J Neurosurg 75:783-786, 1991
Trigeminal neuralgia caused by compression from arteries transfixing the nerve Report of three cases HARUHIKO TASHIRO, M.D., AKINORI KONDO, M.D., IKUHIRO AOYAMA, M.D., K l v o s m NtN, M.D., KATSUMI SHIMOTAKE,M.D., TATSUYA NISHIOKA,M.D., YOSHIAKI IKAI, M.D., AND JUN TAKAHASHI,M.D.
Department of Neurosurgery, Kitano Medical Research Institute and Hospital, Osaka, Japan ~" The authors present three patients with trigeminal neuralgia due to compression by an artery that transfixed the sensory root of the fifth cranial nerve. These cases represented 0.8% of 384 patients with trigeminal neuralgia treated by microvascular decompression at the authors' clinic during the past 12 years. In the remaining 381 cases, the compressing vessels were successfully removed from the trigeminal nerve without much difficulty, for an initial cure rate of 94.3%. In the three cases reported, however, the compressing artery penetrating the nerve could not easily be maneuvered away from the nerve. In the first two cases, partial rhizotomy perpendicular to the axis of the nerve at the site of arterial transfixion made it possible to separate the artery from the nerve. However, these two patients developed postoperative facial sensory impairment. In the third case, rhizotomy was performed longitudinal to the axis of the nerve at the site of arterial transfixion, making it possible to reposition the artery peripherally beyond the root entry zone of the nerve without causing any postoperative sensory deficits of the face. No recurrent pain has developed in more than 289 years since surgery in any of these three cases. When performing microvascular decompression surgery on patients in whom the compressing artery penetrates the nerve, the technique used in our third patient is the procedure of choice. KEY WORDS
9 trigeminal neuralgia
RIGEMINAL nerve decompression was first used by Gardner and Sava4 as a surgical treatment for trigeminal neuralgia and was greatly improved and popularized by Jannetta 5 after the introduction of microsurgical techniques. We have performed trigeminal nerve decompression surgery in 384 patients with trigeminal neuralgia during a 12-year period from 1977 to 1989, with an initial recovery rate of 94.3%. In this series, there were three cases (0.8%) in which the compressing vessel, the superior cerebellar artery (SCA) or the anterior inferior cerebellar artery (AICA), transfixed the trigeminal nerve. The standard vascular decompression procedure, which consists of separating the offending vessel from the nerve, was greatly complicated in these cases because of the unusual course of the vessel. Since passage of the compressing vessel through the trigeminal nerve is an extremely rare cause of trigeminal neuralgia, we decided to report these three cases and discuss the surgical procedures employed.
T
J. Neurosurg. / Volume 75/November, 1991
compression
9 rhizotomy
9 root entry zone
Case Reports
Case 1 This 50-year-old woman had experienced severe pain on the fight side of her face for about 10 years. Such treatments as oral carbamazepine uptake and nerve block had failed to provide complete pain relief. Examination. At admission, she reported pain in the areas of the fight second and third divisions of the trigeminal nerve; there were no other abnormal neurological symptoms. Operation. A fight retromastoid suboccipital craniectomy was performed. Immediately after emerging from the pons, the portio major of the trigeminal nerve was pierced by a looped AICA passing from its medial aspect below to its lateral aspect above (Fig. 1). The SCA was also compressing the trigeminal nerve superomedially in the same area, causing strangulation of the nerve between these two blood vessels. We suc783
H. Tashiro, et al.
FIG. 1. Intraoperative photograph (h~/i) and drawing (right) of the pathology in Case 1. The right anterior inferior cerebellar arte~ ~hort open arrow) presses on the sensory, root of the trigeminal nerve (long open arrow). The closed arrow points to the site of pressure on the portio major of the right fifth cranial nerve.
ceeded in releasing the SCA from the trigeminal nerve, but it was impossible to free the nerve from the AICA, which was very crooked in the area where it transfixed the nerve. We therefore performed a partial rhizotomy on a rather small portion of the portio major of the trigeminal nerve lateral to the area transfixed, freeing the vessel; we could then reposition the vessel laterally. As the final step in the decompression procedure, prostheses were placed between the brain stem and the two freed vessels. Postoperative Course. The patient suffered loss of nociception in the area of the first and second divisions of the trigeminal nerve on the fight side and tactile hypesthesia in the area of the third division; however, her trigeminal neuralgia was completely relieved. Three years postoperatively, her tactile disorder has improved somewhat, and there has been no recurrence of the trigeminal neuralgia.
