Diabetic neuropathy

Distal symmetric polyneuropathy (DSPN) presents in 10% to 15% of patients with newly diagnosed type 2 diabetes.

 

 

The rate increases  to 50% after 10 years’ duration. 

 

 

Diabetic neuropathy is the most common type of neuropathy, representing 75% of patient cases. 

 

 

DSPN signs include loss of sensory, proprioception, temperature, and pain discrimination. 

 

 

It is a bilateral problem.

 

 

It leads to unsteadiness and increased risk of falls. 

 

 

Progresses to a loss of protective sensation that renders patients unable to sense pain. 

 

 

It is estimated that 50% of patients with diabetes have lost protective sensation.

 

Found in 10-50% of patients with diabetes.

A minority of patients with polyneuropathy will be symptomatic with either burning tingling or numbness and weakness.

Categorized as a focal or diffuse.

Diabetic neuropathy-focal neuropathies include focal appendicular mononeuropathies, such as the median neuropathy at the wrist, the ulnar neuropathy at the elbow, cranial mono neuropathies or lumbar-sacral radiculolexoneuropathy.

Diffuse diabetic neuropathy’s include diabetic polyneuropathy, which produces generalized, predominantly distal, relatively symmetrical dysfunction with sensory aspects affect more than motor function.

Diabetes can cause a number of patterns of neuropathy including mononeuropathies, thoracic radiculopathy, length independent polyradiculoneuropathy and diabetic lumbosacral radiculoplexus neuropathy.

Diabetic radiculoplexus plexus neuropathy affects 1% of patients with diabetes and begins with severe pain, often involving the thigh, with weakness of the limb limbs and often associated with weight loss.

Less common manifestations include: autonomic neuropathy, nerve entrapment, and polyradiculopathy including diabetic amyotrophy.

While diabetic neuropathy can take many forms a chronic, length- dependent, sensorimotor peripheral neuropathy is the most common form.

Diabetic neuropathy is a late complication of poorly controlled diabetes usually occurs with other late microvascular complications, namely retinopathy and nephropathy.

If there is no clinical evidence of retinopathy or nephropathy peripheral neuropathy is unlikely to be due to diabetes.

Most common cause of polyneuropathy in Western countries.

The prevalence of diabetic polyneuropathy ranges from 28 to 55%.

Depending on criteria used, can affect 50-90% of patients.

Prevalence increases with age, duration of diabetes and poor control of the diabetes.

Estimated that 39% of patients remain untreated, and 1 in 8 do not report the condition to their physicians.

In a study of 4400 patients with diabetes followed for more than 25 years 50% of individuals had polyneuropathy by the 25th year of study (Pirart J).

The Europe and Diabetes study indicated a prevalence of diabetic polyneuropathy of 28% 3250 insulin dependent diabetics.

In a study from Minnesota 55% of insulin-dependent and 54% of non-insulin-dependent diabetics have polyneuropathy, but only 15% of the insulin-dependent group and 13% of the non-insulin-dependent group were symptomatic (Dyck P).

Patients with type II diabetes develop polyneuropathy at a rate of 6.1 per hundred person-years (Sands ML).

Patients may present with symmetric involvement or asymmetric involvement, autonomic, peripheral sensory or somatic involvement.

Is often asymptomatic, and evidence of its presence can be found only on clinical examination.

Thirty percent of diabetics suffer from chronic, painful symptoms and have impaired quality of life.

Radiculopathy must be considered and asymmetric findings on sensation and reflex exam suggest this diagnosis rather than diabetic polyneuropathy.

Diabetic patients with predominantly large fiber peripheral neuropathy tend to experience numbness and tingling in the feet, whereas patients with small fiber involvement describe sharp, burning and shooting pain sensations.

Large fiber peripheral neuropathy often preceded by an insensate foot.

Almost half of patients with diabetic foot ulcers lack pain and numbness.

Generally small fiber neuropathy develops before, involvement of large fibers, and most patients complain of burning discomfort in the feet.

A significant number of patients, however present with large fibers, symptoms and numbness, weakness or disturbance in gait.

Microvascular complications of erectile dysfunction, nephropathy, and retinopathy predict for the development of peripheral neuropathy.

Distal symmetric sensorineural polyneuropathy is the most common form of diabetic peripheral neuropathy, but it may progress from distal to proximal over time,

Most identifiable feature of diabetic polyneuropathy is impaired pinprick sensation with normal proximal function.

All diabetic patients should be to screened with a 10-g monofilament to report sensation of pressure at four sites on the lower extremity.

