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Spectrum disorder of neuromyelitis optica in a patient presenting with intractable vomiting and hiccups, transverse myelitis and acute encephalopathy
Journal of Clinical Neuroscience 19 (2012) 1576–1578
Contents lists available at SciVerse ScienceDirect
Journal of Clinical Neuroscience journal homepage: www.elsevier.com/locate/jocn
Case Reports
Spectrum disorder of neuromyelitis optica in a patient presenting with intractable vomiting and hiccups, transverse myelitis and acute encephalopathy Vishal Patel, Neil C. Griffith ⇑, Emma Blackwood, Manu Dias, Dennis J. Cordato Department of Neurophysiology, Liverpool Hospital, Elizabeth Drive, Liverpool 2170, NSW, Australia
a r t i c l e
i n f o
Article history: Received 2 December 2011 Accepted 14 March 2012
Keywords: Encephalopathy Hiccups Intractable vomiting Neuromyelitis optica Transverse myelitis
a b s t r a c t Optic neuropathy and transverse myelitis (TM) are common symptoms of multiple sclerosis (MS) but may also be seen in association with the antibody-mediated autoimmune disorder, neuromyelitis optica (NMO). We report a female patient presenting with intractable vomiting and hiccups and TM shortly followed by an acute encephalopathy, most likely due to NMO spectrum disorder. Serum and cerebrospinal fluid NMO antibodies were negative. Serial MRI abnormalities included longitudinally extensive TM of the cervical cord, focal T2-weighted hyperintensity of the area postrema and lesions in both thalami and the hypothalamus. Clinical and MRI involvement of these brain regions, which have high aquaporin expression, in conjunction with a spinal lesion extending over three vertebral segments strongly favoured a diagnosis of NMO. She required several courses of intravenous methylprednisolone and plasmapheresis before receiving intravenous rituximab therapy. NMO spectrum disorder should be considered in the differential diagnosis of atypical central nervous system presentations such as intractable vomiting and hiccups and acute encephalopathy. Recognition of this syndrome has significant implications as its treatment and prognosis differs from MS. Ó 2012 Elsevier Ltd. All rights reserved.
1. Introduction Neuromyelitis optica (NMO) is an antibody-mediated autoimmune disorder characterised by optic neuropathy and transverse myelitis (TM).1–4 Disease-specific NMO immunoglobulin G antibodies bind to aquaporin 4 (AQP4) water channels in the optic nerves and spinal cord.1–4 Recent studies have identified intractable vomiting and hiccups and other central nervous system (CNS) manifestations including encephalopathy and hypothalamic dysfunction as additional symptoms.1,4 We report a patient presenting with intractable vomiting and hiccups and spastic quadraparesis due to longitudinally extensive transverse myelitis (LETM) followed by an acute encephalopathy, most likely due to NMO spectrum disorder.
2. Case report A 38-year-old Laotian woman presented to hospital with acute onset of vomiting and hiccups. There was no fever or diarrhoea. Two weeks later, she developed upper and lower limb weakness. Clinical examination revealed normal cranial nerves and asymmetric, left worse than right, pyramidal weakness of grade 3–4/5 affecting upper and lower limbs, exaggerated reflexes and extensor plantar responses. Sensory examination revealed bilateral reduction in pain and light touch of the upper and lower limbs. ⇑ Corresponding author. Tel.: +61 2 87383646; fax: +61 2 87383648. E-mail address: nc_griffi[email protected] (N.C. Griffith).
