Chronic Encephalitis Subacute Sclerosing Panencephalitis Rare progressive demyelinating disease of the CNS Progressive Multifocal Leukoencephalopathy assoc with a chronic infection of brain tissue with A. Clinical Features & Pathology measles virus Progressive disorder characterized pathologically by: Hx of primary measles infection at an early age (2 multifocal areas of demyelination of varying size y/o) distributed throughout the CNS followed after a latent interval of 6 to 8 years by the cytologic alterations in both astrocytes & development of insidious intellectual decline and oligodendrocytes mood and personality changes Astrocytes: Typical signs of a CNS viral infection, including fever Enlarged & headache, do not occur Hyperchromatic, deformed Bizarre nuclei As the disease progresses, there is the occurrence of: Frequent mitotic figures Focal and/or generalized seizures Oligodendrocytes: Myoclonus Enlarged Ataxia Densely staining nuclei that contain viral Visual disturbances inclusions formed the crystalline arrays of JC virus particles EEG: characteristic periodic pattern with bursts every Clinical features: 3-8s of high-voltage, sharp slow waves, followed by Visual defects (45%) periods of attenuated ("flat") background Homonymous hemianopia CSF: acellular with a normal or mildly elevated Mental impairment—dementia, confusion, protein level & a markedly elevated ?-globulin level personality changes (38%) (>20% of total CSF protein) Motor weakness—not present early in the disease CSF anti-measles antibody levels: invariably but eventually occurs in 75% of cases elevated; oligoclonal anti-measles antibodies are Almost all pxs have an underlying immunosuppressive often present disorder CT and MRI show evidence of multifocal white matter lesions & generalized atrophy. B. Diagnostic Studies Measles virus can be cultured from brain tissue MRI reveals multifocal asymmetric, coalescing white Viral genome can be detected by in situ hybridization matter lesions located: or PCR amplification Periventricularly In the centrum semiovale Treatment In the parietal-occipital region Isoprinosine (Inosiplex) (100 mg/kg per day): alone In the cerebellum or in combination with intrathecal or intraventricular These lesions have: interferon ↑ T2 & ↓ T1 signal generally nonenhancing or show only minimal Progressive Rubella Panencephalitis peripheral enhancement Extremely rare disorder not assoc with edema or mass effect Primarily affects males with congenital rubella MRI for the diagnosis of PML: show hypodense syndrome nonenhancing white matter lesions After a latent period of 8-19 years, pxs develop CSF findings: progressive neurologic deterioration Typically normal Manifestations: similar to SSPE Although, mild elevation in CHON &/or IgG CSF shows: Pleocytosis (25%)—predominantly mononuclear & a. mild lymphocytic pleocytosis rarely >25cells/uL b. slightly elevated protein level PCR amplification of JC virus from CSF: an impt c. markedly increased ?-globulin diagnostic tool d. rubella virus-specific oligoclonal bands. high specificity, but sensitivity has varied among No therapy is available studies Diagnostic of PML: (+) CSF PCR for JC virus DNA in association with typical MRI lesions in the appropriate clinical setting Pxs 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 No effective therapy is available. Brain Abscess Most common pathogens in brain abscesses Focal, suppurative infection within the brain associated with paranasal sinusitis: parenchyma streptococci (especially S. milleri) Surrounded by a vascularized capsule Haemophilus spp. Bacteroides spp. Cerebritis Pseudomonas spp., and Often employed to describe a nonencapsulated brain S. aureus. abscess - Dental infections are associated with ~2% of brain A. Epidemiology abscesses, although it is often suggested that many A bacterial brain abscess is a relatively uncommon "cryptogenic" abscesses are in fact due to dental intracranial infection infections. Incidence: ~1 in 100,000 persons/yr The most common pathogens in this setting are Predisposing conditions: a. streptococci otitis media & mastoiditis b. staphylococci paranasal sinusitis c. Bacteroides and pyogenic infections in the chest or other body d. Fusobacterium spp. sites penetrating head trauma or neurosurgical - Hematogenous abscesses account for ~25% of brain procedures abscesses. dental