Case Studies In Painful Diabetic Neuropathy
Approximately 800,000 new cases of diabetes mellitus are diagnosed each year. The disease affects over 18 million people, approximately 6 percent of the population of the United States.1 Type 2 diabetes, which is typically not diagnosed in patients under age 45, is overwhelmingly the most prevalent of all types of diabetes as it affects nearly 17 million Americans.1 Symptoms of Type 2 diabetes are often not detected until they are severe or until patients seek treatment for related complications.2 Diabetes complications can result in blindness, end-stage renal disease, stroke, heart disease and neuropathy.2
Diabetic peripheral neuropathy (DPN) is the most common and debilitating complication of diabetes mellitus. It affects up to 62 percent of Americans with diabetes and is one of the most commonly encountered neuropathic pain syndromes in clinical practice.3 According to both the American Diabetes Association and the National Institute of Diabetes and Digestive and Kidney Disease (NIDDK), about 60 to 70 percent of the 18.2 million Americans with diabetes will develop some form of diabetic neuropathy and about 3 million people with diabetes will experience painful neuropathy.
Diabetic neuropathy has three broad types of manifestations: sensory, motor and autonomic. The most prevalent form is somatic or sensorimotor neuropathy, which is often simply referred to as diabetic neuropathy. Symptoms often exhibit a distal symmetric pattern, beginning distally at the base of the toes and ascending proximally up the lower leg as the disease progresses. These symptoms are often described as burning, tingling, stabbing and a pins-and-needles sensation in a stocking and glove distribution. Patients may also display muscle weakness, incoordination and ataxia. The paresthesias often result in the loss of pain perception. This loss of protective sensation can lead to the formation of foot ulcerations, infections, even amputations, and cause significant morbidity and mortality.
Despite being the focus of current research, the sequence of physiological events that result in this debilitating condition is poorly understood. The pathogenesis of DPN is believed to be multifactorial with hyperglycemia being the primary risk factor.4,5 Suggested theories that postulate the etiopathogeny of diabetic neuropathy include abnormalities of protein glycation, sorbitol accumulation, polyol pathway flux, protein kinase C activation, advanced glycation endproducts (AGE), receptor for advanced glycation endproducts (RAGE), a decrease in neuronal nitric oxide synthase (nNOS) protein, and microvascular hypoxia, resulting in oxidative stress.5-11
Diabetic peripheral neuropathy is a significant public health issue that is often associated with negative physical, psychological and social sequelae.12,13 Pain perception and interpretation is further complicated by cognitive, cultural and environmental interaction on the quality of patient life.14 The association between neuropathic pain and decreased quality of life (QoL) in people with DPN is well documented.15,16
In one study, patients with painful DPN reported greater sleep interference in comparison with the general U.S. population, and significant impairment in both physical and mental functioning compared to diabetic people without neuropathy.17 Researchers have shown that painful diabetic neuropathy (>or=4 on 0-10 scales) not only interferes with activities of daily living (ADLs) but substantially affects patients’ moods and their enjoyment of life.17,18 Patients reported moderate ADL interference despite 91 percent of them using prescription medications for painful DPN.18 Moreover, 43 percent of the patients in this study reported concurrent use of prescription medication for anxiety, depression or sleep disturbance while disruption in employment was reported by 35 percent of the patients.18