PNP and PCP neurology. Finger-nose test to assess coordination of movements and their disorders

Parkinsonism-plus syndromes are a group of parkinsonian disorders that differ from IPD in the presence of distinct additional neurological abnormalities. In these pathological conditions, cerebellar, autonomic, pyramidal, oculomotor, sensory cortical, bulbar, cognitive and psychiatric impairments may be observed, as well as apraxia and movement disorders that are not characteristic of IPD (for example, myoclonus, dystonia or chorea).

These neurological and mental disorders may appear in the early stages of the disease. Rapid development of gait disturbances and falls or postural instability, absence of resting tremor, early dementia, and supranuclear gaze palsy are signs that should be considered as a basis for the assumption of Parkinsonism-plus syndrome. The Parkinsonian components of these pathological conditions, such as akinesia and rigidity, usually do not respond well to treatment with levodopa, although transient benefits may be observed early in the course of treatment.

Such diseases in general, they appear in the fifth or sixth decade of life with an average survival time of 5-15 years. The cause of death is usually intercurrent infections - pneumonia or sepsis. The etiopathogenesis of this group of diseases is in most cases unknown.

Despite the obvious clinical differences between UPS and "parkinsonism-plus" syndromes, distinguishing between these conditions can be difficult. During a clinicopathological study, 24% of patients with clinically established IPD at autopsy revealed various variants of parkinsonism syndrome. In “parkinsonism-plus” syndromes, CT or MRI of the brain may be uninformative. They may detect widespread cerebral or cerebellar atrophy and may sometimes reveal focal changes in the caudate nucleus, globus pallidus, cerebellum, or midbrain.

General and biochemical blood tests, serological tests, EMG, and evoked brain potentials are usually uninformative. The EEG may detect nonspecific abnormalities such as slowing of background activity. Specific features of individual variants of this syndrome are described below.

Progressive supranuclear palsy (PSP)

Clinical picture of supranuclear palsy. Early onset of gait disturbances and loss of postural reflexes with falling backwards and freezing when walking, combined with supranuclear gaze palsy (initially limited downward gaze), suggest PSP. Additional signs supporting the diagnosis are axial rigidity and cervical dystonia with a predominance of extension positions, generalized bradykinesia, “apraxia” of opening and closing of the eyelids, blepharospasm, a frozen facial expression with a wrinkled forehead and a monotonous voice (but not hypophonia).

Cognitive impairment usually mild, but may vary. Executive functions are especially affected. The presence of severe bradykinesia and a typical frozen facial expression suggests Parkinson's disease in such patients, however, impaired mobility of the eyeballs, the frequent absence of tremor and the effect of levodopa administration help to establish the correct diagnosis.

Neuroimaging methods for supranuclear palsy. CT and MRI sometimes reveal clear signs of atrophy in the midbrain area, and later in the pons.

Pathomorphology of supranuclear palsy. Signs of neuronal death and gliosis are observed. Predominantly cholinergic neurons of the basal ganglia and brainstem nuclei are affected, with obvious preservation of cortical structures. Inclusions containing aggregates of hyperphosphorylated tau protein are found in the cytoplasm of neurons.

Corticobasal degeneration (CBD)

Clinical picture of corticobasal degeneration. CBD may appear as a severely asymmetric or unilateral akinetic-rigid syndrome accompanied by limb apraxia, alien limb phenomenon, cortical sensory disturbances, stimulus-sensitive myoclonus, action tremor, or positional tremor. Signs of supranuclear gaze palsy, cognitive impairment, and pyramidal symptoms may also be observed.

Neuroimaging methods for corticobasal degeneration. MRI and CT scans in some patients reveal asymmetric atrophy of the frontoparietal regions of the brain. with Pathomorphology. In the frontoparietal regions and substantia nigra, gliosis and a decrease in the number of neurons are detected. Swollen achromatic neurons and basophilic nigral inclusions are characteristic, which resembles the picture of changes in Pick's disease. Abundant inclusions containing aggregates of hyperphosphorylated tau protein are found in the cytoplasm.

> Polyneuropathy

This information cannot be used for self-medication!
Consultation with a specialist is required!

What is polyneuropathy?

Polyneuropathy (PNP) is a disease of the peripheral nervous system, resulting from damage to the nerves by some negative factor. As a result of the influence of this factor, the conduction of impulses along the nerve fiber is slowed down or completely blocked.

What are the symptoms of the disease?

PSP is manifested by the following symptoms: decreased sensitivity in the arms and legs, severe muscle weakness, pain in the limbs. If the disease progresses rapidly, trophic ulcers may develop. The appearance of the limbs with PSP is pale, with areas of hyperemia (redness), and cold to the touch. In an advanced case of the disease, the patient has difficulty raising an arm or leg - so-called flaccid paralysis develops.

Classification of polyneuropathies

Based on the nature of the primary damaging factor, PNS are divided into inflammatory, post-traumatic, allergic (autoimmune), and toxic. Depending on the speed of development of the disease and the severity of clinical manifestations, acute, subacute and chronic forms of the disease can be distinguished.

Who is at risk for developing this pathology?

