University of Groningen
Facial palsy: treatment, quality of life, and assessment
van Veen, Tijn
DOI:
10.33612/diss.131756313
IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from
it. Please check the document version below.
Document Version
Publisher's PDF, also known as Version of record
Publication date:
2020
Link to publication in University of Groningen/UMCG research database
Citation for published version (APA):
van Veen, T. (2020). Facial palsy: treatment, quality of life, and assessment. University of Groningen.
https://doi.org/10.33612/diss.131756313
Copyright
Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).
Take-down policy
If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.
Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum.
Part I
General introduction
and outline of this thesis
10
This thesis focuses on surgical and non-surgical treatment of facial palsy, facial palsy-related quality of life, and the assessment of facial function in facial palsy patients. A brief introduction into the anatomy of the facial nerve, facial palsy and the clinical presentation will be provided here. A more detailed introduction into treatment, quality of life, and assessment of facial palsy will be provided in each corresponding part of this thesis.
Facial nerve anatomy
The facial nerve is the seventh cranial nerve. The nucleus of the facial nerve is located in the brainstem.1 The nerve leaves the brainstem at the cerebellopontine angle and then
passes through the temporal bone. After leaving the styloid mastoid foramen, the facial nerve classically divides in five terminal branches – frontal, zygomatic, buccal, marginal mandibular and cervical – although this typical pattern is present in only 33% of all people.2
This thesis focuses on the mimic function of the facial nerve. However, the intermediate nerve runs along the facial nerve from the brainstem and separates from the facial nerve in the temporal bone, containing sensory and parasympathetic fibres related to taste and lacrimal control and saliva production.1
Facial palsy
Any disorder in the course of the facial nerve can lead to a disturbance in facial mimic movement, called ‘facial palsy’. Many different causes of facial palsy have been described.3,4 Firstly, facial palsy can be either congenital or acquired. Acquired facial
palsy can have many causes such as viral infection (e.g. Bell’s palsy and Ramsay-Hunt syndrome), cerebellopontine angle tumours, trauma, iatrogenic injury to the nerve, benign and malignant tumours, etcetera. Depending on the anatomical location, and type and magnitude of insult to the facial nerve (Table 1), facial palsy can present in myriad ways.
Table 1. Comparison of Seddon5 and Sunderland6 classifications of nerve injury.
Seddon Sunderland Description
Neuropraxia 1 Local conduction block with paralysis but no anatomical disturbance of the nerve.
Axonotmesis 2 Axon injury with degeneration of the distal segment. Intact endoneurium and perineurium.
3 Endoneurial damage with subsequent scarring and incomplete regeneration.
4 Nerve damage with complete internal structural disorganization. Epineurium remains intact. Neurotmesis 5 Nerve trunk cut completely.
One end of the spectrum is presented by flaccidity. Complete discontinuation of the facial nerve (neurotmesis) – or an absent facial nerve in the case of congenital facial palsy – leads to denervation of facial muscles and thus paralysis or the inability to move the mimetic muscles of the face. This flaccid facial palsy can range from weakness of one muscle to full paralysis of the (hemi)face.
I
The other end of the spectrum is represented by synkinesis. With axonotmesis – for example due to compression in the facial canal in case of viral facial palsy or because of traction during surgery for head and neck tumours – nerve regeneration can be expected. Because of the discontinuity of the endoneurial (and perineurial) sheet, regenerating growth cones can grow into a non-native distal endoneurial tube (i.e. an endoneurial tube previously not inhabited by that axon and leading to a different muscle of facial expression), leading to the innervation of a non-native muscle. Clinically this will present as facial synkinesis: the involuntary movement of one muscle (group) with the voluntary movement of another muscle group. This theory of aberrant regeneration is the most widely accepted mechanism of synkinesis.7 A second suggested mechanism of synkinesis development results from
the loss of the myelin sheath.7 After regeneration, the resulting uninsulated axons will
electrically stimulate each other, and thus create synkinesis. As a third mechanism, some literature offers evidence of facial nuclear hyperexcitability as a cause for synkinesis.7
Facial palsy can also result from a lesion of the central motor neuron. Clinically, central facial palsy can be distinguished from peripheral facial palsy by studying the mimic function of the upper half of the face.1 Eye closure and movement of the eyebrows remains intact
in central facial palsy because of cross innervation between both cerebral hemispheres.
