Abstract
Preservation of neuronal tissue is crucial for recovery after stroke, but studies suggest that prolonged neuronal loss occurs following acute ischaemia. This study assessed the temporal pattern of neuronal loss in subacute ischemic stroke patients using 1H magnetic resonance spectroscopy, in parallel with functional recovery at 2, 6 and 12 weeks after stroke. Specifically, we measured N-acetylaspartate (NAA), choline, myoinositol, creatine and lactate concentrations in the ipsilesional and contralesional thalamus of 15 first-ever acute ischaemic stroke patients and 15 control participants and correlated MRS concentrations with motor recovery, measured at 12 weeks using the Fugl–Meyer scale. NAA in the ipsilesional thalamus fell significantly between 2 and 12 weeks (10.0 to 7.97 mmol/L, p = 0.003), while choline, myoinositol and lactate concentrations increased (p = 0.025, p = 0.031, p = 0.001, respectively). Higher NAA concentrations in the ipsilesional thalamus at 2 and 12 weeks correlated with higher Fugl Meyer scores at 12 weeks (p = 0.004 and p = 0.006, respectively). While these results should be considered preliminary given the modest sample size, the progressive fall in NAA and late increases in choline, myoinositol and lactate may indicate progressive non-ischaemic neuronal loss, metabolically depressed neurons and/or diaschisis effects, which have a detrimental effect on motor recovery. Interventions that can potentially limit this ongoing subacute tissue damage may improve stroke recovery.
Highlights
Stroke remains the leading cause of acquired adult disability, with up to 30% of survivors suffering from permanent disability [1]
Many cellular elements involved in these processes have distinctive chemical signatures, which can be measured with Proton Magnetic Resonance Spectroscopy (1H-MRS) [9,10]
The longitudinal changes observed in NAA and CBF between 2 and 12 weeks after stroke provide an insight into subacute neuronal loss after ischaemic stroke and its relationship to recovery
Summary
Stroke remains the leading cause of acquired adult disability, with up to 30% of survivors suffering from permanent disability [1]. Preservation of neuronal tissue after injury is key to recovery and is dependent upon several processes in the post-infarction phase, including further ischaemic damage, reperfusion, inflammation, gliosis and neuronal repair [2,3]. These processes take place in the core of the infarct and in structurally and functionally connected areas, remote from the infarct site.
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