Initial brain MRI was normal but MRI cervical spine demonstrated C2–3 to C5–6 T2-weighted hyperintensity consistent with LETM (Fig. 1a). Lumbar puncture identified 13 mononuclear cells and normal concentrations of cerebrospinal fluid (CSF) protein and glucose. Oligoclonal bands were not detected in the CSF. CSF polymerase chain reaction was negative for herpes simplex, varicella zoster, cytomegalovirus and Epstein Barr viruses. She received intravenous (IV) acyclovir (10 mg/kg per day for 10 days) and IV methylprednisolone (1 g/day for 5 days). Her spastic paraparesis resolved. The patient was readmitted with ongoing intractable vomiting and hiccups. Gastrointestinal consultation was negative for alternative diagnoses. A second MRI brain revealed T2-weighted hyperintensity in the area postrema/floor of the fourth ventricle (Fig. 1b, c) but was otherwise normal (Fig. 1c). Serum and CSF NMO antibodies were negative. She received five treatments of plasmapheresis with resolution of vomiting and hiccups. She was discharged home on oral prednisolone and azathioprine. Two months post-discharge, the patient was readmitted to hospital with a recurrence of left arm and bilateral lower limb paraesthesia and pyramidal weakness. She received a further 5 g IV methylprednisolone followed by plasmapheresis. Azathioprine was discontinued and she was given 1000 mg IV rituximab. A few days later, she developed an acute confusional state with impaired level of consciousness. Her clinical signs included new onset of a right internuclear ophthalmoplegia. A third MRI brain identified new lesions in the thalami, the hypothalamus (Fig. 1d), periaqueductal grey matter as well as parasagittal cortical T2weighted hyperintensities in both frontal, parietal and occipital
Case Reports / Journal of Clinical Neuroscience 19 (2012) 1576–1578
1577
Fig. 1. (a) Sagittal cervical spine T2-fluid attenuated inversion recovery (FLAIR) MRI showing high signal within the cervical cord and cord swelling from C2–3 to C5–6 consistent with longitudinally extensive transverse myelitis; (b) axial brain T2-weighted FLAIR MRI showing a small focus of high signal (4 mm 3 mm 8 mm) in the posterior medulla to the right of the midline at the floor of the fourth ventricle; (c) sagittal brain T2-weighted FLAIR MRI showing hyperintensity in the area postrema; and (d) axial brain T2-weighted FLAIR MRI (the third MRI) showing high signal within the hypothalamus.
lobes. She was given four further treatments of plasmapheresis. She began to improve before receiving a second dose of 1000 mg IV rituximab. She was mobilising with stand-by assistance before transfer for in-patient rehabilitation therapy. 3. Discussion Optic neuritis and TM are two major diagnostic criteria for a diagnosis of NMO.3 NMO-specific antibodies may not be detected in up to 30% of patients with NMO.2 Hence, a diagnosis is often reliant on clinical and radiological findings. Atypical presentations include intractable vomiting and hiccups, which have recently been considered as symptoms that may distinguish NMO from multiple sclerosis (MS).1 The clinical and MRI involvement in our patient of brain regions with high AQP4 expression including the area postrema and hypothalamus3 in conjunction with a spinal lesion extending over three vertebral segments3 strongly favoured a diagnosis of NMO despite negative NMO serology. Brainstem lesions involving the mesencephalon and medulla oblongata causing pathological laughter and intractable hiccups
have been rarely described in MS.5 However, the area postrema, an emetic centre that contains unmyelinated fibres, is not typically involved in MS.1 Disruption of AQP4 channels, which are abundant in the area postrema and floor of the fourth ventricle, may constitute a distinct syndrome, specific to NMO.1 Pathological studies have shown that area postrema lesions in NMO are non-destructive with relative preservation of axons, neurons and myelin, which may account for the reversibility of clinical and MRI findings.1 Area postrema lesions in NMO, as seen in our patient, may be pathologically distinct rather than a rostral extension of cervical lesions.1 The hypothalamus and ependyma also have high expression of AQP4 and their involvement constitute supportive criteria for a diagnosis of NMO.3 Less common central nervous system (CNS) manifestations seen in association with NMO spectrum disorder include impaired consciousness and acute confusional state, diabetes insipidus and other endocrinopathies such as amenorrhoea, galactorrhoea and hyperphagia.3 Treatment of acute relapses of NMO and MS are similar whereas long-term treatments differ vastly. Agents such as prednisolone,
1578
Case Reports / Journal of Clinical Neuroscience 19 (2012) 1578–1580
azathioprine and rituximab are considered appropriate in NMO whereas immunomodulating agents used in MS are unproven or relatively ineffective.3,4 IV methylprednisolone resolved our patient’s quadraparesis but not her vomiting and hiccups, which responded to plasmapheresis. Following her acute encephalopathy, which included new MRI abnormalities in her thalami and hypothalamus, she was changed from maintenance azathioprine and prednisolone therapy to rituximab. Thus, we report a patient with a rapid succession of symptoms including intractable vomiting and hiccups, TM and acute encephalopathy, most probably due to NMO spectrum disorder. NMO should be considered in the differential diagnosis of atypical CNS presentations such as intractable vomiting and hiccups and acute encephalopathy. Recognition of this syndrome has significant implications as its treatment and prognosis differs from MS.
