scholarly journals Hemodynamic correlates of transient cognitive impairment after transient ischemic attack and minor stroke: A transcranial Doppler study

2016 ◽  
Vol 11 (9) ◽  
pp. 978-986 ◽  
Author(s):  
Sara Mazzucco ◽  
Linxin Li ◽  
Maria A Tuna ◽  
Sarah T Pendlebury ◽  
Rose Wharton ◽  
...  

Background and aims Transient cognitive impairment (TCI) on the Mini Mental State Evaluation score is common after transient ischemic attack/minor stroke and might identify patients at increased risk of dementia. We aimed to replicate TCI using the Montreal Cognitive Assessment (MoCA), compare it with persistent Mild Cognitive Impairment (PMCI), and to determine whether global cerebral hemodynamic changes could explain transient impairment. Methods Consecutive patients with transient ischemic attack/minor stroke (NIHSS ≤ 3) were assessed with the MoCA and transcranial Doppler ultrasound acutely and at 1 month. We compared patients with TCI (baseline MoCA < 26 with ≥ 2 points increase at 1 month), PMCI (MoCA < 26 with < 2 points increase), and no cognitive impairment (NCI; MoCA ≥ 26). Results Of 326 patients, 46 (14.1%) had PMCI, 98 (30.1%) TCI, and 182 (55.8%) NCI. At baseline, TCI patients had higher systolic blood pressure (150.95 ± 21.52 vs 144.86 ± 22.44 mmHg, p = 0.02) and lower cerebral blood flow velocities, particularly end-diastolic velocity (30.16 ± 9.63 vs 35.02 ± 9.01 cm/s, p < 0.001) and mean flow velocity (48.95 ± 12.72 vs 54 ± 12.46 cm/s, p = 0.001) than those with NCI, but similar clinical and hemodynamic profiles to those with PMCI. Systolic BP fell between baseline and 1 month (mean reduction = 14.01 ± 21.26 mmHg) and end-diastolic velocity and mean flow velocity increased (mean increase = + 2.42 ± 6.41 and 1.89 ± 8.77 cm/s, respectively), but these changes did not differ between patients with TCI, PMCI, and NCI. Conclusions TCI is detectable with the MoCA after transient ischemic attack and minor stroke and has similar clinical and hemodynamic profile to PMCI. However, TCI does not appear to be due to exaggerated acute reversible global hemodynamic changes.

2016 ◽  
Vol 12 (3) ◽  
pp. 264-272 ◽  
Author(s):  
Leka Sivakumar ◽  
Parnian Riaz ◽  
Mahesh Kate ◽  
Thomas Jeerakathil ◽  
Christian Beaulieu ◽  
...  

Background Temporary and permanent cognitive changes following transient ischemic attack/minor stroke have been described previously. It is unknown if persisting cognitive deficits in these patients are correlated with acute infarction identified using magnetic resonance imaging. Aims We tested the hypothesis that persistent cognitive impairment after transient ischemic attack/minor stroke can be predicted by the volume of diffusion-weighted imaging lesions. Methods Acute transient ischemic attack/minor stroke (NIH stroke scale score ≤ 3) patients were prospectively recruited within 72 h of onset. Patients underwent Montreal cognitive assessment and magnetic resonance imaging, including diffusion-weighted imaging and Fluid-Attenuated Inverse Recovery sequences, at baseline, days 7 and 30. Cognitive testing was repeated at day 90. Diffusion-weighted imaging lesion and Fluid-Attenuated Inverse Recovery chronic white matter hyperintensity volumes were measured planimetrically. Cognitive impairment was defined a priori as Montreal cognitive assessment score < 26. Results One hundred fifteen patients were imaged at a median (inter-quartile range) of 24.0 (16.6) h after onset. Acute ischemic lesions were present in 91 (79%) patients. Cognitive impairment rates were similar in patients with (47/91, 52%) and without diffusion-weighted imaging lesions (13/24, 54%; p = 0.83). Although linear regression indicated no relationship between acute diffusion-weighted imaging lesion volume and day 30 Montreal cognitive assessment scores (β = −0.163, [−2.243, 0.334], p = 0.144), white matter hyperintensity volumes at baseline were predictive of persistent cognitive deficits after 30 days (β = 2.24, [1.956, 45.369], p = 0.005). Conclusions In most transient ischemic attack/minor stroke patients who suffer acute cognitive impairment post event, deficits are temporary. Deficits after 30 days of onset are correlated with chronic white matter hyperintensity, suggesting subclinical cognitive impairment and/or impaired ability to compensate for the effects of acute ischemic infarcts.


2016 ◽  
Vol 125 (3) ◽  
pp. 730-736 ◽  
Author(s):  
Nohra Chalouhi ◽  
Badih Daou ◽  
Toshimasa Okabe ◽  
Robert M. Starke ◽  
Richard Dalyai ◽  
...  

