Leg neuropathy: diabetic, alcoholic, peripheral, sensory, toxic

Any neurological disease of the legs, defined as neuropathy of the lower extremities, is associated with damage to the nerves that provide motor and sensory innervation of their muscles and skin. This can lead to weakening or complete loss of sensitivity, as well as loss of the ability of muscle fibers to tense and tone, that is, to carry out locomotion of the musculoskeletal system.

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Epidemiology

In patients with diabetes, the incidence of lower extremity neuropathy exceeds 60%. And CDC statistics indicate that 41.5 million Americans, or nearly 14% of the U.S. population, have peripheral neuropathy. Such figures may seem unrealistic, but experts at the National Institute of Diabetes note that about half of patients do not even know that they have this pathology, because the disease is in its early stages, and they do not even complain to the doctor about some discomfort from numbness in the toes.

According to experts, peripheral neuropathy is detected in 20-50% of HIV-infected people and in more than 30% of cancer patients after chemotherapy.

Charcot-Marie-Tooth hereditary neuropathy affects 2.8 million people worldwide, and the incidence of Guillain-Barré syndrome is 40 times lower, as is the incidence of multiple myeloma.

The incidence of alcoholic neuropathy (sensory and motor) varies from 10% to 50% of alcoholics. However, if electrodiagnostic methods are used, neurological problems with the legs can be detected in 90% of patients with long-term alcohol dependence.

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Causes neuropathies of the lower extremities

In modern neurology, the most common causes of neuropathy of the lower extremities are:

• injuries in which broken bones or their tight plaster fixation (splints, splints) can exert pressure directly on the motor nerves;
• stenosis (narrowing) of the spinal canal, in which the trunk of the spinal nerve is located, as well as compression of its ventral branches or inflammation of individual nerve roots;
• traumatic brain injury, stroke, brain tumors (primarily in the areas of the extrapyramidal system, cerebellum and subcortical motor nuclei);
• infections, including herpetic myelitis caused by the Varicella zoster virus, Guillain-Barré syndrome (developing with infection by the herpes virus type IV of the Gammaherpesvirinae subfamily), diphtheria, hepatitis C, Lyme disease (tick-borne borreliosis), AIDS, leprosy (caused by the bacterium Mycobacterium leprae), meningoencephalitis of various etiologies;
• metabolic and endocrine diseases – diabetes mellitus of both types, porphyria, amyloidosis, hypothyroidism (deficiency of thyroid hormones), acromegaly (excess growth hormone);
• autoimmune diseases: rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis (with destruction of the myelin sheaths of the nerves), acute disseminated encephalomyelitis;
• hereditary diseases: Charcot-Marie-Tooth neuropathy, Friedreich's neurodegenerative ataxia, hereditary sphingolipidosis or Fabry disease; glycogenesis imperfection type 2 (Pompe disease, caused by a defect in the gene for the lysosomal enzyme maltase);
• motor neuron disease - amyotrophic lateral sclerosis;
• subcortical atherosclerotic encephalopathy with atrophic changes in the white matter of the brain (Binswanger's disease);
• multiple myeloma or multiplex plasma cell myeloma (in which malignant transformation affects plasma B-lymphocytes);
• Lambert-Eaton syndrome (noted in small cell lung cancer), neuroblastoma. In such cases, neuropathies are called paraneoplastic;
• systemic vasculitis (inflammation of blood vessels), which can provoke the development of nodular periarthritis with impaired innervation of the lower extremities;
• radiation and chemotherapy of malignant neoplasms;
• toxic effects of ethyl alcohol, dioxin, trichloroethylene, acrylamide, herbicides and insecticides, arsenic and mercury, heavy metals (lead, thallium, etc.);
• side effects of certain long-term medications, such as the anti-tuberculosis drug isonicotinic acid, anticonvulsant drugs of the hydantoin group, fluoroquinolone antibiotics, lipid-lowering statins, and overdose of pyridoxine (vitamin B6);
• insufficient levels of cyanocobalamin and folic acid (vitamins B9 and B12) in the body, leading to the development of funicular myelosis.

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Risk factors

Doctors unanimously attribute weakened immunity, which affects the body's resistance to bacterial and viral infections, as well as heredity (family history of the disease) to risk factors for the development of neuropathy of the lower extremities.

In addition, obesity and metabolic syndrome, poor kidney and liver function contribute to the development of diabetes; multiple sclerosis – diabetes, intestinal problems and thyroid pathologies.

Risk factors for systemic vasculitis include HIV, hepatitis and herpes viruses, and increased sensitization of the body of various etiologies. And plasma cell myeloma develops more easily in those who are overweight or alcohol dependent.

