Nerve conduction tests may show reduced functioning of the peripheral nerves, but seldom correlate with the severity of diabetic peripheral neuropathy and are not appropriate as routine tests for the condition. Small fiber neuropathy measured by QST and Sudomotor function tests, through electrochemical skin conductance, is more and more indicated to assess early signs of diabetic neuropathy and autonomic neuropathy. Classification
Diabetic neuropathy encompasses a series of different neuropathic syndromes which can be categorized as follows:
Focal and multifocal neuropathies:
Mononeuropathy which affects one nerve
Amyotrophy or radiculopathy such as proximal diabetic neuropathy, affecting a specific pattern of nerves
Multiple lesions, affecting nerves that dont follow a specific pattern, also called "mononeuritis multiplex"
Nerve damage from entrapment (e.g. median, ulnar, peroneal)
Symmetrical neuropathies:
Sensory
Autonomic
Distal symmetrical polyneuropathy (DSPN), the diabetic type of which is also known as diabetic peripheral neuropathy (DPN) (most common presentation)

Prevention
Diabetic neuropathy can be largely prevented by maintaining blood glucose levels and lifestyle modifications. Enhanced glucose control methods include more frequent subcutaneous insulin administration, continuous insulin infusion, oral antidiabetic agents, while lifestyle modifications may include exercise alone, or in combination with dietary modifications. Enhanced glucose control prevents the development of clinical neuropathy and reduces nerve abnormalities in type 1 diabetes, and delays the onset of neuropathy in both types of diabetes. However, such methods may increase the likelihood of experiencing a hypoglycemic event, and many of these more aggressive methods require more frequent insulin use which has been associated with excessive risk of falls. Treatment
Blood glucose management
Treatment of early manifestations of sensorimotor polyneuropathy involves improving glycemic control.
Antiepileptic drugs
Multiple guidelines from medical organizations such as the American Association of Clinical Endocrinologists, American Academy of Neurology, European Federation of Neurological Societies, and the National Institute of Clinical Excellence recommend AEDs, such as pregabalin, as first-line treatment for painful diabetic neuropathy. Pregabalin is supported by low-quality evidence as more effective than placebo for reducing diabetic neuropathic pain but its effect is small. Studies have reached differing conclusions about whether gabapentin relieves pain more effectively than placebo. Available evidence is insufficient to determine if zonisamide or carbamazepine are effective for diabetic neuropathy. The first metabolite of carbamazepine, known as oxcarbazepine, appears to have a small beneficial effect on pain. A 2014 systematic review and network meta-analysis concluded topiramate, valproic acid, lacosamide, and lamotrigine are ineffective for pain from diabetic peripheral neuropathy. The most common side effects associated with AED use include sleepiness, dizziness, and nausea. Serotonin-norepinephrine reuptake inhibitors
As above, the serotonin-norepinephrine reuptake inhibitors (SNRIs) duloxetine and venlafaxine are recommended in multiple medical guidelines as first or second-line therapy for DPN. A 2017 systematic review and meta-analysis of randomized controlled trials concluded there is moderate quality evidence that  duloxetine and venlafaxine each provide a large benefit in reducing diabetic neuropathic pain. Common side effects include dizziness, nausea, and sleepiness. Tricyclic antidepressants
TCAs include imipramine, amitriptyline, desipramine, and nortriptyline. They are generally regarded as first or second-line treatment for DPN. Of the TCAs, imipramine has been the best studied. These medications are effective at decreasing painful symptoms but lead to multiple side effects that are dose-dependent.