- Email: [email protected]
Isolated Subcallosal Artery Infarction Secondary to Localized Cerebral Vasospasm of Anterior Communicating Artery Complex Following Subarachnoid Hemorrhage
Accepted Manuscript Isolated subcallosal artery infarction secondary to localised cerebral vasospasm of anterior communicating artery complex following subarachnoid haemorrhage Santhosh Kumar Kannath, Virender Malik, Jayadevan Enakshy Rajan PII:
S1878-8750(17)31152-X
DOI:
10.1016/j.wneu.2017.07.052
Reference:
WNEU 6114
To appear in:
World Neurosurgery
Received Date: 17 April 2017 Revised Date:
10 July 2017
Accepted Date: 11 July 2017
Please cite this article as: Kannath SK, Malik V, Rajan JE, Isolated subcallosal artery infarction secondary to localised cerebral vasospasm of anterior communicating artery complex following subarachnoid haemorrhage, World Neurosurgery (2017), doi: 10.1016/j.wneu.2017.07.052. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT Title page: Isolated subcallosal artery infarction secondary to localised cerebral vasospasm of anterior communicating artery complex following subarachnoid haemorrhage. Author information and affiliations:
RI PT
• Santhosh Kumar Kannath
Phone no:+91-4712524117
• Virender Malik
M AN U
Email:[email protected]
SC
Associate Professor, Neurointervention Center, Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Trivandrum, Kerala, India. Pin no:695011
Senior Resident, Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Trivandrum, Kerala, India. Pin no:695011 Phone no:+91-4712524117
TE D
Email:[email protected] • Jayadevan Enakshy Rajan
EP
Associate Professor, Neurointervention Center, Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Trivandrum, Kerala, India. Pin no:695011 Phone no:+91-4712524117
AC C
Email: [email protected]
Corresponding Author
Jayadevan Enakshy Rajan Associate Professor, Neurointervention Center, Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Trivandrum, Kerala, India. Pin no:695011 Phone no:+91-4712524117 Email: [email protected]
ACCEPTED MANUSCRIPT Running title: Subcallosal infarction due to SAH related vasospasm Key words: isolated; subarachnoid haemorrhage; subcallosal artery infarction; vasospasm
RI PT
Abbreviations:ACOM- anterior communicating artery, ACA-anterior cerebral artery, ScAsubcallosal artery,
Contributions of authors:
• •
Santhosh Kumar Kannath- Concept and design, data analysis, data interpretation, manuscript preparation, critical revision Virender Malik- manuscript preparation,critical revision Jayadevan Enakshy Rajan –Concept and design,data interpretation, critical revision
SC
•
Conflicts of interest:
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EP
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M AN U
The authors have no personal or financial conflict of interest to disclose
ACCEPTED MANUSCRIPT ABSTRACT Background:Subcallosal artery (ScA) infarction is a well-recognised, but uncommon complication of surgical treatment of anterior communicating artery (ACOM) aneurysms. Case description:An elderly man presented with massive subarachnoid haemorrhage due to
RI PT
left posterior communicating artery aneurysm with thick clots in the anterior interhemispheric fissure. The aneurysm was coiled with balloon protection and later, on the fifth day of ictus, the patient became acutely confused and developed memory disturbances. MR evaluation
SC
revealed typical infarcts in the anterior subcallosal region and fornix confirming ScA
infarction. Retrospective analysis of follow up angiograms revealed focal isolated spasm of
M AN U
the ACOM artery and ScA, responding to intrarterial milirinone infusion that was administered in view of neurological worsening and clinical suspicion of cerebral vasospasm. Conclusion:Our case demonstrates a rare case of isolated ScA infarction induced by a local vasospasm and highlights the importance of its recognition. An early identification and
AC C
EP
TE D
intervention could potentially halt irreparable cerebral injury.
