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Chronic_Encephalitis

Chronic_Encephalitis

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Chronic Encephalitis
Progressive Multifocal Leukoencephalopathy
A. Clinical Features & Pathology
\ue000Progressive disorder characterized pathologically
by:
\ue001multifocal areas of demyelination of varying
size distributed throughout the CNS
\ue001cytologic alterations in both astrocytes &
oligodendrocytes
\ue000Astrocytes:
\ue001Enlarged

\ue001Hyperchromatic, deformed
\ue001Bizarre nuclei
\ue001Frequent mitotic figures

\ue000Oligodendrocytes:
\ue001Enlarged
\ue001Densely staining nuclei that contain viral
inclusions formed the crystalline arrays of JC
virus particles

\ue000Clinical features:
\ue001Visual defects (45%)
\ue001Homonymous hemianopia
\ue001Mental impairment\u2014dementia, confusion,

personality changes (38%)
\ue001Motor weakness\u2014not present early in the
disease but eventually occurs in 75% of cases
\ue000Almost all pxs have an underlying
immunosuppressive disorder
B. Diagnostic Studies
\ue000MRI reveals multifocal asymmetric, coalescing
white matter lesions located:

\ue001Periventricularly
\ue001In the centrum semiovale
\ue001In the parietal-occipital region
\ue001In the cerebellum

\ue000These lesions have:
\ue001\u2191T2 & \u2193T1 signal
\ue001generally nonenhancing or show only minimal
peripheral enhancement
\ue001not assoc with edema or mass effect
\ue000MRI for the diagnosis of PML: show hypodense
nonenhancing white matter lesions
\ue000CSF findings:
\ue001Typically normal
\ue001Although, mild elevation in CHON &/or IgG
\ue001Pleocytosis (25%)\u2014predominantly mononuclear
& rarely >25cells/uL
\ue000PCR amplification of JC virus from CSF: an impt
diagnostic tool
\ue001high specificity, but sensitivity has varied
among studies
\ue000Diagnostic of PML: (+) CSF PCR for JC virus DNA in
association with typical MRI lesions in the
appropriate clinical setting
\ue000Pxs with (-) CSF PCR studies may require brain

biopsy for definitive diagnosis; JC virus antigen and
nucleic acid can be detected by
immunocytochemistry, in situ hybridization, or PCR
amplification

C. Treatment
\ue000No effective therapy is available.
Subacute Sclerosing Panencephalitis
\ue000Rare progressive demyelinating disease of the CNS
assoc with a chronic infection of brain tissue with
measles virus
\ue000Hx of primary measles infection at an early age (2
y/o)
\ue000followed after a latent interval of 6 to 8 years by
the development of insidious intellectual decline
and mood and personality changes
\ue000Typical signs of a CNS viral infection, including
fever & headache, do not occur
As the disease progresses, there is the occurrence of:
\u2022
Focal and/or generalized seizures
\u2022
Myoclonus
\u2022
Ataxia
\u2022
Visual disturbances
\ue000EEG: characteristic periodic pattern with bursts

every 3-8s of high-voltage, sharp slow waves,
followed by periods of attenuated ("flat")
background

\ue000CSF: acellular with a normal or mildly elevated
protein level & a markedly elevated ?-globulin level
(>20% of total CSF protein)
\ue000CSF anti-measles antibody levels: invariably
elevated; oligoclonal anti-measles antibodies are
often present
\ue000CTand MRI show evidence of multifocal white
matter lesions & generalized atrophy.
\ue000Measles virus can be cultured from brain tissue
\ue000Viral genome can be detected by in situ
hybridization or PCR amplification
Treatment
\ue000Isoprinosine (Inosiplex) (100 mg/kg per day): alone
or in combination with intrathecal or
intraventricular interferon
Progressive Rubella Panencephalitis
\ue000Extremely rare disorder
\ue000Primarily affects males with congenital rubella
syndrome
\ue000After a latent period of 8-19 years, pxs develop
progressive neurologic deterioration
\ue000Manifestations: similar to SSPE
\ue000CSFshow s:

a. mild lymphocytic pleocytosis
b. slightly elevated protein level
c. markedly increased ?-globulin
d. rubella virus-specific oligoclonal bands.

