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Herpetic encephalitis prognosis: Herpes Meningoencephalitis | Johns Hopkins Medicine

Herpes Meningoencephalitis | Johns Hopkins Medicine

What is herpes meningoencephalitis?

The meninges are the layers of thin tissue that cover your brain. If these tissues become infected, it’s called meningitis. When your brain becomes inflamed or infected, the problem is called encephalitis. If both the meninges and the brain are infected, the condition is called meningoencephalitis.

Encephalitis involving herpes is a medical emergency. It needs to be promptly diagnosed and treated. This disease is often fatal when it is not treated. Many people who survive it have long-term problems afterward.

What causes herpes meningoencephalitis?

Meningitis and encephalitis may be caused by bacteria, fungi, or other types of germs. But many are caused by viruses, and many kinds of viruses can be to blame.

Encephalitis is caused by the herpes simplex virus. Most are caused by herpes simplex virus type 1 (HSV1), the virus that also causes cold sores. The disease may also be caused by herpes virus type 2 (HSV2). This virus can be spread by sexual contact or from an infected mother to her baby during childbirth. HSV1 infection can also be sexually transmitted to the genital area. These viruses remain in the body throughout a person’s life, even when they’re not causing signs of infection.

Sometimes the meningoencephalitis occurs during the initial infection with the herpes simplex virus, but most often it is caused by reactivation of the virus from an earlier infection.

What are the symptoms of herpes meningoencephalitis?

If you have viral meningitis, symptoms may include fever, light sensitivity, headache, and a stiff neck. If you have other symptoms, such as confusion, seizures, sleepiness, or a focal neurologic deficit—a nerve function problem that affects a specific area — these may suggest that your brain is also affected, and your healthcare provider may diagnose it as meningoencephalitis.

These are possible symptoms of meningoencephalitis:

  • Headache

  • Fever

  • Neck stiffness

  • Sensitivity to light

  • Seizures

  • Trouble thinking clearly

  • Personality changes

  • Hallucinations, visual and auditory

  • Unusual behaviors

  • Unconsciousness

Click image to enlarge.

How is herpes meningoencephalitis diagnosed?

If, after reviewing your medical history and symptoms, your healthcare provider thinks you may have herpes meningoencephalitis, he or she will order various tests and exams to confirm the diagnosis. Other tests may include:

  • Neurological exam. Your provider will do a neurological exam to look for changes in motor and sensory function, vision, coordination and balance, mental status, and in mood or behavior.

  • Lumbar puncture. In this procedure, your provider will take a sample of spinal fluid. Cells and other substances in this fluid may give your provider important clues.

  • Imaging. Your provider may want to create images of your brain using a CT or MRI scan.

  • EEG. An EEG measures brain waves by placing electrodes onto your scalp.

  • Blood tests. Testing the blood helps identify infection.

If your healthcare providers think that a newborn has herpes encephalitis resulting from infection with HSV2 while passing through the birth canal, they may check samples of the baby’s blood and spinal fluid.

How is herpes meningoencephalitis treated?

Treating the cause of your infection is the primary treatment. Since most cases of meningoencephalitis are caused by the herpes virus, the antiviral acyclovir is used to treat it. You may need to take this medicine through an intravenous (IV) line for 10 to 14 days. Your healthcare provider may also give you medicine to reduce swelling in the brain and to treat or prevent seizures.

Healthcare providers may treat babies with this disease with acyclovir for several weeks.

Depending on the severity of your infection, you may need to be treated in the hospital.

What are the complications of herpes meningoencephalitis?

With treatment, most people with this disease start to improve within a day or two and tend to recover fully within about a month. But without treatment, very serious complications can set in, including death.

Even with treatment, some people with severe cases may have long-term brain damage. They may have trouble thinking, controlling their body, and hearing, seeing, or speaking. They may need to take medicines for a long time, and they may require long-term care.

Can herpes meningoencephalitis be prevented?

