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Chronic Encephalitis

Progressive Multifocal Leukoencephalopathy


A. Clinical Features & Pathology Subacute Sclerosing Panencephalitis
 Progressive disorder characterized pathologically  Rare progressive demyelinating disease of the CNS
by: assoc with a chronic infection of brain tissue with
 multifocal areas of demyelination of varying measles virus
size distributed throughout the CNS  Hx of primary measles infection at an early age (2
 cytologic alterations in both astrocytes & y/o)
oligodendrocytes  followed after a latent interval of 6 to 8 years by
 Astrocytes:
the development of insidious intellectual decline
 Enlarged and mood and personality changes
 Hyperchromatic, deformed  Typical signs of a CNS viral infection, including
 Bizarre nuclei
fever & headache, do not occur
 Frequent mitotic figures
 Oligodendrocytes:
As the disease progresses, there is the occurrence of:
 Enlarged
• Focal and/or generalized seizures
 Densely staining nuclei that contain viral • Myoclonus
inclusions formed the crystalline arrays of JC
virus particles • Ataxia
 Clinical features: • Visual disturbances
 Visual defects (45%)
 Homonymous hemianopia  EEG: characteristic periodic pattern with bursts
 Mental impairment—dementia, confusion, every 3-8s of high-voltage, sharp slow waves,
personality changes (38%) followed by periods of attenuated ("flat")
 Motor weakness—not present early in the background
disease but eventually occurs in 75% of cases  CSF: acellular with a normal or mildly elevated
 Almost all pxs have an underlying protein level & a markedly elevated ?-globulin level
immunosuppressive disorder (>20% of total CSF protein)
 CSF anti-measles antibody levels: invariably
B. Diagnostic Studies elevated; oligoclonal anti-measles antibodies are
 MRI reveals multifocal asymmetric, coalescing often present
white matter lesions located:  CT and MRI show evidence of multifocal white
 Periventricularly matter lesions & generalized atrophy.
 In the centrum semiovale
 In the parietal-occipital region
 Measles virus can be cultured from brain tissue
 In the cerebellum  Viral genome can be detected by in situ
 These lesions have: hybridization or PCR amplification
 ↑ T2 & ↓ T1 signal Treatment
 generally nonenhancing or show only minimal
peripheral enhancement  Isoprinosine (Inosiplex) (100 mg/kg per day): alone
 not assoc with edema or mass effect or in combination with intrathecal or
intraventricular interferon
 MRI for the diagnosis of PML: show hypodense
nonenhancing white matter lesions
Progressive Rubella Panencephalitis
 CSF findings:
 Typically normal  Extremely rare disorder
 Although, mild elevation in CHON &/or IgG  Primarily affects males with congenital rubella
 Pleocytosis (25%)—predominantly mononuclear syndrome
& rarely >25cells/uL  After a latent period of 8-19 years, pxs develop
 PCR amplification of JC virus from CSF: an impt progressive neurologic deterioration
diagnostic tool  Manifestations: similar to SSPE
 high specificity, but sensitivity has varied  CSF shows:
among studies a. mild lymphocytic pleocytosis
 Diagnostic of PML: (+) CSF PCR for JC virus DNA in b. slightly elevated protein level
association with typical MRI lesions in the c. markedly increased ?-globulin
appropriate clinical setting d. rubella virus-specific oligoclonal bands.
 Pxs with (-) CSF PCR studies may require brain  No therapy is available
biopsy for definitive diagnosis; JC virus antigen and
nucleic acid can be detected by
immunocytochemistry, in situ hybridization, or PCR
amplification