References 1. Popescu BF, Lennon VA, Parisi JE, et al. Neuromyelitis optica unique are postrema lesions: nausea, vomiting, and pathogenic implications. Neurology 2011;76: 1229–37. 2. Lennon VA, Wingerchuk DM, Kryzer TJ, et al. A serum autoantibody marker of neuromyelitis optica: distinction from multiple sclerosis. Lancet 2004;364:2106–12. 3. Sellner J, Boggild M, Clanet M, et al. EFNS guidelines on diagnosis and management of neuromyelitis optica. Eur J Neurol 2010;17:1019–32. 4. Jacob A, Weinshenker BG, Violich I, et al. Treatment of neuromyelitis optica with rituximab: retrospective analysis of 25 cases. Arch Neurology 2008;65:1443–8. 5. De Seze J, Zephir H, Hautecouer P, et al. Pathological laughing and intractable hiccups can occur early in multiple sclerosis. Neurology 2006;67:1684–6.
doi:http://dx.doi.org/10.1016/j.jocn.2012.03.007
Microsurgical clipping of an unruptured lenticulostriate aneurysm M. Yashar S. Kalani, Nikolay L. Martirosyan, Peter Nakaji, Robert F. Spetzler ⇑ Division of Neurological Surgery, Barrow Neurological Institute, St. Joseph’s Hospital and Medical Center, 350 West Thomas Road, Phoenix, AZ 85013, USA
a r t i c l e
i n f o
Article history: Received 12 March 2012 Accepted 17 March 2012
Keywords: Aneurysm Clipping Hunterian ligation Lenticulostriate Moyamoya
a b s t r a c t Aneurysms of the lenticulostriate artery have been associated with hypertension, vasculopathy, tumors, and arteriovenous malformations. Although several cases of microsurgical treatment of ruptured lenticulostriate artery aneurysms have been reported, to our knowledge there is no published case of microsurgical treatment of an unruptured lenticulostriate artery aneurysm. We report a 66-year-old woman with a history of moyamoya disease, previously treated with a right-sided middle cerebral artery-tosuperficial temporal artery bypass who presented with an unruptured aneurysm of a lenticulostriate artery. We report successful microsurgical treatment of this rare lesion and discuss the rationale for our treatment strategy. Ó 2012 Elsevier Ltd. All rights reserved.
1. Introduction Aneurysms of the lenticulostriate artery are rare lesions that may occur at the junction of the middle cerebral artery trunk or distally within the basal ganglia. These lesions have been reported in the setting of a diverse array of pathologies including tumors, vascular malformations, various vasculitides (including moyamoya and lupus), and hypertension.1–4 Although the microsurgical and endovascular treatment of almost 20 ruptured aneurysms of the lenticulostriate artery has been reported,1–9 we found no case that reported successful microsurgical clipping of an unruptured lenticulostriate aneurysm. We now describe a rare unruptured aneurysm of the lenticulostriate artery treated with microsurgical clipping in a woman with moyamoya disease.
bypass in 2000. Postoperatively, the patient was started on aspirin. Immediately after that surgery she had slight aphasia, but she recovered well and was neurologically intact. One year before her current presentation, she developed gait imbalance. As part of the evaluation ordered by her neurologist, formal cerebral angiography (Fig. 1A, B) and MRI (Fig. 1C, D) showed a complex multilobulated 6 mm 6 mm 9 mm aneurysm involving a right lenticulostriate artery. Given the size and complex nature of this aneurysm, it was thought that treatment was warranted. The patient underwent two attempts at endovascular embolization of this aneurysm, but the tortuous, small caliber of the vessels (likely caused by her moyamoya disease) made endovascular catheterization challenging. The patient was subsequently referred to our clinic for microsurgical treatment of this unruptured aneurysm.
2. Case report 2.1. History and physical examination A 66-year-old woman with a history of hypercholesterolemia, hypertension, and moyamoya disease had undergone a right-sided middle cerebral artery-to-superficial temporal artery (MCA-STA) ⇑ Corresponding author. Tel.: +1 602 406 3593; fax: +1 602 406 4104. E-mail address: [email protected] (R.F. Spetzler).
