Acute basilar artery (BA) occlusion is a key etiology of devastating posterior circulation stroke, unless recanalization is performed early. Recanalization therapy is determined synthetically based on symptom onset time, stroke severity, and brain imaging. Herein, we report the case of a 72-year-old male patient presenting with minor neurological symptoms, but with thrombotic occlusion at the BA tip. Transcranial Doppler (TCD) showed systolic flow reversal along the vertebrobasilar arteries, and the patient benefited from endovascular thrombectomy. This case highlights the critical role of TCD in identifying hemodynamic insufficiency and determining the implementation of endovascular interventions to mitigate stroke progression.

Eagle’s syndrome is caused by an elongated styloid process or calcified stylohyoid ligament that interferes with adjacent structures. Herein, we present the case of a 26-year-old man who presented to the emergency department due to sudden onset pain in the right occipital area, dysarthria, left hemiparesis, and left arm paresthesia. Computed tomography (CT) angiography revealed an intimal flap and thrombus in the proximal right internal carotid artery (ICA), indicative of carotid artery dissection, as well as direct contact between the styloid process and ICA on both sides. The patient underwent anticoagulation with intravenous heparin for 7 days, followed by 75 mg of clopidogrel per day. Following treatment, the patient gradually improved and was discharged with slight paresthesia in the left arm two weeks after symptom onset. Carotid artery dissection is a rare manifestation of Eagle’s syndrome caused by an elongated styloid process.

Background: Blood viscosity (BV) reflects blood thickness and stickiness, crucial for vascular health. Elevated BV is linked to stroke risk factors, suggesting a role in transient ischemic attacks (TIA). Methods: This retrospective observational study investigated BV levels in TIA patients with and without cerebral artery stenosis. Patients admitted within 24 hours of symptom onset between March 2017 and December 2021 were included. Baseline characteristics, including demographics and vascular risk factors, were assessed. BV measurements were obtained within 24 hours of symptom onset using a scanning capillary-tube viscometer. Patients were categorized into TIA groups based on the presence or absence of cerebral artery stenosis. Results: Of the 153 TIA patients screened, 86 were included for analysis. The mean age was 62.6 years, with a predominance of hypertension (59%) and dyslipidemia (45%). Patients with cerebral artery stenosis (TIA-AT group, n=56) exhibited significantly higher BV levels within 24 hours of symptom onset compared to those without stenosis (TIA-E group, n=30). This finding suggests a potential link between underlying pathophysiological mechanisms of TIA and BV levels. Conclusion Despite the limitations of a single-center, retrospective study, this research suggests that there is evidence of increased blood viscosity in patients with TIA who have cerebral artery stenosis, implying that blood viscosity may play a role in the pathophysiology of TIA. Further research involving larger cohorts is warranted to elucidate the precise mechanisms linking BV to TIA and to validate its utility as a prognostic marker and therapeutic target in TIA management.

Background: Carotid plaque formation is a major global health issue and contributes in pathogenesis of vascular diseases. Lipoprotein(a), similar to low-density lipoprotein, may influence atherogenesis by promoting inflammation and thrombosis. However, the association between lipoprotein(a) levels and presence of carotid plaques has been debated. This study investigated the correlation between these parameters. Methods: We retrospectively analyzed 4,896 individuals who underwent lipoprotein(a) measurement and carotid ultrasonography at Gangnam Severance Hospital between January 2017 and December 2022. The relationship between lipoprotein(a) levels and the presence of carotid plaques was evaluated using logistic regression analysis adjusted for factors such as age, sex, hypertension (HTN), dyslipidemia, and diabetes mellitus (DM). Results: Among the 4,896 enrolled participants, those with carotid plaques were older, more likely to be men, and had a higher prevalence of HTN, DM, and dyslipidemia. The analysis showed a significant association between the presence of carotid plaques and a level of lipoprotein(a) ≥50 mg/dL in both univariable (unadjusted odds ratio=1.508, p<0.001, 95% confidence interval: 1.192–1.907) and multivariable (adjusted odds ratio=1.335, p=0.029, 95% confidence interval: 1.030–1.731) models. Conclusion Elevated lipoprotein(a) level emerged as an independent risk factor for carotid plaque formation, emphasizing the need for integrated risk assessment. Targeting lipoprotein(a) could enhance preventive strategies against cerebrovascular events. Therefore, further research is warranted to elucidate this disease’s underlying mechanisms and evaluate therapeutic interventions.

Acute basilar artery (BA) occlusion is a key etiology of devastating posterior circulation stroke, unless recanalization is performed early. Recanalization therapy is determined synthetically based on symptom onset time, stroke severity, and brain imaging. Herein, we report the case of a 72-year-old male patient presenting with minor neurological symptoms, but with thrombotic occlusion at the BA tip. Transcranial Doppler (TCD) showed systolic flow reversal along the vertebrobasilar arteries, and the patient benefited from endovascular thrombectomy. This case highlights the critical role of TCD in identifying hemodynamic insufficiency and determining the implementation of endovascular interventions to mitigate stroke progression.