Clinical presentation
Patients suffering from facial palsy may present with a wide variety of clinical symptoms. Inability to move the muscles around the mouth can lead to problems with eating, drinking and speaking.8,9 The inability to close the eyes, and its resulting sequelae, are
often described by patients to be most limiting.10,11 Complaints include a dry or irritated
eye, excessive tearing, and exposure keratitis, of which the latter can ultimately lead to blindness if not treated adequately. Furthermore, advancing age usually leads to an increase in static asymmetry, thereby aggravating complaints. Depending on the location of the lesion, movement disorders can be accompanied by a variety of symptoms resulting from dysfunction of the intermediate nerve.
Psychosocial problems are also very prevalent. Depression and anxiety are more common amongst facial palsy patients (approximately 25% and 30% respectively) compared to the general population (approximately 5% and 10%).12 Diminished control of the muscles
of facial expression limits articulation, pronunciation and the expression of emotions – and therefore influences both verbal and non-verbal communication.9,13,14
Together, these physical and psychosocial limitations can decrease a patients' quality of life severely.
Aim
The research described in this thesis aimed to study aspects of surgical and non-surgical treatment of facial palsy, facial palsy-related quality of life, and the assessment of facial function in facial palsy patients.
12
OUTLINE OF THIS THESIS
Part I provides a general introduction and outline of this thesis. Part II presents comparative studies of smile reanimation surgery.
Part III consists of studies of mime therapy and the treatment of synkinesis.
Part IV describes factors explaining and associated with facial palsy-related quality of life. Part V presents an insight in assessment methods of facial function in facial palsy. Part VI provides a summary of the findings and general discussion including future
perspectives.
I
REFERENCES – I
1. Nervus facialis (VII). In: Schunke M, ed.
Pro-metheus anatomische atlas. Houten: Bohn
Stafleu van Loghum; 2007:78-81.
2. Katz AD, Catalano P. The clinical significance of the various anastomotic branches of the fa-cial nerve: Report of 100 patients. Arch
Otolar-yngol Head Neck Surg. 1987;113(9):959-962.
3. Hohman MH, Hadlock TA. Etiology, diagno-sis, and management of facial palsy: 2000 patients at a facial nerve center.
Laryngo-scope. 2014;124(7):e283-e293.
4. Kleiss IJ. Assessment of facial function in
periph-eral facial palsy. Radboud University; 2015.
5. Seddon HJ. A classification of nerve injuries.
Br Med J. 1942;2(4260):237-239.
6. Sunderland S. The anatomy and phys-iology of nerve injury. Muscle & nerve. 1990;13(9):771-784.
7. Husseman J, Mehta RP. Management of synk-inesis. Facial Plast Surg. 2008;24(2):242-249.
8. de Swart BJM, Verheij JC, Beurskens CHG. Problems with eating and drinking in pa-tients with unilateral peripheral facial paral-ysis. Dysphagia. 2003;18(4):267-273.
9. Moverare T, Lohmander A, Hultcrantz M, Sjogreen L. Peripheral facial palsy: Speech, communication and oral motor function.
Eur Ann Otorhinolaryngol Head Neck Dis.
2017;134(1):27-31.
10. van Veen MM, Dijkstra PU, le Coultre S, Mureau MAM, Werker PMN. Gracilis trans-plantation and temporalis transposition in longstanding facial palsy in adults: Pa-tient-reported and aesthetic outcomes. J
Cra-niomaxillofac Surg. 2018;46(12):2144-2149.
11. Hamour AF, Mendez AI, Biron VL, et al. De-velopment of the alberta facial clinical evalu-ation (A-FaCE) scale: A patient-centered out-comes instrument for facial nerve paralysis.
Clin Otolaryngol. 2019 [Epub ahead of print].
12. Pouwels S, Beurskens CHG, Kleiss IJ, Ingels KJAO. Assessing psychological distress in patients with facial paralysis using the hos-pital anxiety and depression scale. J Plast
Re-constr Aesthet Surg. 2016;69(8):1066-1071.
13. Coulson SE, O'dwyer NJ, Adams RD, Crox-son GR. Expression of emotion and quality of life after facial nerve paralysis. Otol Neurotol. 2004;25(6):1014-1019.
14. Bogart KR, Tickle-Degnen L, Ambady N. Communicating without the face: Holis-tic perception of emotions of people with facial paralysis. Basic Appl Soc Psych. 2014;36(4):309-320.
