**2. Facial palsy**

Facial palsy is defined as the control loss of the facial muscles due to a dysfunction of the seventh cranial nerve (facial nerve). It can be categorized as complete in the case of the inability to contract the facial muscles voluntarily, hyperacusis, and partial or total taste loss [2–4]. The person who suffers it has a severe disability as the facial nerve is the backbone in facial mimic [4–10].

### **2.1 Pathology description**

The facial nerve has a high-frequency damage rate than any other nerve in the body. It does make peripheral facial palsy the most common cranial mononeuropathy; however, in some cases, when it is not possible to determine or define the cause of origin and only when it is the case, it is designated as Bell's palsy. Although, the origin is attributed as a result of the swelling or facial nerve entrapment in its bony canal within the temporal bone [2, 5–14]; usually, only one side of the face is affected. It might reduce the functionality of both sides. Although, it is uncommon, it is called bilateral facial palsy [1, 2, 4]. Due to the lack of etiology, the treatment of Bell's palsy is deficient in most cases. Fortunately, spontaneous recovery is common [13]. The clinical picture of peripheral facial palsy lies on the lesion localization. Owing to the damage, it inhibits the electrical connections among the facial nerve and the muscles closely related to the affected area. In case that the damage occurs in the nerve conduit that connects the brain to the facial muscles, it is called central facial palsy.

#### **2.2 Facial nerve**

The seventh cranial nerve, also known as facial nerve shown in **Figure 1**, originates from the brainstem and travels through the internal auditory and fallopian canals as well as the large parotid. It innervates the orbicularis oris, salivary glands, lacrimal glands, and 23 paired facial muscles via the posterior auricular, temporal, zygomatic, buccal, marginal mandibular, and cervical branches [12].

### **2.3 Etiology**

Facial palsy causes have been encompassed into four possible mechanisms: genetic, due to hereditary factors that have shown to be important. Vascular, where the edema occurs due to insufficient blood supply. Infectious causes. Undetermined etiologies and autoimmune processes. **Table 1** lists the peripheral facial palsy, and **Table 2** lists bilateral facial palsy causes found in the literature [2, 11, 12, 16]. Moreover, viral infections, ischemia, or autoimmune diseases have been postulated as possible pathomechanisms for Bell's palsy [2, 4, 14, 17].

*Medical System to Evaluate the Seventh Cranial Nerve through the Main Facial Mimic Muscles DOI: http://dx.doi.org/10.5772/intechopen.107134*

#### **Figure 1.**

*Schematic diagram that features the facial nerves. The green lines show the parasympathetic fibers. The purple line is the visceral afferent fibers [15]. The labels states for: (a) lacrimal gland, (b) pterygopalatine ganglion, (c) trigeminal ganglion, (d) V n, (e) geniculate ganglion, (f) motor nucleus VI n, (g) superior salivatory nucleus, (h) motor nucleus VII n, (i) fasciculus solitarius, (j) nucleus fasciculus solitarius, (k) VII n, (l) major superficial petrosal nerve, (m) to nasal and palatine glands, (n) chorda tympani, (o) lingual nerve, (p) submandibular gland, (q) sublingual gland, and (r) submandibular gland.*



#### **Table 1.**

*Potential causes for peripheral facial nerve palsy [2, 4, 11, 12, 14, 16–21].*


**Table 2.**

*Potential causes of bilateral facial nerve palsy [2, 22, 23].*

### **2.4 Syntomatology**

One of the main tasks that the facial nerve has is to provide motor innervation. As a consequence, when it is damaged, the patients can present decreased facial expression, abnormal muscle tone, syncynesia, hyperacusis, tearing, irritation, dry eyes, inability to blink, loose lips corners, numbness, pain around the ear and temple,

*Medical System to Evaluate the Seventh Cranial Nerve through the Main Facial Mimic Muscles DOI: http://dx.doi.org/10.5772/intechopen.107134*

temperature variation sensation, altered sense of taste, and flow of saliva out of the mouth [4, 5, 12, 17, 24, 25]. Those symptoms are closely related to the lesion location in the facial nerve [11]. Others are produced due to the facial nerve generating a sensation in one part of the ear. Moreover, the taste is produced at the anterior (twothirds) of the tongue via the chorda tympani and to the innervation to the lacrimal gland and submandibular one [2, 26].

#### **2.5 Diagnosis**

The facial palsy is diagnosed by an abrupt facial expression alteration due to unilateral or bilateral facial weakness of the facial nerve branches. The healthcare professionals take into account the presence of typical symptoms and signs mentioned elsewhere [2, 4]. Although, Bell's palsy diagnosis is reserved to be used when whole set of peripheral facial palsy causes are excluded. Nevertheless, Bell's palsy can coexist with the diseases that cause peripheral facial palsy [2]. In some cases, blood chemistries, cerebrospinal fluid analysis, mastoids, and crane X-rays, magnetic resonance imaging, or nerve conduction studies for facial nerve prognosis [2]. In contrast, therapeutic functional evaluation includes patient history, initial photographs or video recording of facial movements, electromyographic readings, observations of muscle tone, movement, and synsynesias [5, 12, 27].

Additionally, the weakness progression is evaluated by reviewing old photographs in order to compare it with the current status. The damage degree can also be assessed by the conduction of the facial nerve. A nerve conduction study measures the potential action, amplitude, and latencies through the facial nerve (**Table 3**). The study can identify nerve damage, as an example, the damage degree can also be assessed by nerve conduction of the facial nerve. Decreased muscle-action potentials suggest axon degeneration while increased latency suggests nerve demyelination [2, 28]. Along the test, several electrodes are inserted into the facial muscles. The muscles used to fix the electrodes are the orbicularis oculi or the oblicularis oris, mentalis, messetere, and temporalis. Two electrodes are needed for each muscle. The first electrode sends an electrical stimulation, and the other one is used as an electrical impulse receptor. The received signal is used to calculate the nerve conduction velocity [29]. However, prospective analyses are needed to assess the relevance of nerve conduction studies [27].

