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Facial palsy is one of the most frequent mononeuropathies expressed in muscular weakness. The condition is produced by lesions in the seventh cranial nerve that causes esthetic, functional, and psychosocial alterations. The disorder has a qualitative diagnosis, and as a consequence, it does hinder the disease timely monitoring. As time is a key factor for the patient’s recovery, we developed a system capable to quantify the condition and/or damage in the seventh cranial nerve. It allows us to provide the best treatment available that offers the best response to each patient. To know the seventh cranial nerve state is possible due to the connections between whole muscular system and neurons. The system quantifies the muscles activity and displays the differential information of both hemifaces. Our proposal features a mask in which an array of sensors is placed across the frontal, zygomatic minor, risorio, zygomatic major muscles of each hemiface. The data collected are analyzed and displayed in a user-friendly interface.
Research Centre for Applied Science and Engineering (CUCEI), Universidad de Guadalajara, Mexico
Gregorio Guadalupe-Carbajal Arizaga
Research Centre for Applied Science and Engineering (CUCEI), Universidad de Guadalajara, Mexico
Orfil González-Reynoso
Research Centre for Applied Science and Engineering (CUCEI), Universidad de Guadalajara, Mexico
Mario Alberto García-Ramírez*
Research Centre for Applied Science and Engineering (CUCEI), Universidad de Guadalajara, Mexico
Research Centre for Translational Medicine (CiMeT), Guadalajara, Mexico
*Address all correspondence to: mario.garcia@academicos.udg.mx
1. Introduction
“The facial expressions of human beings fascinate me because they convey both the lowest, most bestial pleasures and the strongest and gentlest emotions of the spirit.” This is how Sir Charles Bell described the facial mimic importance [1]. Facial palsy is a disease that reduces the facial symmetry, and as a consequence, it causes functional and esthetic alterations that affect the person mental health as well as the activities they perform on daily basis.
Facial palsy is a disorder that, in most cases, is evaluated qualitatively; therefore, it is essential to find an adequate method to use for diagnosis regardless of the evaluator perception. In this manner, a system capable to quantify the paralyzed hemiface was proposed and developed. Our proposal considers the healthy hemiface as the base control one for the facial palsy and for a bilateral one, the system will use both to evaluate the paralysis degree and to provide an accurate and safer diagnosis in contrast with the nerve conduction diagnosis. Muscular information based on the current status as well as the muscular evolution movement will be gathered by the set of sensors array that would be able to measure the acceleration caused by the muscular movement at each hemiface. As a result of such analysis, it would be possible to deliver an optimal treatment as well as to execute it for each particular case.
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, 3, 4]. The person who suffers it has a severe disability as the facial nerve is the backbone in facial mimic [4, 5, 6, 7, 8, 9, 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, 6, 7, 8, 9, 10, 11, 12, 13, 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].
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.
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].
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, 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 (two-thirds) 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].
Bilateral facial palsy causes
Bulbospinal atrophy
Pontine gliomas
Mononucleosis
Borreliosis
Pontine hemorrhage
Sífilis
Diabetes
Infections
Sarcoidosis
Pregnancy
Leprosy
Guillain-Barré
Encephalitis
Leukemia
Miller-Fisher
Hansen’s disease
Systemic lupus erythematosus
Moebius
Fractures
Cryptococcal meningitis
Linezolid therapy
Table 3.
Potential causes of bilateral facial nerve palsy [2, 22, 23].
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].
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, 35, 36, 37, 38, 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].
Grade
HBS
Y system (%)
Normal, symmetric functions in all areas.
I
40
Mild weakness on close inspection, complete closure of eyes with minimal effort, asymmetrical weakness of smile with maximal effort, weak synkinesis, no contractures or spasms.
II
32–38
Obvious but not disfiguring weakness of the face, inability to raise the eyebrow, full and forceful eye closures, asymmetric movement of the mouth with maximal effort, obvious but not disfiguring synkinesis, mass movement or twitching.
III
24–30
Obvious disfigurement due to weakness, inability to raise the eyebrows, incomplete closure of the eyes, asymmetry of the mouth with maximum effort, severe synkinesis, mass movements, spasms.
IV
16–22
Barely perceptible movement, incomplete closure of eyes, weak movement at the corner of the mouth, synkinesis, contracture, spasms usually absent.
V
8–14
No movement, low muscle tone, no synkinesis, contracture and spasms.
VI
0–6
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].
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 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, 47, 48, 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].
