- Email: [email protected]
Microsurgical treatment of patients with vestibular and cochlear symptoms
Surg Neurol
141
1987;27:141-6
Microsurgical Cochlear
Treatment
of Patients
and
Symptoms
Toshisuke
Sakaki,
Shozaburo
Utsumi,
M.D.,
Tetsuya
M.D.,
Department of Neurosurgery
Morimoto,
and Yukikazu
M.D.,
KEY WORDS: Vertigo; Tinnitus; Hearing disturbance; Microvascular decompression; Neurovascular compression; Vestibular nerve; Cochlear nerve
symptoms
in the eighth cranial nerve,
which carries hearing and balance functions, hyperacusis,
M.D.,
Kikuo
Kyoi, M.D.,
and Otology, Nara Medical University, Kasihihara, Nara, Japan
Eighteen patients with vertigo, tinnitus, and various hearing disturbances were treated by posterior fossa exploration and microvascular decompression of the eighth cranial nerve; they were followed for more than 3 years. After successful decompression of the eighth nerve from offending vessels, the attacks of vertigo disappeared in 11 patients, improved markedly in 3 patients, and improved mildly in 4 patients. The tinnitus vanished in three patients and decreased in nine. The hearing disturbance improved in only five patients and worsened in three. Because of the satisfactory improvement of the attacks of vertigo, which are the most distressing symptoms for patients, we recommend surgical exploration for patients with severe symptoms of vestibular disturbances.
The hyperactive
Seiji Miyamoto,
Hyo, M.D.
Sakaki T, Morimoto T, Miyamoto S, Kyoi K, Utsumi S, Hyo Y. Microsurgical treatment of patients with vestibular and cochlear symptoms. Sug Neural 1987;27:141-6.
tinnitus,
with Vestibular
diplacusis,
hearing
tigo and may vary in frequency
may include loss, and ver-
and intensity.
These
symptoms are considered to be caused by an abnormality of the intracranial course of the nerve that is almost always a vascular compression, similar to trigeminal neuralgia and hemifacial spasm. During the last 8 years our experience with vascular decompression in cases of trigeminal neuralgia and hemifacial spasm, which was suggested by Jannetta [5], showed good results. Furthermore, two patients who suffered severe vertigo, tinnitus, hearing disturbances, and hemifacial spasm underwent vascular decompression of the seventh and eighth nerve complex for the treatment of Address reprint requests to: Toshisuke Sakaki, M.D., Department Neurosurgery and Otology, Kashihihara, Nara, Japan. 0 1987 by Elsevier Science Publishing Co., Inc.
of
the hemifacial spasm; the hemifacial spasm disappeared immediately after surgery and so did the vertigo. In accordance with these results, we performed vascular decompression on the hyperactive symptoms of the eighth cranial nerve when other conservative treatments failed. In these functional operations, long-term follow-up results are important. We followed 18 patients for more than 3 years. The results of relief of tinnitus and vertigo were satisfactory.
Clinical
Material
and Methods
In our series of 18 cases, 6 were men and 12 were women. Their ages ranged from 47 to 70 years. Table 1 shows a synopsis of their preoperative status. The main indication for surgery was intractable vertigo, which was present in all patients. The most common symptom was a whirling or fainting sensation that occurred when the patient moved his head in a particular position, and was commonly associated with nausea and occasionally with vomiting. Most patients were severely disabled with vertigo, either with strict limitations of their everyday activities or loss of occupation. The preoperative duration varied between 1 and 7 years, with an average of 2.7 years. Tinnitus, which is a constant pulsating or buzzing noise in the ears of variable intensity, was a frequent complaint. Four patients (cases 4, 8, 13, and 16) complained of not being able to sleep and were exhausted because of continuous distressing tinnitus. Three patients (cases 2, 3, and 10) had the coexistent symptom of hemifacial spasm. In these patients, surgical exploration of the cerebellopontine angle was indicated for this condition. Neuroradiologic preoperative work-up consisted of plain roentgenograms of the skull, polytomography of the internal auditory canal, computed tomography (CT) scans with and without contrast medium , bilateral vertebral angiography, and CT metrizamide-cisternography of the cerebellopontine angle area. In all 18 cases, the results were normal except for mild brain atrophy ob-
142
Surg Neurol 1987;27:141-6
Sakaki et al
served on some of the CT scans and moderate cerebral arterial sclerotic changes observed on the angiograms. Other than demonstrating vascularlization at the level of the internal auditory meatus and ruling out abnormal mass lesions, the offending vessels could not be identified. Audiometry revealed a varying neurosensory loss. All patients had a significant amount of hearing loss; three patients (cases 8, 9, and 16) were deaf. Audiograms generally showed that the loss of hearing became more marked in the range above 2000 Hz. Vestibular investigation with caloric testing and electronystagmography revealed hypoexcitability in all but one case (case 2). In two cases (cases 8 and 16) the reflex was not recognized at all, even though the stimulus used was > ice-cold water. We also routinely observed nystagmus with positional stimulation in seven different head positions and recognized nystagmus to the contralateral side in all cases of the head position in which the patients complained of vertigo. All patients underwent