Radiation induced necrosis

bluerose

The first time I heard the word 'necrosis' was in the ER when I went in for an extremely painful spot on my left thigh and the ER doc said it could be 'fat necrosis'. Of course I knew what the word probably meant so looked it up when I got home, hmmm.

Wondered if you can have necrosis all through your body anywhere that you have been radiated? Would it produce pain like the horrible pain I had in my thigh? It wasn't really all that deep a pain but not surface pain either.

Can anyone comment on this subject? I have read the brain necrosis statements but wonder if this can apply to anywhere in the body that radiation has hit? If so then how would it present itself in the patient?

Thanks for your time.

Blessings,

Bluerose

irishangel32

There are great meds for pain relief, when that time comes.
Kathy here,
I have had hip and shoulder necrosis since 1980. It became a pain issue in 1986, first I was taking Daypro 600mg,twice daily. Total relief for 27 years,life was beautiful. I did water exercise and dance plus yoga. Around 2008 I was getting break through pain,my doctor added Cymbalta 60mg. Now in 2011 I have some pain and need to fine tune something. My necrosis is in the bones of my joints.

gdpawel

Radiation-induced necrosis
BlueRose

When brain tumors are treated with radiation therapy, there is always a risk of radiation-induced necrosis of healthy brain tissue. Insidious and potentially fatal, radiation necrosis of the brain may develop months or even years after irradiation.

This poorly understood side effect can occur even when the most stringent measures are taken to avoid exposing healthy tissue to harmful levels of radiation. In most cases, radiation necrosis of the brain occurs at random, without known genetic or other predisposing risk factors. The only treatment options typically available for radiation necrosis of the brain are surgery to remove dead tissue and use of the steroid dexamethasone to provide limited symptom control. But clinicians have not found a way to stop the progression of necrosis, despite having tested a range of therapies including anticoagulants, hyperbaric oxygen, and high-dose anti-inflammatory regimens.

However, recent studies at M. D. Anderson have shown that the monoclonal antibody bevacizumab (Avastin) may be able to stop radiation necrosis of the brain and allow some of the damage to be reversed. Victor A. Levin, M.D., a professor in the Department of Neuro-Oncology and the senior researcher on the studies, said the findings suggest that radiation necrosis of the brain can be successfully managed—and perhaps even prevented—with bevacizumab or similar drugs.

The need for such a breakthrough is as old as radiation therapy for cancers in the brain. “No matter what we do or how good we do it, we know a small percentage of patients who receive radiation therapy to the central nervous system will suffer late-occurring radiation necrosis,” Dr. Levin said. “We used to think it was the dose that was causing problems. Then we did a study and found that there was little to no relation to radiation dose or radiation volume—the necrosis occurred simply by chance. So it is impossible to say which patients will develop this problem; we just have to monitor them and hope for the best.”

Like necrosis, the discovery that bevacizumab has an effect on necrosis can also be attributed to chance. Bevacizumab, a newer drug that prevents blood vessel growth in tumors by blocking vascular endothelial growth factor (VEGF), was originally approved in the United States for the treatment of metastatic colon cancer and non–small cell lung cancer. An M. D. Anderson group that included Dr. Levin decided to test the drug in patients who had VEGF-expressing brain tumors. “Some of these patients also had necrosis from prior radiation therapy, and we were struck by the positive response of those patients to bevacizumab,” Dr. Levin said. “We had never seen such a regression of necrotic lesions with any other drug like we did in those patients.” The observation prompted the researchers to design a placebo-controlled, double-blind, phase II trial sponsored by the U.S. Cancer Therapy Evaluation Program in which bevacizumab would be tested specifically for the treatment of radiation necrosis of the brain.

