History
The earliest descriptions about hemifacia spasm is by Shultze in 1875 and Gowers in 1899. The etiology of hemifacial spasm and location of the abnormality have been debated for more than a century. Surgical treatment for hemifacial spasm in the early 20th century included neurolysis (destruction of nerve tissue), stretching the facial nerve (seventh cranial nerve), and high-pressure irrigation of the nerve with lactate ringer's solution. The medical regimens of that time involved injection of the nerve with ethanol, electrical stimulation, application of toxic compounds (nitrate of silver, zinc, arsenic, bromides) as well as medications such as Dilantin or other anticonvulsants.
Additional advances in understanding the etiology and improving treatments for hemifacial spasm did not occur until the mid-seventies. In 1977, 47 cases of hemifacial spasm underwent microvascular decompression of the facial nerve using the operating microscope. The results illustrated nerve-vessel conflicts (or cholesteatoma) to be located at the root exit zone of the facial nerve in all cases. The root exit zone is where the central glial axonal insulation of the nerve ends and the peripheral nerve axonal myelination begins. Biopsies of the root exit zone demonstrated degeneration of axons, denuded axis cylinder and interrupted myelin. The results of the experiment strengthened the theory that vascular compression of the facial nerve was the primary cause of hemifacial spasm, and proposed a specific region of the facial nerve where the effects of longstanding compression results in nerve dysfunction.
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