Mild Acute Ischemic Stroke Research Articles

Neuromelanin magnetic resonance imaging of nigral volume loss in patients with Parkinson’s disease

Parkinson’s disease (PD) is characterized by progressive degeneration of melanin-containing neurons in the substantia nigra pars compacta (SNc). Pathological change has not been detected by neuroimaging techniques in patients with PD in vivo. We examined 80 patients with PD to determine whether degeneration of the SNc is detectable in vivo by MRI. The age-matched controls consisted of 54 patients who had suffered mild acute ischemic stroke. Axial T1-weighted MRI were obtained with a 3-Tesla MRI scanner. The border of the neuromelanin-sensitive region in the SNc was traced manually on these images, and the volume of this area was calculated. The mean volumes for the left and right SNc were significantly reduced in patients with PD compared to the controls. Volume loss became marked in parallel with disease severity and duration. Neuromelanin MRI may be considered as a biomarker of nigral degeneration in patients with PD.

Reduction of Neuromelanin-Positive Nigral Volume in Patients with MSA, PSP and CBD

Diseases presenting extrapyramidal symptoms are accompanied by nigral cell loss. In the previous study, we demonstrated the reduction of the neuromelanin-positive volume of substantia nigra (SN) pars compacta (SNc) in patients with Parkinson's disease (PD) using 3-Tesla MRI. In the present study we investigated the neuromelanin-positive SNc volume in patients with the other parkinsonian disorders including multiple system atrophy (MSA), progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) and compared the results with those with PD, spinocerebellar ataxia (SCA) and controls. Axial T1-weighted (T1W) images were obtained with a 3-Tesla MRI scanner. The border of the neuromelanin-positive region of the SNc was traced manually on these images with a pentablet pointing device and the SNc volume was calculated. The SNc volumes of 28 patients with MSA, 11 patients with PSP and 10 patients with CBD were compared with those of 80 patients with PD, 9 patients with SCA and 54 patients who had suffered mild acute ischemic stroke as controls. The mean volumes for the left and right SN were used for statistical analyses. The volumes of the neuromelanin-positive SNc region in patients with MSA, PSP and CBD, but not SCA were reduced to the same extent as PD patients compared with controls. Reduced volume of the neuromelanin-positive SNc region of patients with MSA, PSP and CBD was detected by neuromelanin MR imaging. Volumetric evaluation of neuromelanin MR imaging may provide a biomarker of nigral degeneration in patients with MSA, PSP and CBD as in patients with PD.

Effect of Telmisartan on Functional Outcome, Recurrence, and Blood Pressure in Patients With Acute Mild Ischemic Stroke

High blood pressure (BP) is common in acute ischemic stroke and associated independently with a poor functional outcome. However, the management of BP acutely remains unclear because no large trials have been completed. The factorial PRoFESS secondary stroke prevention trial assessed BP-lowering and antiplatelet strategies in 20 332 patients; 1360 were enrolled within 72 hours of ischemic stroke, with telmisartan (angiotensin receptor antagonist, 80 mg/d, n=647) vs placebo (n=713). For this nonprespecified subgroup analysis, the primary outcome was functional outcome at 30 days; secondary outcomes included death, recurrence, and hemodynamic measures at up to 90 days. Analyses were adjusted for baseline prognostic variables and antiplatelet assignment. Patients were representative of the whole trial (age 67 years, male 65%, baseline BP 147/84 mm Hg, small artery disease 60%, NIHSS 3) and baseline variables were similar between treatment groups. The mean time from stroke to recruitment was 58 hours. Combined death or dependency (modified Rankin scale: OR, 1.03; 95% CI, 0.84-1.26; P=0.81; death: OR, 1.05; 95% CI, 0.27-4.04; and stroke recurrence: OR, 1.40; 95% CI, 0.68-2.89; P=0.36) did not differ between the treatment groups. In comparison with placebo, telmisartan lowered BP (141/82 vs 135/78 mm Hg, difference 6 to 7 mm Hg and 2 to 4 mm Hg; P<0.001), pulse pressure (3 to 4 mm Hg; P<0.002), and rate-pressure product (466 mm Hg.bpm; P=0.0004). Treatment with telmisartan in 1360 patients with acute mild ischemic stroke and mildly elevated BP appeared to be safe with no excess in adverse events, was not associated with a significant effect on functional dependency, death, or recurrence, and modestly lowered BP.