the recording of brainstem auditory evoked potentials. Four patients (cases 4, 5, 13, and 17) had increased latencies between peaks I and III, similar to those seen in patients with surgically confirmed acoustic nerve tumors [S], and 3 patients (cases 8, 9, and 16) had absent acoustic middle ear reflex. All patients underwent a mannitol test to rule out Meniere’s disease and did not notice any improvement. Operative Findings Exploration of the cerebellopontine angle was done through a small retromastoid craniectomy with the patient in the lateral decubitus position. Adequate cerebellar collapse was obtained by lumbar drainage and proper head positioning. Soft cerebellar retraction is necessary to lessen postoperative morbidity. Under the operative microscope, the entire seventh and eighth nerve complex was inspected from the meatus to the brainstem in each patient. Contrary to the general finding in hemifacial spasm or trigeminal neuralgia [3,5,13], the offending vessels were not necessarily located at the root-entry zone near the brainstem but were visualized at different points between the brainstem and the auditory meatus. In three patients (cases 6, 11, and 12) the eighth nerve was distorted by a single tortuous or elongated arterial loop of the posterior inferior cerebellar artery (Figure 1). In seven patients (cases 1, 4, 5, 7, 9, 14, and 18) the compressing artery of the eighth nerve was the anterior inferior cerebellar artery (Figure 2). In four patients (cases 8, 13, 15, and 17) several unidentified elongated and tortuous small arteries were found running close to or crossing the eighth nerve. In three patients (cases 2, 3, and 10) an elongated vertebral artery distorted the facial-acous-
++ ++
+ +
+ +++++++++++++++ ++++++++++++++++++
Treatm lent of Vestibular
Surg Neutol 1987;27: 141-6
and Cochlear Symptoms
Figure 1. Lateralsuboccipital exposure of the cerebellopontine angle on the left side of case no. 6. The posterior inferior cerebellar artery (arrow) cornpre.&g the eighth nerve (x, is demonstrated.
tic ner ve complex dorsolaterally. These the co Iexistent symptom of hemifacial differs :nt degrees of indentation and in eighth nerve were demonstrated
patients suffered spasm. After the distortion of the each patient, the
143
arterial loop was mobilized and a small prosthesis was inserted between the artery and the nerve. In one patient (case 16) an abnormally thick arachnoid membrane compressed the dorsal side of the eighth nerve; it was excised and removed. Figure 2.
LateraL suboccipital exposure of the right cerebellopontine angle of case no. 4. The anterior inferior rerebellar artery (arrow) compressing the eighth nerve (XI is demorutrated.
144
Surg Nemo1 1987;27:141-6
Sakaki et al
Results
Discussion
The results of the operations are shown in Table 2. Two complications occurred in this series. One patient (case 10) was a 4%year-old male with the coexistent symptom of hemifacial spasm. To mobilize the vertebral artery that deeply indented the root-entry zone of the facialacoustic nerve complex, retraction of the cerebellar hemisphere was required. The patient awoke soon after surgery, but on the third postoperative day, he complained of a severe headache and left cerebellar signs. A CT scan revealed a left cerebellar hematoma, and evacuation of the hematoma was performed immediately. His cerebellar signs disappeared completely on the eighth postoperative day. Another patient (case 16), a 61-year-old female, had a moderate degree of right cerebellar signs postoperatively. However, the CT scan showed no cerebellar abnormalities and her symptoms improved considerably 5 days after surgery. In four patients (cases 4, 6, 10, and 17) hearing disturbances improved in the range of 20 to 40 dB. But in three patients (cases 7, 8, and 18), postoperative audiometry showed a decrease of 10, 30, and 20 dB, respectively, although the patients did not notice worsening of their hearing. Results in relieving vertigo were good in all cases. Eleven patients experienced no attacks of vertigo after surgery. Three patients (cases 4,5, and 14) noticed marked improvement in spite of a mild dizzy sensation in a particular head posture. These patients were able to return to their preoperative occupations. Only four patients (cases 7, 8, 12, and 18) still suffered frequent attacks of vertigo 6 months to 2 years after the surgery, although they did have good results in their early postoperative course. Two patients (cases 8 and 12) returned to their occupations despite partial disability. Another two patients (cases 7 and 18) were still disabled but could return to everyday activities. The relief of tinnitus was less predictable. Three patients (cases 4, 6, and 10) noticed the disappearance of tinnitus immediately after the surgery and experienced no recurrence. Two patients (cases 8 and 16) had marked improvement (8OoJo), and one patient (case 13) had moderate improvement (50$%). In six patients (cases 2, 3, 5, 9, 14, and 17) tinnitus was absent or of slight degree during the early stages after surgery, but gradually returned (6 months to 3 years postoperatively) to the slightly improved level (20%-30%) in comparison with the preoperative state. In six patients (cases 1, 7, 11, 12, 15, and 18) tinnitus occurred soon after the surgery and has not changed postoperatively. Three patients (cases 2, 3, and 10) with coexistent symptoms of hemifacial spasm noticed complete disappearance immediately after the operation and have had no recurrence.