infections - show a predilection for the territory of the middle Modern causes: cerebral artery (i.e., posterior frontal or parietal lobes). Toxoplasma gondii - often located at the junction of the gray and white Aspergillus spp. matter Nocardia spp. - often poorly encapsulated. Mycobacteria spp. - often multiple C. neoformans - microbiology of these hematogenous abscesses is The said organisms are almost exclusively dependent on the primary source of infection restricted to immunocompromised hosts: Examples: a. HIV infection 1. brain abscesses that develop as a complication b. organ transplantation of infective endocarditis are often due to viridans c. cancer streptococci or S. aureus. d. immunosuppressive therapy 2. Abscesses associated with pyogenic lung infections such as lung abscess or bronchiectasis are often B. Etiology due to Streptococci, staphylococci, or Bacteroides or A brain abscess may develop: Fusobacterium spp. 3. Enterobacteriaceae and P. aeruginosa are by direct spread from a contiguous cranial site important causes of abscesses associated with urinary of infection, such as paranasal sinusitis, otitis sepsis. media, mastoiditis, or dental infection; 4. Abscesses that follow penetrating head trauma following head trauma or a neurosurgical or neurosurgical procedures are frequently due to procedure; or staphylococci, Enterobacteriaceae, and Pseudomonas as a result of hematogenous spread from a species. remote site of infection 25% of cases: no obvious primary source of - Congenital cardiac malformations that produce a right- infection to-left shunt (congenital cyanotic heart disease), such as 1/3 of brain abscesses: assoc with otitis media & tetralogy of Fallot, patent ductus arteriosus, and atrial mastoiditis, often with an cholesteatoma and ventricular septal defects, allow bloodborne bacteria Otogenic abscesses occur predominantly in the: to bypass the pulmonary capillary bed and reach the temporal lobe (55 to 75%) brain. cerebellum (20 to 30%) - Similar phenomena can occur with pulmonary Common organisms: arteriovenous malformations. The decreased arterial Streptococci oxygenation and saturation from the right-to-left shunt Bacteroides spp. and polycythemia may cause focal areas of cerebral P. aeruginosa ischemia, thus providing a nidus for microorganisms that Enterobacteriaceae bypassed the pulmonary circulation to multiply and form Abscesses that develop as a result of direct spread an abscess. of infection from: - Streptococci are the most common pathogens in this Frontal setting. Ethmoidal Sphenoidal sinuses PATHOGENESIS AND HISTOPATHOLOGY Those that occur due to dental infections: usually located in the frontal lobes -intact brain parenchyma is relatively resistant to ~10% of brain abscesses: assoc with paranasal infection sinusitis Prerequisite for effective bacterial invasion - and its absence should not exclude the a. preexisting brain ischemia diagnosis. b. necrosis, or c. hypoxia Focal neurologic deficits -new onset of focal or generalized seizure - Once infection is established, brain abscess frequently activity is a presenting sign in 15 to 35% of patients. evolves through a series of stages, influenced by: - includes hemiparesis, aphasia, or visual field a. the nature of the infecting organism and defects b. by the immunocompetence of the host - part of the initial presentation in >60% of patients. Early cerebritis stage (days 1 to 3) - characterized by a perivascular infiltration of The clinical presentation of a brain abscess depends on: inflammatory cells, which surround a central core of a. location coagulative necrosis. b. the nature of the primary infection if - Marked edema surrounds the lesion present, and c. the level of the ICP Late cerebritis stage (days 4 to 9) - pus formation leads to enlargement of the Hemiparesis necrotic center, which is surrounded at its border by an - most common localizing sign of a frontal lobe inflammatory infiltrate of macrophages and fibroblasts. abscess. - A thin capsule of fibroblasts and reticular fibers gradually develops, and the surrounding area of cerebral A temporal lobe abscess may present with: edema becomes more distinct than in the previous stage. a. disturbance of language (dysphasia) or b. upper homonymous quadrantanopia. Early capsule formation (days 10 to 13) - characterized by the formation of a