The Facial Nerve (The Seventh Cranial Nerve) Three theories exist to explain the facial nerve dysfunction found in<unk> . The first proposed theory is ephaptic transmission, which is electrical activity crossing from one demyelinated neuron to another resulting in a false synapse. The second theory involves abnormal activity of axons at the facial nerve root end zone secondary to compressive damage/demyelination. The third theory or "Kindling theory" involves increased excitability of the facial nerve nucleus due to feedback from a damaged facial nerve. It is generally accepted as compression of the facial nerve by vessels of the posterior circulation. In detail compression of the seventh cranial nerve by a dolichoectatic (a distorted, dilated, and elongated) vertebral artery is accepted to be the general cause of<unk> . Less than 1% of cases are caused by tumor.<unk>  is much more common in some Asian populations. Several families with<unk>  have been reported, suggesting a genetic etiology or predisposition in some cases. There appears to be an autosomal dominant pattern of inheritance in these families with low penetrance, and except for a younger age at onset, the clinical features overlap with the idiopathic cases. Evaluation of single-nucleotide polymorphisms in genes related to vascular change causing compression of blood vessels did not show an association with<unk> . Clarifying the role of genetic susceptibility in<unk>  may help to better understand the pathogenesis of this disease.
Hemifacial spasm
Trismus
Anismus
Facial weakness
Barodontalgia
Strabismus
Oscillopsia
Palatal myoclonus