In the presence of the hyperactive symptoms of the cranial nerves, one must consider the possibility of an irritative or compressive mechanism on the cranial nerve in its course in the posterior cranial fossa. From the clinical point of view, one must suspect a lesion of the cerebellopontine angle such as a tumor, a malformation or an anomaly of the artery, or arachnoidal adhesions which induce symptoms of an irritative nature. Campbell and Keedy [2] found ectatic vessels in two patients with trigeminal neuralgia and hemifacial spasm. In 1962, Gardner and Sava [3] first applied a piece of Gelfoam prosthesis between the compressing vessel and the facial nerve for decompression and elegantly correlated this to hemifacial spasm. Jannetta IS], a pioneer of modern microvascular decompressive surgery of the cranial nerve, reported his experience with treating the trigeminal neuralgia and hemifacial spasm by decompression of the trigeminal and facial nerve of anomalous arteries; he cut adhesions or removed tumors with the aid of microsurgical instruments and excellent microsurgical techniques without injuring these nerves. During the investigation of patients with symptoms pertaining to the trigeminal and facial nerves, there were coexistent symptoms relevant to the eighth cranial nerve such as severe vertigo, tinnitus, and hearing loss. On the other hand, patients investigated for symptoms relevant to the eighth nerve frequently had symptoms of the fifth or seventh cranial nerves. Yeh et al [14] reported 10 cases of hemifacial spasm due to a vascular loop anomaly and arachnoid adhesion. In one of the 10 patients, severe vertigo, ataxia, and hearing loss coexisted and compression of the seventh and eighth nerve complex by two independent arterial loops was found. This patient was symptom-free after operation. We treated two patients with hemifacial spasm, severe vertigo, tinnitus, and hearing loss before this study. After microvascular decompression of the facial-acoustic nerve complex for the relief of hemifacial spasm, severe vertigo also was relieved. We postulated that eighth nerve hyperactivity may be caused by the same mechanism as the trigeminal neuralgia or hemifacial spasm. At autopsy, Ouaknine et al [lo] reported that cochlear and vestibular parts of the eighth nerve were compressed by a redundant loop of the posterior inferior cerebellar artery in a patient who suffered for 21 years with tinnitus, hypoacousis, and occasional dizziness. Bertrand et al El] reported that in five patients with eighth cranial nerve dysfunction and other cranial nerve symptoms, the exploration of the cerebellopontine angle with decompression of the cranial nerves led to improvement of these symptoms. Leclercq et al [7] reported on 10 patients with complaints of tinnitus, vertigo, or both. Eight patients with intractable vertigo were
Free Mildly improved
Unchanged
18
Mildly improved
11-82
17
None
1 l-82
13 14 15 16
Free Mildly improved Free Markedly improved Free Free
11 12
Unchanged Unchanged Moderately improved Mildly improved Unchanged Markedly improved
6-82 9-82 9-82 9-82 10-82 1 l-82
9 10
Improved (30 dB) Worse (10 dB)
Unchanged Unchanged Unchanged Improved (20 dB) Unchanged Unchanged
Unchanged Improved (30 dB)
(20 dB)
Worse
Mildly improved
improved
Markedly Free Free
5-82 6-82
8 Mildly improved Free
5-82
5 6 7
Unchanged Unchanged Unchanged Improved (30 dB) Unchanged Improved (10 dB) Worse (10 dB)
Hearing
Free Free Free Markedly improved Markedly improved Free Mildly improved
Vertigo
Unchanged Mildly improved Mildly improved Free Mildly improved Free Unchanged
Tinnitus
Result
None Cerebellar hemorrhage None None None None None Transient cerebellar sign None
None
11-81 l-82 2-82 4-82 5-82
3 4
None None None None None None None
9-81
11-81
1
Complications
2
G3.W no.