The trial is small, having accrued 13 of a planned 16 patients, and is limited to those with progressive symptoms, lower-grade primary brain tumors, and head and neck cancers. But the results have been unlike anything the researchers have seen before in radiation necrosis therapy. All of the patients receiving bevacizumab responded almost immediately to treatment, with regression of necrotic lesions evident on magnetic resonance images, while none of the patients receiving the placebo showed a response. The results were striking, and all of the patients who switched from placebo showed a response to bevacizumab as well. So far, responses have persisted over 6 months even after the end of bevacizumab treatment.

Side effects seen in the trial so far included venous thromboembolism in one patient, small vessel thrombosis in two patients, and a large venous sinus thrombosis in one patient. Dr. Levin is unsure whether the side effects were caused by therapy or the radiation necrosis itself. “We’re also not absolutely sure what is causing the positive effects against the radiation necrosis,” he said. “We presume it’s related to the release of cytokines like VEGF, since bevacizumab is very specific and only reduces VEGF levels. We think aberrant production of VEGF is involved with radiation necrosis of the brain, and the fact that even short treatment with bevacizumab seems to turn off the cycle of radiation damage further confirms the central role of VEGF in the process.”

The multidisciplinary research team has also postulated that radiation therapy damages astrocytes, a cell type involved in various brain functions, and causes them to leak VEGF. This leaked VEGF might then cause further damage to brain cells and further leakage of VEGF. “It gets to be a very vicious cycle,” Dr. Levin said. “The question is, is that all that’s going on?”

Dr. Levin hopes that the answers to that question and others may lead to preventive measures against radiation necrosis, beyond what is already done to control the development of radiation itself. Perhaps bevacizumab can be given in low doses before radiation or intermittently afterward to reduce VEGF levels and protect the brain from abnormally high levels of the protein. He hopes such approaches can be tested in future studies. “Just the fact that bevacizumab works has helped us understand so much more about what happens in radiation necrosis,” he said. “Everything we’ve tried up until now has been a brick wall.”

Source: OncoLog, May 2009, Vol. 54, No. 5

Visualizing the effects of Avastin (bevacizumab)

http://www2.mdanderson.org/depts/oncolog/articles/09/5-may/pop.html

Bevacizumab (Avastin) Reverses Cerebral Radiation Necrosis

http://jco.ascopubs.org/content/26/34/5649.full.pdf

bluerose

irishangel32 said:

There are great meds for pain relief, when that time comes.
Kathy here,
I have had hip and shoulder necrosis since 1980. It became a pain issue in 1986, first I was taking Daypro 600mg,twice daily. Total relief for 27 years,life was beautiful. I did water exercise and dance plus yoga. Around 2008 I was getting break through pain,my doctor added Cymbalta 60mg. Now in 2011 I have some pain and need to fine tune something. My necrosis is in the bones of my joints.

Hi Kathy
Thanks for your response to my posting. My pain was in the tissue on my hip because when I even touched the area it hurt like crazy and hurt all the time even if I didn't touch it. I haven't had the pain now in awhile and hope it has gone away for good but nothing seems to leave me ever - totally except for a heart arythmia so am greatful for that.

Thank you for your info.

Blessings,

Bluerose

bluerose

gdpawel said:

Radiation-induced necrosis
BlueRose

When brain tumors are treated with radiation therapy, there is always a risk of radiation-induced necrosis of healthy brain tissue. Insidious and potentially fatal, radiation necrosis of the brain may develop months or even years after irradiation.

This poorly understood side effect can occur even when the most stringent measures are taken to avoid exposing healthy tissue to harmful levels of radiation. In most cases, radiation necrosis of the brain occurs at random, without known genetic or other predisposing risk factors. The only treatment options typically available for radiation necrosis of the brain are surgery to remove dead tissue and use of the steroid dexamethasone to provide limited symptom control. But clinicians have not found a way to stop the progression of necrosis, despite having tested a range of therapies including anticoagulants, hyperbaric oxygen, and high-dose anti-inflammatory regimens.

However, recent studies at M. D. Anderson have shown that the monoclonal antibody bevacizumab (Avastin) may be able to stop radiation necrosis of the brain and allow some of the damage to be reversed. Victor A. Levin, M.D., a professor in the Department of Neuro-Oncology and the senior researcher on the studies, said the findings suggest that radiation necrosis of the brain can be successfully managed—and perhaps even prevented—with bevacizumab or similar drugs.

The need for such a breakthrough is as old as radiation therapy for cancers in the brain. “No matter what we do or how good we do it, we know a small percentage of patients who receive radiation therapy to the central nervous system will suffer late-occurring radiation necrosis,” Dr. Levin said. “We used to think it was the dose that was causing problems. Then we did a study and found that there was little to no relation to radiation dose or radiation volume—the necrosis occurred simply by chance. So it is impossible to say which patients will develop this problem; we just have to monitor them and hope for the best.”

Like necrosis, the discovery that bevacizumab has an effect on necrosis can also be attributed to chance. Bevacizumab, a newer drug that prevents blood vessel growth in tumors by blocking vascular endothelial growth factor (VEGF), was originally approved in the United States for the treatment of metastatic colon cancer and non–small cell lung cancer. An M. D. Anderson group that included Dr. Levin decided to test the drug in patients who had VEGF-expressing brain tumors. “Some of these patients also had necrosis from prior radiation therapy, and we were struck by the positive response of those patients to bevacizumab,” Dr. Levin said. “We had never seen such a regression of necrotic lesions with any other drug like we did in those patients.” The observation prompted the researchers to design a placebo-controlled, double-blind, phase II trial sponsored by the U.S. Cancer Therapy Evaluation Program in which bevacizumab would be tested specifically for the treatment of radiation necrosis of the brain.

The trial is small, having accrued 13 of a planned 16 patients, and is limited to those with progressive symptoms, lower-grade primary brain tumors, and head and neck cancers. But the results have been unlike anything the researchers have seen before in radiation necrosis therapy. All of the patients receiving bevacizumab responded almost immediately to treatment, with regression of necrotic lesions evident on magnetic resonance images, while none of the patients receiving the placebo showed a response. The results were striking, and all of the patients who switched from placebo showed a response to bevacizumab as well. So far, responses have persisted over 6 months even after the end of bevacizumab treatment.

Side effects seen in the trial so far included venous thromboembolism in one patient, small vessel thrombosis in two patients, and a large venous sinus thrombosis in one patient. Dr. Levin is unsure whether the side effects were caused by therapy or the radiation necrosis itself. “We’re also not absolutely sure what is causing the positive effects against the radiation necrosis,” he said. “We presume it’s related to the release of cytokines like VEGF, since bevacizumab is very specific and only reduces VEGF levels. We think aberrant production of VEGF is involved with radiation necrosis of the brain, and the fact that even short treatment with bevacizumab seems to turn off the cycle of radiation damage further confirms the central role of VEGF in the process.”

The multidisciplinary research team has also postulated that radiation therapy damages astrocytes, a cell type involved in various brain functions, and causes them to leak VEGF. This leaked VEGF might then cause further damage to brain cells and further leakage of VEGF. “It gets to be a very vicious cycle,” Dr. Levin said. “The question is, is that all that’s going on?”

Dr. Levin hopes that the answers to that question and others may lead to preventive measures against radiation necrosis, beyond what is already done to control the development of radiation itself. Perhaps bevacizumab can be given in low doses before radiation or intermittently afterward to reduce VEGF levels and protect the brain from abnormally high levels of the protein. He hopes such approaches can be tested in future studies. “Just the fact that bevacizumab works has helped us understand so much more about what happens in radiation necrosis,” he said. “Everything we’ve tried up until now has been a brick wall.”