Eagle’s syndrome is caused by an elongated styloid process or calcified stylohyoid ligament that interferes with adjacent structures. Herein, we present the case of a 26-year-old man who presented to the emergency department due to sudden onset pain in the right occipital area, dysarthria, left hemiparesis, and left arm paresthesia. Computed tomography (CT) angiography revealed an intimal flap and thrombus in the proximal right internal carotid artery (ICA), indicative of carotid artery dissection, as well as direct contact between the styloid process and ICA on both sides. The patient underwent anticoagulation with intravenous heparin for 7 days, followed by 75 mg of clopidogrel per day. Following treatment, the patient gradually improved and was discharged with slight paresthesia in the left arm two weeks after symptom onset. Carotid artery dissection is a rare manifestation of Eagle’s syndrome caused by an elongated styloid process.

Background: Blood viscosity (BV) reflects blood thickness and stickiness, crucial for vascular health. Elevated BV is linked to stroke risk factors, suggesting a role in transient ischemic attacks (TIA). Methods: This retrospective observational study investigated BV levels in TIA patients with and without cerebral artery stenosis. Patients admitted within 24 hours of symptom onset between March 2017 and December 2021 were included. Baseline characteristics, including demographics and vascular risk factors, were assessed. BV measurements were obtained within 24 hours of symptom onset using a scanning capillary-tube viscometer. Patients were categorized into TIA groups based on the presence or absence of cerebral artery stenosis. Results: Of the 153 TIA patients screened, 86 were included for analysis. The mean age was 62.6 years, with a predominance of hypertension (59%) and dyslipidemia (45%). Patients with cerebral artery stenosis (TIA-AT group, n=56) exhibited significantly higher BV levels within 24 hours of symptom onset compared to those without stenosis (TIA-E group, n=30). This finding suggests a potential link between underlying pathophysiological mechanisms of TIA and BV levels. Conclusion Despite the limitations of a single-center, retrospective study, this research suggests that there is evidence of increased blood viscosity in patients with TIA who have cerebral artery stenosis, implying that blood viscosity may play a role in the pathophysiology of TIA. Further research involving larger cohorts is warranted to elucidate the precise mechanisms linking BV to TIA and to validate its utility as a prognostic marker and therapeutic target in TIA management.

Background: Carotid plaque formation is a major global health issue and contributes in pathogenesis of vascular diseases. Lipoprotein(a), similar to low-density lipoprotein, may influence atherogenesis by promoting inflammation and thrombosis. However, the association between lipoprotein(a) levels and presence of carotid plaques has been debated. This study investigated the correlation between these parameters. Methods: We retrospectively analyzed 4,896 individuals who underwent lipoprotein(a) measurement and carotid ultrasonography at Gangnam Severance Hospital between January 2017 and December 2022. The relationship between lipoprotein(a) levels and the presence of carotid plaques was evaluated using logistic regression analysis adjusted for factors such as age, sex, hypertension (HTN), dyslipidemia, and diabetes mellitus (DM). Results: Among the 4,896 enrolled participants, those with carotid plaques were older, more likely to be men, and had a higher prevalence of HTN, DM, and dyslipidemia. The analysis showed a significant association between the presence of carotid plaques and a level of lipoprotein(a) ≥50 mg/dL in both univariable (unadjusted odds ratio=1.508, p<0.001, 95% confidence interval: 1.192–1.907) and multivariable (adjusted odds ratio=1.335, p=0.029, 95% confidence interval: 1.030–1.731) models. Conclusion Elevated lipoprotein(a) level emerged as an independent risk factor for carotid plaque formation, emphasizing the need for integrated risk assessment. Targeting lipoprotein(a) could enhance preventive strategies against cerebrovascular events. Therefore, further research is warranted to elucidate this disease’s underlying mechanisms and evaluate therapeutic interventions.

Acute basilar artery (BA) occlusion is a key etiology of devastating posterior circulation stroke, unless recanalization is performed early. Recanalization therapy is determined synthetically based on symptom onset time, stroke severity, and brain imaging. Herein, we report the case of a 72-year-old male patient presenting with minor neurological symptoms, but with thrombotic occlusion at the BA tip. Transcranial Doppler (TCD) showed systolic flow reversal along the vertebrobasilar arteries, and the patient benefited from endovascular thrombectomy. This case highlights the critical role of TCD in identifying hemodynamic insufficiency and determining the implementation of endovascular interventions to mitigate stroke progression.

Eagle’s syndrome is caused by an elongated styloid process or calcified stylohyoid ligament that interferes with adjacent structures. Herein, we present the case of a 26-year-old man who presented to the emergency department due to sudden onset pain in the right occipital area, dysarthria, left hemiparesis, and left arm paresthesia. Computed tomography (CT) angiography revealed an intimal flap and thrombus in the proximal right internal carotid artery (ICA), indicative of carotid artery dissection, as well as direct contact between the styloid process and ICA on both sides. The patient underwent anticoagulation with intravenous heparin for 7 days, followed by 75 mg of clopidogrel per day. Following treatment, the patient gradually improved and was discharged with slight paresthesia in the left arm two weeks after symptom onset. Carotid artery dissection is a rare manifestation of Eagle’s syndrome caused by an elongated styloid process.