People who abuse alcohol and have diabetes are at risk for developing PSP. The risk of developing this disease increases when working in hazardous conditions: in smoky, dusty, gas-filled rooms, in hot workshops of metallurgical production. Polyneuropathy can be provoked by factors such as hypothermia of the extremities, frequent infectious diseases, serum sickness, oral poisoning with salts of heavy metals, and vitamin deficiency.

A special case of this pathology is Guillain-Barré syndrome, the main cause of which is considered to be autoimmune damage to nervous tissue. Previous diphtheria can also provoke polyneuropathy.

Methods for diagnosing the disease

A general practitioner can suggest a diagnosis of polyneuropathy, but to make a final diagnosis, he must refer the patient to a neurologist who will conduct the necessary examinations. Comprehensive diagnostics includes general clinical blood and urine tests, and examination of neurological status. Of the specific diagnostic methods, electroneuromyography is used, which helps determine the degree of damage to the nerve fiber by slowing down the conduction of the nerve impulse. If Guillain-Barre disease is suspected, the cerebrospinal fluid (CSF) is examined for the presence of antibodies.

Basic principles of treatment

Neurologists treat any type of neuropathy. Drugs that improve nerve conduction are used. For autoimmune lesions, glucocorticosteroids are prescribed. Vitamin therapy plays an important role, especially in cases of alcoholic polyneuropathy and PSP caused specifically by hypovitaminosis or vitamin deficiency. For toxic PSP, plasmapheresis is used to remove toxins from the body. Massage, exercise therapy, acupuncture help maintain muscle tone at a sufficient level.

Forecast and prevention of polyneuropathy

The prognosis for neuropathy depends on the cause of the disease. With Guillain-Barré syndrome, recovery occurs in 70% of cases. For other types of PSP, the cure rate is also quite high. In the case of alcoholic etiology of PSP, the prognosis is determined by the patient’s ability to stop drinking alcohol. In diabetic PSP, the prognosis depends on the effectiveness of hypoglycemic therapy. Untreated diabetes can lead to gangrene of the lower extremities and amputation.

Prevention of polyneuropathy involves maintaining a healthy lifestyle and giving up bad habits (smoking, drinking alcohol). In the presence of chronic diseases, it is necessary to monitor the general condition of the body, carry out all medical prescriptions and, if necessary, correct treatment.

The brachiocephalic arteries are the vessels that are responsible for supplying blood to the brain, tissues of the head, shoulder girdle and arms. They are separated from the aorta at shoulder level. The research method is based on the use of the Doppler effect, which is named after the Austrian scientist Christian Doppler who discovered it.

The main advantages of Dopplerography of neck vessels:

Dopplerography is a non-invasive and therefore painless method;
it does not require much time - the examination takes only a few minutes;
it is an inexpensive study;
At the same time, Doppler ultrasound is informative and will help the doctor make the correct diagnosis.

Ultrasound of the BCA allows you to determine:

condition of the vascular walls;
vascular damage even in the early stages;
presence and severity of atherosclerosis;
presence and severity of stenosis;
speed and nature of blood flow.

Doppler ultrasound also shows the anatomical features of the vessels of the neck - for example, how strongly they twist around the spine.

With all these advantages, keep in mind that Doppler ultrasound is a more primitive method compared to duplex and triplex vascular scanning. They are more informative, but require more sophisticated equipment and are more expensive.

A duplex or triplex scan will provide more information to help your doctor choose the right treatment. The information content is further enhanced by the use of color mapping method during ultrasound diagnostics.

Indications and contraindications

The risk group for the development of cerebrovascular accidents includes people with diseases such as:

diabetes;
hypertension;
cervical osteochondrosis;
autoimmune vascular lesions (vasculitis);
obesity;
angina pectoris;
cardiac ischemia;
history of heart attack and stroke;
heart attacks, strokes, hypertension and atherosclerosis in the anamnesis of relatives;
age over 40 years.

In the presence of these diseases, periodic (once a year or every two years) scheduled ultrasound examination of the neck vessels is indicated. It is also recommended that people with a smoking history of 15 years or more undergo this examination regularly.

Direct indications for undergoing ultrasound scanning of the brachiocephalic trunk are also:

headache;
dizziness;
fainting;
sleep disorders;
permanent or transient visual disturbances;
flickering of flies, a veil before the eyes;
tinnitus, ringing in the head;
coordination problems;
disturbance of tactile sensations, weakness in the arms and legs;
impaired concentration;
memory impairment.

For more information about the indications and examination, watch the video:

Rules for preparing for the procedure and procedure

To prepare for the study, you need to adjust your diet. The day before the study, it is necessary to exclude foods that affect vascular tone:

drinks containing caffeine (tea, coffee, energy drinks);
alcohol;
salty foods.

Two hours before the procedure, refrain from taking hot baths and smoking, as well as staying in smoky rooms: in the first case, arteries and veins expand, in the second, they contract.

In addition, the results of BCA ultrasound are distorted by drugs that change vascular tone and affect the nature of blood flow. You should consult with your doctor about which medications need to be stopped before testing.

As noted above, Doppler ultrasound takes very little time. An experienced ultrasound specialist will only need a few minutes to perform all the necessary manipulations.

