Rehabilitation Therapy of Neurological Training of Facial Paralysis

Abstract

Facial paralysis is vulgo of facial neuritis and facioplegia, which is also called Bell disease [1]. It is non-purulent inflammation of facial nerve, which usually occur in winter and spring. The pathological change is neural edema, degeneration of myelin sheath and axon to varying degrees. The patients are recovered to varying degrees in 2 months after disease attack and some patients are recovered 1 year later. Some got persistent sequelae.

• 1. Causes: Facial neuritis can be induced by various factors.

  Facial neuritis usually is induced by cranial nerve diseases. This may be because facial nerve canal is a long bony pipeline. If petrosal bone develops abnormally, there usually is facial nerve canal stenosis, which is the internal pathogenic factor of facial neuritis. The external pathological factor of facial neuritis remains unclear. The early pathological change is edema of facial nerve, degeneration of myelin sheath and axon to varying degrees. The reason may be that cold air blast induces nutritional microvascular spasm of facial nerve and then lead to ischemia and anoxia of local tissue. Someone think that it is related to virus infection [2]. However, until now, no one can isolate virus. In recent years, some reports think that it may be a immunoreaction. Ramsay-Hunt Syndrome is induced by infection of herpes zoster virus and inflammation of geniculate ganglion and facial nerve.

  In short, the factors that can affect functional nucleus of facial nerve and neural axon functions can lead to dysfunction of facial muscles dominated by them such as infectious, compressive, traumatic, physical and neurogenic factors.

  Infectious factor accounts for 42.5% of the total number. It is the herpes zoster virus in dormant state, which usually hides in sensory ganglion of facial nerve. The virus is activated when local immunity is low. It can also be induced by inflammatory diseases such as meningitis, mumps, influenza, scarlet fever, malaria, multiple cranial neuropathy, local infection and otogenic infection (otitis media, labyrinthitis, mastoiditis).

  Compressive factor can induce facial neuritis, which is usually observed in tumors such as acoustic neuroma, parotid gland and primary acquired cholesteatoma and accounts for 5.5% of the total number.

  The common traumatic factors of facial paralysis include temporal bone fracture, facial trauma, surgery and injection of neurotoxic drug in facial nerve distribution area and account for 8.2% of the total patients.

  Neurogenic facial paralysis accounts for 13.5% of the total patients, which is usually induced by cerebrovascular disease, encephalic and non-traumatic neurogenic disease. If cold wind blows the face for a long time, undercooling in face can directly stimulate local nerve trophic vessels and induce spasm, which can induce ischemia and edema of neural tissue and dysfunctions. It is the common factor to induce facial paralysis.

  In addition, poisoning, metabolic disturbance such as diabetes mellitus and vitamin deficiency, vascular function insufficiency and congenital facial nucleus hypoplasia is one of the pathological factors.

• 2. Types: Facioplegia is divided into peripheral type and central type. The majority is peripheral type.

  • (a) Central type is paralysis of muscle in lower part of the face on the offside of lesion induced by injury of supranuclear tissue includes cortex, cortex and brainstem fiber, medullary triangle and pons, which are usually observed in cerebrovascular disease, brain tumor and encephalitis.

  • (b) Peripheral type is paralysis of all facial muscles in the ipsilateral of the lesion induced by injury of facial nerve nucleus or facial nerve, which is usually observed in catching cold, ear or meninx infection, peripheral facioplegia induced by neurofibroma. In addition, there is dysgeusia in the front two third of tongue and unclear speaking.

• 3. Dysfunctions mainly are motor and sensory dysfunctions of facial muscle.

  According to the motor dysfunction part of facial muscle, there are different clinical manifestations such as palpebral fissure enlargement, unable to frown or close eyes, forehead wrinkle disappearance, grinningly, agitating cheek and unable to whistle. There are also clinical manifestations such as forehead wrinkle disappearance, palpebral fissure enlargement, nasolabial groove becoming shallow, droop, stretching face to offside, lacrimation or salivation.

  The dysfunctions are different in different injured part of facial nerve. It can be summarized as follows:

• (a) Facial nerve branch below stylomastoid foramen is injured, which can induce peripheral facial paralysis. The main manifestations are forehead wrinkle disappearance in injured side, unable to crinkle forehead and frown, palpebral fissure enlargement, unable to close or close incompletely, Bell syndrome (eyeball rotate upward and outside when closing eyes and white sclera is exposed), nasolabial groove becoming shallow, corner of the mouth skews to uninjured side, corner of the mouth deviate to uninjured side when exposing teeth, air leakage in agitating cheek or whistle, food retention in teeth buccal space when eating.

• (b) Facial nerve branch above tympanic cord is injured. Besides peripheral facial paralysis, there is dysgeusia in two third front of tongue in the ipsilateral.

• (c) Facial nerve branch above stapedius is injured. Besides peripheral facial paralysis and dysgeusia in two third front of tongue in the ipsilateral, there is hyperakusis.

• (d) Geniculate ganglion is injured. Besides peripheral facial paralysis, dysgeusia in two third front of tongue in the ipsilateral and hyperakusis, there is pain in mastoidea, hypaesthesia of auricle and external auditory canal, herpes of external auditory canal or tympanic membrane, which is called Hunt syndrome [3].

• 4. Sequelae: Facial dysfunction still exists half a year after the disease.

  The main signs include no raising eyebrow movement or incomplete raising eyebrow movement, incomplete opening eyes, corner of the mouth going upward when raising eyebrow, stretching the corner of the mouth when closing eyes, eyes becoming small when agitating mouth (synkinetic movement of mouth and eye), shallow nasolabial groove, facial stiffness, food retention, tears, secondary prosopospasm and denervated muscle atrophy.

  Sequelae are due to delay of the illness or improper therapy method. Some reports deem that half a day after attach is the best therapeutic opportunity. Nerve in injured side is not recovered timely, which lead to incomplete conduction of neural impulse or conduction generalization. In addition, some sequelae are due to irreversible injury of facial nerve.