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Diabetic Neuropathy Diagnosis

Diabetic Neuropathy Diagnosis

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Published by: kijokobodro on Oct 18, 2011
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Diabetic Neuropathy Diagnosis
A doctor reaches a diabetic neuropathy diagnosis based on symptoms, aphysical exam, and certain tests. To make a definitive diabetic neuropathydiagnosis, the doctor will do a comprehensive foot exam to assess the skin,circulation, and sensation. Tests used to reach a diabetic neuropathy diagnosisinclude nerve conduction studies, electromyography (EMG), and ultrasound.
Neuropathies are characterized by a progressive loss of nerve fiber function. Awidely accepted definition of diabetic peripheral neuropathy is "the presence ofsymptoms and/or signs of peripheral nerve dysfunction in people with diabetes afterexclusion of other causes."
 Neuropathies are the most common complication of diabetes mellitus (DM), affectingup to 50% of patients with type 1 and type 2 DM. In type 1 diabetes mellitus,distal polyneuropathy typically becomes symptomatic after many years of chronicprolonged hyperglycemia. Conversely, patients with type 2 diabetes mellitus may present with distal polyneuropathy after only a few years of known poor glycemiccontrol; sometimes, these patients already have neuropathy at the time of diagnosis.(See Clinical Presentation.)Neuropathies severely decrease patients' quality of life (QOL). Furthermore, whilethe primary symptoms of neuropathy can be highly unpleasant, the secondarycomplications (eg, falls, foot ulcers,cardiac arrhythmias, and ileus) are even more serious and can lead to fractures, amputations, and even death in patients with DM.Since diabetic neuropathy can manifest with a wide variety of sensory, motor, andautonomic symptoms, a structured list of symptoms can be used to help screen alldiabetic patients for possible neuropathy (see History). Physical examination ofpatients with suspected distal sensory motor or focal (ie, entrapment ornoncompressive) neuropathies should include assessments for both peripheral andautonomic neuropathy (see Physical Examination).Multiple consensus panels recommend the inclusion of electrophysiologic testing inthe evaluation of diabetic neuropathy. An appropriate array of electrodiagnostic testsincludes both nerve conduction testing and needle EMG of the most distal musclesusually affected. (See Workup.)Management of diabetic neuropathy should begin at the initial diagnosis of diabetes.The primary care physician needs to be alert for the development of neuropathy
oreven its presence at the time of initial diabetes diagnosis
because failure todiagnose diabetic polyneuropathy can lead to serious consequences, includingdisability and amputation. In addition, the primary care physician is responsible foreducating patients about the acute and chronic complications of diabetes (seePatient Education). Patients with diabetic peripheral neuropathy require morefrequent follow-up, with particular attention to foot inspection to reinforce the need forregular self-care. (See Treatment Strategies and Management.)Management of diabetic neuropathy includes 2 approaches: therapies forsymptomatic relief and those that may slow the progression of neuropathy. Of alltreatments, tight and stable glycemic control is probably the most important for
slowing the progression of neuropathy. Many medications are available for thetreatment of diabetic neuropathic pain, although most of them are not specificallyapproved by the United States Food and Drug Administration for this use.Nonpharmacologic treatment includes rehabilitation, which may comprise physical,occupational, speech, and recreational therapy. (See Medication.)A review of the anatomy of the peripheral nervous system can facilitateunderstanding of the classification of diabetic peripheral neuropathy. Peripheralneurons can be categorized broadly as motor, sensory, or autonomic.Motor neurons originate in the central nervous system (CNS) and extend to theanterior horn of the spinal cord. From the anterior horn, they exit the spinal cord (viaventral roots) and combine with other fibers in the brachial or lumbar plexuses andinnervate their target organs through peripheral nerves.Sensory neurons originate at the dorsal root ganglia (which lie outside the spinalcord) and follow a similar course with motor neurons. Sensory neurons aresubdivided into categories according to the sensory modality they convey (see theTable below).Autonomic neurons consist of sympathetic and parasympathetic types. In theperiphery, preganglionic fibers leave the CNS and synapse on postganglionicneurons in the sympathetic chain or in sympathetic ganglia.The smaller fibers are affected first in DM. With continued exposure tohyperglycemia, the larger fibers become affected. Fibers of different size mediatedifferent types of sensation, as shown in the table below.Table. Subdivisions of Sensory Neurons (Open Table in a new window) 
Fiber Type
 A-alpha (I) 13-20 micrometers Limb proprioception YesA-beta (II) 6-12 micrometers Limb proprioception, vibration, pressure YesA-delta (III) 1-5 micrometers Mechanical sharp pain YesC (IV) 0.2-1.5 micrometers Thermal pain, mechanical burning pain No
The factors leading to the development of diabetic neuropathy are not understoodcompletely, and multiple hypotheses have been advanced.
It isgenerally accepted to be a multifactorial process. Development of symptomsdepends on many factors, such as total hyperglycemic exposure and other riskfactors such as elevated lipids, blood pressure, smoking, increased height, and highexposure to other potentially neurotoxic agents such as ethanol. Genetic factors may
also play a role.
Important contributing biochemical mechanisms in thedevelopment of the more common symmetrical forms of diabetic polyneuropathylikely include the polyol pathway, advanced glycation end products, and oxidativestress.For more information, see Type 2 Diabetes and TCF7L2. 
Polyol pathway
Hyperglycemia causes increased levels of intracellular glucose in nerves, leading tosaturation of the normal glycolytic pathway. Extra glucose is shunted into the polyolpathway and converted to sorbitol and fructose by the enzymes aldose reductaseand sorbitol dehydrogenase.
Accumulation of sorbitol and fructose lead to reducednerve myoinositol, decreased membrane Na
-ATPase activity, impaired axonaltransport, and structural breakdown of nerves, causing abnormal action potentialpropagation. This is the rationale for the use of aldose reductase inhibitors toimprove nerve conduction.
Advanced glycation end products
The nonenzymatic reaction of excess glucose with proteins, nucleotides, and lipidsresults in advanced glycation end products (ACE) that may have a role in disruptingneuronal integrity and repair mechanisms through interference with nerve cellmetabolism and axonal transport.
Oxidative stress
The increased production of free radicals in diabetes may be detrimental via severalmechanisms that are not fully understood. These include direct damage to bloodvessels leading to nerve ischemia and facilitation of AGE reactions. Despite theincomplete understanding of these processes, use of the antioxidant alpha-lipoicacid may hold promise for improving neuropathic symptoms.
Related contributing factors
Problems that are a consequence of or co-contributors to these disturbedbiochemical processes include altered gene expression with altered cellularphenotypes, changes in cell physiology relating to endoskeletal structure or cellulartransport, reduction in neurotrophins, and nerve ischemia.
Clinical trials of the best-studied neurotrophin, human recombinant nerve growth factor, were disappointing.With future refinements, however, pharmacologic intervention targeting one or moreof these mechanisms may prove successful.In the case of focal or asymmetrical diabetic neuropathy syndromes, vascular injuryor autoimmunity may play more important roles.
 Risk factors that are associated with more severe symptoms include the following
Poor glycemic control
Advanced age

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