scholarly journals Clinical Case of Facial Muscles Function Recovery in a Patient With Idiopathic Lesions of the Facial Nerve With Unfavorable Myographic Predictors

2021 ◽  
Vol 10 (1) ◽  
pp. 216-223
Author(s):  
K. I. Chekhonatskaya ◽  
L. B. Zavaliy ◽  
M. V. Sinkin ◽  
L. L. Semenov ◽  
G. R. Ramazanov ◽  
...  

The facial nerve (fn) palsy is a disease of the peripheral nervous system that leads to aesthetic, organic and functional disorders. The causes of the disease are different, the most common is the idiopathic form bell’s palsy. With a conservative approach to therapy, up to 80% of patients note the complete recovery of the lost functions of facial muscles, the others have the likelihood of severe consequences. Electroneuromyography is used to assess the risk of a negative outcome of the disease. In cases of confirmation of severe nerve damage, surgical treatment is suggested. The article presents a clinical case of complete recovery of the function of facial muscles in a patient with severe damage to the a nerve and an unfavorable prognosis. The course of the disease, complications of bell’s palsy and methods of their correction are described. Timely correct choice of treatment tactics and prevention of complications minimizes negative consequences. When working with a patient, a differentiated approach is important depending on the clinical situation.

2021 ◽  
pp. 83-87
Author(s):  
D.S. Khapchenkova ◽  
◽  
S.О. Dubyna ◽  
K.Yu. Yena ◽  
◽  
...  

Bell's palsy is an acute peripheral paralysis of the facial nerve of unknown etiology. The facial nerve is the seventh cranial nerve. One part of the facial nerve is the motor fibers that innervate the facial muscles. The facial nerve emerges from the brain between the posterior edge of the pons and the medulla oblongata with two roots. The main motor nucleus is responsible for the voluntary control of facial muscles. There are central and peripheral paresis of the facial nerve. Central paresis occurs during а stroke. Peripheral paresis (unilateral muscle weakness of the entire half of the face) develops when the facial nerve is affected from the motor nucleus to the exit from the stylomastoid foramen. Among the various localizations of damage to the peripheral part of the facial nerve, the most common is Bell's palsy as a result of edema and compression of the nerve in the bone canal. Clinical symptoms of facial nerve neuropathy are characterized by acute paralysis or paresis of facial muscles: smoothed skin fold on the affected side of the face; swelling of the cheeks; an inability to close the eyelid, Bell's symptom; facial muscle weakness. The degree of damage is determined by the House Brackmann scale. Treatment with glucocorticosteroids, antiviral drugs, physiotherapy procedures. Purpose — to present a clinical case of a patient with Bell's palsy as an example of delayed diagnosis, treatment and, as a result, long-term restoration of the facial muscles functions. Clinical case. The boy after suffering from the flu, began to complain of acute ear pain, vomiting, lack of movement in the right half of the face, dizziness, insomnia. Asymmetry of the face, lack of movement of the right side of the face, inability to completely close the right eye, a symptom of sailing on the right, muscle weakness were revealed during examination. The general condition of the patient improved, facial expressions were restored, sleep was normalized after hormonal, metabolic therapy, physiotherapy procedures. Conclusions. The article describes a case of inflammation of the facial nerve or Bell's palsy in a teenager who developed on the background of the flu. Timely diagnosis and treatment of the above pathology is the key to a satisfactory prognosis for the restoration of facial expressions, prevention of negative consequences of the the disease. The research was carried out in accordance with the principles of the Helsinki Declaration. The informed consent of the patient was obtained for conducting the studies. No conflict of interest was declared by the authors. Key words: facial nerve, Bell's palsy, flu, inflammation.


2021 ◽  
Vol 09 (3) ◽  
pp. 650-656
Author(s):  
Ram Lakhan Meena ◽  
Santoshkumar Bhatted ◽  
Nilam Meena

Bell’s palsy, also known as acute idiopathic lower motor neuron facial paralysis, is characterized by sud-den onset paralysis or weakness of the muscles to one side of the face controlled by the facial nerve. In contemporary science, administration of steroids is the treatment of choice for complete facial palsy. Cer-tain Panchakarma procedures and internal Ayurvedic medicines have been proved to be beneficial in the management of Ardita vata. The present report deals with a case of 62-year-old male patient diagnosed as Ardita vata was treated with various Panchakarma procedures like Nasya, Shirobasti, Kukkutanda Swedana, Dashmoola Ksheer Dhoom, Gandoosh and oral Ayurveda medicines. Criteria of assessment was based on the scoring of House-Brackmann Facial Nerve Grading scale. After completion of Ayurveda treatment, the patient Shown almost complete recovery without any adverse effects. This case is an evi-dence to demonstrate the effectiveness of Ayurveda treatment in case of Ardita vata (Bell’s palsy).


