Reduced cerebral blood flow velocity and impaired cerebral autoregulation in patients with Fabry disease

Abstract. In Fabry disease, there is glycosphingolipid storage in vascular endothelial and smooth muscle cells and neurons of the autonomic nervous system. Vascular or autonomic dysfunction is likely to compromise cerebral blood flow velocities and cerebral autoregulation. This study was performed to evaluate cerebral blood flow velocities and cerebral autoregulation in Fabry patients. In 22 Fabry patients and 24 controls, we monitored resting respiratory frequency, electrocardiographic RR-intervals, blood pressure, and cerebral blood flow velocities (CBFV) in the middle cerebral artery using transcranial Doppler sonography. We assessed the Resistance Index, Pulsatility Index, Cerebrovascular Resistance, and spectral powers of oscillations in RR-intervals, mean blood pressure and mean CBFV in the high (0.15–0.5 Hz) and sympathetically mediated low frequency (0.04–0.15 Hz) ranges using autoregressive analysis. Cerebral autoregulation was determined from the transfer function gain between the low frequency oscillations in mean blood pressure and mean CBFV. Mean CBFV (P < 0.05) and the powers of mean blood pressure (P < 0.01) and mean CBFV oscillations (P < 0.05) in the low frequency range were lower,while RR-intervals, Resistance Index (P < 0.01), Pulsatility Index, Cerebrovascular Resistance (P < 0.05), and the transfer function gain between low frequency oscillations in mean blood pressure and mean CBFV (P < 0.01) were higher in patients than in controls. Mean blood pressure, respiratory frequency and spectral powers of RR-intervals did not differ between the two groups (P > 0.05). The decrease of CBFV might result from downstream stenoses of resistance vessels and dilatation of the insonated segment of the middle cerebral artery due to reduced sympathetic tone and vessel wall pathology with decreased elasticity. The augmented gain between blood pressure and CBFV oscillations indicates inability to dampen blood pressure fluctuations by cerebral autoregulation. Both, reduced CBFV and impaired cerebral autoregulation, are likely to be involved in the increased risk of stroke in patients with Fabry disease.     

Cardiovascular and cerebrovascular responses to lower body negative pressure in type 2 diabetic patients

In diabetic patients, vascular disease and autonomic dysfunction might compromise cerebral autoregulation and contribute to orthostatic intolerance. The aim of our study was to determine whether impaired cerebral autoregulation contributes to orthostatic intolerance during lower body negative pressure in diabetic patients. Thirteen patients with early-stage type 2 diabetes were studied. We continuously recorded RR-interval, mean blood pressure and mean middle cerebral artery blood flow velocity at rest and during lower body negative pressure applied at -20 and -40 mm Hg. Spectral powers of RR-interval, blood pressure and cerebral blood flow velocity were analyzed in the sympathetically mediated low (LF: 0.04-0.15 Hz) and the high (HF: 0.15-0.5 Hz) frequency ranges. Cerebral autoregulation was assessed from the transfer function gain and phase shift between LF oscillations of blood pressure and cerebral blood flow velocity. In the diabetic patients, lower body negative pressure decreased the RR-interval, i.e. increased heart rate, while blood pressure and cerebral blood flow velocity decreased. Transfer function gain and phase shift remained stable. Lower body negative pressure did not induce the normal increase in sympathetically mediated LF-powers of blood pressure and cerebral blood flow velocity in our patients indicating sympathetic dysfunction. The stable phase shift, however, suggests intact cerebral autoregulation. The dying back pathology in diabetic neuropathy may explain an earlier and greater impairment of peripheral vasomotor than cerebrovascular control, thus maintaining cerebral blood flow constant and protecting patients from symptoms of presyncope.     

Inspiratory muscle weakness is associated with autonomic cardiovascular dysfunction in patients with type 2 diabetes mellitus

Introduction  

Diabetic autonomic neuropathy is a complication of diabetes mellitus (DM) that can cause cardiovascular and respiratory abnormalities. The association between respiratory muscle weakness and autonomic cardiovascular neuropathy has not yet been studied. The aims of the present study were to assess respiratory muscle strength, pulmonary function, and heart rate (HR) variability in diabetic patients with and without diabetic autonomic neuropathy.     

