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Hemifacial Spasm, Glossodynia, and Dolichoectasia of the Basilar Artery
Case Report
Hemifacial Spasm, Glossodynia, and Dolichoectasia of the Basilar Artery Ambar Chakravarty, MD, FRCP
The case of a 77-year-old hypertensive man presenting with hemifacial spasm and glossodynia is reported. Imaging studies revealed gross dolichoectasia of the vertebrobasilar arterial system with pontine compression. It is suggested that the neurologic symptoms most likely resulted from pontine compression, rather than from any compression of the cranial nerves. Key Words: Hemifacial spasm—glossodynia— vertebrobasilar dolichoectasia—brainstem compression—basilar artery ectasia. Ó 2012 by National Stroke Association
Hemifacial spasm (HFS), characterized by irregular involuntary and recurrent tonic and clonic contractions of muscles innervated by the ipsilateral facial nerve,1 is usually attributed to compression of the facial nerve at the root entry zone by an aberrant blood vessel or cerebellopontine angle masses.2,3 The offending vessels are usually arterial, such as the anterior or posterior inferior cerebellar arteries.4 Some HFSs develop after recovery from ipsilateral facial nerve paresis5 or might be due to arteriovenous malformation or multiple sclerosis plaque. The disorder can be bilateral, but the 2 sides of the face do not spasm in synchrony. Definitive treatment involves surgery to decompress the nerve,6 although many patients prefer botulinum toxin treatment, which can be highly effective.7 Glossodynia (or stomatopyrosis or orodynia) is considered a disorder with a wide range of possible associations,8 including hematologic diseases, vitamin deficiencies, dental work, hormonal factors, diabetes, and infection. In addition, psychological disorders, such as neuroses, depression, and phobias, have been purported to play a role, but robust evidence is lacking. The oral mucosa is normal From the Department of Neurology, Vivekananda Institute of Medical Science, Calcutta, India. Received December 10, 2009; accepted March 9, 2010. The author has no conflicts of interest to disclose. Address correspondence to Ambar Chakravarty, MD, FRCP, 1E 1202 AVISHIKTAII, Calcutta 700078, India. E-mail: [email protected]. 1052-3057/$ - see front matter Ó 2012 by National Stroke Association doi:10.1016/j.jstrokecerebrovasdis.2010.03.011
78
in most affected patients. Typically, patients awake without pain, but note increasing symptoms through the day and into the night, when sleep is disturbed. The condition is generally treated with antidepressants (eg, tricyclics), based on the notion that it is essentially a psychosomatic disorder. No specific neurologic conditions have been associated with glossodynia. Vertebrobasilar dolichoectasia (VBD) is an anatomical variation of the vertebrobasilar system involving arterial enlargement and dilatation, often associated with tortuosity and elongations.9 VBD probably results from marked thinning of the internal elastic lamina and media, most likely due to prolonged systemic arterial hypertension.10 Various clinical syndromes have been related to the pulsatile compression by the aberrant vessel, including cerebellar dysfunction, hydrocephalus, ischemic stroke, transient or permanent motor deficits, central sleep apnea, trigeminal neuralgia, and brain stem compression syndrome.7,11,12 Treatment by microvascular decompression has been advocated;9 a new approach is to combine this with repositioning of the ectatic vessel.13 Here I report a patient presenting with HFS and glossodynia in whom investigation revealed the presence of a grossly dolichoectatic basilar artery.
Case Report A 77-year-old hypertensive, nondiabetic man presented with severe burning pain in the front part of the tongue.