Avoiding herpes virus infections in the first place can help you prevent herpes meningoencephalitis. Ways to avoid infections from herpes viruses include:

  • Abstain from sex or have only one sex partner who has been tested for the virus and isn’t infected.

  • Use a latex condom, which can reduce — but not entirely prevent — the risk of infection.

  • Avoid kissing people with cold sore blisters. It’s important to keep in mind that most people have already been infected with HSV1 virus by the time they’re 20 years old. If you’ve already been infected, the virus goes dormant inside your body except during outbreaks.

Some pregnant women who have had genital herpes outbreaks may want to have their babies delivered by cesarean section. This may prevent meningoencephalitis in newborns.

When should I call my healthcare provider?

Treating herpes meningoencephalitis as soon as possible is essential. If you’re feeling neck stiffness, having any neurological problems (including seizures, changes in consciousness, or feeling sleepy), are sensitive to light, or are running a fever along with a bad headache, call your healthcare provider and have the problem treated promptly.

If you have already been diagnosed with herpes meningoencephalitis and are being treated, it’s very important to let your healthcare providers know if any of your symptoms get worse or if you develop any new symptoms, as these could be signs that the infection is getting worse despite treatment.

Key points

  • Herpes meningoencephalitis is an infection of the brain and brain covering (meninges) caused by the herpes simplex virus. It is a medical emergency that requires treatment right away.

  • Symptoms can include headache, fever, changes in consciousness, confusion, neck stiffness, sensitivity to light, seizures, and changes in mood, personality, or behavior.

  • Treatment is with antiviral medicine, sometimes along with other medicines such as steroids and drugs to prevent seizures.

Long-term outcome of severe herpes simplex encephalitis: a population-based observational study

1. Whitley RJ, Soong SJ, Dolin R, Galasso GJ, Ch’ien LT, Alford CA. Adenine arabinoside therapy of biopsy-proved herpes simplex encephalitis. National Institute of Allergy and Infectious Diseases collaborative antiviral study. N Engl J Med. 1977;297:289–94. doi: 10.1056/NEJM197708112970601. [PubMed] [CrossRef] [Google Scholar]

2. Hjalmarsson A, Blomqvist P, Sköldenberg B. Herpes simplex encephalitis in Sweden, 1990–2001: incidence, morbidity, and mortality. Clin Infect Dis. 2007;45:875–80. doi: 10.1086/521262. [PubMed] [CrossRef] [Google Scholar]

3. Raschilas F, Wolff M, Delatour F, Chaffaut C, De Broucker T, Chevret S, et al. Outcome of and prognostic factors for herpes simplex encephalitis in adult patients: results of a multicenter study. Clin Infect Dis. 2002;35:254–60. doi: 10.1086/341405. [PubMed] [CrossRef] [Google Scholar]

4. Barnett GH, Ropper AH, Romeo J. Intracranial pressure and outcome in adult encephalitis. J Neurosurg. 1988;68:585–8. doi: 10.3171/jns.1988.68.4.0585. [PubMed] [CrossRef] [Google Scholar]

5. Durand ML, Calderwood SB, Weber DJ, Miller SI, Southwick FS, Caviness VS, et al. Acute bacterial meningitis in adults. A review of 493 episodes. N Engl J Med. 1993;328:21–8. doi: 10.1056/NEJM199301073280104. [PubMed] [CrossRef] [Google Scholar]

6. van de Beek D, de Gans J, Spanjaard L, Weisfelt M, Reitsma JB, Vermeulen M. Clinical features and prognostic factors in adults with bacterial meningitis. N Engl J Med. 2004;351:1849–59. doi: 10.1056/NEJMoa040845. [PubMed] [CrossRef] [Google Scholar]

7. Kumar G, Kalita J, Misra UK. Raised intracranial pressure in acute viral encephalitis. Clin Neurol Neurosurg. 2009;111:399–406. doi: 10.1016/j.clineuro.2009.03.004. [PubMed] [CrossRef] [Google Scholar]

