Vasomotor Reactivity In Patients Research Articles

Statin treatment intensity and cerebral vasomotor reactivity response in patients with ischemic stroke.

Cerebral vasomotor reactivity (VMR) is vital for regulating brain blood flow and maintaining neurological function. Impaired cerebral VMR is linked to a higher risk of stroke and poor post-stroke outcomes. This study explores the relationship between statin treatment intensity and VMR in patients with ischemic stroke. Seventy-four consecutive patients (mean age 69.3 years, 59.4% male) with recent ischemic stroke were included. VMR levels were assessed 4 weeks after the index stroke using transcranial Doppler, measuring the breath-holding index (BHI) as an indicator of the percentage increase in middle cerebral artery blood flow (higher BHI signifies higher VMR). Multistep multivariable regression models, adjusted for demographic and cerebrovascular risk factors, were employed to examine the association between statin intensity treatment and BHI levels. Forty-one patients (55%) received high-intensity statins. Patients receiving high-intensity statins exhibited a mean BHI of 0.85, whereas those on low-intensity statins had a mean BHI of 0.67 (mean difference 0.18, 95% confidence interval: 0.13-0.22, p-value<.001). This significant difference persisted in the fully adjusted model (adjusted mean values: 0.84vs. 0.68, p-value:.008). No significant differences were observed in BHI values within patient groups on high-intensity or low-intensity statin therapy (all p-values>.05). Furthermore, no significant association was found between baseline low-density lipoprotein (LDL) levels and BHI. High-intensity statin treatment post-ischemic stroke is linked to elevated VMR independent of demographic and clinical characteristics, including baseline LDL level. Further research is needed to explore statin therapy's impact on preserving brain vascular function beyond lipid-lowering effects.

Vasomotor reactivity in patients with cerebral small vessel disease vs. internal border zone infarction and its correlation with disease outcome

BackgroundAvailable data collected from patients of different types of cerebrovascular strokes can detect risk factors, severity and clinical outcome of these patients. Differentiating between different types of strokes is mandatory for early diagnosis and proper management. The aim of this study is to compare between cerebral small vessel disease with lacunar infarctions and internal border zone infarctions regarding vasomotor reactivity by using transcranial color-coded duplex and its correlation with their MRI perfusion, disease severity and outcome.ResultsOn admission, 56.7% of patients in lacunar stroke had impaired reactivity vs. 100% of patients in internal border zone group. At 3 months follow-up, this number dropped to 23.3% in lacunar group, but persisted as 100% in internal border zone group. On comparing the 3 perfusion parameters between the 2 groups, there was statistically significant impairment in all parameters in patients with internal border zone infarction than patients with lacunar infarction (longer time to peak, decreased cerebral blood flow and cerebral blood volume). By comparing the severity of the stroke by using National Institute of Health and Stroke Scale, it was found that patients with internal border zone infarction had higher disability than patients with lacunar infarction on admission and on discharge. At 3 months follow-up, the lacunar group had a better outcome than of the border zone group.ConclusionPatients having internal border zone infarction had higher clinical disability and worse prognosis, together with more impairment in vasomotor reactivity and MRI perfusion parameters than patients having lacunar infarction.

Assessment of cerebral vasomotor reactivity in patients with acute stroke and transient ischemic attack (TIA) with different etiopathogenesis: Preliminary results

An impaired vasomotor reactivity (VMR) represents a negative prognostic factor for vascular and degenerative cognitive deterioration. Only few studies have addressed VMR in acute phase of stroke. We aim to investigate if VMR, calculated through the breath holding index (BHI), is a prognostic marker of clinical outcome in stroke/TIA patients.

The Effects of Melatonin Treatment on Headache and Vasomotor Reactivity in Patients with Chronic Tension-Type Headache

Objectives: Chronic tension-type headache (TTH) is a serious disease that disrupts quality of life. In this study, the effect of prophylactic oral melatonin treatment on headache and cerebral vasomotor reactivity (VMR) was investigated in patients diagnosed with chronic TTH per the International Classification of Headache Disorders criteria. Subjects and Methods: Twenty patients with chronic TTH and 20 healthy individuals were included in the study. The patients were administered a melatonin treatment at 3 mg/day for 12 weeks. The number of monthly painful days and pain severity were recorded with the “Visual Analog Scale” before and after the treatment. Cerebral VMR measurements were performed at baseline in the control group and in patients before and after the treatment. Results: The median number of monthly painful days was 20 (15–27) before the treatment and 10 (4–18) after the treatment; the median pain severity score was 70.00 (45–80) before the treatment and 42.50 (15–75) after the treatment. The difference was statistically significant (P = 0.001). No statistically significant difference between the VMR values was observed (P &gt; 0.05). Conclusions: Melatonin treatment was effective in reducing the pain severity and decreasing the number of monthly painful days in patients with chronic TTH but demonstrated no effect on the cerebral VMR.