Journal of Stroke and Cerebrovascular Diseases, Vol. 21, No. 1 (January), 2012: pp 78-81
HEMIFACIAL SPASM, GLOSSODYNIA, AND DOLICHOECTASIA OF THE BASILAR ARTERY
He reported that the pain had started about 3 months earlier at the tip and had spread over the 2 sides and the dorsal and ventral aspects of the anterior half or more of the tongue. The pain was not present on waking but started late in the morning and continue throughout the day and into then night, when it disturbed his sleep. It was so severe that he could not eat. The patient had consulted dentists and oral pathologists, who could not find any dental cause and deemed his oral mucosa to be healthy. For the past 25 years, the patient had been experiencing continuous muscle contractions of the left side of his face, which was diagnosed as HFS. Medical treatment (with cerbamazepine and clonazepam) had been unsuccessful, and although several neurologists had suggested treatment with botulinum toxin, the patient refused, noting that he had learned to live with the HFS and was not bothered by it. He was greatly disturbed by the development of glossodynia, however. Examination revealed classical tonic and clonic movements of the left facial musculature. There was no facial motor paralysis. General and taste sensations in the anterior part of the tongue were intact. The tongue demonstrated no motor paralysis or wasting. The rest of the neurologic examination was normal. No cerebellar signs were evident. Routine hematology and biochemical profiles, including estimation of serum B12 level, were normal. Brain magnetic resonance imaging (MRI) in T2weighted sequences revealed focal and confluent hyperintensities in the periventricular and subcortical white matter, as well as in both basal ganglia. Compression on the pons, cerebellum, and left middle cerebellar peduncle by a dilated and tortuous basilar artery (ie, signal void) was seen (Fig 1). Parenchymal signals of the brainstem
Figure 1. T2-weighted MRI of the brain showing pontine compression by a dolichoectatic basilar artery.
79
and cerebellum were otherwise normal. Ventricular sizes were normal. Magnetic resonance angiography (MRA) revealed no abnormalities of the anterior circulation arteries. Both vertebral arteries and the basilar artery were tortuous and ecstatic, with fusiform dilatation of the proximal part of the basilar artery for 3 cm, measuring about 1.6 cm in diameter at its widest part (Fig 2). The bifurcation of the basilar artery was elevated; the distal basilar artery measured 0.6 cm in diameter. Both posterior cerebral arteries were patent. The patient was offered microvascular decompression, but he refused, citing his advanced age. Because of the clinical association with HFS and the imaging demonstration of pontine compression, the glossodynia was indeed believed to be a neuropathic pain disorder. Thus, the patient was started on gabapentin, with the dosage gradually increased to 300 mg 3 times daily. Within 1 month, the patient noticed significant improvement in his glossodynia, and could sleep and eat well. The symptomatic relief persisted over the next several months.
Discussion In the present case, both hemifacial spasm and glossodynia resulted from pontine compression by a large fusiform dolichoectatic basilar artery. HFS caused by VBD has been reported previously.3,14,15,16 In those cases, compression of the facial nerve at the root entry zone in the cerebellopontine region was considered to be responsible for the facial spasm. Fahn and Jankovic17 proposed that HFS might result from 2 different mechanisms, which they termed the ‘‘nerve origin hypothesis’’
A. CHAKRAVARTY
80
pulled the ectatic vessel away from the brain stem and fixed it to the nearby dura with unabsorbable nylon.13 Satisfactory brain stem decompression was achieved, with subsequent symptom improvement. It should be noted that VBD with brain stem compression is an uncommon condition, and thus the reported surgical techniques and benefits claimed are merely anecdotal. Acknowledgment: I thank Dr. Sumita Kundu (EKO Imaging Institute, Calcutta) for the imaging interpretations.
References
Figure 2.
MRA showing a dolichoectatic basilar artery.
