vitamin b6 to treat neuropathy

vitamin b6 to treat neuropathy

vitamin b6 to treat depression

Vitamin B6 To Treat Neuropathy

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If damaged myelin is at the heart of the trigeminal nerve’s short-circuiting pain, then fixing it seems to be a logical goal.  Neurosurgeons address this problem by seeking to move a blood vessel away from the area where the vessel is hitting the nerve as blood pumps through it and consequently wears down the myelin sheath. The nutritional approach encourages the body to heal injured myelin.  Because Vitamin B-12 is thought to play a role in myelin production, it is one of the most common nutrients used in trying to combat TN and neuropathic facial pain. Researchers explored Vitamin B-12 injections and pills as a TN treatment as early as the 1940s and 1950s.  In three separate studies between 1952 and 1954, more than three-quarters of the 49 patient participants got complete or marked relief from Vitamin B-12 shots given daily for 10 days.  The daily doses ranged from 100 to 1000 micrograms.  The studies do not, however, follow up to determine the length of time patients received pain relief.




When Dilantin and Tegretol became available, B-12 research was largely abandoned.  Therefore, the only recent study, from Japan, linked the methylcobalamin form of B-12 to the prevention and treatment of chronic fatigue syndrome, Parkinson’s disease, neuropathies, Alzheimer’s disease, and muscular dystrophies. The researchers suggest that high doses of methylcobalamin may help regenerate myelin and nerve cells.  Because there have been no detailed, double-blind studies of its effectiveness, there is no protocol for the use of B-12 in neuropathic facial pains like TN.The Trigeminal Neuralgia and Face Pain Handbook, references several TN patients who have reported good results from using B-12. FPA is compiling a list of patients who are willing to talk about their experiences. Nutritionist Patricia Hausman reports in her book, The Right Dose:  How to Take Vitamins and Minerals Safely, that there is little risk of taking too much B-12.  She says that Swedish doctors found no problems in patients who took single doses as high as 100,000 micrograms or in patients who took 500 to 1000 micrograms daily for three to five years. 




Nevertheless, it is always a good idea to discuss any therapy with a trusted health practitioner. The most common form of B-12 is cynocobalamin.  This is also the least expensive and is found in most drug stores.  However, nutritional experts suggest that the most effective form is methylcobalamin.  The human body does not utilize cynocobalamin and must convert cynocobalamin to methylcobalamin.  The most effective ways to utilize B-12 is by injection or by a sublingual form that is placed under the tongue until dissolved.  B-12 also is available in the form of a gel that is placed in the nasal passages.  Tablets that must be swallowed are usually distorted by stomach acid and have a very low utilization. Check with your local health food store for sublingual methylcobalamin. Injectable methylcobalamin must be made by a compounding pharmacist because it is not commonly available. Check out more resources on our Shop Page, where we have books with a lot of information. Other terms:  peripheral neuropathy, numbness and tingling.




The body's nervous system is divided into two major systems; system and the peripheral nervous system.  The peripheral nervous system is also divided into two major parts, the somatic nervous system and the autonomicThe somatic nervous system consists of peripheral nerve fibers that send sensory information to the central nervous system and motor nerve fibers that send signals to skeletal muscle.  The autonomic nervous system controls smooth muscle of the viscera (internal organs) and glands. Peripheral neuropathy results from some type of damage to the peripheral nerves. Certain chemotherapy drugs can cause peripheral neuropathy such as vinca alkaloids (vincristine), cisplatin, paclitaxel, and the podophyllotoxins (etoposide and tenoposide). Other drugs used to treat cancer such as thalidomide and interferon also can cause Individuals at greatest risk of peripheral neuropathy associated with chemotherapy are those with preexisting peripheral neuropathy from conditions such as:




