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Compressive effect of large persistent trigeminal artery upon pituitary gland: importance of MRI and MRA
European Journal of Radiology Extra 51 (2004) 65–67
Compressive effect of large persistent trigeminal artery upon pituitary gland: importance of MRI and MRA Mustafa Harman a,∗ , Necmi Kýymaz b , Hayati Ayakta c , Mustafa Kayan a a
Department of Radiology, University of Yuzuncu Yýl Faculty of Medicine, 65200 VAN, Turkey Department of Neurochirur, University of Yuzuncu Yýl Faculty of Medicine, 65200 VAN, Turkey Department of Endocrinology, University of Yuzuncu Yýl Faculty of Medicine, 65200 VAN, Turkey
b c
Received 20 February 2004; received in revised form 30 April 2004; accepted 3 May 2004
Abstract Persistent trigeminal artery (PTA) is a relatively frequent type of carotid-basilar anastomosis. Most of PTA has no symptoms and are noticed incidentally. We report a case of PTA compressing the right side pituitary gland, in a patient with hormonal disorder. In this report, we emphasize importance of MR imaging and MR angiography on demonstrating the relationship between the pituitary gland and PTA. © 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: Persistent trigeminal artery; Magnetic resonance imaging; Magnetic resonance angiography
1. Introduction Persistent trigeminal artery (PTA) is the most common carotid-basilar anastomic channel observed in adult life and has been reported as an incidental finding in 0.1–0.6% of consecutive cerebral angiograms or autopsy cases [1–3]. While PTA is diagnosed incidentally in most of the cases, it rarely causes hormonal disorder by compressing the pituitary gland [4,5]. We present MRI and MRA findings in a case of PTA compressing the pituitary gland.
2. Case report A 22-year-old-woman was referred to the hospital with hirsutism and oligomenorrhea. Clinical abdominal ultrasonography examinations were normal. MRI examination (0.3 T, Hitachi AIRIS I, Tokyo, Japan) of the pituitary gland demonstrated that a vascular structure arising from the posteromedial part of the cavernous segment of the right internal carotid artery was compressing the right side of the pituitary gland (Fig. 1). Although endocrinological examination showed pituitary hormone disorder [(blood prolactin ∗
Tel.: +90 532 223 8483; fax: +90 432 216 8352. E-mail address: [email protected] (M. Harman).
level: 54 ng/ml (↑), TSH: 0.22 uIU/ml (↓), total T3 : 50 ng/dl (↓), GH: 7.02 ng/ml (↑)], micro or macro adenoma could not be detected in the pituitary gland with standard MRI investigation. Dynamic MRI investigation with contrast was applied to exclude the presense of microadenoma. Three slices in coronal orientation through the hypophysis in ten dynamic images per slice were acquired at 11 s intervals. All scans had 3 mm of slice thickness and no interslice gap. Dynamic imaging was initiated simultaneously with the bolus injection of contrast material (gadopentetate dimeglumine, 0.2 ml/kg). Magnetic resonance angiography (MRA) was performed with a pre-diagnosis PTA using the three dimensional time of flight (TOF) technique (repetition time: 33.3–57 ms, echo time: 2.9–4.6 ms, Field of view: 16 cm × 16 cm, matrix: 256 × 192). On MRA it was observed that the persistent trigeminal artery arising from the cavernous segment of the right internal carotid artery continued posterolaterally and communicated with the basilar artery. Basilar artery proximal to the PTA connection was hypoplastic (Fig. 2). We did not perform digital subtraction angiography because MRI and MRA findings were sufficient. Since the pituitary gland was interpreted as normal for adenoma on dynamic MRA, we assumed that the reason for the hormonal disorder was related to the compression of the pituitary gland by the PTA.
1571-4675/$ – see front matter © 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ejrex.2004.05.001
66
M. Harman et al. / European Journal of Radiology Extra 51 (2004) 65–67
Fig. 2. Three-dimensional time of flight magnetic resonance angiography in the cranio-caudal view plane. Vascular structure arising from the cavernous segment of the internal carotid artery and extending to the basilar artery is consistent with the PTA (arrows). Basilar artery proximal to the PTA connection is hypoplastic (arrowhead). Right internal carotid artery is hyperplasic.
Fig. 1. T1-weighted two consecutive MR images in the coronal plane (A and B). Signal void tubular structure arising from the cavernous segment of the right internal carotid artery compressing the right side of the pituitary gland (arrows). No other pathologies was detected in this location on dynamic MRI sequence.
