Diabetic Neuropathy: Practice Essentials, Background, Anatomy

Practice Essentials

Diabetic neuropathy is the most common complication of diabetes mellitus (DM), affecting as many as 50% of patients with type 1 and type 2 DM. Diabetic peripheral neuropathy involves the presence of symptoms or signs of peripheral nerve dysfunction in people with diabetes after other possible causes have been excluded. 

Signs and symptoms

In type 1 DM, distal polyneuropathy typically becomes symptomatic after many years of chronic prolonged hyperglycemia, whereas in type 2, it may be apparent after only a few years of known poor glycemic control or even at diagnosis. Symptoms include the following:

• Sensory – Negative or positive, diffuse or focal; usually insidious in onset and showing a stocking-and-glove distribution in the distal extremities
• Motor – Distal, proximal, or more focal weakness, sometimes occurring along with sensory neuropathy (sensorimotor neuropathy)
• Autonomic – Neuropathy that may involve the cardiovascular, gastrointestinal, and genitourinary systems and the sweat glands

Physical examination should include the following assessments:

• Peripheral neuropathy testing – Gross light touch and pinprick sensation; vibratory sense; deep tendon reflexes; strength testing and muscle atrophy; dorsal pedal and posterior tibial pulses; skin assessment; Tinel testing; cranial nerve testing
• Autonomic neuropathy testing – Objective evaluation of cardiovagal, adrenergic, and sudomotor function in a specialized autonomic laboratory; may be preceded by bedside screening to assess supine and upright blood pressure and heart rate, with measurement of sinus arrhythmia ratio

Two classification systems for diabetic neuropathy are the Thomas system and the symmetrical-versus-asymmetrical system. The Thomas system (modified) is as follows:

• Hyperglycemic neuropathy
• Generalized symmetrical polyneuropathies
• Sensory neuropathy
• Sensorimotor neuropathy
• Autonomic neuropathy
• Focal and multifocal neuropathies
• Superimposed chronic inflammatory demyelinating polyneuropathy

Distal symmetrical sensorimotor polyneuropathy is commonly defined according to the following 3 key criteria:

• The patient must have diabetes mellitus consistent with a widely accepted definition
• Severity of polyneuropathy should be commensurate with duration and severity of diabetes
• Other causes of sensorimotor polyneuropathy must be excluded

Pure autonomic diabetic neuropathy is rare.

Asymmetrical neuropathies include the following:

• Median neuropathy of the wrist (carpal tunnel syndrome)
• Other single or multiple limb mononeuropathies
• Thoracic radiculoneuropathy
• Lumbosacral radiculoplexus neuropathy
• Cervical radiculoplexus neuropathy

Diabetic polyneuropathy is commonly staged as follows:

• NO - No neuropathy
• N1a - Signs but no symptoms of neuropathy
• N2a - Symptomatic mild diabetic polyneuropathy; sensory, motor, or autonomic symptoms; patient is able to heel-walk
• N2b - Severe symptomatic diabetic polyneuropathy; patient is unable to heel-walk)
• N3 - Disabling diabetic polyneuropathy

Read more: Peripheral neuropathy - Symptoms and causes

Diagnosis

Laboratory tests that may be helpful include the following:

• Fasting plasma glucose
• Hemoglobin A1c
• Complete blood count
• Complete metabolic panel (electrolytes and liver function panel)
• Vitamin B-12 and folate levels
• Thyroid function tests
• Erythrocyte sedimentation rate
• C-reactive protein
• Serum protein electrophoresis with immunofixation electrophoresis
• Antinuclear antibody
• Anti-SSA and SSB antibodies
• Rheumatoid factor
• Paraneoplastic antibodies
• Rapid plasma reagin
• Genetic screens
• Hematology screen (for anemia)
• Sequential multiple analysis-7 (renal function and electrolyte imbalances)/complete metabolic panel (CMP)

Other diagnostic modalities that may be considered are as follows:

• Electromyography and nerve conduction velocity testing
• Electrophysiologic studies
• Magnetic resonance imaging
• Computed tomography (including single-photon emission computed tomography)
• Nuclear imaging
• Doppler imaging
• Microdialysis
• Electrocardiography
• Nerve and skin biopsy (now rarely recommended for clinical purposes)

Management

Key components of the management of diabetic neuropathy include the following:

• Foot care, including regular follow-up, patient education, and referral as appropriate
• Tight, stable glycemic control (most important for slowing progression of neuropathy)
• Pain management (eg, with pregabalin, gabapentin, sodium valproate, dextromethorphan, morphine sulfate, tramadol, oxycodone, duloxetine, topical capsaicin, transdermal lidocaine)
• Treatment of diabetic gastroparesis (eg, with erythromycin, cisapride [not available in the United States], metoclopramide, polyethylene glycol 3350, tegaserod [currently available only on an emergency basis])
• Experimental therapies include aldose reductase inhibitors, alpha-lipoic acid, actovegin, and spinal cord stimulators.

Treatment of autonomic dysfunction must address the following:

• Erectile dysfunction
• Orthostatic hypotension
• Gustatory sweating

Surgical treatment may be considered as follows:

• Aggressive debridement or amputation for recalcitrant foot necrosis or infection
• Jejunostomy for intractable gastroparesis
• Implantation of a penile prosthesis for ongoing impotence
• Bracing, special boots, or, in some cases, surgery for Charcot foot
• Pancreatic transplantation for diabetes with end-stage renal disease

See Treatment and Medication for more detail: http://www.theneuropathysolution.com/