2.2. Surgical procedure The patient underwent a right orbitozygomatic craniotomy for clipping of the aneurysm. Intraoperatively, the lesion was visualized, but it was felt that given the distal and deep location of the aneurysm, direct clipping might cause damage to adjacent eloquent neural structures. Therefore, we sought to proximally occlude the vessel leading to the aneurysm (Fig. 2). The decision was made to place the clip adjacent to the aneurysm dome to block
Contents lists available at SciVerse ScienceDirect
Journal of Clinical Neuroscience journal homepage: www.elsevier.com/locate/jocn
Case Reports
Spectrum disorder of neuromyelitis optica in a patient presenting with intractable vomiting and hiccups, transverse myelitis and acute encephalopathy Vishal Patel, Neil C. Griffith ⇑, Emma Blackwood, Manu Dias, Dennis J. Cordato Department of Neurophysiology, Liverpool Hospital, Elizabeth Drive, Liverpool 2170, NSW, Australia
a r t i c l e
i n f o
Article history: Received 2 December 2011 Accepted 14 March 2012
Keywords: Encephalopathy Hiccups Intractable vomiting Neuromyelitis optica Transverse myelitis
a b s t r a c t Optic neuropathy and transverse myelitis (TM) are common symptoms of multiple sclerosis (MS) but may also be seen in association with the antibody-mediated autoimmune disorder, neuromyelitis optica (NMO). We report a female patient presenting with intractable vomiting and hiccups and TM shortly followed by an acute encephalopathy, most likely due to NMO spectrum disorder. Serum and cerebrospinal fluid NMO antibodies were negative. Serial MRI abnormalities included longitudinally extensive TM of the cervical cord, focal T2-weighted hyperintensity of the area postrema and lesions in both thalami and the hypothalamus. Clinical and MRI involvement of these brain regions, which have high aquaporin expression, in conjunction with a spinal lesion extending over three vertebral segments strongly favoured a diagnosis of NMO. She required several courses of intravenous methylprednisolone and plasmapheresis before receiving intravenous rituximab therapy. NMO spectrum disorder should be considered in the differential diagnosis of atypical central nervous system presentations such as intractable vomiting and hiccups and acute encephalopathy. Recognition of this syndrome has significant implications as its treatment and prognosis differs from MS. Ó 2012 Elsevier Ltd. All rights reserved.
1. Introduction Neuromyelitis optica (NMO) is an antibody-mediated autoimmune disorder characterised by optic neuropathy and transverse myelitis (TM).1–4 Disease-specific NMO immunoglobulin G antibodies bind to aquaporin 4 (AQP4) water channels in the optic nerves and spinal cord.1–4 Recent studies have identified intractable vomiting and hiccups and other central nervous system (CNS) manifestations including encephalopathy and hypothalamic dysfunction as additional symptoms.1,4 We report a patient presenting with intractable vomiting and hiccups and spastic quadraparesis due to longitudinally extensive transverse myelitis (LETM) followed by an acute encephalopathy, most likely due to NMO spectrum disorder.
2. Case report A 38-year-old Laotian woman presented to hospital with acute onset of vomiting and hiccups. There was no fever or diarrhoea. Two weeks later, she developed upper and lower limb weakness. Clinical examination revealed normal cranial nerves and asymmetric, left worse than right, pyramidal weakness of grade 3–4/5 affecting upper and lower limbs, exaggerated reflexes and extensor plantar responses. Sensory examination revealed bilateral reduction in pain and light touch of the upper and lower limbs. ⇑ Corresponding author. Tel.: +61 2 87383646; fax: +61 2 87383648. E-mail address: nc_griffi[email protected] (N.C. Griffith).
