Letter to the Editor: Pure arterial malformations of the posterior cerebral artery

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To The Editor: We read with great interest the report by McLaughlin et al.1 (McLaughlin N, Raychev R, Duckwiler G, et al: Pure arterial malformation of the posterior cerebral artery: importance of its recognition. Case report. J Neurosurg 119:655–660, September 2013) on pure arterial malformations of the posterior cerebral artery. We would like to briefly illustrate a similar case that supports these authors' claim that indeed the vascular anomaly described may represent a separate pathological entity. In August 2010, a 10-year-old girl complained of a short-lasting, primarily left-sided headache that woke her up from sleep. Axial imaging studies did not show any acute bleeding but raised the suspicion of a complex vascular anomaly involving the supraclinoid internal carotid artery (ICA). This was confirmed by a subsequent catheter angiography (Fig. 1). After seeking multiple opinions, she was referred to our institution. We interpreted the lesion as representing a possible complex dissecting pseudoaneurysm of the posterior communicating/posterior cerebral artery and proceeded to perform coil embolization of the larger, saccular-type, pseudoaneurysm component. Three years later, the girl remains well and very active in various sports. Axial imaging studies have shown stability of the lesion over time.

Fig. 1.
Fig. 1.

Sequential arterial phase lateral (A–C), anteroposterior (D), and 3D (E) angiograms of the left ICA show a complex vascular anomaly involving the posterior communicating artery. Anteroposterior left vertebral artery angiogram (F), obtained during balloon test occlusion of the left ICA, demonstrates the abnormally dilated caliber of the proximal left posterior cerebral artery (arrow) and the anomaly involving the posterior communicating artery. The patient underwent uneventful coil embolization of the larger, pseudoaneurysm component (G), which resulted in flow disruption and contrast stasis (arrowhead, H) into this component.

Years ago, William Sweet wrote a thoughtful article on the difference between one and zero and how new concepts and descriptions of pathological conditions often start with a single observation not always fully appreciated by the unprepared mind.2 The striking resemblance between the case reported by McLaughlin and coworkers and our case seems to indeed confirm, as boldly proposed by these authors, that we may be dealing with a separate pathological entity. We commend the authors for their keen and original observation, and we encourage more reports of similar cases so that the natural history and the true clinical significance of this entity can be better defined.

Disclosure

The authors report no conflict of interest.

Referencess

  • 1

    McLaughlin NRaychev RDuckwiler GMartin NA: Pure arterial malformation of the posterior cerebral artery: importance of its recognition. Case report. J Neurosurg 119:6556602013

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  • 2

    Sweet W: The difference between zero and one. Clinical Neurosurg 23:32511976

Response

We appreciate the letter written by Lanzino and colleagues and read with interest the case illustrated therein. In addition to suspecting a complex dissecting pseudoaneurysm of the posterior communicating/posterior cerebral artery, the diagnosis of a congenital intracranial dilative arteriopathy could have been considered in this young patient. Contributing factors such as genetic, inflammatory, immunological, and degenerative conditions should be sought. However, we agree with Lanzino and colleagues that the case they shared is similar to the pure arterial malformation we reported.

Since the time of publication of our case report, we encountered an additional patient with a vascular lesion suggestive of a pure arterial malformation. An 8-yearold girl was referred for management of an arteriovenous malformation. At age 3 years, she underwent head imaging (CT and CT angiography) in the context of a sinus infection. Her neurologist diagnosed a brain arteriovenous malformation and recommended conservative treatment. Five years later, after having experienced new episodes of isolated headaches in the absence of other symptoms, the patient underwent new brain imaging (CT angiography and MR angiography). At this time, there was no significant change in the mass of the coiled abnormal vessels in comparison to previous images. Contributing factors to congenital intracranial dilative arteriopathy had been sought and ruled out by her neurologist. An angiogram was recommended to better characterize the abnormal vessels. The angiogram again showed the dilated supraclinoid left ICA and proximal aspect of the left M1 segment (Fig. 1). Supporting the hypothesis that this was a pure arterial malformation, the dilative appearance extended beyond the main vessel (ICA and M1), involving the origins of the left ophthalmic artery, left anterior choroidal artery, and left lateral lenticulostriate arteries. Similar to the case we reported and the case shared by Lanzino and colleagues, this additional case also had a saccular aneurysm arising from the supraclinoid segment of the left ICA. Given the superposition of tortuous vessel and the difference in technique, it was challenging to determine if the aneurysm was present on previous images acquired at outside facilities. The patient was managed conservatively and recommended to undergo follow-up catheter angiography with 6-second frames and 3D acquisition in 9 months.

Fig. 1.
Fig. 1.

Lateral (left) and anteroposterior (right) left common carotid artery injection angiograms acquired via femoral catheter, showing the dilated supraclinoid left ICA and proximal aspect of the left M1, representing a coiled mass of dilated elongated and tortuous vessels with no early venous drainage, suggestive of a pure arterial malformation.

Other cerebrovascular surgeon colleagues have written to the senior author (N.A.M.) following the publication of the case report on pure arterial malformations, recollecting similar cases in their practice. In order to better study the natural history and clinical significance of this new entity, we propose the coordination of a registry of such potential cases. We thank Dr. Lanzino and colleagues for sharing their case and encourage others to report other descriptions of similar cases and to consider entering the case in the ongoing registry.

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Article Information

Please include this information when citing this paper: published online November 15, 2013; DOI: 10.3171/2013.7.JNS131478.

© AANS, except where prohibited by US copyright law.

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Figures

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    Sequential arterial phase lateral (A–C), anteroposterior (D), and 3D (E) angiograms of the left ICA show a complex vascular anomaly involving the posterior communicating artery. Anteroposterior left vertebral artery angiogram (F), obtained during balloon test occlusion of the left ICA, demonstrates the abnormally dilated caliber of the proximal left posterior cerebral artery (arrow) and the anomaly involving the posterior communicating artery. The patient underwent uneventful coil embolization of the larger, pseudoaneurysm component (G), which resulted in flow disruption and contrast stasis (arrowhead, H) into this component.

  • View in gallery

    Lateral (left) and anteroposterior (right) left common carotid artery injection angiograms acquired via femoral catheter, showing the dilated supraclinoid left ICA and proximal aspect of the left M1, representing a coiled mass of dilated elongated and tortuous vessels with no early venous drainage, suggestive of a pure arterial malformation.

References

  • 1

    McLaughlin NRaychev RDuckwiler GMartin NA: Pure arterial malformation of the posterior cerebral artery: importance of its recognition. Case report. J Neurosurg 119:6556602013

    • Search Google Scholar
    • Export Citation
  • 2

    Sweet W: The difference between zero and one. Clinical Neurosurg 23:32511976

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