Assessment of Cerebral Vasomotor Reactivity in Patients With Primary Open-angle Glaucoma and Ocular Hypertension Using the Breath-Holding Index.

Patients with ocular hypertension (OHT) do not show impaired cerebral vasodilation responses to hypercapnia but patients with primary open-angle glaucoma (POAG) do. Impaired vasoreactivity in patients with POAG may have neuronal or vascular origins and increase stroke risk. To investigate changes in cerebral blood flow and cerebral vasomotor reactivity using the breath-holding index in patients with POAG and OHT, to examine whether these parameters contribute to the risk of ischemic stroke. Thirty patients with POAG, 30 patients with OHT, and 30 age- and sex-matched healthy control subjects were included in this university hospital-based, cross-sectional, and observational study. Eyes with a greater degree of visual field loss and/or more severe optic disc damage were selected for the study in patients with POAG, whereas in patients with OHT and controls, the study eye was chosen randomly. The mean blood flow velocity and breath-holding index were measured in the middle cerebral artery ipsilaterally in patient and control groups, by using transcranial Doppler ultrasonography. The mean blood flow velocity and breath-holding indexes were significantly lower in patients with POAG than in the control group (all P<0.05). In the OHT group, the mean blood flow velocity and breath-holding indexes were not different from those in the control group. Patients with POAG have impaired vasodilation response to hypercapnia. Presumably, the neuronal changes and deterioration of the endothelium-mediated vasodilatation in patients with glaucoma may disrupt the regulation of arteries and potentially present functional insufficiency on vasoreactivity. Moreover, impaired cerebral vascular regulation may contribute to the increased risk of stroke in patients with POAG.

Right-to-left shunts and hormonal therapy influence cerebral vasomotor reactivity in patients with migraine with aura.

Patent Foramen Ovale and impaired cerebral hemodynamics were proposed among the pathophysiological mechanisms explaining the increased risk for stroke in patients with Migraine with Aura (MA). Our study aimed at comparing the vasomotor reactivity (VMR) of the anterior and the posterior cerebral circulation in patients with Migraine with Aura, in patients with acute vascular ischemic accidents, and in controls. We hypothesized that VMR in MA patients is preserved in the anterior circulation and reduced in the posterior circulation. We prospectively assessed with Transcranial Doppler the vasomotor reactivity to breath holding of the Middle and Posterior Cerebral Arteries (MCA, PCA) in MA patients, in acute vascular patients and healthy controls. We also evaluated the possible effect of clinical characteristics of MA (attack frequency, aura length or type, disease history), vascular factors and the presence of right-to-left shunt on VMR. Diverging from our hypothesis, MA patients displayed a higher breath-holding index (BHI) than controls in the MCA (1.84±0.47%/s vs 1.53±0.47%/s, p = .001) as well as in the PCA (1.87±0.65%/s vs 1.47±0.44%/s, p < .001). In MA patients, MCA BHI was higher in those with large right-to-left shunts (2.09±0.42 vs 1.79±0.47, p = .046) and lower in those taking estrogens (1.30±0.30%/s vs 1.9±0.45%/s, p = .009). We did not observe an effect of MA characteristics on BHI. The increased BHI in MA patients with large right-to-left shunts could be explained by the vasoactive effect in the cerebral circulation of substances bypassing the deactivating pulmonary filters or by a constitutional trait of the vascular system associating persistent right-to-left shunts and hyper-reactive hemodynamics. Our results discourage the hypothesis that altered hemodynamics contribute to increasing the stroke risk in all MA patients. However, estrogens can lower VMR, curtailing the hemodynamic resources of MA patients.

