Diabetic peripheral neuropathy in the elderly
Introduction
Introduction to diabetic peripheral neuropathy in the elderly Neuropathy is one of the most common complications of diabetes, and its prevalence can reach 7% to 50%. If it includes various subclinical neuropathy, it can be as high as 90%, which is an important cause of disability and death in diabetic patients. Threatening the health of people with diabetes. Any part of the nervous system (peripheral nerve, spinal cord and brain) can be involved, can be single or combined, of which peripheral neuropathy is most common, especially in the peripheral neuropathy of the elderly, diabetes is the most common cause of disease. Peripheral neuropathy refers to the dysfunction of the spinal cord and brainstem motor neurons, the primary sensory neurons and the surrounding autonomous axons and supporting tissues. A variety of clinical manifestations can occur. Its neuropathology revealed Schwann cell edema, axonal degeneration and segmental demyelination. basic knowledge Sickness ratio: 30-50% Susceptible people: the elderly Mode of infection: non-infectious Complications: cardiac arrest and cardiopulmonary resuscitation
Cause
The cause of diabetic peripheral neuropathy in the elderly
Blood vessels (30%):
From the animal models of diabetes and tissue biopsy of diabetic patients, it is concluded that small blood vessels, especially microangiopathy, are closely related to diabetic peripheral neuropathy, mainly characterized by thickening of capillary basement membrane, enlargement of area, proliferation of vascular endothelial cells or hypertrophy. , edema and hyaline degeneration, glycoprotein deposition, luminal stenosis, resulting in neuro-ischemia and hypoxia, in addition, neuro-ischemia and hypoxia may also be related to hypertensive state caused by hyperglycemia caused by hemorheological changes, such as blood Increased viscosity, decreased red blood cell deformability, glycosylated protein product formation, etc. In streptozotocin (STZ)-induced diabetic rats, neurological blood flow is reduced to 2/3 of normal, and clinical and Animal models have shown that prostaglandin E2, angiotensin-converting enzyme inhibitors and calcium antagonists can relax vascular smooth muscle, dilate blood vessels, increase blood flow, and restore and improve the nerve conduction function of diabetic neuropathic patients or rats. , further illustrating the occurrence of diabetic neuropathy and vasculopathy caused by God Ischemia and hypoxia, mostly single neuropathy are more likely to support vascular insufficiency caused by vascular mechanisms.
Metabolism (20%):
The long-term hyperglycemia state of diabetes leads to a series of metabolic disorders. Abnormal metabolites directly damage the nerves, affecting the nutrition and blood supply of the nerves, and then cause the body's immune response, eventually leading to the occurrence of diabetic neuropathy. Most bilateral symmetric multiple nerves The lesion supports this doctrine.
(1) Increased activity of the polyol metabolic pathway: Aldose reductase (AR) is a highly substrate-dependent enzyme in the polyol metabolic pathway. Normally, AR activity is very low, but in hyperosmolar state of diabetes. Under the AR activity, the higher activity of the glucose is reduced to produce more sorbitol, and the sorbitol must be converted to fructose by the dehydrogenase to gradually oxidize, and the sorbitol dehydrogenase activity is reduced. It causes a large accumulation of sorbitol in the cells, and the accumulation of sorbitol directly acts on nerve cells, causing an increase in osmotic pressure, swelling and necrosis of nerve cells. On the other hand, glucose can competitively inhibit hyperglycemia. Inositol is taken up by nerve tissue, and inositol synthesis is reduced due to enhanced activity of sorbitol pathway. The inositol levels of nerve cells are greatly reduced, the inositol phospholipids synthesized by cells are reduced, and the metabolites are correspondingly reduced. The decrease in protein kinase C (PKC) activity ultimately leads to a decrease in Na+-K+-ATPase activity, which changes the depolarization of the membrane. When the normal conduction of nerve impulses is affected, the activity of the enzyme decreases, which inevitably leads to a slowing of the nerve conduction velocity. In severe cases, the intracellular sodium ion concentration increases, the Langfei knot edema causes demyelination changes, and at the same time, the PKC activity decreases. Influencing the activity of other enzymes in the cell, resulting in decreased intake of nutrients such as amino acids by nerve cells, decreased energy utilization, and impaired neurotrophic function.