ACCEPTED MANUSCRIPT Introduction Subcallosal artery infarction is a well-recognised, but very uncommon complication of surgical treatment of anterior communicating artery aneurysms.1 Vascular damage to the perforators arising from the anterior communicating artery complex supplying the calloso-
RI PT
forniceal region is presumed to be the underlying mechanism of these infarcts. Its incidence following endovascular coiling is extremely rare,with only two of such cases being reported in the literature.2,3 We report an unusual case of isolated callosal infarction in a patient with
SC
acute subarachnoid haemorrhage due to ruptured right posterior communicating artery
aneurysm. The observation is interesting as the infarction occurred in the absence of any
M AN U
thromboembolic complications or operative interference in the region of ACOM complex. The plausible pathomechanism of infarction is discussed. Case description
A 60-year-old hypertensive man, presented with acute severe intensity headache associated
TE D
with vomiting, photophobia and single episode of seizure. Urgent plain CT of brain showed massive subarachnoid hemorrhage (Fisher grade 4) with conspicuous clot concentration in interhemispheric fissure. Digital subtraction angiography (DSA) showed a wide neck right
EP
posterior communicating artery aneurysm measuring 6 x 7 mm. Balloon assisted coiling of
AC C
the aneurysm was done on 3rd day of the ictus, achieving aneurysm occlusion of class 3a modified Raymond-Roy classification (figure 1). On day 5 of ictus, the patient developed acute phase of confusion, memory disturbances and somnolence, raising the suspicion of cerebral vasospasm syndrome. Immediate CT study showed no rebleed or acute infarcts. Emergent DSA showed mild spasm of proximal M1 middle cerebral artery on both sides. He was treated with intraarterial milirinone bolus of 4 mg in each internal carotid artery (ICA) territory and the intravenous infusion was continued till 10th day of ictus. Over next 2 days, the confusion state improved; however patient developed anterograde amnesia. MRI
ACCEPTED MANUSCRIPT obtained at the time of discharge revealed acute infarct in the genu of corpus callosum and in the anterior commissure. The DSA images were retrospectively reviewed to identify the probable etiology of ScA infarction. There were neither thromboembolic complications during the procedure nor any
RI PT
catheter or wire manipulations in the anterior cerebral artery (ACA) or ACOM artery. A1 and A2 segments of ACA appeared normal in calibre. There was reduced opacification of
bilateral A2 segments, however a delay in cerebral perfusion or perfusion defect was not
SC
evident. Careful analysis of initial angiogram revealed a prominent ScA artery arising from ACOM artery. Subsequent angiogram prior to milirinone administration revealed that there
M AN U
was possible mild spasm of ACOM artery with non-visualisation of ScA.(figure 2). However, following chemical angioplasty, the ScA could be normally visualised confirming the presence of isolated spasm of ACOM-ScA complex, responding to milirinone. A follow-up comprehensive assessment (cognitive, behavioural, and psychosocial ) of the
Discussion
TE D
patient at 3 months showed no persistent abnormality.
Perforator injury is an important complication during the surgery of ACOM artery aneurysm
EP
or midline interhemispheric tumors and hence, its preservation is of utmost importance to
AC C
avoid postoperative complications.4 Several important perforators arise from the ACOM complex that perfuses critical regions such as subcallosal area, corpus callosum, hypothalamus and optic chiasm. Depending on their vascular territories, Serigawa categorised these arteries into three types such as subcallosal, hypothalamic or chiasmatic arteries.5 The subcallosal artery usually arises from posterior or posterior-superior aspect of ACOM artery as a single, large branch with a diameter range of 0.4 mm to 0.8 mm. The artery courses vertically through the cistern of lamina terminalis and ultimately, terminates in the subcallosal region. The regions supplied this artery include genu and rostrum of corpus
ACCEPTED MANUSCRIPT callosum, anterior cingulate gyrus, paraolfactory and paraterminal gyrus, columns of fornix and septum pellucidum. In more than a third of patients, it may give off branches to hypothalamus as well.5,6 The typical presentation of subcallosal artery infarction is antegrade amnesia, which may
RI PT
develop immediately or several days later after the insult. Other symptoms such as retrograde amnesia, behavioural or personality changes, psychomotor retardation or Korsarkoff’s
psychosis are also described.2,4 It is presumed that the pathophysiology of antegrade amnesia
SC
is due to the involvement of columns of fornix, which forms an important constituent of
Papez circuit. The fornix is a major white matter output tract that connects hippocampus with
M AN U
hypothalamus and basal forebrain. It is thought to play an important role in the registration of episodic information and hence any damage would likely cause disturbances in declarative memory. Forniceal infarcts are usually bilateral, due to the unpaired nature of the subcallosal artery.4
TE D
In a recent study, Mugikura et al described typical patterns of subcallosal infarction on imaging in patients with amnesia following ACOM aneurysm surgery. The most common sites of involvement were forniceal columns, anterior commissure and paraterminal gyrus.
