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Low-intensity LED therapy in facial paralysis: Case report

Low-intensity LED therapy in facial paralysis: Case report

MARCELLO DE SOUZA SILVA1 | RENATA AMADEI NICOLAU1 | MATHEUS AUGUSTO PEREIRA1 | CARLOS EDUARDO DIAS COLOMBO2

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ABSTRACT

Peripheral facial palsy (PFP) is characterized by the interruption of the neuronal stimulus of the branches of the VII cranial pair due to several etiological factors that acutely affect the total or partial motor information of the facial muscles. PFP may be related to infectious, traumatic, neoplastic, autoimmune, metabolic and iatrogenic processes. The objective of this article is to present the case report of a 41-year-old, Caucasian, male patient, PFP compatible with Ramsay Hunt Syndrome type II, treated with pharmacological approach associated with low intensity LED therapy (640 ± 20 nm), applied all the nerve path, for 30 seconds, with energy density of 1.7 J/cm², energy of 3 J and power of 100 mW. After the first session, there was an expressive improvement in the clinical picture, promoting increased muscle tone and greater contracture of the facial mimic, such as frowning, beak, smile and completely closing the eye. For 15 days, five applications were performed, resulting in the absence of any signal or symptom referring to paralysis. It was concluded that low intensity LED therapy was effective in the treatment of PFP, with the protocol tested.

Keywords: Facial paralysis. Low-level light therapy. Facial nerve.

1 Universidade do Vale do Paraíba, Departamento de Cirurgia e Traumatologia Buco-Maxilo-Facial (São José dos Campos/SP, Brazil).

2 Universidade do Vale do Paraíba, Departamento de Patologia Bucal (São José dos Campos/SP, Brazil). How to cite: Silva MS, Nicolau RA, Pereira MA, Colombo CED. Low-intensity LED therapy in facial paralysis: Case report. J Braz Coll Oral Maxillofac Surg. 2021 Jan-Apr;7(1):61-7. DOI: https://doi.org/10.14436/2358-2782.7.1.061-067.oar

» The authors report no commercial, proprietary or financial interest in the products or companies described in this article.

» Patients displayed in this article previously approved the use of their facial and intraoral photographs.

Submitted: August 08, 2018 - Revised and accepted: February 07, 2019

Contact address: Renata Amadei Nicolau E-mail: renatanicolau@hotmail.com

INTRODUCTION

Facial paralysis (FP) is characterized by the interruption of neuronal stimulation of branches of cranial nerve VII due to several etiological factors that acutely affect the total or partial motor information of the facial musculature, either unilaterally or bilaterally.1 Facial paralysis can present as an idiopathic form, according to reports in the literature; however, it is possible to identify the presence of infectious, traumatic, neoplastic, autoimmune, metabolic and/or iatrogenic disorders. Pregnancy, diabetes mellitus and severe systemic hypertension are also considered risk factors. Among the etiological factors described, Bell’s palsy is the most common, with an estimated incidence of 20 to 30 cases per 100,000 inhabitants, with prevalence in the third and eighth decades of life, being rare before ten years old, affecting both genders, even though some authors cite higher prevalence in women.2

Due to its high incidence, trauma is the second most frequent cause of FP and is relevant due to the long intracranial path of the facial nerve, increasing the risk of injuries that affect its functions, partially or totally. The main traumas include fracture of the temporal bone (most frequent), fracture of facial bones, firearm injuries, blunt injuries of the face, birth trauma and iatrogenic. The nerve is rarely completely sectioned, and longitudinal involvement of the temporal bone presents higher incidence and better prognosis in relation to transverse fractures.3

Viral infection by herpes simplex or other pathogens has been discussed as the main pathophysiological agent. It is believed that its reactivation occurs in the geniculate ganglion, due to climatic factors, fever, stress and trauma in oral surgeries. According to Lazarini et al.4, a clinical study found DNA of herpes simplex virus type 1 (HSV-1) in 11 cases of 38 patients evaluated, presenting a significant result, suggesting that viral reactivation may be the etiology of disease, not interfering with the prognosis.

The Ramsay Hunt syndrome, also known as herpes zoster oticus, is one of the etiological factors associated with FP, due to reactivation of varicella zoster virus in the geniculate ganglion. It is prevalent between the second and third decades of life but can occur at any age. Clinically, vascular lesions are observed in the pinna and ipsilateral otalgia, which can cause vertigo, vomiting and nausea.5

Another triggering factor for FP is anesthesia of the inferior alveolar nerve, cited by Viegas et al.6 in their clinical cases, in which the movements were normalized after drug therapy, laser therapy, physiotherapy and waiting for three hours, respectively.

