Sensory neuropathy of the lower and upper extremities

Axonal polyneuropathy is a pathology of the peripheral nervous system that develops as a result of damage to the peripheral nerves. The basis of the pathology - the defeat of the axons, myelin sheaths or the bodies of nerve cells. Axonal polyneuropathy impairs the patient and develops severe complications: diabetic foot syndrome, paralysis, anesthesia.

Polyneuropathy is manifested by a decrease in muscle strength, impaired sensitivity and local autonomic lesions in the area of ​​neuropathy. Usually the nerves are affected symmetrically in distant areas of the body: arms or legs. The lesion in the course of development smoothly moves to close areas: foot → ankle → shin → hip → pelvis.

Polyneuropathy is caused by the following reasons:

  1. Chronic diseases: diabetes mellitus (50% of all cases of neuropathy), HIV infection (HIV-infected polyneuropathy develops in 30% of cases), tuberculosis.
  2. Acute intoxication: arsenic, methyl alcohol, organophosphorus compounds, carbon monoxide, chronic alcohol consumption (developed in 50% of alcoholics).
  3. Metabolic states: deficiency of B vitamins, uremia.
  4. Long-term medication: Isoniazid, Metronidazole, Vincristine, Dapsone.
  5. Hereditary predisposition, autoimmune diseases.

The above factors cause endogenous and exogenous intoxication. Metabolic and ischemic disorders occur in the nerve. The nerve tissue and the secondary myelin sheath are damaged.

Toxic compounds that come from the environment, metabolites affect the peripheral nerve. More often it happens in case of liver failure, when untreated hazardous chemical compounds accumulate in the bloodstream, in cases of lead, lithium and arsenic poisoning.

Among endogenous intoxications, metabolic disturbances and accumulation of toxic substances in diabetes mellitus and renal failure are more common. As a result, the cylindrical axis of the axon is affected. Peripheral nerve damage due to endogenous intoxication can reach a point where sensitivity is completely lost. This is demonstrated by electroneuromyography, when a stimulus is applied to the skin and there is no sensory response in the nerve.

With strong exposure to chemical agents, complex axonal demyelinating polyneuropathy develops. Axonal-demyelinating polyneuropathy occurs against the background of uremic intoxication, severe lead poisoning, and chronic administration of Amiodarone in non-therapeutic doses. The most severe lesions are observed in insulin-dependent diabetes mellitus, when malignant glucose values ​​are observed in the blood.

The clinical picture develops slowly. Signs are divided into groups:

  • Vegetative disturbances. Axonal polyneuropathy of the lower extremities is manifested by local sweating of the legs, hot flashes, cooling.
  • Sensory disturbances. Manifested by a decrease in tactile and temperature sensitivity. The threshold of sensitivity of low temperatures rises: the patient may keep his foot in the cold for a long time and not feel it, which causes frostbite. Often there are paresthesias: numbness, crawling, tingling.
  • Pain syndrome. It is characterized by neuropathic aching or sharp, like electrical shocks pains in the affected area.
  • Movement disorders. Due to damage to the nerve and myelin sheaths, motor activity is disturbed: the muscles are weakened and atrophy, even paralysis.

There are positive (productive) symptoms: convulsions, small tremor, twitching (fasciculation), restless legs syndrome.

Axonal sensorimotor polyneuropathy is manifested by systemic symptoms: increased blood pressure and heart rate, pain in the intestines, excessive sweating, frequent urination.

Axonopathies are acute, subacute and chronic. Acute axonal polyneuropathy develops on the background of heavy metal poisoning, and the clinical picture develops in 3-4 days.

Subacute neuropathies develop within 2-4 weeks. Subacute course is characteristic of metabolic disorders.

Chronic axonopathies develop over a period of 6 months to several years. Chronic axonal polyneuropathy is characteristic of alcoholism, diabetes, cirrhosis of the liver, cancer, uremia. Chronic course is also observed with uncontrolled intake of Metronidazole, Isoniazid, Amiodarone.

Diagnosis and treatment

Diagnosis begins with anamnesis. The circumstances of the disease are being clarified: when the first symptoms appeared, what was manifested, whether there was contact with heavy metals or poisoning, what medicines the patient was taking.

Concomitant symptoms are investigated: are there any impairments of coordination, mental disorders, decreased intelligence, how large are lymph nodes, complexion. Blood is collected and sent: the level of glucose, the number of erythrocytes and lymphocytes are examined. Calcium, glucose, urea and creatinine levels are examined in the urine. Liver samples are collected through a biochemical blood test - this is how the liver is examined.