and the ‘‘facial nucleus hypothesis.’’ In the present case, HFS apparently resulted from a facial nuclear pathology (or involvement of the intrapontine facial nerve fibers) resulting from pontine compression by the VBD. This is supported by the association with glossodynia affecting the entire anterior portion of the tongue. Compression of the trigeminal nerve at its root entry zone would have caused only unilateral symptoms. This patient’s glossodynia, which started at the tip of the tongue and then spread to involve the whole anterior part of the tongue, is highly suggestive of compression by the VBD of the decussating second-order neuronal fibers (trigeminal lemniscus) originating from the principal sensory nucleus of the trigeminal located at the pons. Thus, the patient’s symptoms can be considered entirely related to pontine compression by the ‘‘giant’’ VBD. Pontine compression was demonstrated on brain MRI (Fig 1). The absence of any pyramidal, cerebellar, or sensory signs, as well as the sparing of the sixth nerve nucleus, remain unexplained, however. An ischemic lesion in the pons from associated hypertension remains a possibility, given the demonstration of ischemic changes in the cerebrum by brain MRI, but this was not be detected on imaging. No specific neurologic association of glossodynia has been reported to date. This patient’s therapeutic response to gabapentin is suggestive of neuropathic pain, which would be consistent with the proposed mechanism. It has been reported that brainstem compression by VBD cannot be satisfactorily treated using ordinary microvascular decompression.13 In the surgical approach to this condition, simply inserting a prosthesis between the vessel and the brainstem is insufficient to achieve decompression, because the size and stiffness of the dilated artery makes standard microsurgery difficult. Alternative techniques have been suggested. Ogawa et al18 reported the use of a synthetic vascular graft sutured to the clival dura to move the ectatic vessel away from cranial nerves. Others have used a silicone sling to reposition the basilar artery.19 A recent report described how the surgeon
1. Wang A, Jankovic J. Hemificial spasm: Clinical findings and treatment. Muscle Nerve 1998;21:1740-1747. 2. Sharma RR, Pawar SJ, Kharangate PP, et al. Symptomatic ependymal cysts of the perimesencephalic and cerebellopontine angle cisterns. J Clin Neurosci 2000;7:552-554. 3. Rahman EA, Trobe JD, Gebarski SS. Hemifacial spasm caused by vertebral artery dolichoectasia. Am J Ophthalmol 2002;133:854-856. 4. Jannetta PJ, Abbasy M, Maroon JG, et al. Etiology and definitive microsurgical treatment of hemifacial spasm: Operative techniques and results in 47 patients. J Neurosurg 1977;47:321-328. 5. Colosimo C, Bologna M, Lamberti S, et al. A comparative study of primary and secondary hemifacial spasm. Arch Neurol 2006;63:441-444. 6. Samii M, Gunther T, Iaconetta G, et al. Microvascular decompression to treat hemifacial spasm: Long-term results for a consecutive series of 143 patients. Neurosurgery 2002;50:712-713. 7. Tan EK, Fook-Chong S, Lum SY, et al. Botulinum toxin improves quality of life in hemifacial spasm: Validation of a questionnaire (HFS-30). J Neurol Sci 2004;218: 151-155. 8. Reiss M, Reiss G. Some aspects of glossodynia. Wochenschr Schweiz Med 1999;129:1461-1466. 9. Ubogu EE, Zaidat OO. Vertebrobasilar dolichoectasia diagnosed by magnetic resonance angiography and risk of stroke and death: A cohort study. J Neurol Neurosurg Psychiatry 2004;75:22-26. 10. Schulz R, Fegbeutel C, Althoff A, et al. Central sleep apnea diaphragmatic paralysis associated with vertebral artery compression of the medulla oblongata. J Neurol 2003;250:503-505. 11. Tomasello F, Alafaci C, Salpietro FM, et al. Bulbar compression by an ectatic vertebral artery: A novel neurovascular construct relieved by microsurgical decompression. Neurosurgery 2005;56:117-124. 12. Milandre L, Bonnefol B, Pestre P, et al. Vertebrobasilar arterial dolichoectasia: Complications and prognosis. Rev Neurol (Paris) 1991;147:714-772. 13. Pereira-Filho A, Faria M, Bleil C, et al. Brainstem compression syndrome caused by vertebrobasilar dolichoectasia: Microvascular repositioning technique. Arq Neuropsiquiatr 2008;66:408-411. 14. Arantes M, Carcia R, Pereira JR, et al. Hemifacial spasms and vertebral dolicheoectasias. Rev Neurol 2008;47: 468-470. 15. Papapetropoulos S, Andreas A, Guevara A, et al. Hemifacial spasm and pontine compression caused by a giant vertebrobasilar dolichoectasia. Cerebrovasc Dis 2009; 27:413-414.
HEMIFACIAL SPASM, GLOSSODYNIA, AND DOLICHOECTASIA OF THE BASILAR ARTERY 16. Hau IB, Chong JH, Chong JN, et al. Unusual causes and presentations of hemifacial spasm. Neurosurgery 2009; 65:130-137. 17. Fahn S, Jankovic J. Restless legs syndrome and peripheral movement disorders. In: Fahn S, Jankovic J, eds. Principles and Practice of Movement Disorders. Philadelphia: Churchill Livingstone, 2007:577-588.
81
18. Ogawa A, Suzuki M, Shirane R, et al. Repositioning of the tortuous vertebrobasilar artery for trigeminal neuralgia: A technical note. Surg Neurol 1992;38:232-235. 19. Stone JL, Lichtor T, Crowell RM. Microvascular sling decompression for trigeminal neuralgia secondary to ectatic vertebrobasilar compression. J Neurosurg 1993; 79:943-945.
