Vera Parkhutik

A Neuroscience Approach to Virtual Reality Experience Using Transcranial Doppler Monitoring

Virtual reality enables people to behave and feel as if they were present in a virtual environment and therefore is a useful tool in many fields. In order to study the usefulness of virtual environments, the concept of presence is examined. Up to now, the most common method to measure presence has been to use subjective measures based on validated questionnaires about user experience. However, more objective measurements, such as physiological measurements, are now being considered. In this study, transcranial Doppler (TCD) sonography is presented as a brain activity measurement technique that can be used to study presence in virtual environments. Thirty-two subjects navigated in a virtual environment in different immersive conditions while TCD was monitored. The results show that there are changes in blood flow velocity in the subjects during moments associated with different levels of presence.

Brain activity and presence: a preliminary study in different immersive conditions using transcranial Doppler monitoring

Transcranial Doppler (TCD) sonography is a brain activity measurement technique that monitors the hemodynamic characteristics of the major cerebral arteries in normal and pathological conditions. As it is not invasive, it can be easily used in combination with virtual environments (VE). In the present study, TCD has been used to analyze brain activity variations in different presence conditions during the exposure to a VE. Forty-two subjects have taken part in the experience grouped in two different visualization conditions: a CAVE-like and a single screen projection configuration. In each session, two different navigation conditions were used: a free navigation (controlled by the subject) and an automatic navigation (controlled by the system). Results show that these immersion and navigation modifications in the VE generate changes in brain activity that can be detected using TCD techniques. Several factors, one of them being presence, could be having an influence on this behavior.

Postradiosurgery Hemorrhage Rates of Arteriovenous Malformations of the Brain Influencing Factors and Evolution With Time

Background and Purpose— The long-term benefit of radiosurgery of brain arteriovenous malformations (AVM), especially nonhemorrhagic cases, is controversial. We calculated hemorrhage rates pre- and posttreatment and analyzed the risk factors for bleeding based on cases followed at our site. Methods— One hundred eight patients, age 36±17 years, 56 men. The mean follow-up was 65±44 months (median, 54; interquartile range, 33–94). Most AVMs were small (74.1% <3 cm in diameter); 48.1% were located in an eloquent area, 27.8% had deep drainage, and 39.8% presented with hemorrhage. Results— The annual hemorrhage rate for any undiagnosed AVM was 1.2%, and 3.3% for AVMs with hemorrhagic presentation. Older patients, cortical or subcortical AVMs, and cases with multiple draining veins were less likely to present with bleeding. During the first 36 months postradiosurgery, hemorrhagic AVMs had a rebleeding rate of 2.1%, and a rate of 1.1% from 3 years onwards. Nonhemorrhagic AVMs had a hemorrhage rate of 1.4% during the first 3 years and 0.3% afterward. Arterial hypertension and nidus volume were independent predictors of bleeding after treatment. Mean nidus obliteration time was 37±18 months (median, 32; interquartile range, 25–40), with hemorrhage rate of 1.3% before and 0.6% after obliteration, and 1.9% for AVMs that were not closed at the end of follow-up. Conclusions— Both hemorrhagic and nonhemorrhagic AVMs benefit from radiosurgical therapy, with gradual decrease in their bleeding rates over the years. Albeit small, the risk of hemorrhage persists during the entirety of follow-up, being higher for cases with hemorrhagic presentation and nonobliterated AVM.

Circulating MicroRNAs as Novel Biomarkers of Stenosis Progression in Asymptomatic Carotid Stenosis

Background and Purpose— Progression of asymptomatic carotid artery stenosis (ACAS) in patients with >50% luminal narrowing is considered a potential risk factor for ischemic stroke; however, subclinical molecular biomarkers of ACAS progression are lacking. Recent studies suggest a regulatory function for several microRNAs (miRNAs) on the evolution of carotid plaque, but its role in ACAS progression is mostly unknown. The aim of our study was to investigate a wide miRNA panel in peripheral blood exosomes from patients with ACAS to associate circulating miRNA expression profiles with stenosis progression. Methods— The study included 60 patients with ACAS carrying >50% luminal narrowing. First, miRNA expression profiles of circulating exosomes were determined by Affymetrix microarrays from plasma samples of 16 patients from the cohort. Second, those miRNAs among the most differentially expressed in patients with ACAS progression were quantified by real-time polymerase chain reaction in a separate replication cohort of 39 subjects within the patient sample. Results— Our results showed that ACAS progression was associated with development of stroke. MiR-199b-3p, miR-27b-3p, miR-130a-3p, miR-221-3p, and miR-24-3p presented significant higher expression in those patients with ACAS progression. Conclusions— In conclusion, our study supports that specific circulating miRNA expression profiles could provide a new tool that complements the monitoring of ACAS progression, improving therapeutic approaches to prevent ischemic stroke.