(2) Protein glycosylation: glucose, fructose, etc. in the body can undergo non-enzymatic glycosylation with various proteins in the body, especially long-lived proteins. Glycosylation of neural structural proteins is the formation of diabetic peripheral neuropathy. One of the important reasons is that when plasma proteins and albumin are glycosylated, they are permeable, while the vascular wall cells and basement membrane are glycosylated, the permeation barrier is destroyed, so the osmotic substances enter the inner lining and accelerate the nerve fibers. Degeneration, glycosylation of myelin proteins makes demyelinated fibers more sensitive to external damage, and glycosylation of the perineurium membrane leads to compression of the perivascular artery due to changes in permeability and further neuroendometrial ischemia. In addition, microtubules and glycosylation of neurofilaments alter cell phosphorylation and dephosphorylation cycles, severely affecting axonal conduction, leading to atrophy of distal axons and axonal atrophy. Ryle et al. The structural proteins of the central nervous system are more susceptible to glycosylation, which is consistent with clinically more likely to cause peripheral neuropathy.
(3) Abnormal lipid metabolism: It has been found that the abnormal lipid synthesis of the nerve in the diabetic patient and the lipid ratio of the myelin sheath are abnormal, resulting in loss of function and shrinkage of the synapse, but no consensus has been obtained.
(4) Reduction of prostacyclin: Prostacyclin (PG12) is a potent platelet aggregation inhibitor that prevents platelets and other blood cells from collecting in the lumen of the vascular lumen and increases cAMP in vascular smooth muscle cells. Local vasodilation, and thrombospondin (TXA2) (from PTI2 from the same precursor) can induce platelet aggregation and vasoconstriction, the opposite effect, maintaining a dynamic balance in normal, diabetes, due to arachidonic acid metabolism The abnormality caused the imbalance of PGI2 and TXA2, the increase of platelet synthesis of TXA2, the inhibition of vascular endothelial cell production of PGI2, the platelet showed hypercoagulable state, the microvascular contraction enhanced, the nerve tissue ischemia, leading to the occurrence of diabetic peripheral neuropathy.
Reduced neurotrophic factor (15%):
Neurotrophic factor is a protein that promotes neuronal survival, morphological development and physiological function differentiation. Among them, nerve growth factor (NGF) is important, and NGF is necessary for sensory neurons and sympathetic neurons to maintain normal function. Especially for the sensory neurons of fine fibers, animal experiments have shown that the axonal transport of NGF in diabetic rats is significantly reduced, the level of endogenous NGF in NGF-sensitive neurons and their dominant target organs is significantly reduced, and the expression of NGF-mRNA in target tissues is significantly reduced. The decrease suggests that the reduction of NGF is related to the pathogenesis of diabetes.
Prevention
Elderly diabetic peripheral neuropathy prevention
Strict diet control and control of blood sugar are fundamental measures to prevent diabetic peripheral neuropathy.
Complication
Elderly diabetic peripheral neuropathy complications Complications, cardiac arrest and cardiopulmonary resuscitation
Common concomitant foot ulcers, joint lesions and sympathetic autonomic dysfunction, oculomotor and nerve damage, breathing, myocardial arrest.
Symptom
Symptoms of diabetic peripheral neuropathy in the elderly Common symptoms Inability to dizziness, visual impairment, standing heart rate difference, loss of appetite, nutritional disorders, sensory disturbance, dull pain, gait, unstable bacterial infection
In the elderly, because the glucose metabolism disorder is often very mild, it is difficult to be observed. Peripheral neuropathy may be the main clinical manifestation of diabetes. The lesions may involve the sensory, motor and autonomic nerves, resulting in various clinical manifestations, but overall Can be divided into bilateral symmetric multiple neuropathy and asymmetric single neuropathy.
