Background and purpose: Metabolic syndrome has been proposed as a risk factor for stroke and transient ischaemic attack. One pathophysiological mechanism could be impairment of endothelial function. Thus, we hypothesized that cerebral vasomotor reactivity would be decreased in patients with metabolic syndrome, compared to patients without metabolic syndrome.Methods: In this retrospective analysis, 83 consecutive patients (aged 59.19 ± 15.98; 33 women) underwent Doppler examination for carotid artery disease including bi‐hemispherical vasomotor reactivity assessment using transcranial Doppler monitoring. Vasomotor reactivity data were analyzed from the hemisphere with no or low‐grade carotid stenosis (<40%). Cerebral vasomotor reactivity was calculated as percent increase in mean flow velocity per mmHg pCO2 during 2 min of 5% CO2 inhalation delivered by anesthesia mask (normal if ≥2%/mmHg). Univariate and multivariable linear regression models were used to determine factors, including metabolic syndrome, that were independently associated with pathologic vasomotor reactivity.Results: After adjusting for the presence of contralateral carotid stenosis and ipsilateral stroke in the multivariable model, metabolic syndrome was independently associated with lower vasomotor reactivity values (2.27 ± 1.24% vs. 2.68 ± 1.37; ß = −0.258, P = 0.033). In this model, there was no association of cerebral vasomotor reactivity with age, gender, race, cardiac disease, current statin therapy, or small vessel disease.Conclusions: Our findings suggest that impaired cerebral vasomotor reactivity may be a mediator of stroke in patients with metabolic syndrome, a syndrome affecting a significant and growing proportion of the population. A prospective longitudinal study is warranted to study the cerebral haemodynamic effect of metabolic syndrome.

Sir, We thank Drs Tsivgoulis and Heliopoulos for their thoughtful comments [1]. In our study, metabolic syndrome (MetS) was associated with lower cerebral vasomotor reactivity (VMR) [2]. Based on our findings, we proposed a possible physiological mechanism to explain the higher risk of stroke and cardiovascular mortality in patients with MetS. With regard to the authors’ suggestion to evaluate the potential interaction of contralateral carotid stenoses with MetS, we would like to note that in the univariate model, mean VMR values were higher and not lower in the presence of contralateral carotid stenoses; the explanation may be cohort-specific. In our multivariable analysis, MetS remained significantly and independently associated with lower VMR values [2]. It is established that high-grade carotid stenosis is strongly associated with impaired VMR [3,4]; therefore, in our approach, we included VMR values only from patients or the hemisphere with <40% carotid stenosis. We do note that the cohort under investigation contained a high prevalence of frank atherosclerotic disease. Therefore, we cannot -exclude the possibility that the correlation between MetS and VMR might be different in a non-atherosclerotic population. Indeed, there is mounting evidence underscoring impaired VMR as the intermediate link between stroke risk and various disease states including sleep apnoea syndrome [5,6]. Adding to the significance of VMR, our findings suggest that lower VMR or impaired cerebrovascular reserve might be the mediator of the higher rate of cerebrovascular ischaemic events in patients with MetS [2] and underscores the need for early identification of these patients. Dr Sotirios Giannopoulos was supported by Stavros Niarchos Foundation with a Visiting Scholar Award for Greek Neurologists. This study was supported by NINDS P50NS049060 project SWIFT (RSM, Program project PI).