1977 ◽  
Vol 86 (4) ◽  
pp. 549-558 ◽  
Author(s):  
Ruth Gussen

The pathogenesis of Bell's palsy is presented as retrograde epineurial compression edema with ischemia of the facial nerve. Although the etiology is unknown, an attractive theory is vasospasm, from any cause, along any facial nerve branch, with the chorda tympani, perhaps, the usual primary involvement. Retrograde vascular distension and edema, within the epineurium of the bony facial canal, compresses the nerve from outside its perineurial sheath. The compression force may be mild or severe, resulting in varying degrees of reversible or irreversible ischemic degeneration of myelin sheaths and axons, with varying degrees of cellular reaction to myelin breakdown. The edema may be resorbed, leaving reversible or irreversible nerve damage, or may stimulate collagen formation within the epineurium, with persisting fibrous compression (entrapment) neuropathy of the facial nerve. This concept is consistent with the varying results of Bell's palsy, and depends on the severity and duration of edema, and whether fibrosis occurs within the epineurium of the facial canal. Epineurial fibrosis also results in disturbance of metabolic exchange through the epineurial-permeurial-endoneurial tissues, and may ultimately result in obliteration of vascular drainage. Two temporal bone cases of Bell's palsy, one occurring ten years before death, with residual paralysis. and one two years before death, with clinical recovery, are added to the previously described four cases in the literature, three of early Bell's palsy, and one of remote palsy with almost complete recovery.


2021 ◽  
Vol 14 (12) ◽  
pp. 733-741
Author(s):  
Frith Cull ◽  
Holli Coleman

Bell's palsy is the term given to an idiopathic lower motor neurone facial nerve paresis or paralysis. It is of rapid onset, almost always unilateral, and may be associated with facial or retro-auricular pain or otalgia. It is the most common diagnosis associated with facial nerve palsy; a GP will see a case approximately every 2 years in practice in the United Kingdom. Early diagnosis and steroid treatment increase the likelihood of full recovery, whereas ocular complications can be prevented by lubricants and lid taping. Over 70% of patients recover within a year. Options to improve facial appearance and function, in those who do not experience a complete recovery, include surgery.


1968 ◽  
Vol 6 (7) ◽  
pp. 25-26

There is controversy on the management of the idiopathic facial nerve palsies (Bell’s palsy). About two out of every three patients have a nerve conduction block alone and recover completely in less than one month.1 The rest develop denervation of the facial muscles to a varying degree and never recover completely. In addition, contracture of the facial muscles may occur, with severe disfigurement. About 10% of all patients with facial palsy have complete denervation and serious sequelae.2 Using electromyography3 and measurement of the anodal galvanic threshold4 an accurate prognosis can be given within the first week.


