Spontaneous thrombosis of giant intracranial aneurysm with parent artery occlusion is uncommon. We present an unusual case of a 28-year-old female who presented with a hemispheric infarct probably secondary to dissection of the cervical internal carotid artery (ICA). The cervical ICA occlusion simultaneously induced total thrombosis of pre-existing incidental giant cavernous ICA aneurysm. We discuss the various theories and probable mechanisms involved.

Background and Purpose: Delayed intraparenchymal hemorrhages (DIPHs) are one of the most serious complications of cerebral aneurysm treatment with flow diverters (FD), yet their causes are largely unknown. This study analyzes distal hemodynamic alterations induced by the treatment of intracranial aneurysms with FDs.Methods: A realistic model of the brain arterial network was constructed from MRA images and extended with a constrained constructive optimization technique down to vessel diameters of approximately 50μm. Different variants of the circle of Willis were created by alternatively occluding communicating arteries. Collateral vessels connecting different arterial trees were then added to the model, and a distributed lumped parameter approach was used to model the pulsatile blood flow in the arterial network. The treatment of an ICA aneurysm was modeled by changing the local resistance, flow inertia, and compliance of the aneurysmal segment.Results: The maximum relative change in distal pressure induced by the aneurysm treatment was below 1%. However, for certain combinations of the circle of Willis and distal collateralization, important flow reversals (with a wall shear stress larger than approximately 1.0 dyne/cm2) were observed in collateral vessels, both ipsilaterally and contralaterally to the treated aneurysm.Conclusion: This study suggests the hypothesis that flow diverters treatment of intracranial aneurysms could cause important flow reversal in distal collaterals. Flow reversal has previously been shown to be pro-inflammatory and pro-atherogenic and could therefore have a detrimental effect on these collateral vessels, and thus could be a suitable explanation of DIPHs, while the small distal pressure increase is not.

Background: Traumatic basal ganglia hematomas (TBGH) are rare entities. They are situated in the deep cerebral parenchyma and have also been termed as intermediate coup contusions. Available literature is sparse with regards to the characteristics and prognosis of TBGH. We aim to share our experience in the management, outcomes, and prognostic factors of TBGH. Methods: A 4-year retrospective study which included all cases of TBGH, except dot contusions (<2 mL) and those with coagulopathies. Admission variables were correlated with Glasgow Outcome Scale score at discharge and 12 months. Results: Thirty-two patients were analyzed. The mean age was 39.2 years. Two-thirds were due to road traffic accidents. Around 60% were severe head injuries. The mean Glasgow coma scale (GCS) score at presentation was 8.5. Twenty patients had moderate-to-severe hemiparesis. The mean hematoma volume was 18.1 mL. Associated traumatic intracranial lesions were seen in 28 cases. Only 7 patients (22%) underwent surgery. The mean follow-up was 17.4 months (range 14–34 months). The mortality rate was 12.5% (n = 4). Among the survivors, only 39% (n = 11) had good outcomes at discharge which showed modest improvement to 54% (n = 15) at 12 months. Conclusion: Our study noted that poor admission GCS scores, poor motor response, presence of significant hemiparesis, and larger hematoma volumes (>20 mL) correlated with poor outcomes at 12 months. The overall outcomes have been mostly unfavorable as observed in majority of studies due to deeper location of these hematomas, high proportion of severe head injuries, and high proportion of residual weakness in survivors.

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