\ue000No therapy is available
Brain Abscess
\ue000Focal, suppurative infection within the brain
parenchyma
\ue000Surrounded by a vascularized capsule
Cerebritis
\ue000Often employed to describe a nonencapsulated
brain abscess
A. Epidemiology
\ue000A bacterial brain abscess is a relatively
uncommon intracranial infection
\ue000Incidence: ~1 in 100,000 persons/yr
\ue000Predisposing conditions:
\u2022
otitis media & mastoiditis
\u2022
paranasal sinusitis
\u2022
pyogenic infections in the chest or other
body
\u2022
sites
\u2022
penetrating head trauma or neurosurgical
\u2022
procedures
\u2022
dental infections
\ue000Modern causes:
\u2022
Toxoplasma gondii
\u2022
Aspergillus spp.
\u2022
Nocardia spp.
\u2022
Mycobacteria spp.
\u2022
C. neoformans
\ue000The said organisms are almost exclusively

restricted to immunocompromised hosts:
a. HIV infection
b. organ transplantation
c. cancer
d. immunosuppressive therapy

B. Etiology
\ue000A brain abscess may develop:
\u2022

by direct spread from a contiguous cranial
site of infection, such as paranasal sinusitis,
otitis media, mastoiditis, or dental infection;

\u2022
following head trauma or a neurosurgical
procedure; or
\u2022
as a result of hematogenous spread from a
remote site of infection
\ue00025% of cases: no obvious primary source of
infection
\ue0001/3 of brain abscesses: assoc with otitis media &
mastoiditis, often with an cholesteatoma
\ue000Otogenic abscesses occur predominantly in the:
\u2022
temporal lobe (55 to 75%)
\u2022
cerebellum (20 to 30%)
\ue000Common organisms:
\u2022
Streptococci
\u2022
Bacteroides spp.
\u2022
P. aeruginosa
\u2022
Enterobacteriaceae
\ue000Abscesses that develop as a result of direct
spread of infection from:
\u2022
Frontal
\u2022
Ethmoidal
\u2022
Sphenoidal sinuses
\ue000Those that occur due to dental infections: usually
located in the frontal lobes
\ue000~10% of brain abscesses: assoc with paranasal
sinusitis
\ue000Most common pathogens in brain abscesses
associated with paranasal sinusitis:
\u2022
streptococci (especially S. milleri)
\u2022
Haemophilus spp.
\u2022
Bacteroides spp.
\u2022
Pseudomonas spp., and
\u2022
S. aureus.
\ue000

- Dental infections are associated with ~2% of brain
abscesses, although it is often suggested that many
"cryptogenic" abscesses are in fact due to dental
infections.
The most common pathogens in this setting are

a. streptococci
b. staphylococci
c. Bacteroides and
d. Fusobacterium spp.

- Hematogenous abscesses account for ~25% of brain
abscesses.
- show a predilection for the territory of the middle
cerebral artery (i.e., posterior frontal or parietal lobes).
- often located at the junction of the gray and white
matter
- often poorly encapsulated.
- often multiple
- microbiology of these hematogenous abscesses is
dependent on the primary source of infection

Examples:

1. brain abscesses that develop as a complication
of infective endocarditis are often due to viridans
streptococci or S. aureus.

2. Abscesses associated with pyogenic lung
infections such as lung abscess or bronchiectasis are often
due to Streptococci, staphylococci, or Bacteroides or
Fusobacterium spp.

3. Enterobacteriaceae and P. aeruginosa are
important causes of abscesses associated with urinary
sepsis.

4. Abscesses that follow penetrating head trauma
or neurosurgical procedures are frequently due to
staphylococci, Enterobacteriaceae, and Pseudomonas
species.