Source: OncoLog, May 2009, Vol. 54, No. 5

Visualizing the effects of Avastin (bevacizumab)

http://www2.mdanderson.org/depts/oncolog/articles/09/5-may/pop.html

Bevacizumab (Avastin) Reverses Cerebral Radiation Necrosis

http://jco.ascopubs.org/content/26/34/5649.full.pdf

Thanks GD
Yes I had read that about brain necrosis but I was wondering if necrosis can happen in other spots on the body, like in the tissue of my hip? I don't know if having brain necrosis (are we talking chemo brain stuff here??) could be part of what causes the hip pain too or what you mean? I know that when radiation hits healthy cells too they can die from exposure so are we talking about that as necrosis or something more complex?

Thank you for your post. As usual you present fascinating information. I appreciate it.

Blessings,

Bluerose

bluerose

gdpawel said:

Radiation-induced necrosis
BlueRose

When brain tumors are treated with radiation therapy, there is always a risk of radiation-induced necrosis of healthy brain tissue. Insidious and potentially fatal, radiation necrosis of the brain may develop months or even years after irradiation.

This poorly understood side effect can occur even when the most stringent measures are taken to avoid exposing healthy tissue to harmful levels of radiation. In most cases, radiation necrosis of the brain occurs at random, without known genetic or other predisposing risk factors. The only treatment options typically available for radiation necrosis of the brain are surgery to remove dead tissue and use of the steroid dexamethasone to provide limited symptom control. But clinicians have not found a way to stop the progression of necrosis, despite having tested a range of therapies including anticoagulants, hyperbaric oxygen, and high-dose anti-inflammatory regimens.

However, recent studies at M. D. Anderson have shown that the monoclonal antibody bevacizumab (Avastin) may be able to stop radiation necrosis of the brain and allow some of the damage to be reversed. Victor A. Levin, M.D., a professor in the Department of Neuro-Oncology and the senior researcher on the studies, said the findings suggest that radiation necrosis of the brain can be successfully managed—and perhaps even prevented—with bevacizumab or similar drugs.

The need for such a breakthrough is as old as radiation therapy for cancers in the brain. “No matter what we do or how good we do it, we know a small percentage of patients who receive radiation therapy to the central nervous system will suffer late-occurring radiation necrosis,” Dr. Levin said. “We used to think it was the dose that was causing problems. Then we did a study and found that there was little to no relation to radiation dose or radiation volume—the necrosis occurred simply by chance. So it is impossible to say which patients will develop this problem; we just have to monitor them and hope for the best.”

Like necrosis, the discovery that bevacizumab has an effect on necrosis can also be attributed to chance. Bevacizumab, a newer drug that prevents blood vessel growth in tumors by blocking vascular endothelial growth factor (VEGF), was originally approved in the United States for the treatment of metastatic colon cancer and non–small cell lung cancer. An M. D. Anderson group that included Dr. Levin decided to test the drug in patients who had VEGF-expressing brain tumors. “Some of these patients also had necrosis from prior radiation therapy, and we were struck by the positive response of those patients to bevacizumab,” Dr. Levin said. “We had never seen such a regression of necrotic lesions with any other drug like we did in those patients.” The observation prompted the researchers to design a placebo-controlled, double-blind, phase II trial sponsored by the U.S. Cancer Therapy Evaluation Program in which bevacizumab would be tested specifically for the treatment of radiation necrosis of the brain.

The trial is small, having accrued 13 of a planned 16 patients, and is limited to those with progressive symptoms, lower-grade primary brain tumors, and head and neck cancers. But the results have been unlike anything the researchers have seen before in radiation necrosis therapy. All of the patients receiving bevacizumab responded almost immediately to treatment, with regression of necrotic lesions evident on magnetic resonance images, while none of the patients receiving the placebo showed a response. The results were striking, and all of the patients who switched from placebo showed a response to bevacizumab as well. So far, responses have persisted over 6 months even after the end of bevacizumab treatment.

