Idiopathic facial nerve palsy, also known as facial neuritis and Bell’s palsy, is a peripheral facial palsy caused by nonspecific inflammation of the facial nerve in the foramen magnum, and its pathogenesis is still inconclusive. Most scholars believe that it may be due to vascular nerve dysfunction caused by wind and cold, resulting in small artery spasm and local ischemia in the facial nerve canal and stem mammary foramen area. In recent years, more and more studies have shown that the main cause of facial nerve palsy is the activation of the herpes virus latent in the cerebral ganglia.
Brief description of the case
The patient was a 31-year-old male who presented to the clinic with a 1-day history of weakness in left eye closure and shallowing of the left nasolabial fold. He woke up in the morning and found weakness in closing the left eye, shallowing of the left nasolabial fold, and salivation at the left corner of the mouth. The patient had no obvious physical activity disorder.
The left frontal stripe was shallower than the contralateral side, the left eye closure was incomplete, the left nasolabial sulcus was shallow, the right angle of the mouth was deviated, the muscle strength of the limbs was grade 5, and the bilateral pathological signs were negative.
The cranial magnetic resonance imaging (MRI) did not show any significant abnormalities, and the electromyography showed incomplete damage to the left facial nerve (43% decrease in the wave amplitude of motor nerve conduction in both facial nerves compared with the right side).
After admission, he was considered to have facial nerve palsy and was treated with prednisone, acyclovir, vitamin B1 and vitamin B12, as well as physical therapy and rehabilitation exercises. One week after the onset of the disease, the condition was stable and he was discharged after 2 weeks of treatment. Follow-up after discharge showed that the symptoms basically recovered 2 months after the onset.
Clinical presentation
The disease can be seen in people of any age, mostly between 20 and 40 years old, with no gender difference. It is mostly unilateral facial paralysis, but rarely bilateral. The onset is usually acute, with sudden paralysis of the facial expression muscles on one side, which can reach a peak within a few hours. Some patients have pain in the postauricular mastoid area of the affected external ear canal one to three days before the onset of the disease, which is often detected in the morning when washing or by others.
The following signs are seen on physical examination.
① disappearance of ipsilateral forehead lines and inability to frown in the patient.
(2) The eyelid cannot be closed or is incompletely closed when the eye is closed because the orbicularis oculi muscle is paralyzed and the eye fissure is enlarged, while the eyeball turns outward and exposes the white sclera, which is called Bell’s phenomenon.
(iii) The lower eyelid is ectropion and the tears do not flow easily into the nasolacrimal duct and mostly overflow out of the eye.
④ shallowing of the nasolabial folds on the affected side, drooping of the corners of the mouth, and the corners of the mouth being drawn to the healthy side when showing the teeth.
⑤ Inability to pout and whistle, and air leakage from the affected side of the mouth when puffing the cheeks.
⑥When eating and washing the mouth, water can leak out from the affected corner of the mouth, and because the patient’s buccal muscle is paralyzed, food is often trapped between the teeth and cheeks.
If the lesion involves the bulbar nerve, in addition to the above symptoms, the patient may also have a decreased or absent sense of taste in the anterior 2/3 of the ipsilateral tongue. If the facial nerve is involved above the pedunculopontine branch, ipsilateral auditory hypersensitivity may also occur. If the geniculate ganglion is involved, in addition to facial palsy, taste disorder and auditory hypersensitivity, the patient may also have ipsilateral salivary and lacrimal gland secretion disorder, pain in the ear and behind the ear, and herpes zoster symptoms in the external auditory canal and auricular area.
Auxiliary examinations
Imaging tests Cranial X-ray, CT, MRI can help in the differential diagnosis of the disease. For example, otitis media, labyrinthitis, and mastoiditis can be diagnosed by cranial radiography or CT; while cranial MRI helps to differentiate the disease from vascular diseases, cerebral bridge cerebellar tumors, intracranial infections, and multiple sclerosis.
Laboratory tests.
① glycated hemoglobin test and glucose tolerance test to exclude facial nerve palsy due to diabetes mellitus.
(ii) Lyme virus antibody titers can help diagnose facial nerve palsy due to Lyme disease.
(iii) Herpes virus antibody titer test is valuable for the diagnosis of herpes virus infection, but is not a reliable diagnostic basis for facial nerve palsy.
④Lumbar puncture cerebrospinal fluid examination is helpful in differentiating from facial nerve palsy due to Grimballi syndrome.
Other The transient reflex can reflect the whole conduction function of the facial nerve, which can be used for early diagnosis of nerve damage and localization of damage to the central or peripheral segment of the facial nerve. This method, combined with facial nerve conduction velocity, can localize damage to the proximal or distal facial nerve and help determine prognosis. EMG abnormalities correlate with the duration of the patient’s disease and can directly reflect the extent of his or her nerve damage. The combination of the above three methods is important for the early diagnosis, localization and prognosis of Bell’s palsy.
