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Ashfaq Shuaib

Publications and source records attributed to Ashfaq Shuaib.

At least 19 recordsLinked to original sources
PubMed2006

Clinical deterioration after intravenous recombinant tissue plasminogen activator treatment: a multicenter transcranial Doppler study.

BACKGROUND AND PURPOSE: Patients may experience clinical deterioration (CD) after treatment with intravenous recombinant tissue plasminogen activator (rt-PA). We evaluated the ability of flow findings on transcranial Doppler to predict CD and outcomes on modified Rankin Scale. METHODS: Patients with acute stroke received intravenous rt-PA within 3 hours of symptom onset at four academic centers. CD was defined as an increase in the National Institutes of Health Stroke Scale (NIHSS) score by 4 points or more within 24 hours. Poor long-term outcome was defined by modified Rankin Scale > or =2 at 3 months. Transcranial Doppler findings were interpreted using the Thrombolysis in Brain Ischemia flow grading system as persistent arterial occlusion, reocclusion, or complete recanalization. Multiple regression analysis was used to identify transcranial Doppler flow as a predictor for CD after controlling for age, sex, baseline NIHSS, hypertension, and glucose. RESULTS: A total of 374 patients received intravenous rt-PA at 142+/-60 minutes (median pretreatment NIHSS score 16 points). At the end of intravenous rt-PA infusion, transcranial Doppler showed persistent arterial occlusion in 219 patients (59%), arterial reocclusion in 54 patients (14%), and complete recanalization in 101 patients (27%). CD occurred in 44 patients: 36 had persistent arterial occlusion or reocclusion (82%), 13 symptomatic intracerebral hemorrhage (29%), and both persistent occlusion/reocclusion and symptomatic intracerebral hemorrhage in 10 patients (23%). After adjustment, patient risk for CD with persistent occlusion was OR 1.7 (95% CI: 0.7 to 4) and with arterial reocclusion 4.9 (95% CI: 1.7 to 13) (P=0.002). Patient risk for poor long-term outcomes with persistent occlusion, partial recanalization, or reocclusion was OR 5.2 (95% CI: 2.7 to 9, P=0.001). CONCLUSIONS: Inability to achieve or sustain vessel patency at the end of rt-PA infusion correlates with the likelihood of clinical deterioration and poor long-term outcome. Early arterial reocclusion on transcranial Doppler is highly predictive of CD and poor outcome.

Adult↗
PubMed2006

Additional outcomes and subgroup analyses of NXY-059 for acute ischemic stroke in the SAINT I trial.

BACKGROUND AND PURPOSE: NXY-059 is a free radical-trapping neuroprotectant demonstrated to reduce disability from ischemic stroke. We conducted analyses on additional end points and sensitivity analyses to confirm our findings. METHODS: We randomized 1722 patients with acute ischemic stroke to a 72-hour infusion of placebo or intravenous NXY-059 within 6 hours of stroke onset. The primary outcome was disability at 90 days, as measured by the modified Rankin Scale (mRS), a 6-point scale ranging from 0 (no residual symptoms) to 5 (bed-bound, requiring constant care). Additional and exploratory analyses included mRS at 7 and 30 days; subgroup interactions with final mRS; assessments of activities of daily living by Barthel index; and National Institutes of Health Stroke Scale (NIHSS) neurological scores at 7 and 90 days. RESULTS: NXY-059 significantly improved the distribution of the mRS disability score compared with placebo at 7, 30, and 90 days (Cochran-Mantel-Haenszel test P=0.002, 0.004, 0.038, respectively; 90-day common odds ratio 1.20; 95% CI, 1.01 to 1.42). The benefit was not attributable to any specific baseline characteristic, stratification variable or subgroup interaction. Neurological scores were improved at 7 days (odds ratio [OR], 1.46; 95% CI, 1.13, 1.89; P=0.003) and the Barthel index was improved at 7 and 30 days (OR, 1.55; 95% CI, 1.22, 1.98; P<0.0001; OR, 1.27; 95% CI, 1.01, 1.59; P=0.02). CONCLUSIONS: NXY-059 within 6 hours of acute ischemic stroke significantly reduced disability. Benefit on neurological scores and activities of daily living was detectable early but not significant at 90 days; however, our trial was underpowered to measure effects on the neurological examination. The benefit on disability is not confounded by interactions and is supported by other outcome measures.

