Diabetic peripheral neuropathy

Introduction to diabetic peripheral neuropathy Diabetic peripheral neuropathy is one of the most common chronic complications of diabetes. It is a group of peripheral neuropathy with sensory and autonomic symptoms as the main clinical manifestations. It forms a triad of diabetes with diabetic nephropathy and diabetic retinopathy, which seriously affects diabetics. Quality of life. basic knowledge The proportion of sickness: 0.6% Susceptible people: no specific population Mode of infection: non-infectious Complications: Diabetic nephropathy

Causes of diabetic peripheral neuropathy

Metabolic disorder (30%):

(1) Tissue glycosylation: elevated blood glucose can cause glycosylation of tissue proteins, and glycosylation protein end products are not only an important factor causing systemic complications of diabetes, but also destroy the myelin structure of peripheral nerves. Causes the loss of myelin, microfilament, and glycosylation of tubulin can lead to axonal degeneration. The glycosylation process of this tissue protein in diabetic patients can continue after the blood glucose level returns to normal, resulting in persistent peripheral nerves. damage.

(2) Abnormal inositol metabolism: Inositol is a substrate for the synthesis of phosphatidylinositol, and phosphatidylinositol can not only affect the activity of cell membrane Na-K-ATPase, but also an important substance for cell transmembrane information transmission. Inositol intake requires a Na-dependent carrier. Inositol is similar in structure to glucose. Hyperglycemia competitively inhibits Na-dependent carriers, reduces cellular uptake of inositol, and decreases intracellular inositol levels. Neural structure and function.

(3) sorbitol fructose metabolism disorder: hyperglycemia can increase the activity of aldose reductase in peripheral nerve Schwann (Swanwang) cells, accelerate the process of glucose conversion to sorbitol, and sorbitol in sorbitol dehydrogenase Oxidation produces fructose, which causes excessive accumulation of sorbitol and fructose in the cells, causing an increase in intracellular osmotic pressure and retention of sodium and water. As a result, peripheral nerve cells (Schwann cells) are degenerated, myelin loss and axonal mutation Sex.

Microcirculatory disorders (25%):

(1) microvascular disease and ischemia and hypoxia: hyperglycemia can make glycosylation of microvascular structural proteins, resulting in vascular endothelial proliferation, thickening of intima, hyaline degeneration and thickening of basement membrane and increased capillary permeability, severe It can cause vascular stenosis and even thrombosis, causing ischemia and hypoxia damage of peripheral nerve tissue. A comparative study of wrinkle cycle in patients with diabetes mellitus and diabetes mellitus complicated with peripheral neuropathy shows that the visibility of microcirculation in diabetic patients with peripheral neuropathy is obvious. Decline, the field of view is dark red, most of the tube is blurred, and the number is reduced. At the same time, the tube becomes thinner and shorter, and the input branch and microangioma are present. The periorbital exudation, the blood flow velocity is obviously slowed down, and the sediment is sediment. A cluster of fluids.

(2) Reduction of vasoactive factors: reduction of vasoactive factors (NO) in diabetic peripheral neuropathy, decreased sensitivity of endometrial trophoblasts to vasodilators, abnormal dysfunction of smooth muscles, microcirculation disturbance, and metabolism of arachidonic acid The abnormality causes the ratio of prostacyclin (PGl2) and thromboxane (TXA2) to decrease, the blood vessels contract, and the blood is hypercoagulable, and the result is ischemia and hypoxia of nerve tissue.

Immune mechanism (25%):

Studies have shown that 12% of patients with diabetic peripheral neuropathy are positive for anti-GM1 antibodies and are associated with distal symmetric polyneuropathy, 88% of patients are positive for antiphospholipid antibodies, and only 32% of patients without neurological complications are positive for this antibody. It indicates that the pathogenesis of diabetic peripheral neuropathy is related to autoimmunity.

The main pathological features of diabetic peripheral neuropathy are axonal degeneration and segmental demyelination, accompanied by significant remyelination and unmyelinated fibroplasia. The spatial distribution characteristics of sciatic nerve, sural nerve and vagus neuropathy show that The axon mutation and demyelination are reverse dying back, that is, the distal axonal degeneration is heavier, the proximal end is relatively light, and multiple segmental myelin loss can be primary. Can also be secondary, some patients have pathological features of hypertrophic neuropathy, manifested as Schwann cell proliferation to form onion-like structure, visible collagen fibrosis with collagen sac formation, clinical manifestations of painful neuropathic patients with gastrocnemius biopsy visible Selective fine myelinated fiber loss with unmyelinated fibrous axon buds, autopsy pathological observation of diabetic peripheral neuropathy can sometimes reveal loss of posterior root ganglion cells and spinal anterior horn cells, and axonal degeneration of nerve roots and posterior cord .