EP
The typical imaging features include bow-tie-like appearance (representing bilateral
AC C
involvement of anterior commissure associated with infarcted foci in column of the fornix) and sagittally elongated infarction along the medial aspect of the brain. Involvement of adjacent brain structures such as corpus callosum or medial frontal lobes are also common, however the patients may remain asymptomatic unless significant brain parenchyma is affected.7 In our case, the postoperative symptoms were mistaken for cerebral vasospasm syndrome and the ScA infarction was identified only after the follow up MR imaging that showed typical findings. Retrospective analysis showed the ScA was poorly visualised in the postoperative
ACCEPTED MANUSCRIPT angiography, which demonstrated normalisation of the arterial calibre following milirinone infusion. Operative manipulations inducing spasm were ruled out, as the aneurysm was located in a different vascular territory. Also, there were no thromboembolic complications during the procedure. Our patient was treated with dual antiplatelet medications for his
RI PT
cardiac ailments and hence, deranged hemostasis in the setting of aneurysmal rupture might have resulted in the massive subarachnoid haemorrhage and formation of large cisternal clots. A large clot in the interhemispheric fissure might precipitate narrowing of ScA by mass effect
SC
or vasospasm, making the patient vulnerable to ischemia, especially when ScA is prominent arterial branch. Indeed, Abla et al had shown that the incidence of radiological or
M AN U
symptomatic was higher for pericallosal artery, even with a lesser clot burden and this observation was attributed to smaller calibre of the arteries.8 Though bilateral anterior cerebral arteries were unaffected by the vasospasm, narrowing of ScA and probable involvement of microscopic anastomotic communications between ACA-ScA would have
TE D
rendered the patient vulnerable to infarction of ScA territory. Isolated ScA infarction secondary to cerebral vasospasm is previously unreported. However, moderate or severe angiographic cerebral vasospasm is observed in up to one third of the patients with
EP
aneurysmal SAH, which would lead to delayed cerebral infarction in 15% of the patients. More than half of these vasospasm related infarcts were observed in the anterior cerebral
AC C
artery territory.9
Our case highlights the importance of early recognition of the ScA syndrome, so that an appropriate and if needed, aggressive intervention could be instituted if vasospasm of ACA or ScA is identified as the possible etiology.
Funding: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
ACCEPTED MANUSCRIPT
RI PT
Conflicts of interest: None
References
SC
1. DeLuca J, Diamond BJ. Aneurysm of the anterior communicating artery: a review of
neuroanatomical and neuropsychological sequelae. J Clin Exp Neuropsychol 1995;17:100–
M AN U
121.
2.Meila D,Saliou G,Krings T. Subcallosal artery stroke: infarction of the fornix and the genu of the corpus callosum. The importance of the anterior communicating artery complex. Case series and review of the literature. Neuroradiology 2015;57:41–47.
TE D
3.Mosimann PJ, Saint-Maurice JP, Lenck S, Puccinelli F, Houdart E. Fornix infarction and Korsakoff dementia after coiling of a large anterior communicating artery aneurysm. Neurol Clin Pract 2012;2: 260–262.
EP
4.Mugikura S,Kikuchi H,Fujii T,Murata T,Takase K,Mori E,Marinkovic S,Takahashi S. MR imaging of subcallosal artery infarct causing amnesia after surgery for anterior
AC C
communicating artery aneurysm. AJNR Am J Neuroradiol 2014;35:2293–2301. 5.Serizawa T,Noakatsu S,Akira Y. Microsurgical anatomy and clinical significance of the anterior communicating artery and its perforating branches. Neurosurgery 1997;40:12111218.
6.Marinkovc S, Milisavljevic M, Marinkovic Z: Branches of the anterior communicating artery: microsurgical anatomy. Acta Neurochir 1990;106:78-85. 7.Moudgil SS,Azzouz M,Al-Azzaz A,Haut M,Gutman L. Amnesia due to fornix infarction. Stroke. 2000;31:1418- 1419.