In most cases, lack of blood supply to the brain causes necrosis of its tissues, but when the myelin sheath of nerve fibers does not receive enough oxygen, its gradual degeneration occurs. And this condition can be observed in patients with cerebrovascular diseases.

In principle, all of the diseases listed above can be attributed to factors that increase the likelihood of developing a neurological disorder of motor functions.

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Pathogenesis

The pathogenesis of neurological problems with the legs depends on the causes of their occurrence. Physical injuries can be accompanied by compression of nerve fibers, exceeding their ability to stretch, which disrupts their integrity.

The pathological effect of glucose on the nervous system has not yet been clarified, however, with prolonged excess of glucose levels in the blood, disturbances in the conduction of nerve signals along the motor nerves are an indisputable fact. And with insulin-dependent diabetes, not only a violation of carbohydrate metabolism is observed, but also a functional insufficiency of many endocrine glands, affecting the general metabolism.

The pathophysiological component of neuropathy in Lyme disease has two versions: Borrelia bacteria can provoke an immune-mediated attack on the nerve or directly damage its cells with their toxins.

In the development of amyotrophic lateral sclerosis, the main pathogenetic role is played by the replacement of dead motor neurons of the corresponding structures of the brain with nodes of glial cells that do not perceive nerve impulses.

In the pathogenesis of demyelinating neuropathies (the most common of which is hereditary peroneal amyotrophy or Charcot-Marie-Tooth disease), genetic disorders of the synthesis of the substance of the nerve fiber sheaths, myelin, by Schwann cells, consisting of 75% lipids and 25% neuregulin protein, have been identified. Spreading along the nerve along its entire length (with the exception of small unmyelinated nodes of Ranvier), the myelin sheath protects nerve cells. Without it, due to degenerative changes in axons, the transmission of nerve signals is disrupted or completely stops. In the case of Charcot-Marie-Tooth disease (with damage to the peroneal nerve, transmitting impulses to the peroneal muscles of the lower extremities, extending the foot), mutations are noted on the short arm of chromosome 17 (genes PMP22 and MFN2).

Multiple myeloma affects B-lymphocytes that have emerged from the germinal center of the lymph node, disrupting their proliferation. This is the result of a chromosomal translocation between the immunoglobulin heavy chain gene (in 50% of cases, on chromosome 14, in locus q32) and the oncogene (11q13, 4p16.3, 6p21). The mutation leads to dysregulation of the oncogene, and the growing tumor clone produces abnormal immunoglobulin (paraprotein). And the antibodies produced in this case lead to the development of amyloidosis of the peripheral nerves and polyneuropathy in the form of paraplegia of the legs.

The mechanism of poisoning with arsenic, lead, mercury, tricresyl phosphate is an increase in the content of pyruvic acid in the blood, disruption of the balance of thiamine (vitamin B1) and a decrease in the activity of cholinesterase (an enzyme that ensures synaptic transmission of nerve signals). Toxins provoke the initial breakdown of myelin, which triggers autoimmune reactions that manifest themselves in swelling of myelin fibers and glial cells with their subsequent destruction.

In alcoholic neuropathy of the lower extremities, acetaldehyde reduces intestinal absorption of vitamin B1 and reduces the level of thiamine pyrophosphate coenzyme, which leads to disruption of many metabolic processes. Thus, the level of lactic, pyruvic and d-ketoglutaric acids increases; glucose absorption deteriorates and the level of ATP necessary to maintain neurons decreases. In addition, studies have revealed damage to the nervous system in alcoholics at the level of segmental demyelination of axons and loss of myelin at the distal ends of long nerves. Metabolic effects of liver damage associated with alcoholism, in particular, lipoic acid deficiency, also play a role.

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Symptoms neuropathies of the lower extremities

Typical clinical symptoms of lower extremity neuropathy are related to the type of nerve affected.

If a sensory nerve is damaged, the first signs are tingling and a crawling sensation on the skin, and these are symptoms of paresthesia (numbness).

In addition, the following may be noted: a burning sensation of the skin and increased sensitivity (hyperesthesia); inability to feel changes in temperature and pain or, conversely, hypertrophied pain sensations (hyperalgesia, hyperpathy or allodynia); loss of coordination of movements (ataxia) and orientation of the position of the limbs (proprioception).

Motor neuropathy affects the muscles and manifests itself as:

• muscle twitching and cramps;
• periodic involuntary contractions of individual muscle fibers (fasciculations);
• weakening or absence of reflexes of the biceps femoris, patellar and Achilles tendons;
• weakness and atrophy of the leg muscles, leading to instability and difficulty in movement;
• flaccid unilateral or bilateral partial paralysis (paresis);
• unilateral hemiplegia or bilateral complete paralysis of the legs (paraplegia).