Aged↗
PubMed2006

High-density lipoprotein cholesterol regulates endothelial progenitor cells by increasing eNOS and preventing apoptosis.

OBJECTIVE: Endothelial progenitor cells (EPCs) are implicated as an important marker of endothelial function and cardiovascular risk. In the present study, we examined whether high-density lipoprotein (HDL) cholesterol plays a role in the peripheral EPC levels and its underlying mechanisms in the HDL cholesterol-induced elevation of EPCs. METHODS: For the clinical study, vascular risk factors and blood markers were measured and EPC colony forming units were counted after 7 days of culture. For the in vitro study, after 7 days of culture, EPCs were incubated in the presence or absence of HDL for 24h followed by measurements of eNOS and pro-MMP-9 expression and caspase-3 activity. RESULTS: EPC colony levels significantly correlated with HDL levels (P=0.017). HDL treatment significantly increased eNOS protein expression in EPCs (P<0.001) while it significantly decreased pro-MMP-9 levels at the concentration of 50 microg/mL (P=0.002). Homocysteine treatment significantly increased caspase-3 activity whereas HDL significantly decreased it as compared to the homocysteine-only treated group. INTERPRETATION: The data demonstrate that EPC colony levels are significantly lower in individuals with low HDL and that HDL increases eNOS and decreases pro-MMP-9 in EPCs. HDL also prevents EPC apoptosis through inhibition of caspase-3 activity suggesting a possible mechanism for its positive effects on circulating EPC numbers.

Aged↗
PubMed2006

Matrix metalloproteinase activation and blood-brain barrier breakdown following thrombolysis.

Thrombolysis with tissue plasminogen activator (tPA) is the only pharmacotherapy available for cerebral ischemia. However, the use of tPA can increase the risk of hemorrhage due to blood-brain barrier (BBB) breakdown. Recent evidence suggests that increased activation of matrix metalloproteinases (MMPs) may be involved in this breakdown. This study examines the temporal profile of MMP-2 and -9 following tPA administration to ischemic rats. Male Sprague-Dawley rats were randomly assigned to one of four groups (Sham-tPA; Sham-Saline; Ischemia-tPA; Ischemia-Saline; group n = 6, total N = 120). Focal embolic ischemia was induced by middle cerebral artery occlusion through injection of an autologous clot. One hour post-surgery, tPA (10 mg/kg) or saline was delivered intravenously and animals were euthanized at 3, 6, 12, or 24 h after onset of ischemia. Infarct volume was measured by TTC staining; BBB components examined immunohistochemically; and MMP activation measured by gelatin zymography. Our results show that tPA significantly reduced infarct volumes (overall infarct volume-Sham-tPA: 5.80 +/- 4.55 [mean +/- SE]; Sham-Saline: 5.00 +/- 4.23; Ischemia-tPA: 186.1 +/- 73.45; Ischemia-Saline: 284.8 +/- 88.74; all P < 0.05). Treatment with tPA was also associated with the activation of MMP-9 at 6, 12, and 24 h following ischemia. No temporal changes were observed in MMP-2 activation, although tPA administration increased its activity compared to saline treatment. Analyses of immunohistochemistry showed that destruction of components of the BBB followed MMP-9 activation. Thus, increased MMP-9 activation may, in part, be responsible for the increases in hemorrhagic transformation reported with use of tPA. Our study is the first to demonstrate the temporal profile of MMP activation following thrombolysis with tPA in a model of thrombotic focal cerebral ischemia.

Animals↗
PubMed2006

The relationship between diffusion anisotropy and time of onset after stroke.

