What Is Cn Vii Palsy?

Botulinum toxin injections for facial nerve palsy

The motor and sensory root of the nerve are in the intracranial portion and travel through the internal acoustic meatus to the temporal bone. The lacrimal glands are responsible for parasympathetic innervation. The sensory functions of CN 7 are due to the rise of the greater petrosal nerve that travels through the foramen.

Patients should be asked about their past skin cancer history since it can lead to facial pain and eventually lead to facial nerve palsy. Medical management should be pursued if conservative management fails. It is important to inject botulinum toxin into the upper lid because it can cause ptosis of the upper lid for up to 6 weeks.

Facial Nerves

The facial nerve goes from the brain stem to the fossa and then to the temporal bone. The nerve runs through the facial canal into the labyrinthine, tympanic, and mastoid segments. The second bend in the facial nerve is called the pyramidal eminence.

The nerve that goes to the stapedius muscle and the tympani goes in the temporal part of the facial canal. The taste fibers of the anterior two thirds of the tongue are supplied by the tympani. The submandibular ganglion has postsynaptic fibers.

The facial nerve has cell bodies in the nucleus or ganglia. The taste sensation is caused by the cell bodies for the afferent nerves. The superior salivatory nucleus contains the cell bodies for the parasympathetic efferent nerves.

Tastes of Facial Fate

The key to detecting subtle signs of weakness in muscles is to watch carefully. The blink, nasolabial folds, and corners of the mouth are important. Asymmetry is the clue to weakness and is best seen when the patient is not aware of it.

The tastes are bitter, sweet, sour and salty. There are disorders of sweet or salty taste. If the patient's eyes are closed, take a tongue blade and spread a small amount of salt or sugar on the side of the tongue.

The patient should tell you the substance's identity. If you want to repeat the test on the other side, rinse the mouth thoroughly. The lower facial muscles are paralyzed due to the bilateral supranuclear innervation of the upper muscles.

It is difficult to confirm weakness. Many normal individuals have mild lower facial asymmetries, making interpretation difficult. The characteristics of the structures involved in the disease make anatomic localization of the lesions possible.

The location of the clinical manifestations is given in Table 62.4 Refer to Figure 62.1 to see where the lesions occur. Patients with a disease like Addison's disease, or a condition like pituitary insufficiency, have an increased ability to detect the four primary tastes.

Preventing Corneal Drying by using natural tears, isotonic saline drops and patchy patches

Patients may feel a heavy feeling in their face. The affected side becomes flat and expressionless, and the ability to blink, grimace, and wrinkling the forehead is limited or absent. In severe cases, the palpebral fissure widens and the eye does not close, which can cause irritation to the eye and drying of the cornea.

The other disorders that cause peripheral facial nerve palsy take longer to develop than the one that causes facial nerve palsy. If patients have any other neurologic symptoms or signs, they should have an Magnetic Resonance Investigation done. For all patients, a chest x-ray is done, and the patient's blood pressure is measured.

The blood sugar is measured to check for diabetes. The benefits of viral titers are not helpful. The extent of nerve damage is what determines outcome in facial nerve palsy.

Full recovery occurs within several months if function remains. Nerve conduction studies and electrical studies are done to help predict outcome. If nerve branches in the face retain normal excitability to supramaximal electrical stimulation, the likelihood of complete recovery is about 80%.