Diabetic Neuropathies

Abstract

Objective: This article provides an up-to-date review of the diagnosis and management of the most common neuropathies that occur in patients with diabetes.

Latest developments: The prevalence of diabetes continues to grow worldwide and, as a result, the burden of diabetic neuropathies is also increasing. Most diabetic neuropathies are caused by hyperglycemic effects on small and large fiber nerves, and glycemic control in individuals with type 1 diabetes reduces neuropathy prevalence. However, among people with type 2 diabetes, additional factors, particularly metabolic syndrome components, play a role and should be addressed. Although length-dependent distal symmetric polyneuropathy is the most common form of neuropathy, autonomic syndromes, particularly cardiovascular autonomic neuropathy, are associated with increased mortality, whereas lumbosacral radiculoplexus neuropathy and treatment-induced neuropathy cause substantial morbidity. Recent evidence-based guidelines have updated the recommended treatment options to manage pain associated with distal symmetric polyneuropathy of diabetes.

Essential points: Identifying and appropriately diagnosing the neuropathies of diabetes is key to preventing progression. Until better disease-modifying therapies are identified, management remains focused on diabetes and metabolic risk factor control and pain management.

Figure 1:

Graphs for two separate patients depicting heart rate response to deep breathing – (A) is for the patient in Case 2, compared to (B) a normal study. This test is an assessment of parasympathetic cardiovagal function. The heart rate increases at the end of inspiration and decreases at the end of expiration. The R-R interval is the distance in milliseconds between successive QRS complexes on a single-lead ECG tracing. A graph of the R-R interval versus time should have a clear sinusoidal shape that mimics the patient’s respiratory rate, as seen in (B), when parasympathetic cardiovagal function is intact. This response is blunted in the patient from Case 2 as seen in (A).

Figure 2:

Nerve conduction studies show decreased CMAPs in the left tibial and peroneal motor nerves as well as an absent sural sensory response. There is increased positive sharpwaves and fibrillations in muscles in the left leg with absent voluntary motor unit action potentials in muscles innervated by the peroneal, tibial, obturator, and femoral nerves. There is asymmetry between the sides. These findings are typical for diabetic lumbosacral radiculoplexus neuropathy.

Figure 3:

MRI without contrast of the pelvis in a patient with asymmetric leg weakness. Asymmetric increased T2 signal and thickening of the left lumbosacral plexus coronal STIR image (A) and thickening of the left femoral nerve on the axial FLAIR (B). In the appropriate clinical context, these findings are consistent with a diagnosis of diabetic lumbosacral radiculoplexus neuropathy.