Hemifacial Spasm, Glossodynia, and Dolichoectasia of the Basilar Artery Ambar Chakravarty, MD, FRCP
The case of a 77-year-old hypertensive man presenting with hemifacial spasm and glossodynia is reported. Imaging studies revealed gross dolichoectasia of the vertebrobasilar arterial system with pontine compression. It is suggested that the neurologic symptoms most likely resulted from pontine compression, rather than from any compression of the cranial nerves. Key Words: Hemifacial spasm—glossodynia— vertebrobasilar dolichoectasia—brainstem compression—basilar artery ectasia. Ó 2012 by National Stroke Association
Hemifacial spasm (HFS), characterized by irregular involuntary and recurrent tonic and clonic contractions of muscles innervated by the ipsilateral facial nerve,1 is usually attributed to compression of the facial nerve at the root entry zone by an aberrant blood vessel or cerebellopontine angle masses.2,3 The offending vessels are usually arterial, such as the anterior or posterior inferior cerebellar arteries.4 Some HFSs develop after recovery from ipsilateral facial nerve paresis5 or might be due to arteriovenous malformation or multiple sclerosis plaque. The disorder can be bilateral, but the 2 sides of the face do not spasm in synchrony. Definitive treatment involves surgery to decompress the nerve,6 although many patients prefer botulinum toxin treatment, which can be highly effective.7 Glossodynia (or stomatopyrosis or orodynia) is considered a disorder with a wide range of possible associations,8 including hematologic diseases, vitamin deficiencies, dental work, hormonal factors, diabetes, and infection. In addition, psychological disorders, such as neuroses, depression, and phobias, have been purported to play a role, but robust evidence is lacking. The oral mucosa is normal From the Department of Neurology, Vivekananda Institute of Medical Science, Calcutta, India. Received December 10, 2009; accepted March 9, 2010. The author has no conflicts of interest to disclose. Address correspondence to Ambar Chakravarty, MD, FRCP, 1E 1202 AVISHIKTAII, Calcutta 700078, India. E-mail: [email protected]. 1052-3057/$ - see front matter Ó 2012 by National Stroke Association doi:10.1016/j.jstrokecerebrovasdis.2010.03.011
78
in most affected patients. Typically, patients awake without pain, but note increasing symptoms through the day and into the night, when sleep is disturbed. The condition is generally treated with antidepressants (eg, tricyclics), based on the notion that it is essentially a psychosomatic disorder. No specific neurologic conditions have been associated with glossodynia. Vertebrobasilar dolichoectasia (VBD) is an anatomical variation of the vertebrobasilar system involving arterial enlargement and dilatation, often associated with tortuosity and elongations.9 VBD probably results from marked thinning of the internal elastic lamina and media, most likely due to prolonged systemic arterial hypertension.10 Various clinical syndromes have been related to the pulsatile compression by the aberrant vessel, including cerebellar dysfunction, hydrocephalus, ischemic stroke, transient or permanent motor deficits, central sleep apnea, trigeminal neuralgia, and brain stem compression syndrome.7,11,12 Treatment by microvascular decompression has been advocated;9 a new approach is to combine this with repositioning of the ectatic vessel.13 Here I report a patient presenting with HFS and glossodynia in whom investigation revealed the presence of a grossly dolichoectatic basilar artery.
Case Report A 77-year-old hypertensive, nondiabetic man presented with severe burning pain in the front part of the tongue.
