Comprehensive Ultrasound Assessment of the Craniocervical Circulation in Transient Global Amnesia

Objectives Structural changes and metabolic stress have been reported on diffusion-weighted magnetic resonance imaging in the cornu ammonis 1 area of the hippocampus in patients with transient global amnesia (TGA), but a consensus on pathogenesis is still lacking. The aim of our study was to perform a comprehensive ultrasound analysis of the cerebrovascular circulation in our population of patients with TGA. Methods One hundred patients with TGA and 50 age- and sex-matched control participants underwent ultrasound examinations of the cervicocranial circulation. Results The most significant risk factor for TGA was arterial hypertension (P .05). Rarely detected microembolic signals or a right-left cardiopulmonary shunt excluded an emboligenic mechanism of TGA (P > .05). The internal jugular vein valves were incompetent in 54% of patients with TGA, and this condition was associated with an increased risk of TGA (odds ratio, 4.16; 95% confidence interval, 1.91–9.04). The mean values of the breath holding index and pulsatility index, as parameters of small-vessel function, were within normal ranges and without differences between the TGA and control groups (P > .05). Conclusions Our ultrasound examination did not detect significant structural atherosclerotic changes of cervicocranial arteries, and an emboligenic mechanism was excluded. Only a significant rise of blood pressure in TGA and significant valvular insufficiency of the internal jugular vein were established. New research should clarify whether these simultaneous functional circulatory changes have relevance for metabolic stress in the cornu ammonis of the hippocampus

Comprehensive Ultrasound Assessment of the Craniocervical Circulation in Transient Global Amnesia

Objectives Structural changes and metabolic stress have been reported on diffusion-weighted magnetic resonance imaging in the cornu ammonis 1 area of the hippocampus in patients with transient global amnesia (TGA), but a consensus on pathogenesis is still lacking. The aim of our study was to perform a comprehensive ultrasound analysis of the cerebrovascular circulation in our population of patients with TGA. Methods One hundred patients with TGA and 50 age- and sex-matched control participants underwent ultrasound examinations of the cervicocranial circulation. Results The most significant risk factor for TGA was arterial hypertension (P .05). Rarely detected microembolic signals or a right-left cardiopulmonary shunt excluded an emboligenic mechanism of TGA (P > .05). The internal jugular vein valves were incompetent in 54% of patients with TGA, and this condition was associated with an increased risk of TGA (odds ratio, 4.16; 95% confidence interval, 1.91–9.04). The mean values of the breath holding index and pulsatility index, as parameters of small-vessel function, were within normal ranges and without differences between the TGA and control groups (P > .05). Conclusions Our ultrasound examination did not detect significant structural atherosclerotic changes of cervicocranial arteries, and an emboligenic mechanism was excluded. Only a significant rise of blood pressure in TGA and significant valvular insufficiency of the internal jugular vein were established. New research should clarify whether these simultaneous functional circulatory changes have relevance for metabolic stress in the cornu ammonis of the hippocampus

Correlation of Carotid Artery Disease Severity and Vasomotor Response of Cerebral Blood Vessels

We assessed reactivity of cerebral vessels on hypercapnia in patients with carotid occlusive disease. The effects of vascular risk factors on carotid atherosclerosis and vasomotor reactivity (VMR) of cerebral arterioles were also examined. Patients (n = 50) with carotid stenosis (30% in 1 or both sides) were included; 30 patients acted as controls. Hypertension, hyperlipidemia, diabetes, cardiac diseases, inflammation, and smoking were recorded. Vasomotor reactivity was assessed with the apnea test by transcranial Doppler ultrasonography and estimated by flow velocity changes in the middle cerebral artery before and after hypercapnia induction. Vasomotor reactivity was defined by the breath holding index, and values under 0.69 were considered critical for VMR impairment. Vasomotor reactivity reduction was significant (P = .004) in patients with severe carotid stenosis ( GT 70%) and with symptomatic carotid disease (P LT .05). The risk factors did not significantly influence VMR reduction. Severe carotid stenosis impairs VMR and may increase the risk of stroke, especially in symptomatic patients

Type 2 Diabetic Patients with Ischemic Stroke: Decreased Insulin Sensitivity and Decreases in Antioxidant Enzyme Activity Are Related to Different Stroke Subtypes