Diffusion anisotropy changes in stroke lesions less than 24 h after onset have been reported to be elevated, decreased, or both. To address these mixed findings, we sought to characterize temporal changes of diffusion anisotropy by analyzing anatomically distinct ischemic white matter (WM) regions at 3 time phases within the first 34 h of ischemic stroke onset in 26 stroke patients (2 to 5 h, N=7; 7 to 14 h, N=11; 18 to 34 h, N=8). Mean diffusivity (Trace/3 apparent diffusion coefficient (ADC)), fractional anisotropy (FA), and T2-weighted signal intensity were measured for major and subcortical WM in lesions defined by a >or=30% drop in Trace/3 ADC. Major WM tract lesions with mean decreases of approximately 40% in relative (r) Trace/3 ADC showed an increased rFA of 1.11+/-0.18 (P<0.01) during the hyperacute phase (2 to 5 h), whereas rFA declined to 0.90+/-0.20 (P<0.01) and 0.88+/-0.12 (P<0.01) in the acute (7 to 14 h) and subacute (18 to 34 h) phases, respectively. Of those patients with lesions in major WM, 4 of 8 patients <or=7 h showed elevated rFA as opposed to none of the remaining 13 patients after 7 h. A greater proportion of the evaluated WM regions-of-interest (ROI) in the hyperacute phase revealed increases in rFA (60%), whereas conversely large proportions of ROIs (55% and 59%) in the acute and subacute phases showed reduced rFA. Similar anisotropy changes were noted in subcortical WM regions in the gyri.

Adult↗
PubMed2006

NXY-059 for acute ischemic stroke.

BACKGROUND: NXY-059 is a free-radical-trapping agent that is neuroprotective in animal models of stroke. We tested whether it would reduce disability in humans after acute ischemic stroke. METHODS: We conducted a randomized, double-blind, placebo-controlled trial involving 1722 patients with acute ischemic stroke who were randomly assigned to receive a 72-hour infusion of placebo or intravenous NXY-059 within 6 hours after the onset of the stroke. The primary outcome was disability at 90 days, as measured according to scores on the modified Rankin scale for disability (range, 0 to 5, with 0 indicating no residual symptoms and 5 indicating bedbound, requiring constant care). RESULTS: Among the 1699 subjects included in the efficacy analysis, NXY-059 significantly improved the overall distribution of scores on the modified Rankin scale, as compared with placebo (P=0.038 by the Cochran-Mantel-Haenszel test). The common odds ratio for improvement across all categories of the scale was 1.20 (95 percent confidence interval, 1.01 to 1.42). Mortality and rates of serious and nonserious adverse events were each similar in the two groups. NXY-059 did not improve neurologic functioning as measured according to the National Institutes of Health Stroke Scale (NIHSS): the difference between the two groups in the change from baseline scores was 0.1 point (95 percent confidence interval, -1.4 to 1.1; P=0.86). Likewise, no improvement was observed according to the Barthel index (P=0.14). In a post hoc analysis of patients who also received alteplase, NXY-059 was associated with a lower incidence of any hemorrhagic transformation (P=0.001) and symptomatic intracranial hemorrhage (P=0.036). CONCLUSIONS: The administration of NXY-059 within six hours after the onset of acute ischemic stroke significantly improved the primary outcome (reduced disability at 90 days), but it did not significantly improve other outcome measures, including neurologic functioning as measured by the NIHSS score. Additional research is needed to confirm whether NXY-059 is beneficial in ischemic stroke. (ClinicalTrials.gov number, NCT00119626.).

Acute Disease↗
PubMed2006

Magnetic resonance imaging profiles predict clinical response to early reperfusion: the diffusion and perfusion imaging evaluation for understanding stroke evolution (DEFUSE) study.