Journal of Stroke and Cerebrovascular Diseases, Vol. 21, No. 1 (January), 2012: pp 78-81
HEMIFACIAL SPASM, GLOSSODYNIA, AND DOLICHOECTASIA OF THE BASILAR ARTERY
He reported that the pain had started about 3 months earlier at the tip and had spread over the 2 sides and the dorsal and ventral aspects of the anterior half or more of the tongue. The pain was not present on waking but started late in the morning and continue throughout the day and into then night, when it disturbed his sleep. It was so severe that he could not eat. The patient had consulted dentists and oral pathologists, who could not find any dental cause and deemed his oral mucosa to be healthy. For the past 25 years, the patient had been experiencing continuous muscle contractions of the left side of his face, which was diagnosed as HFS. Medical treatment (with cerbamazepine and clonazepam) had been unsuccessful, and although several neurologists had suggested treatment with botulinum toxin, the patient refused, noting that he had learned to live with the HFS and was not bothered by it. He was greatly disturbed by the development of glossodynia, however. Examination revealed classical tonic and clonic movements of the left facial musculature. There was no facial motor paralysis. General and taste sensations in the anterior part of the tongue were intact. The tongue demonstrated no motor paralysis or wasting. The rest of the neurologic examination was normal. No cerebellar signs were evident. Routine hematology and biochemical profiles, including estimation of serum B12 level, were normal. Brain magnetic resonance imaging (MRI) in T2weighted sequences revealed focal and confluent hyperintensities in the periventricular and subcortical white matter, as well as in both basal ganglia. Compression on the pons, cerebellum, and left middle cerebellar peduncle by a dilated and tortuous basilar artery (ie, signal void) was seen (Fig 1). Parenchymal signals of the brainstem
Figure 1. T2-weighted MRI of the brain showing pontine compression by a dolichoectatic basilar artery.
79
and cerebellum were otherwise normal. Ventricular sizes were normal. Magnetic resonance angiography (MRA) revealed no abnormalities of the anterior circulation arteries. Both vertebral arteries and the basilar artery were tortuous and ecstatic, with fusiform dilatation of the proximal part of the basilar artery for 3 cm, measuring about 1.6 cm in diameter at its widest part (Fig 2). The bifurcation of the basilar artery was elevated; the distal basilar artery measured 0.6 cm in diameter. Both posterior cerebral arteries were patent. The patient was offered microvascular decompression, but he refused, citing his advanced age. Because of the clinical association with HFS and the imaging demonstration of pontine compression, the glossodynia was indeed believed to be a neuropathic pain disorder. Thus, the patient was started on gabapentin, with the dosage gradually increased to 300 mg 3 times daily. Within 1 month, the patient noticed significant improvement in his glossodynia, and could sleep and eat well. The symptomatic relief persisted over the next several months.
Discussion In the present case, both hemifacial spasm and glossodynia resulted from pontine compression by a large fusiform dolichoectatic basilar artery. HFS caused by VBD has been reported previously.3,14,15,16 In those cases, compression of the facial nerve at the root entry zone in the cerebellopontine region was considered to be responsible for the facial spasm. Fahn and Jankovic17 proposed that HFS might result from 2 different mechanisms, which they termed the ‘‘nerve origin hypothesis’’
A. CHAKRAVARTY
80
pulled the ectatic vessel away from the brain stem and fixed it to the nearby dura with unabsorbable nylon.13 Satisfactory brain stem decompression was achieved, with subsequent symptom improvement. It should be noted that VBD with brain stem compression is an uncommon condition, and thus the reported surgical techniques and benefits claimed are merely anecdotal. Acknowledgment: I thank Dr. Sumita Kundu (EKO Imaging Institute, Calcutta) for the imaging interpretations.
References
Figure 2.
MRA showing a dolichoectatic basilar artery.
