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Transient oculomotor nerve palsy due to non-aneurysmal neurovascular compression
Journal of Clinical Neuroscience xxx (2017) xxx–xxx
Contents lists available at ScienceDirect
Journal of Clinical Neuroscience journal homepage: www.elsevier.com/locate/jocn
Case report
Transient oculomotor nerve palsy due to non-aneurysmal neurovascular compression Stuti Joshi a,⇑, William Wei Han Tee b, Catherine Franconi a, David Prentice c a
Department of Neurology, Royal Perth Hospital, Perth, Australia Department of Neuroradiology, Royal Perth Hospital, Perth, Australia c Department of Internal Medicine, Royal Perth Hospital, Perth, Australia b
a r t i c l e
i n f o
Article history: Received 5 January 2017 Accepted 11 July 2017 Available online xxxx Keywords: Neurovascular Compression Oculomotor
a b s t r a c t Acute oculomotor nerve palsy requires urgent exclusion of aneurysmal compression. We report a 62 year old man with a transient right third nerve palsy with pupillary involvement, who was found to have neurovascular compression of the cisternal oculomotor nerve as it curved over a duplicated superior cerebellar artery on high resolution MR imaging. Direct vascular compression should be considered in patients with isolated cranial neuropathies in whom other pathologies have been excluded. Crown Copyright Ó 2017 Published by Elsevier Ltd. All rights reserved.
1. Case A 62 year old plumber was referred to our centre with an acute onset of binocular diplopia whilst performing strenuous physical work. He experienced a sudden warm flush in his face, followed by an acute onset of binocular diplopia, described as both horizontal and vertical. This was associated with some periorbital discomfort. His past medical history was significant for ischaemic heart disease, hypertension and hyperlipidaemia. On examination, the patient’s blood pressure was 205/105 mmHg and heart rate was 60 beats per minute and regular. There was a partial ptosis on the right. The right pupil was 6 mm and left 4 mm in size. Both were reactive to light. There was no obvious restriction of eye movements, however the patient did complain of ongoing diplopia. There was no fatigability with sustained upgaze. The upper and lower limb examination was within normal limits. The patient was admitted, and within 24 h his signs and symptoms resolved completely. Investigations including full blood count, electrolytes, renal and liver function tests were normal. ESR was 2 mm/hr and ANA was negative. Acetylcholine receptor antibodies were normal. A CTscan of the head and CT angiogram of the head and neck vessels showed no intracranial pathology and there was no evidence of vascular aneurysms or dissections. ⇑ Corresponding author at: Department of Neurology, Royal Perth Hospital, Perth, Western Australia 6000, Australia. E-mail address: [email protected] (S. Joshi).
The patient went on to have an MRI scan of the head which showed that the right oculomotor nerve branched into its superior and inferior divisions early at its cisternal segment, curving over a duplicated superior cerebellar artery (SCA). There was flattening and elevation of the right oculomotor nerve as it passed over the SCA (Fig. 2), as compared to the left side (Fig. 1). There were no areas of restricted diffusion to suggest acute infarct and no aneurysm or other pathology Fig. 3. 2. Discussion In the subarachnoid space, the oculomotor nerves run between the posterior cerebral artery and the superior cerebellar artery, across the basilar artery and parallel to the posterior communicating artery. Enlargement or displacement of these arteries could lead to compression. The parasympathetic fibres of the oculomotor nerve that control pupillary constriction are located superficially and superomedially. Their blood supply is derived from the pial vessels, whereas the main trunk of the third nerve is supplied by the vasa nervorum. The rule of the pupil is used to distinguish between mass lesions from those caused by infarction, by stating that pupillary involvement generally indicates compression of the pial vessels and the superficial pupillary fibres [1]. An ischaemic lesion is less likely to affect the pupil as these involve the vasa nervorum causing central infarction and sparing of the pupillary fibres. Compressive lesions are commonly secondary to intracranial aneurysms, and non-aneurysmal vascular compression of the third nerve has rarely been reported.
http://dx.doi.org/10.1016/j.jocn.2017.07.006 0967-5868/Crown Copyright Ó 2017 Published by Elsevier Ltd. All rights reserved.