Multiple neuropathy
Sensory disturbances are often typical of gloves or socks, pain, temperature, position and vibration loss or loss, or limb numbness, burning, chills, ants walking and other sensory abnormalities and sensitive skin touch, insidious onset, Symptoms persist, deep sputum or severe pain can occur in the limbs, typically at night, when the deep feeling is damaged, the patient often feels heavy limbs, feeling cotton and gait instability.
The dyskinesia manifests as different degrees of lower motor neuron spasm, and the short extension of the short toe of the foot is an early symptom. The atrophy of the interosseous muscles of the hands and feet can cause a claw-shaped deformity, which can be insidiously attacked. It can rapidly develop and rapidly deteriorate.
The sacral reflex disorder is characterized by its weakening or disappearance, the sputum reflex disappears earlier, and then the knee reflex can disappear, and then the upper limb reflex disappears.
Autonomic dysfunction can be manifested as sweaty or sweaty and nutritive barriers to the skin and nails, such as rough skin, dry nails, brittleness, hyperkeratosis, and nutritional ulcers.
A special manifestation of painful diabetic polyneuropathy is diabetic neuropathic cachexia syndrome, which is characterized by mild diabetes with multiple neuropathy, limb pain, fear of eating, depression, insomnia and obvious weight. The decline has been clinically excluded from malignant tumors and other wasting diseases, and its pathogenesis is still unclear. Some scholars have speculated that the dysfunction of the hypothalamus is.
Diabetic polyneuropathy can have no obvious symptoms and signs for a long period of time, but its clinical symptoms are obvious, and in many patients, it causes long-term severe disability, mainly due to the loss of pain and sensation. The ground is traumatized, forming a painless, penetrating, "nutritive" ulcer, which can easily cause severe necrotizing bacterial infection and osteomyelitis in the deep fascial compartment of the foot. In addition, about 1% of patients have Most of those who are over 50 years of age with a 15-year course of diabetes can have insidious medial humerus, painless destruction of the patellofemoral bone and less common ankles and joints, resulting in significant foot deformities. That is, Charcot's neuroarthropathy.
2. Single neuropathy and multiple neuropathy
(1) cranial nerve single neuropathy: oculomotor involvement is the most common, there are obvious eyelid drooping and eye movement disorders, but the pupil is generally exempt, eye movement disorders generally reach peak in 1 day or several days, lasting for several weeks Gradually recovered, completely recovered within 3 to 5 months, the pathogenesis is generally considered to be caused by ocular nerve ischemia caused by microvascular disease, because the fibers that innervate the pupil are located in the peripheral part of the oculomotor nerve, the effect on ischemia The central part is light, so most exemptions, other cranial nerves that are prone to lesions have nerves and facial nerves, and the involvement of the trochlear nerve alone is rare.
(2) proximal motor neuropathy: also known as "diabetic muscular atrophy", its pathogenesis may be caused by multiple vascular lesions of the vascular disease of the nerve, more common in the 50-year-old longer course, diabetes is also heavier Patients, generally acute or subacute onset, first feeling weak, 2 to 3 weeks of obvious atrophy, mainly involving the quadriceps, iliopsoas and thigh adductor muscles, flexor muscles such as arm muscles, rope and gastrocnemius It is less affected. The main symptoms of exercise are unstable knee joints, difficulty in standing and walking, especially difficulty in upper steps. Generally, there are pains. It is a persistent dull pain in the deep, and it can also be burning pain, and it is heavy at night. The pain begins on the affected side of the lower back or buttocks, or from the hip to the knee, the skin has no obvious paresthesia, and some cases have a positive reaction of tendon reflex.
(3) trunk neuropathy: chest and abdomen neuropathy, more common in patients over 50 years old with long-term diabetes, sudden onset, pain and paresthesia are the earliest symptoms, pain is often deep dull pain, but also pain, thorn Pain or burning pain, usually unilateral or mainly one side, so it is easy to be confused with angina pectoris, lung or gastrointestinal symptoms, night is the heaviest, generally cough force has no effect, pain can appear in 1 or Several skin segments can be found on the heaviest segment of the pain. There is a paresthesia in the acupuncture. It is usually in the chest and the front of the abdomen is obvious. There may be ipsilateral abdominal muscle weakness due to the relaxation of the abdominal muscles. , causing local bulging.