C. Treatment
 No effective therapy is available.
• Bacteroides spp.
• P. aeruginosa
• Enterobacteriaceae
 Abscesses that develop as a result of direct
spread of infection from:
• Frontal
Brain Abscess
• Ethmoidal
 Focal, suppurative infection within the brain
parenchyma • Sphenoidal sinuses
 Surrounded by a vascularized capsule  Those that occur due to dental infections: usually
located in the frontal lobes
Cerebritis  ~10% of brain abscesses: assoc with paranasal
 Often employed to describe a nonencapsulated sinusitis
brain abscess  Most common pathogens in brain abscesses
associated with paranasal sinusitis:
A. Epidemiology • streptococci (especially S. milleri)
 A bacterial brain abscess is a relatively • Haemophilus spp.
uncommon intracranial infection
• Bacteroides spp.
 Incidence: ~1 in 100,000 persons/yr • Pseudomonas spp., and
 Predisposing conditions:
• S. aureus.
• otitis media & mastoiditis 
• paranasal sinusitis - Dental infections are associated with ~2% of brain
• pyogenic infections in the chest or other abscesses, although it is often suggested that many
body "cryptogenic" abscesses are in fact due to dental
infections.
• sites The most common pathogens in this setting are
• penetrating head trauma or neurosurgical a. streptococci
• procedures b. staphylococci
• dental infections c. Bacteroides and
 Modern causes: d. Fusobacterium spp.
• Toxoplasma gondii
- Hematogenous abscesses account for ~25% of brain
• Aspergillus spp.
abscesses.
• Nocardia spp. - show a predilection for the territory of the middle
• Mycobacteria spp. cerebral artery (i.e., posterior frontal or parietal lobes).
• C. neoformans - often located at the junction of the gray and white
 The said organisms are almost exclusively matter
restricted to immunocompromised hosts: - often poorly encapsulated.
a. HIV infection - often multiple
b. organ transplantation - microbiology of these hematogenous abscesses is
c. cancer dependent on the primary source of infection
d. immunosuppressive therapy Examples:
1. brain abscesses that develop as a complication
B. Etiology of infective endocarditis are often due to viridans
 A brain abscess may develop: streptococci or S. aureus.
• by direct spread from a contiguous cranial 2. Abscesses associated with pyogenic lung
site of infection, such as paranasal sinusitis, infections such as lung abscess or bronchiectasis are often
otitis media, mastoiditis, or dental infection; due to Streptococci, staphylococci, or Bacteroides or
• following head trauma or a neurosurgical Fusobacterium spp.
3. Enterobacteriaceae and P. aeruginosa are
procedure; or
important causes of abscesses associated with urinary
• as a result of hematogenous spread from a
sepsis.
remote site of infection 4. Abscesses that follow penetrating head trauma
 25% of cases: no obvious primary source of or neurosurgical procedures are frequently due to
infection staphylococci, Enterobacteriaceae, and Pseudomonas
 1/3 of brain abscesses: assoc with otitis media & species.
mastoiditis, often with an cholesteatoma
 Otogenic abscesses occur predominantly in the: - Congenital cardiac malformations that produce a right-
• temporal lobe (55 to 75%) to-left shunt (congenital cyanotic heart disease), such as
• cerebellum (20 to 30%) tetralogy of Fallot, patent ductus arteriosus, and atrial
 Common organisms: and ventricular septal defects, allow bloodborne bacteria
to bypass the pulmonary capillary bed and reach the
• Streptococci brain.
- Similar phenomena can occur with pulmonary b. fever, and
arteriovenous malformations. The decreased arterial c. a focal neurologic deficit
oxygenation and saturation from the right-to-left shunt
and polycythemia may cause focal areas of cerebral Headache
ischemia, thus providing a nidus for microorganisms that -most common symptom in patients with a brain
bypassed the pulmonary circulation to multiply and form abscess (>75% of patients)
an abscess. -often characterized as a constant, dull, aching
- Streptococci are the most common pathogens in this sensation, either hemicranial or generalized
setting. -becomes progressively more severe and
refractory to therapy.
PATHOGENESIS AND HISTOPATHOLOGY
Fever
-intact brain parenchyma is relatively resistant to - is present in only 50% of patients at the time of
infection diagnosis
- and its absence should not exclude the
Prerequisite for effective bacterial invasion diagnosis.
a. preexisting brain ischemia
b. necrosis, or Focal neurologic deficits
c. hypoxia -new onset of focal or generalized seizure
activity is a presenting sign in 15 to 35% of patients.
- Once infection is established, brain abscess frequently - includes hemiparesis, aphasia, or visual field
evolves through a series of stages, influenced by: defects
a. the nature of the infecting organism and - part of the initial presentation in >60% of
b. by the immunocompetence of the host patients.

