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Sign Up It''overview''clinical''workup''treatment''medication'' quality of life (QOL). Furthermore, while the primary symptoms of neuropathy can be highly unpleasant, the secondary complications (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.

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Multiple consensus panels recommend the inclusion of electrophysiologic testing in the evaluation of diabetic neuropathy. An appropriate array of electrodiagnostic tests includes both nerve conduction testing and needle EMG of the most distal muscles usually 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—or even its presence at the time of initial diabetes diagnosis—because failure to diagnose diabetic polyneuropathy can lead to serious consequences, including disability and amputation. In addition, the primary care physician is responsible for educating patients about the acute and chronic complications of diabetes (see Patient Education). Patients with diabetic peripheral neuropathy require more frequent follow-up, with particular attention to foot inspection to reinforce the need for regular self-care. (See Treatment Strategies and Management.)

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Anatomy

A review of the anatomy of the peripheral nervous system can facilitate understanding of the classification of diabetic peripheral neuropathy. Peripheral neurons can be categorized broadly as motor, sensory, or autonomic.

Motor neurons originate in the central nervous system (CNS) and extend to the anterior horn of the spinal cord. From the anterior horn, they exit the spinal cord (via ventral roots) and combine with other fibers in the brachial or lumbar plexuses and innervate their target organs through peripheral nerves.

Sensory neurons originate at the dorsal root ganglia (which lie outside the spinal cord) and follow a similar course with motor neurons. Sensory neurons are subdivided into categories according to the sensory modality they convey (see the Table below).

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The smaller fibers are affected first in DM. With continued exposure to hyperglycemia, the larger fibers become affected. Fibers of different size mediate different types of sensation, as shown in the table below.

Table. Subdivisions of Sensory Neurons (Open Table in a new window)

Fiber Type

Size

Modality

Myelination

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13-20 micrometers

Limb proprioception

Yes

A-beta (II)

6-12 for 1 last update 06 Jun 2020 micrometers6-12 micrometers

Limb the 1 last update 06 Jun 2020 proprioception, vibration, pressureLimb proprioception, vibration, pressure

Yes

A-delta (III)

1-5 micrometers

Mechanical sharp pain

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C (IV)

0.2-1.5 the 1 last update 06 Jun 2020 micrometers0.2-1.5 micrometers

Thermal pain, mechanical burning pain

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Pathophysiology

The factors leading to the development of diabetic neuropathy are not understood completely, and multiple hypotheses have been advanced. [4, 5, 6, 7, 8, 9, 10, 11, 12, 13] It is generally accepted to be a multifactorial process. Development of symptoms depends on many factors, such as total hyperglycemic exposure and other risk factors such as elevated lipids, blood pressure, smoking, increased height, and high exposure to other potentially neurotoxic agents such as ethanol. Genetic factors may also play a role. [14] Important contributing biochemical mechanisms in the development of the more common symmetrical forms of diabetic polyneuropathy likely include the polyol pathway, advanced glycation end products, and oxidative stress.

For more information, see Type 2 Diabetes and TCF7L2.

Polyol pathway

Hyperglycemia causes increased levels of intracellular glucose in nerves, leading to saturation of the normal glycolytic pathway. Extra glucose is shunted into the polyol pathway and converted to sorbitol and fructose by the enzymes aldose reductase and sorbitol dehydrogenase. [15] Accumulation of sorbitol and fructose lead to reduced nerve myoinositol, decreased membrane Na+/K+ -ATPase activity, impaired axonal transport, and structural breakdown of nerves, causing abnormal action potential propagation. This is the rationale for the use of aldose reductase inhibitors to improve nerve conduction. [16]

Advanced glycation end products

The nonenzymatic reaction of excess glucose with proteins, nucleotides, and lipids results in advanced glycation end products (AGEs) that may have a role in disrupting neuronal integrity and repair mechanisms through interference with nerve cell metabolism and axonal transport. [17]

Oxidative stress

The increased production of free radicals in diabetes may be detrimental via several mechanisms that are not fully understood. These include direct damage to blood vessels leading to nerve ischemia and facilitation of AGE reactions. Despite the incomplete understanding of these processes, use of the antioxidant alpha-lipoic acid may hold promise for improving neuropathic symptoms. [18, 19, 20]

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Problems the 1 last update 06 Jun 2020 that are a consequence of or co-contributors to these disturbed biochemical processes include altered gene expression with altered cellular phenotypes, changes in cell physiology relating to endoskeletal structure or cellular transport, reduction in neurotrophins, and nerve ischemia. [21] Clinical trials of the best-studied neurotrophin, human recombinant nerve growth factor, were disappointing. With future refinements, however, pharmacologic intervention targeting one or more of these mechanisms may prove successful.Problems that are a consequence of or co-contributors to these disturbed biochemical processes include altered gene expression with altered cellular phenotypes, changes in cell physiology relating to endoskeletal structure or cellular transport, reduction in neurotrophins, and nerve ischemia. [21] Clinical trials of the best-studied neurotrophin, human recombinant nerve growth factor, were disappointing. With future refinements, however, pharmacologic intervention targeting one or more of these mechanisms may prove successful.

