Improved Iatrogenic Facial Nerve Paralysis Based on House–Brackmann Facial Nerve Grading System by Using Acupuncture Therapy: A Case Report

INTRODUCTION

Facial nerve is the seventh cranial nerve that is important for facial communication and expressions. Damage to its functions can be very influential to the quality of life.^1,2 The rate of nerve injury published in oral surgery procedure ranges approximately from 2% to 25%. ³ Arthroplasty is the selected surgery for treating bony ankylosis, dislocation or damage of articular disks, and severe joint adhesion. ⁴

In their study, Liu and Granquist ⁵ found that of 21 patients suffering from facial nerve injuries, all of them had an injury on the temporal branch of facial nerve.

One of the standard methods to measure facial nerve functions is the House–Brackmann facial nerve grading system (HBFNGS).^5,6 HBFNGS has been considered as accurate in describing patient's facial function and in supervising patient's status periodically to assess the course of recovery and the effects of treatment. ⁶

Acupuncture therapy has long been the basic therapy for neurologic disorders. ⁷ It has been shown to have neuroprotective effects by activating and enhancing neurotrophic factor (NTF) expressions of the brain, including brain-derived neurotrophic factor (BDNF) and glial-derived neurotrophic factor (GDNF). Therefore, one neurophysiologic mechanism is the neuroplasticity arrangement, that is, neurogenesis. NTF level modulated is related to the life sustainability and proliferation and differentiation of neural stem cells (NSC). ⁸

CASE PRESENTATION

A 22-year-old man came by referral of the oral surgery specialist with physical complaints in forms of inability to completely close the right eyelid, inability to contract right eyebrow muscle, and difficulty in opening jaws (can only be opened with a gap of 1.5 patient's finger). The patient developed these symptoms a month post-gap arthroplasty for temporomandibular joint (TMJ) repair due to right TMJ ankylosis caused by motorcycle accident that happened 2 years before his current health condition.

During physical examination, a weakness in right facial nerve was found, marked by asymmetrical face expression, inability to lift right eyebrow muscle, inexistence of the right side of forehead wrinkles, asymmetric and leaking when puffing out cheeks, asymmetrical lip corner when smiling, as well as 7 mm right lagophthalmos.

HBFNGS examination showed medium to severe dysfunction (4th degree), regional HBFNGS examination showed 4, 4, 3, 3 degrees. During panoramic photograph examination, old fracture on the right caput mandibulae was accompanied by formation of periost that gave an impression of ankylosing on right caput mandibulae. Based on the results of nerve conduction velocity and electromyography (EMG), a description corresponding to the right peripheral N. VII axonal lesion was obtained, with still visible denervation.

The patient's diagnosis was iatrogenic paralysis of right facial nerve post-gap arthroplasty due to TMJ ankylosis, given Mefenamic acid 3 × 500 mg if necessary, and Mecobalamin 1 × 500 mg.

ACUPUNCTURE TREATMENT

Patient was prescribed manual acupuncture with Western medical acupuncture style. The acupoints selected were BL2 Cuanzhu, EX-HN 4 Yuyao, GB1 Tongziliao, GB14 Yangbai, ST3 Juliao, ST4 Dicang, ST7 Xiaguan, and TE17 Yifeng on the affected side. The remote acupoints selected were GV20 Baihui, SP6 Sanyinjiao, ST36 Zusanli, LI11 Quchi, and LI4 Hegu bilateral. The penetration points selected from ninth therapy was EX-HN 3 Yintang toward the top and EX-HN 5 Taiyang to GB8 Shuaigu. All of the needles were pricked in a perpendicular position, but TE17 was pricked toward posterosuperior until a sensation of deqi was felt. It was conducted for 3 times in a week; each session lasted for 30 minutes, and manipulation was conducted every 10 minutes by turning. On 19th therapy, acupuncture penetration technique for 15 minutes was added and manipulation every 5 minutes was conducted by turning by using filiform needle with the dimension of 0.25 × 25 mm. The results of therapy are presented in Table 1.

DISCUSSION

Research by Liu and Granquist ⁵ in Philadelphia reported that of 56.4% (22 patients) who experienced facial nerve dysfunction after undergoing TMJ arthroplasty, 19 of them had their facial nerve functions coming back to normal 18 months post-op, while the rest experienced persistent signs of nerve weakness 6 months post-op.

Repair of iatrogenic paralysis of facial nerve requires a physiologic process of growth known as neurogenesis. Neurogenesis is a mechanism occurring throughout life and is a multistep process in which new neurons are generated by neural progenitor cells (NPCs), followed by maturation and advanced functional integration to the pre-existing circuits. It happens in the 2 areas of brain, subventricular zone of lateral ventricle and subgranular zone of dentate gyrus (DG) of the hippocampus. ⁹

Method of acupuncture employed on this patient followed the steps of Bell's palsy therapy in Korea, where in the healing stage (more than 3 weeks), acupuncture with fine needles or needle implantation was conducted. In terms of acupoint selection, fewer local points were used than those used in Korea, local acupoints on the healthy side were not used, ¹⁰ and SP6, LI11, and GV20 remote points were added for anti-inflammatory and neurogenesis effects.^7,11–14

Acupoint LI4 can reduce abnormal functional connectivity modulated on Bell's palsy patients. ¹⁵ Research by Kong et al. ¹⁶ showed that LI4 activates main region of the brain in the left cerebellum, BA22, BA20, BA5, BA8, BA1/2, and BA6.

