Meningoencephalitis is a neuroinfectious disease that occurs with a combined lesion of the cerebral substance and membranes. It is manifested by infectious, shell-like, variable focal symptoms. It is diagnosed as a result of neurological examination, cerebral MRI / CT, cerebrospinal fluid examination, laboratory diagnostics aimed at finding the pathogen. Treatment is based on etiotropic therapy (antibiotics, antiviral, antimycotic, antiparasitic pharmaceuticals) in combination with pathogenetic, symptomatic agents.
General information
The term “meningoencephalitis” refers to a simultaneous inflammatory lesion of the membranes (“meningea”) and the substance (“encephalon”) of the brain. Combined inflammation may occur initially or be the result of the spread of the pathological process. With secondary involvement of the medulla, meningoencephalitis acts as a complication of meningitis, with the transition of inflammation to the cerebral membranes — a complication of encephalitis. Due to the immaturity of the blood-brain barrier and the immune system, younger children are most susceptible to the disease. Pathology is widespread everywhere. Some etiological forms (mosquito, tick-borne meningoencephalitis) are endemic and seasonal.
Causes
The main etiofactor of the disease is infection. Primary infection of cerebral structures is caused by the direct penetration of neurotropic pathogens into them. Secondary infection occurs when the infectious process spreads from nearby foci (otitis, sinusitis), with common infectious diseases (measles, rubella, flu). The main causative agents of encephalitis are viruses, bacteria, less often — protozoa, pathogenic fungi. Infection is possible due to:
- Getting the pathogen into the nasopharynx. Occurs by airborne, alimentary methods. Penetration into the cranial cavity is realized hematogenically, provokes inflammatory changes in the affected tissues, leading to the development of meningoencephalitis.
- An insect bite. The transmissible transmission pathway is characteristic of a number of viral meningoencephalitis and encephalitis (Japanese mosquito encephalitis, tick-borne encephalitis, St. Louis encephalitis). The insect is a carrier of the pathogen, which, when bitten, enters the bloodstream and enters the cerebral tissues, provoking the disease.
- The presence of infection in the body. With the existence of tuberculous, syphilitic foci, chronic purulent otitis, purulent processes of the maxillofacial region, paranasal sinuses, hematogenic spread of bacterial infection is possible. Viral meningoencephalitis can occur as a complication of individual acute respiratory infections.
- Traumatic brain injury. With an open injury with a violation of the integrity of the skull bones, infection occurs by contact. According to various data, posttraumatic meningoencephalitis is observed in 1.3-3.5% of patients with TBI.
- Vaccinations. The introduction of a live vaccine against the background of weakened immunity is complicated by the development of the infectious process. A post-vaccination complication with the penetration of pathogens through the blood-brain barrier leads to meningoencephalitis.
When pathogens enter the human body, the disease does not always occur. Factors contributing to the development of the disease are considered to be a weakened state of the body, the presence of primary or secondary immunodeficiency, immaturity of the immune system, massive invasion.
Pathogenesis
In response to the introduction of the pathogen in the brain tissues, inflammation develops, the nature of which (serous, purulent) depends on the type of infectious agent. Emerging perivascular inflammatory infiltrates worsen cerebral circulation. Ischemia occurs, acting as a secondary damaging factor. The production of cerebrospinal fluid increases, which causes the development of intracranial hypertension. The lesion of the membranes is accompanied by their irritation, leading to the appearance of meningeal syndrome. Inflammation of the cerebral substance proceeds with the formation of inflammatory foci of various sizes. A violation of the function of neurons located in the foci causes the formation of a corresponding neurological deficit — focal symptoms. The mass death of nerve cells is the cause of the persistent nature of the deficiency that has arisen.
Classification
In clinical neurology , the division of meningoencephalitis into different types is used according to several criteria: etiology, the nature of morphological changes, the type of flow. Verification of the disease is carried out at the diagnostic stage, it is necessary for the correct selection of treatment.
According to the etiology , the following types of encephalitis are distinguished:
- Viral. The causative agents are influenza viruses, herpes simplex, measles, rabies, cytomegalovirus, enteroviruses. The serous nature of inflammatory changes prevails.
- Bacterial. It is caused by strepto-, meningo-, pneumococci, Klebsiella, hemophilic bacillus. The inflammation has a purulent character.
- Protozoan. It is extremely rare. Infectious agents are amoebas, toxoplasmas and other protozoa.
- Fungal. It is observed mainly in immunocompromised individuals.
According to the type of inflammatory process , meningoencephalitis is classified into:
- Serous. Inflammation is accompanied by the formation of serous discharge. Cerebrospinal fluid is transparent, lymphocytosis is typical.
- Purulent. As a result of the inflammatory process, pus forms, causing turbidity of the cerebrospinal fluid. Leukocytes predominate.
- Hemorrhagic. It proceeds with a violation of the permeability of the walls of the cerebral vessels. As a result, petechial hemorrhages form in the tissues.
According to the peculiarities of the clinical course , meningoencephalitis happens:
- Lightning—fast – has rapid development within a few hours. Most cases end in death.
- Acute — symptoms increase more slowly than in the lightning form, within 24-48 hours.
- Subacute — the disease occurs gradually, the symptoms worsen over a period of several days to 1 week.
- Chronic — the inflammatory process lasts for several months, years. Periods of remission and exacerbation are possible. Acute and subacute meningoencephalitis can transform into a chronic form.
