Download Acute viral neurological diseases

Acute viral neurological diseases
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Dr. Mohammed Arif
Associate professor
Consultant virologist
Head of the virology unit
College of medicine & KKUH
Acute viral neurological diseases
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Aseptic meningitis
Encephalitis
Post-infectious encephalomyelitis
Paralysis
1-Aseptic meningitis
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Case definition
A syndrome characterized by acute onset of
meningeal symptoms, fever and cerebrospinal fluid
pleocytosis, with no laboratory evidence of bacterial
or fungal meningitis.
Aseptic meningitis
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Inflammation of the meninges that cover the brain
and spinal cord.
Meninges: duramatter, arachnoid and piamatter.
It is a disease of children and young adults.
Viral etiology
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Enteroviruses (85%).
Arboviruses.
Mumps virus.
Lymphocytic choriomeningitis.
Herpes viruses (HSV-1&2, CMV EBV.HHV-6,7,8)
Symptoms
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Severe headache.
Fever.
Stiffness of neck.
Nausea.
Vomiting.
Sore throat.
Myalgia.
Symptoms ( CONT.)
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Prognosis: recovery is usual in 5 – 14 days.
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Complication : meningoencephalitis.
CSF-picture
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Clear.
Colorless.
Pleocytosis (increased lymphocytes).
Increased protein.
Normal glucose.
Negative for bacterial culture.
2-Acute viral encephalitis
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Inflammation of the brain.
Caused by direct viral invasion of the brain.
The virus replicate in the brain, causing destructive
lesions in the grey matter.
Viral etiology
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HSV-1&2.
Enteroviruses.
Arboviruses.
Rabies virus.
Mumps virus.
Clinical features
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The incubation period 3-7 days.
Starts with the symptoms of aseptic meningitis
followed by :
Drowsiness.
Mental confusion.
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Alteration in the level of consciousness.
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Clinical features (cont.)
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Lack of coordination.
Seizures.
Coma.
Prognosis
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The clinical outcome varies, some are mild with full
recovery.
Others are severe with permanent neurological
sequalae.
Permanent neurological impairments include
memory, speech, vision, and muscle control.
Pathology
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HSV-encephalitis is characterized by:
Edema, hemorrhage and necrosis confined primarily
to the temporal lobes (bilateral or unilateral).
Vascular destruction with infiltrates of neutrophils
and lymphocytes.
Glial proliferation.
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Eosinophilic intranuclear inclusion bodies.
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Pathology
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Rabies encephalitis is characterized by:
Perivascular infiltrate of neutrophils and
lymphocytes.
Glial proliferation.
Negri bodies, intracytoplasmic inclusion bodies, most
prominent in the hippocampus.
Treatment
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For enteroviruses and arboviruses, treatment is
supportive. There is no anti-viral drug therapy.
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For HSV, the recommended dose of acyclovir is 30
mg/ kg per day, in three divided doses for 14 - 21
days.
Methods of Diagnosis
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Detection of the viral genome using PCR.
Isolation of the virus in tissue culture, followed by
identification of the isolated virus.
MRI (magnetic resonance imaging) provides high
quality picture of the brain, useful in the identification
of edema, necrosis and hemorrhage.
Methods of Diagnosis (cont.)
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CT-scan (computer assisted tomography), useful of
identification of internal bleeding. Edema and
necrosis.
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EEG (electroencephalography) shows spikes and
wave activity.
3-Post-infectious encephalomyelitis
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It is uncommon complication of many viruses that do
not usually affect the CNS including measles,
mumps , rubella and varicella.
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Encephalitis develops within 6 – 10 days after
symptoms of viral illness appear.
Post- infectious encephalomyelitis
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The disease is believed to be an auto-immune
phenomenon, in which the immune system is
triggered by exposure to foreign antigen which is
closely related to host proteins normally expressed
in brain tissue.
Pathology
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Characterized by wide spread demyelinating lesions
in the brain and spinal cord.
Lymphocytic infiltration and perivascular cuffing of
adjacent blood vessels.
Clinical features
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Similar to acute viral encephalitis.
Fever.
Headache.
Stiffness of neck.
Alteration in the level of consciousness.
Mental confusion.
Seizures and coma.
Prognosis
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Not good.
Recovery is not complete.
Survivors are left with permanent neurological
sequalae.
Treatment
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Supportive therapy, there is no specific viral drug
therapy.
Lab. diagnosis
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By detection of the viral genome to measles,
mumps and rubella.
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By detection of IgM-Ab to these viruses.
Chronic viral neurological diseases
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Subacute sclerosing pan encephalitis (SSPE).
Progressive multifocal leucoencephalopathy.
Tropical spastic paraparesis (TSP).
SSPE
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Caused by a mutant measles virus.
Measles virus usually does not cause brain damage,
but the mutant virus can invade the brain causing
persistent infection and severe form of encephalitis
and death.
It affects only unvaccinated children.
Clinical features
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It is a rare, slowly progressive disease of the CNS
ending in death.
SSPE develops 6 – 12 years after having a primary
measles infection.
It is due to reactivation of persistent measles virus in
the brain.
Clinical features
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The disease starts with personality changes and
memory defects followed by
Myoclonic.
Intellectual impairment.
Impairment of vision and speech.
Seizures.
Ataxia
Coma & death.
Laboratory Diagnosis
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Presence of high Ab-titre to measles virus in CSF
and serum.
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MRI provides high quality picture of the brain.
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Electro-encephalogram (ECG), is a test for the
electrical activity of the brain, which shows a wave
pattern whish is typical of SSPE.
Treatment
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No cure for SSPE exist.
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A combination of Isoprinosine and alpha
interferon injected directly into the brain
ventricles appears to be the most effective
treatment.
Prevention
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Immunization of children against measles virus is the
only known prevention of SSPE.
Pathology
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SSPE is characterized by atrophy of the cortex, loss
of white matter and ventricular enlargement.
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Perivascular lymphocytic infiltrate and intense
gliosis.
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Intranuclear inclusion bodies.
Progressive multifocal leukoencephalopathy
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Caused by a polyoma virus known as JC virus.
The virus belongs to the family papovaviridae.
Genus: polyoma virus,
The virus is opportunistic, causing brain disorder
only in the immunosuppressive patients.
Infection with JC virus is common, but asymptomatic.
50 – 60% of adults have Ab to the virus.
Clinical features
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It is a slowly progressive disease of the CNS that is
usually fatal.
It is due to reactivation of latent virus in the brain.
The disease is characterized by :
Hemiparesis
Dementia
Impaired vision and speech
Dysphagia
Lack of coordination & seizures.
Prognosis
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Death is very common 1 to 6 months when
symptoms starts.
Laboratory diagnosis
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Detection of the viral genome using PCR.
MRI.
Pathology
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Brain autopsy shows multiple demyelination foci
prominent in the hemispheres and cerebellum.
Destruction of the white matter.
Prominent gliosis.
Eosinophilic intranuclear inclusion bodies.