The symptoms of ischemic neuropathy include: acute pain, swelling, hyperemia of the skin, lack of sensitivity on the dorsum of the foot, and then in the proximal parts of the limb.

Symptoms may develop quickly (as in Guillain-Barré syndrome) or slowly over weeks to months. Symptoms usually occur in both feet and begin at the toes.

Forms

Among neurological disorders, the following types of neuropathy of the lower extremities are distinguished.

Motor neuropathy of the lower extremities, that is, motor, develops due to a disruption of the conductive function of the efferent nerves, which transmit signals from the central nervous system to the peripheral and ensure muscle contraction and leg movement.

Sensory neuropathy of the lower extremities occurs when the

Afferent (sensory) fibers are distributed throughout many peripheral nerves, and their receptors (belonging to the peripheral nervous system) are located in the skin and soft tissues, providing mechanoreception (tactile sensations), thermoreception (sensations of heat and cold), and nociception (pain sensitivity)

Sensorimotor neuropathy of the lower extremities is a simultaneous disturbance of the conduction of motor nerves and sensory fibers, and since the peripheral nervous system is affected, there is a definition - peripheral neuropathy of the lower extremities. It can affect only one nerve (mononeuropathy) or several nerves at the same time (polyneuropathy). When two or more separate nerves in separate areas of the body are affected, it is multifocal (multiple) neuropathy.

Neurological syndromes can be a complication of diabetes type 1 and 2, and in clinical neurology, diabetic neuropathy of the lower extremities is diagnosed (most often sensory, but can also be sensory and sensorimotor).

The most common type of progressive loss of sensory function of individual nerves in patients with diabetes mellitus is distal sensory neuropathy of the lower extremities, i.e. affecting the most distant parts of the nerve - with symmetrical numbness (paresthesia) of the feet. With proximal neuropathy, the absence of mechano- and thermoreception is noted in the area of the shins, thighs and gluteal muscles.

Traumatic or ischemic neuropathy of the lower extremities is usually diagnosed in cases of fractures of the bones - femur and tibia, and is caused by compression of nerve fibers and caudal branches of motor nerves, impaired blood flow and damage to the muscles of the lower extremities.

Alcoholic neuropathy of the lower extremities is detected when the pathology is associated with alcohol abuse.

Toxic neuropathy of the lower extremities is the result of neurotoxic effects of a number of substances (which were listed above).

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Complications and consequences

Neurological pathologies of the lower extremities can have negative consequences and complications, in particular:

• burns and skin injuries due to loss of sensory nerve function;
• infectious lesions of soft tissues (in patients with diabetes);
• Weakness of the foot muscles and loss of coordination can lead to unbalanced pressure being placed on the ankle joint while walking, causing it to become deformed over time.

Peripheral neuropathy affects the motor nerves and can result in a partial or complete inability of muscle fibers to contract and tone to provide musculoskeletal function.

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Diagnostics neuropathies of the lower extremities

Comprehensive diagnostics of neuropathy of the lower extremities includes:

• performing a physical examination (including checking tendon reflexes), a detailed medical history and a detailed analysis of symptoms;
• laboratory tests – blood tests (general and biochemical, for sugar and glucagon levels, for antibodies, for the content of various enzymes, thyroid-stimulating and some other hormones); blood and urine tests for paraprotein.

Instrumental diagnostics include: electromyography (determination of electrical activity of muscles), electroneuromyography (study of nerve conduction), X-ray of the spine, contrast myelography, CT of the spinal cord and MRI of the brain, ultrasound angiography of cerebral vessels.

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Differential diagnosis

Based on symptoms, standard laboratory and additional examinations (nerve and muscle biopsies, as well as biopsies to study peripheral nerves), differential diagnosis is carried out.

Treatment neuropathies of the lower extremities

Treatment that addresses the underlying cause of neuropathy may prevent further nerve damage, but it is not always possible. Symptomatic therapy is then prescribed, as well as methods to maintain muscle tone and physical function of the lower extremities.

For example, in cases of bacterial infection such as leprosy or Lyme disease, antibiotics are used.

Neuropathy of the lower extremities caused by diabetes can be treated by monitoring blood sugar levels, including the use of thioctic acid preparations (Thioctacid, Octolipen, Thiogamma, etc.). These drugs are also used for alcoholic and toxic neuropathies. Read more - Treatment of diabetic neuropathy

When the pathology occurs due to a lack of vitamins, vitamins B1 and B12 are administered intramuscularly, and vitamins A, E, D, as well as calcium and magnesium are taken orally.