The patient is assigned an instrumental diagnosis:

  • Electromyography: the reaction of nerve fibers to the stimulus is investigated, the activity of the autonomic nervous system is assessed.
  • Radiography of the chest cavity.
  • Biopsy of the cutaneous nerve.

Treatment of axonal neuropathy:

  1. Etiological therapy. Aims to eliminate the cause. If it is diabetes mellitus - normalize blood glucose levels, if alcoholism - cancel alcohol.
  2. Pathogenetic therapy. It is aimed at restoring the work of the nerve: vitamins of group B, alphalipolyic acid are introduced. If it is an autoimmune disease, corticosteroids are prescribed - they block the pathological effect on myelin and nerve fibers.
  3. Symptomatic therapy: pain is eliminated (antidepressants, opioid narcotic analgesics).
  4. Rehabilitation: physiotherapy, physiotherapy, occupational therapy, massage.

The prognosis is conditionally favorable: when normalization of glucose level, elimination of pathological mechanisms and implementation of medical recommendations, reinnervation occurs - sensitivity gradually recovers, movements and vegetative disturbances disappear.

Medical expert articles

Peripheral nerve impairment with impaired sensitivity is sensory neuropathy. Consider the main causes of the disease, types, symptoms, methods of treatment.

Neuropathy is a disease that occurs when nerve function is impaired. According to the International Classification of Diseases ICD-10, this pathology belongs to category VI. Diseases of the nervous system.

G60-G64 Polyneuropathy and other lesions of the peripheral nervous system:

  • G60 Hereditary and idiopathic neuropathy.
  • G61 Inflammatory polyneuropathy.
  • G62 Other polyneuropathies.
  • G63 Polyneuropathy in diseases classified elsewhere.
  • G64 Other disorders of the peripheral nervous system. Peripheral nervous system disorder NOS.

Structural abnormalities in the central and peripheral parts of the nervous system are manifested by trophic and vascular disorders in the distal extremities, impaired sensitivity, and peripheral paralysis. In severe cases, the trunk and neck muscles are involved in the pathological process.

, , , , ,


According to medical statistics, sensory neuropathy is diagnosed in 2% of people. In elderly patients, polyneuropathy rate is more than 8%. One of the main causes of the disease is diabetes mellitus, genetic predisposition, chronic vitamin B deficiency, traumatic injuries and severe intoxication of the body.

, , , , , , ,

Causes of sensory neuropathy

Neuropathy develops due to many factors. In most cases, peripheral nerve damage is caused by the following reasons:

  • Violations of the body's immune system. Immunity produces antibodies, attacks its own immune cells and nerve fibers.
  • Metabolic disorders.
  • Intoxication.
  • Tumor diseases.
  • Various infections.
  • Systemic pathology.

Isolated sensitivities are extremely rare. Their appearance is most often caused by damage to thin and / or thick nerve fibers.

Sensory Neuropathy for Diabetes

One of the serious complications of type 1 and type 2 diabetes is sensory neuropathy. In diabetes, about 30% of patients experience this problem. Pathology is characterized by sharp burning pains, crawling on the skin, numbness of the legs and their muscular weakness.

Diabetic neuropathy has several types:

  • Peripheral - symmetrical (sensory, distal), asymmetrical (motor, proximal), radiculopathy, mononeuropathy, visceral.
  • Central - encephalopathy, acute neuropsychiatric disorders due to decompensation of metabolism, acute violation of cerebral circulation.

The process of therapy begins with a comprehensive diagnosis aimed at determining the causes and mechanism of disease development. Patients are shown a clear regulation of the concentration of sugar in the blood, the use of antioxidant, vascular, metabolic drugs. In case of severe pain syndrome, an anesthetic is prescribed. Early diagnosis and treatment can reduce the risk of complications. Fully cure the pathology is impossible.

, ,

Risk factors

The development of neuropathy can be triggered by such factors:

  • Acute deficiency of vitamins of group B - these substances are necessary for the full functioning of the nervous system. A deficiency of nutrients over an extended period of time leads to polyneuropathy and other pathologies.
  • Genetic predisposition - some metabolic disorders of hereditary nature can cause damage to nerve fibers.
  • Endocrine diseases - diabetes mellitus disrupts the vessels that are responsible for the nutrition of the nerves. This leads to metabolic changes in the myelin sheath of nerve fibers. If the disease is caused by diabetes, then neuropathy affects the lower limbs.
  • Intoxication of the body - nerve damage can be triggered by chemicals, various medications, and alcohol. The risk group includes people with infectious diseases. When poisoning the body with carbon monoxide or arsenic, the disease develops over a very short period of time. In some cases, the disease is a complication / side effect of medication.
  • Traumatic injuries - various injuries and surgical interventions in which there was damage to the nerve fibers, can cause not only sensory neuropathy, but also polyneuropathy. Most often, the pathological symptoms are observed in diseases of the spine (osteochondrosis, herniated intervertebral discs).
  • Pregnancy - a specific reaction of the immune system to the fetus, a deficiency of vitamins and minerals, toxicosis and other factors can cause nerve damage. Neuropathy occurs at any stage of pregnancy.