Areas affected by neuropathy: Although some of the signs of neuropathy may appear suddenly, this change in sensation usually builds gradually and can worsen with each additional dose of chemotherapy. It is usually strongest right after a chemo treatment, but tends to lessen just before the next treatment.  The symptoms usually peak about 3-5 months after the last dose of treatment is taken.  The abnormal sensations may disappear completely, or lessen only partially; they may also involve less of the body. If neuropathy diminishes, it is a gradual process usually requiring several months. However, in some cases it may be irreversible and never diminish in intensity or the area of the body affected. Various techniques have been tried by patients and recommended by physicians to prevent, lessen the severity or treat chemotherapy side effects such asThere is no "one-size-fits-all" regimen that works for everyone.  Much of the treatment is based on trial and error,




and finding what combination of interventions works for the individual. Protection and Safety against Peripheral Neuropathy: Measures to relieve constipation induced by neuropathy: Control of neuropathic pain: Note: We strongly encourage you to talk with your health care professional about your specific medical condition and treatments. in this website is meant to be helpful and educational, but is not a substitute is designed to provide the latest information about chemotherapy to patients and their families, caregivers and friends. Volume 91, Issues 23–24, 10 December 2012, Pages 1187–1195Contribution of Intraneuronal Amyloid β Accumulation to Alzheimer’s DiseaseEdited By Colin Combs and Michael Nichols AimsThere is mounting evidence that use of B vitamins can help control neuropathic pain. This study investigated if treatment with B1, B6 and B12 vitamins, alone or in combination with carbamazepine, can ameliorate distinct nociceptive behaviors in a model of trigeminal neuropathic pain.




Main methodsMale Wistar rats were submitted to infraorbital nerve constriction or sham surgery and received a 5-day treatment with one of the B vitamins, a single carbamazepine injection or the association of both treatments and were tested for facial thermal and mechanical hyperalgesia at different time intervals.Key findingsRepeated treatment with B1 (thiamine), B6 (pyridoxine) and B12 (cyanocobalamin) vitamins (at 180, 180 and 18 mg/kg/day, respectively, for 5 days) prevented the development of heat hyperalgesia after infraorbital nerve injury, but only B12 and B6 treatments attenuated cold and mechanical hyperalgesia, respectively. A single injection of carbamazepine (30 mg/kg) significantly reduced thermal, but not mechanical, hyperalgesia after nerve injury. Combinations of lower doses of each B vitamin (B1 and B6 at 18 mg/kg/day and B12 at 1.8 mg/kg/day for 5 days) with carbamazepine (10 mg/kg) markedly reduced heat hyperalgesia after infraorbital nerve injury. Treatment with B12 (1.8 mg/kg/day) combined with carbamazepine (10 mg/kg) also synergized to attenuate cold hyperalgesia at some time points, but combination of B6 (18 mg/kg/day) with carbamazepine (30 mg/kg) failed to modify mechanical hyperalgesia.




SignificanceWe suggest that B vitamins might constitute a relevant adjuvant to control some aspects of the pain afflicting patients suffering from trigeminal neuropathic pain.Chronic neuropathic pain caused by lesions in the peripheral or central nervous system comes in various forms which are still difficult to control and treat. Trigeminal neuralgia, continues to represent a therapeutic challenge as its pathophysiology is not yet fully understood (Adams, 1989; Alves et al., 2004; Chichorro et al., 2006a; Chichorro et al., 2006b; Cuellar et al., 2010; Eide and Rabben, 1998; Fisher et al., 2003; Kleef et al., 2009; Sindrup and Jensen, 2002 ;  Currently, anticonvulsant drugs are commonly used to control symptoms in neuropathic pain, especially for their ability to reduce neuronal excitability by acting through different mechanisms (Attal et al., 2010; Delzell and Grelle, 1999; Finnerup et al., 2010a; Finnerup et al., 2010b; Gill et al., 2011; Martin and Forouzanfar, 2011; Zakrzewska and McMillan, 2011).




The most studied agents are carbamazepine, gabapentin and pregabalin, but lamotrigine, topiramate and oxcarbazepine have also shown analgesic potential in different pain models and in clinical studies (Ambrósio et al., 2002; Cheng and Chiou, 2006; Czapinski et al., 2005; Lynch and Watson, 2006; Siniscalchi et al., 2011 ;  Wilhelmus and Forouzanfar, 2011). Indeed, carbamazepine is currently the first choice for treatment of trigeminal neuralgia, as it has been shown to reduce pain symptoms in about 70% of the cases, and it is also used to diagnose the condition (Ambrósio et al., 2002 ;  Kleef et al., 2009). However, continuous treatment with carbamazepine or other anticonvulsant drugs results in numerous adverse effects such as drowsiness, dizziness, ataxia, diplopia, blurred vision, nausea, dry mouth, constipation and diarrhea (Alves et al., 2004; Attal et al., 2010 ;  Zakrzewska and Patsalos, 1992). In addition, many patients submitted to repeated carbamazepine treatment become refractory to the medication (Attal et al., 2010;