Aerobic Exercise Training and Cerebral Vasomotor Reactivity in Patients with Mild Cognitive Impairment

Aerobic Exercise Training and Cerebral Vasomotor Reactivity in Patients with Mild Cognitive Impairment

Decreased cerebral vasomotor reactivity in patients with obstructive sleep apnea syndrome

ObjectiveIn obstructive sleep apnea syndrome (OSAS), any of the activated neural, vascular, hemodynamic, metabolic, inflammatory, and thrombotic mechanisms may be related to increased cerebrovascular disease and risk of death; however, the possible pathophysiological process between obstructive sleep apnea syndrome and stroke has not been clearly explained. We hypothesize that alterations in vasomotor reactivity in patients may be responsible for their altered cerebral blood flow, and may contribute to the increased risk of ischemic stroke. MethodsA total of 30 untreated patients with severe obstructive sleep apnea and 26 control subjects were included in the study. The mean blood flow velocity and breath holding index were measured in middle cerebral artery bilaterally in both patient and control groups by using transcranial Doppler ultrasound. We compared the values between two groups. ResultsThe mean blood flow velocity and breath holding indexes were significantly decreased in the patient group when compared with the control group. There were no correlations between cerebral hemodynamic parameters and polysomnographic findings in patients. ConclusionOur findings suggest that there was a deteriorated vasodilator response to hypercapnia in patients with OSAS. This deterioration may stem from chemoreceptors or endothelial damages that lead to vascular relaxation and vasodilatation in cerebrovascular circulation. This impaired cerebral vascular regulation may contribute to the increased risk of stroke in patients with OSAS.

P038. Effects of non-invasive vagus nerve stimulation on cerebral vasomotor reactivity in patients with chronic migraine during intercritical phase: a pilot study.

Different strategies of neurostimulation have been developed as treatment tools for migraine. Among them, vagus nerve stimulation (VNS) can be performed both invasively and non-invasively. Recently, “Gammacore” has been approved as a non-pharmacological and non-invasive tool for headache, and a recent study demonstrated its efficacy in 22% of patients with acute migraine attacks[1]. Although the pathophysiology of migraine is not yet fully understood, many studies have shown a role of sterile inflammation of cerebral vessels and of the change in diameter of the intracranial arteries. Blood flow velocities and vasomotor reactivity (VMR) in patients suffering from migraine without aura in the intercritical phase were found either increased or normal compared to non-migraineurs healthy controls[2, 3]. Since the vagus nerve is the largest parasympathetic nerve of the body, it is probable that its neuromodulation can affect cerebral hemodynamics. The purpose of the study was to evaluate the effects of external vagus nerve stimulation on VMR of patients suffering from chronic migraine.

Identification of Disturbances of Autoregulation of Cerebral Hemodynamics and Blood Vessels Reactivity in Patients with Consequences of Mild Traumatic Brain Injuries

The purpose of the current research was to revise the disturbances of autoregulation of cerebral hemodynamics and reactivity of vessels in patients with consequences of mild traumatic brain injuries by using Doppler ultrasonography with hyper-and hypocapnic tests. Methods: We examined 65 patients with consequences of mild traumatic brain injuries. Doppler ultrasonography with hyper-and hypocapnic tests were carried out according to the standard method. Results: During the research by Doppler ultrasonography with the hypercapnic and hypocapnic tests in patients with consequences of mild TBI the coefficient of overshoot of 1.13 ± 0.04 was identified. A paradoxical cerebral vascular response was evident as a delayed response to the tests as carried out. The above response was accompanied by the increase of the LVF after the hypercapnic test to 28.7% (48.8% in the control group) and by the increase of the LVF after the hypocapnic test to 36.8% (27.5% in the control group). Under the hypercapnic load in patients with consequences of mild TBI the coefficient of reactivity was lower than that of the patients in the control group (0.34 ± 0.07 and 0.46 ± 0.03 RVU respectively, p<0.05). Under the hypocapnic load in patients with consequences of mild TBI the coefficient of reactivity was lower than that of healthy subjects (0.44 ± 0.02 and 0.55 ± 0.04 RVU respectively, p<0.05). The index of vasomotor reactivity in patients with TBI consequences was lower, than that of the control group (73.1 ± 0.05 and 97.3 ± 0.02 respectively, p<0.0001). The increase of PI up to 1.73 ± 0.02; and the increase of RI up to 0.97 ± 0.02 (p<0.0001) were present in all the patients in the survey sample with consequences of traumatic brain injuries. Conclusions: During our investigation we detected changes of reactivity of vessels towards the decrease of indicators of linear velocity of blood flow under the tests. A paradoxical vascular response was marked in all the patients under the hyper- and hypocapnic load; a test-induced delayed vessels reaction was marked in 52 out of 65 patients.