Case 2 This 55-year-old man had experienced persistent pain in the left side of the face and oral cavity for about 5 years. His pain was relieved for 2 years by a trigeminal ganglion block, but when it recurred, a second block proved ineffective. Examination. At admission to our department, no abnormalities other than hypertension and neuralgia in the areas of the left second and third divisions of the trigeminal nerve were noted. Operation. A left retromastoid suboccipital craniectomy was performed, and the SCA and AICA were found to be compressing the trigeminal nerve. The SCA was pressing on the entry zone of the portio major of the trigeminal nerve superomedially; the AICA, forming a loop bulging superiorly, pierced one-third of the medial aspect of the entry zone of the portio major and compressed this portion of the nerve (Fig. 2). After freeing the SCA from the nerve, we performed a rhizotomy parallel to the axis of the trigeminal nerve 784
peripheral to the portion penetrated by the AICA and attempted to move the AICA peripheral to what appeared to be the Obersteiner-Redlich zone. This maneuver proved to be impossible, and we were forced to perform a one-third partial rhizotomy on the medial side of the trigeminal nerve in the portion penetrated by this vessel. We were then able to free the penetrating vessel from the nerve and inserted a prosthesis between the vessel and the brain stem; this succeeded in adequately decompressing the trigeminal nerve. Postoperative Course. The patient's trigeminal neuralgia disappeared. Mild tactile hypesthesia was noted in the area of the second division of the nerve. At 289 years after surgery, tactile hypesthesia is much improved and there has been no recurrence of pain.
Case 3 This 67-year-old woman had a 7-year history of pain in the area of the left second and third divisions of the trigeminal nerve. Temporary relief was obtained with a trigeminal nerve block but, because the pain recurred, she requested surgery. Examination. On admission, there were no abnormal findings other than trigeminal neuralgia of the left second and third divisions of the nerve and hypertension. Operation. A left retromastoid suboccipital craniectomy was performed. The SCA was found to bulge inferiofly in a loop and to penetrate the center of the portio major of the trigeminal nerve at its zone of entry from its medial aspect below to its lateral aspect above. It was very crooked in the area where it transfixed and compressed the nerve. Since it was impossible to free the compressing vessel from the nerve, we performed a partial rhizotomy longitudinal to the axis of the nerve from the area of vessel penetration toward the periphery, then moved the SCA approximately 4 to 5 mm peripheral to the entry zone of the portio major, to a position believed to be beyond the root entry zone (Fig. 3). J. Neurosurg. / Volume 75/November, 1991
T r i g e m i n a l n e u r a l g i a d u e to t r a n s f i x i n g a r t e r i e s
Fl(;. 2. Intraoperative photograph (left) and drawing (right) of nerve compression in Case 2. The left anterior inferior cerebellar artery (short open arrow) presses on the sensory root of the left tfigeminal nerve (long open arrow). The closed arrow points to the site of impingement on the portio major of the left fifth cranial nerve.
