© Springer Science+Business Media Dordrecht 2016
Shi-Ting Li, Jun Zhong and Raymond F. Sekula, Jr. (eds.)Microvascular Decompression Surgery10.1007/978-94-017-7366-9_11. The History of Microvascular Decompression Surgery
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Department of Neurosurgery, Allegheny General Hospital, 420 East North Ave, Suite 302, Pittsburgh, PA 15212, USA
Neurosurgery is a very different surgical specialty from the days when this investigator was a research fellow and resident in the years 1957 through 1967. Technological advances have enabled most of these changes from an almost brutal surgical specialty with many poor results to a field wherein a normally sensitive human being can work happily and effectively. These advances, “the four factors,” include application of the binocular dissection microscope to surgery, clinical neurophysiology, neuroradiology imaging, and neuroanesthesia. These advances were all necessary for the work to be described below. Two other important applications of technology but not used here include advances in stereotactic surgery (i.e., focused irradiation) and endovascular techniques. Utilization of these four factors has enabled us to see and do things hitherto thought impossible or at least highly dangerous.
Over the years, starting in 1965, neurosurgeons were able to define a number of cranial nerve diseases caused by pulsatile vascular compression of the centrally myelinated (one or two exceptions) cranial nerves (Jannetta 1977). These entities occur as the arteries of the base of the brain elongate and loop about with aging, so that they impact the nerves. The brain also moves caudally in the posterior fossa with aging contributing to arterial and venous pulsatile compression (Jannetta 1967, 1968, 1975, 1997; Rand and Jannetta 1968)
The best known of the cranial nerve vascular compression problems are trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia (Rand and Jannetta 1968). Other entities include Meniere’s disease, vertigo, tinnitus (Jannetta 1975), and spasmodic torticollis (Jho and Jannetta 1995).
More recently, beginning in 1973 and first published in 1979, brain stem vascular compression was found to be associated with essential hypertension (Jannetta and Gendell 1979; Segal et al. 1979), type 2 diabetes (Jannetta and Hollihan 2004; Jannetta et al. 2010), and most recently Parkinson’s disease (Jannetta et al. 2011). Other entities not yet published include cardiac arrhythmias (left and right heart), hypercholesterolemia and hyperlipidemias, and cerebellomedullary auto-compression syndrome (“hypoplastic posterior fossa” as described by Rosner). The latter is frequently but not always associated with medullary vascular compression.
We will not consider some of these entities in order:
1.1 Trigeminal Neuralgia
Early work by Dandy (1934) and Gardner (1962), concerning vascular compression and other abnormalities of the root entry zone of the trigeminal nerve, forms the basis for our current concepts of the etiology and definitive treatments of this disabling symptom called trigeminal neuralgia (TN). Dandy, starting in 1932, noted abnormalities of the dorsal root in a progressively larger percentage of his patients with TN. This innovative surgeon sectioned the portio major at the brain stem in these patients. He was able to treat TN without giving complete numbness by preserving fascicles which he described and called “accessory sensory fascicle” during the nerve section. In 5.6 % of patients where an extra-axial tumor was the cause of TN, he removed the lesion as treatment. He did not treat the TN by vascular compression. Indeed, it was impressive that he was able to see vascular compression by “normal” (although perhaps elongated) arteries and veins in 60 % of his patients without magnification. Gardner further elaborated upon abnormalities of the dorsal root of the trigeminal nerve and lucidly opined upon the pathophysiological mechanisms involved.
Others more recently described gross lesions such as aneurysms, tumors, and other abnormalities in the cerebellopontine angle of patients with TN. Despite these publications, there was little or no acceptance of this concept until recently. Many reasons for this lack of acceptance may be given. Some of them may include relatively primitive technology, lack of verification by others, inadequate documentation of findings, and rare definitive treatment. However, with the development of safer operative and anesthetic techniques for surgery of the cerebellopointine angle, the use of microsurgical techniques, photographic and videotape documentation findings and definitive treatment, and the concepts of root entry zone abnormality as an etiology of TN and microvascular decompression (MVD) as therapy have had wide acceptance in recent years.
The procedure MVD appears to be indicated in patients of any age with intractable tic douloureux who are in reasonably good health and who are not responding to medical therapy (Sekula et al. 2008, 2011). Almost all of our patients have had a course of carbamazepine which has been stopped for one reason or another. It is unfortunate that the elderly and frail patients appear to be more sensitive to the side effects and complications of this drug. The procedure is contraindicated in those who are in poor health, but the usual older person in generally good health appears to tolerate the procedure easily. A prior unsuccessful procedure or a recurrence is not a contraindication to operation.