The SARS-CoV-2 (COVID-19) infection pandemic has been a major public health issue worldwide. Recent studies have shown that it has an effect on other pathologies such as neurological syndromes [21, 51, 52]. COVID-19 as well as facial palsy disrupts the daily life of our society. Those diseases provoke anguish to those who suffer it due to possible functional and esthetic sequels [21, 51]. Literature has suggested a possible link between COVID-19 and facial palsy, the coronavirus neurotropic nature [21]. The COVID-19 ability to infect different cell types is determined by the ACE2 receptors. The ACE2 inhibitors are located at the endothelial cells of the blood-brain barrier. The binding between ACE2 and COVID-19 allows it to enter the central nervous system [52, 53, 55], even facial palsy has been proposed as the first and only COVID-19 symptom [54, 56].
The COVID-19 incidence has increased along the pandemic development, and some studies focus on the vaccine trial as facial palsy cause [21]. Although, other authors do not find significant differences in the incidence of facial palsy [57], the incidence in pregnant women increases due to the physiological pregnancy stress. This is why they could be more susceptible to neurotropic invasion by the virus [52]. It has been reported an unusual amount of children, a cluster of six, that features facial palsy between March 23 and April 26, 2020 [58]. Despite the low incidence, the bilateral facial palsy case was reported as an asymptomatic COVID-19 [59]. Later, other bilateral facial palsy studies related to COVID-19 were presented [60, 61].
Authors hypothesize in their works that Bell’s palsy may be a neuro-COVID-19 manifestation. Nevertheless, a few authors have claimed that there is not enough evidence to establish a clear cause between the two conditions [21, 52, 56, 57]. Other researchers compile the online databases about COVID-19 and facial palsy, and they concluded that COVID-19 increases the number of neurological deceases and pointed out that SARS-CoV-2 infection may be an underlying etiology in patients with COVID-19, and facial palsy can be the first COVID-19 manifestation [62, 63].
In order to support and help patients that suffer facial palsy as well as the professionals who treat them, a system to analyze the illness was developed. Our proposal features two modules: WaLi that is an electronic device that it is responsible for data aqcuisition and a graphical user-friendly interface called WaL that displays the processed data.
WaLi is a system that features a set of sensors distributed across the face in which are localized the muscles controlled by the seventh nerve. Figure 1 shows a schematic image that features the seventh cranial nerve following an axial symmetry. At each point shown in Figure 2(a), a set of sensors will be distributed on the same spot to measure each muscle in a differential way.
Figure 2.
Schematic diagram that features hardware system. (a) The circles show the sensor location on the most representative muscles of the facial mimic (frontal, minor zygomatic, risorio, and the major zygomatic) and (b) the data bus that links the sensors to the MCU at the rear.
In order to measure the movement provided by the muscles, eight inertial measurement units that features six freedom degrees were used. The sensors were placed at the frontal, zygomaticus minor, zygomaticus major, risorius, and the pairs by following an axial symmetry. The data generated by the muscles and transmitted to the sensors are sent through several data busses. Although, WaLi (Figure 3) is a physical array of electronics devices, it needs software to execute a set of algorithms on the acquired data. The backbone of the software is the acquisition algorithm that is responsible to gather the data and sending it to the serial port by using a serial communication protocol.
Figure 3.
Schematic diagram that shows the sensors distribution across the both hemifaces over the key muscles.
The facial symmetry is the key principle in which the system is based. This is why, the backbone of the entire system focuses on the position at which each sensor is located across the face. In order to keep the position sharp for each sensor, a mask was developed through the fabrication of positive and negative mold. Once the sensors were in place on the key spots, the data busses were positioned in order to not interfere with the facial mimic. Once fixed, the negative mold was used to finish the mask to keep the whole set of arrays in place.
WaL: It is defined as a user-friendly interface that receives, analyzes, and displays the information obtained from the muscles chosen by the user. Figure 4 shows a schematic diagram that displays the interface featuring the mobility behavior of a healthy person.
Figure 4.
Schematic diagram that shows WaL, the user-friendly interface. In here, it shows the mobility graphs of the frontal muscle in a healthy person. The left side exhibits a set of menus that the user can utilize. The options to manipulate are: (a) patient information; (b) study type; (c) start study; (d) display graphs and hemiface; (e) muscle to show; (f) thresholds and standard deviation; (g) maximum threshold; (h) minimum threshold, (i) mobility degree; (k) and (j) standard deviation of left and right hemiface, respectively.