To reduce the risk of developing the disease should be eliminated or to minimize the effect of the above factors.

, , , , , , ,

The mechanism of development of neuropathy depends on its root cause, therefore, pathogenesis is represented by two pathological processes:

  • Damage to the axon (axial cylinder of the nerve fiber) - in this case, the process of functioning of nerve and muscle cells is disturbed. The nerves with long axons are involved in the pathological process, which leads to denervation changes in the muscle. Occurs due to the impact on the nerves of genetic, exogenous or endogenous factors.
  • Nerve fiber demyelination is a violation of the nerve impulse, which leads to a decrease in the speed of the nerve. Against this background, muscular weakness develops, earlier loss of tendon reflexes without muscular atrophy. In most cases, demyelination is associated with autoimmune processes, the formation of antibodies to immune cells, genetic abnormalities, and intoxication.

Both pathological processes are interconnected. As in the case of an axonal lesion, secondary demyelination occurs, and in the demyelination of the nerve fiber an axonal disorder develops. Diabetic sensory neuropathy develops after an acute disorder of carbohydrate metabolism or rapid compensation of insulin hyperglycemia.

, ,

Symptoms of sensory neuropathy

Impaired sensitivity develops due to various causes and factors. Pathology has several types and forms, but they all have similar symptoms:

  • Muscle weakness of the upper and lower extremities.
  • Swelling of the legs and arms.
  • Goosebumps, burning, paresthesia and other strange sensations in the limbs.
  • Decreased sensitivity of the arms and legs.
  • The emergence of unexplained pain and discomfort.
  • Trembling fingers, involuntary muscle twitching.
  • Increased sweating.
  • Coordination disorder, dizziness.
  • Slow wound healing.
  • Heart palpitations.
  • Respiratory disorders.

Sensory neuropathy begins to manifest itself from the fingers, feet. Gradually, the pathological process rises. In severe cases, patients have atrophied both arms and legs, which leads to their disability.

Sensory manifestations of the disease can be positive and negative. The first are:

  • Heightened perception of pain.
  • Burning.
  • Paresthesia.
  • Hypersensitivity to tactile stimuli.
  • Acute pain syndrome.

As for negative sensory symptoms, this is a decrease in sensitivity in the limbs and lower abdomen. Most often, the negative form develops with acute deficiency of vitamins E and B12. Patients are observed movement disorders and severe weakness in the limbs. The muscles of the head, neck, throat, upper body can be involved in the pathological process. Patients have painful cramps, uncontrolled muscle twitching.

The above symptoms can be either pronounced or mild. In most cases, neuropathy develops within a few years, but it can occur suddenly, in a couple of weeks.

Sensory signs of neuropathy completely depend on the degree of involvement of nerve fibers in the pathological process.

  • If large peripheral nerves are affected, then there is a decrease in sensitivity to a light touch. Patients develop unstable atactic gait, weakness of the deep muscles of the limbs.
  • With the defeat of small nerve fibers there is a decrease in temperature and pain sensitivity. Because of this, the level of injury increases.

Many patients note spontaneous pain and contact paresthesias, which indicate the simultaneous destruction of all types of nerve fibers. As the disease progresses, the end of the short nerves of the trunk, chest and abdomen are involved in the pathological process.

Motor sensory neuropathy

Charcot-Marie-Tut disease or motor-sensory neuropathy is peripheral nerve damage with impaired sensitivity.Pathology is characterized by progressive polyneuropathy with damage to the muscles of the distal extremities. In most cases, the disease has a genetic origin.

The first signs of a violation occur at the age of 15-30 years. There is a weakness and atrophy of the muscles of the distal upper extremities. Gradually, the muscles of the distal legs are involved in the pathological process. The tendon reflexes from the hands quickly atrophy, the knee and Achilles reflexes are reduced. All patients develop deformity of the feet.

