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Thread: Loss of function due to blood loss

  1. #1

    Loss of function due to blood loss

    Dr. Young,

    How do you identify where the cord is damaged when the cord damage is a result from lack of blood supply to the cord because of internal bleeding from internal injuries? If the cord wasn't cut or bruised but damaged from lack of blood supply what can be done to help improve the nerves years after injury? Has any research been applied to eschemic injuries? Where can one go for help?

  2. #2
    LJWeber, ischemic injury of the spinal cord have been extensively studied. It produces lesions in the spinal cord that are not dissimilar from contusion injury except for the following three distinctions:

    1. Its location often follows the anatomy of spinal vasculature (I actually started an article on carecure describing the vasculature but decided that it was a bit too time-consuming and complicated to do properly in one sitting... but if you are interested, let me know and I can post it). T4-T6 is considered a "watershed" zone for the spinal cord where occlusion of the aorta and flow to the lower spinal cord will cause a paralysis. A recent study (see Research Forum) suggests that the lumbosacral spinal cord is very vulnerable in cases of cardiac arrests... this is quite interesting and surprising. Several people I know apparently have had cervical spinal cord ischemic lesions but I have been unable to find any description of such in the literature.

    2. There is of course no bony fracture associated with the injury and the damage to the spinal cord may be more widespread than after a traumatic spinal cord injury. For example, as pointed out below, loss of blood pressure for even short periods of time may be associated with lumbosacral cord damage.

    3. Ischemic damage to the spinal cord tends to injure the gray matter and smaller axons selectively, leaving the larger myelinated axons. Note that a contusion injury tends to damage the gray matter (central hemorrhagic necrosis) at the injury site but selectively damages the larger axons, leaving the smaller axons.

    Ischemic damage to the spinal cord is often very difficult to distinguish from transverse myelitis (TM). The cause of TM is still not well-understood although most textbooks still describe it as a form of immunological mediated damage of the spinal cord. The term transverse myelitis means inflammatory damage to the white matter of the spinal cord and that extends across the spinal cord. I suspect that many cases of TM may be ischemia related. The problem is of course that we do not have autopsies to see what the damage is and MRI scans are too crude to provide cellular details of the damage and cause of the damage. TM is also more common that most people think... occurring often in associated with lupus erythematosis (LE), an immunological disease. However, LE is not only immunological... it may also result in increased inflammation of blood vessels that increase the likelihood of thrombosis (clotting) that may lead to ischemic spinal cord injury.

    Most cases if ischemic spinal cord injury are "incomplete". Because they involve gray matter, much of the paralysis may be due to neuronal loss and more atrophy may be present. Recovery from ischemic spinal cord injury, like from TM or traumatic spinal cord injury, tend to be slow. Finally, I think that that demyelination may play a role in ischemic injuries because oligodendroglia tend to be sensitive to loss of blood flow. However, the larger axons tend to survive. So, people with ischemic spinal cord injury should in theory be more responsive to 4-aminopyridine.

    Wise.

  3. #3

    Eschemic Injuries

    Dr. Young,

    Thank you for the great explaination concerning the eschemic injury to spinal cords. In Texas, where would one go to get 4-AP? I have a good feeling 4-AP would benefit me. I just need to be pointed in the right direction wherever that may be. I just want to go ahead and get on a program of 4-AP, just don't know where to go from here, so I would appreciate any info on where I acn go to get started.

    Thanks again...

  4. #4
    You need to find first a doctor who is willing to prescribe it to you. I know that the Neurology Department at Baylor has been prescribing it for people with Multiple sclerosis. Unfortunately, I don't know the doctors personally but you may want to call them and find out.

    Wise.

  5. #5

    Eschemic Injury

    Great, I'll contact Baylor and keep you posted on what I find out about getting 4-AP.
    LJ

  6. #6
    Super Moderator Sue Pendleton's Avatar
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    From what I have found in literature and from doctors who have seen cervical ischemia injuries, they are very rare because they act quickly in paralyzing the the muscles needed to breath, either the diaphram or the intercostals. Because of this unless a thorough autopsy is done and the cord MRId during it a specific cause of death other than acute respiratory arrest is rarely found. Most cervical injuries that survive do so because the person is close to help like Jim Lubin of the quadlist, paramedics across the street, and the brother of one of my therapists who had a C3 stroke while flirting with 2 nursing students (his was a posterior damage mainly). My stroke was small and in the C3-4 or C5-7 range depending on who you talk to but I lost breathing within 3 hours because of the intercostals going. Most lose this a lot faster. And one of my acute doctors said he saw a very small artery below where my stroke was where most don't have an artery.

    I understood that the difference between TM and Guillame Barre Syndrome and ischemia was the first two effect the lower body and ascend while ischemia effects the area of loss of oxygen and descends. Also that TM and GBS move a bit slower than ischemia normally, taking several hours to several days to cause permenant damage.