For the development of WaL, a set of algorithms based on numerical analyses were used. The interface established a serial communication between WaLi and WaL in order to collect the data from the serial port. The data are sent through a serial port as a vector. WaL stores and transforms the vector into a matrix. The columns are classified as a function of the hemiface, muscle name, and the plane in which the movement was performed (x, y, and z). Then, the signal is preprocessed to be analyzed later. No human is symmetrical; hereby, at the interface, the user selects the healthy hemiface. The option selected by the user will be considered by the algorithm as a reference. The robustness of the system allows to be used by anyone due to the user-friendly interface.
Another feature that WaL has is the postprocessing feature. A set of statistical analyses can be performed on WaL such as standard deviation, mean, and correlation coefficient. Furthermore, another measurement unit was proposed [64]. The mobility degree (gM) expressed as a percentage of the weakened hemiface as function of the healthy counterpart is obtained by using the following equation:
gM=100×a2f−a2iaf−aiE1
where a2i: initial component of the weakened hemiface; a2f: final component in x, y or z of the weakened hemiface; ai: initial component of the healthy hemiface; af: final component of the healthy hemiface.
Moreover, WaL is capable to analyze and display the state and the information that each sensor has as well as auto-calibration, patient information, and the option to safe the analysis.
In order to show the effectiveness of the system, a study on muscular trajectory was performed in 18 patients for male and female genders on an age span of 22 and 24 years. Fifteen of the patients were healthy, and three presented peripheral facial palsy. The protocol to analyze the group of patients was as follows: the test subject sat in a chair with a straight back making sure that he/she was comfortable. Once the test subject was in place, he/she put on the mask and adjusted it so that the sensors were on the corresponding muscle. Immediately WaL started to record. The person contracted the muscles to be studied as intensely as possible for a couple of seconds and immediately relaxed them.
The results found from healthy people were used for calibration purposes. The ill individual results corroborate that our system is capable to quantify the muscle movement controlled by the seventh cranial nerve. The system is calibrated to take 12,000 samples of the muscular trajectory in 6.06 seconds, with this information, the standard deviation and the mean for each component are obtained. The correlation among components of the same muscle such as the thresholds that state the point of major and minor displacement, the asymmetry facial, and muscle correlation is expressed as a percentage. The data that the system collected when conducting the study on the 15 healthy people and three people with facial paralysis were used as a reference to establish the thresholds that indicate the state of the user’s facial muscles. The purpose of the system is to provide a tool that contributes with information for an accurate diagnosis. The collected data can reduce the time to find the ideal treatment for the patients. The data measured by the system are graphed and normalized in order to standardize the signal and thus, compare the reaction speed and intensity of the movement of each hemiface.
5.1 Healthy person muscular trajectory
The central trajectory measurements that appear in Figure 5 correspond to a healthy 24-year-old woman, weighing 70 kg and 1.74 m tall. The frontal muscle trajectory shown in Figure 5I has a correlation percentage for all the components of 95.54%, zygomaticus minor (Figure 5II) has a correlation of 94.23%, risorio (Figure 5II) of 96.42% and for zygomaticus major (Figure 5IV) it is 92.61%. Although the study was applied to a healthy person. The asymmetry of the face of this particular person is accentuated in the zygomaticus minor muscle. Therefore, it can be affirmed that the muscular response is attenuated by 7.39%.
Figure 5.
Set of experimental results that shows the muscle movement intensity in a healthy person where the frontal (I), zigomaticus minor (II), risorius (III), and zigomaticus major (IV) are shown. The signals are normalized and plotted against time (a) shows the “x” components of the muscle trajectory, (b) the “y” components, and (c) shows present the components in “z.”
5.2 Facial paralysis muscular trajectory
The person with facial paralysis is shown in Figure 6. It is observed that the similarity of the signals decreases in all the muscles. By having a correlation percentage of 77.14% for the frontal muscle, 73.30% for the zygomatic minor, 84.60% for the risorius, and 5.48% for the zygomaticus major.
Figure 6.
Set of measured results that feature the intensity of frontal (I), zigomaticus minor (II), risorius (III), and zigomaticus major (IV) muscles movement in a person with facial paralysis. The signals were normalized and are plotted against time where (a), (b), and (c) are the x, y, and z components, respectively.
The signals belong to the injured hemiface that reached the maximum point of contraction starting from the minimum state in a longer time with respect to the healthy counterpart. In most cases, the signals are function of the healthy side of the face by reaching the highest intensity in approximately 1 s while the signals from the paralyzed side take twice as long.