OBJECTIVE: To determine whether prespecified baseline magnetic resonance imaging (MRI) profiles can identify stroke patients who have a robust clinical response after early reperfusion when treated 3 to 6 hours after symptom onset. METHODS: We conducted a prospective, multicenter study of 74 consecutive stroke patients admitted to academic stroke centers in North America and Europe. An MRI scan was obtained immediately before and 3 to 6 hours after treatment with intravenous tissue plasminogen activator 3 to 6 hours after symptom onset. Baseline MRI profiles were used to categorize patients into subgroups, and clinical responses were compared based on whether early reperfusion was achieved. RESULTS: Early reperfusion was associated with significantly increased odds of achieving a favorable clinical response in patients with a perfusion/diffusion mismatch (odds ratio, 5.4; p = 0.039) and an even more favorable response in patients with the Target Mismatch profile (odds ratio, 8.7; p = 0.011). Patients with the No Mismatch profile did not appear to benefit from early reperfusion. Early reperfusion was associated with fatal intracranial hemorrhage in patients with the Malignant profile. INTERPRETATION: For stroke patients treated 3 to 6 hours after onset, baseline MRI findings can identify subgroups that are likely to benefit from reperfusion therapies and can potentially identify subgroups that are unlikely to benefit or may be harmed.

Aged↗
PubMed2006

Randomized controlled trial of modafinil for the treatment of fatigue in postpolio patients.

The purpose of this study was to test whether modafinil is effective in alleviating the symptoms of fatigue in postpolio patients, because it has been helpful for such symptoms in other neurologic disorders. Using a double-blind, randomized, placebo-controlled cross-over design, 14 postpolio patients with moderate to severe fatigue were assigned to receive modafinil or placebo first. Piper Fatigue Scale, Epworth Sleepiness Scale, digit span, and reaction time tests were done at baseline and then at weekly intervals. The Piper Fatigue Scale scores improved by 27 +/- 40% (mean +/- SD) following modafinil and by 43 +/- 36% following placebo. Scores for most of the other tests did not change during the study. Therefore, we conclude that modafinil was not effective in alleviating the symptoms of fatigue in postpolio patients.

Benzhydryl Compounds↗
PubMed2006

Therapeutic strategies for the treatment of stroke.

Acute ischaemic stroke is a major health problem with no effective treatments apart from the thrombolytic recombinant tissue plasminogen activator (rt-PA), which must be given within 3h of stroke onset. However, rt-PA increases the risk of symptomatic intracranial haemorrhage and is administered to <5% of stroke patients. New perfusion-enhancing compounds are in development but the risk:benefit ratio remains to be determined. Many neuroprotective drugs have been studied but all those that reached clinical development have failed to demonstrate efficacy. However, adherence to recently published guidelines on preclinical development has resulted in one novel compound (NXY-059) demonstrating efficacy in a Phase III trial, providing encouragement for the validity of the concept of neuroprotection. There are a variety of new neuroprotective compounds in the early stages of investigation and some could prove clinically effective, provided appropriate preclinical development guidelines are observed.

Animals↗
PubMed2006

Derivation of power M-mode transcranial Doppler criteria for angiographic proven MCA occlusion.

BACKGROUND: Stringent transcranial Doppler (TCD) criteria for diagnosing occlusion are needed for more reliable TCD performance at bedside in the acute stroke setting. SUBJECTS AND METHODS: At three academic stroke centers, we performed TCD examination for patients with symptoms of cerebral ischemia who underwent digital subtraction angiography (DSA). We used a standard insonation protocol with power M-mode Doppler (PMD) TCD (TCD 100 M, Spencer Technologies Inc., Seattle, WA). We collected mean flow velocity (MFV), pulsatility indices (PI), and power M-mode resistance signature (absent, high, or low) in symptomatic middle (MCA), anterior (ACA), posterior (PCA), and in affected (a), ipsilateral (i), and contralateral (c-lat) cerebral arteries. Ratios of aMCA/c-lat MCA, aMCA/iACA, and aMCA/iPCA MFV were subsequently calculated. PMD-TCD flow findings were evaluated with a receiver-operating characteristic (ROC) analysis for angiographically proven MCA occlusion. RESULTS: We studied 120 patients with acute cerebral ischemia with PMD-TCD examinations prior to or immediately after DSA. Lower aMCA velocities pointed to higher probability of occlusion (P= .055). The aMCA/iPCA MFV ratio was superior to the aMCA/iACA ratio and strongly predictive of occlusion at a threshold ratio of 0.5 (RR 2.31 CI(95) 2.13-2.51). High resistance or absent M-mode flow signatures in the proximal MCA were present in 87% of M1 and M2 MCA occlusions (probability 87%). In the presence of a low-resistance PMD signature, obtaining the aMCA/iPCA MFV ratio <0.5 increases probability of occlusion to 87%. Normal MFV ratios and low-resistance M-mode signatures are highly predictive of a negative angiogram for MCA occlusion. CONCLUSION: In acute cerebral ischemia, reliable criteria for proximal MCA occlusion have been developed based on combination of MFV ratios and M-mode flow resistance signatures. Validation of these criteria will require multicenter studies.