We analyzed (a) insulin sensitivity (IS) and (b) glutathione peroxidase (GSH-Px), glutathione reductase (GR), and superoxide dismutase (SOD) antioxidant enzyme activity in type 2 diabetic (T2D) patients with atherothrombotic infarction (ATI) (group A), lacunar infarction (LI) (B), or without stroke (C) and in nondiabetics with ATI (D), LI (E), or without stroke (F). ATI and LI were confirmed by brain imaging IS levels were determined by minimal model (Si index), and the enzyme activity by spectrophotometry. In T2D patients, Si was lower in A and B versus C (1.14 ± 0.58, 1.00 ± 0.26 versus 3.14 ± 0.62 min −1 /mU/l × 10 4 , < 0.001) and in nondiabetics in D and E versus F (3.38 ± 0.77, 3.03 ± 0.72 versus 6.03 ± 1.69 min −1 /mU/l × 10 4 , < 0.001). Also, GSH-Px and GR activities were lower in A and B versus C (GSH-Px: 21.96 ± 3.56, 22.51 ± 1.23 versus 25.12 ± 1.67; GR: 44.37 ± 3.58, 43.50 ± 2.39 versus 48.58 ± 3.67 U/gHb; < 0.001) and in D and E versus F (GSH-Px: 24.75 ± 3.02, 25.57 ± 1.92 versus 28.56 ± 3.91; GR: 48.27 ± 6.81, 49.17 ± 6.24 versus 53.67 ± 3.96 U/gHb; < 0.001). Decreases in Si and GR were significantly related to both ATI and LI in T2D. Our results showed that decreased IS and impaired antioxidant enzymes activity influence ischemic stroke subtypes in T2D. The influence of insulin resistance might be exerted on the level of glutathione-dependent antioxidant enzymes

Type 2 Diabetic Patients with Ischemic Stroke: Decreased Insulin Sensitivity and Decreases in Antioxidant Enzyme Activity Are Related to Different Stroke Subtypes

We analyzed (a) insulin sensitivity (IS) and (b) glutathione peroxidase (GSH-Px), glutathione reductase (GR), and superoxide dismutase (SOD) antioxidant enzyme activity in type 2 diabetic (T2D) patients with atherothrombotic infarction (ATI) (group A), lacunar infarction (LI) (B), or without stroke (C) and in nondiabetics with ATI (D), LI (E), or without stroke (F). ATI and LI were confirmed by brain imaging IS levels were determined by minimal model (Si index), and the enzyme activity by spectrophotometry. In T2D patients, Si was lower in A and B versus C (1.14±0.58, 1.00±0.26 versus 3.14±0.62 min−1/mU/l × 104, P<0.001) and in nondiabetics in D and E versus F (3.38±0.77, 3.03±0.72 versus 6.03±1.69 min−1/mU/l × 104, P<0.001). Also, GSH-Px and GR activities were lower in A and B versus C (GSH-Px: 21.96±3.56,  22.51±1.23 versus 25.12±1.67; GR: 44.37±3.58,  43.50±2.39 versus 48.58±3.67 U/gHb; P<0.001) and in D and E versus F (GSH-Px: 24.75±3.02,  25.57±1.92 versus 28.56±3.91; GR: 48.27±6.81,  49.17±6.24 versus 53.67±3.96 U/gHb; P<0.001). Decreases in Si and GR were significantly related to both ATI and LI in T2D. Our results showed that decreased IS and impaired antioxidant enzymes activity influence ischemic stroke subtypes in T2D. The influence of insulin resistance might be exerted on the level of glutathione-dependent antioxidant enzymes

Decreased Insulin Sensitivity and Impaired Fibrinolytic Activity in Type 2 Diabetes Patients and Nondiabetics with Ischemic Stroke

We analyzed (a) insulin sensitivity (IS), (b) plasma insulin (PI), and (c) plasminogen activator inhibitor-1 (PAI-1) in type 2 diabetes (T2D) patients with (group A) and without (group B) atherothrombotic ischemic stroke (ATIS), nondiabetics with ATIS (group C), and healthy controls (group D). IS was determined by minimal model (Si). Si was lower in A versus B (1.18±0.67 versus 2.82±0.61 min−1/mU/L × 104; P<0.001) and in C versus D (3.18±0.93 versus 6.13±1.69 min−1/mU/L × 104; P<0.001). PI and PAI-1 were higher in A versus B (PI: 19.61±4.08 versus 14.91±1.66 mU/L; P<0.001, PAI-1: 7.75±1.04 versus 4.57±0.72 mU/L; P<0.001) and in C versus D (PI: 15.14±2.20 versus 7.58±2.05 mU/L; P<0.001, PAI-1: 4.78±0.98 versus 3.49±1.04 mU/L; P<0.001). Si correlated with PAI-1 in T2D patients and nondiabetics, albeit stronger in T2D. Binary logistic regression identified insulin, PAI-1, and Si as independent predictors for ATIS in T2D patients and nondiabetics. The results imply that insulin resistance and fasting hyperinsulinemia might exert their atherogenic impact through the impaired fibrinolysis