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Year : 2006  |  Volume : 54  |  Issue : 2  |  Page : 177

Invited Comments

Helsinki University Central Hospital, Helsinki, Finland

Correspondence Address:
Perttu Arkkila
Helsinki University Central Hospital, Helsinki
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Source of Support: None, Conflict of Interest: None

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How to cite this article:
Arkkila P. Invited Comments. Neurol India 2006;54:177

How to cite this URL:
Arkkila P. Invited Comments. Neurol India [serial online] 2006 [cited 2022 Aug 10];54:177. Available from: https://www.neurologyindia.com/text.asp?2006/54/2/177/25967

Diabetic peripheral neuropathy is a common complication of diabetes that can cause functional disturbance and clinical morbidity. It is usually characterized by an insidious onset and symmetrical distribution. Sensory features of reduced or absent sensation and altered or painful sensation are present. Mechanisms that may lead to the development of diabetic neuropathy include oxidative stress, sorbitol accumulation (advanced glycation end products), polyol pathway flux and protein kinase C.[1] All these contribute to microvascular disease and nerve dysfunction. Hyperglycemia is considered to be the primary risk factor for diabetic neuropathy which emphasizes the importance of good glycemic control in preventing the development of diabetic neuropathy.

The attempts to treat diabetic neuropathy by manipulating the underlying metabolic pathways have not produced significant symptomatic relief. Symptomatic treatment is generally the only useful measure. Pain relief has been achieved by different medications including tricyclic drugs, different anticonvulsants, tramadol, mexiletine or capsaicin used in topical ointments. Increasing experience has been gained. Also non-steroidal anti-inflammatory drugs, opioid analesics and new anti-depressant drugs have been used as adjuvant agents.

In recent years, several new-generation antiepileptic drugs such as gabapentin and pregabalin have been introduced in clinical practice and they have been shown to be quite effective and well tolerated in the treatment of diabetic neuropathy. New approaches to therapy are still needed, because many patients do not achieve good enough pain relief or they suffer side effects preventing the long term use of the previous drugs. Oxcarbazepine is a second-generation antiepileptic drug, which has been shown to be effective in managing partial epileptic seizures. It has also been shown to have fewer side effects than carbamazepine. Animal studies and two human studies have suggested that oxcarbazepine monotherapy, may be efficacious and may provide clinically meaningful pain relief in diabetic patients with neuropathic pain.[1],[2],[3]

The results of the study published at this journal also shows that oxcarbazepine administered as monotherapy is an efficacious and safe option for the symptomatic treatment of pain associated with symmetrical diabetic neuropathy. Moreover, social interference including general activity, mood, walk, work, people relations, sleep and life enjoyment were improved by the use of oxcarbazepine. None of the patients had prominent side effects. Although these results will need to be confirmed in double-blind, placebo-controlled, randomized clinical trials, oxcarbazepine seem to be very promising new symptomatic treatment for diabetic neuropathy[4].

  References Top

1.Duby JJ, Campbell RK, Setter SM, White JR, Rasmussen KA. Diabetic neuropathy: an intensive review. Am J Health Syst Pharm 2004;61:160-73.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Dogra S, Beydoun S, Mazzola J, Hopwood M, Wan Y. Oxcarbazepine in painful diabetic neuropathy: a randomized, placebo-controlled study. Eur J Pain 2005;9:543-54.   Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Beydoun A, Kobetz SA, Carrazana EJ. Efficacy of oxcarbazepine in the treatment of painful diabetic neuropathy. Clin J Pain 2004;20:174-8.   Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Kiguchi S, Imamura T, Ichikawa K, Kojima M. Oxcarbazepine antinociception in animals with inflammatory pain or painful diabetic neuropathy. Clin Exp Pharmacol Physiol 2004;31:57-64.  Back to cited text no. 4  [PUBMED]  


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