Embolism and impaired washout: A possible explanation of border zone strokes in hypereosinophilic syndrome

We describe 4 patients with stroke caused by hypereosinophilic syndrome, all of whom presented with border zone infarcts, and discuss the possible underlying mechanism. Cardioembolism (endomiocardial fibrosis) would coexist with impaired washout (perfusion disturbance due to high eosinophil count and/or eosinophil-derived substances), explaining the watershed characteristics of the infarcts.

Influence of COX-inhibiting Analgesics on the Platelet Function of Patients with Subarachnoid Hemorrhage

BACKGROUND Platelet function of patients with subarachnoid hemorrhage (SAH) may play an important part in both rebleeding and delayed cerebral ischemia, but little is known about aggregation pathways during the acute phase of stroke. Analgesics are used regularly in the first days after bleeding, and some can potentially inhibit the cyclooxygenase (COX) enzyme. We examined the platelet function of patients with SAH in order to describe their basal situation and determine whether the administration of intravenous nonsteroidal antiinflammatory drugs (NSAIDs) affected platelet aggregation. METHODS Arachidonic acid (AA)-induced aggregation and the platelet function analyzer (PFA)-100 test with collagen/epinephrine cartridges were used to study a group of SAH patients that was treated with dexketoprofen and dipyrone and to compare them to patients that had received no analgesia. RESULTS Ninety-six consecutive SAH patients prospectively enrolled in platelet studies. Twenty-seven patients were taking NSAIDs (10 on dexketoprofen and 17 on dipyrone), and there were 15 cases in the control group. AA-induced aggregation was 10% ± 3.2% for NSAIDs (mean ± standard error), specifically 17.2% ± 7% for dexketoprofen and 5.7% ± 1% for dipyrone. Aggregation in the control group was 72.4% ± 6% (P = .001). Both analgesics slowed the platelet plug formation during the PFA-100 test, with closure times of 237.2 ± 25 seconds for dexketoprofen and 198.4 ± 22 seconds for dipyrone and 138.1 ± 21 seconds in controls (P = .02). CONCLUSIONS The administration of COX-inhibiting analgesics leads to an hypoaggregability state in the first days of SAH. Further insight into their impact on complications such as rebleeding and delayed cerebral ischemia is needed in order to optimize the headache treatment of SAH.

Breaks in presence in virtual environments: An analysis of blood flow velocity responses

One of the techniques used to monitor variations in presence during a virtual reality experience is the analysis of breaks in presence (BIPs). Previous studies have monitored peripheral physiological responses during BIPs in order to find a characteristic physiological response. In this work, blood flow velocity (BFV) in middle cerebral arteries (MCAs) has been monitored using transcranial Doppler ultrasound during the exposure to a virtual environment. Two BIPs of different intensity were forced during the virtual reality experience. Variations in BFV during each BIP and during the recovery periods that followed them have been analyzed. A decreasing trend was observed in BFV signal during the most intense BIP in most subjects. However, during the less intense BIP an oscillating behavior was observed. Significant differences have been found between the maximum percentage variations observed in each BIP. During the recovery periods, an increasing trend was observed. The mean response times (time elapsed since the beginning of the period until the maximum percentage variation in the period occured) ranged between 10.116 s and 12.774 s during the BIPs, and between 11.025 s and 13.345 during the recovery periods, depending on the vessel and on the kind of BIP.

A New Visually Evoked Cerebral Blood Flow Response Analysis Using a Low-Frequency Estimation

Transcranial Doppler (TCD) has been widely used to monitor cerebral blood flow velocity (BFV) during the performance of cognitive tasks compared with repose periods. Although one of its main advantages is its high temporal resolution, only some of the previous functional TCD studies have focused on the analysis of the temporal evolution of the BFV signal and none of them has performed a spectral analysis of the signal. In this study, maximum BFV data in both posterior cerebral arteries was monitored during a visual perception task (10 cycles of alternating darkness and illumination) for 23 subjects. A peak was located in the low-frequency band of the spectrum of the maximum BFV of each subject both during visual stimulation and repose periods. The frequency of this peak was in the range between 0.037 and 0.098Hz, depending on the subject, the vessel and the experimental condition. The component of the signal at this frequency, which is associated with the slow variations caused by the visual stimuli, was estimated. That way, the variations in BFV caused by the experimental stimuli were isolated from the variations caused by other factors. This low-frequency estimation signal was used to obtain parameters about the temporal evolution and the magnitude variations of the BFV in a reliable way, thus, characterizing the neurovascular coupling of the participants.