Acupoints BL2, EX-HN4, GB1, and GB14 were selected based on the patient's complaint, in which he experienced lagophthalmos and that his eyebrow muscles cannot be moved up and down. The points are local points and innervated by branches of facial nerve, namely frontal and temporal nerves.

Acupoint ST3 was used for normalizing mid region of the face that is also innervated by facial nerve. Acupoint ST4 was used for normalizing lip corners. Acupoint TE17 anatomically is the exit of facial nerve from stylomastoid foramen, while acupoint ST7 anatomically is the start of zygomatic nerve branch.

Acupuncture can improve release of activation of glutamate receptors, such as N-methyl-d-aspartate, enhances the entry of Ca²⁺ into the cell and activates kinase, including calcium/calmodulin-dependent protein kinase II (CaMKII) and protein kinase C (PKC) proteins. These kinases are known to stimulate various transcription factors, such as cAMP response element-binding protein (CREB), nuclear factor-κB (NF-κB), activator protein-1 (AP-1) and Wnt/β-catenin/T-cell factor/lymphoid enhancer factor. BDNF is induced in the transcription level by CREB and NF-κB. ⁸

GDNF promotor contains bond for transcription factor, including CREB and NF-κB. GDNF transcription is stimulated by phosphorylated CREB and activation of c-Fos, components of AP-1 transcription factor. CREB activation is usually accompanied by BDNF expression enhanced after acupuncture stimulation. Hence, it can induce BDNF and GDNF in neurons and glial cells through glutamate transmitter stimulations ⁸ (Fig. 1a).

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FIG. 1.

(a) Schematic diagram of the mechanism of acupuncture-induced NTF expression. ⁸ (b) Schematic diagram of the mechanism of neurogenesis induced by acupuncture. ⁸ NTF, neurotrophic factor.

Acupuncture can act as a stimulator or NTF production enhancer, which will act as an autocrine or paracrine signal to promote proliferation of NSC/NPC and differentiation to neuroblast, as well as to promote cell life sustainability. This can lead to the functional integration of new neurons to the central nerve system, resulting in functional recovery (Fig. 1b). ⁸

Scientifically, acupoints GV 20 and ST36 enhance the expressions of BDNF, GDNF, basic fibroblast growth factor, and neuro peptide-Y.^{7,8,11,12,17,18} On depressed mice that were acupunctured on GV20 for 21 days, it was found that the treatment can induce enhancement in BDNF expression in hippocampus. ¹² Acupoint ST36 significantly increases bromodeoxyuridine (BrdU⁺) cells and improves proliferation in DG on gerbils with a stroke, decreases production of TNF-α induced by liposaccharide through vagal modulation, which improves macrophage activity as anti-inflammation measure in the lymph, and induces c-Fos (Fig. 2).^7,17,19

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FIG. 2.

Acupuncture stimulation at GV20 and ST36 points to induce neurogenesis. ¹⁷

Acupoint SP6 was proven to increase interleukin (IL)-10, which functions as anti-inflammation and to decrease extravasation of plasma and neutrophil migration. ¹³

Research by Wang et al. ²⁰ stated that after plug-and-pull stimulation of Acupoint LI11, levels of IL-1β and tumor necrosis factor (TNF)-α were found to be lower, while IL-4 level was found to be higher.

The results of therapy were as follows, right lagophthalmos became invisible after the 8th session, and jaws can open normally after the 12th session. Right eyebrow muscle's functions came back perfectly after the 28th session. In the approximate period of 4.5 months, patient's facial nerve functions came back to normal, proven by subsequent EMG results 6 months post-therapy, which stated that right facial nerve was found within normal limits (Fig. 3).

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FIG. 3.

Clinical picture of the patient showing before and after acupuncture therapy. (a–c) Before acupuncture therapy. (d–f) After acupuncture therapy. Patient photos published with permission.

Acupuncture can stimulate the body in producing neurotrophic and anti-inflammation and reduce side effects and oral drugs usage. The usage and dosage of corticosteroids can be reduced, since they have side effects of immune suppression, blood glucose increase, and peptic ulcer. ² Neurotrophic if consumed continuously can also cause gastrointestinal disorders.

CONCLUSION

Acupuncture should be considered as one of the therapeutic treatments for iatrogenic facial nerve paralysis. Its effects on the patients, especially neurogenesis and anti-inflammatory processes, can be explained by scientific evidence. In neurogenesis acupuncture stimulates the expression of neurotransmitters, neuropeptides, neurotrophic, and growth factors, while in the anti-inflammatory process it stimulates IL-10, IL-4, c-Fos and reduces levels of TNF-α, IL-1β, cyclooxygenase-2.