Journal of neurological surgery. Part A, Central European neurosurgery · 2023
Delayed Internal Carotid Artery Dissection Mimicking Cerebral Vasospasms after Subarachnoid Hemorrhage: A Case Report.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Lampmann Tim, Dorn Franziska, Schievelkamp Arndt-Hendrik, Banat Mohammed, Vatter Hartmut, Hamed Motaz
Аннотация
BACKGROUND: Delayed cerebral ischemia (DCI) is usually caused by cerebral vasospasm (CVS). To detect DCI and CVS, a cranial computed tomography (CT) scan will be performed, but cervical vessels are not necessarily displayed.
METHODS: A 63-year-old female patient who suffered from aneurysmal subarachnoid hemorrhage (SAH) was treated at the authors' institution. After an initially unremarkable clinical course, she developed aphasia on day 11. CT angiography (CTA) and perfusion imaging revealed significant hypoperfusion of the left hemisphere. In addition, the CTA showed a subtotal stenosis of the internal carotid artery (ICA) at the level of the petrous segment, suspicious for a dissection. This was not detectable angiographically in the final control of the intervention and was also not clinically evident until day 11.
RESULTS: Cerebral perfusion as well as the clinical symptoms normalized rapidly after stent reconstruction of the ICA.
CONCLUSION: Even though CVS is the most common cause of hypoperfusion in patients after an SAH, a peri-interventional dissection can also lead to relevant stenosis and thus to a disturbed cerebral perfusion and corresponding neurologic deficits. The time delay between the intervention and the clinical and CTA manifestation in our case is remarkable.
METHODS: A 63-year-old female patient who suffered from aneurysmal subarachnoid hemorrhage (SAH) was treated at the authors' institution. After an initially unremarkable clinical course, she developed aphasia on day 11. CT angiography (CTA) and perfusion imaging revealed significant hypoperfusion of the left hemisphere. In addition, the CTA showed a subtotal stenosis of the internal carotid artery (ICA) at the level of the petrous segment, suspicious for a dissection. This was not detectable angiographically in the final control of the intervention and was also not clinically evident until day 11.
RESULTS: Cerebral perfusion as well as the clinical symptoms normalized rapidly after stent reconstruction of the ICA.
CONCLUSION: Even though CVS is the most common cause of hypoperfusion in patients after an SAH, a peri-interventional dissection can also lead to relevant stenosis and thus to a disturbed cerebral perfusion and corresponding neurologic deficits. The time delay between the intervention and the clinical and CTA manifestation in our case is remarkable.