ACCEPTED MANUSCRIPT 8.Abla AA,Wilson DA,Williamson RW,Nakaji P,McDougall CG,Zabramski JM.Albuquerque FC,Spetzler RF. The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial. J Neurosurg 2014;120:391–
RI PT
397. 9.Brown RJ,Kumar A,Dhar R,Sampson TR,Diringer MN. The relationship between delayed infarcts and angiographic vasospasm after aneurysmal subarachnoid haemorrhage.
SC
Neurosurgery 2013;72:702-708.
M AN U
Figure legends Figure 1
Plain CT scan of the brain on day 1 of ictus reveals massive subarachnoid haemorrhage in the sylvian and basal cisterns (A) with most conspicuous clot concentration in interhemispheric
TE D
fissure(B. Right internal carotid artery angiogram obtained on day shows a right posterior communicating artery aneurysm (C) that was occluded by balloon assisted coiling (arrow in D).
EP
Figure 2
Bilateral internal carotid artery angiogram obtained on the same shows mild spasm of M1
AC C
middle cerebral artery both sides, A1 anterior cerebral artery are normal in caliber(A,B). Note that the ACOM complex is not distinctly visualised (B). Initial angiogram obtained at the time of balloon assisted coiling shows a prominent ScA artery (arrow in C) that is not identifiable in the angiogram obtained at the time of clinical suspicion of vasospasm (arrow in D). The ScA artery is visible following the chemical angioplasty (arrow in E) with improved opacification of distal ACA branches. Axial section of apparent diffusion coefficient map shows acute infarction in the anterior commissure and fornix (arrow in F)
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT
ACCEPTED MANUSCRIPT Highlights
RI PT
SC M AN U
•
TE D
•
EP
•
Subcallosal infarction presents with typical clinical features of confusion and antegrade amnesia Subarachnoid hemorrhage with localised thick clot in the anterior interhemispheric fissure can result in localized spasm of anterior communicating artery complex and subcallosal artery Accurate recognition of symptoms and careful analysis of prior angiograms help in the early diagnosis and its subsequent management Chemical angioplasty is effective in reversing the local vasospasm and it could potentially prevent an irreparable brain injury
AC C
•
S1878-8750(17)31152-X
DOI:
10.1016/j.wneu.2017.07.052
Reference:
WNEU 6114
To appear in:
World Neurosurgery
Received Date: 17 April 2017 Revised Date:
10 July 2017
Accepted Date: 11 July 2017
Please cite this article as: Kannath SK, Malik V, Rajan JE, Isolated subcallosal artery infarction secondary to localised cerebral vasospasm of anterior communicating artery complex following subarachnoid haemorrhage, World Neurosurgery (2017), doi: 10.1016/j.wneu.2017.07.052. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT Title page: Isolated subcallosal artery infarction secondary to localised cerebral vasospasm of anterior communicating artery complex following subarachnoid haemorrhage. Author information and affiliations:
RI PT
• Santhosh Kumar Kannath
Phone no:+91-4712524117
• Virender Malik
M AN U
Email:[email protected]
SC
Associate Professor, Neurointervention Center, Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Trivandrum, Kerala, India. Pin no:695011
Senior Resident, Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Trivandrum, Kerala, India. Pin no:695011 Phone no:+91-4712524117
TE D
Email:[email protected] • Jayadevan Enakshy Rajan
EP
Associate Professor, Neurointervention Center, Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Trivandrum, Kerala, India. Pin no:695011 Phone no:+91-4712524117
AC C
Email: [email protected]
Corresponding Author
Jayadevan Enakshy Rajan Associate Professor, Neurointervention Center, Department of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Trivandrum, Kerala, India. Pin no:695011 Phone no:+91-4712524117 Email: [email protected]
ACCEPTED MANUSCRIPT Running title: Subcallosal infarction due to SAH related vasospasm Key words: isolated; subarachnoid haemorrhage; subcallosal artery infarction; vasospasm
RI PT
Abbreviations:ACOM- anterior communicating artery, ACA-anterior cerebral artery, ScAsubcallosal artery,
Contributions of authors:
• •
Santhosh Kumar Kannath- Concept and design, data analysis, data interpretation, manuscript preparation, critical revision Virender Malik- manuscript preparation,critical revision Jayadevan Enakshy Rajan –Concept and design,data interpretation, critical revision
SC
•
Conflicts of interest:
AC C
EP
TE D
M AN U
The authors have no personal or financial conflict of interest to disclose