A double-blind crossover study of oral xamoterol in postural hypotension due to diabetic autonomic neuropathy

Recent reports have suggested that xamoterol, a beta₁ adrenoceptor partial agonist with 43% intrinsic sympathomimetic activity improves symptomatic postural hypotension in patients with primary autonomic failure. To evaluate the use of xamoterol in eleven insulin dependent patients with diabetes mellitus who had postural hypotension (over 20 mmHg systolic blood pressure) secondary to autonomic neuropathy, we performed a double-blind, randomized, placebo controlled crossover study with xamoterol (200 mg bd orally) for 1 month. Treatment with xamoterol raised supine systolic blood pressure by 11 mmHg but a reduced standing systolic blood pressure by 11 mmHg with an increase in the standing-supine systolic blood pressure difference. No significant differences were observed in symptom score, HbA₁ or plasma glucose. We conclude that oral xamoterol raises supine systolic blood pressure but paradoxically lowers standing systolic blood pressure further in insulin dependent diabetes mellitus, Xamoterol is unlikely to be of value in the management of postural hypotension in diabetic patients with autonomic neuropathy.     

Comment on "Changing cerebral blood flow velocity by transcranial Doppler during head up tilt in patients with diabetes mellitus" by Asil et al

Transcranial Doppler is often employed for the assessment of cerebral autoregulation. The study by Asil et al. [Asil T, Utku U, Balci K, Uzunca I. Changing cerebral blood flow velocity by transcranial Doppler during head up tilt in patients with diabetes mellitus. Clin Neurol Neurosurg 2007;109:1-6] raises some important issues regarding the better understanding of the influence of autonomic nervous system in cerebral autoregulation. We suggest including some additional parameters, especially carbon dioxide levels, transcranial Doppler waveform patterns and their characteristics to further elucidate cerebral hemodynamics and the mechanisms of cerebral autoregulation. Vasomotor reactivity testing under controlled circumstances may add to the quantification of cerebral autoregulation.     

Vasomotor reflexes in the fingertip skin of patients with type 1 diabetes mellitus and leprosy

Fingertip skin blood flow was measured by laser Doppler flowmetry (as LDflux) under environmental conditions promoting vasodilatation in Scottish patients with diabetes mellitus and Indian patients with leprosy. The reflex control of fingertip blood flow was assessed by measuring the reduction in LDflux induced by deep inspiratory gasp (IG) and cold challenge (CC) of immersing the contralateral hand in cold water.The uncomplicated diabetic patients showed normal vasomotor reflexes and an increased, though non significant, LDflux level (p < 0.06). The patients with diabetic neuropathy had resting LDflux levels significantly less than the uncomplicated group and also had substantial impairment of both IG and CC reflexes. Those with retinopathy (but no clinically apparent neuropathy) had LDflux within the normal range, but they showed minor evidence of impairment of the vasomotor reflexes.The uncomplicated newly registered leprosy patients had reduced LDflux and substantial impairment of CC reflexes. These changes were more marked in newly registered leprosy patients with clinical evidence of neuropathy. Leprosy patients with long-standing neuropathy requiring orthopaedic treatment had LDfluxes so greatly reduced that measurement of vasomotor reflexes was not practicable. The CC reflex was more severely affected than the IG reflex and more frequently absent in leprosy patients, possibly because of associated sensory neuropathy affecting the afferent limb of this response.Thus laser Doppler flowmetry can detect impairment of reflex control of fingertip blood flow in both diabetes mellitus and leprosy, but there are functional differences in the pattern of autonomic impairment between the diseases, suggesting differences in the pathogenesis of nerve damage.     

老年2型糖尿病合并脑梗死患者的血脂分析

目的 对老年2型糖尿病合并脑梗死患者的血脂特点进行分析.方法 收集2型糖尿病合并脑梗死患者与无糖尿病的脑梗死患者,通过统计学分析比较两组间的血脂特点.结果 2型糖尿病合并脑梗死组患者的TG、LDL-C和apoB较无糖尿病的脑梗死患者显著升高,而HLD-C和apoA1较对照组显著下降.结论 糖尿病患者的高血糖状态对患者的血脂代谢具有重要影响,可能是促使糖尿病患者动脉粥样硬化、引起脑梗死的重要原因.     

