The facial nerve (VII-7^th) is the most commonly affected motor nerve. Facial nerve is responsible for controlling movement of the face. It is a much smaller nerve than the trigeminal nerve and is intimately related to the acoustic nerve (VIII-8^th) responsible for hearing and balance.  The facial nerve and the acoustic nerve emerge from the brainstem in very close proximity and share a confined space before entering the bone into the inner ear through a common opening called the internal auditory canal.

Figure 1: The close relationship of the facial (VII) and acoustic (VIII) nerve are demonstrated.  The two are shown here separated by a black line, but in reality they are superimposed one on top of the other. Compression of the facial nerve most often occurs directly at the level of the brainstem where it emerges into the fluid space. This is commonly not recognized by inexperienced surgeons.  The nerve is located under and deep to the hearing and balance nerve making access particularly challenging.  The blood vessel causing the compression maybe small and even a vein maybe responsible.

Figure 2: a small artery is seen (circled area) causing compression of the facial nerve (VII) at the origin of the brainstem. It is postulated that the compression creates stimulation of the nerve in a reverse direction (retrograde transmission).  This results in formation going backwards into the origin of the nerve (Facial nucleus). The nerve unable to process the unusual stimulation responds by firing creating uncontrolled facial twitching.

The development of the symptomatic twitching is generally predictable. It initially starts in the eye lid occurring primarily with activity and movement.  Eventually the twitching marches down the face through the cheek, jaw and into the neck.  The twitching becomes uncontrolled and occurs even when the patient is trying to quietly rest the face.  In more severe cases the twitching progresses to sustained facial contractures referred to as “tonus phenomena”.  Tonus phenomena behaves like a “Charlie horse of the face” creating periods where the face becomes locking in place with eyes closed, cheeked contracted and jaw clenched. In addition to being painful this can be dangerous as it creates uncontrolled loss of binocular vision by closing one eye.  These situations can lead to sudden and unpredictable loss of depth perception and 3-dimensional vision.

Treatment for Hemifacial Spasm can also be divided into the 3 general categories discussed for Trigeminal Neuralgia:

• Medical Therapy
• Ablative Therapy
• Microvascular Decompressio

Medical Therapy:

Several drugs have been attempted to treat Hemifacial spasm with little consistent success.  Most commonly these drugs fall into the general category of muscle relaxants or sedatives.  Unlike Trigeminal neuralgia, Hemifacial Spasm is rarely responsive to medication on a consistent basis.

Ablative Therapy:

Botox therapy has been used to create a functional chemical block between the fine nerve endings of the facial nerve and their insertion into the muscles of the face.  The Botox is applied to the muscles by a series of injections.  Over time the Botox has a potential of reduced efficacy requiring more frequent injections to provide ongoing control. Often this will require injections at 9, 6, then 3-month intervals. The effects of Botox may potentially create facial weakness overtime.

Microvascular Decompression:

This procedure is intended to move the offending vessel and create a cushion or pad between the facial nerve and the offending blood vessel.  The decompression addresses the root cause of Hemifacial Spasm by dealing with vessel that is causing the compression.  The approach involves a minimally invasive key whole retromastoid approach.  This approach involves making a small incision behind the ear and a keyhole opening in the bone. Using the natural space that is created when the cerebrospinal fluid is drained direct access to the nerve and offending vessel is provided.  Using this space there is little need for manipulation of the brain and nerve.  Small pads of Teflon are placed between the facial nerve and pulsating vessel. 
View Microvascular Decompression surgery 

Over 90% of patients benefit from significant relief of their HFS following an MVD. The risk of hearing loss on the in one ear (the side of the HFS) can range from 1-6%.

Figure 3: A small keyhole craniotomy (shadowed circle) is created behind the ear and a path (arrow) using the space created by the drainage of the CSF is used to access the facial nerve and compressing artery.  The artery is carefully mobilized using a microscope, endoscope or combination of both. Small pieces of Teflon (white circles) are placed to keep the vessel away from the nerve.