As the pathology progresses, all types of sensitivity decrease. A number of patients show signs of static and dynamic cerebellar ataxia. In the pathological process may be involved proximal leg, the development of scoliosis.


Hereditary sensory neuropathy

According to studies, about 70% of neuropathies are hereditary. Genetically heterogeneous disease occurs with a progressive lesion of peripheral nerves.

Clinical manifestations of the disease:

  • Weakness and atrophy of the muscles of the distal extremities.
  • Deformation of the limbs.
  • Impaired sensitivity.
  • Tendon hypo / areflexia.
  • Coordination Disorders.

This form of sensory neuropathy has a strong resemblance to other types of this disease, therefore it requires differentiation at the clinical level. Treatment and prognosis of the disease depends on its early diagnosis.

, , ,

Peripheral sensory neuropathy

Peripheral nerve damage leads to impaired sensitivity. The disease develops due to many reasons, among which are the most common:

  • Trauma to the nerve.
  • Tumor lesions.
  • Immune disorders.
  • Intoxication.
  • Acute deficiency of vitamins in the body.
  • Vascular diseases.
  • Vasculitis
  • Blood diseases.
  • Metabolic disorders.

Peripheral nerve damage occurs in endocrine diseases, viral and bacterial infections, drug intoxication. The presence of a huge number of possible risk factors significantly complicates the process of identifying the root cause.

Signs of peripheral nerve damage:

  • Atrophy of the muscles of the limbs.
  • Weakness in arms and legs.
  • The sensation of burning and paresthesia of the arms and legs.
  • Reduction of reflexes or their loss.
  • Peripheral paralysis.

For diagnosis, a comprehensive examination of the patient. The patient is prescribed CT, MRI, neuroelectromyography, biopsy of the skin / nerve. For the treatment of used drugs, physiotherapy and various rehabilitation techniques aimed at the restoration of motor function and nervous sensitivity.


Distal sensory neuropathy

This type of disease most often acts as a form of diabetic polyneuropathy and occurs in 33% of people with diabetes. Pathology is manifested symmetric lesion of the lower extremities. Loss of sensation occurs, pain and tingling of varying intensity occur. Atrophy of the muscles of the foot is also possible.

Sensory symptoms and pathological signs dominate over motor ones. With the defeat of large fibers there is a decrease in sensitivity to a light touch. This leads to a lack of coordination, the development of weakness of the deep muscles of the limbs.

If the small nerve fibers are damaged, then there is a decrease in pain and temperature sensitivity. The disease develops slowly, therefore, with early detection reduces the risk of ulceration and other life-threatening complications.


Sensory Neuropathy of the Limbs

One of the possible causes of impaired limb sensitivity is sensory neuropathy. Nerve disease most often occurs against the background of metabolic disorders of the body. Damage to nerve fibers is characterized by the following symptoms:

  • Loss of sensation
  • Numbness of the arms, legs.
  • Immunity of cold, heat, tactile impact.

But in some cases, the sensitivity on the contrary becomes acute and pronounced. Neuropathy of the lower limbs is more common than the upper. This is due to the increased load on the legs. At the same time, the causes and symptoms of lesions in both upper and lower extremities are similar.

In most cases, muscle cramps occur, due to malnutrition of the skin dryness appears and protective functions are reduced. In combination, this leads to slower healing of various injuries, minor purulent processes. Treatment begins by identifying the cause of the disease. Often it is diabetes and a hereditary predisposition. All patients are prescribed B vitamins, painkillers and anti-depressants.

, ,

Sensory neuropathy of the lower extremities

Nerve fibers are divided into several types: motor, sensitive and vegetative. The defeat of each of them has its own symptoms. For sensory neuropathy of the lower extremities is characterized by damage to the sensory nerve fibers.

The main causes of the disease include:

  • Hereditary predisposition
  • Autoimmune diseases.
  • Tumor lesions.
  • Drug intoxication.
  • Metabolic disorders.
  • Alcohol abuse.
  • Diabetes.
  • Poisoning the body.
  • Impaired renal function and liver.

Depending on the cause of the peripheral nerve fibers, these types of foot neuropathy are distinguished: dismetabolic, toxic, diabetic, alcoholic. The success of treating a pathology depends on determining and eliminating its root cause.

A, p.Arg204Gln) "target =" _ blank "rel =" noopener noreferrer "> 43,,

Sensory axonal neuropathy

Sensory-type axonal neuropathy is a disease with damage to sensory nerve fibers. It develops against the background of endocrine pathologies, vitamin deficiency, failure of the immune system, after acute intoxications and for a number of other reasons.