Angiography, Digital Subtraction↗
PubMed2005

Simvastatin reduced ischemic brain injury and perfusion deficits in an embolic model of stroke.

Simvastatin is cholesterol lowering agent and also a modulator of cytokine in the nervous system. The functional significance and neuroprotectiove mechanism of simvastatins in ischemic brain injury is controversial. The purpose of study is to evaluate the effect of simvastatin on ischemic brain injury and to investigate the perfusion capability of brain microvessels in the ischemic injury. This study included two series of experiments. In the first series, we studied if simvastatin is neuroprotective in an embolic model of stroke. The treatments began 2 weeks before middle cerebral artery (MCA) occlusion. Infarct volume was measured at 48 h post stroke. Neurological deficits were assessed at 2 h, 24 h and 48 h post stroke. Results showed that infarct volume in rats which received saline and simvastatin was 32.5 +/- 9.3% (mean +/- SD) and 18.7 +/- 6.5%, respectively. The infarct volume in the simvastatin group was significantly smaller than in the controls (P < 0.002). Treatment with simvastatin also improved neurological deficits and reduced brain edema significantly (P < 0.05). In the second series, we studied if simvastatin can improve microvascular reperfusions after ischemia. Perfusion deficits were detected at 8 h post stroke using Evens blue dye. Neurological deficits were assessed at 2 h and 8 h post stroke. Results showed that perfusion deficit in saline and simvastatin-treated groups were 58.7 +/- 8.7% and 23.4 +/- 7.5%, respectively. The perfusion deficit in simvastatin-treated group was decreased 61% (P < 0.01). These studies thus suggest that simvastatin is a protective agent in ischemic brain injury and this protective effect may be partially due to its action in the improvement of microvascular reperfusion.

Animals↗
PubMed2005

Derivation of transcranial Doppler criteria for rescue intra-arterial thrombolysis: multicenter experience from the Interventional Management of Stroke study.

BACKGROUND AND PURPOSE: Transcranial Doppler (TCD) has the potential to identify acute stroke patients with arterial occlusion when treatment with intravenous recombinant tissue plasminogen activator (rtPA) may fail to open the vessel. We examined clinical utility and prognostic value of TCD flow findings in patients enrolled in an intravenous/intra-arterial rtPA pilot trial (Interventional Management of Stroke [IMS] study). METHODS: Patients enrolled in the IMS trial who underwent urgent TCD performed before intra-arterial rtPA treatment were included. TCD findings were analyzed by a mean flow velocity (MFV) ratio using reciprocal middle carotid artery (MCA) depths bilaterally (affected MCA-to-contralateral MCA MFV ratio [aMCA/cMCA MFV ratio]). The clinical utility of TCD was determined by its ability to predict outcome and identify a proximal arterial occlusion that requires intra-arterial lysis per protocol. RESULTS: Twenty-nine of 80 patients enrolled in IMS trial had pre-intra-arterial lysis TCD (mean age, 61+/-11; men-to-women ratio: 17:12; median baseline National Institutes of Health Stroke Score, 17). No temporal window was found in 3 patients (10%). Cerebral angiography was performed at mean 174+/-36 minutes from stroke onset. TCD was performed at median 93.5 minutes from onset. The aMCA/cMCA MFV ratio <0.6 had a sensitivity of 94% (95% confidence interval [CI], 63% to 99%), specificity of 100% (97.5%; lower CI of 54%), positive predictive value of 100% (lower CI, 80%); and negative predictive value of 86% (CI, 42% to 99%) for identifying proximal occlusion in the anterior circulation that require intra-arterial lysis. All patients with absent MCA flow (n=6) had poor outcomes (modified Rankin Scale > or =3) (P=0.014). CONCLUSIONS: TCD is a useful modality for evaluating the arterial circulation in acute ischemic stroke patients; it may have significant potential as a screening tool for intravenous/intra-arterial lysis protocols.

