Re: Neuropathy
 

Really taking a hit with this neuropathy. All nails are separating from nail bed & discolored. My index finger on my left hand is swollen and it hurts to relax my hand in a straight position. I'm keeping it cupped for a little relief. There is intense throbbing pain and I have been taking tylenol pm to get a little relief. But tonight I'm thinking I will pull out an old bottle of percocet. I will call my oncologist tomorrow to see what can be done. Anyone else have throbbing pain with the neuropathy?

Re: Neuropathy
 

The boots are definitely the last straw. Hopefully the neuropathy will pass with time-from your photo I can't imagine you in clogs! All the best,
Trish

Re: Neuropathy
 

Greetings all,
I finished Taxol in September '09 and still have significant neuropathy in my in my fingers and feet/toes (feels like pin and needles 24/7, and only slightly better -- I can now get on shoes, and no, they are no nearly as stylish as I wore before, but beat the flip flops I lived while I was on taxol. I have not tried any of the medication yet, preferring to adjust to a new normal, and see if I can cope with natural remedies. I have tried tonic water, and vitamin B but not much effect. I would like to try the apple cider soak, but don't know the details (how frequently; amount of vinegar to be added to water). If anyone knows this please let me know.

Thanks.

Estelle

Diagnosed 12/08
Bilateral mastectomy
Unsuccessful Tykerb Trial (could not tolorate)
Switched to Herceptin
Finished Chemo 9/09
Finished Herceptin 7/10
Candidate for Vaccine Trial

Re: Neuropathy
 

Found two recent report by researchers in Europe (underline emphasis is mine):

Nat Rev Neurol. 2011 Jan 25
Monoclonal antibody therapy – associated neurological disorders
Bosch X, Saiz A, Ramos-Casals M, the BIOGEAS Study Group
Department of Internal Medicine, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital ClÃ*nic, University of Barcelona, Villarroel 170, 08036-Barcelona, Spain
Abstract
Several neurological disorders have been associated with the use of monoclonal antibodies (mAbs), especially those targeting tumor necrosis factor (TNF) and its receptors. These disorders include, among others, multiple sclerosis, optic neuritis, and various forms of peripheral demyelinating neuropathy. Progressive multifocal leukoencephalopathy, the natural course of which is lethal within months, has been mainly associated with the anti-α4-integrin mAb natalizumab and, to a lesser extent, with rituximab, alemtuzumab and efalizumab. The prevalence of demyelinating disease induced by biological therapies, as reported in randomized controlled trials and postmarketing studies, has been estimated to range from 0.02-0.20%. Peripheral neuropathies can occur early or late after initiation of therapy. Short-term follow-up indicates relatively good outcomes, sometimes after mAb discontinuation alone, although corticosteroids or intravenous immunoglobulin may be necessary to reverse and stabilize the condition. Definitive cessation of the biological therapy should be discussed on a case-by-case basis. Prospective postmarketing studies in which the control group includes patients with rheumatic autoimmune diseases-most notably rheumatoid arthritis-treated with conventional therapies could help us to evaluate the real risks and outcomes in patients receiving mAbs who develop neurological diseases.

Curr Treat Options Neurol. 2010 Dec31
Chemotherapy-induced neuropathy
Cavaletti G, Alberti P, Frigeni B, Piatti M, Susani E.
Department of Neuroscience and Biomedical Technology, University of Milano-Bicocca, Via Cadore 48, 20052, Monza, Italy, guido.cavaletti@unimib.it.
Abstract
OPINION STATEMENT: Chemotherapy-induced peripheral neurotoxicity (CIPN) is one of the most severe and unpredictable side effects of modern anticancer treatment. In recent years, a clear understanding of the importance of an integrated approach to CIPN has become evident, and efforts are increasing to better characterize its features and to identify more accurate methods to report and grade its occurrence. The clinically relevant impact of CIPN on cancer patients has been known for a long time, but knowledge of its pathogenetic aspects is still very limited. This incomplete knowledge is one of the major limitations in identifying targets for evidence-based neuroprotective strategies. Nevertheless, several studies have been devoted to the prevention or at least the effective treatment of symptoms secondary to peripheral nerve damage and to the early identification of patients at high risk of developing severe CIPN. Unfortunately, none of these studies has been successful and the optimal management of CIPN patients is still an unmet clinical need. Therefore, the modification of chemotherapy is currently the only available approach to limit the severity of neuropathy in the vast majority of patients. The indications for treatment modification are not universally accepted and they can differ among the various drugs. Generally, treatment modification should be considered as soon as symptoms and signs impair the daily life activities of the patient, but the possibility of a delayed worsening of CIPN after treatment withdrawal ("coasting") should always be considered, and delay of modification decisions should be avoided.

Re: Neuropathy
 

Here's the information from Livestrong about how to treat it 'naturally' (Apple cider recipe included):

http://www.livestrong.com/article/74...ts-neuropathy/

Re: Neuropathy
 

My lovely onco nurse said equal parts warm water to apple cider VINEGAR.

Re: Neuropathy
 

So I developed neuropathy during TCH and was told it was from the taxotere. When I went to my appointment for my third herceptin only infusion my neuropathy was the same as it had been when I finished 9 weeks earlier. AFter the infusion within about 3 hours all my neuropathy got worse. Larger areas and has stayed that way for a week. It is the worst it has been. Does anyone have any thoughts about this??? Thanks

Re: Neuropathy
 

While doing my paper on Taxol, I came across a molecular basis for the peripheral pain from it. It appears to be caused when the drug binds to a protein and initiates improper calcium signaling, researchers at Yale School of Medicine reported in a study published in the Proceedings of the National Academy of Sciences.

This response leads to side effects such as acute hypersensitivity, slower heart rhythms, tingling, numbness, and other symptoms. These serious side effects limit the drug's effectiveness. Peripheral pain becomes worse with continued use and increased dosages lead to persistent and irreversible pain.

The binding protein is called neuronal calcium sensor (NCS-1). When paclitaxel (taxol) binds to NCS-1, it makes the cell more sensitive to normal signals and increases the magnitude and frequency of changes in calcium. Over time, increased calcium levels activate an enzyme (calpain) that degrades proteins, especially NCS-1.

Calcium signals are needed for nerves to be stimulated and to respond and the loss of NCS-1 makes it more difficult to generate any calcium signals. While the loss of NCS-1 stops the protein interaction that is causing the inappropriate calcium signals, it also decreases the ability to have normal responses (PNAS 104: 11103-11108 June 20, 2007).

Someone had asked, does the intake of calcium in your diet have any bearing on any of this? Believe it or not, the Mayo Clinic has a clinical trial going on using calcium and magnesium in preventing peripheral neuropathy caused by another Bristol-Myers Squibb drug Ixempra (ixabepilone) in patients with breast cancer (NCT00998738).

http://clinicaltrials.gov/ct2/show/NCT00998738