BACKGROUND AND PURPOSE: Endovascular brain cooling as a method for rapid and selective induction of hypothermic neuroprotection has not been systematically studied in humans. In this clinical pilot study we investigated the feasibility, safety, and physiologic responses of short-term brain cooling with IC-CSI. MATERIALS AND METHODS: We studied 18 patients (50 ± 10 years old, 9 women) undergoing follow-up cerebral angiography after previous treatment of vascular malformations. Isotonic saline (4–17°C) was infused into 1 internal carotid artery at 33 mL/min for 10 minutes. Brain (JVB) and bladder/esophageal temperature measurements (n = 9) were performed. Both MCAs were monitored with transcranial Doppler sonography (n = 13). Arterial and JV blood were sampled to estimate hemodilution and brain oxygen extraction. RESULTS: JVB temperature dropped ∼0.84 ± 0.13°C and systemic temperature by 0.15 ± 0.08°C from baseline (JVB versus systemic temperature: P = .0006). Systolic MCA-flow velocities decreased from 101 ± 27 to 73 ± 18 cm/s on the infused side and from 83 ± 24 to 78 ± 21 cm/s on the contralateral side (relative changes, −26 ± 8% versus −4 ± 27%; P = .009). Changes in hematocrit (−1.2 ± 1.1%) and cerebral arteriovenous oxygen difference (0.2 ± 1.0 mL O2/100 mL) were not significant. Doppler data showed no signs of vascular spasm or microemboli. No focal neurologic deficits occurred. Pain was not reported. CONCLUSIONS: The results of this pilot study suggest that brain cooling can be achieved safely, rapidly, and selectively by means of IC-CSI, opening a new potential avenue for acute neuroprotection. Clinical investigations with control of infusion parameters and measurements of CBF, oxygen consumption, and brain temperature are warranted.

Objective: Some patients with brain arteriovenous malformation (BAVM) present with focal neurological deficits (FNDs) unrelated to clinically discernable seizure activity or hemorrhage. The aim of this study is to determine demographic and morphological AVM characteristics associated with FNDs.Methods: The 735 patients of the prospective Columbia AVM Databank were analyzed. Univariate and multivariate statistical models were used to test the association of demographic (age, gender), and morphological characteristics (BAVM size, anatomic location, arterial supply, venous drainage pattern, venous ectasia) with the occurrence of FNDs at the time of initial BAVM diagnosis.Results: Fifty-three patients (7%, mean age 40 +/- 16 years, 70% women) presented with FNDs. The multivariate logistic regression model revealed an independent association of FNDs with increasing age (OR 1.03; 95%-CI 1.00-1.05), female gender (OR 2.14: 95%-CI 1.15-3.97), deep brain location (OR 2.46; 95%-CI 1.24-4.88), brainstem location (OR 5.62; 95%-CI 1.65-19.23), and venous ectasia (OR 1.91; 95%-CI 1.01-3.64). No association was found for BAVM size, lobar location, arterial supply and venous drainage pattern.Interpretation: Focal neurologic deficits unrelated to seizures or hemorrhage are a rare initial presentation of BAVMs. The predominance of FNDs among brainstem and deeply located BAVMs and the lack of a significant association of BAVM size with FNDs indicate selective white matter pathway-specific vulnerability, the association with patient age a time dependent effect The higher frequency of FNDs among women suggests gender-specificity of brain tissue vulnerability. (C) 2009 Elsevier B.V. All rights reserved.

Background: Endovascular revascularization for intracranial atherosclerotic stenoses is being increasingly performed at major medical centers and has been reported to be technically feasible and safe. The authors report their experience with patients who underwent such a procedure for impending stroke and neurologic instability. Method: All 18 patients (21 intracranial lesions) treated between 1997 and 2002 at the authors' institution with endovascular revascularization were retrospectively reviewed. Each patient had failed maximal medical therapy and was thought to be at high risk for an imminent stroke. Results: Endovascular revascularization was performed on eight distal internal carotid artery lesions, six middle cerebral artery lesions, four intracranial vertebral artery lesions, and three basilar artery lesions. Recanalization was complete in 5 arteries (Thrombolysis in Myocardial Infarction [TIMI] Grade III), partial in 14 arteries (TIMI Grade II), and complete occlusion (TIMI 0) developed in 1 artery. In a patient with a tight basilar stenosis, no angioplasty could be performed because of the inability to cross the stenosis with the guidewire. Major periprocedural complications occurred in 9 (50%) patients: intracranial hemorrhage in 3 (17%), disabling ischemic stroke in 2 (11%), and major extracranial hemorrhage in 4 (22%). Three patients died: one from intracerebral hemorrhage and two from cardiorespiratory failure. Conclusions: Endovascular revascularization of intracranial vessels is technically feasible and may be performed successfully. However, periprocedural complication and fatality rates in neurologically unstable patients are high. The results suggest that patient selection, procedure timing, and periprocedural medical management are critical factors to reduce periprocedural morbidity and mortality.