To carry out the procedure, you must undress to the waist. During the examination, the patient lies on the couch, periodically changing position - on his back, on his side, on his stomach - so that the diagnostic specialist can examine all the vessels that need to be checked.

Also, during ultrasound diagnostics of neck vessels, additional functional tests can be performed:

holding your breath;
changing the horizontal position of the body to a vertical one;
taking certain medications (most often nitroglycerin).

Principles for deciphering results and normal indicators

A diagnostic specialist can prepare a report immediately after the procedure is completed. When interpreting the results, the data obtained during the study is compared with normal indicators of the condition of the arterial walls and the nature of blood flow in each of them.

The conclusion states:

condition of the walls of blood vessels;
description of pathological changes, if any;
nature of blood flow.

Normally, there are no narrowings or atherosclerotic plaques in the vessels that would impede the movement of blood; the blood flow has no turbulence. In this case, blood moves freely through the arteries and veins, providing the brain, tissues of the head and arms with sufficient oxygen and nutrients.

The ultrasound specialist’s conclusion must be shown to the attending physician, who will compare the data obtained with the clinical picture, advise you on all issues and, if necessary, prescribe treatment.

Deviations from the norm and possible diagnoses

With changes in blood vessels and the nature of blood flow, the following concepts may appear in the conclusion:

stenosis is a pathological narrowing of the lumen of a vessel, as a result of which blood cannot freely pass through them;
aneurysm - a protrusion of a vessel wall as a result of its thinning, in which the wall of an artery or vein expands more than twice (learn about carotid artery aneurysm);
atherosclerosis - the formation of cholesterol plaques on the walls of blood vessels, which impede blood flow, resulting in an increased risk;
occlusion - disruption of the patency of a vessel due to damage to its wall;
turbulent flow - when blood moves through a vessel, turbulence is formed.

Average prices in Russia and abroad

The price of ultrasound Dopplerography in Russia ranges from 500 to 5000 rubles. The specific cost depends on the region and varies from one hospital or clinic to another, but the average price is 1000-1500 rubles. In neighboring countries the price is lower - for example, in Ukraine it is about 300 hryvnia.

At the same time, as noted above, ultrasound examination of the BCA is rarely used. In our country, it is mainly used in public clinics for treatment under the compulsory medical insurance policy. In paid clinics both in Russia and in other countries, today more advanced methods are used - duplex and triplex scanning of the brachiocephalic arteries with color mapping.

It does not require special preparation, with the exception of minor adjustments to the diet and the withdrawal of certain medications the day before the procedure, and at the same time it allows you to accurately assess not only the condition of the arteries, but also the nature of the blood flow in them. The procedure will allow the doctor to choose the right treatment to restore normal blood supply to the head and arms if it is disrupted, and to avoid the development of serious health problems - for example, to prevent a stroke.

However, this research method can already be considered outdated, and if possible, it is worth paying attention to more modern duplex scanning of the brachiocephalic arteries.

Polyneuropathy (PNP) is multiple lesions of peripheral nerves, which are manifested by flaccid paralysis, vegetative-vascular and trophic disorders, and sensitivity disorders. In the structure of diseases of the peripheral nervous system, polyneuropathy ranks second after vertebrogenic pathology. However, in terms of the severity of clinical signs and consequences, polyneuropathy is one of the most serious neurological diseases.

This pathology is considered an interdisciplinary problem, since it is encountered by doctors of different specialties, but primarily by neurologists. The clinical picture of polyneuropathy is characterized by decreased tendon reflexes, muscle atrophy and weakness, and sensitivity disorders. Treatment of the disease is symptomatic and aimed at eliminating the factors that provoked it.

Classification of polyneuropathies

Based on the predominant clinical manifestations, polyneuropathy is divided into the following types:

sensitive (symptoms of involvement of sensory nerves in the process predominate);
motor (predominance of symptoms of damage to motor fibers);
autonomic (symptoms show signs of involvement of autonomic nerves in the process, which ensure the normal functioning of internal organs);
mixed (symptoms of damage to all nerves).

Depending on the distribution of the lesion, distal limb lesions and multiple mononeuropathy are distinguished. According to the nature of the course, polyneuropathy can be acute (symptoms appear within a couple of days), subacute (the clinical picture takes a couple of weeks to form), chronic (symptoms of the disease bother from a couple of months to several years).

Based on pathogenetic characteristics, diseases are divided into demyelinating (myelin pathology) and axonal (primary damage to the axial cylinder). The following types of disease are distinguished depending on its etiology:

hereditary (Refsum disease, Dejerine-Sotta syndrome, Roussy-Levi syndrome);
autoimmune (axonal type of GBS, Miller-Flesher syndrome, paraneoplastic neuropathies, paraproteinemic polyneuropathies);
metabolic (uremic polyneuropathy, diabetic polyneuropathy, hepatic polyneuropathy);
nutritional;
infectious-toxic;
toxic.

Etiology and pathogenesis of polyneuropathies

Polyneuropathy is based on metabolic (dismetabolic), mechanical, toxic and ischemic factors that provoke the same type of morphological changes in the myelin sheath, connective tissue interstitium and axial cylinder. If the pathological process, in addition to the peripheral nerves, also includes the roots of the spinal cord, then the disease is called polyradiculoneuropathy.