Side effects seen in the trial so far included venous thromboembolism in one patient, small vessel thrombosis in two patients, and a large venous sinus thrombosis in one patient. Dr. Levin is unsure whether the side effects were caused by therapy or the radiation necrosis itself. “We’re also not absolutely sure what is causing the positive effects against the radiation necrosis,” he said. “We presume it’s related to the release of cytokines like VEGF, since bevacizumab is very specific and only reduces VEGF levels. We think aberrant production of VEGF is involved with radiation necrosis of the brain, and the fact that even short treatment with bevacizumab seems to turn off the cycle of radiation damage further confirms the central role of VEGF in the process.”

The multidisciplinary research team has also postulated that radiation therapy damages astrocytes, a cell type involved in various brain functions, and causes them to leak VEGF. This leaked VEGF might then cause further damage to brain cells and further leakage of VEGF. “It gets to be a very vicious cycle,” Dr. Levin said. “The question is, is that all that’s going on?”

Dr. Levin hopes that the answers to that question and others may lead to preventive measures against radiation necrosis, beyond what is already done to control the development of radiation itself. Perhaps bevacizumab can be given in low doses before radiation or intermittently afterward to reduce VEGF levels and protect the brain from abnormally high levels of the protein. He hopes such approaches can be tested in future studies. “Just the fact that bevacizumab works has helped us understand so much more about what happens in radiation necrosis,” he said. “Everything we’ve tried up until now has been a brick wall.”

Source: OncoLog, May 2009, Vol. 54, No. 5

Visualizing the effects of Avastin (bevacizumab)

http://www2.mdanderson.org/depts/oncolog/articles/09/5-may/pop.html

Bevacizumab (Avastin) Reverses Cerebral Radiation Necrosis

http://jco.ascopubs.org/content/26/34/5649.full.pdf

Thanks GD
site glitch

bluerose

gdpawel said:

Radiation-induced necrosis
BlueRose

When brain tumors are treated with radiation therapy, there is always a risk of radiation-induced necrosis of healthy brain tissue. Insidious and potentially fatal, radiation necrosis of the brain may develop months or even years after irradiation.

This poorly understood side effect can occur even when the most stringent measures are taken to avoid exposing healthy tissue to harmful levels of radiation. In most cases, radiation necrosis of the brain occurs at random, without known genetic or other predisposing risk factors. The only treatment options typically available for radiation necrosis of the brain are surgery to remove dead tissue and use of the steroid dexamethasone to provide limited symptom control. But clinicians have not found a way to stop the progression of necrosis, despite having tested a range of therapies including anticoagulants, hyperbaric oxygen, and high-dose anti-inflammatory regimens.

However, recent studies at M. D. Anderson have shown that the monoclonal antibody bevacizumab (Avastin) may be able to stop radiation necrosis of the brain and allow some of the damage to be reversed. Victor A. Levin, M.D., a professor in the Department of Neuro-Oncology and the senior researcher on the studies, said the findings suggest that radiation necrosis of the brain can be successfully managed—and perhaps even prevented—with bevacizumab or similar drugs.

The need for such a breakthrough is as old as radiation therapy for cancers in the brain. “No matter what we do or how good we do it, we know a small percentage of patients who receive radiation therapy to the central nervous system will suffer late-occurring radiation necrosis,” Dr. Levin said. “We used to think it was the dose that was causing problems. Then we did a study and found that there was little to no relation to radiation dose or radiation volume—the necrosis occurred simply by chance. So it is impossible to say which patients will develop this problem; we just have to monitor them and hope for the best.”

Like necrosis, the discovery that bevacizumab has an effect on necrosis can also be attributed to chance. Bevacizumab, a newer drug that prevents blood vessel growth in tumors by blocking vascular endothelial growth factor (VEGF), was originally approved in the United States for the treatment of metastatic colon cancer and non–small cell lung cancer. An M. D. Anderson group that included Dr. Levin decided to test the drug in patients who had VEGF-expressing brain tumors. “Some of these patients also had necrosis from prior radiation therapy, and we were struck by the positive response of those patients to bevacizumab,” Dr. Levin said. “We had never seen such a regression of necrotic lesions with any other drug like we did in those patients.” The observation prompted the researchers to design a placebo-controlled, double-blind, phase II trial sponsored by the U.S. Cancer Therapy Evaluation Program in which bevacizumab would be tested specifically for the treatment of radiation necrosis of the brain.