Postoperative Course. The patient's trigeminal neuralgia disappeared and there were no complications such as facial sensory impairment. At present, -2 years postoperatively, there have been no signs of recurrence. Discussion
Pathogenesis Various hypotheses have been proposed as to the etiology of trigeminal neuralgia. Gardner, 3 believing nerve compression was caused by vessels at the entry zone of the trigeminal nerve, succeeded in relieving pain by freeing the blood vessel from the nerve and decompressing it. Jannetta 5 improved the procedure by using microsurgical techniques. In our own experience comprising 384 cases of trigeminal neuralgia in which we have performed decompression surgery, pain has
completely disappeared after surgery in 94.3% of cases. Thus, we believe that the etiology oftrigeminal neuralgia is vascular compression of the nerve in the Obersteiner-Redlich zone. The question arises as to why such nerve dysfunction develops with increasing age. We have investigated the vascular structure of the vertebral artery system of patients with trigeminal neuralgia and hemifacial spasm, and found that the diameter of either the left or the right vertebral artery enlarges with age. It appears that the hemodynamic effect of long-term high blood flow through the enlarged artery, hypertension, and arteriosclerotic changes produce crookedness and tortuosity of the artery and that the crooked vessel gradually compresses the nerve. In our three patients in whom the compressing vessel transfixed the nerve, symptoms of trigeminal nerve
FIG. 3. Drawings of the intraoperative findings in Case 3. a: The left superior cerebellar artery (short open arrow) compresses the portio major of the fifth cranial nerve (long open arrow). The closed arrow indicates the site of impingement on the ponio major, b: Selective partial rhizotomy of the portio major was performed longitudinal to the axis of the nerve (short arrow). The superior cerebellar artery was held away from the peripheral part of the Obersteiner-Redlich zone of the fifth nerve by a prosthesis (long arrow). J. Neurosurg. / Volume 75/November, 1991
785
H. Tashiro, et al. compression did not develop until the patient reached a certain age even though the vessel had been in contact with the trigeminal nerve since the fetal period. If the site of compression is outside the junction zone, symptoms will not develop. In the case of the trigeminal nerve, the true Obersteiner-Redlich zone is a site approximately 2.2 mm from the nerve's zone of entry. into the pons. In all three cases, the region of the trigeminal nerve transfixed by the compressing vessel was within what is considered the junction zone.
Literature Review There are few reports of cases in which blood vessels transfix the trigeminal nerve in this way. Gardner 3 described a 73-year-old trigeminal neuralgia patient with this finding and, Dandy 2 reported that in 30 of his 215 rhizotomy cases the petrosal vein transfixed or came into contact with the trigeminal nerve. There were three cases (0.8%) in our series of 384 cases in which the nerve was transfixed by the compressing artery. Axial Rhizotomy and Transposition In the three cases reported here, the blood vessel transfixed the root entry zone portion of the trigeminal nerve; since the area of penetration was almost at the center of the nerve, there was no choice but to free the vessel from the nerve by partial rhizotomy. In Case 3, it was possible both to obtain postoperative pain relief and to preserve facial tactile perception. In Cases 1 and 2, impairment of facial tactile sensation remained, although pain relief was achieved. As indicated above, the etiological mechanism for trigeminal neuralgia is compression of the nerve by an offending vessel in the Obersteiner-Redlich zone. If nerve compression by a blood vessel occurs at a site remote from this zone, no symptoms develop. Thus, it seemed logical to avoid postrhizotomy impairment of facial sensation by performing an axial rhizotomy peripheral to the area of the nerve transfixed by the vessel, then moving the compressing vessel peripherally in the direction of the nerve's vertical axis and fixing it in a position believed to be beyond the Obersteiner-Redlich zone. We did this in Case 3 and achieved postoperative preservation of facial sensation and adequate pain relief, with no recurrence of symptoms 289 years later. The Obersteiner-Redlich zone of the trigeminal nerve is wider than the corresponding zone of the facial nerve and, since it extends a little further peripherally, the vessel must be moved enough to obtain reliable pain
786
relief; this is believed to be the "trick" of this surgical procedure. There has been no recurrence of pain during the 289to 3 years of the follow-up period; however, this is considered long enough for symptoms to recur after partial rhizotomy alone for treatment of trigeminal neuralgia. Conclusions