Please cite this article in press as: Joshi S et al. Transient oculomotor nerve palsy due to non-aneurysmal neurovascular compression. J Clin Neurosci (2017), http://dx.doi.org/10.1016/j.jocn.2017.07.006
2
Case report / Journal of Clinical Neuroscience xxx (2017) xxx–xxx
Fig. 1. CISS 3D Sagittal; The left Oculomotor nerve ( ) traverses normally through is seen just the ponto-cerebellar cistern. The left superior cerebellar artery inferior to the oculomotor cisternal-cavernous junction without nerve displacement.
Fig. 2. CISS 3D Sagittal; In contradistinction, the right Oculomotor nerve ( ) is significantly displaced superiorly by the duplicated right superior cerebellar arteries ( ) near it’s brainstem origin.
To our knowledge, there is only one previously reported case of superior cerebellar artery causing third nerve compression. Albayram et al. report a case of oculomotor nerve compression from a duplicated superior cerebellar artery and a posterior communicating artery [2]. A handful of cases of isolated oculomotor nerve palsy secondary to vascular compression have been summarised by Tan et al. [3]. Suzuki et al. report a case of a 78 year old man with partial left third nerve palsy with pupillary involvement who was found to have a small internal carotid-posterior communicating artery aneurysm [4]. The patient went on to have surgical clipping, however during the procedure it became evident that the aneurysm was not compressing the oculomotor nerve and in fact the nerve was pinched between arteriosclerotic posterior cerebral and superior cerebellar arteries. Microvascular decompression was performed with improvement in the third nerve palsy. In our case, we believe that focal compression from the adjacent superior cerebellar artery was responsible for the mydriasis, ptosis
Fig. 3. CISS 3D Axial; The duplicated right superior cerebellar arteries ( ) intimately abuts and displaces the anteriorly traversing right oculomotor nerve ( ). Normal contralateral left oculomotor nerve (}).
and diplopia. We speculated that the transient nature of symptoms was due to the acute hypertension contributing to change in blood flow through the posterior circulation and therefore vascular compression by the SCA. Tsai et al. report 10 patients with idiopathic strabismus, who underwent high resolution MRI [5]. In one patient with a third nerve palsy, an ectatic PCA caused flattening of the ipsilateral third nerve, and in two patients with unexplained sixth nerve palsy, ectatic basilar arteries were noted to cause compression ipsilaterally. High resolution MR imaging can reliably depict the anatomical relationships between arteries and cranial nerves [6]. Our patient’s MRI was performed on a SIEMENS 3T scanner. Anatomical delineation is best appreciated on Axial CISS (modified fully refocused steady-state sequence) with sagittal-oblique 3D reformats. This heavily CSF-weighted sequence accentuates structures within the inter-peduncular and pontocerebellar cisterns without significant susceptibility, motion or flow artefacts. Direct vascular compression should be considered in patients with isolated cranial nerve palsies in whom other causes have been excluded. References [1] Ikeda K, Tamura M, Iwasaki Y, et al. Relative pupil-sparing third nerve palsy: etiology and clinical variables predictive of a mass. Neurology 2001;57 (9):1741–2. PubMed PMID: 11706136. [2] Albayram S, Ozer H, Sarici A, et al. Unilateral mydriasis without ophthalmoplegia–a sign of neurovascular compression? Case report. Neurosurgery 2006;58(3):E582–3 [discussion E582-3]. [3] Tan T, Tee JW, Wang YY. Oculomotor nerve palsy secondary to aberrant posterior cerebral artery. BMJ Case Rep 2014;2014. http://dx.doi.org/10.1136/ bcr-2014-205063. Review. [4] Suzuki K, Muroi A, Kujiraoka Y, et al. Oculomotor palsy treated by microvascular decompression. Surg Neurol 2008;70(2):210–2. http://dx.doi.org/10.1016/ j.surneu.2007.04.001. Epub 2008 Feb 11. [5] Tsai TH, Demer JL. Nonaneurysmal cranial nerve compression as cause of neuropathic strabismus: evidence from high-resolution magnetic resonance imaging. Am J Ophthalmol 2011;152(6):1067–1073.e2. http://dx.doi.org/ 10.1016/j.ajo.2011.05.031. Epub 2011 Sep 8. [6] Liang C, Du Y, Lin X, et al. Anatomical features of the cisternal segment of the oculomotor nerve: neurovascular relationships and abnormal compression on magnetic resonance imaging. J Neurosurg. 2009;111(6):1193–200. http://dx. doi.org/10.3171/2009.1.JNS081185.
