Glioblastoma multiform with ipsilateral carotid artery stenosis: carotid artery stent promote tumor growth?

Ischemic stroke is a leading health problem in China, and is the most common disease in elderly people [1]. Glioblastoma multiforme (GBM) is a World Health Organization (WHO) grade IV tumor with a dismal prognosis; <10 % of patients are alive after 2 years [2]. Co-existing ischemic stroke with carotid artery stenosis and GBM is rare. The patient described herein presented three times with ischemic strokes complicated by left carotid artery severe stenosis. Magnetic resonance imaging (MRI) showed an infarct pattern consistent with a watershed infarction. Two months after left carotid artery stent (CAS), multiple lesions were noted in the left cerebral hemisphere with massive edema, and a GBM was diagnosed post-operatively. There are some issues worthy of discussion about the clinical diagnosis, therapy, and blood flow after CAS-induced deterioration.

A 55-year-old male patient complained of dysphasia for 4 weeks and continuous deterioration for 5 days. The patient had a history of ischemic stroke (Fig. 1a, b), which manifested as right limb numbness and amaurosis 1 year ago. He had a history of hypertension for 10 years, a myocardial infarction 3 years ago, and cigarette smoking for 40 years, but no history of diabetes, hyperlipidemia, and alcohol consumption. The patient exhibited a disorder of linguistic expression and long-term memory impairment without a limb motor disorder. Cranial MRI confirmed an ischemic stroke at a local hospital (Fig. 1c, d). The symptoms were relieved after medical treatment. The dysphasia relapsed 5 days before admission. Cranial computed tomography (CT) showed a hypodense lesion in the left temporal and occipital lobes (Fig. 1e). Cerebral infarction was considered based on serial cranial MRI, which showed hyperintensity at the internal border zone and the border zone between the left temporal and occipital lobes, and Doppler ultrasound revealed severe left carotid artery stenosis. The patient was transferred to our stroke center for further treatment. At the time of admission, the vital signs were normal. A neurologic examination showed mild dysphasia, normal cranial nerves, normal limb motor function, and negative Babinski signs bilaterally. CT perfusion imaging showed mild ischemic in the territory of the left middle cerebral artery (Fig. 1f). Cervical computed tomography angiography (CTA) confirmed the first segment of the carotid artery with severe stenosis (Fig. 1g). An electrocardiogram revealed an abnormal Q-wave involving the inferior wall, which was consistent with an inferior myocardial infarction. Homocysteine (35.3 μmol/L) and the following laboratory investigations were normal: triglycerides, total cholesterol, low-density lipoprotein cholesterol, antinuclear antibodies, anti-neutrophil cytoplasmic antibodies, prothrombin time, and tumor markers. The patient was given medical treatment consisting of aspirin (100 mg per day), clopidogrel (75 mg), and atorvastatin (20 mg). The patient received combined anti-platelet treatment with 100 mg of aspirin and 75 mg of clopidogrel daily for a week prior to the intervention. Under local anesthesia, the patient underwent placement of a left carotid artery stent (Fig. 1h, i). The patient was discharged 3 days post-operatively. Two months after CAS, the patient experienced right limb numbness and mild dysphasia with a severe headache. The recurrent symptoms and each episode lasted approximately 2 min. An emergency cranial MRI showed massive hyperintense lesions in the left temporal and occipital lobes with ventricular compression (Fig. 2a, b). The cranial CT performed on the same day indicated no cerebral hemorrhage (Fig. 2c). A neurologic examination was also negative. On the basis of a detailed medical history, a diagnosis of hyperfusion was proposed; an anti-hypertensive and mannitol were introduced, and aspirin was discontinued. Despite the medical treatment, the headache worsened. A repeat cranial CT revealed that the cerebral edema had worsened (Fig. 2d). Based on the failed medical treatment and imaging features, a brain tumor was considered. Repeat MRI showed multiple ring-enhanced lesions in the left temporal, parietal, and occipital lobes complicated by massive brain edema (Fig. 2e, f). The patient underwent whole-body positron emission tomography–computed tomography (PET/CT), which showed that the increased FDG metabolism in the left parietal and temporal lobes was consistent with malignant lesions. Revised medical treatment included albumin, furosemide, and dexamethasone. Then, the patient was transferred to the neurosurgery ward pre-operatively. The final pathologic diagnosis was glioblastoma multiforme (WHO grade IV). A post-operative intracranial CT showed regression of the cerebral edema (Fig. 2g, h).

A GBM is a high-grade tumor with a dismal prognosis; complication with severe ipsilateral carotid artery stenosis is rare. Although ischemic stroke is a common disease, we should make the diagnosis cautiously to avoid misdiagnosis. There is insufficient evidence that stent therapy for carotid artery stenosis will aggravate an ipsilateral GBM. Thus, we should be careful in performing CAS when a patient has a concomitant GBM.