3. Diabetic autonomic neuropathy
(1) Cardiovascular system:
1 abnormal heart rate: There are two main manifestations: one is tachycardia when quiet, and the other is fixed heart rate, which means that the heart rate changes obviously less than normal people.
2 Postural hypotension: refers to the systolic blood pressure drop from the lying position to the standing position when the systolic blood pressure drops more than (4kPa) 30mmHg, the patient may have postural weakness, dizziness, visual impairment, and even syncope. The mechanism of occurrence is mainly reflective compensatory. There are obstacles to the vasoconstriction mechanism.
(2) Gastrointestinal system: Autonomic neuropathy can affect any part of the gastrointestinal tract, causing loss of appetite, nausea, vomiting, diarrhea, constipation and other symptoms.
(3) genitourinary system:
1 Abnormal bladder function: the patient's early manifestation is prolonged urination interval, morning urine volume increase, detrusor involvement, weak urinary flow, prolonged urination, more force when urinating, and unclean, drip, etc. There is urinary retention and overflow urinary incontinence.
2 Sexual dysfunction: one of the most common symptoms of autonomic neuropathy in male diabetic patients, most of which have impotence, reduced sperm, etc., male infertility, female patients with sexual dysfunction are generally mild, manifested as decreased libido, menstrual disorders .
(4) hypoglycemia reaction: under normal circumstances, there will be a mild parasympathetic reaction when blood glucose is lowered, followed by a sympathetic response, so the patient will perceive hypoglycemia and provide an antagonistic mechanism to avoid hypoglycemic coma, that is, parasympathetic response through vagus Glucagon release; sympathetic reaction promotes hepatic glycogen decomposition by releasing adrenaline, and autonomic neuropathy patients may lose early sympathetic response, thus appearing hypoglycemia without self-consciousness, and due to the above-mentioned lack of antagonistic function, no Symptoms suddenly enter a hypoglycemic coma.
The elderly peripheral neuropathy is classified according to the cause, and usually has the following types:
1 idiopathic peripheral neuropathy;
2 nutritional peripheral neuropathy: chronic alcoholism, malabsorption syndrome, malnutrition;
3 metabolic peripheral neuropathy: diabetes, uremia, water and electrolyte disorders;
4 toxic peripheral neuropathy: drug-like, heavy metal;
5 compression and circulatory peripheral neuropathy: deformable cervical spondylosis, carpal tunnel syndrome, cubital tunnel syndrome, arteriosclerosis ischemic;
6 cancerous peripheral neuropathy
Despite the different causes of various peripheral neuropathies, clinical manifestations are often the same, with sensory, motor, reflex, autonomic and nutritional disorders.
Electromyography can be seen as a denervated potential at rest, when the contraction is free, the normal motor potential is reduced with multiphase wave potential, and the myoelectricity of the biceps, triceps, tibialis anterior and tibialis muscles is detected. At times, it is often seen that the amplitude is increased, mostly around 2mV, and the duration is prolonged. In the early stage, the nerve conduction velocity (NCV) can be slowed down and the amplitude is reduced. Generally speaking, the change of nerve conduction velocity is obvious in the lower limbs than in the upper limbs. The abnormal rate of sensory nerve conduction velocity (SCV) is higher than that of motor nerve conduction velocity (MCV), but if hyperglycemia is controlled, the conduction velocity often returns to normal and is a reversible change.
Examine
Examination of diabetic peripheral neuropathy in the elderly
Blood sugar, urea nitrogen, elevated creatinine, abnormal potassium, sodium, and chlorine.
Neurological biopsy, electromyography, and neurophysiological examination showed abnormalities.
Diagnosis
Diagnosis and diagnosis of diabetic peripheral neuropathy in the elderly
According to the patient's clear history of diabetes, the above-mentioned clinical manifestations of different symptom combinations and abnormalities in neurophysiological examination can diagnose diabetic peripheral neuropathy and differentiate it from other peripheral neurological diseases.
Clinical and tumor-related peripheral neuropathy, uremia peripheral neuropathy.
