Título
Post-Clipping Cerebrovascular Compliance in an Infant With Bilateral Anterior Circulation Aneurysms
Autor
Christopher Jones
Jacob Fairhall
Venkataraman Balakrishnan
Agadha Wickremesekera
Fecha
Mayo 2004
Lugar de Realización
Department of Neurosurgery, Wellington Hospital, Wellington, New Zealand
Correspondencia
wickremesekera@ccdhb.org.nz
Texto
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Documento sin título
Rev. Argent. Neuroc. 2004, 18 (S2): 18
Department of Neurosurgery, Wellington Hospital, Wellington, New Zealand
Correspondencia: Agadha Wickremesekera MBChB, FRACS, Department of Neurosurgery, Wellington Hospital, Capital and Coast District Health Board, Riddiford St, Private Bag 7902. Wellington South, New Zealand.
Email: agadha.wickremesekera@ccdhb.org.nz
CASE REPORT
A 12 month old female infant presented with a week of a flu-like illness and a generalized tonic clonic seizure lasting 5 minutes. She was born at term by normal vaginal delivery, and she did not have a past medical history of intracranial hemorrhage or a family history of cerebrovascular disease. On initial examination she was afebrile, with generalized hypotonia, reduced responsiveness and normal blood pressure, but moving all limbs to stimuli. Fundoscopy was unremarkable. She was reusable maintaining a good airway.
Lumbar puncture revealed bloodstained cerebrospinal fluid with xanthochromia. No organisms were seen on gram stain and culture. The serum white cell count was elevated, but c-reactive protein and coagulation profile were normal. Intravenous fluid and nimodipine were commenced.
Computed tomography (CT) of the brain revealed extensive subarachnoid hemorrhage particularly in the interhemispheric cistern, extending into the ventricular system with moderate hydrocephalus (Fig. 1).
Cerebral angiography demonstrated tortuosity of anterior cerebral (Al) and pericallosal (A2) arteries. The angiogram revealed a 5 mm Al /A2 junction aneurysm; the anterior communicating segment was hypoplastic (Fig. 2).
At operation, a right pterional craniotomy exposed a partially thrombosed 15 mm right Al /A2 junction aneurysm, which was clipped with a Sugita bayonet clip. A 2-3 mm loculus/aneurysm on the distal right Al, not seen on angiography, was also clipped with a curved Sugita miniclip. Postoperatively, on day 2 she suffered focal seizures with left-sided twitching, but no loss of consciousness. She recovered with no neurological deficit and was discharged on day 14.
Check cerebral angiography 5 months later confirmed absence of the right Al /A2 aneurysm, but also showed loss of the right Al (Fig. 3). The same angiogram also showed a de novo 5 mm left Al /A2 junction aneurysm (Fig. 4), not visualized on the initial angiogram (Fig. 5). When comparing similar projections of the interval angiograms, the left sided aneurysm clearly appeared to be at a de novo site, be it adjacent to the anterior cerebral complex.
Fig 1. Admission CT: subarachnoid hemorrhage and yentriculomegaly
Fig 2. Right carotid angiogram on admission demonstrating 5 mm Al /A2 junction aneurysm
Fig 3. Post-operative angiogram following clipping of the right Al /A2 aneurysm, showing absence of right anterior cerebral artery
Fig 4. Post-operative left internal carotid injection showing de novo left Al aneurysm
Fig 5. Left carotid angiogram on admission: no aneurysm seen
The de novo aneurysm was clipped electively by a left pterional approach. At operation a 10 mm partially thrombosed aneurysm was seen, which was separate from the site of the right aneurysm and its clip. The postoperative period was uneventful and she was discharged on day 5.
Repeat check cerebral angiography 5 months following the second operation showed no aneurysms, continued loss of flow in the right Al and significantly reduced flow in the left Al. A further four vessel cerebral angiogram after 12 months showed no aneurysms and no flow in either A 1 segments, with collateral flow via the posterior communicating and the posterior cerebral arteries, especially on the left side (Fig. 6). The patient has continued to develop normally. She has had a normal cardiac and renal ultrasound. Follow up is planned with cerebral CT angiography.
Fig 6. Left internal carotid injection demonstrating collateral flow to the posterior circulation via the posterior communicating and posterior cerebral arteries.