8. Ropper AH. Hyperosmolar therapy for raised intracranial pressure. N Engl J Med. 2012;367:746–52. doi: 10.1056/NEJMct1206321. [PubMed] [CrossRef] [Google Scholar]

9. Schwab S, Junger E, Spranger M, Dorfler A, Albert F. Craniectomy An aggressive treatment approach in severe encephalitis. Neurology. 1997;42(2):412–7. doi: 10.1212/WNL.48.2.412. [PubMed] [CrossRef] [Google Scholar]

10. Yan HJ. Herpes simplex encephalitis: the role of surgical decompression. Surg Neurol. 2002;57:20–4. doi: 10.1016/S0090-3019(01)00688-7. [PubMed] [CrossRef] [Google Scholar]

11. Mellado P, Castillo L, Andresen M, Campos M, Pérez C, Baudrand R. Decompressive craniectomy in a patient with herpetic encephalitis associated to refractory intracranial hypertension. Rev Med Chil. 2003;131:1434–8. doi: 10.4067/S0034-98872003001200011. [PubMed] [CrossRef] [Google Scholar]

12. Midi I, Tuncer N, Midi A, Mollahasanoglu A, Konya D, Sav A. Effects of decompressive surgery on prognosis and cognitive deficits in herpes simplex encephalitis. Behav Neurol. 2007;18:245–9. doi: 10.1155/2007/534982. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

13. Di Rienzo A, Iacoangeli M, Rychlicki F, Veccia S, Scerrati M. Decompressive craniectomy for medically refractory intracranial hypertension due to meningoencephalitis: report of three patients. Acta Neurochir (Wien) 2008;150:1057–65. doi: 10.1007/s00701-008-0019-1. [PubMed] [CrossRef] [Google Scholar]

14. González Rabelino GA, Fons C, Rey A, Roussos I, Campistol J. Craniectomy in herpetic encephalitis. Pediatr Neurol. 2008;39:201–3. doi: 10.1016/j.pediatrneurol.2008.06.006. [PubMed] [CrossRef] [Google Scholar]

15. Taferner E, Pfausler B, Kofler A, Spiss H, Engelhardt K, Kampfl A, et al. Craniectomy in severe, life-threatening encephalitis: a report on outcome and long-term prognosis of four cases. Intensive Care Med. 2001;27:1426–8. doi: 10.1007/s001340101027. [PubMed] [CrossRef] [Google Scholar]

16. Maraite N, Mataigne F, Pieri V, Dang T, Diederich NJ. Early decompressive hemicraniectomy in fulminant herpes simplex encephalitis. Bull Soc Sci Med Grand Duche Luxemb. 2010;(2):279–82. PMID: 20882746. [PubMed]

17. Pili-Floury S, Valentin L, Blasco G, Godard J, Samain E. Hypertension intracrânienne réfractaire et tardive, traitée par craniectomie de décompression dans un cas d’encéphalite herpétique. Ann Fr Anesth Reanim. 2009;28:709–10. doi: 10.1016/j.annfar.2009.05.012. [PubMed] [CrossRef] [Google Scholar]

18. Adamo MA, Deshaies EM. Emergency decompressive craniectomy for fulminating infectious encephalitis. J Neurosurg. 2008;108:174–6. doi: 10.3171/JNS/2008/108/01/0174. [PubMed] [CrossRef] [Google Scholar]

19. Venkatesan A, Tunkel AR, Bloch KC, Lauring AS, Sejvar J, Bitnun A, et al. Case definitions, diagnostic algorithms, and priorities in encephalitis: consensus statement of the international encephalitis consortium. Clin Infect Dis. 2013;57:1114–28. doi: 10.1093/cid/cit458. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

20. Institut national de la statistique et des études économiques or in english: national institute of statistics and economic studies. http://www.insee.fr. Accessed on June 9th 2015.