Less prevalent factors are also cited in the literature, such as acute and chronic otitis media, malignant external otitis, Melkersson Rosenthal syndrome, Lyme disease, congenital anomalies and association between facial paralysis and intracranial hypertension.

Several treatments have been described, aimed at the recovery of nerve fibers, elimination of possible sequelae and mainly normalization of facial movements. Although facial paralysis has an unknown etiology in most cases, the indicated treatments have been effective in the improvement of patients who did not have spontaneous recovery of symptoms.

Physiotherapy is an important treatment method for cases of FP, for the recovery of muscle tone, with associations with other types of therapies. The main guideline is the implementation of measures that avoid one of the worst complications, such as corneal ulcer, due to lack of complete eye closure. It is recommended to lubricate the eyes with artificial tears, applied at every 60 minutes during the day, and the use of sunglasses to protect against foreign bodies. Corticosteroids, according to Viegas et al.6, have a potent anti-inflammatory action, which can minimize the damage of nerve fibers and improve the prognosis of patients with this condition.

A clinical study conducted by Ferraria et al.7 demonstrated the association of antiviral and corticosteroids, evaluating 180 cases of Bell’s palsy, in which the main therapy used was the combination of corticosteroids and antivirals, in 67.2% of cases. The total recovery rate using this combination was 65.5% (57 out of 87 patients) versus 72.4% (21 out of 29 patients) with isolated corticosteroid therapy. The combination did not present difference in the recovery rate compared to corticosteroid therapy alone. Surgical intervention, according to Paraguassú et al.2, aims to decompress the facial nerve; however, many risks are involved, including seizures, deafness, leakage of cerebrospinal fluid and facial nerve damage. Thus, surgery is not widely used in the treatment of FP.

A new treatment method has been used in FP, the low-level LED therapy, due to its beneficial characteristics to biological tissues, such as increased microcirculation, genesis of new blood capillaries, stimulating

growth and cell regeneration, besides anti-inflammatory and analgesic effects.8 The basic principle of low-level LED therapy is the absorption of light in irradiated tissues. This light is only a visible part of the electromagnetic spectrum composed of oscillatory and vibrating energies, in which the different types differ according to the frequency of oscillation.

According to Bispo,9 these reactions occur by the capture of light by photoreceptors called chromophores, present in the crest of cytoplasmic organelle, called mitochondria, in which the captured energy is stored as adenosine triphosphate (ATP) and transformed into adenosine diphosphate (ADP). When released, this alters the Krebs cycle, stimulating oxidative phosphorylation with the purpose of promoting greater cellular energy and, consequently, increasing its metabolic functions, such as: collagen production, analgesia, reduction of enzymes that degrade the skin, reduction of edema and erythema, stimulation of the immune system, production of hormones, better oxygenation of tissues and normalization of pH, accelerating the tissue repair process and minimizing the use of drugs.

Scientific studies involving low-level LED therapy in FP are scarce, justifying research in this field, so that this innovative, non-invasive, effective and relatively lowcost method can be widely disseminated in the dental field. Thus, the aim of the present study is to present and discuss a clinical case of FP treated with low-level LED.

CASE REPORT

This case report was approved by the Institutional Review Board of the University of Vale do Paraíba, under report N. 2529129. A 41-year-old male Caucasoid patient initially presented with a painful whiteopaque vesicle of approximately 2 mm on the lateral tongue edge on the right side, evolving within a few days to inflammation in the right ear, with the presence of vesicles in the pinna, which was swollen. Two days after the diagnosis of otitis, the condition evolved to facial paralysis on the right side. The patient also had tinnitus in the right ear and vertigo.

In the emergency room, the patient underwent computed tomography of the skull, which showed a normal aspect, discarding the hypothesis of etiology in the central nervous system, suggesting facial paralysis resulting from peripheral nerve impairment. With the hypothesis of viral infection, the patient was medicated with fanciclovir 500 mg (1 tablet orally 8/8h for 7 days), prednisolone 20 mg (1 tablet orally 24/24h for 7 days), injection solution containing 100 mg of thiamine hydrochloride (vitamin B1), 100 mg of pyridoxine hydrochloride (vitamin B6) and 5000 mcg of cyanocobalamin (vitamin B12), intramuscularly at every 72 hours for 16 days, besides continuous use of lubricating eye drops (2 drops 8/8h).

Serological tests were negative for antibodies against herpes simplex virus (HSV-1 and HSV-2) and positive for IgG against varicella zoster virus (VZV). The patient reported chickenpox in childhood. The condition was diagnosed as neuritis affecting the facial nerve, compatible with Ramsay Hunt type II syndrome. This syndrome is caused by reactivation of VZV, previously latent in the sensory ganglion of the facial nerve, which, by acute inflammatory reaction of the facial nerve and vestibulocochlear nerve, can cause vesicular eruptions in the pinna, which may extend through the neck, as well as vertigo, fever, dry eyes, changes in taste, severe earache and facial paralysis.