DISCUSSION
Aneurysmal subarachnoid hemorrhage in the pediatric population is rare, with an incidence of one to three cases per one million populations. Pediatric aneurysms are reported to represent 0.5 to 4.6% of all cerebral aneurysmsl. Due to their rarity, it is uncommon for any one center to have a large series, but a recent review found 63 of 85 infants with cerebral aneurysms presented with subarachnoid hemorrhage2. Some report, that pediatric aneurysms usually present as subarachnoid hemorrhage rather than mass effect, most arising from the anterior circulation3, but others suggest that aneurysms in the pediatric population commonly occur in the posterior circulation4-5. Delayed diagnosis of subarachnoid hemorrhage in infants, especially neonates is associated with a high mortality and morbidity6. Aneurysmal subarachnoid hemorrhage in infancy also has a significant mortality. Postmortem histological studies following a right middle cerebral artery hemorrhage in an infant revealed disruption of the internal elastic lamina of both middle cerebral arteries, reinforcing the theory of dysembryogenesis and the congenital nature of aneurysms in infancy7. Pediatric cerebral aneurysms differ from those that occur in adults in several ways. Pediatric aneurysms appear more common in the posterior circulation4 5, although due to small numbers this varíes markedly between series8 overall 21% in children compared with 7% in adults. Male predominance of pediatric aneurysms is converse to the trend in adults1.
Children appear to be either less susceptible to or more tolerant ofvasospasm3. One series, noting severe angiographic vasospasm in 6 symptomatic children, concluded that vasospasm seemed to be well tolerated in children8.
Pediatric cerebral aneurysms are recognized to be associated with a number of conditions, including but not limited to aortic coarctation, arteriovenous malformation, birth trauma, cardiac myxoma, fibromuscular dysplasia, head injury, tuberous sclerosis, polycystic kidney disease and other vascular anomalies5.
The incidence of adult de novo aneurysms, may be calculated as 1.8% per annum, and more common with a history of multiple aneurysms9. Adult de novo aneurysms are more common in the anterior cerebral circulation, and are often seen some years after initial diagnosis of the first aneurysm, but have been detected 3 months after initial presentation10-11. The incidence of childhood de novo aneurysms remains uncertain.
Spontaneous thrombosis of an aneurysm has been attributed to hemodynamic flow factors, ratio of neck to fundus diameter, and the age of the aneurysm. Clipping of a posterior cerebral aneurysm in a child was suggested to lead to spontaneous thrombosis of a second superior cerebellar artery aneurysm. The mechanism was unclear and there was no parent artery thrombosis12.
In our case, we are unable to attribute any specific cause for the partial thrombosis of both aneurysms. Tortuous abnormal vessels and postsubarachnoid hemorrhage vasospasm may con ceivably explain partial thrombosis within the aneurysms, as well as the loss of A1s postoperatively. In our case, the absence of a left Al /A2 junction aneurysm on the initial angiogram raised the possibility of recanalization and/or enlargement of a thrombosed aneurysm. The disappearance and reappearance of a cerebral aneurysm in an infant after 6 months, has been described recently13. Another possible mechanism may be that, cessation of flow in the right Al increased flow in the left Al contributing to enlargement of a thrombosed aneurysm, in a similar fashion to compaction of coils within an aneurysm. On the other hand the left Al /A2 junction aneurysm may be de novo, as described aboye", but the true mechanism of formation of short term de novo aneurysms remains unclear. In this reported case both aneurysms were partially thrombosed, but complete spontaneous thrombosis occurs in infants, in particular the larger cerebral aneurysms14.
Another explanation is that the left aneurysm is part of the same complex of the right aneurysm. Nevertheless, in comparing interval angiograms, it is compelling that the left aneurysm was not seen on the first angiogram, and has developed since the first operation.
In our case, despite the loss of Als, anterior cerebral infarction was prevented by sustained collateral perfusion by the posterior cerebral arteries. Children are considered to have superfluous cerebrovascular compliance and greater toleran-ce to surgery. These features may be attributed to minimal vasospasm after subarachnoid hemorrhage, absence of systemic hypertension and /or the absence of endothelial changes seen in adults.