    If you do find time to write that article in the future Wise I'd like to read it but no hurry....damage is already done. :-(

    I think most people who have ischemia in the throrasic and lumbar areas where they recover some movement or sensation do so because of heart attacks or heart surgery where an artery is clamped too long and from epidurals during labor that effect the lumbar region. Both types of injuries are most often in the hospital when they happen and can be treated immediately while a torn or ruptured main thorasic artery during a major car accident causes serious loss of blood pressure and those people tend to remain complete injuries.

  7. #7
    Sue, instead of posting it on the site, let me post what I have here and then polish it up for an article later.

    In theory, immunogenic transverse myelitis should cause only demyelination. This is because an immune reaction cannot attack the neurons themselves or else the person would be brain-dead or have all sorts of other neurological syndromes. Guillian-Barre should affect only the peripheral nervous system. Of course, multiple sclerosis is believed to be immune mediated and attacks primarily central myelin.

    From that perspective, both the lesion and the solutions for TM and GB should differ from ischemia. However, I am not yet convinced that TM is really an autoimmune problem. Yes, indeed it does ascend and takes place over time. However, TM often manifest several characteristics that suggest that many people assumed to have TM (such as Cody Unser) may have had spinal cord ischemia. I apologize to Cody for using her as an example but I hope that she doesn't mind being used as a example for a scientific discussion. Here is the reasoning:

    1. Level of loss. In TM, the neurological loss usually starts in the lower thoracic spinal cord and ascends to about T4. While it may occasionally go into the cervical region, most people come back down to the T4-T6 level. The T4-T6 region is special because this is considered the watershed zone of the spinal cord. The blood flow for 50% of the spinal cord comes from the anterior spinal artery (ASA) which receives its blood supply from the vertebral arteries in the upper cervical cord and the Artery of Adamkiwicz (ARM) which enters the spinal canal at T9-11 but anastomoses with the anterior spinal artery at T4-6. If ARM is blocked (and it is a very small artery with a characteristic hair-pin turn where it enters the spinal canal at T9-11), it causes ischemia of the spinal cord up to the cervical region. But because blood flow from the vertebral artery from above will feed the ASA, the eventually level that most people with ARM occlusion will get to is T4-T6. Most people that I know with TM and traumatic aortic aneurysms have T4-T6 levels.

    2. Vascular occlusion. TM is common in people with lupus erythrematosis (LE). Incidence rates range from several percent to the double digit percentage levels depending on the study. However, this is a autoimmune disease that affects the blood vessels. Vasculitis or inflammation of the blood vessels commonly cause clots that block the vessels. Because the human spinal cord relies on essentially two sources of blood for over 50% of the spinal cord with the thoracic spinal cord being supplied mostly by ARM up to T4-T6, it is not inconceivable that some people with LE may have clotted off their ARM. If this is the case, one would expect TM with a T4-T6 level.

    3. Vasculitis. A number of viral diseases cause vasculitis. Although it is not a consistent finding, as many as 50% of people who develop TM have a prior history of a viral fever in the days before the development of the TM. However, because most people survive TM and autopsies are only rarely done these days by knowledgeable pathologists, precious little or no data is available to show the pathology of the spinal cord in TM. Also, unless the person dies within days after the acute attack, the vasculitis may have subsided. Also, I suspect that most coroners are not steeped in the anatomy of the vasculature of the spinal cord sufficiently to make the diagnosis.

    In any case, what has been puzzling to me is the lack of mention in the medical literature about cervical spinal cord ischemia. I have not seen any systematic study of cervical spinal cord ischemia published to date. You and Chuck Close both may have had cervical spinal cord ischemia. By the way, his symptoms are similar to yours except that his arms are less strong than yours (if you can really belt a person across the room).

    The cervical spinal cord is vascularized by three arteries: the ASA and two posterior spinal arteries (PCA). The ASA supplies most of the gray matter and anterior white matter. The PCA supplies the dorsal columns, horns, and lateral columns. The ASA receives blood from two branches of the vertebral artery that converge, as shown in the following diagram.

    This diagram shows an anterior view of the brainstem and spinal cord, pointing out the vertebral arteries (1), the anterior spinal artery (2), the posterior inferior cerebellar artery (3), the basilar artery (4), the anterior inferior cerebellar artery (5), the pontine perforating branches(6), the posterior cerebellar artery (7). Unfortunately, you cannot see the posterior spinal artery which can be better appreciated in a three dimensional figure from www.vesalius.com:.



    The ASA is supplied from the bottom by the Artery of Adamkievicz which enters the spinal canal through the T9-T11 foramen (usually on the left), takes a hairpin curve (called the radiculomedullary artery in the figure), and ascends to T6-T4 where it then joins with the ASA. This is very difficult to explain in words or in regular diagrams. The only way to see the anatomy is in three dimensions, shown below.