3. Discussion Four different persistent embryonic communicating arteries are described between the carotid and vertebro-basilar systems: hypoglossal; otic; proatlantal; and trigeminal arteries. The PTA is the most common of the persistent carotid-basilar anastomoses with an incidence of 0.6% as seen on angiography [3]. The PTA arise where the internal carotid artery exits the carotid canal and enters the
cavernous sinus. It then runs posterolaterally along the trigeminal nerve or crosses over through the dorsum sellae before joining the basilar artery. Saltzman [6] classified the PTA into two types. Type I PTA join the basilar artery between the anterior inferior cerebellar and superior cerebellar arteries and are usually associated with the small posterior communicating artery and the vertebral artery and a hypoplastic basilar artery caudal to the anastomosis. Type II PTA join only superior cerebellar arteries, in which case posterior cerebral arteries receive their blood through the posterior communicating arteries. There are different ways to classify the intracranial course of the PTA, the latest and most widely accepted belonging to Salas et al. [1]. The relationship of PTA with the abducens nerve helps to distinguish between the lateral (petrosal) and medial (sphenoidal) variations. Our case is a medial variations with the PTA arising from the posteromedial C4 part of the cavernous segment of the right internal carotid artery with a course medial to the abducens nerve. Most of PTA has no symptoms and noticed incidentally, but there have been reports of PTA with several clinical manifestations. In cases with severe internal carotid artery (ICA) occlusion, vascular steal phenomena can occur between the basilar and carotid systems through the PTA [3]. Aneurysms have been reported generally at the origin of the PTA and at the connection with the basilar artery [7,8]. If the aneurysm happens at the carotid connection, isolated sixth cranial nerve palsies can occur due to the compression caused by the aneurysm. The petrosal variant has been re-
M. Harman et al. / European Journal of Radiology Extra 51 (2004) 65–67
ported with clinical symptoms of trigeminal neuralgia and diplopia [8]. There are three PTA cases reported in the literature with intrasellar course [4,9,10]. There are two cases reported hormonal disorder due to compressive effect of PTA on pituitary gland [4,5]. In one of these cases hyperprolactinemia due to compression by PTA was reported and in the other case anomalies of different hypophyseal hormones were reported as found in our case. Our patient did not have findings of pituitary adenoma but we assumed that the elevated and decreased pituitary hormone levels might result from the compression caused by the PTA. In most cases reported, PTA variants have been found incidentally. Yet, PTA variants can cause trigeminal neuralgia, and preoperative recognition of PTA variants is very important during surgical treatment of parasellar lesions, percutaneous gasserian ganglion procedure, and endovascular therapies [11]. MRA can detect PTA non-invasively. Some prior reports of MRI and MRA of PTA variants reveal that PTA variants were identified by MRA [11,12]. In our case, PTA variants could be shown successfully by MRA. While there are many reasons of pituitary hormone disorders, one of the rare causes as in our case is the compression by a persistent trigeminal artery with an intrasellar course, which may cause hormonal disorder without pituitary adenoma. Compressive effect of PTA on the pituitary gland can be demonstrated with MRI and MRA.
67
References [1] Salas E, Ziyal IM, Sekhar LN, Wright DC. Persistent trigeminal artery: an anatomic study. Neurosurgery 1998;43:557–61. [2] Fields WS. The significance of persistent trigeminal artery. Radiology 1968;91:1096–101. [3] Stern J, Correll JW, Bryan N. Persistent hypoglossal artery and persistent trigeminal artery presenting with posterior fossa transient ischemic attacks. J Neurosurg 1978;49:614–9. [4] Ekinci G, Baltacioglu F, Kilic T, et al. A rare cause of hyperprolactinemia: persistent trigeminal artery with stalk section effect. Eur Radiol 2001;11:648–50. [5] Osztie E, Czirjak S, Racz K, Martos J. Hormone disorders caused by intrasellar persistent trigeminal artery. Ideggyogy Sz 2002;20(55):395–8. [6] Saltzman GF. Patent primitive trigeminal artery studied by cerebral angiography. Acta Radiol 1959;51:329–36. [7] Kunilic T, Pamir N, Erzen C. MR angiography of the persistent trigeminal artery associated with an aneurysm. Turk Neurosurg 1997;7:91–3. [8] Blom RJ, Vinuela F. Aneurysm of a persistent trigeminal artery. AJNR 1985;6:651–2. [9] Richardson DN, Elster AD, Ball MR. MR intrasellar trigeminal artery. AJNR 1989;10:205. [10] Tulsi RS, Locket NA. Persistent trigeminal artery: an anatomical study. Aust NZ J Surg 1985;55:397–402. [11] Hirai T, Korogi Y, Sakamoto Y. MR angiography of the persistent trigeminal artery variant. J Comput Assist Tomogr 1995;19:495–7. [12] Uchino A, Kato A, Takase Y, Kudo S. Persistent trigeminal artery variants detected by MR angiography. Eur Radiol 2000;10: 1801–14.
