Basilar Perforator Artery Aneurysm: Spontaneous Subarachnoid Hemorrhage Caused by the Rupture of a Small Aneurysm of a Pontine Perforating Vessel Originating from the Upper Basilar Artery Trunk; Conservative Management, with Fatal Outcome after Recurrent Hemorrhages and Due to Severe Vasospasm

  • Victoria Hellstern
  • Marta Aguilar Pérez
  • Muhammad AlMatter
  • Patricia Kohlhof-Meinecke
  • Hansjörg Bäzner
  • Hans HenkesEmail author
Living reference work entry


A 62-year-old male patient presented to a local hospital with an acute onset of headache and nuchal stiffness. Non-contrast cranial CT (NCCT) showed subarachnoid hemorrhage (SAH) in the basal cisterns and also a minor intraventricular hemorrhage (Hunt and Hess I, Fisher IV). The patient was transferred to our hospital for further treatment. A diagnostic angiogram (DSA) performed on the following day did not reveal the site of the bleeding, notably there was no aneurysm present. The contour of the V4 segment of the left vertebral artery (VA) appeared irregular and a dissection was suspected and presumed to be the source of the SAH. Therefore, a second DSA examination was planned 10 days after the bleeding. However, 2 days later the patient deteriorated clinically. NCCT images showed repeat bleeding with early hydrocephalus. After placement of an external ventricular drain (EVD) the patient improved significantly. However, the patient refused to have a second DSA examination. Another 9 days later, and 12 days after the first hemorrhage, the patient suddenly became comatose. The CCT scan showed a third episode of hemorrhage with herniation of the cerebellar tonsils and occlusive hydrocephalus. The patient underwent a DSA at this stage, which showed vasospasm of the basilar artery (BA) and the cerebellar arteries and a small aneurysm of a perforating pontine artery. A dissection of the left VA was not confirmed. Another 4 h after the DSA the patient deteriorated further and bilateral pupils became dilated. MRI revealed early signs of severe ponto-cerebellar infarct with downward tonsillar herniation. NCCT on the following day confirmed ascending transtentorial herniation. A sequence of three recurrent SAHs, post-hemorrhagic vasospasm of the BA artery and cerebellar arteries and eventually a ponto-cerebellar infarct had occurred. The patient died 4 h after the final NCCT scan. Autopsy revealed a small aneurysm of a perforating pontine artery originating from the basilar artery. The phenomenon of small aneurysms of perforating pontine arteries, their natural history and management options are the topics of this chapter.


Basilar perforator artery Small aneurysm SAH Posterior circulation Conservative management Recurrent aneurysm hemorrhage Vasospasm 


A 62-year-old male patient, otherwise healthy, presenting with severe headaches and nuchal rigidity due to spontaneous SAH (Hunt and Hess I, Fisher IV).

Diagnostic Imaging

A NCCT was carried out on the same day as the onset of the headache, which demonstrated SAH in the prepontine cistern. The DSA examination on the following day was essentially within normal limits. The preliminary diagnosis was “benign perimesencephalic hemorrhage” (Fig. 1). A second DSA examination was planned 10 days after the first bleeding but 2 days later the patient deteriorated clinically. A further NCCT scan showed recurrent hemorrhage with early hydrocephalus (Fig. 2). After placement of an external ventricular drain, the patient improved significantly. He refused, however, a second DSA examination. Nine days later the patient suddenly became comatose. The NCCT scan showed a new hemorrhage with herniation of the cerebellar tonsils and occlusive hydrocephalus. The patient underwent a DSA examination, which showed vasospasm of the basilar and ponto-cerebellar arteries and a small aneurysm of a perforating pontine artery originating from the upper third of the BA. Another 4 h after the DSA the patient deteriorated further and developed bilaterally pupillary dilatation. MRI revealed signs of ponto-cerebellar infarct and tonsillar herniation. NCCT on the following day confirmed the ponto-cerebellar infarct with upward transtentorial herniation. The patient passed away 4 h later (Fig. 3).
Fig. 1

CT (a–f) immediately following the onset of headache and nuchal rigidity in a 62-year-old man shows a SAH around the pons and in the interpeduncular fossa. A DSA examination was performed on the following day and did not reveal the source of this hemorrhage (g–m)

Fig. 2

The clinical condition of the patient deteriorated 2 days later. CT confirmed a second SAH with unchanged blood around the pons (a, b) but an increase in the volume of the subarachnoid blood in the basal cisterns (c). The patient developed a post-hemorrhagic hydrocephalus during the following hours, which required the insertion of an external ventricular drain. The level of consciousness improved thereafter and remained stable. A routine CT examination 5 days later showed no new hemorrhage (d, e, f)