21. Grammatico-Guillon L, Baron S, Gettner S, Lecuyer AI, Gaborit C, Rosset P, et al. Bone and joint infections in hospitalized patients in France, 2008: clinical and economic outcomes. J Hosp Infect. 2012;82:40–8. doi: 10.1016/j.jhin.2012.04.025. [PubMed] [CrossRef] [Google Scholar]

22. Defez C, Fabbro-Peray P, Cazaban M, Boudemaghe T, Sotto A, Daurès JP. Additional direct medical costs of nosocomial infections: an estimation from a cohort of patients in a French university hospital. J Hosp Infect. 2008;68:130–6. doi: 10.1016/j.jhin.2007. 11.005. [PubMed] [CrossRef] [Google Scholar]

23. Grammatico-Guillon L, Maakaroun Vermesse Z, Baron S, Gettner S, Rusch E, Bernard L. Paediatric bone and joint infections are more common in boys and toddlers: a national epidemiology study. Acta Paediatr. 2013;102:e120–5. doi: 10.1111/apa.12115. [PubMed] [CrossRef] [Google Scholar]

24. George BP, Schneider EB, Venkatesan A. Encephalitis hospitalization rates and inpatient mortality in the United States, 2000–2010. PLoS One. 2014;9:e104169–14. doi: 10.1371/journal.pone.0104169. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

25. Thakur KT, Motta M, Asemota AO, Kirsch HL, Benavides DR, Schneider EB, et al. Predictors of outcome in acute encephalitis. Neurology. 2013;81:793–800. doi: 10.1212/WNL.0b013e3182a2cc6d. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

26. Sonneville R, Gault N, de Montmollin E, Klein IF, Mariotte E, Chemam S, et al. Clinical spectrum and outcomes of patients with encephalitis requiring intensive care. Eur J Neurol. 2014;22:6. doi: 10.1111/ene.12541. [PubMed] [CrossRef] [Google Scholar]

27. Pillai SC, Hacohen Y, Tantsis E, Prelog K, Merheb V, Kesson A, et al. Infectious and autoantibody-associated encephalitis: clinical features and long-term outcome. Pediatrics. 2015;135:e974–84. doi: 10.1542/peds.2014-2702. [PubMed] [CrossRef] [Google Scholar]

28. Cruz-Flores S, Berge E, Whittle IR. Surgical decompression for cerebral oedema in acute ischaemic stroke. Cochrane Database Syst Rev. 2012;1:CD003435. [PubMed] [Google Scholar]

29. Jüttler E, Unterberg A, Woitzik J, Bösel J, Amiri H, Sakowitz OW, et al. Hemicraniectomy in older patients with extensive middle-cerebral-artery stroke. N Engl J Med. 2014;370:1091–100. doi: 10.1056/NEJMoa1311367. [PubMed] [CrossRef] [Google Scholar]

30. Campbell JTP, Bray BD, Hoffman AM, Kavanagh SJ, Rudd AG, Tyrrell PJ, et al. The effect of out of hours presentation with acute stroke on processes of care and outcomes: analysis of data from the Stroke Improvement National Audit Programme (SINAP) PLoS One. 2014;9:e87946. doi: 10.1371/journal.pone.0087946. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

31. Grammatico-Guillon L, Baron S, Gaborit C, Rusch E, Astagneau P. Quality assessment of hospital discharge database for routine surveillance of hip and knee arthroplasty-related infections. Infect Control Hosp Epidemiol. 2014;35:646–51. doi: 10.1086/676423. [PubMed] [CrossRef] [Google Scholar]

32. Sunder S, Grammatico-Guillon L, Baron S, Gaborit C, Bernard-Brunet A, Garot D, et al. Clinical and economic outcomes of infective endocarditis. Infect Dis. 2015;47:80–7. doi: 10.3109/00365548.2014.968608. [PubMed] [CrossRef] [Google Scholar]