The main manifestations of axonal neuropathy:

  • Spastic and flaccid paralysis of the limbs.
  • Muscle twitching and cramps.
  • Change in sensitivity: tingling, burning, paresthesia.
  • Circulatory disorders: limb swelling, dizziness.
  • Coordination violation.
  • Changing tactile, temperature and pain.

To diagnose the pathological process and identify its localization is conducted electroneuromyography. With this procedure, it is possible to establish the degree of damage to the nervous tissue. Treatment is complex, aimed at eliminating the cause of the disease and preventing possible complications.


There are several forms of neuropathy, one of them is sensory, which is characterized by the involvement of sensory nerve fibers (numbness, pain, burning) in the pathological process. Most often, sensory impairment is distal and symmetrical.

Consider the main types of neuropathy, taking into account the types of affected sensory fibers:

  1. Sensory neuropathy in the defeat of thick nerve fibers:
  • Diphtheria
  • Diabetic
  • Acute Sensory Atactic
  • Dysproteinemic
  • Chronic inflammatory demyelinating
  • Against the background of biliary cirrhosis
  • In critical conditions.
  1. With predominant lesion of fine nerve fibers:
  • Hereditary (amyloid, autonomous)
  • Idiopathic
  • Diabetic
  • MGUS neuropathy
  • In diseases of the connective tissue
  • Vasculitis
  • Paraneoplastic pathology
  • Against the backdrop of renal failure
  • With sarcoidosis
  • Intoxication
  • HIV infection.

Each type of disease requires a comprehensive diagnosis with the study of pathogenesis. The treatment process depends on the stage and severity of the pathology.

, ,

The clinical picture of axonal neuropathy

If the work of the nerve is seriously impaired by squeezing or stretching, axonal neuropathy is diagnosed. There are also signs of tingling, numbness, and most patients complain of a burning sensation in the limbs. Sometimes this disease affects the work of some internal organs. Symptoms felt in the limbs may have varying degrees of pain. In exceptional cases, with axonal neuropathy, itching occurs, as well as chronic pain in combination with the main symptoms.

As a rule, severe axon damage is a definite consequence of a significant nerve injury. The anatomical structure of the nerve will be preserved by stretching or slight squeezing. Recovery of the functions of such a nerve is possible in a period from a couple of minutes to one month, depending on the severity of edema and the degree of ischemia. However, more serious injuries, for example, after a strong blow, can greatly disrupt the necessary integrity of the axons themselves, but the myelin sheath is not damaged.

Severe distal rupture of many axons often occurs during nerve degeneration. This pathology is called Wallerian rebirth. This nerve regeneration is characteristic of the growth of axons inside the myelin preserved shells. In this case, axons grow only in the direction of their direct terminal branching at approximately 1 mm per day.

With an even stronger injury, neuromesis is observed, in other words, an anatomical complete break of the entire nerve. This is often followed by the inevitable Wallerian rebirth. It is believed that the necessary regeneration of axons, due to severe injury, is always incomplete. Some motor fibers can sometimes replace any sensitive fibers, or even head towards the so-called "alien" muscles.

Axonal degeneration is a completely different mechanism for the development of axonal neuropathy. It is this degeneration caused by a serious violation of the typical metabolism directly in the body of the neuron. As a consequence, the necessary axoplasmic current is then significantly hampered. The most distant large areas of the nerve are always the first to suffer greatly, after which this dangerous process also spreads in a proximal direction.

This mechanism is considered the main factor of all distal axonal neuropathies. Significant damage to the motor neuron bodies in motor neuropathies could be attributed to various diseases of the spinal cord, if the clinical picture was caused only by nerve damage. That is why this type of disease is considered along with axonal neuropathies.

It should be noted that the characteristic symptoms of motor-type axonal neuropathies are fasciculation, atrophy and muscle weakness. With prolonged damage in severe cases, all tendon reflexes are noticeably weakened. It is also often found loss of reflexes, as a rule, only at the beginning of the disease. It has been observed that with axonal neuropathies of the sensory type, different sensitivity zones are often violated, approximately equally.

Schwann cells suffer a second time with distal axonal neuropathies and Wallerian degeneration. In most cases, their number decreases, or they disappear altogether.

Expert Editor: Pavel Alexandrovich Mochalov | D.M.N. general practitioner

Education: Moscow Medical Institute. I. M. Sechenov, specialty - “Medicine” in 1991, in 1993 “Occupational diseases”, in 1996 “Therapy”.

Watch the video: Peripheral Neuropathy (December 2019).