Early cerebritis stage (days 1 to 3) The clinical presentation of a brain abscess depends on:
- characterized by a perivascular infiltration of a. location
inflammatory cells, which surround a central core of b. the nature of the primary infection if
coagulative necrosis. present, and
- Marked edema surrounds the lesion c. the level of the ICP
Late cerebritis stage (days 4 to 9) Hemiparesis
- pus formation leads to enlargement of the - most common localizing sign of a frontal lobe
necrotic center, which is surrounded at its border by an abscess.
inflammatory infiltrate of macrophages and fibroblasts.
- A thin capsule of fibroblasts and reticular fibers A temporal lobe abscess may present with:
gradually develops, and the surrounding area of cerebral a. disturbance of language (dysphasia) or
edema becomes more distinct than in the previous stage. b. upper homonymous quadrantanopia.
Early capsule formation (days 10 to 13) - Nystagmus and ataxia are signs of a cerebellar abscess.
- characterized by the formation of a capsule
that is better developed on the cortical than on the - Signs of raised ICP — papilledema, nausea and vomiting,
ventricular side of the lesion. and drowsiness or confusion — can be the dominant
-This stage correlates with the appearance of a presentation of some abscesses, particularly those in the
ring-enhancing capsule on neuroimaging studies. cerebellum
Late capsule formation (day 14 and beyond) Meningismus
- defined by a well-formed necrotic center -not present unless the abscess has ruptured into
surrounded by a dense collagenous capsule. the ventricle or the infection has spread to the
- surrounding area of cerebral edema has subarachnoid space.
regressed, but marked gliosis with large numbers of
reactive astrocytes has developed outside the capsule. DIAGNOSIS
- gliotic process may contribute to the
development of seizures as a sequelae of brain abscess. - made by neuroimaging studies
CLINICAL PRESENTATION MRI
- better than CT for demonstrating abscesses in
- typically presents as an expanding intracranial mass the early (cerebritis) stages
lesion, rather than as an infectious process. - superior to CT for identifying abscesses in the
- evolution of signs and symptoms is extremely variable, posterior fossa
ranging from hours to weeks or even months - A mature brain abscess appears on CT as a focal
- most patients present to the hospital 11 to 12 days area of hypodensity surrounded by ring enhancement.
following onset of symptoms. - CT and MRI appearance, particularly of the
capsule, may be altered by treatment with glucocorticoids
The classic clinical triad (present in <50% of cases)
a. headache
Microbiologic diagnosis of the etiologic agent - generally reserved for multiloculated abscesses
- is most accurately determined by Gram's stain or those in which stereotactic aspiration is unsuccessful.
and culture of abscess material obtained by stereotactic
needle aspiration - Medical therapy alone is not optimal for treatment of
- Up to 10% of patients will also have positive brain abscess and should be reserved for patients whose
blood cultures. abscesses are:
a. neurosurgically inaccessible
- LP168 should not be performed in patients with known b. for patients with small nonencapsulated
or suspected focal intracranial infections such as abscess abscesses (cerebritis), and
or empyema c. patients whose condition is too tenuous to
- CSF analysis contributes nothing to diagnosis or therapy allow performance of a neurosurgical procedure

Laboratory studies - All patients should receive a minimum of 6 to 8 weeks of


- may provide clues to the diagnosis of brain parenteral antibiotic therapy.
abscess in patients with a CNS mass lesion. - Patients should also receive prophylactic anticonvulsant
a. 50% of patients have a peripheral leukocytosis therapy because of the high risk of seizures.
b. 60% an elevated ESR - Anticonvulsant therapy is continued for at least 3 months
c. 80% an elevated C-reactive protein. after resolution of the abscess
- decisions regarding withdrawal are then based on the
DIFFERENTIAL DIAGNOSIS EEG.

Conditions that can cause headache, fever, focal EEG is abnormal - continue anticonvulsant therapy
neurologic signs, and seizure activity include: EEG is normal - anticonvulsant therapy can be slowly
a. brain abscess withdrawn, with close follow-up and repeat EEG after the
b. subdural empyema medication has been discontinued.
c. bacterial meningitis
d. viral meningoencephalitis Glucocorticoids
e. superior sagittal sinus thrombosis - should not be given routinely to patients with
f. acute disseminated encephalomyelitis. brain abscesses.
- IV dexamethasone therapy (10 mg every 6 h) is
- When fever is absent, primary and metastatic brain usually reserved for patients with substantial periabscess
tumors become the major differential diagnosis edema and associated mass effect and increased ICP.
- Dexamethasone should be tapered as rapidly as
TREATMENT possible to avoid delaying the natural process of
encapsulation of the abscess.
Combination of high-dose parenteral antibiotics and
neurosurgical drainage Serial MRI or CT scans
- optimal therapy of brain abscesses - should be obtained on a monthly or twice-
monthly basis to document resolution of the abscess
Empirical therapy of community-acquired brain abscess in - A small amount of enhancement may remain for
an immunocompetent patient typically includes: months after the abscess has been successfully treated.
a. a third-generation cephalosporin
(e.g., cefotaxime or ceftriaxone) and
b. metronidazole
PROGNOSIS
- In patients with penetrating head trauma or
recent neurosurgical procedures treatment should - In modern series the mortality is typically <15%
include:
a. ceftazidime as the third-generation Significant sequelae includes (occur in 20% of survivors)
cephalosporin to enhance coverage of a. seizures
Pseudomonas spp. b. persisting weakness
b. vancomycin for coverage of c. aphasia, or
staphylococci. d. mental impairment.

- Meropenem plus vancomycin also provides good coverage


in this setting. NONBACTERIAL CAUSES OF INFECTIOUS FOCAL CNS
LESIONS
- Aspiration and drainage of the abscess under stereotaxic
guidance are beneficial for both diagnosis and therapy. ETIOLOGY
- Empirical antibiotic coverage should be modified based
on the results of Gram's stain and culture of the abscess Neurocysticercosis
contents -is the most common parasitic disease of the CNS
worldwide.
Complete excision of a bacterial abscess via craniotomy or - Humans acquire cysticercosis by the ingestion
craniectomy of food contaminated with the eggs of the parasite T.
solium.
- Eggs are contained in undercooked pork or in - In the presence of the characteristic neuroimaging
drinking water or other foods contaminated with human abnormalities of this parasitic infection, serum anti-T.
feces. gondii antibodies should be obtained; if positive, the
T. gondii is a parasite that is acquired from the patient should be treated.
ingestion of undercooked meat and from handling cat
feces.
TREATMENT
CLINICAL PRESENTATION
Anticonvulsant therapy
New-onset partial seizures with or without secondary - initiated when the patient with
generalization neurocysticercosis presents with a seizure.
- most common manifestation of
neurocysticercosis Albendazole and praziquantel
-used in the treatment of neurocysticercosis.
Cysticerci may develop in:
a. brain parenchyma - Approximately 85% of parenchymal cysts are destroyed
- cause seizures or focal neurologic by a single course of albendazole (15 mg/kg per day in
deficits two doses for 8 days)
b. subarachnoid or ventricular spaces, - ~75% are destroyed by a single course of praziquantel(50
- produce increased ICP by interference mg/kg per day for 15 days)
with CSF flow.
c. Spine Long-term antiepileptic therapy
- mimic the presentation of intraspinal - recommended when seizures occur after
tumors. resolution of edema and resorption or calcification of the
degenerating cyst.
- When the cysticerci first lodge in the brain, they
frequently cause little in the way of an inflammatory CNS toxoplasmosis is treated with a combination of:
response. a. sulfadiazine, 1.5 to 2.0 g orally qid, plus
b. pyrimethamine, 100 mg orally to load then
Cysticercal cyst degeneration 75 to 100 mg orally qd, plus
- elicits an inflammatory response that may c. folinic acid, 10 to 15 mg orally qd.
present clinically as a seizure.
- Eventually the cyst dies, a process that may - Folinic acid is added to the regimen to prevent
take several years, and is typically associated with megaloblastic anemia.
resolution of the inflammatory response and often - Therapy is continued until there is no evidence of active
abatement of seizures. disease on neuroimaging studies, which typically takes at
least 6 weeks, and then the dose of sulfadiazine is
Primary toxoplasma infection reduced to 2 to 4 g/d and pyrimethamine to 50 mg/d.
- often asymptomatic
- however, during this phase parasites may spread Clindamycin plus Pyrimethamine
to the CNS, where they become latent. - an alternative therapy for patients who cannot
- Reactivation of CNS infection is almost tolerate sulfadiazine, but the combination of
exclusively associated with immunocompromised hosts, pyrimethamine and sulfadiazine is more effective.
particularly those with HIV176 infection
- patients present with headache, fever, seizures,
and focal neurologic deficits.
SUBDURAL EMPYEMA
DIAGNOSIS
- collection of pus between the dura and arachnoid
- The lesions of neurocysticercosis are readily visualized membranes
by MRI or CT scans
EPIDEMIOLOGY
Parenchymal brain calcifications
- most common finding. - rare disorder that accounts for 15 to 25% of focal
suppurative CNS infections
- The scolex can often be visualized on MRI
- A very early sign of cyst death is hypointensity of the Sinusitis
vesicular fluid on T2-weighted images when compared -most common predisposing condition
with CSF. -typically involves the frontal sinuses, either
- MRI findings: of multiple lesions in the deep white alone or in combination with the ethmoid and maxillary
matter, the thalamus, and basal ganglia and at the gray- sinuses.
white junction in the cerebral hemispheres
- With contrast administration, the majority of the lesions - Sinusitis-related Subdural empyema has a striking
enhance in a ringed, nodular, or homogeneous pattern and predilection for young males
are surrounded by edema. -~3:1 male:female predominance
- 70% of cases occurring in the second and third decades - then becomes more severe and generalized.
of life.
Contralateral hemiparesis or hemiplegia
-SDE may also develop as a complication of head trauma - most common focal neurologic deficit
or neurosurgery. - can occur from the direct effects of the SDE on
-Secondary infection of a subdural effusion may also result the cortex or as a consequence of venous infarction
in empyema, although secondary infection of hematomas, - Seizures begin as partial motor seizures that then
in the absence of a prior neurosurgical procedure, is rare. become secondarily generalized