In order to show the trajectory analysis, a set of box plots were used to graphically represent the scatter, symmetry, and outliers found in the muscle trajectory signal. On the graph of the healthy person (Figure 7), it can be seen that the upper quartile is larger than the lower one. In addition, the mean values of both sides are closer to last mentioned.
Figure 7.
Muscular trajectory box diagrams in normal state. The names along the x–axis represent the sensor number. (a) Represents the left hemiface side with sensors 1–4 and (b) the right hemiface side with sensors 5–8. Notches were added in the diagrams of the healthy hemiface for purposes of distinction.
The patient that presents facial palsy (Figure 8), it is observed that the interquartile distribution of the injured half-face with respect to the healthy half-face is irregular. It does imply that those are not close to any particular quartile. In addition, outliers are presented in the diagram between the lower quartile and the minimum threshold; likewise, the distance between the outer quartiles and the thresholds is greater compared with the diagrams in Figure 7.
Figure 8.
Muscle trajectory box plots, those represent a person with facial palsy. (a) Shows the components of the left hemiface side muscles on the left hemiface side and (b) the right hemiface side. In addition, both hemifaces display an odd behavior (a) and (b), in contrast with a healthy person shown elsewhere (Figure 7).
The outliers denoted by “+” signs outside the quartiles are neither present in the healthy person (Figure 7) nor in the healthy person half-face with paralysis box plot (Figure 8a). As the study results show, WaL is effective in quantifying the trajectory of the frontalis, zygomaticus minor, risorius, and zygomaticus major muscles. The data obtained from the tests performed on 15 healthy persons and three with facial paralysis suggest that the facial correlation percentage of a healthy person is in a span between 89.57% and 97.87%, with a deviation standard between 0.34822 and 0.3433.
Due to the fact that having a healthy face does not guarantee having a symmetrical face, the system does a precalibration, by showing an error coefficient in order to express the asymmetry. Under the assumption that all faces are asymmetric, the facial muscles are normal when the error coefficient is below 10.43%.
According to the graphs generated by the system (Figure 5), when one side of the face is in a normal state, the average response speed from the point of largest relaxation to the point of largest contraction is 2.49 seconds while for the injured hemifaces, it was 3.52 seconds. Furthermore, it was observed in the experimental data that when the correlation is high, the data dispersion marked by the standard deviation increases.
From the analyses shown in Figures 7 and 8, it is observed that if the contraction muscle time is larger than the relaxation time, the length of the upper quartiles increase; on the other hand, it decreases if the contraction is lower, so it can be stated that the length of the quartiles depends on the muscle contraction as well as the mean. Although the possibility of anomalous values + that appear in the box plots of normalized signals from healthy half-faces is not ruled out, in the 18 studies on which this research is based, outliers were only present in the normalized paralyzed hemifaces.
The person whose results are shown in Figure 6 was diagnosed with peripheral facial paralysis. It shows weakness on the left side of the face, which was confirmed by the system with an average standard deviation of 0.32232 and a facial correlation coefficient of 72.63%. A value that is outside of the range previously established for healthy people, which means that the electrical potentials presented the muscles of the left side of the face were attenuated by 27.37% due to the paralysis, by making it impossible for the person to perform a symmetrical contraction affecting their muscular excursion.
A full system to quantify the degree of facial palsy that will help to know the degree of muscle re–education improvement or not with the help of therapy was proposed and fabricated. By broadening the panorama of possible disease causes and keeping a timely record. An important point in performing the study with WaLi and WaL system is the placement of the mask, as the sensors are not located on the muscle to which they have been assigned, the result will be affected. By accentuating the degree of error of the system in the axis from which it was erroneously offset with respect to the point of interest.
For a face to be classified as healthy, it must have a high correlation, which means that the movement of both sides is very similar in intensity and time. According to the results provided by the system, healthy faces have a shorter response time between the largest relaxation point to the longest contraction that causes the difference between the mean of the signal and the data by increasing the standard deviation. So, it can be concluded that the greater the deviation, the correlation coefficient, and the arithmetic mean, the greater the symmetry of the face and the smaller the difference in reaction time.
We express our gratitude to the Mexican National Council of Science and Technology (CONACYT) for their support under the Scholarship 1023006 and the Research Project 319712 as well as the Chemistry & Electronics Department and the Methabolic and Bioinformatic Lab of University of Guadalajara.
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