QTc interval, and autonomic and somatic nerve function in diabetic neuropathy

QTc intervals were measured using an electrocardiogram and other autonomic function tests, in 66 neuropathy patients with non-insulin-dependent diabetes mellitus (59.0±12.5 years; mean ± SD). The change in R-R interval did not influence the QTc interval, as calculated by the equation: QTc =QT+(1000-R-R)/7 (ms), compared with the conventional Bazett's equation which appeared to overcompensate in the case of a small R-R interval. The QTc interval in the diabetic patients was significantly longer than that in age-matched controls. The QTc interval showed an inverse correlation with the coefficient of variation of the R-R interval and skin blood flow at rest. However, no correlation was found between QTc interval and blood pressure change, change in heart rate on standing, or results of the sympathetic skin response. The QTc interval did not correlate significantly with motor or sensory nerve conduction parameters. We conclude that the QTc interval can be a simple and useful autonomic indicator for diabetic neuropathy relatively independent of other abnormalities of autonomic and somatic nervous system function. Clin Auton Res 8:139–143     

Vitamin D and Nerve Conduction In Pediatric Type-1 Diabetes Mellitus

IntroductionThe aim of this study is to investigate a possible association between vitamin D deficiency and diabetic peripheral neuropathy in pediatric patients with type 1 diabetes mellitus.Materials-methodsTwenty-nine patients with type 1 diabetes mellitus and 19 healthy controls were included to the study. All individuals were evaluated for diabetic peripheral neuropathy with nerve conduction studies. Complete blood cell count, biochemical investigations, serum vitamin D levels, hemoglobin A1c levels were recorded.ResultsNo statistically significant differences between the diabetes and control groups in terms of gender, age, body weight, height, body mass index, systolic and diastolic blood pressures, laboratory investigations, serum vitamin D levels and nerve conduction studies was found. Patients with diabetes were grouped as patients with normal serum vitamin D levels and patients with vitamin D deficiency. Sensory nerve action potential of sural nerve and motor peroneal nerve velocity were statistically significantly lower in diabetic patients with vitamin D deficiency compared to diabetic patients with normal vitamin D levels (p 0.009 and 0.005 respectively).ConclusionOur results suggested that hypovitaminosis D might lead to development of neuropathic changes particularly on the lower limb nerves even in the early stages of the disease. It should be kept in mind that patients with hypovitaminosis D should be elaborately examined and closely followed up for the development of diabetic neuropathic changes, even if glucose control is achieved.     

Neuropathy is a major contributing factor to diabetic erectile dysfunction

Abstract

Erectile dysfunction (ED) in diabetes is multifactorial. So far, the impact of neuropathy has not been well determined. This study was performed to assess the frequency of abnormal neurophysiological tests in patients with ED due to diabetes compared to patients with ED due to nondiabetic neuropathies in order to estimate the contribution of neuropathy in diabetic ED. Forty-nine men with ED were studied. We classified ED as 'diabetic', 'neuropathic' or 'ED of other origin'. 26.6% of the men fulfilled the criteria of diabetic ED, 42.9% had neuropathic ED. In every patient history taking, a questionnaire focusing on autonomic symptoms other than ED, clinical examination, nerve conduction studies (NCS), sphincter ani electromyography (EMG), heart rate variability testing (HRV) and quantitative sensory testing (QST) was performed. Vascular function was assessed by the intracavernosal prostaglandin E1 (PGE1) injection test. The frequency of abnormal results in diabetic and neuropathic patients was compared. Vascular function was abnormal in only one patient with diabetic ED and three patients with neuropathic ED. Both groups had similar frequencies of autonomic symptoms other than ED (64% in diabetic vs. 64% in neuropathic patients), abnormal EMG (33% vs. 40%) and abnormal QST (vibratory perception 83% vs. 84%, cold perception 9% vs. 19%, warm perception 42% vs. 43%). Abnormal clinical findings (50% vs. 33%), NCS (75% vs. 50%) and HRV (39% vs. 25%) were slightly, but not significantly more frequent in men with diabetic ED than neuropathic ED. The tests indicating neuropathy showed abnormalities in men with diabetic ED as frequently as in men with neuropathic ED. Some tests even suggested neuropathy more often in diabetic than in neuropathic ED. The findings support the hypothesis that neuropathy contributes significantly to the pathophysiology of ED in diabetes mellitus. [Neurol Res 2001; 23: 651-654]     