Reduced breath holding index in patients with chronic migraine

Migraine is a neurovascular disorder characterized by autonomic nervous system dysfunction and severe headache attacks. Studies have shown that changes in the intracranial vessels during migraine have an important role in the pathophysiology. Many studies have been conducted on the increased risk of stroke in patients with migraine, but insufficient data are available on the mechanism underlying the increase. This study aimed to evaluate basal cerebral blood flow velocity and vasomotor reactivity in patients with chronic migraine. We evaluated 38 patients with chronic migraine. Three of them were excluded because they had auras and four of them were excluded because of their use of medication that can affect cerebral blood flow velocity and breath holding index (beta or calcium channel blockers). Our study population consisted of 31 patients with chronic migraine without aura and 29 age- and gender-matched healthy individuals who were not taking any medication. The mean blood flow velocity and breath holding index were measured on both sides from the middle cerebral artery and posterior cerebral artery, with temporal window insonation. The breath holding index for middle cerebral artery and posterior cerebral artery was significantly lower in the migraine group compared to that of the control group (p < 0.05).The vasomotor reactivity indicates the dilatation potential of a vessel, and it is closely related to autoregulation. According to our results, the vasodilator response of cerebral arterioles to hypercapnia was lower in patients with chronic migraine. These findings showed the existence of impairments in the harmonic cerebral hemodynamic mechanisms in patients with chronic migraine. This finding also supports the existing idea of an increased risk of stroke in patients with chronic migraine due to impaired vasomotor reactivity.

Vasomotor reactivity as a predictor for syncope in patients with orthostatism

Syncope in patients with orthostatic hypotension (OH) may be the result of impaired cerebral autoregulation. Cerebral autoregulation status can be determined by assessing cerebral vasomotor reactivity (VMR). We assessed and compared VMR in patients with OH with and without syncope. Twenty-nine patients with OH underwent transcranial Doppler (TCD) and the Diamox test (1 g acetazolamide IV) for assessing VMR during elaboration of their OH syndrome. The percent difference between cerebral blood flow velocities (BFV) in the middle cerebral (MCA) and vertebral (VA) arteries before and after acetazolamide was defined as VMR%. We considered increases of BFV of ≥ 40% as being indicative of good VMR and classified our study patients as having good or impaired VMRs accordingly. Mean VMR% values of the MCA and VA in patients with OH with syncope (n = 12) were significantly lower as compared with patients with OH without syncope (n = 17): 25.2 ± 20.5% and 42.5 ± 18.6%; 20.9 ± 15.5% and 40.8 ± 28.5%, respectively (P < 0.05). Among patients with OH, we found an association between the presence of syncope and impaired VMR. Assessment of VMR among patients with OH may predict those who are at higher risk to faint and fall and to support more aggressive intervention.

Evaluation of cerebral vasomotor reactivity in Parkinson's disease: Is there any association with orthostatic hypotension?

Objective Our aim was to look for a probable relationship between cerebral vasomotor reactivity (VMR) and orthostatic hypotension (OH) in Parkinson's disease (PD). Materials and methods This study was conducted on 44 patients with PD. Assessment of cerebral VMR was performed by means of transcranial Doppler (TCD) of middle cerebral artery (MCA) before and after a vasodilatory stimulus, carbon dioxide test. Moreover, orthostatic hypotension was evaluated. Results OH was presented in 12 (27.3%) Parkinson's patients. The average resting blood flow velocity (BFV) in the MCA was 30.20 (SD = 9.58) cm s −1 which significantly increased to 46.25 (SD = 16.23) cm s −1 after carbon dioxide test ( P < 0.001). Impaired VMR was observed in 15 (34.1%) of the subjects, while it was not associated with the presence of OH ( P = 0.770). Conclusion Evaluation of VMR in patients affected by PD, could assist in early diagnosis of cerebral autonomic dysfunction and prevent its serious consequences prior and more valid to OH.