Polyneuropathy can be provoked by various intoxications: lead, thallium, mercury, arsenic and alcohol. Drug-induced polyneuropathies occur in the case of treatment with antibiotics, bismuth, emetine, gold salts, isoniazid, sulfonamides, meprobamate. The causes of polyneuropathy can be different:

diffuse connective tissue pathologies;
cryoglobulinemia;
avitaminosis;
vasculitis;
viral and bacterial infections;
malignant neoplasms (lymphogranulomatosis, cancer, leukemia);
diseases of internal organs (kidneys, liver, pancreas);
diseases of the endocrine glands (hyper- and hypothyroidism, diabetes, hypercortisolism);
genetic enzyme defects (porphyria).

Polyneuropathy is characterized by two pathological processes - demyelination of the nerve fiber and axon damage. Axonal polyneuropathies arise due to problems with the transport function of the axial cylinder, which leads to disruption of the normal functioning of muscle and nerve cells. Due to disturbances in the trophic function of the axon, denervation changes occur in the muscles.

The process of demyelination is characterized by a violation of the saltatory conduction of the nerve impulse. This pathology is manifested by muscle weakness and decreased tendon reflexes. Demyelination of nerves can be triggered by autoimmune aggression, which is accompanied by the formation of antibodies to peripheral myelin protein components, exposure to exotoxins, and genetic disorders.

Clinical picture of polyneuropathy

The symptoms of polyneuropathy depend on the etiology of the disease. However, it is possible to identify common symptoms for all types of disease. All etiological factors that provoke the disease irritate the nerve fibers, after which the functions of these nerves are impaired. The most pronounced symptoms of irritation of nerve fibers are muscle cramps (cramps), tremor (trembling of the limbs), fasciculations (involuntary contractions of muscle bundles), muscle pain, paresthesia (a feeling of crawling on the skin), increased blood pressure, tachycardia (rapid heartbeat) .

Signs of nerve dysfunction include:

muscle weakness in the legs or arms (it develops first in the muscles furthest from the head);
atrophy (thinning) of muscles;
decreased muscle tone;
hypoesthesia (decreased skin sensitivity);
unsteadiness of gait while walking with eyes closed;
hypohidrosis (dry skin);
dizziness and flashing spots before the eyes when trying to get up from a lying position, fixed pulse.

Autoimmune polyneuropathies

The acute inflammatory form of the disease occurs with a frequency of one to two cases per hundred thousand people. It is diagnosed in men aged 20-24 and 70-74 years. It is characterized by the occurrence of symmetrical weakness in the limbs. The typical course of the disease is characterized by painful sensations in the calf muscles and paresthesia (numbness and tingling sensation) in the fingers, which are quickly replaced by flaccid paresis. In the proximal sections, muscle wasting and weakness are observed, and palpation reveals pain in the nerve trunks.

The chronic form of the pathology is accompanied by a slow (about two months) worsening of motor and sensory disorders. This pathology often occurs in men (40-50 years old and over 70 years old). Its characteristic symptoms are muscle hypotonia and hypotrophy in the arms and legs, hypo- or areflexia, paresthesia or numbness in the extremities. In a third of patients, the disease manifests itself with cramps in the calf muscles.

The vast majority of patients (about 80%) complain of autonomic and polyneuritic disorders. In 20% of patients, there are signs of central nervous system damage - cerebellar, pseudobulbar, pyramidal symptoms. Sometimes the cranial nerves are also involved in the process. The chronic form of the disease has a severe course and is accompanied by serious complications, so a year after its onset, half of the patients have partial or complete loss of ability to work.

Inflammatory polyneuropathies

The diphtheria form of the disease is characterized by the early appearance of oculomotor disorders (mydriasis, ptosis, diplopia, limited mobility of the eyeballs, paralysis of accommodation, decreased pupillary reactions to light) and bulbar symptoms (dysphonia, dysphagia, dysarthria). One to two weeks after the onset of the disease, paresis of the extremities, predominant in the legs, becomes evident in its clinical picture. All these symptoms are often accompanied by manifestations of intoxication of the body.

HIV-associated polyneuropathy is accompanied by distal symmetrical weakness in all extremities. Its early symptoms are mild leg pain and numbness. In more than half of cases, the following symptoms are observed:

distal paresis in the lower extremities;
loss or decreased Achilles reflexes;
decreased vibration, pain or temperature sensitivity.

All these symptoms appear against the background of other signs of HIV infection - fever, weight loss, lymphadenopathy.

Lyme borreliosis polyneuropathies are considered a neurological complication of the disease. Their clinical picture is represented by severe pain and parasthesia of the limbs, which are then replaced by amyotrophies. The disease is characterized by more severe damage to the arms than to the legs. In patients, deep reflexes in the hands may completely disappear, but the Achilles and knee reflexes are preserved.