Autonomic dysfunction and hemodynamics in vitamin B12 deficiency

Orthostatic hypotension in patients with cobalamin (Cbl) deficiency has been reported previously in isolated cases but we are not aware of detailed systematic studies of hemodynamic and autonomic nervous system function in patients with cobalamin deficiency. We investigated hemodynamic and autonomic responses to 60 degrees passive head up tilt (HUT) in 21 patients with vitamin B12 deficiency, 21 healthy age-matched control subjects and 9 age-matched patients with diabetes mellitus (DM) and established diabetic neuropathy. To systematically assess hemodynamic and autonomic nervous system function, we performed measurements of heart rate, beat-to-beat systolic and diastolic blood pressure, stroke index, cardiac index, total peripheral resistance index, total power, low (LF) and high (HF) frequency oscillatory component of heart rate variability, LF/HF ratio and spontaneous baroreflex sensitivity. As compared to controls, we found a significant fall of systolic blood pressure during 60 consecutive beats directly after head up tilt; furthermore, a significantly blunted fall of stroke index, cardiac index and a lack of increase of total peripheral resistance index for the duration of tilt in patients with diabetes mellitus and in patients with vitamin B12 deficiency. As compared to controls, we observed an altered response of spectral indices of sympathetic activation and vagal withdrawal and an impaired modulation of baroreflex sensitivity during head up tilt suggestive of a complex modification in the neural control activities in patients with cobalamin deficiency, which was comparable to that observed in patients with diabetes mellitus and established autonomic neuropathy. The results suggest that vitamin B12 deficiency causes autonomic dysfunction with similar hemodynamic consequences and patterns of autonomic failure as seen in diabetic autonomic neuropathy. Defective sympathetic activation may be the cause for orthostatic hypotension, which is occasionally seen in patients with vitamin B12 deficiency. It is concluded that patients with orthostatic hypotension should be screened for cobalamin deficiency.     

Autonomic neuropathy in type-2 diabetes, lessons from Okamoto Diabetes Study]

Clinically important diabetic autonomic neuropathy includes constipation, diarrhea, neurogenic bladder, impotence, dry skin, arterio-venous shunt in the lower extremities, reduced heart rate variability with tachycardia, orthostatic hypotension, and dysautoregulation of the cerebral blood flow. To investigate the prevalence, clinical characteristics and risk factor for diabetic complications, prospective epidemiological study (Okamoto Diabetes Study) has been started since 1991. Autonomic neuropathy was judged from the results of RR interval variation (CV < or = 1.5) and/or orthostatic change of systolic blood pressure (deltaSBP > or = 30 mmHg). The prevalence of autonomic neuropathy was 28% in type-2 diabetes enrolled in the Okamoto Diabetes Study. Aging, duration of diabetes, higher systolic blood pressure and HbA1c levels were independent risk factors for autonomic neuropathy. Frequent association with macrovascular complications in the subjects with autonomic neuropathy resulted in poor prognosis, especially due to cardiovascular events. The 55 subjects (19% of the 286 subjects already died) had died suddenly. Cause of sudden death in these subjects is still unclear, but silent myocardial infarction due to autonomic neuropathy may be, at least in part, one of the major causes of unexpected sudden death in type-2 diabetes.     

Exosomes from miRNA‐126‐modified endothelial progenitor cells alleviate brain injury and promote functional recovery after stroke

AimsWe previously showed that the protective effects of endothelial progenitor cells (EPCs)‐released exosomes (EPC‐EXs) on endothelium in diabetes. However, whether EPC‐EXs are protective in diabetic ischemic stroke is unknown. Here, we investigated the effects of EPC‐EXs on diabetic stroke mice and tested whether miR‐126 enriched EPC‐EXs (EPC‐EXs^miR126) have enhanced efficacy.MethodsThe db/db mice subjected to ischemic stroke were intravenously administrated with EPC‐EXs 2 hours after ischemic stroke. The infarct volume, cerebral microvascular density (MVD), cerebral blood flow (CBF), neurological function, angiogenesis and neurogenesis, and levels of cleaved caspase‐3, miR‐126, and VEGFR2 were measured on day 2 and 14.ResultsWe found that (a) injected EPC‐EXs merged with brain endothelial cells, neurons, astrocytes, and microglia in the peri‐infarct area; (b) EPC‐EXs^miR126 were more effective than EPC‐EXs in decreasing infarct size and increasing CBF and MVD, and in promoting angiogenesis and neurogenesis as well as neurological functional recovery; (c) These effects were accompanied with downregulated cleaved caspase‐3 on day 2 and vascular endothelial growth factor receptor 2 (VEGFR2) upregulation till day 14.ConclusionOur results indicate that enrichment of miR126 enhanced the therapeutic efficacy of EPC‐EXs on diabetic ischemic stroke by attenuating acute injury and promoting neurological function recovery.     