2. Postoperative Findings
Date of operation (mo-yd
Table
Free
Free Free
Facial spas*
to to to to to to
work work work work work work Back to work Still disabled Return to everyday
Back Back Back Back Back Back
Back to work Back to work Back to work Back to work Back to work Back to work Still disabled Return to everyday Partially disabled Back to work Back to work Back to work
Postoperative
activity
activity
status
146
Surg Neurol 1987;27:141-6
severely disabled. After neurovascular decompression of the eighth nerve, they noticed marked improvement of the vertigo. Jannetta [4] reported that, of 38 patients with eighth cranial nerve dysfunction, there was vascular compression at the root-entry zone by an artery in 26 cases, by a vein in 8 cases, and by both an artery and a vein in 4 cases. In this report, relief of vertigo was much more satisfactory than that of tinnitus or hearing loss. Samii et al El l] reported on four cases of vascular decompression in vestibulocochlear dysfunction. In two cases with preoperative vertigo, attacks of vertigo ceased and, in all cases, the tinnitus vanished or decreased. But, improvement in hearing loss was unsatisfactory. Mprller et al 191 reported on 21 patients operated on consecutively for the management of disabling positional vertigo. In all cases, one (or more) artery or vein was found on the eighth nerve when the nerve was exposed for microvascular decompression. After the operation, 16 of the 21 patients were either free of symptoms, or the symptoms were so much improved that the patients were able to return to their normal activities. In our series of 18 cases, relief of vertigo was much more satisfactory than relief of other symptoms. These results are similar to many other reports. Though the vertigo was relieved or markedly improved in 14 cases (77.7%), the tinnitus was relieved or markedly improved in only 5 cases (27.8%). We do not think that tinnitus alone-except in a highly selective case such as the one reported by Kudo and Ito [6]-is an indication for surgical treatment. Janetta [S] found that the offending vessels compressed the root-entry zone of the nerve in trigeminal neuralgia and hemifacial spasm. However, in our series of 18 cases with dysfunctional symptoms of the eighth nerve, the offending vessels were not necessarily located at the root-entry zone near the brainstem but were located at different points between the brainstem and the internal auditory meatus. The same operative findings were reported by Leclercq et al f7] and Yasuoka et al 1131. We speculate that a portion of the central glial segments of the cranial nerve is sensitive to compression because it is not protected by the Schwann sheath. According to Tarlov [ 12], the length of the trigeminal or facial nerve glial segments are short, whereas the central glial segments of the vestibular and cochlear nerves are long and extend near the porus acousticus. In cases of trigeminal neuralgia or hemifacial spasm, the offending vessels coincide with the cross compression vessels of the root-entry zone of the trigeminal or facial nerve. But in the case of dysfunctional symptoms of the eighth nerve, the arteries that compress the nerve root between the portion near the brainstem and the porus acousticus may be regarded as the offending vessels.
Sakaki et al
No particular test is completely diagnostic of the vascular compression syndrome of the eighth nerve. It is our opinion that abnormal stimulation of the vestibular or cochlear nerves, whether by tumor, abnormal vessels, or arachnoid adhesion, can produce the symptoms relating to these nerves, and that removal of the abnormal stimulants could relieve the symptoms. The patient with severe vertigo, evoked by moving the head in a particular position, usually is considered a good candidate for this surgery. Surgery should be reserved for cases where serious disability is present and the patient’s activity is significantly affected. In the hands of an experienced the nontraumatic, microsurgical apneurosurgeon, proach carries a low morbidity and usually good results.
References 1. Bertrand RA, Morina P, Hardy J. Vestibular syndrome and vascular anomaly in the cerebella-pontine angle. Acta Otolaryngol 1977; 831187-94. 2. Campbell E, Keedy C. Hemifacial spasm. A note on the etiology in two cases. J Neurosurg 1974;4:342-7. 3. Gardner WJ, Sava GA. Hemifacial spasm-a physiologic state. J Neurosurg 1962;19:240-7.
reversible patho-
4. Jannetta PJ. Neurovascular cross-compression of the eighth cranial nerve in patients with vertigo and tinnitus. In: Samii M, Jannetta PJ, eds. The cranial nerve. Berlin: Springer-Verlag, 1981:552-5. 5. Jannetta PJ. Observation on the etiology of trigeminal neuralgia, hemifacial spasm, acoustic nerve dysfunction and glossophatyngeaI neuralgia. Definitive microsurgical treatment and results in 117 patients. Neurochirurgia (Stuttg) 1977;20:145-54. 6. Kudo T, Ito K. Microvascular decompression of the eighth cranial nerve for disabling tinnitus without vertigo: a case report. Neurosurgery 1984;14:338-40. 7. Leclercq ‘IA, Hill CL, Grisoli F. Retromastoid microsurgical approach to vascular compression of the eighth cranial nerve. Laryngoscope 1980;90:1011-7. 8. Moller MB, Moller AR. Brainstem auditory evoked potentials in patients with cerebella-pontine angle tumors. Ann Otol Rhino1 Laryngol 1983;92:645-50. 9. Moller MB, Moller AR, Jannetta PJ, Sekhar L. Diagnosis and surgical treatment of disabling positional vertigo. J Neurosurg 1986;64:21-8. 10. Ouaknine GE, Robert F, Molina-Negro P, Hardy J. Geniculate neuralgia and audio-vestibular disturbances due to compression of the intermediate and eighth nerve by the posteroinferior cerebellar artery. Surg Neural 1980;13:147-50. 11. Samii h$, Ohlemutz A. Early experiences in vascular decompression for vertebro-cochlear malfunction. In: Samii M, Jannetta PJ, eds. The cranial nerve. Berlin: Springer-Verlag, 1981:556-8. 12. Tarlov IM. Structure of the nerve root. II. Differentiation of sensory from motor roots; observation on identification of function in roots of mixed cranial nerves. Arch Neurol Psychiatry 1937;37:1338-55. 13. Yasuoka S, Takakura K, Fukaya T. Tinnitus, vertigo and loss of carolic response due to neurovascular compression. Brain Nerve (Tokyo) 1983;35:1097-101. 14. Yeh HS, Tew JM, Ramirez RM. Microsurgical treatment of intractable hemifacial spasm. Neurosurgery 1981;9:383-6.