Influence of Galantamine on Vasomotor Reactivity in Alzheimer’s Disease and Vascular Dementia Due to Cerebral Microangiopathy

Recent reports suggest that vascular factors play a crucial role in the development and progression of Alzheimer's disease. We aimed to assess vasomotor reactivity in patients with Alzheimer's disease and vascular dementia due to microangiopathy using transcranial Doppler sonography and near-infrared spectroscopy during a CO(2) exposition task. The normalized CO(2) reactivity assessed at the middle cerebral artery and the oxygenated and deoxygenated hemoglobin of the frontal cortex were obtained. To investigate the impact of cholinergic deficiency known for Alzheimer's disease on vasomotor reactivity, both groups were reinvestigated during treatment with the acetylcholine esterase inhibitor galantamine. Transcranial Doppler analysis revealed significantly reduced normalized CO(2) reactivity for Alzheimer's disease and vascular dementia. Vasomotor reactivity assessed by near-infrared spectroscopy was decreased in patients with vascular dementia, but not in Alzheimer's disease. Galantamine treatment showed a beneficial effect, normalizing these parameters close to age-matched control levels. Our results suggest that Alzheimer's disease is associated with a lack of vasomotor reactivity, which might be associated with disturbed autoregulation indicating a potential risk for a decreased protection of brain tissue against blood pressure changes. Additionally, a diminished increase of cortical oxygenated hemoglobin during the CO(2) test was apparent in patients with vascular dementia. Galantamine treatment influenced vascular reactivity in the CO(2) test, thus providing evidence for the cholinergic deficiency, thereby adding to vascular dysregulation in Alzheimer's disease, but also indicating an important role of cholinergic system dysfunction for vascular dementia.

Evaluation of Vasomotor Reactivity by Transcranial Doppler Sonography in Patients With Acute Stroke Who Have Symptomatic Intracranial and Extracranial Stenosis

In patients with large artery disease, determining the cerebral hemodynamic state and following its alterations may be a good marker for predicting long-term outcome. The aim of our study was to compare the changes in vasomotor reactivity (VMR) of patients with symptomatic intracranial and extracranial artery stenosis. We also examined whether VMR after stroke influences the long-term prognosis for these patients. Forty-one patients were included in the study. To determine the cerebral hemodynamic state, transcranial Doppler ultrasound examinations and acetazolamide tests were performed after acute stroke and repeated after 6 months. We compared the VMR on admission and at 6 months, together with changes in VMR, of the patients with symptomatic intracranial and extracranial artery stenosis. By calculating the Barthel index at 6 months, we examined whether VMR had an effect on an improvement in their quality of life. We observed a significantly higher initial VMR of the ipsilateral hemisphere in patients with intracranial stenosis (22.4 +/- 9.1 versus 13.4 +/- 12.8; P = .013). At 6 months, the VMR obtained from the ipsilateral hemisphere was better in patients with extracranial stenosis than in the patients with intracranial stenosis (P = .01). The ipsilateral VMR measured on admission showed a positive correlation with the Barthel index at 6 months (P = .007; r = 0.434). Our study showed that VMR in patients with acute stroke who have extracranial and intracranial artery stenosis measured by using a transcranial Doppler examination may have value in predicting long-term outcome.

Statins and Cerebral Vasomotor Reactivity

See related article, pages 2540-2545. Animal models have shown that cholesterol-lowering therapy with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (commonly called statins) may augment absolute cerebral blood flow (CBF) by enhancing nitric oxide synthase (eNOS).1 Statins upregulate type III endothelial eNOS in thrombocytes, decrease platelet activation, and protect from cerebral ischemia in normocholesterolemic mice.2 Statins may also provide additional beneficial effects by upregulating endogenous tissue plasminogen activator and enhancing clot lysis in a mouse model of embolic focal ischemia.3 Statins given 24 hours after experimental ischemia can enhance CBF, angiogenesis, neurogenesis and sinaptogenesis.4 How can these findings be applied in the clinical setting? A meta-analysis of published clinical trials showed that low-density lipoprotein–lowering with statins may decrease the risk of stroke in diabetic or hypertensive patients with normal low-density lipoprotein cholesterol at baseline, and in patients with coronary artery disease, with respectively 48%, 27% and 25% reduction in stroke incidence.5 Does any relationship exist among statins and cerebral vasomotor reactivity? Functional transcranial Doppler (TCD) ultrasonography permits the assessment of cognitively induced CBF velocity changes6 and the evaluation of cerebral vasomotor reactivity.7 TCD can be used to reliably evaluate age-related changes in the physiological response of the human cerebral circulation. A diminished nitric oxide–mediated cerebral vasomotor response may exist in aging subjects and in patients with vascular risk factors.8 Because there are no reliable markers for the functional status of the cerebral small vessels in elderly patients at risk of stroke, TCD studies may be useful. Although some parameters …

Cerebral vasomotor reactivity testing in head injury: the link between pressure and flow

Background: It has been suggested that a moving correlation index between mean arterial blood pressure and intracranial pressure, called PRx, can be used to monitor and quantify cerebral vasomotor reactivity...