Dysmetabolic polyneuropathies

Diagnosed in 60-80% of patients with diabetes. Early symptoms of this pathology are the development of paresthesia and dysesthesia in the distal parts of the extremities, as well as loss of Achilles reflexes. If the disease progresses, patients begin to complain of severe pain in the legs, which intensifies at night, as well as disturbances in temperature, vibration, tactile and pain sensitivity. Later, weakness of the foot muscles, trophic ulcers, and finger deformities are added to the symptoms of the disease. This disease is characterized by autonomic disorders: cardiac arrhythmia, orthostatic hypotension, impotence, gastroparesis, sweating disorder, impaired pupillary reactions, diarrhea.

Nutritional polyneuropathy

Alimentary polyneuropathy is caused by a lack of vitamins A, E, B. It is characterized by such manifestations as paresthesia, burning sensation, dysesthesia in the lower extremities. In patients, the Achilles and knee reflexes decrease or completely disappear, and amyotrophies appear in the distal parts of the arms and legs. The clinical picture of the pathology also includes heart pathology, swelling in the legs, weight loss, orthostatic hypotension, anemia, stomatitis, cheilosis, diarrhea, dermatitis, and corneal atrophy.

Alcoholic polyneuropathy

Alcoholic polyneuropathy is considered a variant of nutritional polyneuropathy. It is caused by a lack of vitamins PP, E, A and group B, which is caused by exposure to ethanol on the body. This disease manifests itself as pain in the legs, dysesthesia, and cramps. Patients experience pronounced vegetative-trophic disorders: changes in skin tone, anhidrosis of the hands and feet. In the distal parts of the legs and arms, a symmetrical decrease in sensitivity is detected.

Polyneuropathy of critical illness

Polyneuropathies of critical conditions occur due to severe injuries, infections or intoxication of the body. Such conditions are characterized by multiple organ failure. Pronounced signs of the disease are the early appearance of muscle weakness and contractures in the distal arms and legs, loss of deep reflexes, and lack of spontaneous breathing after stopping mechanical ventilation, which is not caused by cardiovascular or pulmonary pathology.

Hereditary polyneuropathies

Polyneuropathy, which has a hereditary etiology, usually manifests itself in patients aged 10-16 years. This disease is characterized by the following triad of symptoms: impaired superficial types of sensitivity, atrophy of the hands and feet, hypo- or areflexia. Patients also experience foot deformities.

Diagnosis of polyneuropathies

Diagnosis of polyneuropathy begins with collecting a medical history and patient complaints. Namely, the doctor should ask the patient how long ago the first symptoms of the disease appeared, in particular muscle weakness, numbness of the skin and others, how often he drinks alcohol, whether his relatives had this disease, and whether he suffers from diabetes. The doctor also asks the patient whether his activities involve the use of chemicals, especially salts of heavy metals and gasoline.

At the next stage of diagnosis, a thorough neurological examination is carried out to detect signs of neurological pathology: muscle weakness, areas of skin numbness, impaired skin trophism. Blood tests are required to identify all kinds of toxins, determine protein products and glucose levels.

For an accurate diagnosis, the neurologist may additionally prescribe electroneuromyography. This technique is necessary to identify signs of nerve damage and assess the speed of impulse transmission along nerve fibers. A nerve biopsy is performed, which involves examining a piece of nerves that is taken from the patient using a special needle. Additionally, consultation with an endocrinologist and therapist may also be required.

Treatment of polyneuropathies

Treatment tactics for polyneuropathy are chosen depending on its etiology. To treat a hereditary disease, symptomatic therapy is chosen, aimed at eliminating the most pronounced signs of pathology that worsen the patient’s quality of life. The goal of the autoimmune form of polyneuropathy will be to achieve remission. Treatment of alcoholic, diabetic and uremic polyneuropathies is reduced to slowing the course of the disease and eliminating its symptoms.

An important place in the treatment of all types of polyneuropathy is occupied by physical therapy, which helps prevent the appearance of contractures and maintain normal muscle tone. If the patient has respiratory problems, he is indicated for mechanical ventilation. There is currently no effective drug treatment for polyneuropathy that would get rid of it forever. Therefore, doctors prescribe maintenance therapy aimed at reducing the severity of the symptoms of the disease.

Treatment of porphyritic polyneuropathy involves prescribing glucose, symptomatic and painkillers to the patient.
For the treatment of chronic inflammatory demyelinating polyneuropathy, membrane plasmapheresis is used (a method of purifying the patient’s blood outside his body). If this technique turns out to be ineffective, then the doctor prescribes glucocorticosteroids. After starting therapy, the patient's condition improves within 25-30 days. After two months of treatment, you can begin to reduce the dose of the drug.
In addition to the neurologist, an endocrinologist plays an important role in the treatment of diabetic polyneuropathy. The goal of treatment is to gradually lower blood sugar levels. To eliminate the intense pain from which the patient suffers, drugs such as gabapentin, pregabalin, carbamazepine, and lamotrigine are prescribed.
Therapy for uremic polyneuropathy involves correcting the level of uremic toxins in the blood through kidney transplantation or program hemodialysis.
The success of treatment of toxic polyneuropathy depends on how quickly the patient’s contact with the toxic substance is stopped. If the disease is a consequence of taking medications, its treatment should begin with reducing their dosage. Timely administration of antitoxic serum will help prevent the worsening of diphtheria polyneuropathy with a confirmed diagnosis of diphtheria.