We have reported three rare cases of trigeminal neuralgia in which the compressing vessel transfixed the trigeminal nerve and provoked symptoms. Treatment in the first two cases consisted of partial rhizotomy perpendicular to the axis of the nerve in the area transfixed by the vessel and separation of the vessel from the nerve; however, facial sensory impairment remained postoperatively. To avoid this outcome, in the third case partial rhizotomy longitudinal to the trigeminal nerve was performed, and the artery was moved peripherally beyond the Obersteiner-Redlich zone. This procedure resulted in both relief of facial pain and preservation of facial sensation, and is considered a more suitable technique. References
1. Burchiel KJ, Steege TD, Howe JF, et al: Comparison of percutaneous radiofrequency gangliolysis and microvascular decompression for the surgical management of tic douloureux. Neurosurgery 9:111-119, 1981 2. Dandy WE: Concerning the cause of trigeminal neuralgia. Am J Surg 24:447-455, 1934 3. Gardner WJ: Concerning the mechanism of trigeminal neuralgia and hemifacial spasm. J Neurosurg 19: 947-958, 1962 4. Gardner WJ, Sara GA: Hemifacial spasm - - a reversible pathophysiologic state. J Neurosurg 19:240-247, 1962 5. Jannetta PJ: Arterial compression of the trigeminal nerve at the pons in patients with trigeminal neuralgia. J Neurosurg 26:159-162, 1967 6. Kondo A, Ishikawa J, Ito H, et al: [Hemifacial spasm: its mechanism and operative results by a microvascular decompression for the facial nerve.] Neurosurgeons 2: 239-249, 1982 (Jpn) 7. Kondo A, Ishikawa J, Konishi T, et al: [Mechanism of vascular compression of cranial nerves - - role of changes of vertebrobasilar vasculatures.] Neurol Med Chir 21: 287-293, 198t (Jpn) Manuscript received May l, 1990. Accepted in final form February 25, 1991. Address reprint requests to: Haruhiko Tashiro, M.D., Department of Neurosurgery, Kitano Medical Research Institute and Hospital, 13-3, Kamiyama-cho, Kita-ku, Osaka 530, Japan.
J. Neurosurg. / Volume 75/November, 199I
Trigeminal neuralgia caused by compression from arteries transfixing the nerve Report of three cases HARUHIKO TASHIRO, M.D., AKINORI KONDO, M.D., IKUHIRO AOYAMA, M.D., K l v o s m NtN, M.D., KATSUMI SHIMOTAKE,M.D., TATSUYA NISHIOKA,M.D., YOSHIAKI IKAI, M.D., AND JUN TAKAHASHI,M.D.
Department of Neurosurgery, Kitano Medical Research Institute and Hospital, Osaka, Japan ~" The authors present three patients with trigeminal neuralgia due to compression by an artery that transfixed the sensory root of the fifth cranial nerve. These cases represented 0.8% of 384 patients with trigeminal neuralgia treated by microvascular decompression at the authors' clinic during the past 12 years. In the remaining 381 cases, the compressing vessels were successfully removed from the trigeminal nerve without much difficulty, for an initial cure rate of 94.3%. In the three cases reported, however, the compressing artery penetrating the nerve could not easily be maneuvered away from the nerve. In the first two cases, partial rhizotomy perpendicular to the axis of the nerve at the site of arterial transfixion made it possible to separate the artery from the nerve. However, these two patients developed postoperative facial sensory impairment. In the third case, rhizotomy was performed longitudinal to the axis of the nerve at the site of arterial transfixion, making it possible to reposition the artery peripherally beyond the root entry zone of the nerve without causing any postoperative sensory deficits of the face. No recurrent pain has developed in more than 289 years since surgery in any of these three cases. When performing microvascular decompression surgery on patients in whom the compressing artery penetrates the nerve, the technique used in our third patient is the procedure of choice. KEY WORDS
9 trigeminal neuralgia
RIGEMINAL nerve decompression was first used by Gardner and Sava4 as a surgical treatment for trigeminal neuralgia and was greatly improved and popularized by Jannetta 5 after the introduction of microsurgical techniques. We have performed trigeminal nerve decompression surgery in 384 patients with trigeminal neuralgia during a 12-year period from 1977 to 1989, with an initial recovery rate of 94.3%. In this series, there were three cases (0.8%) in which the compressing vessel, the superior cerebellar artery (SCA) or the anterior inferior cerebellar artery (AICA), transfixed the trigeminal nerve. The standard vascular decompression procedure, which consists of separating the offending vessel from the nerve, was greatly complicated in these cases because of the unusual course of the vessel. Since passage of the compressing vessel through the trigeminal nerve is an extremely rare cause of trigeminal neuralgia, we decided to report these three cases and discuss the surgical procedures employed.