ETIOLOGY Seizures may be due:


a. direct irritative effect of the SDE on
Most common causative organisms of sinusitis-associated the underlying cortex or
SDE: b. result from cortical venous infarction
a. Aerobic and anaerobic streptococci
b. Staphylococci - In untreated SDE, the increasing mass effect and
c. Enterobacteriaceae, and increase in ICP cause progressive deterioration in
d. anaerobic bacteria consciousness, leading ultimately to coma.

Staphylococci and gram-negative bacilli DIAGNOSIS


-often the etiologic organisms when SDE follows
neurosurgical procedures or head trauma. -MRI is superior to CT186 in identifying SDE1 and any
associated intracranial infections
-Administration of gadolinium
PATHOPHYSIOLOGY greatly improves diagnosis by enhancing the rim
of the empyema and allowing the empyema to be clearly
-Sinusitis-associated SDE182 develops as a result of either: delineated from the underlying brain parenchyma
(1) retrograde spread of infection from septic
thrombophlebitis of the mucosal veins draining the sinuses Cranial MRI also extremely valuable in:
(2) contiguous spread of infection to the brain a. identifying sinusitis
from osteomyelitis in the posterior wall of the frontal or b. other focal CNS infections
other sinuses. c. cortical venous infarction
d. cerebral edema, and
-may also develop from direct introduction of bacteria e. cerebritis.
into the subdural space as a complication of a
neurosurgical procedure. - CT may show a crescent-shaped hypodense lesion over
-evolution of SDE can be extremely rapid because the one or both hemispheres or in the interhemispheric
subdural space is a large compartment that offers few fissure.
mechanical barriers to the spread of infection - Frequently the degree of mass effect, exemplified by
- suppuration typically begins in the upper and anterior midline shift, ventricular compression, and sulcal
portions of one cerebral hemisphere and then extends effacement, is far out of proportion to the mass of the
posteriorly. SDE.

SDE is often associated with other intracranial infections CSF examination


including -avoided in patients with known or suspected
a. epidural empyema (40%) SDE188 as it adds no useful information and is associated
b. cortical thrombophlebitis (35%), and with the risk of cerebral herniation.
c. intracranial abscess or cerebritis (>25%).
DIFFERENTIAL DIAGNOSIS
- Cortical venous infarction produces necrosis of
underlying cerebral cortex and subcortical white matter, The differential diagnosis of the combination of headache,
with focal neurologic deficits and seizures (see below). fever, focal neurologic signs, and seizure activity that
progresses rapidly to an altered level of consciousness
CLINICAL PRESENTATION includes:
a. subdural hematoma
-SDE typically presents with fever and a progressively b. bacterial meningitis
worsening headache. c. viral encephalitis
-diagnosis of SDE should always be suspected in a patient d. brain abscess
with known sinusitis who presents with new CNS1 signs or e. superior sagittal sinus thrombosis, and
symptoms f. acute disseminated encephalomyelitis.