ACCEPTED MANUSCRIPT ABSTRACT Background:Subcallosal artery (ScA) infarction is a well-recognised, but uncommon complication of surgical treatment of anterior communicating artery (ACOM) aneurysms. Case description:An elderly man presented with massive subarachnoid haemorrhage due to
RI PT
left posterior communicating artery aneurysm with thick clots in the anterior interhemispheric fissure. The aneurysm was coiled with balloon protection and later, on the fifth day of ictus, the patient became acutely confused and developed memory disturbances. MR evaluation
SC
revealed typical infarcts in the anterior subcallosal region and fornix confirming ScA
infarction. Retrospective analysis of follow up angiograms revealed focal isolated spasm of
M AN U
the ACOM artery and ScA, responding to intrarterial milirinone infusion that was administered in view of neurological worsening and clinical suspicion of cerebral vasospasm. Conclusion:Our case demonstrates a rare case of isolated ScA infarction induced by a local vasospasm and highlights the importance of its recognition. An early identification and
AC C
EP
TE D
intervention could potentially halt irreparable cerebral injury.
ACCEPTED MANUSCRIPT Introduction Subcallosal artery infarction is a well-recognised, but very uncommon complication of surgical treatment of anterior communicating artery aneurysms.1 Vascular damage to the perforators arising from the anterior communicating artery complex supplying the calloso-
RI PT
forniceal region is presumed to be the underlying mechanism of these infarcts. Its incidence following endovascular coiling is extremely rare,with only two of such cases being reported in the literature.2,3 We report an unusual case of isolated callosal infarction in a patient with
SC
acute subarachnoid haemorrhage due to ruptured right posterior communicating artery
aneurysm. The observation is interesting as the infarction occurred in the absence of any
M AN U
thromboembolic complications or operative interference in the region of ACOM complex. The plausible pathomechanism of infarction is discussed. Case description
A 60-year-old hypertensive man, presented with acute severe intensity headache associated
TE D
with vomiting, photophobia and single episode of seizure. Urgent plain CT of brain showed massive subarachnoid hemorrhage (Fisher grade 4) with conspicuous clot concentration in interhemispheric fissure. Digital subtraction angiography (DSA) showed a wide neck right
EP
posterior communicating artery aneurysm measuring 6 x 7 mm. Balloon assisted coiling of
AC C
the aneurysm was done on 3rd day of the ictus, achieving aneurysm occlusion of class 3a modified Raymond-Roy classification (figure 1). On day 5 of ictus, the patient developed acute phase of confusion, memory disturbances and somnolence, raising the suspicion of cerebral vasospasm syndrome. Immediate CT study showed no rebleed or acute infarcts. Emergent DSA showed mild spasm of proximal M1 middle cerebral artery on both sides. He was treated with intraarterial milirinone bolus of 4 mg in each internal carotid artery (ICA) territory and the intravenous infusion was continued till 10th day of ictus. Over next 2 days, the confusion state improved; however patient developed anterograde amnesia. MRI
ACCEPTED MANUSCRIPT obtained at the time of discharge revealed acute infarct in the genu of corpus callosum and in the anterior commissure. The DSA images were retrospectively reviewed to identify the probable etiology of ScA infarction. There were neither thromboembolic complications during the procedure nor any
RI PT
catheter or wire manipulations in the anterior cerebral artery (ACA) or ACOM artery. A1 and A2 segments of ACA appeared normal in calibre. There was reduced opacification of
bilateral A2 segments, however a delay in cerebral perfusion or perfusion defect was not
SC
evident. Careful analysis of initial angiogram revealed a prominent ScA artery arising from ACOM artery. Subsequent angiogram prior to milirinone administration revealed that there
M AN U
was possible mild spasm of ACOM artery with non-visualisation of ScA.(figure 2). However, following chemical angioplasty, the ScA could be normally visualised confirming the presence of isolated spasm of ACOM-ScA complex, responding to milirinone. A follow-up comprehensive assessment (cognitive, behavioural, and psychosocial ) of the
Discussion
TE D
patient at 3 months showed no persistent abnormality.