Prognosis for polyneuropathy

Patients diagnosed with chronic inflammatory demyelinating polyneuropathy have a favorable health prognosis. The mortality rate of patients with this diagnosis is very low. However, it is impossible to completely cure the pathology, so treatment involves eliminating its symptoms. Immunosuppressive therapy can achieve remission of the disease in more than 90% of cases. However, it must be remembered that the disease polyneuropathy is accompanied by numerous complications.

Hereditary polyneuropathy progresses very slowly, making its treatment difficult and the prognosis for patients poor. However, many patients manage to adapt and learn to live with their illnesses. A favorable prognosis for diabetic polyneuropathy is possible only if it is treated in a timely manner. Usually doctors manage to normalize the patient's condition. Only in the later stages of polyneuropathy can the patient complain of severe pain. The prognosis for the life of a patient with uremic polyneuropathy depends on the severity of chronic renal failure.

Polyneuropathy is a damage to the peripheral nerves and blood vessels that provide them with nutrition.

This pathological process is sometimes called polyneuropathy, changing one letter, neuropathy, polyradiculoneuropathy or polyneuritis, but the latter (polyneuritis) is perceived as inflammation, and for peripheral nerves the true inflammatory process is somehow not typical, if it occurs, it is very rare.

The basis of polyneuropathy is made up of other factors: metabolic disorders (a striking example is diabetic polyneuropathy), ischemic factors, mechanical damage, which give rise to morphological changes in nerve fibers. And even an infection that has entered the nerve fibers does not produce typical inflammation, but manifests itself as an allergic reaction. That is why the word “polyneuritis” is gradually disappearing from terminology.

If, in addition to the peripheral nerves, disorders affect the roots of the spinal cord, the disease is called polyradiculoneuropathy. The pathological process is most noticeable when the distal parts of the legs are affected (polyneuropathy of the lower extremities) - it is indicated by the characteristic “cock gait” of the patient.

The reasons for the development of this pathology are very diverse; almost any factor that has a negative impact on the body at least once can lead to the onset of the disease, while individual cases of the disease forever remain a mystery.

In most cases, patients see not just the word “polyneuropathy” in the “diagnosis”; usually some definition is added to it. And if the words “alcoholic” or “toxic” are more or less clear to people, then other terms (“axonal” and “demyelinating”) raise questions. In order for the reader to understand the meaning of these definitions, it will be necessary, based on data from various sources, to make an attempt to somehow classify this pathology, since a generally accepted version of the classification has not yet been developed.

Based on their origin, the following forms of polyneuropathy are distinguished:

Nutritional.
Hereditary.
Autoimmune.
Metabolic (hepatic, uremic, diabetic polyneuropathy).
Toxic.
Infectious-toxic.

Meanwhile, in the literature one can find another division of the disease according to the etiological factor, where they distinguish: inflammatory, although true inflammation is considered extremely rare, toxic, allergic And traumatic options.

demyelination due to neuropathy

Depending on the type of pathological process, two forms of the disease have been identified and it seems that opinions do not differ here:

Axonal polyneuropathy - it occurs when the axon is damaged;
Demyelinating – formed from demyelination of nerve fibers.

It should be noted that these two forms do not exist for long, and therefore do not always exist in their pure form: with primary damage to the axon, a demyelinating component is added as a secondary pathology, and with demyelination – an axonal one.

There is no particular disagreement regarding the classification of polyneuropathy according to the nature of its course, therefore in the description of the disease one can find:

Acute processes;
Subacute variant;
Chronic course.

In addition, depending on the predominance of symptoms of a particular type of neuropathy, motor, sensory vegetative forms are distinguished, which, however, in isolated form occur quite rarely, are more often observed motor-sensory or sensory-vegetative types of disease.

It is quite difficult to describe (or just list) all types of neuropathy - there are a lot of them, but it should be borne in mind that regardless of the etiological factor, all forms have common clinical manifestations, which, to the same extent as their origin, determine the therapeutic approach and prognosis of the disease .

Symptoms of polyneuropathy

typical areas affected by polyneuropathy

Systemic damage to the peripheral nerves is considered to be the main clinical manifestations characteristic of the entire group of neuropathies and is not so important: what type the pathological process belongs to and in what direction the pathological process moves - the main symptoms will be present:

Muscle weakness and atrophy;
Decreased tendon reflexes;
Peripheral paresis;
Sensitivity disorder in the distal extremities (hyposthesia, parasthesia, hypersthesia);
Trophic vegetative-vascular disorders.

Demyelinating PSP is manifested mainly by the suffering of large myelinated (motor and sensory) nerve fibers, while unmyelinated autonomic and sensory nerves, which provide superficial sensitivity, without being particularly involved in the process, remain intact and intact. This variant of the disease is manifested by loss of deep reflexes and disturbance of vibration sensations with relative preservation of surface sensitivity. Demyelination, affecting not only the distal parts of the limbs, over time expands its boundaries and begins to spread to the roots, manifesting itself:

Peripheral paresis;
Weakness of the limbs (distal parts);
Thickening of nerves in case of chronic course.

