# The Effect of Custom Insoles on Muscle Activity in Diabetic Individuals with Neuropathy
## 1 Introduction  
Diabetes is a chronic, metabolic disease affecting about 422 million people worldwide and about 1.5 million deaths are directly attributed to diabetes each year [1]. Diabetes is characterized by elevated levels of blood glucose which over time leads to serious damage to the heart, blood vessels, eyes, kidneys, and nerves [1]. Type 2 diabetes mellitus individuals are at increased risk for multiple and complexorbidities related to macrovascular disease (e.g., coronary heart disease, stroke, and peripheral arterial disease) and microvascular disease (e.g., nephropathy, retinopathy, and neuropathy) [1]. After 10 years of disease duration, up to 50% of individuals with type 2 diabetes mellitus develop diabetic peripheral neuropathy (PN), a major risk factor for diabetic foot related problems [1,2]. The second major risk factor is peripheral arterial disease, and both are extremely common in elderly patients. The estimated prevalence of peripheral arterial disease is 60.6% in individuals aged \(\geq\)70 (mean age 78 years), while the prevalence of PN can be as high as 35% in adults aged \(\geq\)80. It has been estimated that every 30 s a lower limb is lost somewhere in the world as a consequence of type 2 diabetes mellitus [3, 4, 5]. It is expected that 19 to 34% of diabetic individuals will develop an ulcer, and it is well known that ulcers precede 80% of all diabetic lower limb amputations [6]. The pathways to ulceration are similar in most cases and affect individuals with diabetes and simultaneously two or more risk factors. Within PN, sensory neuropathy results in the loss of the body's protective feedback mechanism, and motor neuropathy can affect balance and spatial awareness; while autonomic neuropathy contributes to skin becoming dry and thin andmore susceptible to damage [7]. All these dysfunctions contribute to the reduced tissue perfusion that causes a reduction in tissue oxygenation, and may result in an increased vulnerability to mechanical stresses. Furthermore, changes in the foot structure, the rigidity of the connective tissue, and the loss of foot and ankle muscle volume and strength are all recognized as being responsible for abnormal ground reaction forces during gait, the major cause of friction or pressure-related lesions (i.e., callus, corns, blisters, abrasions) [8]. On the other hand, peripheral arterial disease is a progressive disease caused by atherosclerosis that leads to the ischemia of the lower limb tissue and promotes the development of ulcers. People with diabetes have four times the risk of PAD than people without diabetes. The typical symptoms are intermittent claudication, characterized by the cramping pain in legs after short walks which results in altered spatiotemporal gait parameters such as decreased step length, cadence, and velocity [9]. Both PN and peripheral arterial disease are known to be responsible for changes in gait biomechanics and specifically for causing alterations in plantar pressure, lower limb joint kinematics, ground reaction forces, and muscle activity [8; 9; 10; 11; 12; 13; 14; 15]. Recently, physical exercise programs focused on gait training through strengthening, stretching, and balancing have shown positive results towards the prevention of foot ulcers, amputation, and fall risk [16]. However, the crucial factor in diabetic foot prevention remains the increase in pressure and shear forces, related to changes in foot structure, which produces hyperkeratosis presenting as callus. For instance, areas of plantar callus are commonly seen when the pressures relating to gait and footwear are abnormal [7]. If the pressure on the affected area of the skin and the subsequent callus that develops are not relieved (i.e., offloading and/or mechanical debridement), localized trauma to the tissues are generated [7]. Approximately 50% of diabetic foot ulcers occur on the plantar aspect of the foot and can progress into chronic and non-healing ulcers if not treated appropriately [17].