Prevalence and Associated Risk Factors of Cerebral Microbleeds in Egyptian Patients with Acute Ischemic Stroke and Atrial Fibrillation

BackgroundFew studies addressed the prevalence of cerebral microbleeds (CMB) and associated risk factor profile in Egyptian ischemic cerebral stroke patients with atrial fibrillation (AF).MethodsThe prevalence of CMB was estimated in 150 cases of AF ischemic stroke patients and compared to the prevalence in 150 age- and sex-matched controls of ischemic stroke patients without AF. CMB-associated risk factors were identified by comparing AF ischemic stroke patients with and without CMB. All participants were subjected to complete general, neurological examination, and magnetic resonance imaging.ResultsThe prevalence of CMBs in ischemic stroke with and without AF was 40.7% and 49.3%, respectively. Age, hypertension, diabetes mellitus, past history of stroke, antiplatelet, anticoagulant, National Institutes of Health Stroke Scale, CHA₂DS₂VASc, and white matter lesions (WML) were significant risk factors associated with CMB on univariate analysis. On multivariable logistic regression analysis, age (odds ratio [OR] 1.1, confidence interval [CI] 1.02-1.13), hypertension (OR 3.2, CI 1.19-8.81), anticoagulant (OR 3.3, CI 1.17-9.40), and WML (OR 9.6, CI 3.49-26.3) were the only independent risk factors associated with the presence of CMBs.ConclusionsAF in ischemic stroke patients was not associated with higher prevalence of CMBs. Old age, hypertension, anticoagulant treatment, and WML were the independent risk factors associated with CMB in AF ischemic stroke patients. Our results suggest that elderly hypertensive AF ischemic stroke patients maintained on anticoagulant therapy should be screened for the incidence of CMBs and monitored regularly for the development of intracerebral hemorrhage.     

Diabetic neuropathy

Peripheral nerve disorders are important late complications of diabetes mellitus. Polyneuropathy, which may involve varying proportions of sensory, motor, and autonomic fibers, is considered the consequence of metabolic derangements that result from chronic hyperglycemia. Symmetrical proximal motor neuropathy ("diabetic amyotrophy") also may have a metabolic basis. Mononeuropathies in diabetes may have an ischemic or compressive cause. Advances have been made in understanding the biochemical basis for diabetic polyneuropathy. The treatment of symptomatic diabetic neuropathy should be directed toward long-term normalization of blood glucose until more specific therapies become available.     

Stellate ganglion block reduces inflammation and improves neurological function in diabetic rats during ischemic stroke

Diabetes mellitus is an independent risk factor for ischemic stroke.Both diabetes mellitus and stroke are linked to systemic inflammation that aggravates patient outcomes.Stellate ganglion block can effectively regulate the inflammatory response.Therefore,it is hypothesized that stellate ganglion block could be a potential therapy for ischemic stroke in diabetic subjects.In this study,we induced diabetes mellitus in rats by feeding them a high-fat diet for 4 successive weeks.The left middle cerebral artery was occluded to establish models of ischemic stroke in diabetic rats.Subsequently,we performed left stellate ganglion block with 1%lidocaine using the percutaneous posterior approach 15 minutes before reperfusion and again 20 and 44 hours after reperfusion.Our results showed that stellate ganglion block did not decrease the blood glucose level in diabetic rats with diabetes mellitus but did reduce the cerebral infarct volume and the cerebral water content.It also improved the recovery of neurological function,increased 28-day survival rate,inhibited Toll like receptor 4/nuclear factor kappa B signaling pathway and reduced inflammatory response in the plasma of rats.However,injection of Toll like receptor 4 agonist lipopolysaccharide 5 minutes before stellate ganglion block inhibited the effect of stellate ganglion block,whereas injection of Toll like receptor 4 inhibitor TAK242 had no such effect.We also found that stellate ganglion block performed at night had no positive effect on diabetic ischemic stroke.These findings suggest that stellate ganglion block is a potential therapy for diabetic ischemic stroke and that it may be mediated through the Toll like receptor 4/nuclear factor kappa B signaling pathway.We also found that the therapeutic effect of stellate ganglion block is affected by circadian rhythm.     