CONCLUSIÓN
This case presented with abnormal anterior cerebral arteries, seen to be tortuous with irregularities seen at angiography and surgery. There was no anterior communicating artery seen despite cross compression. The anterior cerebral arteries were prone to aneurysm formation and thrombosis. The post-operative loss of Al flow could be explained by clip obliteration of the parent Als, although this was clearly not the case at surgery, or collapse of pre-existing abnormal arteries with/ without vasospasm, enhanced by surgical manipulation. If the anterior cerebral arteries were normal and there was no collateral perfusion, one
would expect cerebral infarction. The presence of well-developed posterior circulation collaterals with angiographic loss of the Al s after clipping of the aneurysms, suggest a pre-existing abnormality of the anterior cerebral arteries. Such cerebrovascular compliance without the development of neurological sequelae in this case, implicates not only the hypothesis of abnormal neurovascular embryogenesis of the anterior cerebral/anterior communicating arteries, but also the pre-existence of an easily accessible protective collateral perfusion.
References
1. Wojtacha M, Bazowski P, Mandera M, Krawczyk I, Rudnik A. Cerebral aneurysms in childhood. Childs Nerv Syst 2001; 17: 37-41.
2. Elgamal EA, Murshid WR, Abu-Rahma HM, Samir
D. Aneurysmal subarachnoid hemorrhage in the first year of life: case report and review of the literature. Childs Nerv Syst 2004.
3. Young WF, Pattisapu JV. Ruptured cerebral aneurysm in a 39-day-old infant. Clin Neurol Neurosurg 2000; 102: 140-3.
4. Kasahara E, Murayama T, Yamane C. Giant cerebral arterial aneurysm in an infant: report of a case and review of 42 previous cases in infants with cerebral arterial aneurysm. Acta Paediatr Jpn 1996; 38: 684-8.
5. Khoo LT, Levy ML. Intracranial aneurysms. In: Albright A.L, Adelson P.D., Pollack I.F.(eds) Principies and Practice of Pediatric Neurosurgery; Thieme Medical Publishers. New York, Stuttgart, pp 973-1001.
6. Maroun F, Squarey K, Jacob J, Murray G, Cramer B, Barron J, Weir B. Rupture of middle cerebral artery aneurysm in a neonate: case report and review of the literature. Surg Neurol 2003; 59:114-9.
7. Hulsmann S, Moskopp D, Wassmann H. Management of a ruptured cerebral aneurysm in infancy. Report of a case of a ten-month-old boy. Neurosurgery 1998; 21:161-6.
8. Proust F, Toussaint P. Garnieri J, Hannequin D, Legars D, Houteville JP. Freger P. Pediatric cerebral aneurysms. J Neurosurg 2001; 94:733-9.
9. David, CA, Vishteh AG. Spetzler RF, Lemole M, Lawton MT, Partovi S. Late angiographic follow-up review of surgically treated aneurysms. J Neurosurg 1999; 91: 396-401.
10. Sim JH, Kim SC, Kim MS. Early development and rupture of de novo aneurysm—case report. Neurol Med Chir (Tokyo) 2002; 42: 334-7.
11. Matheus MG, Castillo M. Development of de novo intracranial aneurysm in three months: case report and literature review. AJNR 2003; 24(4): 709-10.
12. Nanda A, Drury BT. Posterior circulation aneurysms in a child: clipping of one leads to spontaneous thrombosis of the other. Pediatr Neurosurg 1997; 26: 41-7.
13. Motohashi O, Kameyama M, Imaizumi S, Mino M, Naganuma H, Ishii K, Onuma T. A distal anterior cerebral artery aneurysm in infant: disappearance and reappearance of the aneurysm. J Clin Neurosci 2004; 11: 86-8.
14. Russegger L, Grunert V. A thrombosed giant MCA aneurysm in a ten-week-old infant. Neurochirurgia (Stuttg) 1987; 30: 186-9.
Post-Clipping Cerebrovascular Compliance in an Infant With Bilateral Anterior Circulation Aneurysms
Christopher Jones, Jacob Fairhall, Venkataraman Balakrishnan, Agadha WickremesekeraDepartment of Neurosurgery, Wellington Hospital, Wellington, New Zealand
Correspondencia: Agadha Wickremesekera MBChB, FRACS, Department of Neurosurgery, Wellington Hospital, Capital and Coast District Health Board, Riddiford St, Private Bag 7902. Wellington South, New Zealand.