Please cite this article in press as: Joshi S et al. Transient oculomotor nerve palsy due to non-aneurysmal neurovascular compression. J Clin Neurosci (2017), http://dx.doi.org/10.1016/j.jocn.2017.07.006
Contents lists available at ScienceDirect
Journal of Clinical Neuroscience journal homepage: www.elsevier.com/locate/jocn
Case report
Transient oculomotor nerve palsy due to non-aneurysmal neurovascular compression Stuti Joshi a,⇑, William Wei Han Tee b, Catherine Franconi a, David Prentice c a
Department of Neurology, Royal Perth Hospital, Perth, Australia Department of Neuroradiology, Royal Perth Hospital, Perth, Australia c Department of Internal Medicine, Royal Perth Hospital, Perth, Australia b
a r t i c l e
i n f o
Article history: Received 5 January 2017 Accepted 11 July 2017 Available online xxxx Keywords: Neurovascular Compression Oculomotor
a b s t r a c t Acute oculomotor nerve palsy requires urgent exclusion of aneurysmal compression. We report a 62 year old man with a transient right third nerve palsy with pupillary involvement, who was found to have neurovascular compression of the cisternal oculomotor nerve as it curved over a duplicated superior cerebellar artery on high resolution MR imaging. Direct vascular compression should be considered in patients with isolated cranial neuropathies in whom other pathologies have been excluded. Crown Copyright Ó 2017 Published by Elsevier Ltd. All rights reserved.
1. Case A 62 year old plumber was referred to our centre with an acute onset of binocular diplopia whilst performing strenuous physical work. He experienced a sudden warm flush in his face, followed by an acute onset of binocular diplopia, described as both horizontal and vertical. This was associated with some periorbital discomfort. His past medical history was significant for ischaemic heart disease, hypertension and hyperlipidaemia. On examination, the patient’s blood pressure was 205/105 mmHg and heart rate was 60 beats per minute and regular. There was a partial ptosis on the right. The right pupil was 6 mm and left 4 mm in size. Both were reactive to light. There was no obvious restriction of eye movements, however the patient did complain of ongoing diplopia. There was no fatigability with sustained upgaze. The upper and lower limb examination was within normal limits. The patient was admitted, and within 24 h his signs and symptoms resolved completely. Investigations including full blood count, electrolytes, renal and liver function tests were normal. ESR was 2 mm/hr and ANA was negative. Acetylcholine receptor antibodies were normal. A CTscan of the head and CT angiogram of the head and neck vessels showed no intracranial pathology and there was no evidence of vascular aneurysms or dissections. ⇑ Corresponding author at: Department of Neurology, Royal Perth Hospital, Perth, Western Australia 6000, Australia. E-mail address: [email protected] (S. Joshi).
The patient went on to have an MRI scan of the head which showed that the right oculomotor nerve branched into its superior and inferior divisions early at its cisternal segment, curving over a duplicated superior cerebellar artery (SCA). There was flattening and elevation of the right oculomotor nerve as it passed over the SCA (Fig. 2), as compared to the left side (Fig. 1). There were no areas of restricted diffusion to suggest acute infarct and no aneurysm or other pathology Fig. 3. 2. Discussion In the subarachnoid space, the oculomotor nerves run between the posterior cerebral artery and the superior cerebellar artery, across the basilar artery and parallel to the posterior communicating artery. Enlargement or displacement of these arteries could lead to compression. The parasympathetic fibres of the oculomotor nerve that control pupillary constriction are located superficially and superomedially. Their blood supply is derived from the pial vessels, whereas the main trunk of the third nerve is supplied by the vasa nervorum. The rule of the pupil is used to distinguish between mass lesions from those caused by infarction, by stating that pupillary involvement generally indicates compression of the pial vessels and the superficial pupillary fibres [1]. An ischaemic lesion is less likely to affect the pupil as these involve the vasa nervorum causing central infarction and sparing of the pupillary fibres. Compressive lesions are commonly secondary to intracranial aneurysms, and non-aneurysmal vascular compression of the third nerve has rarely been reported.
http://dx.doi.org/10.1016/j.jocn.2017.07.006 0967-5868/Crown Copyright Ó 2017 Published by Elsevier Ltd. All rights reserved.
Please cite this article in press as: Joshi S et al. Transient oculomotor nerve palsy due to non-aneurysmal neurovascular compression. J Clin Neurosci (2017), http://dx.doi.org/10.1016/j.jocn.2017.07.006
2
Case report / Journal of Clinical Neuroscience xxx (2017) xxx–xxx
Fig. 1. CISS 3D Sagittal; The left Oculomotor nerve ( ) traverses normally through is seen just the ponto-cerebellar cistern. The left superior cerebellar artery inferior to the oculomotor cisternal-cavernous junction without nerve displacement.