OBJECTIVE Cerebral vasospasm (cVSP) is a frequent complication of aneurysmal subarachnoid hemorrhage (aSAH), with a significant impact on outcome. Beta blockers (BBs) may blunt the sympathetic effect and catecholamine surge associated with ruptured cerebral aneurysms and prevent cardiac dysfunction. The purpose of this study was to investigate the association between preadmission BB therapy and cVSP, cardiac dysfunction, and in-hospital mortality following aSAH. METHODS This was a retrospective cohort study of patients with aSAH who were treated at a tertiary high-volume neurovascular referral center. The exposure was defined as any preadmission BB therapy. The primary outcome was cVSP assessed by serial transcranial Doppler with any mean flow velocity ≥ 120 cm/sec and/or need for endovascular intervention for medically refractory cVSP. Secondary outcomes were cardiac dysfunction (defined as cardiac troponin-I elevation > 0.05 μg/L, low left ventricular ejection fraction [LVEF] < 40%, or LV wall motion abnormalities [LVWMA]) and in-hospital mortality. RESULTS The cohort consisted of 210 patients treated between February 2009 and September 2010 (55% were women), with a mean age of 53.4 ± 13 years and median Hunt and Hess Grade III (interquartile range III–IV). Only 13% (27/210) of patients were exposed to preadmission BB therapy. Compared with these patients, a higher percentage of patients not exposed to preadmission BBs had transcranial Doppler-mean flow velocity ≥ 120 cm/sec (59% vs 22%; p = 0.003). In multivariate analyses, lower Hunt and Hess grade (OR 3.9; p < 0.001) and preadmission BBs (OR 4.5; p = 0.002) were negatively associated with cVSP. In multivariate analysis, LVWMA (OR 2.7; p = 0.002) and low LVEF (OR 1.1; p = 0.05) were independent predictors of in-hospital mortality. Low LVEF (OR 3.9; p = 0.05) independently predicted medically refractory cVSP. The in-hospital mortality rate was higher in patients with LVWMA (47.4% vs 14.8%; p < 0.001). CONCLUSIONS The study data suggest that preadmission therapy with BBs is associated with lower incidence of cVSP after aSAH. LV dysfunction was associated with higher medically refractory cVSP and in-hospital mortality. BB therapy may be considered after aSAH as a cardioprotective and cVSP preventive therapy.


2012 ◽  
Vol 32 (2) ◽  
pp. 146-149 ◽  
Author(s):  
BB Lakhkar ◽  
BN Lakhkar ◽  
P Vaswani

Introduction: Role of transcranial Doppler in prevention of stroke in sickle cell children has been well appreciated. Studies are being done to develop the protocol in children. Since we don’t find stroke very commonly in this part of the world, this study was done in order to see the prevalence of abnormal flow velocity in sickle children attending sickle cell clinic. The aims of this study were to measure mean flow velocity in different vessels in homozygous sickle cell patients using transcranial Doppler study, to compare the mean velocity in sickle children with age and sex matched controls and to correlate mean velocity with headache or stroke if any and also to correlate mean velocity with number of transfusions. Materials and Methods: The study was done in Paediatric wards. It was a prospective crosssectional comparative study. Twenty six children below 14yrs of age with homozygous sickle cell disease attending the Sickle cell clinic were selected as the cases. Forty cases of similar age and sex were recruited as normal control group. Transcranial Doppler was done in six different vessels in both the groups and mean flow velocity was measured. Mean flow velocity was correlated with symptoms and number of transfusions. Velocity was classified as normal (<170cm/sec), conditional (170-199cm/sec) or abnormal (>200cm/sec). Statistical analysis was done using SPSS 10 software. Results: In normal age and sex matched controls mean blood flow velocity was 50cm/sec where as in the cases of sickle cell disease was 180cm/sec. Maximum mean velocity was observed in middle and posterior cerebral artery. In two Sickle cell cases (8%) blood flow velocity was abnormal, these children had headache though received 5-10 transfusions/year. In only 4% sickle cell children flow velocity was normal and rest had conditional velocity. Among these children 39% received less than 5 and rest received 5-9 transfusions /yr and had no symptoms of stroke. Conclusions: Flow velocity measured by Transcranial Doppler is highest in middle cerebral artery and Posterior cerebral artery which appear to be the best arteries for this test in this region. Flow velocity was significantly high in children with sickle cell disease as compared to normal children. Prevalence of abnormal flow velocity in our children was 8% and children with abnormal mean flow velocity presented with headache. J. Nepal Paediatr. Soc. 32(2) 2012 146-149 doi: http://dx.doi.org/10.3126/jnps.v32i2.5681


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