141
1987;27:141-6
Microsurgical Cochlear
Treatment
of Patients
and
Symptoms
Toshisuke
Sakaki,
Shozaburo
Utsumi,
M.D.,
Tetsuya
M.D.,
Department of Neurosurgery
Morimoto,
and Yukikazu
M.D.,
KEY WORDS: Vertigo; Tinnitus; Hearing disturbance; Microvascular decompression; Neurovascular compression; Vestibular nerve; Cochlear nerve
symptoms
in the eighth cranial nerve,
which carries hearing and balance functions, hyperacusis,
M.D.,
Kikuo
Kyoi, M.D.,
and Otology, Nara Medical University, Kasihihara, Nara, Japan
Eighteen patients with vertigo, tinnitus, and various hearing disturbances were treated by posterior fossa exploration and microvascular decompression of the eighth cranial nerve; they were followed for more than 3 years. After successful decompression of the eighth nerve from offending vessels, the attacks of vertigo disappeared in 11 patients, improved markedly in 3 patients, and improved mildly in 4 patients. The tinnitus vanished in three patients and decreased in nine. The hearing disturbance improved in only five patients and worsened in three. Because of the satisfactory improvement of the attacks of vertigo, which are the most distressing symptoms for patients, we recommend surgical exploration for patients with severe symptoms of vestibular disturbances.
The hyperactive
Seiji Miyamoto,
Hyo, M.D.
Sakaki T, Morimoto T, Miyamoto S, Kyoi K, Utsumi S, Hyo Y. Microsurgical treatment of patients with vestibular and cochlear symptoms. Sug Neural 1987;27:141-6.
tinnitus,
with Vestibular
diplacusis,
hearing
tigo and may vary in frequency
may include loss, and ver-
and intensity.
These
symptoms are considered to be caused by an abnormality of the intracranial course of the nerve that is almost always a vascular compression, similar to trigeminal neuralgia and hemifacial spasm. During the last 8 years our experience with vascular decompression in cases of trigeminal neuralgia and hemifacial spasm, which was suggested by Jannetta [5], showed good results. Furthermore, two patients who suffered severe vertigo, tinnitus, hearing disturbances, and hemifacial spasm underwent vascular decompression of the seventh and eighth nerve complex for the treatment of Address reprint requests to: Toshisuke Sakaki, M.D., Department Neurosurgery and Otology, Kashihihara, Nara, Japan. 0 1987 by Elsevier Science Publishing Co., Inc.
of
the hemifacial spasm; the hemifacial spasm disappeared immediately after surgery and so did the vertigo. In accordance with these results, we performed vascular decompression on the hyperactive symptoms of the eighth cranial nerve when other conservative treatments failed. In these functional operations, long-term follow-up results are important. We followed 18 patients for more than 3 years. The results of relief of tinnitus and vertigo were satisfactory.
Clinical
Material
and Methods
In our series of 18 cases, 6 were men and 12 were women. Their ages ranged from 47 to 70 years. Table 1 shows a synopsis of their preoperative status. The main indication for surgery was intractable vertigo, which was present in all patients. The most common symptom was a whirling or fainting sensation that occurred when the patient moved his head in a particular position, and was commonly associated with nausea and occasionally with vomiting. Most patients were severely disabled with vertigo, either with strict limitations of their everyday activities or loss of occupation. The preoperative duration varied between 1 and 7 years, with an average of 2.7 years. Tinnitus, which is a constant pulsating or buzzing noise in the ears of variable intensity, was a frequent complaint. Four patients (cases 4, 8, 13, and 16) complained of not being able to sleep and were exhausted because of continuous distressing tinnitus. Three patients (cases 2, 3, and 10) had the coexistent symptom of hemifacial spasm. In these patients, surgical exploration of the cerebellopontine angle was indicated for this condition. Neuroradiologic preoperative work-up consisted of plain roentgenograms of the skull, polytomography of the internal auditory canal, computed tomography (CT) scans with and without contrast medium , bilateral vertebral angiography, and CT metrizamide-cisternography of the cerebellopontine angle area. In all 18 cases, the results were normal except for mild brain atrophy ob-
142
Surg Neurol 1987;27:141-6
Sakaki et al
served on some of the CT scans and moderate cerebral arterial sclerotic changes observed on the angiograms. Other than demonstrating vascularlization at the level of the internal auditory meatus and ruling out abnormal mass lesions, the offending vessels could not be identified. Audiometry revealed a varying neurosensory loss. All patients had a significant amount of hearing loss; three patients (cases 8, 9, and 16) were deaf. Audiograms generally showed that the loss of hearing became more marked in the range above 2000 Hz. Vestibular investigation with caloric testing and electronystagmography revealed hypoexcitability in all but one case (case 2). In two cases (cases 8 and 16) the reflex was not recognized at all, even though the stimulus used was > ice-cold water. We also routinely observed nystagmus with positional stimulation in seven different head positions and recognized nystagmus to the contralateral side in all cases of the head position in which the patients complained of vertigo. All patients underwent the recording of brainstem auditory evoked potentials. Four