T
J. Neurosurg. / Volume 75/November, 1991
compression
9 rhizotomy
9 root entry zone
Case Reports
Case 1 This 50-year-old woman had experienced severe pain on the fight side of her face for about 10 years. Such treatments as oral carbamazepine uptake and nerve block had failed to provide complete pain relief. Examination. At admission, she reported pain in the areas of the fight second and third divisions of the trigeminal nerve; there were no other abnormal neurological symptoms. Operation. A fight retromastoid suboccipital craniectomy was performed. Immediately after emerging from the pons, the portio major of the trigeminal nerve was pierced by a looped AICA passing from its medial aspect below to its lateral aspect above (Fig. 1). The SCA was also compressing the trigeminal nerve superomedially in the same area, causing strangulation of the nerve between these two blood vessels. We suc783
H. Tashiro, et al.
FIG. 1. Intraoperative photograph (h~/i) and drawing (right) of the pathology in Case 1. The right anterior inferior cerebellar arte~ ~hort open arrow) presses on the sensory, root of the trigeminal nerve (long open arrow). The closed arrow points to the site of pressure on the portio major of the right fifth cranial nerve.
ceeded in releasing the SCA from the trigeminal nerve, but it was impossible to free the nerve from the AICA, which was very crooked in the area where it transfixed the nerve. We therefore performed a partial rhizotomy on a rather small portion of the portio major of the trigeminal nerve lateral to the area transfixed, freeing the vessel; we could then reposition the vessel laterally. As the final step in the decompression procedure, prostheses were placed between the brain stem and the two freed vessels. Postoperative Course. The patient suffered loss of nociception in the area of the first and second divisions of the trigeminal nerve on the fight side and tactile hypesthesia in the area of the third division; however, her trigeminal neuralgia was completely relieved. Three years postoperatively, her tactile disorder has improved somewhat, and there has been no recurrence of the trigeminal neuralgia.
Case 2 This 55-year-old man had experienced persistent pain in the left side of the face and oral cavity for about 5 years. His pain was relieved for 2 years by a trigeminal ganglion block, but when it recurred, a second block proved ineffective. Examination. At admission to our department, no abnormalities other than hypertension and neuralgia in the areas of the left second and third divisions of the trigeminal nerve were noted. Operation. A left retromastoid suboccipital craniectomy was performed, and the SCA and AICA were found to be compressing the trigeminal nerve. The SCA was pressing on the entry zone of the portio major of the trigeminal nerve superomedially; the AICA, forming a loop bulging superiorly, pierced one-third of the medial aspect of the entry zone of the portio major and compressed this portion of the nerve (Fig. 2). After freeing the SCA from the nerve, we performed a rhizotomy parallel to the axis of the trigeminal nerve 784
peripheral to the portion penetrated by the AICA and attempted to move the AICA peripheral to what appeared to be the Obersteiner-Redlich zone. This maneuver proved to be impossible, and we were forced to perform a one-third partial rhizotomy on the medial side of the trigeminal nerve in the portion penetrated by this vessel. We were then able to free the penetrating vessel from the nerve and inserted a prosthesis between the vessel and the brain stem; this succeeded in adequately decompressing the trigeminal nerve. Postoperative Course. The patient's trigeminal neuralgia disappeared. Mild tactile hypesthesia was noted in the area of the second division of the nerve. At 289 years after surgery, tactile hypesthesia is much improved and there has been no recurrence of pain.