Eleven days after FP, the patient attended the Polyclinic of the Dentistry course at the University of Vale do Paraíba to treat the condition. After anamnesis and physical examination, it was clinically observed that the right side of the face showed asymmetry and the musculature was deficient, with difficulty in contracting the forehead, pouting, smiling and completely closing the eye on that side of the face. The patient also reported feeling of heaviness on the right eye.

The selected treatment was low-level LED therapy, applied throughout the path of the facial nerve and its branches, at equidistant points of 1 cm, wavelength of 640±20 nm (GaAlAs diode, red region of the electromagnetic spectrum), for 30 seconds, with energy density of 1.7 J/cm², energy of 3 J and power of 100 mW. This therapy was performed in five applications for fifteen days, with one application per session.

The severity of facial paralysis was classified as grade IV according to the House-Brackmann classification table.

To check the improvement of signs and symptoms of the disease, analyses were performed by photogrammetry comparatively between sessions. The measurements were obtained by calibrating the Image J program, considering the anatomical references of the software itself, so that the minimum measurement error could be incorporated into the analyses (Fig 1).

The evaluated points were eyelid occlusion, elevation of the eyebrow in relation to the pupillary center, angulation of the midline/lip commissure and area of dental exposure and distance between lip commissures (Fig 2).

After the patient started the treatment, in the second session it was observed that after the first application there was significant improvement in the clinical status, promoting an increase in muscle tone and greater contraction of mimic muscles, such as frowning, smiling and closing the eye. The patient also reported greater sensation of lightness on the right eye.

From the third to the fifth session, there was progression in the improvement of contraction of the facial musculature.

Comparisons of measurements were made between points on the affected side and the normal side of the patient’s face at completion of each session (Tab. 1 and Fig 3).

It can be observed in this analysis that, soon after the first session, there was proximity of measurements of the affected side in relation to the contralateral side. In the second session, the distance between the contraction of commissures normalized to 3.6 cm in reference to the contralateral side and there was complete eyelid occlusion. The midline/pupil/commissure angulation was normalized, according to the reference (28 degrees), in the third session. In the fourth session, the distance of commissural distension reached the standard of 6.3 cm.

Finally, in the fifth and last session, the values of dental exposure area were normalized, with 6.3 cm2, and the eyebrow/nose tip distance, with 6.7 cm.

Only the eyebrow/pupil distance (2.7 cm) showed a small discrepancy from the final value (2.9 cm). The final values presented were considered as reference of the patient’s face. The treatment resulted in absence of any signs or symptoms related to the paralysis.

A

B C

Figure 1: Measurement between commissures and calibration of the digital image analysis system.

A B

C D

Figure 2: Points analyzed to assess the clinical status: A) eyelid occlusion; B) eyebrow elevation; C) midline/commissure angulation and dental exposure area; and D) commissural distance.

Table 1: Progression and comparison of measurements during treatment on the affected side, in relation to the contralateral side.

Sessions

Eyelid occlusion Eyebrow/pupil distance (cm) Eyebrow/nose tip distance (cm) Distance of commissure distention (cm) Distance of contraction between commissures (cm)

Affected side

1st

2nd

3rd

4th

5th

Contralateral side 5th No Yes Yes Yes Yes Yes 1.7 2.3 2.3 2.6 2.7 2.9 5.9 6.4 6.6 6.6 6.7 6.7 5.7 5.9 6 6.3 6.3 6.3 4.7 3.6 3.6 3.6 3.6 3.6

A B

C D

Figure 3: Example of the clinical status in the first (A) and fifth (B) session of low-level LED therapy.

DISCUSSION

Several types of treatments have been described in the literature, aiming to recover the nerve fibers, eliminating possible sequelae and mainly normalizing the facial movements. Such treatments include drug therapy with the use of corticosteroids and antivirals, physiotherapy, acupuncture, surgery, laser therapy and, more recently, LED therapy. According to Barros, Barros and Nascimento,10 acupuncture aims to treat diseases by stimulating the so-called acupoints on the skin, with several beneficial effects in the treatment of facial paralysis. These authors reported a clinical case of FP treated with drug therapy and acupuncture, which at treatment completion presented mild weakness, small asymmetry of the mouth during movement, persistence of tearing, greater control in keeping food in the mouth and small activity of the mentalis muscle. The use of corticosteroids and antivirals has been the treatment most accepted and described in the literature.6 A clinical study by Ferraria et al.7 demonstrated the effectiveness of the combination of antiviral and corticosteroids in patients with Bell’s palsy. The use of isolated corticosteroids showed inferior results in relation to the association. Accordingly, Magalhaes et al.5, in a clinical case of facial