Usually, electromyography is often performed at the same time. The study measures the muscular electrical activity. It shares the same methodology as the nerve conduction study. The main difference lies in the electrodes distribution. In here, it used superficial electrodes while in the nerve conduction study, the electrodes are invasive. Both studies are searching the damage location in the facial nerve or in the muscles innervated by it [29].

In addition, magnetic resonance imaging is used to detect lesions in the facial nerve [30]. Magnetic resonance imaging or MRI is a technique that uses the magnetic field to generate images of the human body. MRI assesses the underlying disease. In patients with facial palsy, the MRI is used to measure facial muscle volumes by monitoring the decease development [31]. Other authors concluded that contrast enhancement of the paralytic nerve can be indicative of a nerve inflammation. Furthermore, through the MRI image, it is possible to estimate the recovery [30]. Moreover, older facial nerve studies have shown that abnormalities displayed by the MRI were not conclusive to diagnose Bell's palsy [32]. Nevertheless, in 2000, according to the authors, it was find an abnormal MRI in bilateral Bell's palsy [33].


**Table 3.**

*Potential causes of bilateral facial nerve palsy [2, 22, 23].*

#### **2.6 Palsy grade analysis**

Measurement scales to clinically assess facial palsy severity and population studies differ among researchers [34]. In order to standardize the paralysis classification, several scales have been developed such as the Sunderland, Sunnybrook, the Yanagihara classification system, and the most widely used, the House-Brackmann system shown in **Table 4** [2, 4, 12, 34–39]. The most used systems rely on the resting symmetry assessment, facial-muscles excursion degree, and triggered synkinesis by performing voluntary specific movements [2, 40].

The palsy-degrees qualitative descriptions make a clinical evaluation quite complicated. Furthermore, a misunderstood etiology makes the prognosis unpredictable. It also provokes a sluggish pathological process that as a consequence affects the patient recovery [13].

#### **2.7 Rehabilitation**

Rehabilitation focuses on regaining voluntary muscle contraction, improving movement quality, synkinesis control, enhancing symmetry, and increasing the percentage of facial functionality. It is important to achieve a fast recovery to reach a complete restoration of muscle function. Literature shows that the faster the recovery, the less sequelae will be [5, 11, 12, 14, 41]. In addition, the recovery time is key between the second and the fourth week. Thence, to find the most suitable treatment for each patient in the shortest time is essential. A facial palsy poorly treated might cause functional difficulties that decrease the patient's ability to communicate. Psychological help is also essential as it also generates cosmetic deformities that provide serious social stigma to the person who suffers it [2, 5, 12, 14].

Peripheral facial palsy rehabilitation is based on treating the underlying disorder. However, for Bell's palsy case (unknown etiology), the treatment has been controversial due to the lack of scientific evidence. Moreover, it is possible that the diseases listed as the triggers for facial palsy are also present in patients with paresis without being the cause for Bell's palsy [2, 11, 42]. On the other hand, anti-inflammatories and antivirals have shown a major recovery index in patients with Bell's palsy [14, 43, 44].

Balliet in 1982 focused on the study of facial mimic. He proposed a set of key therapeutic exercises to activate muscles or to evoke localized movements [27, 45]. In *Medical System to Evaluate the Seventh Cranial Nerve through the Main Facial Mimic Muscles DOI: http://dx.doi.org/10.5772/intechopen.107134*


**Table 4.**

*House-Brackmann (HBS) and Yanagihara classification systems to rate the severity of facial nerve palsy by evaluating the forehead motility, eyes, nose, and mouth [2, 37].*

addition, in order to increase the operative facial movements, inhibit abnormal movements, maintain trophism, and provide tactile stimulation, techniques such as neuromuscular retraining, isolated exercises, stimulation of sensory modulation, acupuncture, application butyllium toxin, electrical stimulation, surgery, massage, and vibratory therapy are highly used [4, 5, 12]. However, further research is needed regarding specific indications, duration of rehabilitation and potential recovery [2, 5, 12, 14].

### **2.8 Prevalence**

The facial palsy incidence is estimated between 11 and 40 cases per 100,000 inhabitants annually [2, 4, 11, 14, 15]. The peak incidence occurs between 15 and 45 years. However, one in 60 people will experience it in their lifetime [15]. The prevalence of bilateral facial palsy spans from 0.3 to 2%, it increases in pregnant women, diabetic patients, respiratory diseases, influenza or has attended an extraction of a tooth root. It is not common in children under 2 years of age [2, 17].

#### **2.9 Prognosis**

The people prognosis with paresis depends on two main factors, the paralysis degree, and the individual age. The younger the patient, the better the prognosis. When a facial palsy is incomplete, over 94% of patients recover their face functionality [6, 27, 46–49]. In a facial palsy, if recovery does not occur within the first 6 months, the long-term clinical picture includes speech distortion, difficulty to eat, syncynesia, atrophy, soft tissue adherence, and muscle lengthening [12]. Some patients also mentioned otalgia or mild retroarticular pain. When the patients present those sequels, their life quality decreases drastically causing impediments in their work and social life [14]. By receiving therapy, the rate of facial palsy recovery may improve after 1 year, in contrast to those who did not receive any treatment [2, 4, 26, 27, 50].
