Man in a Vegetative State Responds to Questions


This has been all over the web, but Wesley Smith at his Human Exceptionalism blog on the National Review Online web site has probably the best take on it.

A Canadian man named Scott Routley suffered severe brain damage in a car accident 12 years ago, and since then, he has not provided physicians with any evidence that he is conscious.  Several physical assessments by health care professionals have not indicated that Mr. Routley shows any signs of awareness, or has the ability to communicate.

What types of assessments are given to these patients?  The Royal Hospital for Neuro-disability (RHN) in Putney, London, specializes in the rehabilitation of brain-injured patients.  The RHN invented a complex assessment technique for brain-damaged patients that has been given the clever acronym “SMART.”  SMART tests all five senses, and a SMART assessment asks patients to track objects with their eyes, press switches, look at photographs, and even gives them things to taste and smell.

Patients who uniformly fail to show any signs of sensation in a SMART assessment (and others) are thought to be in a “persistent vegetative state.”  Essentially the brain stem still works to get the heart pumping and the lungs breathing, but these are autonomic functions provided by vital centers in the brain stem.  There cerebral cortex and the so-called “higher brain functions” that many people equate with being a human person, are thought to be gone.

Sometimes, patients in a persistent vegetative state will awaken to a kind of coma, in which their eyes are open, but they do not seem to have any perception of themselves or the outside world.

This view of severely brain-damaged patient will need to be rewritten, according to British neuroscientist Prof Adrian Owen.  Owen directed a neurological research team at the Brain and Mind Institute at the University of Western Ontario that examined Mr Routley’s brain with fMRI (fiunctional magnetic resonance imaging).  Their data, in Owen’s view shows that Mr. Routley is clearly not vegetative.

According the Dr. Owen, “”Scott has been able to show he has a conscious, thinking mind. We have scanned him several times and his pattern of brain activity shows he is clearly choosing to answer our questions. We believe he knows who and where he is.”

Dr. Owen continued: “Asking a patient something important to them has been our aim for many years. In future we could ask what we could do to improve their quality of life. It could be simple things like the entertainment we provide or the times of day they are washed and fed.”

Folks, being able to answer questions is not something that patients in persistent vegetative states do.  This chap and probably hundreds or more like him are alive and their brains are functioning.  Their brains however are too damaged to make their bodies move beyond so-called “core reflexes.”

Wesley Smith brings up the poignant point to be taken from all this:  “People such as Routley are dehydrated to death every day in all fifty states and in many countries around the world by having their tube-supplied sustenance withdrawn–supposedly based on their lack of personhood. But don’t expect this to stop the dehydration imperative. Bioethicists will merely say this is even more reason to kill them since they are aware of their profound disabilities and suffering. Indeed, that argument has already started.”

Smith is dead-on.  There are plenty of cases of supposedly brain-dead patients suddenly regaining abilities after being out of it for a long time.  For example, Haleigh Poutre, who was beaten into a coma by her stepfather Jason Strickland and her maternal aunt Holli Strickland.  The Department of Social Services, which had failed to rescue her from an obviously abusive situation in the first place, took custody of her and ordered her to be killed by dehydration and starvation.  However, this order was stayed after Haleigh began to breathe on her own and follow simple commands.  There are many other cases like this and do not get me started on Terry Schiavo (no I am not going to let that one go).

We are putting people down as though they were our pets just because they do sit up a bark when we say so.  Our original moral instincts were correct in the first place – that people are people regardless of whether or not they can follow our instructions.  May God forgive us for what we have done to the most disabled among us.  Hopefully, brain scans such as these will become mandatory before a patient is starved to death in the name of “mercy killing,” which is just simple murder.

A New Blood Vessel-Generating Stem Cell Discovered With Therapeutic Potential


The laboratory of Petri Salven at the University of Helsinki, Helsinki, Finland, has discovered a new type of stem cell that play a decisive role in the growth of new blood vessels. These stem cells are found in the walls of blood vessels and if protocols are developed to isolated these stem cells, they might very well provide news ways to treat cardiovascular diseases, cancer and many other diseases.

