There are several hypotheses of vasoconstriction mechanism after CAS and carotid endarterectomy (CEA). The first hypothesis was that debris or thrombus in stent expansion sites might have caused vasoconstriction due to ischemia or inflammatory conditions [3]. This is supported by the fact that CAS using covered stents caused less neurological complications [7] and the incidence of postoperative complications was high [2]. We suspected an inflammatory condition and administered methylprednisolone. As a result, vasoconstriction improved substantially. However, a pathological search is necessary to identify the effects of glucocorticoids and underlying cause. The second hypothesis was the occurrence of reversible cerebral vasoconstriction syndrome (RCVS). Few reports showed the occurrence of RCVS after CEA, characterized by headache [8, 9]. However, we dismissed the occurrence of RCVS, because the patient did not suffer from headache and vasoconstriction on the image did not show segmental narrowing and dilatation, which is a characteristic of RCVS [10]. Moreover, we administrated methylprednisolone. In general, glucocorticoids are ineffective and can worsen RCVS [11]. The final hypothesis was that cerebral autoregulations became dysfunctional. The pathophysiological hallmark of hyperperfusion syndrome acutely increased the CBF in a hypoperfused brain with maximally dilated vessels. These vessels cannot control increased CBF due to autoregulatory mechanism loss [12]. It was reported that vasoconstriction and hyperperfusion syndrome were developed after CEA [8]. Although completely opposite conditions were observed in the same patient, it may have been the result of disturbances in cerebral autoregulations, which belong to the same spectrum. Chronic severe carotid artery stenosis is observed to cause disturbances in cerebral autoregulations, and relative hypertension in these arteries after CAS or CEA may play a role in developing vasoconstriction. Our patient did not strictly control blood pressure after vasoconstriction, but the patient’s blood pressure was not too high. It is unclear as to why the patient developed hyperperfusion, but the disturbances in cerebral autoregulations may be associated.
This is the first case report on CAS complications, which include vasoconstriction and hyperperfusion syndrome. In general, surgeons know the risk of hyperperfusion syndrome. The operated side is hypoperfused even before the surgery, thus making it difficult to consider hypoperfusion as an unusual manifestation. Hence, surgeons should be aware of the vasoconstriction risk. Hyperperfusion syndrome and vasoconstriction represent two opposite ends of the pathophysiological condition, and the management of both complications is challenging. Thus, regional saturation of oxygen and transcranial Doppler ultrasonography should be performed, and treatment must be given in a timely manner.
There are no data showing the appropriate glucocorticoid treatment for vasoconstriction. Additional cases should be collected and assessed to better understand the pathology of this condition.