Diagnosis and differential diagnosis
The diagnosis of Bell’s palsy is based on a combination of medical history, general examination, specialist examination, audiological assessment, electrophysiological examination and imaging findings. The physician can confirm the diagnosis when the patient has a low immune system, a history of upper respiratory tract infection or cold 1~2 weeks before the onset of the disease, sudden unilateral facial nerve palsy with taste disturbance in the anterior 2/3 of the tongue, auditory hypersensitivity, auricular and external auditory sensory loss, and pain in the affected mastoid region, and after excluding diseases with a clear etiology of peripheral facial palsy.
Differential diagnosis
Guillain-Barre syndrome This disease may have peripheral facial nerve palsy, often bilateral, and most patients have symmetrical paralysis of other cranial nerves and limbs. Cerebrospinal fluid examination 1 to 2 weeks after the onset of the disease shows separation of cerebrospinal fluid protein cells.
Lyme disease This disease may present as unilateral or bilateral lateral paresis with other manifestations of cerebral nerve involvement. There may be fever, headache, skin erythema, arthritis, and a history of exposure to high-risk environments or tick bites. Laboratory tests suggest a positive test for Burkholderia spirochetes.
Middle ear disease and complications The disease may present with fever, pain, and ear symptoms. Abnormalities are seen on otoscopy and CT of the temporal bone.
Tumors This disease presents with progressive facial nerve palsy, parotid swelling, localized pain, tinnitus, or ipsilateral hearing loss. tumor lesions (along the facial nerve or located in the internal auditory canal, pontocerebellar horn, parotid gland, temporal bone) are seen on MRI.
Diabetic neuropathy This disease is often associated with paralysis of other cerebral nerves, most commonly the motoneurone, abducens, and facial nerves, and may occur alone. Laboratory tests show abnormal blood glucose and glucose tolerance.
Stroke The disease may present as central facial palsy with limb paralysis or aphasia, without frontalis involvement. Cranial imaging may show associated lesions.
Facial nerve injury Most patients have a history of trauma or surgery (e.g. parotidectomy), and CT of the temporal bone reveals temporal bone fractures or facial nerve lesions.
Treatment
Drug treatment
Glucocorticoids These drugs can inhibit the inflammatory response of the facial nerve in the acute phase, thus reducing the degree of facial nerve compression by the facial nerve canal due to edema and thickening, as well as microcirculatory disorders. Therefore, glucocorticoids are the primary and main drugs for the treatment of this disease, but they should not be used for a long time.
Dexamethasone 10-20 mg/d can be given for 7-10 days as a course of treatment; or prednisone 1 mg/(kg?d), given orally in 2 doses for 5 days, followed by a gradual reduction in dosage for 7-10 days. In addition, they should be used with caution in patients with diabetes, tuberculosis, gastric ulcer and pregnant women or children.
Antiviral drugs These drugs interfere with herpes virus deoxyribonucleic acid (DNA) polymerase and inhibit DNA replication. Acyclovir, ganciclovir, etc. are commonly used.
B vitamins These drugs can promote the recovery of nerve myelin, and are administered as vitamin B1 100 mg and vitamin B12 500 μg intramuscularly, and can be replaced by oral B vitamin therapy at a later stage.
Other drugs Baclofen can reduce muscle tone and improve local circulation, and should be given orally in small doses (5 mg), 2-3 times/day, gradually increasing to 30-40 mg/d. Individual patients cannot tolerate the adverse effects of this drug such as nausea, vomiting and drowsiness.
Ginkgo biloba extract and other drugs are used to dilate blood vessels and improve microcirculation.
In addition, patients can apply eye ointment to the affected eye at night and protect the eye with an eye shield. When tears decrease, artificial tears can be applied in drops.
Rehabilitation exercises
Functional training and rehabilitation should be started as early as possible when the affected side muscles are slightly mobile, such as frowning in the mirror, raising the forehead, closing the eyes, showing the teeth, puffing the cheeks and whistling several times a day. Each time 10-15 minutes, supplemented by facial muscle massage.
Surgical treatment
Facial nerve decompression is feasible in some patients, but this method carries the risk of complications that can lead to seizures, deafness, cerebrospinal fluid leakage and facial nerve damage, and in severe cases, permanent hearing loss.
For severe facial nerve palsy with 2 years of onset without recovery, facial nerve-paraglottic nerve, facial nerve-subglottic nerve, or facial nerve-phrenic nerve anastomosis is feasible, but the efficacy is uncertain and is only indicated for severe patients. In addition, cosmetic surgery is also feasible in severe patients.
Other treatments
Chinese medicine treatment This method can play an auxiliary treatment role. Treatment with strong stimulation (e.g., acupuncture, etc.) is not recommended during the acute phase (1-2 weeks), and acupuncture can be used after the acute phase. Drugs to activate blood circulation and remove blood stasis have an auxiliary effect on improving microcirculation of facial nerve. Heat-clearing and detoxifying drugs can also be used for antiviral treatment.
Hot compresses, physiotherapy, massage, etc. In the acute stage, warmth therapy, magnetic therapy, electromagnetic therapy, ultrashort wave or microwave therapy can be used as adjunctive treatment. Physiotherapy, such as muscle massage and training, can be used during the recovery period. Facial muscle spasm can be treated with spastic muscle motor point block therapy (such as botulinum toxin injection, etc.).