- Congenital cardiac malformations that produce a right-
to-left shunt (congenital cyanotic heart disease), such as
tetralogy of Fallot, patent ductus arteriosus, and atrial
and ventricular septal defects, allow bloodborne bacteria
to bypass the pulmonary capillary bed and reach the
brain.

- Similar phenomena can occur with pulmonary
arteriovenous malformations. The decreased arterial
oxygenation and saturation from the right-to-left shunt
and polycythemia may cause focal areas of cerebral
ischemia, thus providing a nidus for microorganisms that
bypassed the pulmonary circulation to multiply and form
an abscess.
- Streptococci are the most common pathogens in this
setting.

PATHOGENESIS AND HISTOPATHOLOGY
-intact brain parenchyma is relatively resistant to
infection
Prerequisite for effective bacterial invasion
a. preexisting brain ischemia
b. necrosis, or
c. hypoxia
- Once infection is established, brain abscess frequently

evolves through a series of stages, influenced by:
a. the nature of the infecting organism and
b. by the immunocompetence of the host

Early cerebritis stage (days 1 to 3)

- characterized by a perivascular infiltration of
inflammatory cells, which surround a central core of
coagulative necrosis.

- Marked edema surrounds the lesion
Late cerebritis stage (days 4 to 9)

- pus formation leads to enlargement of the
necrotic center, which is surrounded at its border by an
inflammatory infiltrate of macrophages and fibroblasts.

- A thin capsule of fibroblasts and reticular fibers
gradually develops, and the surrounding area of cerebral
edema becomes more distinct than in the previous stage.

Early capsule formation (days 10 to 13)

- characterized by the formation of a capsule
that is better developed on the cortical than on the
ventricular side of the lesion.

-This stage correlates with the appearance of a
ring-enhancing capsule on neuroimaging studies.
Late capsule formation (day 14 and beyond)
- defined by a well-formed necrotic center
surrounded by a dense collagenous capsule.

- surrounding area of cerebral edema has
regressed, but marked gliosis with large numbers of
reactive astrocytes has developed outside the capsule.

- gliotic process may contribute to the
development of seizures as a sequelae of brain abscess.
CLINICAL PRESENTATION

- typically presents as an expanding intracranial mass
lesion, rather than as an infectious process.
- evolution of signs and symptoms is extremely variable,
ranging from hours to weeks or even months
- most patients present to the hospital 11 to 12 days
following onset of symptoms.

The classic clinical triad (present in <50% of cases)
a. headache
b. fever, and
c. a focal neurologic deficit
Headache
-most common symptom in patients with a brain
abscess (>75% of patients)
-often characterized as a constant, dull, aching
sensation, either hemicranial or generalized
-becomes progressively more severe and
refractory to therapy.
Fever
- is present in only 50% of patients at the time of
diagnosis- and its absence should not exclude the
diagnosis.
Focal neurologic deficits
-new onset of focal or generalized seizure
activity is a presenting sign in 15 to 35% of patients.
- includes hemiparesis, aphasia, or visual field
defects
- part of the initial presentation in >60% of
patients.
The clinical presentation of a brain abscess depends on:
a. location
b. the nature of the primary infection if
present, and
c.the level of the ICP
Hemiparesis
- most common localizing sign of a frontal lobe
abscess.

A temporal lobe abscess may present with:
a. disturbance of language (dysphasia) or
b. upper homonymous quadrantanopia.

- Nystagmus and ataxia are signs of a cerebellar abscess.

- Signs of raised ICP \u2014 papilledema, nausea and vomiting,
and drowsiness or confusion \u2014 can be the dominant
presentation of some abscesses, particularly those in the
cerebellum

Meningismus

-not present unless the abscess has ruptured into
the ventricle or the infection has spread to the
subarachnoid space.

DIAGNOSIS
- made by neuroimaging studies
MRI
- better than CT for demonstrating abscesses in
the early (cerebritis) stages
- superior to CT for identifying abscesses in the
posterior fossa
- A mature brain abscess appears on CT as a focal
area of hypodensity surrounded by ring enhancement.
- CT and MRI appearance, particularly of the
capsule, may be altered by treatment with glucocorticoids

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