(1)Laboratório de Raiva e Encefalites Virais, Instituto Biológico de São Paulo, São Paulo, SP, Brasil. [email protected] This study was aimed to. (2)Laboratório de Raiva e Encefalites Virais, Instituto Biológico, São Paulo, SP, Brazil. (3)Departamento de Estatística, Universidade Federal de Mato Grosso. Craniectomia descompressiva para encefalite viral: relato de dois casos. Ricardo Lourenço . 9 Silva GMM. Encefalites Virais Agudas.
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While systemic viral infections are exceptionally common, symptomatic viral infections of the brain parenchyma itself are very rare, but a serious neurologic condition.
It is estimated that viral encephalitis occurs at a rate of 1. Geography is a major determinant of encephalitis caused by vector-borne pathogens.
In this review, the most common viral encephalitis will be discussed, with focus on ecology, diagnosis, and clinical management. Estima-se que a encefalite viral ocorra em 1,4 casos por The term encephalitis corresponds to an inflammation of the brain parenchyma caused by both infectious and non-infectious diseases. Viruses are the most common infectious agents associated with acute encephalitis.
The cardinal symptoms and signs of acute viral encephalitis are fever, altered level of consciousness, headache, focal neurological deficits, and seizure.
The most common viruses that cause encephalitis are listed in Table 1. It is of primordial importance a detailed epidemiological history about recent ivrais or animal contacts, since some viruses are common in some regions and not seen in others. The most important agents worldwide are the herpes viruses and the arboviruses.
However, numerically Japanese encephalitis is encefwlites most common encephalitis worldwide, while the West Nile virus is the most widespread virus and can be encountered in parts of Europe, Russia, Africa, the Middle East, India, Indonesia, and North America.
Noteworthy, it is estimated that even in the Occident, the larger, undiagnosed proportion of encephalitis cases are encfalites by one of the arboviruses.
Differential diagnosis of viral encephalitis is wide and includes other infections of the central nervous system CNSautoimmune diseases such as ADEM, limbic encephalitis, Rasmussen’s syndrome, and metabolic diseases. This paper will focus on some specific viral encephalitis. The incidence is estimated in 2. After CNS invasion, a focal inflammatory and necrotizing lesion is observed specially in the temporal lobes, orbital frontal cortex, and limbic structures.
Generally, neurological findings are acute, with less than one week in duration. Majority of patients will present fever and headache besides one of the above symptoms. Meningeal sings are uncommon. Immunosuppressed patients may exhibit a more indolent clinical course see Figure 1. A year old HIV-infected man presented in May with anxious disorders, psychomotor agitation, discrete memory impairment, and visual hallucination started 2 weeks before admission.
A brain CT performed in the emergency sector of a peripheral hospital was normal. He was ehcefalites of this hospital with 2 mg daily of risperidone and with a psychiatric consultation scheduled within 6 weeks.
He had a severe memory impairment, but no focal neurologic deficit was present. A lumbar puncture was performed, showing a discrete lymphocytic pleocytosis and protein elevation. IV acyclovir was started immediately. A new PCR test was done before patient’s discharge and was negative. He was left with a mild memory deficit only. EEG shows unilateral or bilateral periodic lateralized epileptiform discharges, while brain MRI discloses hyperintensity in fluid-attenuated inversion recovery FLAIR and T2-weigthed images in one or both of the temporal and orbitofrontal lobes, often extending to the insular and cingulate gyri.
Pleocytosis diminishes with antiviral therapy, but can persist at a low level for weeks or even months.
Glucose levels are normal in majority of cases, but hypoglycorrhachia has been reported in neonatal cases of HSV-2 encephalitis. The presence of red blood cells is neither sensitive nor specific for HSV encephalitis. After antiviral therapy, the rate of positive HSV-1 PCR decrease over time, usually beginning after a full week of therapy 5.
A second lumbar puncture with PCR analysis after 2 weeks of treatment is suggested by some; if positive, continuing therapy is recommended. Favorable prognosis is seen in patients who are treated early, who are younger than 30 years of age, have short duration of illness, a Glasgow Coma Scale score of more than 6, and who have a low viral load on CSF 2. VZV cerebral vasculopathy may also be seen in immunocompetent patients.
VZV vasculopathy presents with acute focal neurological deficits due to involvement of large cerebral arteries following trigeminal distribution of zoster by weeks to months. In immunocompromised patients, VZV vasculopathy presents as a multifocal vasculopathy involving small and medium-size arteries, resulting in mental status changes, focal deficits, and mononuclear pleocytosis in the CSF.
Mixed ischemic and hemorrhagic infarcts in subcortical gray and white matter and demyelinate lesions are noted both in brain MRI and pathological studies.
Noteworthy, typical rash of zoster may be absent in these patients 6. The glucose level is normal in the majority of cases.
VZV vasculopathy should be treated with a combination encegalites acyclovir and a pulse of corticosteroid. Beyond the neonatal period, CMV encephalitis is extremely uncommon in immunocompetent patients.
CMV encephalitis is characterized by nonspecific febrile encephalopathy, with or without focal features. Necefalites can present acutely – encevalites nodular encephalitis – with delirium and confusion, or subacutely — ventriculoencephalitis – characterized by confusion and cranial nerves dysfunction. One quarter of patients have brainstem involvement with vertical or horizontal gaze-evoked nystagmus, internuclear ophtalmoplegia, and cranial neuropathies CMV encephalitis rncefalites a consequence of reactivation of previously latent virus infection.