Such polyneuropathy of the lower extremities does not belong to irreversible processes. Provided that the etiological factor is eliminated and adequate treatment is carried out, the myelin sheaths are restored and neurological symptoms regress within 1.5 - 2 months.

Axonal neuropathies can affect different types of fibers with the gradual development of the pathological condition. Typical symptoms of this type of PSP include:

Sensory (pain, temperature) disorders;
Autonomic disorders;
Absence of deep reflex impairments in the early stages of the disease.

It is unlikely that one can expect a complete restoration of lost functional abilities in the case of axonopathy. Axons regenerate slowly, and the processes of surviving axons, although they try to compensate for the loss, are not able to do this fully.

However, given that to obtain a good effect from therapeutic measures, the causative factor is first of all important, special attention is paid to its search.

What factors cause peripheral nerves to suffer?

NK damage in diabetes

Diabetes mellitus is the main cause

Most often, neuropathy is meant when talking about complications of a very common disease throughout the globe - diabetes mellitus (diabetic neuropathy), so one cannot help but emphasize its dominant position in the list of causes. Damage to small vessels in diabetes mellitus is observed in half or more of patients with diabetes mellitus.

It is difficult to predict when the disease will manifest itself; this may happen at the beginning of the disease and become the first symptoms of diabetes, or the development of the disease may be delayed for an indefinite period, estimated in many years.

The main factor triggering the development of diabetic neuropathy is the ischemic component and metabolic disorders in the nerve fiber. The appearance of the first neurological signs of diabetic polyneuropathy (the sensation of vibration in the ankles is shortened, the Achilles reflexes are reduced) does not give reason to believe that the disease will begin to develop rapidly. A diabetic can live with these symptoms for many years without any other complaints until the process begins to progress, when

The clinical picture takes on a typical coloration for neuropathy:
A strong, very painful pain appears in the feet and legs, which becomes even more acute in warmth and at rest;
The feet become weak;
Autonomic innervation begins to suffer;
The intensity of the pain continues to increase over time - it becomes unbearable;
Simultaneously with the increase in pain, itching appears (not always, but very often), the color of the skin changes (from purple to black);

A diabetic foot develops, which not only leads to a decrease in the functionality of the lower extremities, but is often the reason for their amputation.

Polyneuropathy of the lower extremities, developing against the background of diabetes mellitus, is the most common serious complication of type 2 diabetes mellitus and a headache for endocrinologists, therefore, an established diagnosis (DM) is already a reason for the prevention of damage to nerve fibers, and the appearance of the first signs is for a revision of therapy in side of increasing efficiency. In addition to measures aimed at compensating for the underlying disease (DM), treatment is prescribed to improve blood supply, relieve swelling, and prevent infection (local antibacterial therapy).

Diabetic neuropathy, video – program “Live Healthy!” there may be other diseases: hematological pathology, collagenosis, biliary cirrhosis, neoplasms, hypothyroidism, multiple myeloma, etc.

B vitamin deficiency

Deficiency of individual vitamins from group B (B1, B12, B6), which by nature have a neurotropic effect (positively affect the central nervous system and peripheral nerves), therefore, in medicinal form, are used as important means of pathogenetic treatment. Naturally, if for some reason the body develops a deficiency of these vitamins, which is not quickly replenished, then the symptoms of chronic axonal polyneuropathy will soon manifest themselves:

Vitamin B1 (thiamine) deficiency causes neuropathy of the lower extremities, reminiscent of diabetic or alcoholic;
Lack of B6 (pyridoxine) – forms mainly sensory disturbances, manifested by numbness and tingling;
(cyanocobalomin) - most often leads to degeneration of the spinal cord and damage to the posterior cords, sometimes to the development of sensory disorders with numbness and tingling.

The main method of treating polyneuropathy of this type is the introduction of B vitamins and ascorbic acid in therapeutic doses, as well as a diet rich in these beneficial substances.

Toxic form

A toxic form of the disease with damage to the cranial nerves can develop as a complication of an infectious process caused by agents such as Loeffler's bacillus (diphtheria bacillus - diphtheria neuropathy), herpes virus, human immunodeficiency virus (HIV).

Severe intoxications that develop as a result of the penetration into the blood of substances alien to the human body, which enter there accidentally or intentionally with the aim of committing suicide: arsenic, methanol, which is confused with ethanol, carbon monoxide, dichlorvos and other organophosphorus (or simply toxic) chemical compounds. Toxic polyneuropathy is also caused by chronic consumption of alcoholic beverages, the only difference is that the above poisons act very quickly and affect the nerves in 2-4 days, causing acute axonal polyneuropathy, while an alcoholic poisons his body for months and years, creating the ground for the progression of the pathological process. In most cases, within six months, a person suffering from alcoholism “uses his chances” of getting this disease.

Alcoholic polyneuropathy develops in 2–3% of people who do not drink alcohol in moderation, and is in second place after diabetic polyneuropathy.

