Central facial palsy.
Damage to any part of the superior facial nucleus pathway can cause central facial palsy, the most common place of damage being the internal capsule. Possible causes are: occlusion of the internal carotid artery system, especially of the main trunk and branches of the middle cerebral artery, intracranial hemorrhage due to hemangioma or hypertensive vascular lesions, and intracranial tumors.
In central facial nerve palsy, the muscles in the upper part of the face do not appear paralyzed, because the eyes are closed, the eyebrows are raised, and the frown is normal. The depth of the facial forehead lines is equal to that of the contralateral side, and the height of the eyebrows and the size of the lid fissure are the same as those of the contralateral side. In central facial nerve palsy, the lower facial muscles are paralyzed, i.e., the buccal muscles, orbicularis oris muscle are paralyzed, so the nasolabial fissure on the patient’s side becomes shallow in the resting position, the corners of the mouth droop, and the corners of the mouth are distorted to the healthy side when the teeth are shown.
The facial asymmetry is not obvious in mesostyle facial nerve palsy, and it is extremely rare to see it migrate to facial muscle spasm. Central facial palsy is often accompanied by other signs of hemiplegia, such as abnormal tendon reflexes and Babinski’s sign.
Peripheral facial palsy.
It refers to idiopathic facial nerve palsy, also known as Bell’s palsy, which is a unilateral peripheral facial nerve palsy of unknown origin and acute onset. It is a common disease.
Clinical manifestations: It can occur at any age, but is slightly more common in males. The onset is usually acute, with a peak within a few hours or 1-2 days. There may be pain at the angle of the jaw or behind the ear at the beginning of the disease. The main symptom is paralysis of the facial expression muscles on one side. When trying to close the eye, the eye on the paralyzed side turns upward and outward, revealing the white sclera, which is called the phenomenon of beriberi. The nasolabial fissure on the sick side becomes shallow, the corners of the mouth droop, and the teeth are crooked to the healthy side when exposed. If the lesion is above the bulbar involvement of the facial nerve, there may be ipsilateral loss of taste sensation.
Diagnosis and differential diagnosis: The diagnosis is based on the acute onset of peripheral facial palsy. However, it needs to be differentiated from the following diseases.
1, Green-Barre syndrome can have peripheral facial palsy, but mostly bilateral, with symmetrical limb paralysis and cerebrospinal fluid protein-separation phenomenon.
2. Otogenic facial nerve palsy complicated by various otitis media, vaginitis, mastoiditis, etc., mostly with specific symptoms and history of the original disease.
3. Peripheral facial palsy caused by tumors or meningitis in the posterior cranial fossa mostly has a slow onset and manifestations of other cranial nerve damage or primary disease.
There are many causes of peripheral facial palsy, which are summarized as follows.
(1) Infectious lesions herpes zoster of the ear, meningitis, mumps, scarlet fever, malaria, multiple cranial neuritis, and local infections.
(2) Otogenic diseases such as otitis media, labyrinthitis, mastoiditis, septic inflammation of the temporal bone.
(3)Tumor basilar artery aneurysm, skull base tumor, auditory neuroma, jugular venous bulb tumor.
(4)Trauma skull base fracture, facial trauma.
(5) Intoxication such as alcoholism.
(6) Metabolic disorders such as diabetes mellitus, vitamin deficiency.
(7)Vascular insufficiency
(8) Congenital facial nucleus hypoplasia
In central facial palsy, the muscles in the upper part of the face do not appear paralyzed; therefore, the eyes are closed, the eyebrows are raised, and the frown is normal. The frontal lines are equal in depth to the contralateral side, and the height of the eyebrows and the size of the lid fissure are not different from the contralateral side. It is often differentiated from peripheral facial palsy based on this point.
The distinction between central and peripheral facial palsy is obvious in those with obvious paralysis, but difficult in those with very mild paralysis. One can rely on the following aspects to differentiate: firstly, expression movement, central palsy does not show paralysis when crying or laughing, while peripheral palsy is more obvious; secondly, palmar chin reflex, central palsy is present or hyperactive, while peripheral palsy is absent or diminished, but this method is not very reliable; thirdly, the most reliable method is to determine by linking other physical signs.
For example, when it is not easy to determine whether the facial palsy is central or peripheral, if the patient has a combination of mild paralysis of the upper and lower limbs on one side, and the paralyzed upper and lower limbs are on the opposite side of the facial nerve paralysis, the facial palsy must be peripheral; if the paralyzed upper and lower limbs are on the same side of the facial nerve paralysis, the facial palsy must be central, and it is similar to this when it is associated with ophthalmic muscle paralysis.