Case 3 This 67-year-old woman had a 7-year history of pain in the area of the left second and third divisions of the trigeminal nerve. Temporary relief was obtained with a trigeminal nerve block but, because the pain recurred, she requested surgery. Examination. On admission, there were no abnormal findings other than trigeminal neuralgia of the left second and third divisions of the nerve and hypertension. Operation. A left retromastoid suboccipital craniectomy was performed. The SCA was found to bulge inferiofly in a loop and to penetrate the center of the portio major of the trigeminal nerve at its zone of entry from its medial aspect below to its lateral aspect above. It was very crooked in the area where it transfixed and compressed the nerve. Since it was impossible to free the compressing vessel from the nerve, we performed a partial rhizotomy longitudinal to the axis of the nerve from the area of vessel penetration toward the periphery, then moved the SCA approximately 4 to 5 mm peripheral to the entry zone of the portio major, to a position believed to be beyond the root entry zone (Fig. 3). J. Neurosurg. / Volume 75/November, 1991
T r i g e m i n a l n e u r a l g i a d u e to t r a n s f i x i n g a r t e r i e s
Fl(;. 2. Intraoperative photograph (left) and drawing (right) of nerve compression in Case 2. The left anterior inferior cerebellar artery (short open arrow) presses on the sensory root of the left tfigeminal nerve (long open arrow). The closed arrow points to the site of impingement on the portio major of the left fifth cranial nerve.
Postoperative Course. The patient's trigeminal neuralgia disappeared and there were no complications such as facial sensory impairment. At present, -2 years postoperatively, there have been no signs of recurrence. Discussion
Pathogenesis Various hypotheses have been proposed as to the etiology of trigeminal neuralgia. Gardner, 3 believing nerve compression was caused by vessels at the entry zone of the trigeminal nerve, succeeded in relieving pain by freeing the blood vessel from the nerve and decompressing it. Jannetta 5 improved the procedure by using microsurgical techniques. In our own experience comprising 384 cases of trigeminal neuralgia in which we have performed decompression surgery, pain has
completely disappeared after surgery in 94.3% of cases. Thus, we believe that the etiology oftrigeminal neuralgia is vascular compression of the nerve in the Obersteiner-Redlich zone. The question arises as to why such nerve dysfunction develops with increasing age. We have investigated the vascular structure of the vertebral artery system of patients with trigeminal neuralgia and hemifacial spasm, and found that the diameter of either the left or the right vertebral artery enlarges with age. It appears that the hemodynamic effect of long-term high blood flow through the enlarged artery, hypertension, and arteriosclerotic changes produce crookedness and tortuosity of the artery and that the crooked vessel gradually compresses the nerve. In our three patients in whom the compressing vessel transfixed the nerve, symptoms of trigeminal nerve
FIG. 3. Drawings of the intraoperative findings in Case 3. a: The left superior cerebellar artery (short open arrow) compresses the portio major of the fifth cranial nerve (long open arrow). The closed arrow indicates the site of impingement on the ponio major, b: Selective partial rhizotomy of the portio major was performed longitudinal to the axis of the nerve (short arrow). The superior cerebellar artery was held away from the peripheral part of the Obersteiner-Redlich zone of the fifth nerve by a prosthesis (long arrow). J. Neurosurg. / Volume 75/November, 1991
785
H. Tashiro, et al. compression did not develop until the patient reached a certain age even though the vessel had been in contact with the trigeminal nerve since the fetal period. If the site of compression is outside the junction zone, symptoms will not develop. In the case of the trigeminal nerve, the true Obersteiner-Redlich zone is a site approximately 2.2 mm from the nerve's zone of entry. into the pons. In all three cases, the region of the trigeminal nerve transfixed by the compressing vessel was within what is considered the junction zone.