patients (cases 4, 5, 13, and 17) had increased latencies between peaks I and III, similar to those seen in patients with surgically confirmed acoustic nerve tumors [S], and 3 patients (cases 8, 9, and 16) had absent acoustic middle ear reflex. All patients underwent a mannitol test to rule out Meniere’s disease and did not notice any improvement. Operative Findings Exploration of the cerebellopontine angle was done through a small retromastoid craniectomy with the patient in the lateral decubitus position. Adequate cerebellar collapse was obtained by lumbar drainage and proper head positioning. Soft cerebellar retraction is necessary to lessen postoperative morbidity. Under the operative microscope, the entire seventh and eighth nerve complex was inspected from the meatus to the brainstem in each patient. Contrary to the general finding in hemifacial spasm or trigeminal neuralgia [3,5,13], the offending vessels were not necessarily located at the root-entry zone near the brainstem but were visualized at different points between the brainstem and the auditory meatus. In three patients (cases 6, 11, and 12) the eighth nerve was distorted by a single tortuous or elongated arterial loop of the posterior inferior cerebellar artery (Figure 1). In seven patients (cases 1, 4, 5, 7, 9, 14, and 18) the compressing artery of the eighth nerve was the anterior inferior cerebellar artery (Figure 2). In four patients (cases 8, 13, 15, and 17) several unidentified elongated and tortuous small arteries were found running close to or crossing the eighth nerve. In three patients (cases 2, 3, and 10) an elongated vertebral artery distorted the facial-acous-
++ ++
+ +
+ +++++++++++++++ ++++++++++++++++++
Treatm lent of Vestibular
Surg Neutol 1987;27: 141-6
and Cochlear Symptoms
Figure 1. Lateralsuboccipital exposure of the cerebellopontine angle on the left side of case no. 6. The posterior inferior cerebellar artery (arrow) cornpre.&g the eighth nerve (x, is demonstrated.
tic ner ve complex dorsolaterally. These the co Iexistent symptom of hemifacial differs :nt degrees of indentation and in eighth nerve were demonstrated
patients suffered spasm. After the distortion of the each patient, the
143
arterial loop was mobilized and a small prosthesis was inserted between the artery and the nerve. In one patient (case 16) an abnormally thick arachnoid membrane compressed the dorsal side of the eighth nerve; it was excised and removed. Figure 2.
LateraL suboccipital exposure of the right cerebellopontine angle of case no. 4. The anterior inferior rerebellar artery (arrow) compressing the eighth nerve (XI is demorutrated.
144
Surg Nemo1 1987;27:141-6
Sakaki et al
Results
Discussion
The results of the operations are shown in Table 2. Two complications occurred in this series. One patient (case 10) was a 4%year-old male with the coexistent symptom of hemifacial spasm. To mobilize the vertebral artery that deeply indented the root-entry zone of the facialacoustic nerve complex, retraction of the cerebellar hemisphere was required. The patient awoke soon after surgery, but on the third postoperative day, he complained of a severe headache and left cerebellar signs. A CT scan revealed a left cerebellar hematoma, and evacuation of the hematoma was performed immediately. His cerebellar signs disappeared completely on the eighth postoperative day. Another patient (case 16), a 61-year-old female, had a moderate degree of right cerebellar signs postoperatively. However, the CT scan showed no cerebellar abnormalities and her symptoms improved considerably 5 days after surgery. In four patients (cases 4, 6, 10, and 17) hearing disturbances improved in the range of 20 to 40 dB. But in three patients (cases 7, 8, and 18), postoperative audiometry showed a decrease of 10, 30, and 20 dB, respectively, although the patients did not notice worsening of their hearing. Results in relieving vertigo were good in all cases. Eleven patients experienced no attacks of vertigo after surgery. Three patients (cases 4,5, and 14) noticed marked improvement in spite of a mild dizzy sensation in a particular head posture. These patients were able to return to their preoperative occupations. Only four patients (cases 7, 8, 12, and 18) still suffered frequent attacks of vertigo 6 months to 2 years after the surgery, although they did have good results in their early postoperative course. Two patients (cases 8 and 12) returned to their occupations despite partial disability. Another two patients (cases 7 and 18) were still disabled but could return to everyday activities. The relief of tinnitus was less predictable. Three patients (cases 4, 6, and 10) noticed the disappearance of tinnitus immediately after the surgery and experienced no recurrence. Two patients (cases 8 and 16) had marked improvement (8OoJo), and one patient (case 13) had moderate improvement (50$%). In six patients (cases 2, 3, 5, 9, 14, and 17) tinnitus was absent or of slight degree during the early stages after surgery, but gradually returned (6 months to 3 years postoperatively) to the slightly improved level (20%-30%) in comparison with the preoperative state. In six patients (cases 1, 7, 11, 12, 15, and 18) tinnitus occurred soon after the surgery and has not changed postoperatively. Three patients (cases 2, 3, and 10) with coexistent symptoms of hemifacial spasm noticed complete disappearance immediately after the operation and have had no recurrence.