Effect of cilostazol on vasomotor reactivity in patients with vasospastic angina pectoris

We examined the effects of cilostazol on impaired coronary arterial responses in patients with vasospastic angina (VSA). Thirty patients who were diagnosed with VSA based on an acetylcholine provocation test and 10 subjects with normal coronary arteries were enrolled. The patients were divided into the following 3 groups: no antiplatelet agent treatment group, aspirin treatment, or cilostazol treatment groups. Coronary flow reserve (CFR), coronary flow volume at maximum hyperemia, and epicardial coronary artery diameter after administration of N G-monomethyl- l-arginine ( l-NMMA) were examined using a Doppler flow wire before and 6 months after the start of this study. CFR, coronary flow volume at maximum hyperemia, and diameter changes by l-NMMA were significantly increased in the cilostazol treatment group compared with the other 2 groups. In conclusion, cilostazol increased CFR and flow-dependent coronary dilation; these changes were attributable to nitric oxide. Cilostazol may improve coronary vascular endothelial dysfunction and coronary hemodynamics in patients with VSA.

Association between impaired carbon dioxide reactivity and ischemic lesions in arterial border zone territories in patients with unilateral internal carotid artery occlusion.

Ischemic lesions in patients with internal carotid artery (ICA) steno-occlusive disease can be categorized on the basis of their location and presumed cause: external border zone infarcts, internal border zone infarcts, cortical infarcts, lacunar infarcts, and periventricular lesions. To evaluate the association between the prevalence and size of ischemic lesions and cerebral vasomotor reactivity in patients with unilateral occlusion of the ICA. Cross-sectional study. Referral center. Seventy consecutive patients were included in this study. All patients had a transient or minor disabling retinal or cerebral ischemia that was associated with unilateral occlusion of the ICA. Ischemic lesions on magnetic resonance imaging were identified on hard copies, and volume measurements were obtained by a magnetic resonance workstation. Vasomotor reactivity was assessed with transcranial Doppler ultrasonography with carbon dioxide challenge. Prevalence and size of ischemic lesions. In the hemisphere ipsilateral to the ICA occlusion, we found an increased prevalence of internal border zone infarcts (P =.01), external borders zone infarcts (P<.001), and territorial infarcts (P =.02) compared with the contralateral hemisphere. Hemispheres with a carbon dioxide reactivity less than or equal to 18% demonstrated a significant increase in prevalence (P =.007) and volume (P =.003) of internal border zone infarcts compared with hemispheres with a carbon dioxide reactivity greater than or equal to 19%. No association between carbon dioxide reactivity and any other type of ischemic lesion was found. In patients with an ICA occlusion, only internal border zone infarcts demonstrate a significant association with diminished cerebral hemodynamics.

Lack of gender difference in acetazolamide-induced cerebral vasomotor reactivity in patients suffering from type-1 diabetes mellitus.

The aim of the present work was to investigate the impact of gender on resting cerebral blood flow velocity and cerebrovascular reserve capacity among diabetic patients. Middle cerebral artery mean blood flow velocity (MCAV) was measured in 72 patients suffering from type 1 diabetes mellitus at rest and 5, 10, 15 and 20 min after intravenous administration of 1 g acetazolamide. Cerebrovascular reserve was calculated as the maximal percent increase in MCAV after acetazolamide. Resting MCAV and cerebrovascular reserve capacity were compared between males and females. Resting cerebral blood flow velocity was higher in diabetic females than in males (men, 55.0+/-17.0 cm/s; women, 64.4+/-12.6 cm/s, p=0.0094). Cerebrovascular reserve capacity was similar in diabetic women and men (men, 44.0%+/-18.6%; women, 52.6%+/-32.9%, p=0.17). Comparing MCAV and cerebrovascular reserve capacity among the diabetic subgroups with disease duration < or = 10 years and >10 years, we did not detect any differences between women and men. Duration of diabetes was an important factor in determining cerebrovascular reserve capacity in both sexes: long-term diabetic women and men showed lower CRC values than diabetics with < or = 10 years disease duration. Cerebrovascular reserve capacity is similar in diabetic women and men. Taking into consideration that cerebrovascular reserve is normally higher among women, our finding indicates a relatively more serious worsening of cerebral vasodilatory responses in women suffering from type 1 diabetes.