Integrated brain restoration after ischemic stroke--medical management, risk factors, nutrients, and other interventions for managing inflammation and enhancing brain plasticity.
Brain injury from ischemic stroke can be devastating, but full brain restoration is feasible. Time until treatment is critical; rapid rate of injury progression, logistical and personnel constraints on neurological and cardiovascular assessment, limitations of recombinant tissue plasminogen activator (rtPA) for thrombolysis, anticoagulation and antiplatelet interventions, and neuroprotection all affect outcome. Promising acute neuroprotectant measures include albumin, magnesium, and hypothermia. Long-term hyperbaric oxygen therapy (HBOT) is safe and holds great promise. Eicosanoid and cytokine down-regulation by omega-3 nutrients docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) may help quench stroke inflammation. C-reactive protein (CRP), an inflammatory biomarker and stroke-recurrence predictor, responds favorably to krill oil (a phospholipid-DHA/EPA-astaxanthin complex). High homocysteine (Hcy) is a proven predictor of stroke recurrence and responds to folic acid and vitamin B12. Vitamin E may lower recurrence for individuals experiencing high oxidative stress. Citicoline shows promise for acute neuroprotection. Glycerophosphocholine (GPC) is neuroprotective and supports neuroplasticity via nerve growth factor (NGF) receptors. Stem cells have shown promise for neuronal restoration in randomized trials. Endogenous brain stem cells can migrate to an ischemic injury zone; exogenous stem cells once transplanted can migrate (home) to the stroke lesion and provide trophic support for cortical neuroplasticity. The hematopoietic growth factors erythropoietin (EPO) and granulocyte-colony stimulating factor (G-CSF) have shown promise in preliminary trials, with manageable adverse effects. Physical and mental exercises, including constraint-induced movement therapy (CIMT) and interactive learning aids, further support brain restoration following ischemic stroke. Brain plasticity underpins the function-driven brain restoration that can occur following stroke.
Kidd
Parris M
PM
D000925:Anticoagulants / Q000627:therapeutic use; D001921:Brain / Q000502:physiology; D002545:Brain Ischemia / Q000150:complications*; D006710:Homocysteine / Q000378:metabolism; D006801:Humans; D006931:Hyperbaric Oxygenation; D007249:Inflammation / Q000503:physiopathology / Q000517:prevention & control; D036341:Intercellular Signaling Peptides and Proteins / Q000627:therapeutic use; D009473:Neuronal Plasticity / Q000502:physiology; D018696:Neuroprotective Agents / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D020127:Recovery of Function; D012307:Risk Factors; D055502:Secondary Prevention; D033581:Stem Cell Transplantation; D020521:Stroke / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D015912:Thrombolytic Therapy / Q000379:methods; D014665:Vasodilator Agents / Q000627:therapeutic use
D000925:Anticoagulants; D036341:Intercellular Signaling Peptides and Proteins; D018696:Neuroprotective Agents; D010975:Platelet Aggregation Inhibitors; D014665:Vasodilator Agents; D006710:Homocysteine