In the presence of the hyperactive symptoms of the cranial nerves, one must consider the possibility of an irritative or compressive mechanism on the cranial nerve in its course in the posterior cranial fossa. From the clinical point of view, one must suspect a lesion of the cerebellopontine angle such as a tumor, a malformation or an anomaly of the artery, or arachnoidal adhesions which induce symptoms of an irritative nature. Campbell and Keedy [2] found ectatic vessels in two patients with trigeminal neuralgia and hemifacial spasm. In 1962, Gardner and Sava [3] first applied a piece of Gelfoam prosthesis between the compressing vessel and the facial nerve for decompression and elegantly correlated this to hemifacial spasm. Jannetta IS], a pioneer of modern microvascular decompressive surgery of the cranial nerve, reported his experience with treating the trigeminal neuralgia and hemifacial spasm by decompression of the trigeminal and facial nerve of anomalous arteries; he cut adhesions or removed tumors with the aid of microsurgical instruments and excellent microsurgical techniques without injuring these nerves. During the investigation of patients with symptoms pertaining to the trigeminal and facial nerves, there were coexistent symptoms relevant to the eighth cranial nerve such as severe vertigo, tinnitus, and hearing loss. On the other hand, patients investigated for symptoms relevant to the eighth nerve frequently had symptoms of the fifth or seventh cranial nerves. Yeh et al [14] reported 10 cases of hemifacial spasm due to a vascular loop anomaly and arachnoid adhesion. In one of the 10 patients, severe vertigo, ataxia, and hearing loss coexisted and compression of the seventh and eighth nerve complex by two independent arterial loops was found. This patient was symptom-free after operation. We treated two patients with hemifacial spasm, severe vertigo, tinnitus, and hearing loss before this study. After microvascular decompression of the facial-acoustic nerve complex for the relief of hemifacial spasm, severe vertigo also was relieved. We postulated that eighth nerve hyperactivity may be caused by the same mechanism as the trigeminal neuralgia or hemifacial spasm. At autopsy, Ouaknine et al [lo] reported that cochlear and vestibular parts of the eighth nerve were compressed by a redundant loop of the posterior inferior cerebellar artery in a patient who suffered for 21 years with tinnitus, hypoacousis, and occasional dizziness. Bertrand et al El] reported that in five patients with eighth cranial nerve dysfunction and other cranial nerve symptoms, the exploration of the cerebellopontine angle with decompression of the cranial nerves led to improvement of these symptoms. Leclercq et al [7] reported on 10 patients with complaints of tinnitus, vertigo, or both. Eight patients with intractable vertigo were
Free Mildly improved
Unchanged
18
Mildly improved
11-82
17
None
1 l-82
13 14 15 16
Free Mildly improved Free Markedly improved Free Free
11 12
Unchanged Unchanged Moderately improved Mildly improved Unchanged Markedly improved
6-82 9-82 9-82 9-82 10-82 1 l-82
9 10
Improved (30 dB) Worse (10 dB)
Unchanged Unchanged Unchanged Improved (20 dB) Unchanged Unchanged
Unchanged Improved (30 dB)
(20 dB)
Worse
Mildly improved
improved
Markedly Free Free
5-82 6-82
8 Mildly improved Free
5-82
5 6 7
Unchanged Unchanged Unchanged Improved (30 dB) Unchanged Improved (10 dB) Worse (10 dB)
Hearing
Free Free Free Markedly improved Markedly improved Free Mildly improved
Vertigo
Unchanged Mildly improved Mildly improved Free Mildly improved Free Unchanged
Tinnitus
Result
None Cerebellar hemorrhage None None None None None Transient cerebellar sign None
None
11-81 l-82 2-82 4-82 5-82
3 4
None None None None None None None
9-81
11-81
1
Complications
2
G3.W no.
