Abstract
I N 1934 Dandy 2s stated that whatever the cause of trigeminal neuralgia might be, it must be located in the sensory . This statement was based on his experiences in finding tumors, aneurisms, or angiomas of the sensory in 23 of 215 cases of typical tic, and in finding other causes in 96 patients, such as an artery or a petrosal vein in contact with the root. In 1947 when Gonzalez-Revilla 59,6~ reviewed Dandy's material he found that 16 of the 160 cases of angle neurinomas, five of the 13 angle meningiomas, and l0 of the 13 cholesteatomas had had the typical pain of tic douloureux. GonzalezRevilla, 6~ using the suboccipital approach retrogasserian neurectomy, reported in 1962 that he found changes of a vascular nature in 40 %, tumors of the angle in 5.1%, platybasia in 2.8 %, and multiple sclerosis in 0.5 %. Stookey and Ransohoff 158 indicated that a sensory deficit was the most common finding in such cases. Certainly the presence of sensory defects not due to treatment of the trigeminal neuralgia, as by alcohol block, should suggest neoplasm, aneurism, or angioma. Nevertheless, there are many cases of absolutely typical tic with no sensory or other deficit produced by demonstrable organic lesions; the cholesteatomas are particularly noteworthy examples. Gardner ~4 suggested that this may be because of their extremely slow growth. Moreover, cholesteatomas rarely destroy nerve function but rather displace and surround the nerve roots. Taarnh~j's TM case of cholesteatoma led to his suggestion in 1952 that compression of the posterior was the etiological factor in tic. He had made the clinical diagnosis of probable cholesteatoma on his patient, a man of 31 years with an otherwise typical tic. He based his diagnosis on Olivecrona's 129 report of the syndrome of cholesteatoma of the angle causing typical third-division tic in young adults. The concept of compression at the dural foramen over the petrous tip had been adadvanced in 1937 by Lee, '~ who suggested that decompression might someday be performed by removal of the bony rim of the petrous pyramid. Olivecrona 12s later suggested that the anatomical angulation at this point, which increases with age, might be etiologic in trigeminal neuralgia. TaarnhCj TM performed his first decompression of the posterior tic douloureux on May 9, 1951. In 1954 he reported a group of 76 patients he had treated by this technique, 70 of whom had tic. 16~ He used a subtemporal intradural approach. He incised the dura over the cavum and carried the incision back through the petrosal sinus, then posteriorly for some centimeters, then medially through the free edge of the tentorium. He operated on five patients through a posterior fossa approach, of which more will be said later. Seventeen of his patients had had some hypesthesia preoperatively. None of these had normal sensation postoperatively. Within the first year postoperatively, seven of the patients experienced a return of pain; four of these were of sufficient severity to require reoperation. Love 116 had learned of TaarnhCj's operation from Norl6n and decided to carry out the decompression by the extradural approach using the same technique as section up to the exposure of the dura propria. The dura propria was left closed, however. The temporal dura was then incised, exposing a small portion of the undersurface of the temporal lobe and superior surface of the tentorium. The dense, tense, constrictive fibers overlying the posterior root were then divided. Of the 39 patients originally reported in 1954 by Love, 10 had not been relieved after a follow-up period of I to 13 months; but of these 10, only 3 were considered to have had true tic douloureux. Gardner and Pinto 5~ reported their first nine cases of decompression in 1953. They carried out their first operation using Taarnhr intradural approach but subsequently they used the extradural Frazier approach advocated by Love. They then suggested the idea of an artificial synapse in the sensory fibers where the nerve crosses the petrous apex. They suggested that a tactile stimulus is carried via the somatic afferents to the brain
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have