1.What are the causes of Bell facial palsy?
Bell facial palsy is the most common type of peripheral facial palsy. It mostly strikes suddenly after a cool breeze and manifests as total paralysis of one side of the facial muscles. The etiology of Bell facial palsy is not very clear, but there are three theories.
(1) Nerve ischemia theory: Some of the Bell facial palsy develops after being stimulated by cold and cool wind, so it is presumed that the sudden stimulation of cold or other reasons stimulate the motor nerve reflex of the blood vessels, resulting in spasmodic contraction of the neurotrophic vessels, resulting in nerve ischemia, edema and compression. The facial nerve enters the internal auditory canal and travels in the curved and narrow bony canal, which is the longest nerve in the human body. It travels through the bony canal for about 3.1-3.3 cm, with limited blood flow and poor compensation of the lateral branches, and is prone to ischemic damage.
In addition, the vagus segment of the facial nerve located between the internal auditory canal and the geniculate ganglion lacks peripheral nerve membrane and peripheral nerve tissue, which is less resistant to various stimuli and more prone to damage and edema. After the facial nerve becomes ischemic and edematous, the pressure in the facial nerve canal increases, which affects the blood supply to the facial nerve. These pathological factors are interconnected, forming a vicious circle, causing nerve dysfunction and facial muscle paralysis. Patients with a history of diabetes and vascular sclerosis have a higher incidence of Bell’s facial palsy, which may be related to the ischemia caused by diabetes and vascular sclerosis. Zhao Lijun, Department of Acupuncture and Moxibustion, Shanxi Provincial People’s Hospital
(2) Viral infection theory: Since the onset of Bell facial palsy is accompanied by fever, nasal congestion, sore throat, herpes of the mouth and lips and other symptoms similar to upper respiratory tract viral infection in some patients, scholars suspect that the occurrence of Bell facial palsy may be related to viral infection. The theory that viral infection caused Bell’s facial palsy was proposed as early as the 1970s, and with the widespread use of molecular biology techniques, a large number of clinical and basic studies in the mid- to late-20th century suggested that herpes simplex virus infection might be the cause of Bell’s facial palsy. Some research evidence supporting viral infection was presented, and latent herpes simplex virus was detected in the geniculate ganglion of the facial nerve at autopsy using PCR techniques.
When fluid from the nerve lining was collected for virological analysis during facial nerve decompression surgery, herpes simplex virus DNA was detected in 11 of 14 Bell facial palsy patients, but not in Hunt syndrome (Ramsay Hunt syndrome) or other neurological disorders, suggesting that herpes simplex virus infection is specific in Bell facial palsy patients, and in animal experiments it was found that Herpes simplex virus can cause symptoms similar to those of Bell facial palsy in humans.
In China, some scholars inoculated herpes simplex virus type 1 (HSV-1) in the posterior branch of the facial nerve break could cause temporary facial nerve paralysis in mice, and successfully replicated a model of herpes simplex virus-induced facial neuritis, suggesting that it may be due to retrograde viral transit causing facial neuritis and then nerve swelling and compression, and the occurrence of facial nerve paralysis. These studies suggest a specificity of herpes simplex virus infection in patients with Bell facial palsy.
(3) Inflammatory theory: It may be caused by latent secretory otitis media. During the treatment of this disease, when decompression surgery is performed, it is often found that the mastoid air chamber contains brownish-black viscous fluid, which is quite similar to the secretion in the tympanic chamber of secretory otitis media in non-suppurative otitis media.
2. What are the clinical manifestations and treatment aspects of Bell’s facial palsy?
Most patients have a sudden onset of unilateral facial hemiparesis after being hit by a cool breeze, while a few are involved bilaterally. In unilateral facial palsy, both sides of the face are asymmetrical, and the affected side loses expression movements, cannot frown, frown, close the eyes, and the lower lid turns out and tears for a long time, and the conjunctiva cornea is dry and inflamed due to long-term exposure. The nasolabial folds on the affected side become shallow, and the corners of the mouth droop and skew toward the healthy side, which is obvious when speaking, laughing and doing tooth-exposing actions.
When the cheeks are puffed, the air leaks out, and liquid tends to flow out from the corners of the mouth when eating. In bilateral facial palsy, the face is dull and expressionless. The facial palsy is accompanied by pain around the ear and pressure pain in the mastoid area. The posterior part of the tympanic membrane is congested, but it disappears shortly. Loss of taste sensation in the anterior 2/3 of the tongue on the affected side, but this soon returns.
The principle of treatment for Bell’s facial palsy is to improve local microcirculation, eliminate congestion and edema, and promote the recovery of nerve function. In the acute stage, attention should be paid to keeping warm, and hot compresses or infrared radiation can be used. The commonly used drugs are.
(1) Vasodilators: such as niacin 100mg, 3 times a day, orally; or compound salvia injection 20ml dissolved in 5% glucose solution 500ml as intravenous drip, once a day for 10 days.
(2) Steroid hormone: such as dexamethasone injection 20mg, added to the above liquid for intravenous infusion, once a day; also oral prednisone 30mg, once a day.
(3) Vitamin B group: Vitamin B1 20mg, 3 times daily, orally; Vitamin B12 500μg, 3 times daily, orally.
Chinese medicine calls this disease “crooked mouth and eyes”, and its pathogenesis is mostly due to the lack of solidity outside the guard, wind and phlegm in the luo, congestion of qi and blood, paralysis of the facial veins, so that the face muscle numbness, insensitivity and other symptoms. The treatment is to expel wind and phlegm, and to disperse the evil. This formula is based on the formula of “Zhuanzheng San”.