capsule - Nystagmus and ataxia are signs of a cerebellar abscess. that is better developed on the cortical than on the ventricular side of the lesion. - Signs of raised ICP — papilledema, nausea and vomiting, -This stage correlates with the appearance of a and drowsiness or confusion — can be the dominant ring-enhancing capsule on neuroimaging studies. presentation of some abscesses, particularly those in the cerebellum Late capsule formation (day 14 and beyond) - defined by a well-formed necrotic center Meningismus surrounded by a dense collagenous capsule. -not present unless the abscess has ruptured into - surrounding area of cerebral edema has the ventricle or the infection has spread to the regressed, but marked gliosis with large numbers of subarachnoid space. reactive astrocytes has developed outside the capsule. - gliotic process may contribute to the DIAGNOSIS development of seizures as a sequelae of brain abscess. - made by neuroimaging studies CLINICAL PRESENTATION MRI - typically presents as an expanding intracranial mass - better than CT for demonstrating abscesses in lesion, rather than as an infectious process. the early (cerebritis) stages - evolution of signs and symptoms is extremely variable, - superior to CT for identifying abscesses in the ranging from hours to weeks or even months posterior fossa - most patients present to the hospital 11 to 12 days - A mature brain abscess appears on CT as a focal following onset of symptoms. area of hypodensity surrounded by ring enhancement. - CT and MRI appearance, particularly of the The classic clinical triad (present in <50% of cases) capsule, may be altered by treatment with glucocorticoids a. headache b. fever, and Microbiologic diagnosis of the etiologic agent c. a focal neurologic deficit - is most accurately determined by Gram's stain and culture of abscess material obtained by stereotactic Headache needle aspiration -most common symptom in patients with a brain - Up to 10% of patients will also have positive abscess (>75% of patients) blood cultures. -often characterized as a constant, dull, aching sensation, either hemicranial or generalized - LP168 should not be performed in patients with known -becomes progressively more severe and or suspected focal intracranial infections such as abscess refractory to therapy. or empyema - CSF analysis contributes nothing to diagnosis or therapy Fever - is present in only 50% of patients at the time of Laboratory studies diagnosis - may provide clues to the diagnosis of brain abscess in patients with a CNS mass lesion. a. 50% of patients have a peripheral leukocytosis - Anticonvulsant therapy is continued for at least 3 b. 60% an elevated ESR months after resolution of the abscess c. 80% an elevated C-reactive protein. - decisions regarding withdrawal are then based on the EEG. DIFFERENTIAL DIAGNOSIS EEG is abnormal - continue anticonvulsant therapy Conditions that can cause headache, fever, focal EEG is normal - anticonvulsant therapy can be slowly neurologic signs, and seizure activity include: withdrawn, with close follow-up and repeat EEG after the a. brain abscess medication has been discontinued. b. subdural empyema c. bacterial meningitis Glucocorticoids d. viral meningoencephalitis - should not be given routinely to patients with e. superior sagittal sinus thrombosis brain abscesses. f. acute disseminated encephalomyelitis. - IV dexamethasone therapy (10 mg every 6 h) is usually reserved for patients with substantial periabscess - When fever is absent, primary and metastatic brain edema and associated mass effect and increased ICP. tumors become the major differential diagnosis - Dexamethasone should be tapered as rapidly as possible to avoid delaying the natural process of TREATMENT encapsulation of the abscess. Combination of high-dose parenteral antibiotics and Serial MRI or CT scans neurosurgical drainage - should be obtained on a monthly or twice- - optimal therapy of brain abscesses monthly basis to document resolution of the abscess - A small amount of enhancement may remain for Empirical therapy of community-acquired brain abscess in months after the abscess has been successfully treated. an immunocompetent patient typically includes: a. a third-generation cephalosporin (e.g., cefotaxime or ceftriaxone) and b. metronidazole PROGNOSIS - In patients with penetrating head trauma or - In modern series the mortality is typically <15% recent neurosurgical procedures treatment should include: Significant sequelae includes (occur in 20% of survivors) a. ceftazidime as the third-generation a. seizures cephalosporin to enhance coverage of b. persisting weakness Pseudomonas spp. c. aphasia, or b. vancomycin for coverage of d. mental impairment. staphylococci. - Meropenem plus vancomycin also provides good NONBACTERIAL CAUSES OF INFECTIOUS FOCAL CNS coverage in this setting. LESIONS - Aspiration and drainage of the abscess under stereotaxic ETIOLOGY guidance are beneficial for both diagnosis and therapy. - Empirical antibiotic coverage should be modified based Neurocysticercosis on the results of Gram's stain and culture of the abscess -is the most common parasitic disease of the CNS contents worldwide. - Humans acquire cysticercosis by the ingestion Complete excision of a bacterial abscess via craniotomy or of food contaminated with the eggs of the parasite T. craniectomy solium. - generally reserved for multiloculated abscesses - Eggs are contained in undercooked pork or in or those in which stereotactic aspiration is unsuccessful. drinking water or other foods contaminated with human feces. - Medical therapy alone is not optimal for treatment of T. gondii is a parasite that is acquired from the brain abscess and should be reserved for patients whose ingestion of undercooked meat and from handling cat abscesses are: feces. a. neurosurgically inaccessible b. for patients with small nonencapsulated CLINICAL PRESENTATION abscesses (cerebritis), and c. patients whose condition is too tenuous to New-onset partial seizures with or without secondary allow performance of a neurosurgical procedure generalization - most common manifestation of - All patients should receive a minimum of 6 to 8 weeks of neurocysticercosis parenteral antibiotic therapy. - Patients should also receive prophylactic anticonvulsant Cysticerci may develop in: therapy because of the high risk of seizures. a. brain parenchyma - cause seizures or focal neurologic - Approximately 85% of parenchymal cysts are destroyed deficits by a single course of albendazole (15 mg/kg per day in b. subarachnoid or ventricular spaces, two doses for 8 days) - produce increased ICP by interference - ~75% are destroyed by a single course of praziquantel(50 with CSF flow. mg/kg per day for 15 days) c. Spine - mimic the presentation of intraspinal Long-term antiepileptic therapy tumors. - recommended when seizures occur after resolution of edema and resorption or calcification of the - When the cysticerci first lodge in the brain, they degenerating cyst. frequently cause little in the way of an inflammatory response. CNS toxoplasmosis is treated with a combination of: a. sulfadiazine, 1.5 to 2.0 g orally qid, plus Cysticercal cyst degeneration b. pyrimethamine, 100 mg orally to load then - elicits an inflammatory response that may 75 to 100 mg orally qd, plus present clinically as a seizure. c. folinic acid, 10 to 15 mg orally qd. - Eventually the cyst dies, a process that may take several years, and is typically associated with - Folinic acid is added to the regimen to prevent resolution of the inflammatory response and often megaloblastic anemia. abatement of seizures. - Therapy is continued until there is no evidence of active disease on neuroimaging studies, which typically takes at Primary toxoplasma infection least 6 weeks, and then the dose of sulfadiazine is - often asymptomatic reduced to 2 to 4 g/d and pyrimethamine to 50 mg/d. - however, during this phase parasites may spread to the CNS, where they become latent. Clindamycin plus Pyrimethamine - Reactivation of CNS infection is almost - an alternative therapy for patients who cannot exclusively associated with immunocompromised hosts, tolerate sulfadiazine, but the combination of particularly those with HIV176 infection pyrimethamine and sulfadiazine is more effective. - patients present with headache, fever, seizures, and focal neurologic deficits. DIAGNOSIS SUBDURAL EMPYEMA - The lesions of neurocysticercosis are readily visualized - collection of pus between the dura and arachnoid by MRI or CT scans membranes Parenchymal brain calcifications EPIDEMIOLOGY - most common finding. - rare disorder that accounts for 15 to 25% of focal - The scolex can often be visualized