Polio - Diagnosis

Poliomyelitis is diagnosed based on the characteristic clinical picture (acute onset of the disease with fever, development of meningoradicular syndrome, peripheral paresis, paralysis with hypotension, hypo- or areflexia, hypo- or atrophy without sensory impairment) and epidemiological data: contact with sick or recently vaccinated individuals. The connection with vaccination and the absence or incomplete vaccination are also taken into account. The diagnosis is confirmed by determining the increase in the titer of virus-neutralizing antibodies by 4 times or more in the RSC or RN in paired sera taken at intervals of 14-21 days. Virological studies are also used. The virus can be isolated from feces, less often from nasopharyngeal mucus, cerebrospinal fluid. Isolation of the virus in the absence of clinical manifestations of the disease is not a basis for diagnosing poliomyelitis, especially in areas where vaccination is constantly carried out. To determine whether the isolated virus belongs to a vaccine or “wild” strain, PCR is used.

When examining the cerebrospinal fluid, lymphocytic pleocytosis is detected in several tens to hundreds of cells per 1 μl (sometimes in the first days of the disease it can be neutrophilic). In the acute stage of the disease, the concentration of protein and glucose is usually within normal limits. The paralytic form of poliomyelitis is characterized by a change in cellular-protein dissociation at the onset of the disease to protein-cellular (decreased pleocytosis, increased protein concentration) after 1-2 weeks.

Changes in peripheral blood are not typical. Sometimes moderate leukocytosis is observed.

ENMG is used to identify the level and severity of motor neuron damage. In the paralytic period of poliomyelitis, a change in bioelectrical activity is detected, characteristic of anterior corneal damage: in paralyzed muscles with early-developing atrophy, a complete absence of bioelectrical activity is determined on the electromyogram. When taking an electromyogram from less affected muscles, clear rare potential fluctuations are noted ("picket rhythm").

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Differential diagnosis of poliomyelitis

Differential diagnosis of poliomyelitis is determined by its clinical form.

The abortive form of the disease is clinically indistinguishable from many acute respiratory viral infections or diarrhea caused by enteroviruses of the Coxsackie-ECHO group, rotaviruses and other viral agents.

In the meningeal form, differential diagnostics of poliomyelitis treatment with other serous meningitis (enteroviral, mumps, tuberculosis) is carried out, and in the early stages of the disease with neutrophilic pleocytosis in the cerebrospinal fluid, it is necessary to exclude bacterial purulent meningitis. The meningeal form of poliomyelitis is characterized by the severity of the pain syndrome, the presence of symptoms of tension of the nerve trunks and roots of the spinal nerves, pain in the nerve trunks during palpation, but a definitive diagnosis is possible only using laboratory methods.

The spinal form of paralytic poliomyelitis is differentiated from diseases of the musculoskeletal system, which are characterized by a non-paretic, but gentle gait, pain during passive movements in the joints, preservation of muscle tone, as well as preservation or increase of deep reflexes. Cerebrospinal fluid is normal during examination, and inflammatory changes are noted in the blood. Also, the spinal form of the disease must be differentiated from myelitis, the poliomyelitis form of tick-borne encephalitis, diphtheritic polyneuropathy, polyradiculoneuritis, and Werdnig-Hoffmann spinal amyotrophy.

Paralysis in myelitis has a central character: high muscle tone, brisk reflexes, the presence of pyramidal signs, disturbances of sensitivity, pelvic organ functions, trophic disorders with the formation of bedsores.

In the poliomyelitis form of tick-borne encephalitis, unlike poliomyelitis, the pathological process is localized mainly in the cervical segments and manifests itself as flaccid paresis and paralysis of the muscles of the neck and shoulder girdle. There is no mosaic lesion. In the cerebrospinal fluid - minor lymphocytic pleocytosis (40-60 cells) and an increased protein level (up to 0.66-1.0 g / l). When making a diagnosis, the epidemiological anamnesis is taken into account (tick bite, consumption of raw milk in endemic areas).

Diphtheritic polyneuropathy is characterized by a connection with diphtheria suffered 1.5-2 months before the damage to the peripheral nervous system, symmetry of lesions, gradual increase in paresis over several weeks, detection of disturbances in bioelectrical activity during electroneuromyography, mainly of the demyelinating or axonal-demyelinating type.

In polyradiculoneuritis, there is a slow (sometimes wave-like) development and increase of symmetrical paresis with predominant damage to the distal parts of the limbs, sensitivity disorders of the polyneuritic and radicular types, and an increase in the protein content in the cerebrospinal fluid with normal cytosis.

Spinal amyotrophy of Werdnig-Hoffmann is a hereditary disease characterized by damage to the motor neurons of the spinal cord. The first symptoms of the disease appear before the age of 1.5 years. Paralysis develops gradually and symmetrically: first of the legs, then of the arms, and of the muscles of the trunk and neck. Deep reflexes disappear, and there is no pain syndrome. With a well-defined subcutaneous fat layer, it is often difficult to detect muscle atrophy; the cerebrospinal fluid is unchanged. Death occurs at the age of 4-5 years due to bulbar disorders and paralysis of the respiratory muscles.

In the pontine form of the disease, differential diagnosis and treatment of poliomyelitis is carried out with neuritis of the facial nerve, which is not characterized by general infectious symptoms and at least one of the following symptoms is observed: lacrimation on the affected side, decreased taste sensitivity to sweet and salty on the anterior 2/3 of the tongue on the affected side, soreness of the trigeminal points upon palpation, spontaneous pain and impaired sensitivity on the face.

The bulbar form is differentiated from brainstem encephalitis, in which deep disturbances of consciousness and convulsive syndrome predominate.

Unlike poliomyelitis, damage to the motor cranial nerves in polyradiculoneuritis is usually bilateral and symmetrical: diplegia of the facial muscles, bilateral damage to the oculomotor nerve.

Nervous system lesions that are clinically indistinguishable from poliomyelitis may be caused by enteroviruses of the Coxsackie-ECHO group, and less frequently by other viral agents. In these cases, it is necessary to use the entire range of virological, serological diagnostic methods, as well as PCR.

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