Fig. 3

Twelve days after the first and 9 days after the second SAH, the patient suddenly became comatose. NCCT showed a third massive SAH in the posterior fossa (a–c). DSA demonstrated vasospasm of the right AICA/PICA (d, e), the upper third of the BA and both superior cerebellar arteries (f). A small aneurysm of a pontine perforator originating from the distal third of the BA was visible (g–j). DWI MRI on the same day showed diffusion restriction in the pons and cerebellum (k–m) with increased signal intensity in the PICA territory on T2WI and downward herniation of the cerebellar tonsils. The vasospasm of the upper BA persisted despite the IV administration of nimodipine, as shown by TOF MRA. NCCT on the following day showed the established ponto-cerebellar infarct (q, r) with upward transtentorial herniation (s). The patient died 4 h after this examination

Treatment Strategy

The first DSA examination did not reveal the cause of the SAH. Conservative management with an early follow-up DSA 10 days later was the only option. After the third SAH, DSA revealed an aneurysm of a pontine artery, originating from the upper third of the BA. In retrospect, neither microsurgical clipping nor coil occlusion would have been viable treatment options. The deployment of a flow diverter (e.g., a Pipeline Embolization Device, PED (then ev3, now Medtronic)) would have been a theoretical possibility. The need to put the patient on dual platelet function inhibition medication would certainly have created serious concerns. Once the basilar perforator aneurysm was recognized, the post-hemorrhagic vasospasm with severe ponto-cerebellar ischemia was already determining the clinical course, including the fatal outcome.


No attempt at treating the basilar perforator artery aneurysm was undertaken. Nimodipine IV had been administered since day 2 after the onset of symptoms.

Clinical Outcome

The patient died one day after the angiographic demonstration of the post-hemorrhagic vasospasm and the basilar perforating artery aneurysm. Autopsy confirmed massive infarcts of both the pons and the cerebellum as well as upward and downward herniation. The attempt to find the small aneurysm in the firm clot surrounding the BA trunk failed (Fig. 4).
Fig. 4

Autopsy after recurrent SAHs from a small basilar perforating artery aneurysm, causing severe vasospasm with infarct of cerebellum and pons, resulting in upward and downward herniation. The basilar artery is surrounded by firm clot, which prevented the identification of said aneurysm


Aneurysms of basilar perforator arteries are considered extremely rare. Published cases date back to the 1990s (Ghogawala et al. 1996). In their literature review, Gross et al. (2013) identified only 12 published cases. This number had increased to 18 when Satti et al. (2017) performed their review 4 years later, and 1 year later Chau et al. (2018) reported 52 patients, 49 published and 3 managed by the authors. This rarity is the reason for the limited knowledge surrounding the nature and treatment of these aneurysms. Basilar perforator artery aneurysms are usually found after SAH but may also be associated with pontine ischemia. The first DSA examination following the hemorrhage is sometimes negative and it may take a second or third DSA a few days later to reveal the aneurysm (Ghogawala et al. 1996; Mathieson et al. 2010). These aneurysms are typically located at the level of the mid or distal third of the basilar artery. The clinical course is unpredictable and both spontaneous disappearance and recurrent hemorrhage have been reported. Chau et al. (2018) quote a 15% rate of rebleeding for untreated aneurysms in this location. Successful surgical clipping (Ghogawala et al. 1996; Mathieson et al. 2010), coil occlusion (Chau et al. 2017), telescoping stenting (Chau et al. 2018; Satti et al. 2017), and flow diversion (Peschillo et al. 2016) have all been reported. The risks associated with flow diverter implantation come from the required dual platelet function inhibition. Peschillo et al. (2016) treated three patients with basilar artery perforator aneurysms with flow diversion and encountered two thromboembolic and one hemorrhagic complication. Spontaneous regression of these aneurysms has been reported (Aboukais et al. 2016) and several authors recommend a conservative management as the first-line strategy (Finitsis et al. 2017; Forbrig et al. 2016), which is questioned by the fatal re-hemorrhages in the patient reported in this chapter. Given the flow diverter stents available today, we would rather go for flow diversion than for observation.



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Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  • Victoria Hellstern
    • 1
  • Marta Aguilar Pérez
    • 1
  • Muhammad AlMatter
    • 1
  • Patricia Kohlhof-Meinecke
    • 2
  • Hansjörg Bäzner
    • 3
  • Hans Henkes
    • 1
    Email author
  1. 1.Neuroradiologische Klinik, NeurozentrumKlinikum StuttgartStuttgartGermany
  2. 2.Institut für Pathologie, Klinikum StuttgartStuttgartGermany
  3. 3.Neurologische Klinik, NeurozentrumKlinikum StuttgartStuttgartGermany

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