscles include:
      • Orbicularis oculi
      • Mentalis
      • Platysma
  • Weakening of the depressor anguli oris muscle on the diseased side can result in dramatic improvement in smile dynamics in select patients.
    • Done by chemodenervation or resection
  • Muscle transfer may be done for dynamic smile reanimation
    • Regional (eg, temporalis) or free (eg, gracilis)
    • Considered for cases with severe restriction of oral commissure excursion
  • Targeted nerve transfers are largely ineffective in the setting of PFP

Prognosis

  • Outcomes and prognosis vary based on the etiology of the disease.
  • Overall prognosis is good.
  • Congenital traumatic facial nerve palsy has been shown to resolve spontaneously in 90% of patients within 4 weeks.
  • Evidence shows 80% to 90% recovery rates in adult and pediatric patients with blunt temporal trauma.
  • Time to recovery is longer than in patients with an infectious etiology (about 10 months).
  • Recovery rates of idiopathic facial nerve palsy in children range from 70% to 90%.
  • Systematic tracking of therapeutic outcomes is a paramount to clinical excellence.
  • Outcomes tracking in FP may entail:
    • Patient-reported QoL measures
    • Clinician-assessed grading of facial function
    • Objective measurement of facial displacements
  • QoL impact may be assessed using generalized patient-graded scales such as the SF-36.
  • The House Brackman Scale is a grading tool universally used to grade recovery of facial nerve function
    • It consists of a six point scale with patients grouped into 1 of 6 groups
    • A system made by Brackmann can be used to help place patients in the proper group
      • It involves making measurements of the movement of the eyebrow and corner of the mouth and comparing the results with those on the unaffected side
    • Descriptions of patients in each group are as follows:
      • Group I: Normal facial movement and no weakness or synkinesis
      • Group II: Slight asymmetry of facial movements with a possible slight synkinesis
      • Group III: Obvious asymmetry with obvious secondary defects but some forehead movement
      • Group IV: Obvious asymmetry, no forehead movement, and weakness with possible disfiguring synkinesis or mass action
      • Group V: Only slight movement of the face, no forehead movement, and not enough facial function return to have secondary defects
      • Group VI: Absence of any movement or tone
  • Patient-graded scales specifically designed and validated for use in FP include:
    • The Facial Disability Index
    • The Facial Clinimetric Evaluation
    • The Synkinesis Assessment Questionnaire

Further Reading

  • Zhang W, Xu L, Luo T, Wu F, Zhao B, Li X. The etiology of Bell's palsy: a review. J Neurol. 2020 Jul;267(7):1896-1905. doi: 10.1007/s00415-019-09282-4. Epub 2019 Mar 28. PMID: 30923934; PMCID: PMC7320932.

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