Aged↗
PubMed2005

Hyperthermia masks the neuroprotective effects of tissue plaminogen activator.

BACKGROUND AND PURPOSE: Previously, we have shown that hyperthermia significantly increased neuronal damage after ischemic injury in a focal embolic model of stroke in rats. In the present study, we examined the effects of hyperthermia on the efficacy of thrombolytic therapy in this stroke model. METHODS: In part A, efficacy of tissue plaminogen activator (tPA) treatment was examined in normothermic and hyperthermic rats after embolization of preformed clots into middle cerebral artery (MCA). In part B, brain perfusion deficits were assessed in rats after MCA occlusion. In part C, blood-brain barrier (BBB) permeability was examined in rats after MCA occlusion. In part D, we examined the influence of hyperthermia on fibrinolytic activity of tPA in vitro. RESULTS: Results showed that treatment with tPA significantly reduced infarct volume in normothermic and 38 degrees C hyperthermic rats. When compared with normothermic rats, perfusion deficits in hyperthermic rats were significantly increased at both 3 hours and 6 hours after ischemic injury. Compared with normothermic sham-operated rats, Evans blue dye extravasation was increased in the injured rats with 39 degrees C hyperthermia. In vitro study showed that hyperthermia increased the fibrinolytic activity of tPA. CONCLUSIONS: The present study shows that hyperthermia masks the neuroprotective effects of tPA treatment after ischemic injury and that this may be caused by increased BBB permeability, increased edema, and early progression of ischemic penumbral region to irreversibly damaged tissue as shown by progressively increasing perfusion deficits in hyperthermic rats.

Animals↗
PubMed2005

Interferon gamma induces neurite outgrowth by up-regulation of p35 neuron-specific cyclin-dependent kinase 5 activator via activation of ERK1/2 pathway.

Interferon gamma (IFN-gamma) is a cytokine predominantly involved in antiproliferative and antiviral responses, immune surveillance, and tumor suppression. However, it has been shown that IFN-gamma is also involved in central nervous system development. Here we studied the underlying mechanism for IFN-gamma-induced neuronal differentiation using the human neuroblastoma Paju cell line. Our results indicate that IFN-gamma treatment led to neurite outgrowth followed by growth arrest in the G1 phase of the cell cycle. IFN-gamma induced ERK1/2 phosphorylation and subsequently the transcription factor early gene response 1, which in turn up-regulated p35 expression and increased cyclin-dependent kinase 5 (Cdk5) activity. IFN-gamma-induced neurite outgrowth was abolished by the treatment of MEK1/2 kinase inhibitors, such as U0126 and PD98059, which inhibit the ERK1/2 activation and subsequently prevent the up-regulation of p35 expression and Cdk5 activity. In agreement with the role of p35-Cdk5 in neuronal differentiation, small interfering RNA targeting Cdk5 abrogate the IFN-gamma-induced neurite outgrowth. Together, these results demonstrate for the first time that IFN-gamma-triggered neuronal differentiation mediated through the up-regulation of p35-associated Cdk5 depends on the activation of the ERK1/2 pathway. Therefore, the present study suggests that IFN-gamma is not only involved in tumorigenicity but also involved in neurogenesis by regulating cell proliferation and differentiation.