Compressive effect of large persistent trigeminal artery upon pituitary gland: importance of MRI and MRA Mustafa Harman a,∗ , Necmi Kýymaz b , Hayati Ayakta c , Mustafa Kayan a a
Department of Radiology, University of Yuzuncu Yýl Faculty of Medicine, 65200 VAN, Turkey Department of Neurochirur, University of Yuzuncu Yýl Faculty of Medicine, 65200 VAN, Turkey Department of Endocrinology, University of Yuzuncu Yýl Faculty of Medicine, 65200 VAN, Turkey
b c
Received 20 February 2004; received in revised form 30 April 2004; accepted 3 May 2004
Abstract Persistent trigeminal artery (PTA) is a relatively frequent type of carotid-basilar anastomosis. Most of PTA has no symptoms and are noticed incidentally. We report a case of PTA compressing the right side pituitary gland, in a patient with hormonal disorder. In this report, we emphasize importance of MR imaging and MR angiography on demonstrating the relationship between the pituitary gland and PTA. © 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: Persistent trigeminal artery; Magnetic resonance imaging; Magnetic resonance angiography
1. Introduction Persistent trigeminal artery (PTA) is the most common carotid-basilar anastomic channel observed in adult life and has been reported as an incidental finding in 0.1–0.6% of consecutive cerebral angiograms or autopsy cases [1–3]. While PTA is diagnosed incidentally in most of the cases, it rarely causes hormonal disorder by compressing the pituitary gland [4,5]. We present MRI and MRA findings in a case of PTA compressing the pituitary gland.
2. Case report A 22-year-old-woman was referred to the hospital with hirsutism and oligomenorrhea. Clinical abdominal ultrasonography examinations were normal. MRI examination (0.3 T, Hitachi AIRIS I, Tokyo, Japan) of the pituitary gland demonstrated that a vascular structure arising from the posteromedial part of the cavernous segment of the right internal carotid artery was compressing the right side of the pituitary gland (Fig. 1). Although endocrinological examination showed pituitary hormone disorder [(blood prolactin ∗
Tel.: +90 532 223 8483; fax: +90 432 216 8352. E-mail address: [email protected] (M. Harman).
level: 54 ng/ml (↑), TSH: 0.22 uIU/ml (↓), total T3 : 50 ng/dl (↓), GH: 7.02 ng/ml (↑)], micro or macro adenoma could not be detected in the pituitary gland with standard MRI investigation. Dynamic MRI investigation with contrast was applied to exclude the presense of microadenoma. Three slices in coronal orientation through the hypophysis in ten dynamic images per slice were acquired at 11 s intervals. All scans had 3 mm of slice thickness and no interslice gap. Dynamic imaging was initiated simultaneously with the bolus injection of contrast material (gadopentetate dimeglumine, 0.2 ml/kg). Magnetic resonance angiography (MRA) was performed with a pre-diagnosis PTA using the three dimensional time of flight (TOF) technique (repetition time: 33.3–57 ms, echo time: 2.9–4.6 ms, Field of view: 16 cm × 16 cm, matrix: 256 × 192). On MRA it was observed that the persistent trigeminal artery arising from the cavernous segment of the right internal carotid artery continued posterolaterally and communicated with the basilar artery. Basilar artery proximal to the PTA connection was hypoplastic (Fig. 2). We did not perform digital subtraction angiography because MRI and MRA findings were sufficient. Since the pituitary gland was interpreted as normal for adenoma on dynamic MRA, we assumed that the reason for the hormonal disorder was related to the compression of the pituitary gland by the PTA.
1571-4675/$ – see front matter © 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ejrex.2004.05.001
66
M. Harman et al. / European Journal of Radiology Extra 51 (2004) 65–67
Fig. 2. Three-dimensional time of flight magnetic resonance angiography in the cranio-caudal view plane. Vascular structure arising from the cavernous segment of the internal carotid artery and extending to the basilar artery is consistent with the PTA (arrows). Basilar artery proximal to the PTA connection is hypoplastic (arrowhead). Right internal carotid artery is hyperplasic.
Fig. 1. T1-weighted two consecutive MR images in the coronal plane (A and B). Signal void tubular structure arising from the cavernous segment of the right internal carotid artery compressing the right side of the pituitary gland (arrows). No other pathologies was detected in this location on dynamic MRI sequence.