The virus has a predilection for encefalitds cells of the lateral ventricles and may be suspected when brain MRI shows contrast-enhancing lesions as streaks surrounding the lateral ventricles in a patient with clinical encephalitis.
Characteristically, CSF analysis discloses a polymorphonuclear pleocytosis, depressed glucose, and raised protein levels. Recommended treatment is IV ganciclovir for 3 weeks followed by a maintenance dosing with either IV ganciclovir or oral valganciclovir. Classical manifestation of primary EBV infection is the infectious mononucleosis syndrome, a systemic disease characterized by cervical lymphadenopathy, pharyngitis, and splenomegaly.
EBV encephalitis may present with frank encephalopathy with altered consciousness, coma, seizures, and focal neurological deficits. It can occur before, during, or after infectious mononucleosis or even in its absence. Some patients may exhibit an encephalomyeloradiculitis and some cases may mimic HSV-1 encephalitis.
Pathogenicity of different rabies virus isolates and protection test in vaccinated mice.
None of the currently available antiviral encefalitrs have activity against EBV in vitrobut there are some reports of ganciclovir treatment in EBV meningoencephalitis after bone marrow transplantation.
HHV-6 is encevalites T lymphotropic virus that causes a spectrum of diseases like exanthema subitumlymphadenopathy syndromes, and meningoencephalitis. The virus has also a controversial role in other neurologic conditions, such as febrile seizures in infants, subsequent temporal lobe epilepsy, and cranial nerve palsies. However, it is recognized as an agent in some cases of limbic encephalitis in bone marrow transplant recipients Clinical and radiological picture is similar to paraneoplastic and anti-voltage-gated potassium channel limbic encephalitis.
Patients present generally with behavioral disturbances, severe memory impairment, and agitation. The prognosis is better than in herpetic encephalitis and treatment is generally done with ganciclovir and foscarnet. Enteroviruses EV pertain to Picornaviridae family and comprise over 70 different serotypes. EV are transmitted via a fecal-oral route and certain serotypes predominate in a particular geographical area, causing cyclical outbreaks when there are sufficient non-immunized individuals present, mainly young children.
The EV serotype has been associated with a higher rate of encephalitis, specifically with a focal brainstem dysfunction. Affected patients are usually young children that present fever, myoclonus, ataxia, nystagmus, and cranial nerve palsies. PCR is more sensitive than viral cultures for diagnosis, but most of the studies were conducted in patients with EV meningitis There is no specific treatment, but pleconaril and intravenous immunoglobulin have been tried.
Arbovirus is the acronym for ar thropod- bo rne virusa vast group of viruses that are transmitted to humans by mosquito and tick vectors. Arbovirus are grouped in three families; togaviruses flaviviruses and alphavirusesreoviruses, and encefslites. Considered together, arboviruses represent the leading cause of encephalitis worldwide.
Pathogenicity of different rabies virus isolates and protection test in vaccinated mice.
WNV is transmitted from infected birds to humans by Culex or Aedes mosquitos. Human outbreaks became more frequent and reported nowadays. Neurological manifestations of WNV include meningitis, encephalitis, myelitis, and polio-like illness.
These manifestations are expected in 1 envefalites of infected persons After infection, symptoms and signs of a systemic viral disease appear 2 to 14 days after, and in about half of the patients a rash maculopapular is observed. Pathologically, WNV causes an encephalomyelitis and leptomeningitis, characterized by microglial nodules with neuronal loss in the gray and white matter of the cerebrum, hippocampus, thalamus, medulla, and anterior horn cells, which explain the neurological manifestations observed in these patients.
An abruptly onset of fever and altered mental status is observed in majority of patients. Other clinical manifestations are diffuse proximal muscular weakness, respiratory paralysis, tremor, myoclonus, and Parkinsonism features as seen in Japanese encephalitis. Patients over 65 years of age and those with flaccid paralysis are at greater risk of death. Brain MRI shows bilateral, focal T2 hyperintense lesions in the thalamus, basal ganglia, and pons in severely ill patients.
Electromyography examination may show axonal neuropathy, probably reflecting anterior horn cell involvement, although in some patients a demyelinating neuropathy is seen as well. Among 76 WNM encephalitis patients, vifais More than a half of patients had a polymorphonuclear predominance at presentation and enfefalites No patient had hypoglycorrhachia Dengue fever is caused by 1 of 4 related RNA virus Dengue virus serotypes 1 to 4.
The virus is transmitted mainly by Aedes aegypti from an infected to uninfected person. Infection with one serotype does not confer immunity to the virai virus serotypes. Dengue fever begins after an incubation period of 2 to 7 encwfalites, characterized by fever, headache, myalgia, arthralgia, prostration, abdominal discomfort, and rash.
Dengue hemorrhagic fever viraid the severe form of disease, mainly occurring in persons previously sensitized by infection with a heterologous dengue serotype. Children at are great viraid to severe form of disease. Majority of these patients had a normal CSF study. Dengue diagnosis depends on virus isolation from blood in the early stages or serological tests. Yellow fever occurs in tropical South America and sub-Saharan Africa.
Like dengue, the vector is A. Vaccination with yellow fever vaccine has been associated with rare cases of encephalitis in infants within 30 days after immunization.
Thus, the vaccine is contra-indicated in infants younger than 4 months of age. Encefalitee CNS syndromes are associated with measles: Acute encephalitis is characterized by fever, maculopapular rash, cough, coryza, and Koplik spots.