The trial is small, having accrued 13 of a planned 16 patients, and is limited to those with progressive symptoms, lower-grade primary brain tumors, and head and neck cancers. But the results have been unlike anything the researchers have seen before in radiation necrosis therapy. All of the patients receiving bevacizumab responded almost immediately to treatment, with regression of necrotic lesions evident on magnetic resonance images, while none of the patients receiving the placebo showed a response. The results were striking, and all of the patients who switched from placebo showed a response to bevacizumab as well. So far, responses have persisted over 6 months even after the end of bevacizumab treatment.

Side effects seen in the trial so far included venous thromboembolism in one patient, small vessel thrombosis in two patients, and a large venous sinus thrombosis in one patient. Dr. Levin is unsure whether the side effects were caused by therapy or the radiation necrosis itself. “We’re also not absolutely sure what is causing the positive effects against the radiation necrosis,” he said. “We presume it’s related to the release of cytokines like VEGF, since bevacizumab is very specific and only reduces VEGF levels. We think aberrant production of VEGF is involved with radiation necrosis of the brain, and the fact that even short treatment with bevacizumab seems to turn off the cycle of radiation damage further confirms the central role of VEGF in the process.”

The multidisciplinary research team has also postulated that radiation therapy damages astrocytes, a cell type involved in various brain functions, and causes them to leak VEGF. This leaked VEGF might then cause further damage to brain cells and further leakage of VEGF. “It gets to be a very vicious cycle,” Dr. Levin said. “The question is, is that all that’s going on?”

Dr. Levin hopes that the answers to that question and others may lead to preventive measures against radiation necrosis, beyond what is already done to control the development of radiation itself. Perhaps bevacizumab can be given in low doses before radiation or intermittently afterward to reduce VEGF levels and protect the brain from abnormally high levels of the protein. He hopes such approaches can be tested in future studies. “Just the fact that bevacizumab works has helped us understand so much more about what happens in radiation necrosis,” he said. “Everything we’ve tried up until now has been a brick wall.”

Source: OncoLog, May 2009, Vol. 54, No. 5

Visualizing the effects of Avastin (bevacizumab)

http://www2.mdanderson.org/depts/oncolog/articles/09/5-may/pop.html

Bevacizumab (Avastin) Reverses Cerebral Radiation Necrosis

http://jco.ascopubs.org/content/26/34/5649.full.pdf

Thanks GD
site glitch

gdpawel

bluerose said:

Thanks GD
Yes I had read that about brain necrosis but I was wondering if necrosis can happen in other spots on the body, like in the tissue of my hip? I don't know if having brain necrosis (are we talking chemo brain stuff here??) could be part of what causes the hip pain too or what you mean? I know that when radiation hits healthy cells too they can die from exposure so are we talking about that as necrosis or something more complex?

Thank you for your post. As usual you present fascinating information. I appreciate it.

Blessings,

Bluerose

BlueRose
Necrosis is simply
BlueRose

Necrosis is simply a cell dying, all of its coordinated activities going wrong and things shut down. If a cell gets too much heat or is poisoned by a toxic substance or exposed to chemicals that damage its proteins and membranes or radiation that breaks its DNA molecules, that cell can just stop functioning.

Necrotizing leukoencephalopathy is a form of diffuse white matter injury that can follow chemotherapy. The white matter is the covering of the nerves within the brain. Its function is to speed up the passage of impulses along the nerves.