    In this cutaway diagram of the spinal canal at T11, you can see the intercostal artery coming around the vertebral body and forming a number of different branches. Just before it enters the foramen, it sends a branch that supplies the posterior vertebral process. The branch the enters the foramen splits into three branches, one of which feeds the anterior longitudinal ligament (the white flat structure in the anterior part of the spinal canal), one which supplies the bone of the spinal canal itself, and one (labelled the radiculomedullary artery) takes a hairpin curve, heads up the spinal canal, and joins with the ASA.

    As you can see, the ASA and the arteries that supply the ASA are all small convoluted arteries. Occlusion of the ASA from the top or from the bottom by a clot, vasculitis, or compression could be devastating. I suspect that one reason why ischemia of the spinal cord does not occur as often or at least do not manifest as often is because new arteries can form but it takes a number of days. However, when there is acute and massive occlusion of the artery, part of the spinal cord will become infarcted.

    I happen to be aware of the vasculature of the spinal cord because in the 1980's, I spent a great deal of time working with Alejandro Berenstein at NYU who developed and initiated interventional neuroradiological procedures, where he would embolize arteriovenous malformations of the spinal cord. In the early days, he was causing paralysis in as many as 25% of the patients when he inadvertently embolized the Artery of Adamkiewicz. That was when I started doing somatosensory evoked potential monitoring in the operating room with him. In 1985, we published a paper which reported that the incidence of neurological complications from such procedures could be reduced to nearly 0% when we monitored somatosensory evoked potentials in the spinal cord. When the artery is occluded, the evoked potentials disappeared and this would warn him not to embolize.

    Wise.

    [This message was edited by Wise Young on January 11, 2002 at 09:43 AM.]

  8. #8
    Senior Member TD's Avatar
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    Clarification of my injury/paraplegia

    After wading through your dissertation ( I don't know if I understand it all but then I suffered brain damage) I wondered if you could clarify something for me, Dr. Wise.

    In the accident where I was injured I lost a great deal of blood due to the crushing injuries to my legs and breaking nearly every bone in my face. I received 14 units of blood in intensive care. I have been told I have lesions at T4, T8, and T11. The areas affected on my spine seem to fit your profile for ischemia. Could the blood loss also have affected my brain or would you say the damage was caused by the impact to my face/skull?

    "And so it begins."

  9. #9
    Super Moderator Sue Pendleton's Avatar
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    I'm right handed and while I don't have a full tricep in that arm I can backhand someone pretty good! I do have the left full triceps but my trunk on that side isn't as strong so throwing a forward punch would be difficult. DA? Want to be a sparring partner?

    I was tested almost immediately once I was stablilized for clotting and vascular disorders and for viruses. I had had, almost everyone I know had, hayfever that spring because Europe was having one of its few dry springs and yellow pollen was everywhere. I don't remember any fever though just sniffles bad enough that I couldn't wear my contact lens. I went through all the tests again this last Fall to check for Lupus and other stuff because of missing test results. Again, all negative.

    Considering the incredible and acute pain in my elbows that just came out of nowhere I have always assumed the doctors in Germany were correct in the stroke diagnosis. Within just 10 minutes or so I had lost some sensations and all movement in my hands and fingers and within 30 minutes to my legs. I was one big noodle by the time we got to the first hospital.

    While I had a full brain CT within the first hour that was negative for everything; I didn't have an MRI until day 8 or 9 when I was no longer intubated. There was a lesion shown under contrast at C3/4 on that and again a small area in the same place without contrast a month later while I waited at the army hospital for an evac flight. Where my rehab doc got C2/3 from, I don't know. Currently all my docs agree I am C5-7 incomplete ASIA C and can weight bear. Could that artery have grown in the week between the stroke and the first MRI?

    I do remember a lot of getting poked here and there around my neck and head and questions about my eyes but all my cranial nerves have always been ok when checked. Nice to know I have Chuck Close as such distinquished company in this fun malady. Oh, and I share the same neurologist with Cody Unser. That is one very terrific young lady. I'm glad we have her speaking out for more research money for cure too. But I sure wouldn't want to race her in wheelchairs or otherwise. She's fast!

  10. #10
    TD, the causes of injuries are always difficult to determine. What you say is certainly possible, i.e. significant loss of blood flow requiring 14-unit transfusions (the total blood volume of an average human is 5 liters http://hypertextbook.com/facts/LanNaLee.shtml). Prolonged periods of hypotension cause ischemia damage to the brain and the spinal cord.

    Sue, the spinal cord revascularizes quite rapidly. Within a week or two, there are new blood vessels that have regrown into the spinal cord.

    Wise.

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