Transcript Introduction

Introduction
 Encephalitis is an acute inflammatory process affecting the
brain
 Viral infection is the most common and important cause,
with over 100 viruses implicated worldwide
 Symptoms
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Fever
Headache
Behavioral changes
Altered level of consciousness
Focal neurologic deficits
Seizures
 Incidence of 3.5-7.4 per 100,000 persons per year
Herpes Simplex Encephalitis
 Commonest and gravest form of sporadic acute
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encephalitis.
Between 30 and 70 percent are fatal, and the majority of
patients who survive are left with serious neurologic
abnormalities.
Sporadically throughout the year and in patients of all
ages and in all parts of the world.
Almost always to HSV-1, which is also the cause of the
common herpetic lesions of the oral mucosa.
The type 2 virus may also cause acute generalized
encephalitis, usually in the neonate and in relation to
genital herpetic infection in the mother.
Pathology
 With reactivation in the trigeminal ganglia, the infection
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may spread along nerve fibers that innervate the
leptomeninges of the anterior and middle fossae.
Both direct virus-mediated and indirect immunemediated mechanisms play a role in producing CNS
damage
Intense hemorrhagic necrosis of the inferior and medial
temporal lobes and the medioorbital parts of the frontal
lobes
Temporal lobe lesions are usually bilateral but not
symmetrical
Intranuclear eosinophilic inclusions are found in neurons
and glial cells.
Clinical Features
 Over several days
 Fever, headache, seizures, confusion, stupor, and coma.
 Findings that betray the predilection of this disease for
the inferomedial portions of the frontal and temporal
lobes.
 Olfactory or gustatory hallucinations, anosmia, temporal
lobe seizures, personality change, bizarre or psychotic
behavior or delirium, aphasia, and hemiparesis.
 Swelling and herniation of one or both temporal lobes
through the tentorium may occur
 Status epilepticus is rare.
Herpes Simplex Encephalitis
 The CSF is typically under increased pressure
 Almost invariably shows a pleocytosis (range, 10 to 200 cells
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per cubic millimeter, infrequently more than 500).
The cells are mostly lymphocytes,
In a few cases, 3 to 5 percent in some large series, the spinal
fluid has been normal in the first days of the illness.
In only a minority of cases, red cells, sometimes numbering in
the thousands, and xanthochromia are found
The protein content is increased in most cases.
Rarely, the CSF glucose levels may be reduced to slightly less
than 40 mg/dL, creating confusion with tuberculous and
fungal meningitides
Diagnosis
 CT scans show hypodensity of the affected areas in
50 to 60 percent of cases
 MRI shows signal changes in almost all (increased
signal in T2-weighted images).
 T1-weighted images demonstrate areas of low signal
intensity with surrounding edema and sometimes
with scattered areas of hemorrhage occupying the
inferior parts of the frontal and temporal lobes.
 Almost always the lesions enhance with contrast
Diagnosis
 Detection of HSV antigen in the CSF by the
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application of PCR
The test has extremely high sensitivity (98 percent)
and specificity (94 to 100 percent)
Antiviral treatment did not appear to affect the test.
False-negative tests are most likely to occur in the
first 48 h of febrile infection.
Fluorescent antibody study and by viral culture of
cerebral tissue obtained by brain biopsy
Treatment
 Acyclovir significantly reduces both mortality and
morbidity from the disease
 Initiate treatment while confirmatory testing is being
carried out.
 Early treatment
1. Before loss of consciousness
2. Within 24 hours of the onset of symptoms
3. Glasgow Coma Scale score of 9 to 15
 The duration of treatment of HSV encephalitis in
immunocompetent patients should be 14 to 21 days
Herpes Simplex Encephalitis
 Antiviral therapy may be discontinued if a negative
CSF HSV PCR result is obtained after 72 hours
following onset of neurological signs and symptoms.
 Clinicians must consider alternative reasons for a
false-negative CSF PCR result, including early testing
after the onset of symptoms, or presence of PCR
inhibitors (eg, hemoglobin degradation products in
bloody CSF)