Headache presence of nuchal rigidity


- is the most common complaint at the time of - unusual with brain abscess or epidural
presentation empyema
- initially it is localized to the side of the
subdural infection
-should suggest the possibility of SDE when - rarely result from hematogenous spread of infection
associated with significant focal neurologic signs and from extracranial primary sites.
fever.
The bacteriology of a cranial epidural abscess is similar to
that of SDE
TREATMENT
- etiologic organisms of an epidural abscess that arises
-SDE is a medical emergency. from frontal sinusitis, middle ear infections, or mastoiditis
are usually streptococci or anaerobic organisms.
Burr-hole drainage or craniotomy - Staphylococci or gram-negative organisms are the usual
- definitive step in the management of this cause of an epidural abscess that develops as a
infection. complication of craniotomy or compound skull fracture.

Empirical antimicrobial therapy should include a CLINICAL PRESENTATION


combination of:
a. a third-generation cephalosporin Patients present with:
(e.g., cefotaxime or ceftriaxone) a. fever (60%)
b. vancomycin, and b. headache (40%)
c. metronidazole c. nuchal rigidity (35%)
d. seizures (10%), and
- Parenteral antibiotic therapy should be continued for a e. focal deficits (5%)
minimum of 4 weeks.
-Specific diagnosis of the etiologic organisms is made f. Periorbital edema and Potts puffy
based on Gram's stain and culture of fluid obtained via tumor(~40%) reflecting underlying associated
either burr holes or craniotomy frontal bone osteomyelitis.

- In patients with a recent neurosurgical procedure,


PROGNOSIS wound infection is invariably present, but other symptoms
may be subtle and can include:
Prognosis is influenced by: a. altered mental status (45%)
a. level of consciousness of the patient b. fever (35%), and
at the time of hospital presentation c. headache (20%)
b. size of the empyema, and
c. speed with which therapy is - the diagnosis should also be considered when fever and
instituted. headache follow recent head trauma or occur in the
setting of frontal sinusitis, mastoiditis, or otitis media.
- Long-term neurologic sequelae, which include seizures
and hemiparesis, occur in up to 50% of cases. DIAGNOSIS

- Cranial MRI is the procedure of choice to demonstrate a


cranial epidural abscess
EPIDURAL ABSCESS T2-weighted images - appears as a lentiform or
crescent-shaped fluid collection that is hyperintense
- suppurative infection occurring in the potential space compared to CSF
between the inner skull table and dura T1-weighted images - the fluid collection has a
signal intensity that is intermediate between that of brain
tissue and CSF.
ETIOLOGY AND PATHOPHYSIOLOGY Gadolinium - a significant enhancement of the
dura is seen on T1-weighted images. In distinction to
- less common than either brain abscess or SDE subdural empyema, signs of mass effect or other
-accounts for <2% of focal suppurative CNS infections parenchymal abnormalities are uncommon.

Develops as: - CT appearance of an epidural empyema is that of a lens


a. a complication of a craniotomy or crescent-shaped hypodense extraaxial lesion
b. compound skull fracture or
c. as a result of spread of infection from the
frontal sinuses, middle ear, mastoid, or TREATMENT
orbit.
- Immediate neurosurgical drainage is indicated.
- Infection in the frontal sinus, middle ear, mastoid, or
orbit can reach the epidural space through retrograde - Empirical antimicrobial therapy, pending the results of
spread of infection from septic thrombophlebitis in the Gram's stain and culture of the purulent material obtained
emissary veins that drain these areas or by way of direct at surgery, should include a combination of:
spread of infection through areas of osteomyelitis. a. a third-generation cephalosporin
b. nafcillin or vancomycin
c. metronidazole
-Thrombosis of the superior sagittal sinus is often
- Ceftazidime should be substituted for ceftriaxone or associated with thrombosis of superior cortical veins and
cefotaxime in neurosurgical patients. small parenchymal hemorrhages.

- Meropenem and vancomycin also provide effective Transverse sinuses


empirical therapy in postneurosurgical cases. - drainage of the Superior Sagittal Sinus
- also receive venous drainage from small veins
-Antibiotics should be continued for at least 3 weeks after from both the middle ear and mastoid cells.
surgical drainage. - becomes the sigmoid sinus before draining into
the internal jugular vein.
Septic transverse/sigmoid sinus thrombosis
- can be a complication of acute and chronic
PROGNOSIS otitis media or mastoiditis
- Infection spreads from the mastoid air cells to
-Mortality is <5% in modern series the transverse sinus via the emissary veins or by direct
-full recovery is the rule in most survivors. invasion.