Initial brain MRI was normal but MRI cervical spine demonstrated C2–3 to C5–6 T2-weighted hyperintensity consistent with LETM (Fig. 1a). Lumbar puncture identified 13 mononuclear cells and normal concentrations of cerebrospinal fluid (CSF) protein and glucose. Oligoclonal bands were not detected in the CSF. CSF polymerase chain reaction was negative for herpes simplex, varicella zoster, cytomegalovirus and Epstein Barr viruses. She received intravenous (IV) acyclovir (10 mg/kg per day for 10 days) and IV methylprednisolone (1 g/day for 5 days). Her spastic paraparesis resolved. The patient was readmitted with ongoing intractable vomiting and hiccups. Gastrointestinal consultation was negative for alternative diagnoses. A second MRI brain revealed T2-weighted hyperintensity in the area postrema/floor of the fourth ventricle (Fig. 1b, c) but was otherwise normal (Fig. 1c). Serum and CSF NMO antibodies were negative. She received five treatments of plasmapheresis with resolution of vomiting and hiccups. She was discharged home on oral prednisolone and azathioprine. Two months post-discharge, the patient was readmitted to hospital with a recurrence of left arm and bilateral lower limb paraesthesia and pyramidal weakness. She received a further 5 g IV methylprednisolone followed by plasmapheresis. Azathioprine was discontinued and she was given 1000 mg IV rituximab. A few days later, she developed an acute confusional state with impaired level of consciousness. Her clinical signs included new onset of a right internuclear ophthalmoplegia. A third MRI brain identified new lesions in the thalami, the hypothalamus (Fig. 1d), periaqueductal grey matter as well as parasagittal cortical T2weighted hyperintensities in both frontal, parietal and occipital
Case Reports / Journal of Clinical Neuroscience 19 (2012) 1576–1578
1577
Fig. 1. (a) Sagittal cervical spine T2-fluid attenuated inversion recovery (FLAIR) MRI showing high signal within the cervical cord and cord swelling from C2–3 to C5–6 consistent with longitudinally extensive transverse myelitis; (b) axial brain T2-weighted FLAIR MRI showing a small focus of high signal (4 mm 3 mm 8 mm) in the posterior medulla to the right of the midline at the floor of the fourth ventricle; (c) sagittal brain T2-weighted FLAIR MRI showing hyperintensity in the area postrema; and (d) axial brain T2-weighted FLAIR MRI (the third MRI) showing high signal within the hypothalamus.
lobes. She was given four further treatments of plasmapheresis. She began to improve before receiving a second dose of 1000 mg IV rituximab. She was mobilising with stand-by assistance before transfer for in-patient rehabilitation therapy. 3. Discussion Optic neuritis and TM are two major diagnostic criteria for a diagnosis of NMO.3 NMO-specific antibodies may not be detected in up to 30% of patients with NMO.2 Hence, a diagnosis is often reliant on clinical and radiological findings. Atypical presentations include intractable vomiting and hiccups, which have recently been considered as symptoms that may distinguish NMO from multiple sclerosis (MS).1 The clinical and MRI involvement in our patient of brain regions with high AQP4 expression including the area postrema and hypothalamus3 in conjunction with a spinal lesion extending over three vertebral segments3 strongly favoured a diagnosis of NMO despite negative NMO serology. Brainstem lesions involving the mesencephalon and medulla oblongata causing pathological laughter and intractable hiccups
have been rarely described in MS.5 However, the area postrema, an emetic centre that contains unmyelinated fibres, is not typically involved in MS.1 Disruption of AQP4 channels, which are abundant in the area postrema and floor of the fourth ventricle, may constitute a distinct syndrome, specific to NMO.1 Pathological studies have shown that area postrema lesions in NMO are non-destructive with relative preservation of axons, neurons and myelin, which may account for the reversibility of clinical and MRI findings.1 Area postrema lesions in NMO, as seen in our patient, may be pathologically distinct rather than a rostral extension of cervical lesions.1 The hypothalamus and ependyma also have high expression of AQP4 and their involvement constitute supportive criteria for a diagnosis of NMO.3 Less common central nervous system (CNS) manifestations seen in association with NMO spectrum disorder include impaired consciousness and acute confusional state, diabetes insipidus and other endocrinopathies such as amenorrhoea, galactorrhoea and hyperphagia.3 Treatment of acute relapses of NMO and MS are similar whereas long-term treatments differ vastly. Agents such as prednisolone,
1578
Case Reports / Journal of Clinical Neuroscience 19 (2012) 1578–1580
azathioprine and rituximab are considered appropriate in NMO whereas immunomodulating agents used in MS are unproven or relatively ineffective.3,4 IV methylprednisolone resolved our patient’s quadraparesis but not her vomiting and hiccups, which responded to plasmapheresis. Following her acute encephalopathy, which included new MRI abnormalities in her thalami and hypothalamus, she was changed from maintenance azathioprine and prednisolone therapy to rituximab. Thus, we report a patient with a rapid succession of symptoms including intractable vomiting and hiccups, TM and acute encephalopathy, most probably due to NMO spectrum disorder. NMO should be considered in the differential diagnosis of atypical CNS presentations such as intractable vomiting and hiccups and acute encephalopathy. Recognition of this syndrome has significant implications as its treatment and prognosis differs from MS.