33. Bernard S, Mailles A, Stahl JP. Epidemiology of infectious encephalitis, differences between a prospective study and hospital discharge data. Epidemiol Infect. 2012;141:2256–68. doi: 10.1017/S0950268812002518. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

34. Jennett B, Bond M. Assessment of outcome after severe brain damage. Lancet. 1975;1:480–4. doi: 10.1016/S0140-6736(75)92830-5. [PubMed] [CrossRef] [Google Scholar]

35. Wilson JT, Pettigrew LE, Teasdale GM. Emotional and cognitive consequences of head injury in relation to the Glasgow outcome scale. J Neurol Neurosurg Psychiatry. 2000;69:204–9. doi: 10.1136/jnnp.69.2.204. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

Herpetic encephalitis. What is Herpetic Encephalitis?

IMPORTANT
The information in this section should not be used for self-diagnosis or self-treatment. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For diagnosis and proper treatment, you should contact your doctor.

Herpetic encephalitis is a diffuse or focal lesion of the medulla caused by herpes viruses HSV-1, HSV-2, Varicella Zoster. The main symptoms of the disease: febrile fever, progressive depression of consciousness, convulsive seizures. At the end of the acute period of infection, residual neurological impairment persists for a long time. To establish the diagnosis, it is necessary to carry out PCR diagnostics of cerebrospinal fluid, brain tomography, and an electroencephalogram. Pathology treatment includes antiviral drugs, decongestant, neurometabolic and anticonvulsant therapy.

    ICD-10

    G05.1 Encephalitis, myelitis and encephalomyelitis in viral diseases classified elsewhere

    • Causes
    • Pathogenesis
    • Symptoms of herpetic encephalitis
    • Complications
    • Diagnostics
    • Treatment of herpetic encephalitis

      • Conservative therapy
      • Rehabilitation
    • Prognosis and prevention
    • Treatment prices

    General

    Encephalitis of herpetic origin accounts for up to 15-20% of all viral inflammatory processes in the brain tissue. Symptoms occur with a frequency of 4-5 cases per 1 million population, with up to a third of patients being children, and about 20% more in the age category over 60 years. The disease does not lose its relevance in modern neurology, since for a successful outcome of the pathology it is necessary to make a diagnosis in time and start treatment, and delay in providing medical care is fraught with the death of the patient.

    Herpetic encephalitis

    Causes

    The disease in 95% of cases is caused by the herpes simplex virus type 1, which is explained by the high prevalence of the pathogen. According to WHO, about 2/3 of the world’s population under the age of 50 are infected with HSV-1. In second place in frequency is Varicella Zoster Virus (VZV) – the causative agent of chickenpox, herpes zoster. HSV-2 encephalitis is rare, predominantly in immunocompromised patients.

    The leading risk factor is a reduced immune status. Herpetic infection proceeds latently, is activated against the background of a violation of the general resistance of the organism (with hypothermia, stress, menstruation in women). At risk are people with congenital and acquired immunodeficiencies, patients receiving treatment with immunosuppressive drugs. The triggers include reinfection with other strains of herpes viruses, accompanied by autoimmune reactions.

    Pathogenesis

    Primary infection with HSV-1, as a rule, occurs in childhood when viral particles enter the mucous membranes, after which the pathogen begins to multiply, migrates to the nerve ganglia, where it is in a state of latent infection for a long time. Infection with HSV-2 is observed after the onset of sexual life through the mucous membranes of the genital tract, and the further development of the pathogen is similar to HSV-1.

    Symptoms of the disease in most cases occur when the infection is reactivated under the influence of provoking factors. Herpesviruses enter the brain by the hematogenous route or along the nerve trunks (through the trigeminal or olfactory nerve). From the gasser node, they spread to the thalamus, subcortical nuclei, and the cerebral cortex. When spreading along the olfactory tract, the limbic system (hippocampus, temporal cortex) suffers first.