Fig. 2. CISS 3D Sagittal; In contradistinction, the right Oculomotor nerve ( ) is significantly displaced superiorly by the duplicated right superior cerebellar arteries ( ) near it’s brainstem origin.
To our knowledge, there is only one previously reported case of superior cerebellar artery causing third nerve compression. Albayram et al. report a case of oculomotor nerve compression from a duplicated superior cerebellar artery and a posterior communicating artery [2]. A handful of cases of isolated oculomotor nerve palsy secondary to vascular compression have been summarised by Tan et al. [3]. Suzuki et al. report a case of a 78 year old man with partial left third nerve palsy with pupillary involvement who was found to have a small internal carotid-posterior communicating artery aneurysm [4]. The patient went on to have surgical clipping, however during the procedure it became evident that the aneurysm was not compressing the oculomotor nerve and in fact the nerve was pinched between arteriosclerotic posterior cerebral and superior cerebellar arteries. Microvascular decompression was performed with improvement in the third nerve palsy. In our case, we believe that focal compression from the adjacent superior cerebellar artery was responsible for the mydriasis, ptosis
Fig. 3. CISS 3D Axial; The duplicated right superior cerebellar arteries ( ) intimately abuts and displaces the anteriorly traversing right oculomotor nerve ( ). Normal contralateral left oculomotor nerve (}).
and diplopia. We speculated that the transient nature of symptoms was due to the acute hypertension contributing to change in blood flow through the posterior circulation and therefore vascular compression by the SCA. Tsai et al. report 10 patients with idiopathic strabismus, who underwent high resolution MRI [5]. In one patient with a third nerve palsy, an ectatic PCA caused flattening of the ipsilateral third nerve, and in two patients with unexplained sixth nerve palsy, ectatic basilar arteries were noted to cause compression ipsilaterally. High resolution MR imaging can reliably depict the anatomical relationships between arteries and cranial nerves [6]. Our patient’s MRI was performed on a SIEMENS 3T scanner. Anatomical delineation is best appreciated on Axial CISS (modified fully refocused steady-state sequence) with sagittal-oblique 3D reformats. This heavily CSF-weighted sequence accentuates structures within the inter-peduncular and pontocerebellar cisterns without significant susceptibility, motion or flow artefacts. Direct vascular compression should be considered in patients with isolated cranial nerve palsies in whom other causes have been excluded. References [1] Ikeda K, Tamura M, Iwasaki Y, et al. Relative pupil-sparing third nerve palsy: etiology and clinical variables predictive of a mass. Neurology 2001;57 (9):1741–2. PubMed PMID: 11706136. [2] Albayram S, Ozer H, Sarici A, et al. Unilateral mydriasis without ophthalmoplegia–a sign of neurovascular compression? Case report. Neurosurgery 2006;58(3):E582–3 [discussion E582-3]. [3] Tan T, Tee JW, Wang YY. Oculomotor nerve palsy secondary to aberrant posterior cerebral artery. BMJ Case Rep 2014;2014. http://dx.doi.org/10.1136/ bcr-2014-205063. Review. [4] Suzuki K, Muroi A, Kujiraoka Y, et al. Oculomotor palsy treated by microvascular decompression. Surg Neurol 2008;70(2):210–2. http://dx.doi.org/10.1016/ j.surneu.2007.04.001. Epub 2008 Feb 11. [5] Tsai TH, Demer JL. Nonaneurysmal cranial nerve compression as cause of neuropathic strabismus: evidence from high-resolution magnetic resonance imaging. Am J Ophthalmol 2011;152(6):1067–1073.e2. http://dx.doi.org/ 10.1016/j.ajo.2011.05.031. Epub 2011 Sep 8. [6] Liang C, Du Y, Lin X, et al. Anatomical features of the cisternal segment of the oculomotor nerve: neurovascular relationships and abnormal compression on magnetic resonance imaging. J Neurosurg. 2009;111(6):1193–200. http://dx. doi.org/10.3171/2009.1.JNS081185.
Please cite this article in press as: Joshi S et al. Transient oculomotor nerve palsy due to non-aneurysmal neurovascular compression. J Clin Neurosci (2017), http://dx.doi.org/10.1016/j.jocn.2017.07.006