Detecting and treating the protean manifestations of diabetic autonomic neuropathy

Abstract

The manifestations of diabetic autonomic neuropathy (DAN) are protean and clinically involve multiple systems, including the cardiovascular system, the gastrointestinal system, the genitourinary system as well as the sweat glands (sudomotor dysfunction) and the gallbladder. In addition, cardiac autonomic neuropathy (CAN) is associated with a correctible inability to appreciate and correct hypoglycaemia. While not a clinical problem, pupillary involvement should be the clue and the catalyst to investigate for other manifestations of DAN. This review outlines a practical approach to detecting and investigating the manifestations of DAN. Of particular importance is early detection of cardiovascular involvement where prompt therapy through glycaemic control can decrease the severity of CAN and decelerate the frequency and severity of retinopathy and nephropathy in addition to decreasing cardiovascular events and mortality. CAN also plays a role in accelerating other diabetic complications such as acute ischaemic stroke, heart failure, medial artery calcinosis, foot ulcers, peripheral artery disease and Charcot joints. Many therapies of DAN are available, which should not only decrease morbidity and mortality from DAN, but also improve the patient's quality of life. However, the therapies available are largely symptomatic.

Relationship Between Index of Cardiac Electrophysiological Balance, Frontal QRS-T Angle and Retinopathy in People with Type 2 Diabetes

“… 40 The presence of diabetic autonomic neuropathy accelerates or worsens DR, with impaired haemodynamics/autoregulation and abnormal parasympathetic/sympathetic balance due to diabetic autonomic neuropathy. 42 Previous studies have also found that the QTc interval and QRS-T angle are associated with diabetic autonomic neuropathy. 41 , 43 However, there is also evidence of autonomic dysregulation in prediabetes, especially involving the cardiovascular system.…”

“… 44 Loss of the parasympathetic vagus nerve leads to sympathetic overactivity which, in turn, may lead to arrhythmias by prolonging the QT interval. 42 …”

“…44 Loss of the parasympathetic vagus nerve leads to sympathetic overactivity which, in turn, may lead to arrhythmias by prolonging the QT interval. 42 At present, the pathogenesis of DR is unclear and the mechanism of abnormalities in myocardial repolarization parameters and the electrophysiological balance index is still unclear. The correlations between these parameters and DR may reflect a common or similar pathogenesis.…”

Neurologic Complications of Endocrine Disorders

“…Over time, anesthesia develops seemingly paradoxically alongside neuropathic pain (anesthesia dolorosa) and impairs not only superficial sensory modalities (pain and temperature sensation) but also deeper ones, including proprioception, leading to gait unsteadiness. In severe cases, a generalized autonomic neuropathy develops, leading to urinary urgency, bowel hypomotility, erectile dysfunction, impaired cardiovagal reflexes (leading to orthostatic intolerance), and, in the most extreme cases, impaired pupillary responses 73 …”

The Role of Insulin-like Growth Factor 1, Pro-neurotensin and 25-Hydroxy Vitamin D3 in Type 2 Diabetes Mellitus: Metabolic and Pathophysiological links

“…In 2013, 8.3% of people were affected with diabetes worldwide (International Diabetes Federation, 2013). T2DM has a long asymptomatic pre-clinical phase during which time, 20-30% of patients develop complications such as retinopathy, cardiovascular disease, neuropathy, and nephropathy (Sinnott et al, 2015;Bell, 2023). Therefore, early detection followed by lifestyle modification and/or pharmacotherapy can delay or arrest disease progression (Knowler, 2002; American diabetes association, 2009).…”