Characterisation of DWI-MRI confirmed cerebral infarcts in patients with subarachnoid haemorrhage and their association with MMP-9 levels

Abstract Objectives: It has been suggested that metalloproteinase-9 (MMP-9) could predict the onset of cerebral vasospasm after subarachnoidal haemorrhage (SAH). The aim of this study was to analyse, in patients with SAH, the difference between patients with MRI ischaemic infarcts and patients without, and to investigate the role of metalloproteases as a prognostic factor for ischaemic infarcts. Methods: Sixty eight consecutive patients with SAH and diffusion-weighted magnetic resonance imaging (DWI-MRI) done 3 weeks after SAH. We define two groups, with and without DWI-MRI infarcts. Blood samples were taken at entry, 3 days and 1 week MMP-9 was determined through ELISA method. Results: Forty per cent were male, with a mean age of 54 ± 14 years. Twenty five patients, 36.8%, had DWI-MRI infarcts; in patients with MRI infarcts, SAH was more severe (Fisher = 4 52 vs 25.6%, P = 0.037), with more morbi-mortality (Rankin>3 48 vs 18.6%, P = 0.014), and more symptomatic vasospasm (28 vs 7%, P = 0.031). Levels of MMP-9 were higher than controls, but there were no significant differences between patients with and without infarcts (first determination no infarcts 39.40 ng/ml ± 35.40 vs infarcts 49.75 ng/ml ± 34.54, P>0.005, 3 days no infarcts 72.10 ng/ml ± 70.95 vs infarcts 62.28 ± 33.84, P>0.005, 1 week no infarcts 148.48 ng/ml ± 142.73 vs infarcts 91.51 ng/ml ± 41.20, P>0.005). Conclusion: Thirty eight percent in a well-studied series of patients with SAH have DWI-MRI infarcts; the infarcts were associated to SAH severity, SAH outcome and symptomatic vasospasm. Metalloproteinase-9 was higher in SAH patients than in controls, but it could not discriminate the infarct patients.

TXA2 synthesis and COX1-independent platelet reactivity in aspirin-treated patients soon after acute cerebral stroke or transient ischaemic attack

INTRODUCTION The pharmacological target of aspirin is the inhibition of cyclooxygenase-1 (COX1) and thromboxane-A2 (TX) synthesis. Very few data are available on TX assessment in patients with stroke. We studied platelet TX synthesis, COX1-independent platelet reactivity, the influence of platelet-erythrocyte interactions and the potential association between platelet responses and the severity of stroke, evaluated with a clinical score (NIHSS). MATERIAL AND METHODS We examined 157 aspirin-treated patients with acute stroke or TIA, 128 aspirin-free and 15 aspirin-treated healthy subjects (HS). Collagen-induced TX, platelet recruitment in whole blood and platelets ± erythrocytes (haematocrit 40%) were assessed in patients on daily-aspirin within three days from onset. Arachidonic-acid-, ADP-, thrombin-receptor activating peptide TRAP-, and collagen-induced aggregation were also evaluated. RESULTS Partial TX inhibition (<95% inhibition vs aspirin-free controls) was observed in 13% of patients. This was associated with marked increases in COX1-dependent responses (arachidonic-acid- and collagen-induced aggregation and platelet recruitment; P<0.0001) but not with differences in ADP- or TRAP-induced aggregation. Partial TX inhibition was independently associated with severe stroke (NIHSS ≥ 12) at both admission (P<0.05) and discharge (P<0.05). Among patients with fully blocked TX, those with elevated COX1-independent platelet reactivity (mean+2SD of aspirin-treated HS) were most likely to suffer severe stroke (P<0.05). Platelet-erythrocyte interactions enhanced platelet reactivity in these patients by COX1-dependent and -independent mechanisms (P<0.0001). CONCLUSIONS TX inhibition by aspirin varied across patients. Partial TX inhibition and COX1-independent platelet hyperfunction were associated with more-severe stroke.