Thus, additional therapeutic options are in high demand (Boto, 2010; Zakrzewska et al., 2005a ;  Zakrzewska et al., 2005b).Thiamine, pyridoxine and cyanocobalamin (i.e. B1, B6 and B12 vitamins) are the major vitamins of B complex. They act mainly as coenzymes of different reactions, participating importantly in the metabolism of carbohydrates, proteins and lipids. They also play an important role in the formation of new cells, DNA, RNA and myelin (Dakshinamurti et al., 2003; Depeint et al., 2006a; Depeint et al., 2006b; Healton et al., 1991; McCombe and McLeod, 1984 ;  Selhub et al., 2010). According to some studies, B vitamins present neuroprotective effects, which are suggested to be related to their analgesic action in various models of neuropathic pain (Jolivalt et al., 2009; Mixcoatl-Zecuatl et al., 2008; Reyes-Garcia et al., 2004; Wang et al., 2005 ;  Zimmerman et al., 1990). However, to the best of our knowledge, the influence of the vitamins of B complex on orofacial pain has never been investigated.




Thus, the present study aimed to evaluate the influence of the administration of B1, B6 and B12 vitamins of the B complex, either delivered alone or combined with carbamazepine treatment, in thermal and mechanical hyperalgesia in a model of trigeminal neuropathic pain induced in rats by constriction of the infraorbital nerve.Experiments were conducted on male Wistar rats weighing 180–220 g, maintained five to a cage at controlled temperature (22 ± 1 °C) under a 12/12 h light/dark cycle (lights on at 08:00 h) with free access to chow and tap water. They were acclimatized to the laboratory for at least 48 h before use. The experimental procedures were previously approved by UFPR's institutional Committee on the Ethical Use of Animals (authorization # 471), where the study was carried out, and conducted in accordance with the ethical guidelines of the International Association for the Study of Pain (Zimmermann, 1983) and Brazilian regulations on animal welfare. All efforts were made to minimize the number of animals used and their suffering.




The constriction of the infraorbital nerve (CION) was performed according to the slight modification of the procedure originally proposed by Vos et al. (1994) described by Chichorro et al. (2006a). Briefly, rats were anesthetized with an intraperitoneal (i.p.) injection of a mixture of ketamine and xylazine (50 and 10 mg/kg, respectively) and an incision was made in the skin of the snout, under the right eye, about 3 mm caudal to the mystacial pads. The superior lip elevator and anterior superficial masseter muscles were bluntly dissected to expose the rostral end of the infraorbital nerve, as it emerged from the infraorbital fissure. Special care was taken to not damage the facial nerve. Two silk 4‐0 ligatures were then tied loosely and 2 mm apart around the infraorbital nerve and the wound was closed with additional silk sutures (4‐0). Sham-operated rats were treated identically, but no ligatures were applied to the infraorbital nerve. After surgery, all rats were maintained in a warm room until they recovered from anesthesia.




Before each testing session, animals were placed in individual plastic observation cages and left to adapt to the environment for at least 30 min. After this period, they usually displayed considerable sniffing, but very little locomotor activity. Cold stimulation was applied by the experimenter in the form of a brief 1-s spray of tetrafluoroethane to the center of the right vibrissal pads, while gently restraining the animal in its cage by placing one hand around its trunk. The total duration of bilateral facial grooming behavior with both forepaws directed to the snout was recorded, using a stopwatch, over the first 2 min following application of the cold stimulus, as an index of the intensity of nocifensive responsiveness. In rats subjected to CION, cold responsiveness was evaluated before and on days 2, 4, 6, 9 and 12 after surgery. It is important to point out that cold hyperalgesia peaks on days 4 to 6 after CION surgery, as previously reported by our group (Chichorro et al., 2006a).

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