    Symptoms of herpetic encephalitis

    In a typical course of acute cerebral inflammation, several successive stages are distinguished: early, the period of the peak of the disease, regression of signs, the stage of residual phenomena. In 70%, the pathology manifests itself with a sudden high fever (over 39°C), accompanied by intense headaches in the frontotemporal zone, severe drowsiness, and vomiting not associated with food intake.

    On the second or third day, the symptoms are supplemented by impaired consciousness: patients begin to get confused in time and space, do not recognize relatives, experience various hallucinations. As the severity of the condition worsens, focal or generalized seizures appear. Opercular automatism is occasionally observed – repeated smacking or sucking movements.

    On average, after 3 days, the disease enters the stage of peak. The main manifestation is a deep depression of consciousness up to coma. Patients do not respond to sound and tactile stimuli, but motor responses to pain stimuli remain within the normal range. Symptoms of decortication or decerebration, irregular breathing, and bilateral motor disturbances may also occur.

    If the patient was given complex treatment, the reverse development of the symptoms of herpetic encephalitis begins from 3-4 weeks. This stage lasts from several months to 1 year and is characterized by gradual restoration of temporarily lost neurological functions. At the end of the third stage, about 80% of patients have persistent residual (residual) effects that can persist for life.

    Complications

    In the acute period, the progression of cerebral edema is unfavorable prognostic, which is fraught with its herniation. With the temporo-tentorial form of herniation, a triad of signs occurs: loss of consciousness, hemiparesis, anisocoria. Symptoms of the transtentorial form are the absence of pupillary response to light, fixation of the eyeballs along the midline, bilateral muscle hypertonicity. The work of the respiratory center is often disturbed.

    Pathology has a severe course, in the absence of timely medical care, mortality reaches 70%. Even if etiotropic treatment is carried out, death is recorded in 15-20% of patients, more often in infants, the elderly, patients at risk. In those who have recovered, a complete regression of neurological symptoms is observed only in 20% of cases, while the rest experience residual symptoms.

    The most dangerous chronic complication of the disease is considered to be a progressive vegetative state (akinetic mutism), characterized by the irreversible destruction of higher mental functions. Patients retained consciousness, vital functions (respiration, blood circulation), but cognitive activity is completely absent. Such patients do not speak, do not respond to external stimuli, and require constant care.

    The typical consequences of the herpetic form of encephalitis include Klüver-Bucy syndrome, in which severe long-term disorders of the mental and cognitive sphere develop. Symptoms of the disorder include agitated state, aggressiveness, pathological hypersexuality. There are also intellectual impairments, problems with concentration, memory loss.

    Diagnostics

    The patient is examined by infectious disease specialists, neurologists, doctors of emergency care and intensive care unit. It is possible to suspect encephalitis by an acute onset, the presence of febrile fever, a combination of cerebral and focal symptoms. To confirm the disease, clarify the etiology of the inflammatory process, the following research methods are prescribed:

    • Neuroimaging. The “gold standard” of diagnostics is MRI of the brain, the sensitivity of which in detecting lesions reaches 100% at an early stage of the disease. If this method is not available, or at later stages of herpetic encephalitis, CT of the brain is used.
    • Electroencephalography. In the acute period, the EEG shows focal or diffuse disturbances in the bioelectrical brain activity: high-amplitude delta and theta waves, the appearance of “acute-slow wave” complexes.
    • Lumbar puncture. The cerebrospinal fluid has normal transparency, microscopic examination reveals lymphocytic pleocytosis (about 100 cells per 1 ml), an increase in the amount of protein, and a decrease in glucose levels.
    • DNA diagnostics. The sensitivity of the PCR study of CSF for herpes viruses is 96-98%, and the specificity reaches 94%. Since false-negative results are not excluded in the early period of infection, testing must be repeated on the 4th day of the disease.