The  Ipswich Touch Test is an alternative to the monofilament exam, where the clinician instructs the patient to close his or her eyes while lightly resting a finger on the patient’s first, third, and fifth toes for 1 to 2 seconds, and then is asked  the patient if he or she felt something. 

Testing by pinprick should move from the toes to a proximal point where the sensation is sharp.

An occasional clinical finding is distal hypersensitivity to the pin prick test.

Evaluation includes temperature sensation, sensation to light touch, joint position sense and the ability to detect a 128-Hz tuning fork sensation.

A tuning fork vibration, should be felt for at least 12 seconds as a normal response.

The reliability of vibration sensory testing, has a correlation coefficient as high as 0.93 at the great toe.

Stemmes-Weinstein monofilament determines pressure sensation with normal patients with intact can feel for 4.17 monofilament, which equates in 1 g of linear pressure.

Sensation is lost when patients cannot feel 5.07 monofilament with 10 g of linear pressure on the plantar surface of the foot.

Insensitivity of the monofilament increases eight patients likelihood of developing a foot ulcer on the plantar surface who even future lower extremity amputations.

Patients should be evaluated as to the strength of the toe extensors and flexors and foot dorsiflexion.

Deep tendon reflexes of the arms and knees are normal while they are reduced or absent in the ankles.

Absence of Achilles reflex and reduced vibration perception and position sense at the great toe has a 92.8% positive predictive value for this diagnosis.

Often leads to impaired gait with slower walking speeds, longer stance phases and reduce flexion of the ankle.

Radiculopathy must be considered and asymmetric findings on sensation and reflex exam suggest this diagnosis rather than diabetic polyneuropathy.

Nerve conduction studies and EMG are not mandatory in the evaluation but may be useful with atypical presentations such as with rapid progressive course, marked asymmetry, more weakness than sensory loss in greater upper extremity symptomatology.

Electro-physiologic abnormalities include mild reduction in distal sensory response amplitudes with subsequent reductions in these responses until they are absent.

Motor response amplitudes are generally well preserved early in the disease and decrease as the process advances.

Reduced epidermal nerve fiber density precedes the diagnosis of diabetes.

Examination for large fiber peripheral neuropathy includes: muscle strength, deep tendon reflexes, proprioception, vibration, and pressure sensation.

Reduced epidermal nerve fiber density is more prevalent in diabetic peripheral neuropathy patients compared to diabetic patients without neuropathy.

Diabetic peripheral neuropathy often underdiagnosed.

All diabetic patients should be screened at least annually for diabetic neuropathy.

Positive predictive value of 128-Hz tuning fork is adequate for diagnosis.

Simple screening tests for peripheral neuropathy as a predictor of diabetic foot ulcers indicates that tuning fork has a specificity of 90% and sensitivity of 56%.

Prospective study of 1,172 patients with type 1 diabetes without neuropathy revealed at 7.3 years 23.5% of patients developed neuropathy (Tesfaye).

Most common form is distal symmetrical polyneuropathy with burning, stabbing and shooting pains of the lower extremities and feet.

Pain often increased at night.

Complication of microvascular damage to nerves and impaired nitric oxide synthesis.

Some patients will have loss of sensation from nerve damage and will not be aware of their disability until injury or ulceration occur.

11.6% of type 1 diabetics with neuropathy have pain, while 32.1% of type 2 diabetics with neuropathy have pain.

Sequelae of diabetic neuropathy are Charcot’s arthropathy, ulceration and amputation.

Up to 40-60% of lower extremity amputations are related to diabetic peripheral neuropathy.

The presence of peripheral neuropathy in patients with diabetes mellitus increases the risk of foot ulcers and diabetic foot infections 7 fold (Young MJ).

About 0.5 to 29% of diabetics will have neuropathic joint changes.

Tight glycemic control is the only measure that ameliorates or prevents neuropathy.

Rate of deterioration of glycemic control relates to the risk of neuropathy.

Pain can be relieved year antidepressants, anticonvulsants, tramadol, opioids and topical capsaicin, but the efficaciousness of these agents are limited.

Pregabalin most effcacious drug.

In a randomized trial of 10,251 participants with type 2 diabetes intensive treatment of, glycemic control, and dyslipidemia, but not intensive blood pressure control, reduced progression of diabetic retinopathy: at 4 years rates of progression of DR 7.3% with intensive glycemic treatment vs. 10.4% with standard therapy, 6.5% with intensive dyslipidemia vs. 10.2% for standard treatment, 10.4% with intensive blood pressure therapy vs. 8.8% with standard therapy (Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial).