Physioterapeutic Intervertion on Facial Palsy

Mini Review

J Dent & Oral Disord. 2020; 6(4): 1138.

Physioterapeutic Intervertion on Facial Palsy

Ribeiro MVMR1*, Da Silva AAS2, Alves ALCS2, Ferreira CVO2, Jucá JVO2, Praxedes BSL2, Barbosa FT3 and Ribeiro EAN4

1Master in Health Sciences from the Federal University of Alagoas, Professor at the Centro Universitário Tiradentes Maceió-Alagoas, Specialist in Ophthalmology; Maceió, Alagoas, Brazil

2Medical student at the Centro Universitário Tiradentes Maceió-Alagoas, Maceió, Alagoas, Brazil

3PhD in Health Sciences from the Federal University of Alagoas, Professor at Tiradentes University Maceió-Alagoas; Maceió, Alagoas, Brazil

4PhD in Pharmacology from the Federal University of Paraíba, Professor of the Postgraduate Program in Health Sciences at the Federal University of Alagoas; Maceió, Alagoas, Brazil

*Corresponding author: Marina Moura Rezende, Master in Health Sciences from the Federal University of Alagoas, Professor at the Centro Universitário Tiradentes Maceió-Alagoas, Specialist in Ophthalmology, Maceió, Alagoas, Brazil

Received: May 11, 2020; Accepted: June 01, 2020; Published: June 08, 2020


Peripheral facial palsy is a peripheral facial nerve lesion that affects 8-55 people per 100,000 and is associated with a deficit in the patient’s psychic, physical, and social health. Its main etiology is idiopathic which corresponds to 50-60% of the cases. There are several types of treatment; however, the physiotherapeutic is the most used. This should be associated with other therapies such as pharmacology and surgery. Nevertheless, 10-40% of cases do not progress to full recovery and remain with chronic facial paralysis or paresis.

Keywords: Facial palsy; Rehabilitation; Review; Therapeutic approaches


Since Avicenna (979-1037 DC.) [1], peripheral facial paralysis has been described as a peripheral neural lesion of the facial nerve, and may be at any level of its path, from the nerve nucleus to the neuromuscular junction [2,3]. The involvement of this nerve results in complete or partial paralysis of facial muscles and may be associated with disorders of taste, salivation and lacrimation, hyperacusis and hypoesthesia in the external ear canal [4].

The first major incidence is idiopathic peripheral facial palsy, or Bell’s Palsy, and the second is traumatic, with other associated conditions such as hypertension, diabetes mellitus, virosis, pregnancy and puerperium, herpesviruses, vascular damage and neoplasms [3- 5]. Therefore, Bell’s facial paralysis is defined as primary, and the others, as secondary.

The peripheral facial paralysis’s incidence is of 8-55 cases per 100,000 inhabitants [6-8]. Among these Bell’s palsy has the highest incidence, accounting for 50-60% [6,9].

Maximal deficiency occurs in the first 48-72 hours, and the severity of paralysis is related to duration of facial dysfunction, the extent of recovery time, and deterioration in quality of life [10].

The effects of facial nerve paralysis are debilitating and often depress emotional conditions, with a variety of possible functional and aesthetic problems [11]. Although 60-90% of cases can recover completely, 10-40% will remain with chronic facial paralysis or paresis [6,7,9,12]. It is believed that spontaneous recovery of the facial nerve occurs in up to nine months [13]. The psychological impact of facial disfigurement can result in fear of public places and undermine the socialization [11,14].

Surgical techniques and drug treatment may minimize physical deficits, but rarely improve facial function with respect to selective muscular control and symmetry of expression [14].

The purpose of this narrative review is to list the literature on the concept, diagnosis, and treatment of this pathology, since it is a relevant clinical condition and it causes several aesthetic, psychological, functional and social impairment to the patient.


A review of the PubMed (National Institutes of Health), Scielo and Medline databases was conducted in the Portuguese, English, Spanish and French languages, with the descriptors “facial paralysis”, “physiotherapy”, Bell’s palsy “and” rehabilitation. “We found 50 articles and selected 34 for this review, considering the relevance of the meaning by the authors.

Clinical manifestations

In Bell’s palsy the characteristic findings are acute manifestations of facial motor neuron palsy that affect the upper and lower face muscles with a peak manifestation in 48 to 72 hours [10]. These findings are often accompanied by symptoms of neck, mastoid and ear pain, dysgeusia, hyperacusis or altered facial sensation [10]. Full recovery of the lesion is often impaired by synkinesia [4].

In some cases of chronic evolution of peripheral facial palsy, the most common complication is corneal dryness, which occurs due to the inability to completely close the eyelid, the reduced production of tears and the loss of the eye blinking reflex [4,10]. Lagoftalm may also occur, characterized by depression of the lower eyelid and consequent tearing, a phenomenon called epiphora [6]. Long-term aesthetic or functional sequelae of facial asymmetry include oral dysfunction, contractures, nasal obstruction, difficulty drinking, tasting, salivation and speech, psychosocial problems8, disuse atrophy, lip commissure deviation, tissue adhesion, muscle stretching, hypoesthesia, dysesthesias and hemifacial spasm [4,5].


There are approximately two dozens clinical types of facial paralysis/paresis, being subdivided into group I (perip heral facial paralysis):

1. Peripheral facial palsy (Bell’s palsy)

2. Alternate facial palsy

3. Bilateral facial palsy

4. Facial palsy in multiple cranial neuropathy

5. Recurrent facial palsy

6. Transient facial paralysis

7. Familial facial paralysis, in group II (central facial paralysis):

8. Central facial palsy

9. Emotional facial palsy

10. Paralysis of the face with paradoxical hypermimia and in group III (Others types of facial palsy):

11. Congenital facial palsy in children

12. Ramuscular facial palsy

13. Bilateral volitional facial palsy with preserved emotional motility (Foix-Chavany-Marie syndrome)

14. Facial paralysis of the upper floor - unilateral

15. Paralysis of the upper floor - bilateral

16. Muscular facial palsy and neuromuscular junction

17. Psychogenic facial palsy, these p atrophies are associated with the involvement of one or both of the neural systems, the facial nerve, the myonural plaque, or the facial muscles [15].

Staging system

The best known systems for assess facial palsy are the House- Brackman scale and the Sunnybrook system [10].

The House-Brackman classification consists of six degrees: I - Normal; II - Mild dysfunction; III - Moderate dysfunction; IV - Moderately severe dysfunction (Figure 1); V - Severe dysfunction; VI - Total paralysis, with description of changes that can be observed in each degree, addressing the gross evaluation of the face, static (symmetry and tonus) and in movement - forehead, eye and mouth [16]. It is the most used scale in the international literature [10,15,16], but it fails to provide satisfactory information about regional facial function [6]. For a more detailed analysis, the Sunnybrook [9,10,18] system is used, by evaluating static symmetry, voluntary movement and synkinesia [13,19].

Citation:Ribeiro MVMR, Da Silva AAS, Alves ALCS, Ferreira CVO, Jucá JVO, Praxedes BSL, et al. Physioterapeutic Intervertion on Facial Palsy. J Dent & Oral Disord. 2020; 6(4): 1138.