The main role in the formation of the pathological process is played by 2 factors: 1) the toxic effect of ethanol on the nervous system, 2) metabolic disorders in the nerves. Not only the peripheral nerves are affected by the influence of alcohol; certain changes also affect the brain and spinal cord.

Symptoms of alcoholic polyneuropathy develop gradually:
Pain in the calves, aggravated by pressure, and paresthesia in the distal parts appear first;
Somewhat later comes weakness and paralysis, which affects both the upper and lower limbs;
Paretic muscles quickly begin to atrophy;
Deep reflexes increase, their zones expand;
A disturbance of superficial sensitivity begins to appear, similar to socks and gloves; Intensification of clinical manifestations in the absence of treatment can lead to the fact that the external signs of PSP begin to resemble tabes dorsalis in syphilis, however absence of characteristic symptoms

(RW - positive, difficulty urinating, “lumbago”) indicates another causative factor and another type of neuropathy, which has nothing to do with syphilis.

Sometimes alcoholic polyneuropathy develops rapidly and this usually happens after severe hypothermia. This type is characterized by a wide range of changes in the nervous system; patients, as a rule, have an “eloquent” appearance and present a lot of complaints. Vasomotor, secretory and trophic disorders cause increased sweating, swelling of the distal parts of the lower and upper extremities, changes in temperature and color of the skin.

Pain from alcoholic polyneuropathy may increase over several months. Meanwhile, timely treatment, which includes vitamin therapy, nootropics, physiotherapeutic procedures, proserin, can reverse the development of the process.

In conclusion of this section, we should remember about neuropathy that develops from the use of substances intended for the treatment and prevention of diseases. Drug-induced polyneuropathy develops during treatment with drugs that are difficult to classify as simple: gold salts, bismuth, sulfonamides, anticonvulsants, antibacterial and chemotherapy drugs. In other cases, peripheral nerves may be affected after a vaccination (administration of vaccines and serums).

In this subsection we have collected somewhat similar reasons, because you can often hear that the manifestations of the disease developed after a bruise or hypothermia, sometimes signs of polyneuropathy appeared as a result of infection or as a result of compression syndromes, which are so rich.

Thus, the cause of neuropathy is often:

Of particular interest is polyneuropathy, which was originally called postpartum polyneuritis. Upon further study of this pathological condition, it turned out that it is not so postpartum and can develop at any stage of pregnancy, so now the disease is given a different name - polyneuropathy of pregnancy.

The origin of PNP in pregnant women is associated with:

With a lack of vitamins (group B - especially) during pregnancy;
With increased sensitivity to proteins that enter a woman’s body from the placenta and fetus and are foreign to her;
With toxic effects of metabolic products on peripheral nerves.

Symptoms of polyneuropathy of the lower extremities (paresthesia, paresis, paralysis and pain) appear against the background of complete well-being, but often the development of the disease does not end there and the symptoms of PSP are accompanied by signs of intoxication (general weakness, nausea, vomiting, etc.).

The main treatment for this pathology is the administration of vitamin complexes containing B vitamins and desensitizing therapy.

Heredity

Hereditary neuropathies represent a heterogeneous group of pathological conditions: some gene mutations cause one single symptom, while others, on the contrary, give a lot of different symptoms, among which damage to peripheral nerves manifests itself.

Metabolic neuropathies include inherited amyloidoses, as well as porphyrias and lipid metabolism disorders of the same origin. Mysterious forms are represented by hereditary motor-sensory (Charcot-Marie-Tooth syndrome) and sensory-vegetative types (Fabry disease). As an example of hereditary PSP, let us consider Fabry disease (a sex-linked trait, a lysosomal storage disease), in which neuropathy appears as one of the many symptoms. Since the gene that controls this pathology is located on the X chromosome, men are predominantly affected, which is understandable - they have only one X chromosome and, if it turns out to be defective, the disease is inevitable. However, there are known cases of the disease in women, but why this happens is still not clear from geneticists. The disease has a wide range of symptoms (exertional intolerance, decreased sweating, damage to internal organs) and a characteristic appearance of the patient (acromegaly). Manifestations of neuropathy can equally affect both the lower and upper extremities: the feet and palms experience constant burning, numbness, and soreness. Symptoms are aggravated during a crisis, which is provoked by stress, cold or heat exposure.

Treatment

Although the treatment of polyneuropathy is determined taking into account the causative factor and involves influencing the underlying disease that caused damage to the peripheral nerves, therapeutic measures must be comprehensive with a simultaneous focus on eliminating the symptoms of PSP.

The problem of treating metabolic forms of PSP, which primarily include the most common types: diabetic polyneuropathy (a complication of type 2 diabetes mellitus) and alcoholic polyneuropathy (a consequence of chronic alcohol intoxication). As a rule, these, and often other, neuropathies are accompanied by intense pain and severe sensory impairment. To reduce clinical manifestations, modern medicine offers various treatment methods:

Polyneuropathy (depending on its origin and clinical manifestations) can sometimes chain the patient to bed for a long time. And he himself, and especially his loved ones, must remember that not everything is at the mercy of chemical compounds called drugs. Proper nutrition, rehabilitation measures and, especially, care and concern play a significant role.

Video: peripheral polyneuropathy, program “About the Most Important Thing”

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