Email: agadha.wickremesekera@ccdhb.org.nz
RESUMEN
Se presenta un caso inusual de un niño de 12 meses de edad que consulta por convulsiones debidas a hemorragia subaracnoidea secundaría al sangrado de un aneurisma de la circulacion anterior. Por un abordaje pterional derecho se clipa un aneurisma localizado en la unión de A 1 y A2 de la arteria cerebral anterior derecha. Una angiografia de control, efectuada 5 meses después, mostró un aneurisma "de novo" de la unión Al -A2 izquierda que se clipó a través de un abordaje pterional izquier do. La angiografia de control, 5 meses después, mostró una pérdida del flujo sanguíneo de la arteria cereral anterior izquierda, cuyo territorio pasa a ser irrigado por las arterias cerebrales posteriores. La angiografia de control 8 meses después, mostró el patrón angiográfico antes descripto sin nuevos aneurismas. El niño evolucionó sin déficit neurológico alguno.
Palabras clave: aneurisma cerebral en pediatría, aneurisma de novo
ABSTRACT
We present an uncommon case of an infant aged 12 months, presenting with a seizure due to subarachnoid hemorrhage secondary to an anterior circulation aneurysm. Following angiography, a right A 1 /A2 junction aneurysm was clipped by a right pterional approach. Angiography 5 months after clipping revealed loss offlow in the right anterior cerebral artery and a de novo L Al /A2 aneurysm, which was electively clipped by a left pterional approach. Follow up angiography 5 months later showed loss left anterior cerebral arteryflow and the anterior cerebral artery territory perfused by posterior cerebral arteries. Cerebral angiography 8 months later did not show further aneurysms and demonstrated the posterior circulation vessels perfusing the anterior circulation vascular territory The child remains neurologically intact.
Key words: pediatric cerebral aneurysm, de novo aneurysm
CASE REPORT
A 12 month old female infant presented with a week of a flu-like illness and a generalized tonic clonic seizure lasting 5 minutes. She was born at term by normal vaginal delivery, and she did not have a past medical history of intracranial hemorrhage or a family history of cerebrovascular disease. On initial examination she was afebrile, with generalized hypotonia, reduced responsiveness and normal blood pressure, but moving all limbs to stimuli. Fundoscopy was unremarkable. She was reusable maintaining a good airway.
Lumbar puncture revealed bloodstained cerebrospinal fluid with xanthochromia. No organisms were seen on gram stain and culture. The serum white cell count was elevated, but c-reactive protein and coagulation profile were normal. Intravenous fluid and nimodipine were commenced.
Computed tomography (CT) of the brain revealed extensive subarachnoid hemorrhage particularly in the interhemispheric cistern, extending into the ventricular system with moderate hydrocephalus (Fig. 1).
Cerebral angiography demonstrated tortuosity of anterior cerebral (Al) and pericallosal (A2) arteries. The angiogram revealed a 5 mm Al /A2 junction aneurysm; the anterior communicating segment was hypoplastic (Fig. 2).
At operation, a right pterional craniotomy exposed a partially thrombosed 15 mm right Al /A2 junction aneurysm, which was clipped with a Sugita bayonet clip. A 2-3 mm loculus/aneurysm on the distal right Al, not seen on angiography, was also clipped with a curved Sugita miniclip. Postoperatively, on day 2 she suffered focal seizures with left-sided twitching, but no loss of consciousness. She recovered with no neurological deficit and was discharged on day 14.
Check cerebral angiography 5 months later confirmed absence of the right Al /A2 aneurysm, but also showed loss of the right Al (Fig. 3). The same angiogram also showed a de novo 5 mm left Al /A2 junction aneurysm (Fig. 4), not visualized on the initial angiogram (Fig. 5). When comparing similar projections of the interval angiograms, the left sided aneurysm clearly appeared to be at a de novo site, be it adjacent to the anterior cerebral complex.
Fig 1. Admission CT: subarachnoid hemorrhage and yentriculomegaly
Fig 2. Right carotid angiogram on admission demonstrating 5 mm Al /A2 junction aneurysm
Fig 3. Post-operative angiogram following clipping of the right Al /A2 aneurysm, showing absence of right anterior cerebral artery
Fig 4. Post-operative left internal carotid injection showing de novo left Al aneurysm
Fig 5. Left carotid angiogram on admission: no aneurysm seen
The de novo aneurysm was clipped electively by a left pterional approach. At operation a 10 mm partially thrombosed aneurysm was seen, which was separate from the site of the right aneurysm and its clip. The postoperative period was uneventful and she was discharged on day 5.