Antibodies, Monoclonal↗
PubMed2005

The impact of a stroke prevention clinic in diagnosing modifiable risk factors for stroke.

OBJECTIVE: To evaluate the referral patterns of patients to a stroke prevention clinic (SPC) and to test the adequacy of prereferral diagnosis and management of modifiable risk factors for stroke. METHODS: We collected prospective data on consecutive patients referred to the SPC at University of Alberta Hospital in Edmonton, Alberta, Canada. Outcome measures included: alternate diagnoses to stroke or transient ischemic attack (TIA), uncontrolled or undiagnosed hypertension, hyperlipidemia and diabetes, therapies, and investigations leading to carotid endarterectomy. RESULTS: Two thousand and eleven patients were referred to SPC. Nearly 25% of the referrals originated from the emergency room and the rest from general physicians. Of the referrals, 68.7% were confirmed as TIA or stroke at the SPC. Among 1381 patients with TIA or stroke, 736 had history of hypertension. Uncontrolled hypertension was found in 265 patients (36.0% of those with hypertension: 95% CI: 32.5-39.5) while undiagnosed hypertension was found in 103 (15.9% of those without hypertension: 95%CI: 13.14-18.79). History of hyperlipidemia was present in 451 patients (32.6%) and 356 (78.9%: 95% CI: 75.2-82.69) of these patients were not at target for secondary prevention. Among 930 patients without history of hyperlipidemia, 739 (79.5%: 95% CI: 76.8-82.1) were diagnosed with hyperlipidemia through the SPC. Fasting blood glucose levels above 7.1 mmol/L in patients with and without history of diabetes were 221 (79.2%: 95% CI: 74.5-83.9) and 66 (6%: 95%CI: 4.6-7.4) respectively. CONCLUSIONS: Management of risk factors for stroke needs improvement. SPCs should consider actively managing the classical modifiable risk factors of stroke.

Adult↗
PubMed2005

Bedside emergency transcranial Doppler diagnosis of severe carotid disease using orbital window examination.

BACKGROUND: Identifying internal carotid artery (ICA) stenosis in the acute stroke setting can provide clinically useful information. Transcranial Doppler (TCD) through the orbital window is an easy test to perform and to track and identify different vessels. Previous TCD studies have suggested that a reversed ophthalmic artery (OA) flow is a useful collateral pattern to predict ICA disease. The authors sought to evaluate the TCD orbital window for predicting cervical ICA (cICA) stenosis in the setting of acute stroke and TIA. METHOD: Power M-mode/TCD was performed in acute stroke and transient ischemic attack patients at 2 institutions. Each orbital window depth was detected on M-mode and evaluated for the direction of flow and resistance pattern. Gold standard for comparison was carotid evaluation using carotid duplex, computed tomography angiogram, or conventional angiography. The assessment of cICA disease was categorized by degree of stenosis or occlusion. RESULTS: A total of 216 transorbital exams were performed in 117 patients. Twenty-five cICA occlusions and 8 critical cICA stenoses (>or=95%) were identified by gold standard imaging. Reversed OA flow at 50 to 60 mm depth revealed high specificity (100%; confidence interval [CI], 97.6%-100.0%) and good sensitivity (75%; CI, 53.3%-90.2%) for identifying cICA occlusion or critical stenosis (>or=95%). Low pulsatility index (<1.2) and mean flow velocity (<15 cm/s) discriminated critical severe ICA stenosis or occlusion when OA flow was anterograde with good sensitivity (87.2%) and specificity (95.2%). CONCLUSION: The reversed OA sign at 50 to 60 mm depth is very specific for identifying cICA occlusion or critical stenosis. When OA flow is anterograde, a low mean flow velocity or pulsatility index is also useful to identify cICA critical stenosis or occlusion.

Carotid Artery, Internal↗