Vascular lesions are one of the pathological features of diabetic peripheral neuropathy. The epithelial and intimal small vessel endothelial cells are swollen, the lumen is narrow or even occluded, the adventitia is thickened with mononuclear cell infiltration, and the basement membrane is thickened around the diabetes. Another pathological feature of neuropathy, the basement membrane at the perineurium, Schwann cells and vascular endothelial cells can be significantly thickened, with the most prominent neuromuscular membrane, the longer the course of the distal symmetric neuropathy, the basement membrane The more obvious the thickening, the less severe the single neuropathy is to a lesser extent.

Diabetic peripheral neuropathy prevention

Mainly to prevent and treat diabetes, the primary prevention focus is reasonable diet, moderate exercise, control of blood sugar, and prevention of complications.

Diabetic peripheral neuropathy complications Complications, diabetic nephropathy

All complications of diabetes may be associated with diabetic peripheral neuropathy. The most common is diabetes triad and diabetic retinopathy, which together constitute a triad of diabetes, which seriously affects the quality of life of diabetics, such as diabetic cerebrovascular disease. Genitourinary infections, skin infections, are also more common.

Symptoms of diabetic peripheral neuropathy Common symptoms Responsive nausea, dizziness, dizziness, shaking, cerebral palsy, sensory ataxia, dull pain, intestinal peristalsis, slowing of sensory dysfunction, autonomic nervous system

Distal primary sensory neuropathy

Multiple peripheral neuropathy, which is characterized by distal limb symmetry, is the most common type of diabetic peripheral neuropathy. Multiple onsets are concealed, first involving the distal extremity, progressing from the bottom to the top, rarely affecting the upper limbs, and the fine myelin fibers are involved. Painful peripheral neuropathy or painful temperature sensation, the main symptoms are dull pain from the deep part of the limb, stinging or burning pain, especially at night, both lower extremities have a sore-like feeling of loss or loss, Achilles tendon and knee tendon reflex Or disappear, severe sensory neuropathy can involve the ventral side of the lower part of the trunk, the back side is not tired, called diabetic trunk polyneuropathy, at this time, if you ignore the feeling of the back side of the trunk, the examination is easily misdiagnosed as myelopathy, rough When the myelin fibers are involved, the symptoms are mainly deep sensory disturbances, sensation of ataxia, and easy to fall.

2. Autonomic neuropathy

Almost all patients with long-term diabetes mellitus, sympathetic and parasympathetic fibers can be involved, cardiovascular autonomic dysfunction, the heart rate of activity and deep breathing regulation response is weakened, and even developed into complete cardiac denervation, due to sympathetic contraction Vascular dysfunction, prone to orthostatic hypotension, dizziness, darkness and even syncope when standing up, gastrointestinal autonomic symptoms including esophageal and gastrointestinal motility slow, gastric emptying time prolonged, the so-called diabetic gastroparesis, Other gastrointestinal dysfunctions include nausea, vomiting, bloating, constipation and diarrhea. The autonomic dysfunction of the genitourinary system is characterized by low sexual function, impotence, dysuria, residual urinary retention and urinary retention. This low-tension bladder is easy. Inducing urinary tract infection and renal failure, other autonomic nerve damage symptoms include pupillary abnormalities and sweat secretion disorders, which are characterized by dilated pupils, slow response to light, no sweat in the lower limbs, and compensatory sweating in the head and hands.

3. Diabetic foot

It is a serious complication of sensory neuropathy, which is caused by dry skin, cleft palate, vascular ischemia caused by autonomic dysfunction, limb pain and limb pain, and abnormal position of the foot caused by joint deformation. The clinical manifestation is Long-lasting ulcers on the toes, heels and ankles.

4. In addition to the distal sensory disturbance of the extremities, a small number of patients also have distal muscle weakness and muscle atrophy, reduced or disappeared tendon reflexes, and can also be combined with autonomic dysfunction, so-called diabetic motor sensory neuropathy or chronic progressive exercise. Feeling autonomic neuropathy.