Repeat check cerebral angiography 5 months following the second operation showed no aneurysms, continued loss of flow in the right Al and significantly reduced flow in the left Al. A further four vessel cerebral angiogram after 12 months showed no aneurysms and no flow in either A 1 segments, with collateral flow via the posterior communicating and the posterior cerebral arteries, especially on the left side (Fig. 6). The patient has continued to develop normally. She has had a normal cardiac and renal ultrasound. Follow up is planned with cerebral CT angiography.
Fig 6. Left internal carotid injection demonstrating collateral flow to the posterior circulation via the posterior communicating and posterior cerebral arteries.
DISCUSSION
Aneurysmal subarachnoid hemorrhage in the pediatric population is rare, with an incidence of one to three cases per one million populations. Pediatric aneurysms are reported to represent 0.5 to 4.6% of all cerebral aneurysmsl. Due to their rarity, it is uncommon for any one center to have a large series, but a recent review found 63 of 85 infants with cerebral aneurysms presented with subarachnoid hemorrhage2. Some report, that pediatric aneurysms usually present as subarachnoid hemorrhage rather than mass effect, most arising from the anterior circulation3, but others suggest that aneurysms in the pediatric population commonly occur in the posterior circulation4-5. Delayed diagnosis of subarachnoid hemorrhage in infants, especially neonates is associated with a high mortality and morbidity6. Aneurysmal subarachnoid hemorrhage in infancy also has a significant mortality. Postmortem histological studies following a right middle cerebral artery hemorrhage in an infant revealed disruption of the internal elastic lamina of both middle cerebral arteries, reinforcing the theory of dysembryogenesis and the congenital nature of aneurysms in infancy7. Pediatric cerebral aneurysms differ from those that occur in adults in several ways. Pediatric aneurysms appear more common in the posterior circulation4 5, although due to small numbers this varíes markedly between series8 overall 21% in children compared with 7% in adults. Male predominance of pediatric aneurysms is converse to the trend in adults1.
Children appear to be either less susceptible to or more tolerant ofvasospasm3. One series, noting severe angiographic vasospasm in 6 symptomatic children, concluded that vasospasm seemed to be well tolerated in children8.
Pediatric cerebral aneurysms are recognized to be associated with a number of conditions, including but not limited to aortic coarctation, arteriovenous malformation, birth trauma, cardiac myxoma, fibromuscular dysplasia, head injury, tuberous sclerosis, polycystic kidney disease and other vascular anomalies5.
The incidence of adult de novo aneurysms, may be calculated as 1.8% per annum, and more common with a history of multiple aneurysms9. Adult de novo aneurysms are more common in the anterior cerebral circulation, and are often seen some years after initial diagnosis of the first aneurysm, but have been detected 3 months after initial presentation10-11. The incidence of childhood de novo aneurysms remains uncertain.
Spontaneous thrombosis of an aneurysm has been attributed to hemodynamic flow factors, ratio of neck to fundus diameter, and the age of the aneurysm. Clipping of a posterior cerebral aneurysm in a child was suggested to lead to spontaneous thrombosis of a second superior cerebellar artery aneurysm. The mechanism was unclear and there was no parent artery thrombosis12.
In our case, we are unable to attribute any specific cause for the partial thrombosis of both aneurysms. Tortuous abnormal vessels and postsubarachnoid hemorrhage vasospasm may con ceivably explain partial thrombosis within the aneurysms, as well as the loss of A1s postoperatively. In our case, the absence of a left Al /A2 junction aneurysm on the initial angiogram raised the possibility of recanalization and/or enlargement of a thrombosed aneurysm. The disappearance and reappearance of a cerebral aneurysm in an infant after 6 months, has been described recently13. Another possible mechanism may be that, cessation of flow in the right Al increased flow in the left Al contributing to enlargement of a thrombosed aneurysm, in a similar fashion to compaction of coils within an aneurysm. On the other hand the left Al /A2 junction aneurysm may be de novo, as described aboye", but the true mechanism of formation of short term de novo aneurysms remains unclear. In this reported case both aneurysms were partially thrombosed, but complete spontaneous thrombosis occurs in infants, in particular the larger cerebral aneurysms14.
Another explanation is that the left aneurysm is part of the same complex of the right aneurysm. Nevertheless, in comparing interval angiograms, it is compelling that the left aneurysm was not seen on the first angiogram, and has developed since the first operation.
In our case, despite the loss of Als, anterior cerebral infarction was prevented by sustained collateral perfusion by the posterior cerebral arteries. Children are considered to have superfluous cerebrovascular compliance and greater toleran-ce to surgery. These features may be attributed to minimal vasospasm after subarachnoid hemorrhage, absence of systemic hypertension and /or the absence of endothelial changes seen in adults.
CONCLUSIÓN
This case presented with abnormal anterior cerebral arteries, seen to be tortuous with irregularities seen at angiography and surgery. There was no anterior communicating artery seen despite cross compression. The anterior cerebral arteries were prone to aneurysm formation and thrombosis. The post-operative loss of Al flow could be explained by clip obliteration of the parent Als, although this was clearly not the case at surgery, or collapse of pre-existing abnormal arteries with/ without vasospasm, enhanced by surgical manipulation. If the anterior cerebral arteries were normal and there was no collateral perfusion, one
would expect cerebral infarction. The presence of well-developed posterior circulation collaterals with angiographic loss of the Al s after clipping of the aneurysms, suggest a pre-existing abnormality of the anterior cerebral arteries. Such cerebrovascular compliance without the development of neurological sequelae in this case, implicates not only the hypothesis of abnormal neurovascular embryogenesis of the anterior cerebral/anterior communicating arteries, but also the pre-existence of an easily accessible protective collateral perfusion.
References
1. Wojtacha M, Bazowski P, Mandera M, Krawczyk I, Rudnik A. Cerebral aneurysms in childhood. Childs Nerv Syst 2001; 17: 37-41.
2. Elgamal EA, Murshid WR, Abu-Rahma HM, Samir
D. Aneurysmal subarachnoid hemorrhage in the first year of life: case report and review of the literature. Childs Nerv Syst 2004.
3. Young WF, Pattisapu JV. Ruptured cerebral aneurysm in a 39-day-old infant. Clin Neurol Neurosurg 2000; 102: 140-3.
4. Kasahara E, Murayama T, Yamane C. Giant cerebral arterial aneurysm in an infant: report of a case and review of 42 previous cases in infants with cerebral arterial aneurysm. Acta Paediatr Jpn 1996; 38: 684-8.
5. Khoo LT, Levy ML. Intracranial aneurysms. In: Albright A.L, Adelson P.D., Pollack I.F.(eds) Principies and Practice of Pediatric Neurosurgery; Thieme Medical Publishers. New York, Stuttgart, pp 973-1001.
6. Maroun F, Squarey K, Jacob J, Murray G, Cramer B, Barron J, Weir B. Rupture of middle cerebral artery aneurysm in a neonate: case report and review of the literature. Surg Neurol 2003; 59:114-9.
7. Hulsmann S, Moskopp D, Wassmann H. Management of a ruptured cerebral aneurysm in infancy. Report of a case of a ten-month-old boy. Neurosurgery 1998; 21:161-6.
8. Proust F, Toussaint P. Garnieri J, Hannequin D, Legars D, Houteville JP. Freger P. Pediatric cerebral aneurysms. J Neurosurg 2001; 94:733-9.
9. David, CA, Vishteh AG. Spetzler RF, Lemole M, Lawton MT, Partovi S. Late angiographic follow-up review of surgically treated aneurysms. J Neurosurg 1999; 91: 396-401.
10. Sim JH, Kim SC, Kim MS. Early development and rupture of de novo aneurysm—case report. Neurol Med Chir (Tokyo) 2002; 42: 334-7.
11. Matheus MG, Castillo M. Development of de novo intracranial aneurysm in three months: case report and literature review. AJNR 2003; 24(4): 709-10.
12. Nanda A, Drury BT. Posterior circulation aneurysms in a child: clipping of one leads to spontaneous thrombosis of the other. Pediatr Neurosurg 1997; 26: 41-7.
13. Motohashi O, Kameyama M, Imaizumi S, Mino M, Naganuma H, Ishii K, Onuma T. A distal anterior cerebral artery aneurysm in infant: disappearance and reappearance of the aneurysm. J Clin Neurosci 2004; 11: 86-8.
14. Russegger L, Grunert V. A thrombosed giant MCA aneurysm in a ten-week-old infant. Neurochirurgia (Stuttg) 1987; 30: 186-9.