3. Discussion Four different persistent embryonic communicating arteries are described between the carotid and vertebro-basilar systems: hypoglossal; otic; proatlantal; and trigeminal arteries. The PTA is the most common of the persistent carotid-basilar anastomoses with an incidence of 0.6% as seen on angiography [3]. The PTA arise where the internal carotid artery exits the carotid canal and enters the
cavernous sinus. It then runs posterolaterally along the trigeminal nerve or crosses over through the dorsum sellae before joining the basilar artery. Saltzman [6] classified the PTA into two types. Type I PTA join the basilar artery between the anterior inferior cerebellar and superior cerebellar arteries and are usually associated with the small posterior communicating artery and the vertebral artery and a hypoplastic basilar artery caudal to the anastomosis. Type II PTA join only superior cerebellar arteries, in which case posterior cerebral arteries receive their blood through the posterior communicating arteries. There are different ways to classify the intracranial course of the PTA, the latest and most widely accepted belonging to Salas et al. [1]. The relationship of PTA with the abducens nerve helps to distinguish between the lateral (petrosal) and medial (sphenoidal) variations. Our case is a medial variations with the PTA arising from the posteromedial C4 part of the cavernous segment of the right internal carotid artery with a course medial to the abducens nerve. Most of PTA has no symptoms and noticed incidentally, but there have been reports of PTA with several clinical manifestations. In cases with severe internal carotid artery (ICA) occlusion, vascular steal phenomena can occur between the basilar and carotid systems through the PTA [3]. Aneurysms have been reported generally at the origin of the PTA and at the connection with the basilar artery [7,8]. If the aneurysm happens at the carotid connection, isolated sixth cranial nerve palsies can occur due to the compression caused by the aneurysm. The petrosal variant has been re-
M. Harman et al. / European Journal of Radiology Extra 51 (2004) 65–67
ported with clinical symptoms of trigeminal neuralgia and diplopia [8]. There are three PTA cases reported in the literature with intrasellar course [4,9,10]. There are two cases reported hormonal disorder due to compressive effect of PTA on pituitary gland [4,5]. In one of these cases hyperprolactinemia due to compression by PTA was reported and in the other case anomalies of different hypophyseal hormones were reported as found in our case. Our patient did not have findings of pituitary adenoma but we assumed that the elevated and decreased pituitary hormone levels might result from the compression caused by the PTA. In most cases reported, PTA variants have been found incidentally. Yet, PTA variants can cause trigeminal neuralgia, and preoperative recognition of PTA variants is very important during surgical treatment of parasellar lesions, percutaneous gasserian ganglion procedure, and endovascular therapies [11]. MRA can detect PTA non-invasively. Some prior reports of MRI and MRA of PTA variants reveal that PTA variants were identified by MRA [11,12]. In our case, PTA variants could be shown successfully by MRA. While there are many reasons of pituitary hormone disorders, one of the rare causes as in our case is the compression by a persistent trigeminal artery with an intrasellar course, which may cause hormonal disorder without pituitary adenoma. Compressive effect of PTA on the pituitary gland can be demonstrated with MRI and MRA.
67
References [1] Salas E, Ziyal IM, Sekhar LN, Wright DC. Persistent trigeminal artery: an anatomic study. Neurosurgery 1998;43:557–61. [2] Fields WS. The significance of persistent trigeminal artery. Radiology 1968;91:1096–101. [3] Stern J, Correll JW, Bryan N. Persistent hypoglossal artery and persistent trigeminal artery presenting with posterior fossa transient ischemic attacks. J Neurosurg 1978;49:614–9. [4] Ekinci G, Baltacioglu F, Kilic T, et al. A rare cause of hyperprolactinemia: persistent trigeminal artery with stalk section effect. Eur Radiol 2001;11:648–50. [5] Osztie E, Czirjak S, Racz K, Martos J. Hormone disorders caused by intrasellar persistent trigeminal artery. Ideggyogy Sz 2002;20(55):395–8. [6] Saltzman GF. Patent primitive trigeminal artery studied by cerebral angiography. Acta Radiol 1959;51:329–36. [7] Kunilic T, Pamir N, Erzen C. MR angiography of the persistent trigeminal artery associated with an aneurysm. Turk Neurosurg 1997;7:91–3. [8] Blom RJ, Vinuela F. Aneurysm of a persistent trigeminal artery. AJNR 1985;6:651–2. [9] Richardson DN, Elster AD, Ball MR. MR intrasellar trigeminal artery. AJNR 1989;10:205. [10] Tulsi RS, Locket NA. Persistent trigeminal artery: an anatomical study. Aust NZ J Surg 1985;55:397–402. [11] Hirai T, Korogi Y, Sakamoto Y. MR angiography of the persistent trigeminal artery variant. J Comput Assist Tomogr 1995;19:495–7. [12] Uchino A, Kato A, Takase Y, Kudo S. Persistent trigeminal artery variants detected by MR angiography. Eur Radiol 2000;10: 1801–14.