Author(s):  
A. Pashov

From every 100 cases of Bell’s palsy (idiopathic peripheral facial palsy) from 15 to 30 will not recover completely. Some residuals will remain, and some complications will develop. As residuals, one can name weakness of facial muscles, asymmetry of facial expressions, distortion of taste, hyperacusis, dry eye. Possible complications of long-standing Bell’s palsy (BP) are also numerous: contractures of facial muscles, pathological synkinesis, mass movements, crocodile tears, facial pains, headaches, emotional disbalance etc. Unresolved cases of Bell’s palsy require rehabilitation programs that will address both the issues of general nerve regeneration, complications and irregularities in mimetic movements, and psycho-emotional state of long-standing Bell’s palsy patients. There are several methods and systems to assess the condition of facial nerve and functioning of facial muscles. These scales and systems are either therapist- or patient-graded: House-Brackmann Facial Grading system, Sunnybrook Facial Grading system, Facial Clinimetric Evaluation Scale (FaCE Scale), Synkinesis Assessment Questionnaire (SAQ) and several others. At the same time, to compose a well-balanced and focused rehabilitation program, next to subjective assessments and test-photos of standard facial expressions, it is important to have an objective, instrumentally-measured picture of facial nerve recovery, as well as of the physiological ability of mimetic muscles to perform facial movements, to reflect emotions and to produce articulated speech. In that respect, the surface EMG or Nerve Conduction Study (NCS) is the modality of choice. NCS-examination is non-invasive and is relatively easy to perform. It records Compound Muscle Action Potentials (CMAPs) in response to external stimulation. The analysis of recorded graphs allows to evaluate the level of regeneration and maturity of recovering axons in main branches of the facial nerve. At the same time, the standard protocol of NCS does not offer a detailed assessment of each particular muscle of facial expression. It also requires additional time to swap the active electrode position when changing stimulation side from right to left and vice versa. At Crystal Touch Bell’s palsy clinic, we have developed an amended NCS protocol that addresses all mentioned issues. To allow a more detailed assessment of facial muscles, we have added mm.zygomatici (major et minor) and m.depressor anguli oris to the list of measured facial muscles. In order to perform a more focused stimulation and to receive a more “clean” motor responses from facial muscles, we changed the position of stimulating electrode. In the standard protocol, stimulating electrode is placed either pre- or post-auricularly. In Crystal Touch protocol, we position the stimulating electrode above each particular nerve branch that innervates the measured muscle. Therefore, we use six positions of stimulating electrode that correspond to the six measured facial muscles: m.frontalis, m.orbicularis oculi pars superioris, m.nasalis et m.levator labii superioris, mm.zygomatici (major et minor), m.orbicularis oculi pars superioris, m.depressor anguli oris et m.mentalis. To save time required for the examination, instead of placing reference electrode on the nasal bridge (standard protocol), we use contralateral electrode over the same as measured muscle, as a reference electrode. As there are no anastomoses between left and right facial nerves, stimulation of facial nerve on one side will not evoke CMAPs in contralateral facial muscles. This simple amendment allows to save about 15% of total time required for the examination. In this article we also briefly touch the following issues: distortion in reciprocal inhibition of facial muscles-antagonists, forming of the pathological mimetic patterns in the motor cortex due to lack of proprioceptive feedback during long recovery, and the necessity to further investigate from the electrotechnical, engineering and functional point of view the hypothesis of aberrant regeneration as possible cause of facial synkinesis.


1973 ◽  
Vol 11 (18) ◽  
pp. 69-70

When we discussed facial palsy in 19681 corticotrophin therapy was advocated. Since then oral corticosteroids have been tried and this article discusses their efficacy. Permanent clinical denervation of the affected facial muscles occurs in about a third of patients after Bell’s palsy2 3 and leads to persistent weakness. Some of the patients develop associated movements, or very rarely crocodile tears, due to aberrant regeneration. The movements can be very distressing. The incidence and severity of permanent denervation is related both to the severity of the damage to the facial nerve and to the age of the patient. It is very common over the age of 70 years, but rare below the age of 10 years.


2012 ◽  
Vol 73 (S 02) ◽  
Author(s):  
L. M. Marques ◽  
J. Pimentel ◽  
P. Escada ◽  
G. Neto D'Almeida

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Akira Inagaki ◽  
Sachiyo Katsumi ◽  
Shinji Sekiya ◽  
Shingo Murakami

AbstractIn Bell’s palsy, electrodiagnosis by electroneurography (ENoG) is widely used to predict a patient’s prognosis. The therapeutic options for patients with poor prognostic results remain controversial. Here, we investigated whether early intervention with intratympanic steroid therapy (ITST) is an effective treatment for Bell’s palsy patients with poor electrodiagnostic test results (≤ 10% electroneurography value). Patients in the concurrent ITST group (n = 8) received the standard systemic dose of prednisolone (410 mg total) and intratympanic dexamethasone (16.5 mg total) and those in the control group (n = 21) received systemic prednisolone at the standard dose or higher (average dose, 605 ± 27 mg). A year after onset, the recovery rate was higher in the ITST group than in the control group (88% vs 43%, P = 0.044). The average House-Brackmann grade was better in the concurrent ITST group (1.13 ± 0.13 vs 1.71 ± 0.16, P = 0.035). Concurrent ITST improves the facial nerve outcome in patients with poor electroneurography test results, regardless of whether equivalent or lower glucocorticoid doses were administered. This may be ascribed to a neuroprotective effect of ITST due to a higher dose of steroid reaching the lesion due to dexamethasone transfer in the facial nerve.


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