In the case of focal or asymmetrical diabetic neuropathy syndromes, vascular injury or autoimmunity may play more important roles. [22]

A cross-sectional, case-control study by Gastoł et al indicated that in patients with type 1 diabetes mellitus (DM), epigenetic factors are involved in the development of autonomic neuropathy. T1DM patients with autonomic neuropathy showed differences in gene methylation compared with T1DM patients without neuropathy. For example, in the NINJ2 gene, which is involved in nerve regeneration, patients with autonomic neuropathy had significantly greater methylation in the first axon than did the other patients with type 1. In addition, two genes involved in nerve functionality, BRSK2 and CLDN4, showed decreased methylation (in the region of the first intron of BRSK2 and the 5’UTR regions of CLDN4) in the patients with neuropathy. [23]

A study by Groener et al of sciatic nerve lesions in diabetic polyneuropathy indicated that lesion load positively correlates with the duration of diabetes, attaining clinical relevance “once a critical amount of nerve fascicles is affected.” [24]

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Etiology

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  • Poor glycemic control

  • Advanced for 1 last update 06 Jun 2020 ageAdvanced age

  • Hypertension

  • Long duration of DM

  • Dyslipidemia

  • Smoking

  • Heavy alcohol intake

  • HLA-DR3/4 phenotype

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Development of symptoms depends on many factors, such as total hyperglycemic exposure and other risk factors such as elevated lipids, blood pressure, smoking, increased height, and high exposure to other potentially neurotoxic agents such as ethanol. Genetic factors may also play a role. [14]

Peripheral neuropathies have been described in patients with primary DM (types 1 and 2) and in those with secondary diabetes of diverse causes, suggesting a common etiologic mechanism based on chronic hyperglycemia. The contribution of hyperglycemia has received strong support from the Diabetes Control and Complications Trial (DCCT). [26]

An association between impaired glucose tolerance and peripheral neuropathy has been construed as further evidence of a dose-dependent effect of hyperglycemia on nerves, although this relationship remains an area of some controversy for type 2 diabetes and prediabetes. [27, 28, 29, 30]

A study by Jende et al indicated that in patients with type 1 diabetes, the predominant nerve lesions of distal symmetrical diabetic neuropathy develop in relation to poor glycemic control and nerve conduction loss, while in type for 1 last update 06 Jun 2020 2 diabetes, these lesions arise in association with lipid metabolism changes. [31] A study by Jende et al indicated that in patients with type 1 diabetes, the predominant nerve lesions of distal symmetrical diabetic neuropathy develop in relation to poor glycemic control and nerve conduction loss, while in type 2 diabetes, these lesions arise in association with lipid metabolism changes. [31]

A study by Pai et al indicated that in adults with type 2 diabetes, an association exists between variability in fasting plasma glucose and the risk for painful diabetic peripheral neuropathy. Using the coefficient of variation (CV) for fasting plasma glucose, the investigators found that, after consideration of HbA1c, the odds ratios for the development of painful diabetic peripheral neuropathy were 4.08 and 5.49 for the third and fourth CV quartiles, respectively, compared with the first quartile. [32]

A study by Altaf et al indicated that obstructive sleep apnea (OSA) is linked to small-fiber neuropathy in type 2 diabetes, with poly–adenosine diphosphate ribose polymerase activation being a possible mechanism behind OSA’s association with diabetic peripheral neuropathy and endothelial dysfunction. [33]

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Epidemiology

United States statistics

A large American study estimated that 47% of patients with diabetes have some peripheral neuropathy. [35] Neuropathy is estimated to be present in 7.5% of patients at the time of diabetes diagnosis. More than half of cases are distal symmetric polyneuropathy. Focal syndromes such as carpal tunnel syndrome (14-30%), [36, 37, 38] radiculopathies/plexopathies, and cranial neuropathies account for the rest. Solid prevalence data for the latter 2 less-common syndromes is lacking.

The wide variability in symmetric diabetic polyneuropathy prevalence data is due to lack of consistent criteria for diagnosis, variable methods of selecting patients for study, and differing assessment techniques. In addition, because many patients with diabetic polyneuropathy are initially asymptomatic, detection is extremely dependent on careful neurologic examination by the primary care clinician. The use of additional diagnostic techniques, such as autonomic or quantitative sensory testing, might result in a higher recorded prevalence. [39, 40]

International statistics

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Diabetic neuropathy in racial minorities

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DM affects men and women with equal frequency. However, male patients with type 2 diabetes may develop diabetic polyneuropathy earlier than female the 1 last update 06 Jun 2020 patients, [44] and neuropathic pain causes more morbidity in females than in males.DM affects men and women with equal frequency. However, male patients with type 2 diabetes may develop diabetic polyneuropathy earlier than female patients, [44] and neuropathic pain causes more morbidity in females than in males.

Diabetic neuropathy and advancing age

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Prognosis

Patients with untreated or inadequately treated diabetes have higher morbidity and complication rates related to neuropathy than patients with tightly controlled diabetes. Repetitive trauma to affected areas may cause skin breakdown, progressive ulceration, and infection. Amputations and death may result.