Acupuncture and moxibustion are effective, simple and easy to perform. Buccal car, Di Cang, Shimonoseki, Yang Bai, Fish Waist, Foot San Li, Cataract, and Hegu can be selected. Strong stimulation is not recommended in the acute stage, and weak stimulation is possible in the chronic stage.
According to statistics, if a patient with Bell facial palsy starts to recover within 1 to 2 weeks from the beginning of the disease, he will eventually recover completely, and the time for full recovery does not exceed one month; if the lesion does not improve after treatment from the second week, his prognosis is often poor, and even the recovery is not complete. The beginning of recovery generally starts from the forehead wrinkles, followed by eyelid closure, and the recovery process is top-down.
3. Diagnosis and differential diagnosis.
Bell facial palsy is an unexplained “idiopathic facial nerve palsy”, therefore, for peripheral facial nerve palsy, a clear cause must be excluded before the diagnosis of Bell facial palsy can be made.
Firstly, central facial nerve palsy should be ruled out. Central facial nerve palsy is characterized by the presence of facial muscle movements, normal function of knitting the forehead, closing the eyes and raising the eyebrows, while the lower facial muscles are paralyzed and cannot complete such actions as shrugging the nose, showing the teeth and puffing the cheeks, while the function of taste, lacrimal gland secretion and saliva secretion are normal; secondly, other diseases causing peripheral facial palsy should be ruled out through medical history, ear and head and neck examination;
Secondly, for patients who cannot be identified, clinical audiology, vestibular function and head and neck imaging can be performed to further exclude other central nervous system diseases or ear and posterior cranial fossa diseases, and for recurrent “Bell facial palsy”, a thin-layer temporal bone CT scan or MRI should be performed to exclude facial nerve tumors. Table 1 lists the common clinical sites of facial neuropathy causing facial palsy and the related symptoms, signs and causes, which can be used for reference in the differential diagnosis of Bell’s palsy.
4.What is the history of Bell’s palsy?
The treatment of facial nerve palsy has been documented as early as the 7th century, and the pathophysiological aspects were recorded after the 18th century. Since then, the knowledge of neurophysiology has expanded and enriched the scope of research on this disease. The innervation of muscle contraction and the electrophysiological phenomena of neuromuscular activity were confirmed, and in particular, the ability of damaged nerves to regenerate was discovered.
At the beginning of the 19th century, many excellent neurologists emerged in Europe, and Bell (1774-1842) was one of them. 1829, the British Royal Society published successive reports on facial nerve palsy since 1821, and Bell used a donkey as a test to clearly divide the nerves innervating the face into motor nerves (facial nerve) and sensory nerves (trigeminal nerve), and used this as the basis for research The clinical aspects of facial nerve palsy and related contents were studied on this basis. In particular, facial nerve symptomatology was recorded, with headache on the temporal side at the beginning of the disease, taste disorder, auditory hypersensitivity, pressure pain along the facial nerve trunk, peaking one day after the paralysis, facial swelling, speech, chewing, eye closure disorder, and inability to whistle, which are very similar to the symptoms of Bell’s palsy named today.
In 1849, induction was used to diagnose nerve and muscle diseases, and it was used for the diagnosis and treatment of this disease, and it was possible to distinguish between peripheral and central facial nerve palsy. 1870, an author performed experiments on facial nerve severance and found that the nerve conduction was lost after severance, but the excitability of the muscle was maintained. 1914, Dejerine published “Syndromes of the nervous system”, which is known as the “syndromes of diseases of the nervous system”. In 1914, Dejerine published “Symptomatology of Diseases of the Nervous System”, which is regarded as a classic of neurology, in which the motor disorders and sensory disorders including taste, smell and hearing caused by facial nerve palsy were described in detail, and the causes of facial nerve palsy were trauma, tumor, vascular disease, compression, inflammation (syphilis, otitis media) and neuritis (syphilis, diabetes, polyneuritis). In the late 20th century, the main research was on the etiology of the disease.
5. What is the current understanding of Bell’s palsy?
Bell’s palsy is a peripheral facial nerve paralysis caused by acute nonsuppurative facial neuritis in the foramen ovale. It is also known as facial neuritis in China, and its exact etiology is not yet clear. The exact cause of the disease is not yet clear. Some patients develop the disease due to local wind or cold, so it is usually believed that the disease may be caused by local spasm of the blood vessels that nourish the nerve due to wind and cold, resulting in ischemia, edema, and compression of the nerve tissue; or due to rheumatic facial neuritis, osteochondritis within the foramen caudalis, resulting in swelling and compression of the facial nerve and impaired blood circulation, resulting in nerve paralysis. A few patients have acute nasopharyngitis at the same time. After the facial nerve exits the brain, it passes through the narrow bony canal in the bone, the facial nerve canal, and finally, exits the cranial cavity through the stem mastoid foramen and is distributed to the facial expression muscles.
Therefore, the local neural edema caused by either ischemia or inflammation is bound to cause more severe compression of the nerve by this local anatomical relationship, leading to nerve dysfunction and facial muscle paralysis. Tarerner’s diagnostic criteria for Bell’s palsy are.
① total or partial paralysis of one side of the facial expression muscle;
② sudden onset;
(3) no signs and symptoms of the central nervous system; (4) no signs and symptoms of the ear or posterior cranial recess. However, Adour believed that Bell’s palsy also affects other cranial nerves based on the observation of 2000 cases. Therefore, he concluded that:Bell’s palsy is an acute benign polyneuritis of the cranial nerves and that the loss of function of the motor nerves may be due to neuroinflammation or demyelination rather than ischemic compression. It has been reported in the literature that this disease does have other nerve damage detected with precise examination methods such as evoked potentials and nystagmography, in addition to facial nerve damage. Therefore,the meaning of Bell’s palsy has been revised in recent years.