Literature Review There are few reports of cases in which blood vessels transfix the trigeminal nerve in this way. Gardner 3 described a 73-year-old trigeminal neuralgia patient with this finding and, Dandy 2 reported that in 30 of his 215 rhizotomy cases the petrosal vein transfixed or came into contact with the trigeminal nerve. There were three cases (0.8%) in our series of 384 cases in which the nerve was transfixed by the compressing artery. Axial Rhizotomy and Transposition In the three cases reported here, the blood vessel transfixed the root entry zone portion of the trigeminal nerve; since the area of penetration was almost at the center of the nerve, there was no choice but to free the vessel from the nerve by partial rhizotomy. In Case 3, it was possible both to obtain postoperative pain relief and to preserve facial tactile perception. In Cases 1 and 2, impairment of facial tactile sensation remained, although pain relief was achieved. As indicated above, the etiological mechanism for trigeminal neuralgia is compression of the nerve by an offending vessel in the Obersteiner-Redlich zone. If nerve compression by a blood vessel occurs at a site remote from this zone, no symptoms develop. Thus, it seemed logical to avoid postrhizotomy impairment of facial sensation by performing an axial rhizotomy peripheral to the area of the nerve transfixed by the vessel, then moving the compressing vessel peripherally in the direction of the nerve's vertical axis and fixing it in a position believed to be beyond the Obersteiner-Redlich zone. We did this in Case 3 and achieved postoperative preservation of facial sensation and adequate pain relief, with no recurrence of symptoms 289 years later. The Obersteiner-Redlich zone of the trigeminal nerve is wider than the corresponding zone of the facial nerve and, since it extends a little further peripherally, the vessel must be moved enough to obtain reliable pain
786
relief; this is believed to be the "trick" of this surgical procedure. There has been no recurrence of pain during the 289to 3 years of the follow-up period; however, this is considered long enough for symptoms to recur after partial rhizotomy alone for treatment of trigeminal neuralgia. Conclusions
We have reported three rare cases of trigeminal neuralgia in which the compressing vessel transfixed the trigeminal nerve and provoked symptoms. Treatment in the first two cases consisted of partial rhizotomy perpendicular to the axis of the nerve in the area transfixed by the vessel and separation of the vessel from the nerve; however, facial sensory impairment remained postoperatively. To avoid this outcome, in the third case partial rhizotomy longitudinal to the trigeminal nerve was performed, and the artery was moved peripherally beyond the Obersteiner-Redlich zone. This procedure resulted in both relief of facial pain and preservation of facial sensation, and is considered a more suitable technique. References
1. Burchiel KJ, Steege TD, Howe JF, et al: Comparison of percutaneous radiofrequency gangliolysis and microvascular decompression for the surgical management of tic douloureux. Neurosurgery 9:111-119, 1981 2. Dandy WE: Concerning the cause of trigeminal neuralgia. Am J Surg 24:447-455, 1934 3. Gardner WJ: Concerning the mechanism of trigeminal neuralgia and hemifacial spasm. J Neurosurg 19: 947-958, 1962 4. Gardner WJ, Sara GA: Hemifacial spasm - - a reversible pathophysiologic state. J Neurosurg 19:240-247, 1962 5. Jannetta PJ: Arterial compression of the trigeminal nerve at the pons in patients with trigeminal neuralgia. J Neurosurg 26:159-162, 1967 6. Kondo A, Ishikawa J, Ito H, et al: [Hemifacial spasm: its mechanism and operative results by a microvascular decompression for the facial nerve.] Neurosurgeons 2: 239-249, 1982 (Jpn) 7. Kondo A, Ishikawa J, Konishi T, et al: [Mechanism of vascular compression of cranial nerves - - role of changes of vertebrobasilar vasculatures.] Neurol Med Chir 21: 287-293, 198t (Jpn) Manuscript received May l, 1990. Accepted in final form February 25, 1991. Address reprint requests to: Haruhiko Tashiro, M.D., Department of Neurosurgery, Kitano Medical Research Institute and Hospital, 13-3, Kamiyama-cho, Kita-ku, Osaka 530, Japan.
J. Neurosurg. / Volume 75/November, 199I