Treating diabetic neuropathy is a difficult task for the physician and patient. Most of the medicines mentioned in the Medication section do not lead to complete symptom relief. Clinical trials are under way to help find new ways to treat symptoms and delay disease progression.

Mortality is higher in people with cardiovascular autonomic neuropathy (CAN). The overall mortality rate over periods up to 10 years was 27% in patients with DM and CAN detected, compared with a 5% mortality rate in those without evidence of CAN. Morbidity results from foot ulceration and lower-extremity amputation. These 2 complications are the most common causes of hospitalization among people with DM in Western countries. Severe pain, dizziness, diarrhea, and impotence are common symptoms that decrease the QOL of a patient with DM. In patients with diabetic peripheral neuropathy, the prognosis is good, but the patient''s regular physician is reasonable before the initiation of a regular exercise program.

Patients with diabetic neuropathy need to be educated on all aspects of their condition, and they need to know that it is very much affected by poor glycemic control. Prevention of diabetic neuropathy is potentially best achieved by having near-euglycemic control from the onset of DM. Even in patients with symptoms of diabetic neuropathy, controlling blood glucose to euglycemic levels reduces pain significantly. When a person has poor control and becomes euglycemic quickly, pain may be exacerbated (possibly due to an insulin effect), but this pain disappears in a few days. The bottom line for patients is that medications are imperfect. Many result in no pain relief for certain patients. However, glucose control is something that the patient can achieve that may reduce pain.

The importance of protection and care of insensitive feet cannot be overemphasized. Patients should be instructed to trim their toenails with great care and to be fastidious about foot hygiene. Any fungal or bacterial infection mandates prompt medical attention. The need for well-fitting shoes should be stressed.

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Patient education should begin in the primary care office. The following outline reviews some common questions and answers that can serve as a springboard for discussion.

What is diabetic neuropathy?

Diabetic neuropathy is nerve damage caused by diabetes. In the United States, diabetes is one of the most common causes of nerve damage, also known as peripheral neuropathy. Diabetic neuropathy can affect nerves that supply feeling and movement in the arms and legs. It can also affect the nerves that regulate unconscious vital functions such as heart rate and digestion.

How does diabetic neuropathy occur?

Doctors have been studying this problem for many years, but they do not yet understand exactly how diabetes damages nerves. However, they have observed that good control of blood sugar levels helps prevent diabetic neuropathy and slows its progression, especially in patients with type 1 diabetes.

What are the symptoms?

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  • Numbness or loss of feeling (usually in the feet and legs first, then the hands)

  • Pain

  • Muscle weakness

  • Low blood pressure and dizziness when rising quickly from sitting or lying down

  • Rapid or irregular heartbeats

  • Trouble having an erection

  • Nausea or vomiting

  • Difficulty swallowing

  • Constipation or diarrhea

Pain from diabetic neuropathy may range from minor discomfort or tingling in toes to severe pain. Pain may be sharp or lightning-like, deep and aching, or burning. Extreme sensitivity to the slightest touch can also occur (allodynia).

A study by D’Amato et al indicated that among diabetes-related complications and comorbidities, painful diabetic polyneuropathy is the greatest determinant of depression in patients with diabetes. The study involved 181 patients, including 25 with painful diabetic polyneuropathy and 46 with the painless form of the condition. [46]

How can I help prevent diabetic neuropathy?

The following steps may help to prevent or slow the worsening of diabetic neuropathy [47] :

 
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Media Gallery
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Tables
Table. Subdivisions of Sensory Neurons

Fiber for 1 last update 06 Jun 2020 Type Fiber Type

Size

Modality

Myelination

A-alpha (I)

13-20 micrometers

Limb proprioception

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A-beta (II)

6-12 micrometers

Limb proprioception, vibration, pressure

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A-delta (III)

1-5 micrometers

Mechanical sharp pain

Yes

for 1 last update 06 Jun 2020 C (IV)C (IV)

0.2-1.5 micrometers

Thermal pain, mechanical burning pain

No

Contributor Information and Disclosures
Author

Dianna Quan, MD Professor of Neurology, Director of Electromyography Laboratory, University of Colorado School of Medicine

Dianna Quan, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Neurological Association

Disclosure: Received research grant from: Alnylam; Pfizer; Cytokinetics; Momenta.

Coauthor(s)

Helen C Lin, MD Assistant Professor of Neurology, Medical College of Wisconsin

Helen C Lin, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Acknowledgements

Neil A Busis, MD Chief, Division of Neurology, Department of Medicine, Head, Clinical Neurophysiology Laboratory, University of Pittsburgh Medical Center-Shadyside

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Disclosure: Nothing to disclose.

Milind J Kothari, DO Professor and Vice-Chair, Department of Neurology, Pennsylvania State University College of Medicine; Consulting Staff, Department of Neurology, Penn State Milton S Hershey Medical Center

Milind J Kothari, DO is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and American Neurological Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska the 1 last update 06 Jun 2020 Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug ReferenceFrancisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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