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Hemifacial spasm can be cured by microvascular decompression (MVD) operations of the root exit zone of the facial nerve. This fact was the basis for the (“ephaptic”) hypothesis stating that the anatomical location of the pathology that generates the signs of HFS, spasm in the mimic muscle on one side of the face and synkinesis, was the root exit zone of the facial nerve. However, later intracranial recording from the facial nerve provided strong experimental support of a different hypothesis about the pathology of HFS, namely, that the anatomical location of the pathology is the facial motonucleus.
Intraoperative measurements of neural conduction times provided evidence against the “ephaptic” hypothesis and showed evidence that hyperactivity of the facial motonucleus could explain the symptoms of HFS. Studies of the blink reflex supported the hypothesis that the facial motonucleus is hyperactive in people with HFS. The results of animal experiments showed that signs of HFS could be caused by facial motonucleus hyperactivity.
It was hypothesized that the abnormalities in the facial motonucleus in HFS were caused by activation of maladaptive neuroplasticity that was activated by the irritation of the root of the facial nerve by a blood vessel. These findings were supported by the results of animal studies.
Since a similar close contact with a blood vessel is present in at least 50 % of individuals who do not have any symptoms of spasm, it was concluded that a second factor in addition to vascular contact with the facial nerve root must be present in order to create the signs of HFS.
MVD operations have a success rate of over 85 %, and when combined with monitoring of the abnormal muscle contraction, success rates of 97 % have been reported. No other treatment has been shown to have noticeable success in relieving the signs of HFS.