    Treatment of herpetic encephalitis

    Conservative therapy

    Herpetic encephalitis is characterized by a rapid increase in neurological deficit, progression of cerebral symptoms, so complex treatment should begin as early as possible. The best chances for a full recovery are in patients who started receiving etiotropic drugs on the first day of the disease manifestation. Treatment of the disease includes the following groups of medicines:

    • Antivirals. The drug of choice is acyclovir, administered intravenously by drip in cases of suspected herpetic encephalitis even before laboratory confirmation of the diagnosis. The criterion for the completion of therapy is a negative CSF PCR test.
    • Interferons. In severe forms of encephalitis, it is advisable to combine immunomodulators with etiotropic antiviral drugs. Interferons or interferon inducers are used, which enhance the nonspecific resistance of the body.
    • Glucocorticoids. They are mainly prescribed for the relief of cerebral edema. Hormones are also used in the case of recurrent herpes infection, in which an autoimmune process develops in the body.
    • Diuretics. Medicines are indicated for edema-swelling of the brain. Emergency dehydration is carried out using the osmodiuretic mannitol or the saluretic furosemide. Also recommended are onco-dehydratants (albumin), glycerin solutions for tube introduction into the stomach.
    • Anticonvulsants. The first-line drugs for the elimination of convulsive syndrome are benzodiazepines. With their insufficient effectiveness, treatment is enhanced by drugs for anesthesia, barbiturates.

    Rehabilitation

    Vitamin complexes (vitamins of group B, ascorbic acid) in combination with antioxidants have a beneficial effect on the state of the central nervous system after suffering herpetic encephalitis. Rehabilitation treatments also include nootropics and neurometabolic drugs to improve cognitive brain function. Correction of the immunological status is carried out by adaptogens, actoprotectors, nonspecific immunomodulators.

    To replenish the body’s energy consumption, stimulate reparative processes, adequate enteral nutrition in terms of caloric content and vitamin composition is shown. Much attention is paid to physiotherapy, massage and exercise therapy aimed at improving motor function. If there are indications, classes with speech therapists, speech pathologists are recommended.

    Prognosis and prevention

    Despite ongoing etiotropic treatment, the prognosis for herpetic encephalitis remains unfavorable, the mortality rate is 15-20%. The majority of those who have recovered remain neurologically deficient. To prevent the disease, rational treatment of herpes of the skin and mucous membranes, timely counseling of patients with disseminated herpes infection is necessary.

    Sources

    1. Neurology and neurosurgery. Volume 1 / E.I. Gusev, A.N. Konovalov, V.I. Skvortsova. — 2016.
    2. Meningitis and encephalitis: textbook. settlement for doctors / D. A. Valishin, R. T. Murzabaeva, A. P. Mamon, M. A. Mamon, L. V. Murzagaleeva. – 2012.
    3. Herpetic lesions of the nervous system / M.N. Lebedyuk, M.E. Zapolsky, Yu.I. Goransky // Ukrainian journal of dermatology, venereology, cosmetology. – 2011. – No. 2.
    4. Herpetic encephalitis/ T.V. Matveeva, N.V. Tokareva, G.A. Shakirzyanova // Neurology. – 2006. – No. 16.
    5. This article was prepared based on the materials of the site: https://www.krasotaimedicina.ru/

    IMPORTANT
    Information from this section cannot be used for self-diagnosis and self-treatment. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For diagnosis and proper treatment, you should contact your doctor.

    Herpes simplex encephalitis: symptoms, causes, treatment

    Encephalitis, which is caused by the herpes simplex virus , is a very common clinical manifestation of a severe generalized herpes infection that affects the entire nervous system of the human body. Occurs sporadically. The severity of the course of this disease is associated with the necrotic nature of the process and the subsequent formation of foci of hemorrhagic decay of the brain substance. In addition to herpes encephalitis in newborns, in most other cases, the causative agent of herpes encephalitis is the herpes virus of the first type. The main route of infection is airborne, but contact-household is also possible.