The most common situation in lower facial TN is that the superior cerebellar artery is found coursing cephalad around the pons and then bifurcating, with the medial and lateral branches impinging upon the anterosuperior aspect of the entry zone of the nerve, the motor proprioceptive fascicle side, as it loops back to the brain stem and cerebellum. After sharp and blunt dissection of the widely opened arachnoid from the nerve and the visible part of the artery, the arterial loops are gently teased out from between the trigeminal nerve and the pons. The loops are usually longer in older patients and especially in those with long-standing tic douloureux. They must be manipulated carefully. The arterial loops may be quite adherent to the nerve or easily separable. Perforating branches to the pons have accommodated in length to the loop and will not tear with gentle manipulation of the vessels over the trigeminal nerve.
In the first division TN, a blood vessel is seen compressing the inferolateral portio of the trigeminal nerve entry zone at the pons. The most common cause of isolated V2 neuralgia is compression by the trigeminal vein coursing alongside the nerve. This may run parallel to the nerve.
Quality of survival is excellent in the vast majority of patients as they remain free of pain with no numbness or paresthesias to remind them of their prior syndrome. This author may be accused of bias regarding quality of survival with this procedure versus a destructive operation. Others, without a vested interest, have compared procedures and state strongly that MVD is the procedure of choice in TN.
1.1.1 Discussion
The concept of neurovascular compression as the common cause of trigeminal neuralgia has become generally accepted in recent years. The early reports of Gardner (VF) have been well supported but with inadequate technology. Jannetta reported his experience with vascular findings in 1967 (Jannetta 1968, 1975), but at this time, he had performed only one MVD for TN (with Rand), although he had done a similar procedure for hemifacial spasm prior to this experience. The next verification of the vascular etiology and of the treatments by vascular decompression was by Petty in 1976, and others have continued to report their expanding series. Apfelbaum compared percutaneous radiofrequency lesioning (RFL) for trigeminal neuralgia with MVD and in 1977 (Jannetta 1975) published a large series where the quality of survival and results was clearly superior to the destructive procedure. It must be remembered that destructive procedures may be well indicated in many patients, the frail and elderly.
Vascular compression of the trigeminal nerve can now be clearly stated as causal of almost all cases of trigeminal neuralgia. As operative experience in relieving this compression grows, the results of operation should improve so that relief of the pain with little or no sequelae is a standard goal.
Glossopharyngeal neuralgia is similar to TN except that the pain is tonsillar, in ear, or within the throat. Both cranial nerve IX and X must be decompressed at the brain stem. Results are similar to TN (Resnick et al. 1995).
1.2 Hemifacial Spasm
Hemifacial spasm (HFS) is a symptom complex of hyperactive dysfunction of the facial nerve caused by abnormality at the root entry zone (REZ) of the nerve. This abnormality, almost always vascular cross-compression, most commonly occurs as a result of the aging process just as in other cranial nerves which are subject to hyperactive dysfunction. This problem is well known to the neurosurgical community (Jannetta 1968, 1977; Moussa et al. 2006; McLaughlin et al. 1999; Ruby and Jannetta 1975; Nielsen and Jannetta 1984; Moller and Jannetta 1985).
1.2.1 Clinical-Pathological Correlations
Two major points may be made regarding clinical findings with the pathological abnormality. First, the site of the vascular cross-compression is at or proximal to the REX (the Obersteiner-Redlich Zone) of the nerve. At this point, the myelin of the central nervous system provided by oligodendroglia is replaced by peripheral myelin provided by Schwann cells. By ultrastructural techniques, defects in the myelin are noted to be present here. Second, classical HFS is caused by a blood vessel on the anterior-caudal aspect of the nerve REZ. Atypical HFS is almost always caused by a blood vessel on the posterior-rostral aspect of the REZ. This compression may be venous rather than arterial (i.e., on the intramedullary facial nerve) and may be quite caudal on the medullary side of the pontomedullary junction.
Operative findings show that the abnormality is usually arterial. Multiple vessels, often lying parallel and with one pushing another into the REZ, are common. The posterior interior cerebellar artery is the most common causative vessel.
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