Symptoms
The clinical picture consists of a combination of general infectious, cerebrospinal hypertension, meningeal, focal symptoms. Typical signs of infection are fever, malaise, lack of appetite. Rashes on the skin are possible. In some cases, signs of brain damage occur against the background of a current infectious disease. Cerebrospinal hypertension is manifested by intense headache, nausea, vomiting that does not bring relief. A rapidly increasing increase in intracranial pressure leads to a disorder of consciousness: the patient is excited or sleepy, poorly oriented, falls into a coma with a lightning current.
Meningeal syndrome is characterized by general hyperesthesia — increased light, sound, tactile sensitivity, hypertonicity of the posterior neck muscles, limb flexor muscles. Some patients have seizures. Focal neurological deficit varies widely depending on the localization and type of inflammatory process. Hemiparesis, sensitivity disorders, sensorimotor aphasia, hyperkinesis, cerebellar syndrome, vestibular ataxia, cognitive impairment are observed. With lesions of the cranial nerves, oculomotor and visual disorders, facial distortion, drooping of the upper eyelid, hearing loss, swallowing disorders, dysarthria are noted.
Complications
A massive bacterial infection is accompanied by the release into the blood of a large number of dead cells, bacterial toxins and waste products, which can provoke the development of bacterial-toxic shock. Inflammatory processes occur with the accumulation of exudate in the intercellular space of cerebral tissues, leading to cerebral edema. Intracranial hypertension and increasing cerebral edema are complicated by displacement of brain structures with infringement of the trunk and the development of progressive bulbar paralysis, dangerous cardiac and respiratory failure.
Diagnostics
The diagnostic search begins with a survey of the patient and his relatives regarding the current or recently transferred infectious disease, the detection of a history of TBI, the fact of vaccination, tick bite, etc. Further diagnostic studies include:
- Neurological examination. Allows the neurologist to identify meningeal symptoms, focal neurological deficit, assess the state of consciousness of the patient. The data obtained indicate the involvement of both the membranes and the medulla in the pathological process.
- Laboratory tests. The picture of pronounced inflammatory changes in clinical blood analysis (leukocytosis, accelerated ESR) characterizes acute bacterial meningoencephalitis. Blood culture for sterility, PCR diagnostics allow to verify the pathogen.
- CT, MRI of the brain. Thickening, thickening of the membranes of the brain, diffuse changes in cerebral tissues are determined. The presence of inflammatory foci is not always visualized. In case of parasitic etiology, rounded foci of heterogeneous structure with ring-shaped reinforcement along the periphery are characteristic.
- Lumbar puncture. It is carried out to obtain cerebrospinal fluid. With purulent inflammation, the fluid is cloudy with a flake—like sediment, with serous – transparent, with hemorrhagic — with blood elements. In order to identify the pathogen, the cerebrospinal fluid is examined under a microscope, seeded on various nutrient media, PCR diagnostics.
- Stereotactic brain biopsy. It is necessary in complex diagnostic cases, allows to diagnose meningoencephalitis of parasitic etiology, to exclude the tumor process.
It is necessary to differentiate meningoencephalitis from brain tumors, extensive strokes occurring with shell syndrome, toxic lesions of the central nervous system, progressive degenerative processes. Differential diagnosis is carried out among meningoencephalitis of various etiologies. Finally, the pathogen can only be determined by its isolation from the cerebrospinal fluid, cerebral tissues, and blood.
Treatment
Therapy is carried out comprehensively in the conditions of the intensive care unit or intensive care unit, includes etiotropic, pathogenetic, symptomatic components. Etiotropic treatment is carried out according to the etiology:
- Antibiotics. The most commonly used cephalosporins, their combination with ampicillin. Subsequently, the appointments are adjusted in accordance with the results of determining the sensitivity of the selected flora.
- Antiviral pharmaceuticals. In the case of herpetic etiology, ganciclovir is prescribed, arbovirus — ribavirin. Antiviral therapy is combined with the administration of interferon drugs.
- Antifungal agents. The most effective are amphotericin B, fluconazole. In severe cases, a combination of them is used.
- Antiparasitic drugs. Antiparasitic pharmaceuticals are used in combination with antifungal agents or antibiotics.
The basis of pathogenetic treatment is the fight against cerebral edema: diuretics, glucocorticosteroids. The preservation of the vital activity of neurons is carried out by neuroprotective, neurometabolic means. Symptomatic therapy is aimed at relieving the main manifestations of the disease, including the maintenance of vital body systems (cardiovascular drugs, oxygen therapy, ventilation), anticonvulsants, antipyretics, psychotropic pharmaceuticals. In the stage of regression, the symptomatology begins rehabilitation therapy aimed at maximum recovery of impaired nervous functions (massage, physical therapy, physiotherapy, acupuncture).
Prognosis and prevention
Timely etiotropic therapy increases the chances of recovery, but the outcome of the disease depends on the etiology, the form of the course, the age of the patient, the state of his immune system. Lightning-fast meningoencephalitis has the highest mortality rate. Most of the surviving patients have residual phenomena: paresis, speech disorders, chronic intracranial hypertension, epilepsy, psycho-organic syndrome. In young children, meningoencephalitis provokes a delay in mental development.
Preventive measures include measures aimed at strengthening immunity (fortified nutrition, outdoor exercise, hardening, physical education), timely treatment of infections, elimination of chronic infectious foci in the body. To prevent post-traumatic meningoencephalitis, correct wound treatment, elimination of liquorrhea, prophylactic use of antibiotics allows. Post-vaccination meningoencephalitis can be prevented by careful selection of the vaccinated contingent.