[Causes, spectrum, and treatment of the diabetic neuropathy]

Half of all diabetics are affected by a diabetic neuropathy. Microangiopathy, dysfunctional Schwann cell interactions, accumulation of toxic metabolites, and inflammatory processes all contribute to nerve damage.

Overview and perspectives of the pathophysiology as well as the current and future treatment implications.

Literature search (1990-2020).

Clinically predominant are sensory and autonomic symptoms; however, muscle weakness can occur as well. Complications such as unrecognized myocardial infarctions and the diabetic foot syndrome are potentially life-threatening and can cause major disability. The pathophysiology of neuropathies in type 1 and type 2 diabetes mellitus differs due to additional risk factors of the metabolic syndrome. To reduce the risk of neuropathy, an intensive insulin therapy is superior compared to the conventional insulin therapy. Oral antidiabetic drugs should be chosen based on individual risk profiles. Metformin can cause an iatrogenic vitamin B12 deficiency. In the treatment of neuropathic pain, the calcium channel blocker pregabalin has the highest recommendation level. The tricyclic antidepressant amitriptyline is considered to be equally effective, but it is contraindicated in autonomic dysregulation and cognitive impairment. Alternatively, the serotonin-norepinephrine reuptake inhibitor duloxetine is approved for the symptomatic treatment of diabetic neuropathies. Controversially discussed medications include alpha-lipoic acid, epalrestat, and L‑serine.

The diabetic neuropathy is frequent and causes severe complications. A good understanding of the underlying pathophysiology can contribute to the development of novel treatment strategies in the future.