Seizure-Induced Transient Early Venous Visualization on Angiography in Glioblastoma: A Case Report.
We report a case of seizure-associated transient early venous visualization (EVV) on cerebral angiography in a patient with glioblastoma mimicking arteriovenous shunting pathology.
A 48-year-old woman presented with new-onset generalized tonic-clonic seizures. Brain MRI revealed a poorly demarcated, non-enhancing lesion in the left temporal lobe. Arterial spin labeling (ASL) demonstrated marked hyperperfusion within the lesion and adjacent venous sinuses. Cerebral angiography performed approximately 2 h following seizure cessation showed posterior temporal artery dilation and an EVV pattern, with shunting into the vein of Labbé and the ipsilateral transverse and sigmoid sinuses; this raises suspicion for an arteriovenous shunting lesion. No definitive arteriovenous fistulae or thromboses were identified. The patient was managed with antiepileptic therapy alone, which led to clinical improvement. Follow-up MRI and angiography 2 weeks later revealed complete resolution of ASL hyperperfusion and the EVV pattern. Subsequent histopathological examination of the resected tumor confirmed isocitrate dehydrogenase (IDH)-wild-type small cell glioblastoma. Despite the underlying malignant tumor and persistent seizure susceptibility, the angiographic abnormalities and altered venous drainage were entirely reversible and seizure-induced, rather than structurally pathological.
This case illustrates that ictal or postictal cerebral hyperperfusion can produce transient EVV on cerebral angiography, even with aggressive neoplasms such as glioblastoma. Recognizing this phenomenon is essential to avoid misdiagnosing a true arteriovenous shunting lesion, thereby preventing unnecessary intervention procedures and guiding appropriate management. When interpreting angiographic abnormalities observed shortly after seizures, integration of perfusion-based MRI findings with the temporal evolution of symptoms is crucial.
A 48-year-old woman presented with new-onset generalized tonic-clonic seizures. Brain MRI revealed a poorly demarcated, non-enhancing lesion in the left temporal lobe. Arterial spin labeling (ASL) demonstrated marked hyperperfusion within the lesion and adjacent venous sinuses. Cerebral angiography performed approximately 2 h following seizure cessation showed posterior temporal artery dilation and an EVV pattern, with shunting into the vein of Labbé and the ipsilateral transverse and sigmoid sinuses; this raises suspicion for an arteriovenous shunting lesion. No definitive arteriovenous fistulae or thromboses were identified. The patient was managed with antiepileptic therapy alone, which led to clinical improvement. Follow-up MRI and angiography 2 weeks later revealed complete resolution of ASL hyperperfusion and the EVV pattern. Subsequent histopathological examination of the resected tumor confirmed isocitrate dehydrogenase (IDH)-wild-type small cell glioblastoma. Despite the underlying malignant tumor and persistent seizure susceptibility, the angiographic abnormalities and altered venous drainage were entirely reversible and seizure-induced, rather than structurally pathological.
This case illustrates that ictal or postictal cerebral hyperperfusion can produce transient EVV on cerebral angiography, even with aggressive neoplasms such as glioblastoma. Recognizing this phenomenon is essential to avoid misdiagnosing a true arteriovenous shunting lesion, thereby preventing unnecessary intervention procedures and guiding appropriate management. When interpreting angiographic abnormalities observed shortly after seizures, integration of perfusion-based MRI findings with the temporal evolution of symptoms is crucial.