2. Postoperative Findings
Date of operation (mo-yd
Table
Free
Free Free
Facial spas*
to to to to to to
work work work work work work Back to work Still disabled Return to everyday
Back Back Back Back Back Back
Back to work Back to work Back to work Back to work Back to work Back to work Still disabled Return to everyday Partially disabled Back to work Back to work Back to work
Postoperative
activity
activity
status
146
Surg Neurol 1987;27:141-6
severely disabled. After neurovascular decompression of the eighth nerve, they noticed marked improvement of the vertigo. Jannetta [4] reported that, of 38 patients with eighth cranial nerve dysfunction, there was vascular compression at the root-entry zone by an artery in 26 cases, by a vein in 8 cases, and by both an artery and a vein in 4 cases. In this report, relief of vertigo was much more satisfactory than that of tinnitus or hearing loss. Samii et al El l] reported on four cases of vascular decompression in vestibulocochlear dysfunction. In two cases with preoperative vertigo, attacks of vertigo ceased and, in all cases, the tinnitus vanished or decreased. But, improvement in hearing loss was unsatisfactory. Mprller et al 191 reported on 21 patients operated on consecutively for the management of disabling positional vertigo. In all cases, one (or more) artery or vein was found on the eighth nerve when the nerve was exposed for microvascular decompression. After the operation, 16 of the 21 patients were either free of symptoms, or the symptoms were so much improved that the patients were able to return to their normal activities. In our series of 18 cases, relief of vertigo was much more satisfactory than relief of other symptoms. These results are similar to many other reports. Though the vertigo was relieved or markedly improved in 14 cases (77.7%), the tinnitus was relieved or markedly improved in only 5 cases (27.8%). We do not think that tinnitus alone-except in a highly selective case such as the one reported by Kudo and Ito [6]-is an indication for surgical treatment. Janetta [S] found that the offending vessels compressed the root-entry zone of the nerve in trigeminal neuralgia and hemifacial spasm. However, in our series of 18 cases with dysfunctional symptoms of the eighth nerve, the offending vessels were not necessarily located at the root-entry zone near the brainstem but were located at different points between the brainstem and the internal auditory meatus. The same operative findings were reported by Leclercq et al f7] and Yasuoka et al 1131. We speculate that a portion of the central glial segments of the cranial nerve is sensitive to compression because it is not protected by the Schwann sheath. According to Tarlov [ 12], the length of the trigeminal or facial nerve glial segments are short, whereas the central glial segments of the vestibular and cochlear nerves are long and extend near the porus acousticus. In cases of trigeminal neuralgia or hemifacial spasm, the offending vessels coincide with the cross compression vessels of the root-entry zone of the trigeminal or facial nerve. But in the case of dysfunctional symptoms of the eighth nerve, the arteries that compress the nerve root between the portion near the brainstem and the porus acousticus may be regarded as the offending vessels.
Sakaki et al
No particular test is completely diagnostic of the vascular compression syndrome of the eighth nerve. It is our opinion that abnormal stimulation of the vestibular or cochlear nerves, whether by tumor, abnormal vessels, or arachnoid adhesion, can produce the symptoms relating to these nerves, and that removal of the abnormal stimulants could relieve the symptoms. The patient with severe vertigo, evoked by moving the head in a particular position, usually is considered a good candidate for this surgery. Surgery should be reserved for cases where serious disability is present and the patient’s activity is significantly affected. In the hands of an experienced the nontraumatic, microsurgical apneurosurgeon, proach carries a low morbidity and usually good results.
References 1. Bertrand RA, Morina P, Hardy J. Vestibular syndrome and vascular anomaly in the cerebella-pontine angle. Acta Otolaryngol 1977; 831187-94. 2. Campbell E, Keedy C. Hemifacial spasm. A note on the etiology in two cases. J Neurosurg 1974;4:342-7. 3. Gardner WJ, Sava GA. Hemifacial spasm-a physiologic state. J Neurosurg 1962;19:240-7.
reversible patho-
4. Jannetta PJ. Neurovascular cross-compression of the eighth cranial nerve in patients with vertigo and tinnitus. In: Samii M, Jannetta PJ, eds. The cranial nerve. Berlin: Springer-Verlag, 1981:552-5. 5. Jannetta PJ. Observation on the etiology of trigeminal neuralgia, hemifacial spasm, acoustic nerve dysfunction and glossophatyngeaI neuralgia. Definitive microsurgical treatment and results in 117 patients. Neurochirurgia (Stuttg) 1977;20:145-54. 6. Kudo T, Ito K. Microvascular decompression of the eighth cranial nerve for disabling tinnitus without vertigo: a case report. Neurosurgery 1984;14:338-40. 7. Leclercq ‘IA, Hill CL, Grisoli F. Retromastoid microsurgical approach to vascular compression of the eighth cranial nerve. Laryngoscope 1980;90:1011-7. 8. Moller MB, Moller AR. Brainstem auditory evoked potentials in patients with cerebella-pontine angle tumors. Ann Otol Rhino1 Laryngol 1983;92:645-50. 9. Moller MB, Moller AR, Jannetta PJ, Sekhar L. Diagnosis and surgical treatment of disabling positional vertigo. J Neurosurg 1986;64:21-8. 10. Ouaknine GE, Robert F, Molina-Negro P, Hardy J. Geniculate neuralgia and audio-vestibular disturbances due to compression of the intermediate and eighth nerve by the posteroinferior cerebellar artery. Surg Neural 1980;13:147-50. 11. Samii h$, Ohlemutz A. Early experiences in vascular decompression for vertebro-cochlear malfunction. In: Samii M, Jannetta PJ, eds. The cranial nerve. Berlin: Springer-Verlag, 1981:556-8. 12. Tarlov IM. Structure of the nerve root. II. Differentiation of sensory from motor roots; observation on identification of function in roots of mixed cranial nerves. Arch Neurol Psychiatry 1937;37:1338-55. 13. Yasuoka S, Takakura K, Fukaya T. Tinnitus, vertigo and loss of carolic response due to neurovascular compression. Brain Nerve (Tokyo) 1983;35:1097-101. 14. Yeh HS, Tew JM, Ramirez RM. Microsurgical treatment of intractable hemifacial spasm. Neurosurgery 1981;9:383-6.