Stroke Stem Cell Treatment


Stem Cell Treatment for StrokeStem Cell Treatment for a Stroke is an option

What is a Stroke?

Stroke and Stem Cell Therapy

A stroke (Cerebrovascular Accident or CVA), is the rapid loss of brain function due to the blood supply to the brain being disturbed. This can be from ischemia from the lack of blood flow or from a blockage known as Thrombosis, an Arterial Embolism, or a Haemorrhage where blood is leaking out or inside the brain.

The affected area of the brain is unable to function correctly and may result in an inability to move especially in one or more limbs on one side of the body. Stroke can also cause an inability to understand speech or speak or see properly. 

A stroke is a medical emergency that needs immediate medical attention. Stroke can cause permanent neurological damage and ongoing complications, and death. It is the a leading cause of adult disability in the around the world.

Risk factors for stroke include ederly people,  high blood pressure (hypertension), a previous stroke or from a transient ischemic attack (TIA).

Other related risk conditions include diabetes, high cholesterol, cigarette smoking and atrial fibrillation. High blood pressure is the most important modifiable risk factor of stroke.

A silent stroke is a stroke that does not have any outward symptoms, and the patient is typically unaware they have suffered a stroke. A silent stroke still causes damage to the brain, and places the person at risk for both transient ischemic attack and a major stroke occuring in the future.

People who have suffered a major stroke are at risk of having silent strokes as well.Stem Cell Treatment for Stroke


Stroke rehabilitation.

Lancet. 2011 May 14;377(9778):1693-702

Authors: Langhorne P, Bernhardt J, Kwakkel G

Stroke is a common, serious, and disabling global health-care problem, and rehabilitation is a major part of patient care. There is evidence to support rehabilitation in well coordinated multidisciplinary stroke units or through provision of early supported provision of discharge teams. Potentially beneficial treatment options for motor recovery of the arm include constraint-induced movement therapy and robotics.

Promising interventions that could be beneficial to improve aspects of gait include fitness training, high-intensity therapy, and repetitive-task training. Repetitive-task training might also improve transfer functions. Occupational therapy can improve activities of daily living; however, information about the clinical effect of various strategies of cognitive rehabilitation and strategies for aphasia and dysarthria is scarce. Several large trials of rehabilitation practice and of novel therapies (eg, stem-cell therapy, repetitive transcranial magnetic stimulation, virtual reality, robotic therapies, and drug augmentation) are underway to inform future practice.

PMID: 21571152 [PubMed - in process]


Stem Cell Treatment for Stroke NIH Streaming Database:

Related Articles An introduction to the roles of purinergic signalling in neurodegeneration, neuroprotection and neuroregeneration. Neuropharmacology. 2016 May;104:4-17 Authors: Burnstock G Abstract Purinergic signalling appears to play important roles in neurodegeneration, neuroprotection and neuroregeneration. Initially there is a brief summary of the background of purinergic signalling, including release of purines and pyrimidines from neural and non-neural cells and their ectoenzymatic degradation, and the current characterisation of P1 (adenosine), and P2X (ion channel) and P2Y (G protein-coupled) nucleotide receptor subtypes. There is also coverage of the localization and roles of purinoceptors in the healthy central nervous system. The focus is then on the roles of purinergic signalling in trauma, ischaemia, stroke and in neurodegenerative diseases, including Alzheimer's, Parkinson's and Huntington's diseases, as well as multiple sclerosis and amyotrophic lateral sclerosis. Neuroprotective mechanisms involving purinergic signalling are considered and its involvement in neuroregeneration, including the role of adult neural stem/progenitor cells. This article is part of the Special Issue entitled 'Purines in Neurodegeneration and Neuroregeneration'. PMID: 26056033 [PubMed - indexed for MEDLINE]
Related Articles Effects of the combined treatment of bone marrow stromal cells with mild exercise and thyroid hormone on brain damage and apoptosis in a mouse focal cerebral ischemia model. Metab Brain Dis. 2017 May 25;: Authors: Akhoundzadeh K, Vakili A, Sameni HR, Vafaei AA, Rashidy-Pour A, Safari M, Mohammadkhani R Abstract This study examined whether post-stroke bone marrow stromal cells (BMSCs) therapy combined with exercise (EX) and/or thyroid hormone (TH) could reduce brain damage in an experimental ischemic stroke in mice. Focal cerebral ischemia was induced under Laser Doppler Flowmetry (LDF) guide by 45 min of middle cerebral artery occlusion (MCAO), followed by 7 days of reperfusion in albino mice. BMSCs were injected into the right cerebral ventricle 24 h after MCAO, followed by daily injection of T3 (20 μg/100 g weight S.C) and 6 days of running on a treadmill. Infarct size, neurobehavioral test, TUNEL and BrdU positive cells were evaluated at 7 days after MCAO. Treatment with BMSCs and mild EX alone significantly reduced the infarct volume by 23% and 44%, respectively (both, p < 0.001). The BMSCs + TH, BMSCs + EX, and BMSCs + EX + TH combination therapies significantly reduced the infarct volume by 26%, 51%, and 70%, respectively (all, p < 0.001). A significant improvement in the neurobehavioral functioning was observed in the EX, BMSCs + EX, and BMSCs + EX+ TH groups (p < 0.001). The number of TUNEL-positive cells (a marker of apoptosis) was significantly reduced in the EX, BMSCs, BMSCs + EX, BMSCs + TH, and BMSCs + EX + TH groups (all, p < 0.001). Moreover, the combination therapy considerably increased BrdU-labeled cells in the subventricular zone (SVZ) (p < 0.01). Our findings indicated that the combined treatment of BMSCs with mild EX and TH more efficiently reduces the cerebral infarct size after stroke. More likely, these effects mediate via enchaining generation of new neuronal cells and the attenuation of apoptosis in ischemia stroke in young mice. PMID: 28547077 [PubMed - as supplied by publisher]

Quick Contact Form