Perforator injury is an important complication during the surgery of ACOM artery aneurysm
EP
or midline interhemispheric tumors and hence, its preservation is of utmost importance to
AC C
avoid postoperative complications.4 Several important perforators arise from the ACOM complex that perfuses critical regions such as subcallosal area, corpus callosum, hypothalamus and optic chiasm. Depending on their vascular territories, Serigawa categorised these arteries into three types such as subcallosal, hypothalamic or chiasmatic arteries.5 The subcallosal artery usually arises from posterior or posterior-superior aspect of ACOM artery as a single, large branch with a diameter range of 0.4 mm to 0.8 mm. The artery courses vertically through the cistern of lamina terminalis and ultimately, terminates in the subcallosal region. The regions supplied this artery include genu and rostrum of corpus
ACCEPTED MANUSCRIPT callosum, anterior cingulate gyrus, paraolfactory and paraterminal gyrus, columns of fornix and septum pellucidum. In more than a third of patients, it may give off branches to hypothalamus as well.5,6 The typical presentation of subcallosal artery infarction is antegrade amnesia, which may
RI PT
develop immediately or several days later after the insult. Other symptoms such as retrograde amnesia, behavioural or personality changes, psychomotor retardation or Korsarkoff’s
psychosis are also described.2,4 It is presumed that the pathophysiology of antegrade amnesia
SC
is due to the involvement of columns of fornix, which forms an important constituent of
Papez circuit. The fornix is a major white matter output tract that connects hippocampus with
M AN U
hypothalamus and basal forebrain. It is thought to play an important role in the registration of episodic information and hence any damage would likely cause disturbances in declarative memory. Forniceal infarcts are usually bilateral, due to the unpaired nature of the subcallosal artery.4
TE D
In a recent study, Mugikura et al described typical patterns of subcallosal infarction on imaging in patients with amnesia following ACOM aneurysm surgery. The most common sites of involvement were forniceal columns, anterior commissure and paraterminal gyrus.
EP
The typical imaging features include bow-tie-like appearance (representing bilateral
AC C
involvement of anterior commissure associated with infarcted foci in column of the fornix) and sagittally elongated infarction along the medial aspect of the brain. Involvement of adjacent brain structures such as corpus callosum or medial frontal lobes are also common, however the patients may remain asymptomatic unless significant brain parenchyma is affected.7 In our case, the postoperative symptoms were mistaken for cerebral vasospasm syndrome and the ScA infarction was identified only after the follow up MR imaging that showed typical findings. Retrospective analysis showed the ScA was poorly visualised in the postoperative
ACCEPTED MANUSCRIPT angiography, which demonstrated normalisation of the arterial calibre following milirinone infusion. Operative manipulations inducing spasm were ruled out, as the aneurysm was located in a different vascular territory. Also, there were no thromboembolic complications during the procedure. Our patient was treated with dual antiplatelet medications for his
RI PT
cardiac ailments and hence, deranged hemostasis in the setting of aneurysmal rupture might have resulted in the massive subarachnoid haemorrhage and formation of large cisternal clots. A large clot in the interhemispheric fissure might precipitate narrowing of ScA by mass effect
SC
or vasospasm, making the patient vulnerable to ischemia, especially when ScA is prominent arterial branch. Indeed, Abla et al had shown that the incidence of radiological or
M AN U
symptomatic was higher for pericallosal artery, even with a lesser clot burden and this observation was attributed to smaller calibre of the arteries.8 Though bilateral anterior cerebral arteries were unaffected by the vasospasm, narrowing of ScA and probable involvement of microscopic anastomotic communications between ACA-ScA would have
TE D
rendered the patient vulnerable to infarction of ScA territory. Isolated ScA infarction secondary to cerebral vasospasm is previously unreported. However, moderate or severe angiographic cerebral vasospasm is observed in up to one third of the patients with
EP
aneurysmal SAH, which would lead to delayed cerebral infarction in 15% of the patients. More than half of these vasospasm related infarcts were observed in the anterior cerebral
AC C
artery territory.9
Our case highlights the importance of early recognition of the ScA syndrome, so that an appropriate and if needed, aggressive intervention could be instituted if vasospasm of ACA or ScA is identified as the possible etiology.