Cavernous sinuses
- inferior to the superior sagittal sinus at the
Suppurative Thrombophlebitis base of the skull
 Septic venous thrombosis of cortical veins and - receive blood from the facial veins via the
sinuses. superior and inferior ophthalmic veins.
 May occur as a complication of: - Bacteria in the facial veins enter the cavernous
a. bacterial meningitis sinus via these veins.
b. SDE - Bacteria in the sphenoid and ethmoid sinuses
c. epidural abscess; or can spread to the cavernous sinuses via the small emissary
d. infection in the skin of the face, paranasal veins.
sinuses, middle ear, or mastoid.
Sphenoid and ethmoid sinuses
A. Anatomy & Pathophysiology -most common sites of primary infection
 Cerebral veins and venous sinuses have no valves; resulting in septic cavernous sinus thrombosis.
therefore, blood within them can flow in either
CLINICAL MANIFESTATIONS
direction.
Septic thrombosis of the superior sagittal sinus presents
Superior sagittal sinus
with:
- largest of the venous sinuses
a. headache
- receives blood from the frontal, parietal, and
b. fever
occipital superior cerebral veins and the diploic veins,
c. nausea and vomiting
which communicate with the meningeal veins.
d. confusion, and
e. focal or generalized seizures.
Bacterial meningitis
- a common predisposing condition for septic
- There may be a rapid development of stupor and coma.
thrombosis of the superior sagittal sinus
- Weakness of the lower extremities with bilateral
Diploic veins
Babinski signs or hemiparesis is often present.
- drain into the superior sagittal sinus
- provide a route for the spread of infection from
- When superior sagittal sinus thrombosis occurs as a
the meninges, especially in cases where there is purulent
complication of bacterial meningitis, nuchal rigidity and
exudate near areas of the superior sagittal sinus.
Kernig's and Brudzinski's signs may be present.
- Infection can also spread to the superior sagittal sinus
Structures that pass throuth the cavernous sinus:
from nearby SDE195 or epidural abscess.
a. oculomotor nerve
b. trochlear nerve
Contributory to cerebral venous sinus thrombosis
c. abducens nerve
a. Dehydration from vomiting
b. hypercoagulable states, and d. ophthalmic and maxillary branches of the
c. immunologic abnormalities, including the trigeminal nerve, and
presence of circulating antiphospholipid e. internal carotid artery
antibodies
The symptoms of septic cavernous sinus thrombosis are:
- Thrombosis may extend from one sinus to another, and a. fever
often at autopsy thrombi of different histologic ages can b. headache
be detected in several sinuses. c. frontal and retroorbital pain, and
d. diplopia. T
The classic signs (due to deficits of CN III, IV, and VI) the efficacy of these therapies in septic venous sinus
a. ptosis thrombosis is unknown.
b. proptosis
c. chemosis, and
d. extraocular dysmotility

- hyperesthesia of the ophthalmic and maxillary divisions


of the fifth cranial nerve and a decreased corneal reflex
may be detected.
- There may be evidence of dilated, tortuous retinal veins
and papilledema.

Headache and earache


-most frequent symptoms of transverse sinus
thrombosis.
- may also present with otitis media, sixth nerve
palsy, and retroorbital or facial pain (Gradinego's
syndrome).

- Sigmoid sinus and internal jugular vein thrombosis may


present with neck pain.

DIAGNOSIS

- suggested by an absent flow void within the affected


venous sinus on MRI

Magnetic resonance venography or Venous phase of


cerebral angiography
- for diagnostic confirmatioin

Intracerebral hemorrhage
-suggests the diagnosis of thrombophlebitis of
intracerebral and meningeal veins
-requires cerebral angiography for definitive
diagnosis.

TREATMENT

- usually treated with antibiotics and hydration.

- choice of antimicrobial therapy is based on the bacteria


responsible for the predisposing or associated condition.

- Optimal duration of therapy is unknown, but antibiotics


are usually continued for 6 weeks or until there is
radiographic evidence of resolution of thrombosis.

Anticoagulation with dose-adjusted heparin


- reported to be beneficial in patients with
aseptic venous sinus thrombosis
- also used in the treatment of septic venous
sinus thrombosis complicating bacterial meningitis in
patients who are worsening despite antimicrobial therapy
and intravenous fluids.

- presence of a small intracerebral hemorrhage from


septic thrombophlebitis is not an absolute
contraindication to heparin therapy.

-Successful management of aseptic venous sinus


thrombosis has been reported with urokinase therapy and
with a combination of intrathrombus recombinant tissue
plasminogen activator (rtPA) and intravenous heparin, but