paralysis compatible with Ramsay Hunt Syndrome, indicated treatment with acyclovir, leading to disappearance of lesions in the pinna and partial improvement of facial paralysis after 30 days of monitoring. In the present study, the patient was medicated with a combination of antiviral and corticoids, aiming to control the process of neurodegeneration, pain and inflammation. Low-level laser therapy in FP has been used in recent decades to control pain and inflammation in the acute phase and aid in the process of neuronal recovery and muscle motility.1 Viegas et al.6 presented a clinical case of FP treated with physiotherapy and corticosteroids, in which the paralysis was not solved by drug and physiotherapeutic treatment, with difficulty in moving the mouth and hypotonicity on the affected side. Thus, laser therapy was performed, and the movements of facial mimic muscles normalized in 40 days.

LED therapy has recently been incorporated into the dental, physiotherapy, speech pathology and medical clinic. The difference between laser therapy and LED therapy is the lack of light coherence when LED equipment is used. However, the therapeutic wavelengths employed for both therapies are similar. Thus, the effects promoted by LEDs have been similar to those obtained by laser. LEDs have lower cost and less equipment wear over time, thus being advantageous in relation to lasers, in the case of low level. Regardless of the etiology of FP, treatments have been used to normalize the facial movements; however, complete cure is not always possible. LED therapy has been shown to be efficient in promoting greater cellular energy and, consequently, increasing its metabolic functions, such as stimulation of microcirculation, collagen production, analgesia, reduction of edema and erythema, stimulation of the local immune system, better tissue oxygenation and normalization of pH, accelerating the tissue repair process and minimizing the use of medications.8,9 Facial paralysis evolves differently according to the proposed treatments; therefore, the combination of drug therapy, physiotherapy, acupuncture, and various treatments described is essential, none of which should be replaced by light therapy. However, low-level LED therapy has been very useful, due to the decrease in drug prescription and rapid recovery of nerve fibers and facial muscle movements in a short period of time.

The present clinical case corroborates data in the literature regarding the effectiveness of treatment, which is non-invasive, fast and painless.

FINAL CONSIDERATIONS

It was concluded that low-level LED therapy, in the tested protocol, was effective in the treatment of acute FP, associated with Ramsay Hunt syndrome type II.

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Ter Man. 2012;10(47):34-9. 2. Paraguassú GM, Souza JAC, Ferraz EG. Abordagem clínica e terapêutica da paralisia facial de Bell: uma revisão de literatura. Clipe Odonto - UNITAU. 2011; 3(1):45-9. 3. Jorge JS, Borges GC, Pialarissi PR, Júnior JJJ. Paralisia facial periférica traumática: avaliação clínica e cirúrgica. Rev Fac Ciênc Med Sorocaba. 2013;15(3):68-72. 4. Lazarini PR, Vianna MF, Alcântara MPA, Scalia RA,

Filho HHC. Pesquisa do vírus herpes simples na saliva de pacientes com paralisia facial periférica de Bell.

Rev Bras Otorrinolaringol. 2006;72(1):7-11. 5. Magalhães MJS, Cardoso MS, Gontijo IL. Ramsay Hunt syndrome - case report. Rev Bras Neurol Psiquiatr. 2014;18(3):247-52. 6. Viegas VN, Kreisner PE, Mariani C, Pagnoncelli RN.

Laserterapia associada ao tratamento da Paralisia

Facial de Bell. Rev Port Estomatol Cir Maxilofac. 2006; 47(1):43-8. 7. Ferraria LAM, Silva MIAP, Rosa MHC, Antunes LACJ.

Tipo de terapêutica e fatores de prognóstico na paralisia de Bell: estudo retrospectivo de cinco anos em um hospital português. Sci Med. 2016: 26(1):21384. 8. Cavalcanti PM, Catão MHCV, Lins RDAU, Almeida-Barros RQ, Feitosa APA. Conhecimento das propriedades físicas e da interação do laser com os tecidos biológicos na odontologia. An Bras Dermatol. 2011;86(5):955-60. 9. Bispo LB. A nova tecnologia do laser terapêutico no controle da dor. Rev Bras Odontol. 2009;66(1):107-11. 10. Barros HC, Barros ALS, Nascimento MPR. Uso da acupuntura no tratamento da paralisia facial periférica - estudo de caso. Rev Neurociênc. 2012;20(2):246-53.

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