Funding: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
ACCEPTED MANUSCRIPT
RI PT
Conflicts of interest: None
References
SC
1. DeLuca J, Diamond BJ. Aneurysm of the anterior communicating artery: a review of
neuroanatomical and neuropsychological sequelae. J Clin Exp Neuropsychol 1995;17:100–
M AN U
121.
2.Meila D,Saliou G,Krings T. Subcallosal artery stroke: infarction of the fornix and the genu of the corpus callosum. The importance of the anterior communicating artery complex. Case series and review of the literature. Neuroradiology 2015;57:41–47.
TE D
3.Mosimann PJ, Saint-Maurice JP, Lenck S, Puccinelli F, Houdart E. Fornix infarction and Korsakoff dementia after coiling of a large anterior communicating artery aneurysm. Neurol Clin Pract 2012;2: 260–262.
EP
4.Mugikura S,Kikuchi H,Fujii T,Murata T,Takase K,Mori E,Marinkovic S,Takahashi S. MR imaging of subcallosal artery infarct causing amnesia after surgery for anterior
AC C
communicating artery aneurysm. AJNR Am J Neuroradiol 2014;35:2293–2301. 5.Serizawa T,Noakatsu S,Akira Y. Microsurgical anatomy and clinical significance of the anterior communicating artery and its perforating branches. Neurosurgery 1997;40:12111218.
6.Marinkovc S, Milisavljevic M, Marinkovic Z: Branches of the anterior communicating artery: microsurgical anatomy. Acta Neurochir 1990;106:78-85. 7.Moudgil SS,Azzouz M,Al-Azzaz A,Haut M,Gutman L. Amnesia due to fornix infarction. Stroke. 2000;31:1418- 1419.
ACCEPTED MANUSCRIPT 8.Abla AA,Wilson DA,Williamson RW,Nakaji P,McDougall CG,Zabramski JM.Albuquerque FC,Spetzler RF. The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial. J Neurosurg 2014;120:391–
RI PT
397. 9.Brown RJ,Kumar A,Dhar R,Sampson TR,Diringer MN. The relationship between delayed infarcts and angiographic vasospasm after aneurysmal subarachnoid haemorrhage.
SC
Neurosurgery 2013;72:702-708.
M AN U
Figure legends Figure 1
Plain CT scan of the brain on day 1 of ictus reveals massive subarachnoid haemorrhage in the sylvian and basal cisterns (A) with most conspicuous clot concentration in interhemispheric
TE D
fissure(B. Right internal carotid artery angiogram obtained on day shows a right posterior communicating artery aneurysm (C) that was occluded by balloon assisted coiling (arrow in D).
EP
Figure 2
Bilateral internal carotid artery angiogram obtained on the same shows mild spasm of M1
AC C
middle cerebral artery both sides, A1 anterior cerebral artery are normal in caliber(A,B). Note that the ACOM complex is not distinctly visualised (B). Initial angiogram obtained at the time of balloon assisted coiling shows a prominent ScA artery (arrow in C) that is not identifiable in the angiogram obtained at the time of clinical suspicion of vasospasm (arrow in D). The ScA artery is visible following the chemical angioplasty (arrow in E) with improved opacification of distal ACA branches. Axial section of apparent diffusion coefficient map shows acute infarction in the anterior commissure and fornix (arrow in F)
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT
AC C
EP
TE D
M AN U
SC
RI PT
ACCEPTED MANUSCRIPT
ACCEPTED MANUSCRIPT Highlights
RI PT
SC M AN U
•
TE D
•
EP
•
Subcallosal infarction presents with typical clinical features of confusion and antegrade amnesia Subarachnoid hemorrhage with localised thick clot in the anterior interhemispheric fissure can result in localized spasm of anterior communicating artery complex and subcallosal artery Accurate recognition of symptoms and careful analysis of prior angiograms help in the early diagnosis and its subsequent management Chemical angioplasty is effective in reversing the local vasospasm and it could potentially prevent an irreparable brain injury
AC C
•