In peripheral neuropathy that accompanies autoimmune diseases, multiple motor neuropathy, and also in the initial stage of Guillain-Barr syndrome, plasmapheresis is performed and corticosteroids and immunoglobulins are administered intravenously.

Human immunoglobulin with IgG antibodies (produced under the trade names Intraglobin, Pentaglobin, Sandoglobin, Cytopect, Imbiogam, etc.) is administered intravenously by drip (the dose is determined individually). Drugs of this group are contraindicated in the presence of renal failure, severe allergies and diabetes mellitus. Side effects of immunoglobulins may include chills, fever, headache, general weakness and increased drowsiness; an allergic reaction with coughing and bronchial spasm, as well as nausea and vomiting, are possible.

If patients do not suffer from bronchial asthma, angina or epilepsy, the use of drugs from the group of reversible cholinesterase inhibitors is indicated: Oxazil, Amiridin, Neuromidin, Galantamine hydrobromide, etc. Thus, Oxazil is taken orally (0.01 g three times a day), and a 1% solution of Galantamine is administered subcutaneously - once or twice a day.

Painkillers are used for neuropathy of the lower extremities: tricyclic antidepressants (Nortriptyline), non-steroidal anti-inflammatory drugs (Naproxen, Ketoprofen, Meloxicam or Ibuprofen - one tablet once a day).

Locally, ointments and gels are used for pain in case of neuropathy of the lower extremities: Ketonal (Fastum gel, Bystrumgel) with ketoprofen; Diclofenac (Diklak, Diclofen, Voltaren emulgel); Nise gel (with nimesulide). Doctors also recommend ointments with hot pepper extract capsaicin (Kapsikam, Espole, Finalgon), which not only relieve pain, but also improve tissue trophism.

In cases of nerve damage due to compression or tumor, surgical treatment is used.

In almost all cases, drug therapy is supplemented by physiotherapeutic treatment of neuropathy of the lower extremities: electrophoresis, acupuncture, magnetic therapy, ozone therapy, therapeutic massage, balneological procedures. Physical therapy and exercises for neuropathy of the lower extremities help maintain muscle tone and the functioning of the musculoskeletal system.

In addition, daily exercise for lower extremity neuropathy or an hour-long walk helps control blood sugar levels and stimulate blood circulation.

Folk remedies

Some patients may find that symptoms of peripheral neuropathy can be alleviated by folk remedies:

• taking evening primrose oil orally, which contains alpha-lipoic and gamma-linolenic fatty acids;
• daily consumption of 4 g of fish oil (a source of omega-3 fatty acids) or a tablespoon of flaxseed oil;
• grape seed extract (for nerve demyelination);
• extract of the Eryneceus hericium mushroom (Hericium еrinaceus), which promotes the normal formation of the myelin sheaths of nerve fibers;
• foot massage with castor oil (every other day).

Recommended herbal treatments include decoctions and infusions of St. John's wort, elecampane, blueberry or bilberry leaves, coleus (Coleus forskohlii) and smoke tree (Cotini coggygriae) leaves, and amla or Indian gooseberry (Emblica officinalis) extract.

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Nutrition for neuropathy of the lower extremities

Neurologists do not prescribe a special diet for neuropathy of the lower extremities, but recommendations for proper nutrition must be taken into account.

For example, it is necessary to consume foods rich in omega fatty acids: fresh fish (mackerel, tuna, salmon, herring, sardines, trout), nuts, peanuts, olive oil.

By the way, fish and meat by-products replenish vitamin B12 reserves, and legumes, rice, buckwheat, oatmeal, garlic, sunflower and pumpkin seeds replenish vitamin B1 reserves.

To saturate the body with L-carnitine, the diet should include red meat and dairy products (primarily cheese and cottage cheese).

Prevention

The prevention regimen for diabetic neuropathy includes a diet (to significantly reduce the amount of carbohydrates) and increased physical activity – morning exercises.

Peripheral neuropathies can only be prevented if the diseases that cause them can be avoided. Steps a person can take to prevent potential problems include vaccines against diseases that cause neuropathy, such as polio and diphtheria.

Precautions when using certain chemicals and medications are recommended to prevent neurotoxic effects. And managing chronic conditions such as diabetes can also reduce the chances of developing peripheral neuropathy.

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Forecast

The prognosis for the development and outcome of lower extremity neuropathy varies depending on the underlying cause and nerve damage – from a reversible problem to a potentially fatal complication. In mild cases, the damaged nerve regenerates. Dead nerve cells cannot be replaced, but they can regenerate after damage. And with congenital demyelinating neuropathies, complete recovery is impossible.

Assessing the outlook for patients with alcoholic neuropathy is difficult because it is difficult to persuade chronic alcoholics to stop drinking, although their neurological problems in their legs can lead to severe disability.

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