Letter by Regal Regarding Article, “Serial Montreal Cognitive Assessments Demonstrate Reversible Cognitive Impairment in Patients With Acute Transient Ischemic Attack and Minor Stroke”

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.

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

International Journal of Stroke ◽

10.1177/1747493016661565 ◽

2016 ◽

Vol 11 (9) ◽

pp. 978-986 ◽

Cited By ~ 5

Author(s):

Sara Mazzucco ◽

Linxin Li ◽

Maria A Tuna ◽

Sarah T Pendlebury ◽

Rose Wharton ◽

...

Keyword(s):

Cognitive Impairment ◽

Flow Velocity ◽

Transient Ischemic Attack ◽

Transcranial Doppler ◽

Minor Stroke ◽

Mean Flow ◽

Hemodynamic Changes ◽

Diastolic Velocity ◽

Ischemic Attack ◽

Mean Flow Velocity

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.

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