Learn how you can manage and alleviate your current side effects while actively working to prevent a relapse or secondary cancer using evidence-based, non-toxic therapies.
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Neuropathic pain caused by chemotherapy is not well studied and poorly controlled by conventional oncology. My definition of this sometimes short and/or long-term side effect is simply the tingling, numbness and burning pain in a cancer survivors hands and feet caused by chemo regimens as varied as:
Like my blood cancer, multiple myeloma, if there is no reasonably affective conventional therapy to undergo, patients and survivors will inevitably turn to anything that might help.
The four studies linked and excerpted below offer four different types of evidence-based but non-conventional therapies to try.
For one of the most complete discussion of chemotherapy-induced peripheral neuropathy and potential therapies- click now.
The two posts linked below offer additional evidence-based neuropathic pain therapies.
Are you struggling with neuropathic pain? Scroll down the page, post a question or comment and I will reply to you ASAP.
Hang in there.
“According to research results published in Pain Medicine, intravenous (IV) ketamine has shown to be an effective and safe protocol for the treatment of cancer-related neuropathic pain (CNP) in patients with refractory pain control…
According to researchers, “Each patient’s pain was identified as being secondary to direct tumor compression (n = 13), CIPN (n = 25), surgery (n = 13), or radiation (n = 6).”According to researchers, “Each patient’s pain was identified as being secondary to direct tumor compression (n = 13), CIPN (n = 25), surgery (n = 13), or radiation (n = 6)…”
Overall, 73.7% (P<0.01) of the patients were responders. While on the IV ketamine protocol, all responders reported having improvement in function and mobility. Of the 42 responders, 26.7% (P=0.0003) discontinued treatment due to unsatisfactory pain relief or adverse effects. 71.8% of the responders had pain relief for more than 3 weeks (P< 0.01)…
“Background: Chemotherapy-induced peripheral neuropathy (CIPN) is a common and dosage-limited oxaliplatin-related toxicity. To date, there are no successful interventions for CIPN prevention or treatment. A therapeutic role for cannabis in diabetic and HIV-related peripheral neuropathy and a protective role in CIPN have been suggested. We examined the effect of cannabis on oncologic patients with CIPN…
Results: In total, 513 patients met the inclusion criteria, of whom 248 were treated with cannabis and 265 served as controls. The cannabis-first group included 116 (46.7%) patients and the oxaliplatin-first group included 132 (53.3%) patients. Demographic parameters were comparable between groups.
There was a significant difference in CIPN grade 2–3 between cannabis-exposed patients and controls (15.3% and 27.9%, respectively, p < 0.001).
The protective effect of cannabis was more pronounced among cannabis-first patients compared to oxaliplatin-first patients (75% and 46.2%, respectively, p < 0.001)…
…To date, there are no conventional treatments aimed at neuroprotection or neuroregeneration in CIPN. Numerous trials have been conducted on a number of drugs, including
which are provided in attempts at neuropathy prevention, as well as
which are administered for symptomatic analgesia related to neuropathy treatment. All of these investigations, however, have yielded inconclusive evidence. The use of intravenous calcium and magnesium has also been tested for the prevention of CIPN,16 but there are no large prospective trials that show a substantial decrease in the occurrence of CIPN and specifically oxaliplatin-induced neurotoxicity by any of these measures.17…
The mechanism through which cannabis and cannabinoid products affect neuropathy and neuropathic pain is considered to be through their effect on the peripheral nervous system. The influence may be related to CB2 receptors. CB2 receptors have been identified on peripheral nerve terminals,35,36 as well as throughout the immune system.37 In animal models of tissue and nerve injury-induced nociception, CB2-selective agonists suppressed hyperalgesia and allodynia, and normalized nociceptive thresholds without inducing analgesia.
The effect of cannabis on peripheral neuron CB2 receptors is the presumed primary method of action of cannabis in the present study. The influence of cannabis on CB1 receptors is less well established in the literature in the context of CIPN, but it may have a role in the analgesic effect.38…
Conclusion: The rate of neuropathy was reduced among patients treated with cannabis and oxaliplatin. This reduction was more significant in patients who received cannabis prior to treatment with oxaliplatin, suggesting a protective effect…
“Results- Withdrawal responses to mechanical allodynia and pinch tests were significantly higher in the vitamin D3-treated group (P < 0.05). The electrophysiological analysis also supported these results. Electron microscopic evaluation revealed that the remyelinated nerve fibers in the vitamin D3-treated group (Group 3) had thick myelin sheaths and normal axonal morphology.
Conclusions-Our study demonstrated that vitamin D3 could promote functional and structural recovery in a rat model of VIPN. Further studies should be conducted to elucidate the underlying mechanisms by which vitamin D3 exerts its regenerative effects in VIPN, using alternative administration protocols…”