    CLINICAL PICTURE

    The disease begins acutely, with a rise in body temperature. Meningeal symptoms quickly appear, general epileptic seizures often occur. Focal symptoms are manifested by central mono- and hemiparesis, hyperkinesis. In the cerebrospinal fluid, pleocytosis with a predominance of lymphocytes (up to several hundred cells in 1 μl), an increase in protein content (up to 2-3 g / l), slight xanthochromia or a small admixture of erythrocytes are detected.

    SYMPTOMS

    Early clinical manifestations of encephalitis are not specific. The onset of the disease resembles a flu infection. The first symptoms are an increase in body temperature to high numbers, severe headaches, a decrease or complete loss of appetite, nausea, and there may be repeated vomiting. A state of prostration appears. Further, if the focus of inflammation is localized in the temporal or frontal lobes of the brain, adults and older children may experience inappropriate behavior, psychosensory disturbances, hyperesthesia of the skin, delirium syndrome, gustatory and olfactory hallucinations. All of the above symptoms in young children are almost impossible to recognize. In the future, the course of the disease is in many respects similar to the clinical picture of acute encephalopathy, which is expressed in an increasing impairment of consciousness from somnolence and stupor to cerebral coma.

    One of the main manifestations of encephalitis is local convulsive twitches or attacks of generalized tonic or clonic-tonic convulsions, which in younger children can develop at the very beginning of the disease, which can cause errors in diagnosis. Within a few days, depending on the focus of the inflammatory process, focal neurological symptoms begin to increase in the form of hemiparesis, various sensitivity disorders, and aphasia. In addition, symptoms such as drooping of the corner of the mouth, smoothness of the nasolabial fold on one side, unilateral blepharoptosis, anisocoria, and deviation of the tongue may be noted. As a manifestation of increasing intracranial pressure, when examining the fundus, a congestive optic disc is detected. In most cases, the appearance of a vesicular rash on the skin of the body by the end of the first week of the disease can be considered a sign confirming the herpetic nature of encephalitis. In the absence of treatment, the disease begins to progress steadily and in most cases has an unfavorable prognosis.

    A significant number of surviving patients develop gross persistent residual effects on the part of the neuropsychic sphere in the form of intellectual impairment and the development of paralysis, paresis and contractures.

    TREATMENT

    Treatment should be carried out exclusively by a neurologist. Self-medication is unacceptable. The etiotropic therapy of herpetic encephalitis includes antiviral treatment with acyclovir (zovirax, virolex). This therapy should be based on the results of a clinical examination of the patient. Laboratory-specific examination methods are time-consuming and cannot provide early diagnosis. Therefore, treatment with acyclovir should be started as early as possible, only if the herpetic nature of the disease is suspected, as well as with encephalitis of unclear etiology. To reduce body temperature, physical methods of cooling are used – applying ice to the head and on the region of large vessels, wiping the surface of the body with alcohol or a 1-2% vinegar solution or wrapping in a wet sheet, administering antipyretic drugs such as paracetamol, aspirin, cefecon and etc., the introduction of lytic mixtures.

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    Reception (examination, consultation) of a neurologist, doctor of medical sciences, professor primary

    RUB 5500

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    Appointment (examination, consultation) with a neurologist, doctor of medical sciences repeated

    4000 r.

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    Repeated appointment (examination, consultation) with a neurologist, candidate of medical sciences

    RUB 3000

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    Extended repeated appointment (examination, consultation) with a neurologist (epileptologist)

    3000 r.

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    Primary appointment (examination, consultation) with a neurologist (epileptologist 40 min)

    RUB 3500

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    Primary appointment (examination, consultation) with a neurologist

    2500 rub.

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    Primary appointment (examination, consultation) with a neurologist, doctor of medical sciences

    RUB 4500

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    Primary appointment (examination, consultation) with a neurologist, candidate of medical sciences

    3500 r.