The growth of new blood vessels is known angiogenesis. Angiogenesis is required for the repair of damaged tissues or organs. A downside of angiogenesis is that tumors often secrete angiogenic factors that induce the circulatory system to remodel itself so that new blood vessels grow into the tumor and feed it so that it can grow faster. Thus angiogenesis research tries to promote the growth of new blood vessels when they are needed and inhibit angiogenesis when it is unwanted.

Several drugs that inhibit angiogenesis have been introduced as adjuvant cancer treatments. For example, the drug bevacizumab (Avastin) is a monoclonal antibody that specifically recognizes and binds to an angiogenic factor known as vascular endothelial growth factor or VEGF. When VEGF receptors on the surface of normal endothelial cells. When VEGF binds to receptors on the surfaces of endothelial cells, a signal is sent within those cells that initiate the growth and survival of new blood vessels. Bevacizumab binds tightly to VEGF, which prevents it from binding and activating the VEGF receptor.

Other angiogenesis inhibitors include sorafenib (Nexavar) and sunitinib (Sutent), which are small molecular inhibitors of the receptors that bind the angiogenic factors and the downstream targets of those receptors. Unfortunately, the present crop of angiogenesis inhibitors are not all that effective under certain conditions and they are also extremely expensive and have some very undesirable side effects.

Professor Salven has studied angiogenesis for some time, and his research has focused on the endothelial cells that compose blood vessels. Where do these cells come from and how can we make more or less of them as needed?

A long-standing assumption by scientists in the angiogenesis field was that new endothelial cells came from stem cells found in the bond marrow. This assumption makes sense since there are several stem cell populations in bone marrow that express blood vessel markers and can form blood vessels in culture. However, in 2008, Salven’s group published a paper that demonstrated that new endothelial cells could not come from bone marrow stem cells (see Purhonen S, et al., (2008). Proc Natl Acad Sci U S A. 105(18): 6620-5). Therefore, the mystery remained – from where do new endothelial cells come?

Salven has recently solved this conundrum in his recent paper that appeared in PLoS Biology. According to Salven, “We succeeded in isolating endothelial cells with a high rate of division in the blood vessels of mice. We found that these same cells in human blood vessels and blood vessels growing in malignant tumors in humans. These cells are known as vascular endothelial stem cells, abbreviated VESC. In a cell culture, one such cell is able to produce tends of millions of new blood vessels wall cells.”

Slaven continued: “Our study found that these important stem cells can be found as single cells among the ordinary endothelial cells in blood vessel walls. When the process of angiogenesis is launched, these cells begin to produce new blood vessel wall cells.”

Salven’s colleagues have tested the effects of these new endothelial cells in mice. A particular mouse strain that carries a mutation in the c-kit gene was examined in these experiments. The c-kit gene encodes a cell surface protein called CD117, which is a vital element in the cells that form blood vessels. IN these c-kit mutant mice, new growth of new blood vessels was very poor and the growth of malignant tumors was also quite poor. However, if new stem cells from animals that did not possess a mutation in the c-kit gene were implanted into these mutant mice, blood vessels quickly formed.

As previously mentioned, the cell surface protein CD117 does seem to mark VESCs, but other cells other than VESCs have CD117 on their surfaces. Therefore, isolating all CD177-expression cells only enriches preparations for VESCs; it does not isolate VESCs. Presently, Salven and his group are searching for better surface molecules that can be used to more effectively isolated VESCs from surrounding tissue. If this isolation succeeds, then it will be possible to isolated and propagate VESCs from patients with cardiovascular diseases and expand them in culture for therapeutic purposes.

Another potentially fertile field of research is to find a way to inhibit the activity of VESCs to prevent tumors from remodeling the circulatory system. By cutting of their blood supply, tumors will not only grow slower, but also not spread nearly as quickly.

See: Fang S, Wei J, Pentinmikko N, Leinonen H, Salven P (2012) Generation of Functional Blood Vessels from a Single c-kit+ Adult Vascular Endothelial Stem Cell. PLoS Biol 10(10): e1001407. doi:10.1371/journal.pbio.1001407