and the ‘‘facial nucleus hypothesis.’’ In the present case, HFS apparently resulted from a facial nuclear pathology (or involvement of the intrapontine facial nerve fibers) resulting from pontine compression by the VBD. This is supported by the association with glossodynia affecting the entire anterior portion of the tongue. Compression of the trigeminal nerve at its root entry zone would have caused only unilateral symptoms. This patient’s glossodynia, which started at the tip of the tongue and then spread to involve the whole anterior part of the tongue, is highly suggestive of compression by the VBD of the decussating second-order neuronal fibers (trigeminal lemniscus) originating from the principal sensory nucleus of the trigeminal located at the pons. Thus, the patient’s symptoms can be considered entirely related to pontine compression by the ‘‘giant’’ VBD. Pontine compression was demonstrated on brain MRI (Fig 1). The absence of any pyramidal, cerebellar, or sensory signs, as well as the sparing of the sixth nerve nucleus, remain unexplained, however. An ischemic lesion in the pons from associated hypertension remains a possibility, given the demonstration of ischemic changes in the cerebrum by brain MRI, but this was not be detected on imaging. No specific neurologic association of glossodynia has been reported to date. This patient’s therapeutic response to gabapentin is suggestive of neuropathic pain, which would be consistent with the proposed mechanism. It has been reported that brainstem compression by VBD cannot be satisfactorily treated using ordinary microvascular decompression.13 In the surgical approach to this condition, simply inserting a prosthesis between the vessel and the brainstem is insufficient to achieve decompression, because the size and stiffness of the dilated artery makes standard microsurgery difficult. Alternative techniques have been suggested. Ogawa et al18 reported the use of a synthetic vascular graft sutured to the clival dura to move the ectatic vessel away from cranial nerves. Others have used a silicone sling to reposition the basilar artery.19 A recent report described how the surgeon
1. Wang A, Jankovic J. Hemificial spasm: Clinical findings and treatment. Muscle Nerve 1998;21:1740-1747. 2. Sharma RR, Pawar SJ, Kharangate PP, et al. Symptomatic ependymal cysts of the perimesencephalic and cerebellopontine angle cisterns. J Clin Neurosci 2000;7:552-554. 3. Rahman EA, Trobe JD, Gebarski SS. Hemifacial spasm caused by vertebral artery dolichoectasia. Am J Ophthalmol 2002;133:854-856. 4. Jannetta PJ, Abbasy M, Maroon JG, et al. Etiology and definitive microsurgical treatment of hemifacial spasm: Operative techniques and results in 47 patients. J Neurosurg 1977;47:321-328. 5. Colosimo C, Bologna M, Lamberti S, et al. A comparative study of primary and secondary hemifacial spasm. Arch Neurol 2006;63:441-444. 6. Samii M, Gunther T, Iaconetta G, et al. Microvascular decompression to treat hemifacial spasm: Long-term results for a consecutive series of 143 patients. Neurosurgery 2002;50:712-713. 7. Tan EK, Fook-Chong S, Lum SY, et al. Botulinum toxin improves quality of life in hemifacial spasm: Validation of a questionnaire (HFS-30). J Neurol Sci 2004;218: 151-155. 8. Reiss M, Reiss G. Some aspects of glossodynia. Wochenschr Schweiz Med 1999;129:1461-1466. 9. Ubogu EE, Zaidat OO. Vertebrobasilar dolichoectasia diagnosed by magnetic resonance angiography and risk of stroke and death: A cohort study. J Neurol Neurosurg Psychiatry 2004;75:22-26. 10. Schulz R, Fegbeutel C, Althoff A, et al. Central sleep apnea diaphragmatic paralysis associated with vertebral artery compression of the medulla oblongata. J Neurol 2003;250:503-505. 11. Tomasello F, Alafaci C, Salpietro FM, et al. Bulbar compression by an ectatic vertebral artery: A novel neurovascular construct relieved by microsurgical decompression. Neurosurgery 2005;56:117-124. 12. Milandre L, Bonnefol B, Pestre P, et al. Vertebrobasilar arterial dolichoectasia: Complications and prognosis. Rev Neurol (Paris) 1991;147:714-772. 13. Pereira-Filho A, Faria M, Bleil C, et al. Brainstem compression syndrome caused by vertebrobasilar dolichoectasia: Microvascular repositioning technique. Arq Neuropsiquiatr 2008;66:408-411. 14. Arantes M, Carcia R, Pereira JR, et al. Hemifacial spasms and vertebral dolicheoectasias. Rev Neurol 2008;47: 468-470. 15. Papapetropoulos S, Andreas A, Guevara A, et al. Hemifacial spasm and pontine compression caused by a giant vertebrobasilar dolichoectasia. Cerebrovasc Dis 2009; 27:413-414.
HEMIFACIAL SPASM, GLOSSODYNIA, AND DOLICHOECTASIA OF THE BASILAR ARTERY 16. Hau IB, Chong JH, Chong JN, et al. Unusual causes and presentations of hemifacial spasm. Neurosurgery 2009; 65:130-137. 17. Fahn S, Jankovic J. Restless legs syndrome and peripheral movement disorders. In: Fahn S, Jankovic J, eds. Principles and Practice of Movement Disorders. Philadelphia: Churchill Livingstone, 2007:577-588.
81
18. Ogawa A, Suzuki M, Shirane R, et al. Repositioning of the tortuous vertebrobasilar artery for trigeminal neuralgia: A technical note. Surg Neurol 1992;38:232-235. 19. Stone JL, Lichtor T, Crowell RM. Microvascular sling decompression for trigeminal neuralgia secondary to ectatic vertebrobasilar compression. J Neurosurg 1993; 79:943-945.