Effect of metformin on outcome after acute ischemic stroke in patients with type 2 diabetes mellitus

IntroductionDiabetes mellitus is a well-known risk factor for ischemic stroke and is associated with unfavorable outcome after stroke. Metformin is recommended as first-line treatment in these patients. Pre-stroke metformin use might have neuroprotective properties resulting in reduced stroke severity. However, results of the effects of pre-stroke metformin use on functional outcome are conflicting and has not been previously described in patients with type 2 diabetes mellitus regardless of stroke severity or revascularization treatment. In this study, we aimed to assess the association between metformin use and functional outcome in patients with type 2 diabetes mellitus and acute ischemic stroke.MethodsWe used data from patients with known type 2 diabetes mellitus who were admitted with acute ischemic stroke between 2017 and 2021 in the Isala Hospital Zwolle and Medisch Spectrum Twente (MST) Enschede, the Netherlands. The association between pre-stroke metformin use and favorable functional outcome at 3 months (defined as modified Rankin Scale (mRS) < 3) was expressed as Odds Ratios (ORs) with corresponding confidence intervals (CIs). Adjustments were made for age, sex, hyperglycemia on admission and revascularization treatment by means of multiple logistic regression.ResultsNine hundred thirty seven patients were included of whom 592 patients (63%) used metformin. Six hundred seventy eight (74%) patients were hyperglycemic on admission. Median mRS was 3 (IQR 2–6) and 593 patients (63%) had a favorable outcome. Pre-stroke metformin use was associated with favorable outcome (aOR of 1.94 (95%- CI 1.45–2.59)).ConclusionIn this study, we showed that pre-stroke metformin use was associated with favorable outcome after acute ischemic stroke in patients with diabetes mellitus type 2.     

血压波动对脑梗死后脑灌注的影响

本文主要从脑血管的自动调节与自动调节受损、脑小血管病变可导致脑血管反应性受损、脑梗死患者脑血流速度、脑血流量与血压的相关性,脑梗死侧大脑半球脑灌注降低、低血压对脑主要动脉狭窄者可导致狭窄远端脑组织局部低灌注等几个方面来讨论脑梗死后血压的变化对脑血流速度、脑血流量的影响。给临床医生提出一个思考问题,在脑梗死的急性期把血压控制在多少才是最合适的水平,对患者的功能恢复最有益。     

Effects of cerebrovascular autoregulation and CO2 reactivity in experimental localized brainstem infarction

Abstract

Using the previously reported method of experimental localized brainstem infarct in dogs, we designed this study to elucidate sequential changes of regional cerebral blood flow (rCBF) in three separate regions of the central nervous system: the cerebral cortex, thalamus, and midbrain. The data obtained were referred to in subsequent investigations of cerebrovascular autoregulation and vasomotor reactivity to C0₂. Localized brainstem infarct was produced by permanently occluding the perforators of the posterior cerebral arteries between the bilateral origins of the posterior communicating arteries. The hydrogen clearance method was applied to measure rCBF. Cerebrovascular autoregulation and CO₂ reactivity were assessed in three regions 1, 3, and 5 h after vascular occlusion, respectively. Vascular occlusion resulted in a decrease of rCBF that was 65% in the midbrain and close to 30%–40% in the thalamus. However, no significant change was seen in the cerebral cortex even 5 h after vascular occlusion. Induced hypertension impaired autoregulation in the thalamus, while it was preserved in the cerebral cortex. Induced hypotension did not alter autoregulation in any of the three regions. A marked loss of CO₂ reactivity was observed in the ischemic brainstem, although it was well preserved in the cerebral cortex. The results suggest that noradrenergic fibers originating from the cervical sympathetic ganglia play a main role in the cerebrovascular autoregulation in the cerebral cortex, while noradrenergic fibers possibly originating from the autonomic centers in the brainstem are responsible in the thalamus; that the noradrenergic neuron probably is not involved in the maintenance of cerebral blood flow during hypotension; and that the effect of CO₂ is mediated by its direct effect on the arteriolar wall in the central nervous system. [Neurol Res 2000; 22: 197–203]     

糖尿病与进展性缺血性脑卒中相关性研究

目的 探讨糖尿病与进展性缺血性脑卒中的相关性.方法 我院神经内科2006-05～2009-05收治的缺血性脑卒中患者130例为研究对象,其中伴糖尿病患者64例为糖尿病组,非糖尿病患者66例为非糖尿病组,比较2组发展为进展性缺血性脑卒中的差异.结果 糖尿病组64例中诊断为进展性卒中41例,占64.1%;非糖尿病组66例诊...