5. Acute or subacute proximal motor neuropathy

Also known as proximal diabetic neuropathy or spastic diabetic neuritis, in 1995, Garland was officially named diabetic myoatrophy, the incidence rate was 0.8%, and the pathological findings of muscle biopsy were scattered or small group of muscle fiber atrophy. Both types of fibers can be affected, mainly type 1, sometimes visible target fibers, muscle interstitial hyperplasia, neurobiopsy shows axonal degeneration and demyelination changes simultaneously, neurophysiological examination found proximal muscles and ridges The nerve branches of the muscle are mainly affected, while the distal end is rarely affected.

Proximal diabetic neuropathy can be acute, subacute or insidious onset, seen in various stages of diabetes, can also occur with distal motor neuropathy, mainly involving one or both of the pelvic muscles, especially the quadriceps, In addition, the adductor muscles of the iliopsoas, gluteal muscles and thighs can also be affected. The upper limbs are almost unaffected by the muscles. In the early stage, the proximal muscles of the lower limbs are weak and the muscles are atrophied, and about half of them gradually involve the proximal ends of the lower limbs. It is characterized by standing up, difficulty walking and stairing stairs, often accompanied by sharp pain in the deep thighs and lumbosacral areas.

6. Diabetic mononeuropathy or multiple mononeuropathy

The femoral nerve, sciatic nerve, brachial plexus and median nerve are more common, followed by the sural nerve, ulnar nerve, supraspinal nerve and thoracic nerve. Generally, the onset is more urgent, which is characterized by sudden pain in the affected innervation area. Feeling disorder, muscle weakness.

7. Diabetic-induced cranial nerve damage with oculomotor nerve paralysis

The most common, followed by exhibition, trochle, facial nerve and trigeminal nerve, sometimes can be expressed as the majority of cranial nerve damage, mostly sudden onset, can be unilateral or bilateral, but also repeated attacks.

8. Invasive neuropathy caused by diabetes

Mainly manifested as carpal tunnel syndrome, cubital tunnel syndrome and fistula syndrome.

Electrophysiological examination: patients with diabetic peripheral neuropathy may have slower nerve conduction velocity and prolonged terminal movement latency, reflecting demyelinating damage of peripheral nerves. Electromyography shows a decrease in amplitude of action potential, reflecting axonal degeneration, F wave latency, conduction Changes in velocity, amplitude and time limit reflect the lesions of the proximal nerve and compensate for the lack of measurement of the distal nerve conduction velocity. H-reflex can measure the excitability of a motor neuron and the functional state of the motor fiber, providing a basis for nerve damage. Fibrous electromyography (SFEMG) reflects the germination and nerve re-innervation of axons by fiber density and twitch parameters.

Cerebrospinal fluid examination: 66% of diabetic peripheral neuropathy may have elevated protein, mean 0.6g / L, rarely more than 1.2g / L, mainly with elevated globulin, subclinical stage with abnormal electrophysiological examination but no clinical symptoms There is very little elevated cerebrospinal fluid protein in diabetic peripheral neuropathy.

Examination of diabetic peripheral neuropathy

Laboratory inspection

1. Determination of blood sugar and glucose tolerance.

2. Other blood tests include liver function, kidney function, routine examination of erythrocyte sedimentation rate; rheumatism series, immunoglobulin electrophoresis and other serological tests related to autoimmunity.

3. Detection of serum heavy metals (lead, mercury, arsenic, antimony, etc.).

4. Urine examination includes urine sugar, urine routine, pre-week protein, urinary porphyrin and heavy metal excretion in urine.

5. Cerebrospinal fluid examination.

Film degree exam

1. Electromyography and neurophysiological examination.

2. Organize biopsies (including skin, sural nerves, muscles and kidneys) as necessary to identify other sensory peripheral neuropathies.

Diagnosis and diagnosis of diabetic peripheral neuropathy

Diagnostic criteria:

1. Have a certain diabetes, that is, meet the diagnostic criteria for diabetes.

2. There are persistent pain and/or sensory disturbances in the extremities or lower extremities.

3. One or both sides of the big toe vibration loss.

4. The double pupil reflection disappears.

5. The sacral nerve conduction velocity on the primary side (ie, the hand side) is 1 standard deviation below the normal value of the same age group.

In addition, the determination of F-wave and H-reflection and single-fiber electromyography can provide clues for the diagnosis of proximal and subclinical diabetic peripheral neuropathy.

Differential diagnosis

The first is the diagnosis and identification of diabetes, followed by the identification of other sensory peripheral neuropathy and painful peripheral neuropathy. Diabetic muscular atrophy should be associated with quadriceps myopathy, progressive spinal muscular atrophy and lumbosacral Identification of quadriceps atrophy caused by radiculopathy.

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