It's the damage to this nerves that can cause the peripheral neuropathy. The peripheral nerves that carry information to and from the limbs. The nerves that supply the bowels and other internal organs. The nerves of the head which connect to the ears, eyes, taste buds, etc.

http://cancerfocus.org/forum/showthread.php?t=3439

Greg

gdpawel

bluerose said:

Thanks GD
Yes I had read that about brain necrosis but I was wondering if necrosis can happen in other spots on the body, like in the tissue of my hip? I don't know if having brain necrosis (are we talking chemo brain stuff here??) could be part of what causes the hip pain too or what you mean? I know that when radiation hits healthy cells too they can die from exposure so are we talking about that as necrosis or something more complex?

Thank you for your post. As usual you present fascinating information. I appreciate it.

Blessings,

Bluerose

BlueRose
Necrosis is simply
BlueRose

Necrosis is simply a cell dying, all of its coordinated activities going wrong and things shut down. If a cell gets too much heat or is poisoned by a toxic substance or exposed to chemicals that damage its proteins and membranes or radiation that breaks its DNA molecules, that cell can just stop functioning.

Necrotizing leukoencephalopathy is a form of diffuse white matter injury that can follow chemotherapy. The white matter is the covering of the nerves within the brain. Its function is to speed up the passage of impulses along the nerves.

It's the damage to this nerves that can cause the peripheral neuropathy. The peripheral nerves that carry information to and from the limbs. The nerves that supply the bowels and other internal organs. The nerves of the head which connect to the ears, eyes, taste buds, etc.

http://cancerfocus.org/forum/showthread.php?t=3439

Greg

gdpawel

bluerose said:

Thanks GD
Yes I had read that about brain necrosis but I was wondering if necrosis can happen in other spots on the body, like in the tissue of my hip? I don't know if having brain necrosis (are we talking chemo brain stuff here??) could be part of what causes the hip pain too or what you mean? I know that when radiation hits healthy cells too they can die from exposure so are we talking about that as necrosis or something more complex?

Thank you for your post. As usual you present fascinating information. I appreciate it.

Blessings,

Bluerose

BlueRose
Necrosis is simply
BlueRose

Necrosis is simply a cell dying, all of its coordinated activities going wrong and things shut down. If a cell gets too much heat or is poisoned by a toxic substance or exposed to chemicals that damage its proteins and membranes or radiation that breaks its DNA molecules, that cell can just stop functioning.

Necrotizing leukoencephalopathy is a form of diffuse white matter injury that can follow chemotherapy. The white matter is the covering of the nerves within the brain. Its function is to speed up the passage of impulses along the nerves.

It's the damage to this nerves that can cause the peripheral neuropathy. The peripheral nerves that carry information to and from the limbs. The nerves that supply the bowels and other internal organs. The nerves of the head which connect to the ears, eyes, taste buds, etc.

http://cancerfocus.org/forum/showthread.php?t=3439

Greg

bluerose

gdpawel said:

BlueRose
Necrosis is simply
BlueRose

Necrosis is simply a cell dying, all of its coordinated activities going wrong and things shut down. If a cell gets too much heat or is poisoned by a toxic substance or exposed to chemicals that damage its proteins and membranes or radiation that breaks its DNA molecules, that cell can just stop functioning.

Necrotizing leukoencephalopathy is a form of diffuse white matter injury that can follow chemotherapy. The white matter is the covering of the nerves within the brain. Its function is to speed up the passage of impulses along the nerves.

It's the damage to this nerves that can cause the peripheral neuropathy. The peripheral nerves that carry information to and from the limbs. The nerves that supply the bowels and other internal organs. The nerves of the head which connect to the ears, eyes, taste buds, etc.

http://cancerfocus.org/forum/showthread.php?t=3439

Greg

Gotcha Greg
Okay I understand now. I think that coating of the nerves is mylar sheathing, right? Spelling could be off but it's early here and I'm too tired to look it up. lol.

Thank you for your response. So informative and helpful as usual. Thanks again.

Blessings,

Bluerose