References 1. Popescu BF, Lennon VA, Parisi JE, et al. Neuromyelitis optica unique are postrema lesions: nausea, vomiting, and pathogenic implications. Neurology 2011;76: 1229–37. 2. Lennon VA, Wingerchuk DM, Kryzer TJ, et al. A serum autoantibody marker of neuromyelitis optica: distinction from multiple sclerosis. Lancet 2004;364:2106–12. 3. Sellner J, Boggild M, Clanet M, et al. EFNS guidelines on diagnosis and management of neuromyelitis optica. Eur J Neurol 2010;17:1019–32. 4. Jacob A, Weinshenker BG, Violich I, et al. Treatment of neuromyelitis optica with rituximab: retrospective analysis of 25 cases. Arch Neurology 2008;65:1443–8. 5. De Seze J, Zephir H, Hautecouer P, et al. Pathological laughing and intractable hiccups can occur early in multiple sclerosis. Neurology 2006;67:1684–6.
doi:http://dx.doi.org/10.1016/j.jocn.2012.03.007
Microsurgical clipping of an unruptured lenticulostriate aneurysm M. Yashar S. Kalani, Nikolay L. Martirosyan, Peter Nakaji, Robert F. Spetzler ⇑ Division of Neurological Surgery, Barrow Neurological Institute, St. Joseph’s Hospital and Medical Center, 350 West Thomas Road, Phoenix, AZ 85013, USA
a r t i c l e
i n f o
Article history: Received 12 March 2012 Accepted 17 March 2012
Keywords: Aneurysm Clipping Hunterian ligation Lenticulostriate Moyamoya
a b s t r a c t Aneurysms of the lenticulostriate artery have been associated with hypertension, vasculopathy, tumors, and arteriovenous malformations. Although several cases of microsurgical treatment of ruptured lenticulostriate artery aneurysms have been reported, to our knowledge there is no published case of microsurgical treatment of an unruptured lenticulostriate artery aneurysm. We report a 66-year-old woman with a history of moyamoya disease, previously treated with a right-sided middle cerebral artery-tosuperficial temporal artery bypass who presented with an unruptured aneurysm of a lenticulostriate artery. We report successful microsurgical treatment of this rare lesion and discuss the rationale for our treatment strategy. Ó 2012 Elsevier Ltd. All rights reserved.
1. Introduction Aneurysms of the lenticulostriate artery are rare lesions that may occur at the junction of the middle cerebral artery trunk or distally within the basal ganglia. These lesions have been reported in the setting of a diverse array of pathologies including tumors, vascular malformations, various vasculitides (including moyamoya and lupus), and hypertension.1–4 Although the microsurgical and endovascular treatment of almost 20 ruptured aneurysms of the lenticulostriate artery has been reported,1–9 we found no case that reported successful microsurgical clipping of an unruptured lenticulostriate aneurysm. We now describe a rare unruptured aneurysm of the lenticulostriate artery treated with microsurgical clipping in a woman with moyamoya disease.
bypass in 2000. Postoperatively, the patient was started on aspirin. Immediately after that surgery she had slight aphasia, but she recovered well and was neurologically intact. One year before her current presentation, she developed gait imbalance. As part of the evaluation ordered by her neurologist, formal cerebral angiography (Fig. 1A, B) and MRI (Fig. 1C, D) showed a complex multilobulated 6 mm 6 mm 9 mm aneurysm involving a right lenticulostriate artery. Given the size and complex nature of this aneurysm, it was thought that treatment was warranted. The patient underwent two attempts at endovascular embolization of this aneurysm, but the tortuous, small caliber of the vessels (likely caused by her moyamoya disease) made endovascular catheterization challenging. The patient was subsequently referred to our clinic for microsurgical treatment of this unruptured aneurysm.
2. Case report 2.1. History and physical examination A 66-year-old woman with a history of hypercholesterolemia, hypertension, and moyamoya disease had undergone a right-sided middle cerebral artery-to-superficial temporal artery (MCA-STA) ⇑ Corresponding author. Tel.: +1 602 406 3593; fax: +1 602 406 4104. E-mail address: [email protected] (R.F. Spetzler).
2.2. Surgical procedure The patient underwent a right orbitozygomatic craniotomy for clipping of the aneurysm. Intraoperatively, the lesion was visualized, but it was felt that given the distal and deep location of the aneurysm, direct clipping might cause damage to adjacent eloquent neural structures. Therefore, we sought to proximally occlude the vessel leading to the aneurysm (Fig. 2). The decision was made to place the clip adjacent to the aneurysm dome to block