on MRI suppurative CNS infections - A very early sign of cyst death is hypointensity of the vesicular fluid on T2-weighted images when compared Sinusitis with CSF. -most common predisposing condition - MRI findings: of multiple lesions in the deep white -typically involves the frontal sinuses, either matter, the thalamus, and basal ganglia and at the gray- alone or in combination with the ethmoid and maxillary white junction in the cerebral hemispheres sinuses. - With contrast administration, the majority of the lesions enhance in a ringed, nodular, or homogeneous pattern - Sinusitis-related Subdural empyema has a striking and are surrounded by edema. predilection for young males - In the presence of the characteristic neuroimaging -~3:1 male:female predominance abnormalities of this parasitic infection, serum anti-T. - 70% of cases occurring in the second and third decades gondii antibodies should be obtained; if positive, the of life. patient should be treated. -SDE may also develop as a complication of head trauma or neurosurgery. TREATMENT -Secondary infection of a subdural effusion may also result in empyema, although secondary infection of hematomas, Anticonvulsant therapy in the absence of a prior neurosurgical procedure, is rare. - initiated when the patient with neurocysticercosis presents with a seizure. ETIOLOGY Albendazole and praziquantel Most common causative organisms of sinusitis-associated -used in the treatment of neurocysticercosis. SDE: a. Aerobic and anaerobic streptococci b. Staphylococci c. Enterobacteriaceae, and d. anaerobic bacteria DIAGNOSIS Staphylococci and gram-negative bacilli -often the etiologic organisms when SDE follows -MRI is superior to CT186 in identifying SDE1 and any neurosurgical procedures or head trauma. associated intracranial infections -Administration of gadolinium greatly improves diagnosis by enhancing the rim PATHOPHYSIOLOGY of the empyema and allowing the empyema to be clearly delineated from the underlying brain parenchyma -Sinusitis-associated SDE182 develops as a result of either: (1) retrograde spread of infection from septic Cranial MRI also extremely valuable in: thrombophlebitis of the mucosal veins draining the sinuses a. identifying sinusitis (2) contiguous spread of infection to the brain b. other focal CNS infections from osteomyelitis in the posterior wall of the frontal or c. cortical venous infarction other sinuses. d. cerebral edema, and e. cerebritis. -may also develop from direct introduction of bacteria into the subdural space as a complication of a - CT may show a crescent-shaped hypodense lesion over neurosurgical procedure. one or both hemispheres or in the interhemispheric -evolution of SDE can be extremely rapid because the fissure. subdural space is a large compartment that offers few - Frequently the degree of mass effect, exemplified by mechanical barriers to the spread of infection midline shift, ventricular compression, and sulcal - suppuration typically begins in the upper and anterior effacement, is far out of proportion to the mass of the portions of one cerebral hemisphere and then extends SDE. posteriorly. CSF examination SDE is often associated with other intracranial infections -avoided in patients with known or suspected including SDE188 as it adds no useful information and is associated a. epidural empyema (40%) with the risk of cerebral herniation. b. cortical thrombophlebitis (35%), and c. intracranial abscess or cerebritis (>25%). DIFFERENTIAL DIAGNOSIS - Cortical venous infarction produces necrosis of The differential diagnosis of the combination of underlying cerebral cortex and subcortical white matter, headache, fever, focal neurologic signs, and seizure with focal neurologic deficits and seizures (see below). activity that progresses rapidly to an altered level of consciousness includes: CLINICAL PRESENTATION a. subdural hematoma b. bacterial meningitis -SDE typically presents with fever and a progressively c. viral encephalitis worsening headache. d. brain abscess -diagnosis of SDE should always be suspected in a patient e. superior sagittal sinus thrombosis, and with known sinusitis who presents with new CNS1 signs or f. acute disseminated encephalomyelitis. symptoms presence of nuchal rigidity Headache - unusual with brain abscess or epidural - is the most common complaint at the time of empyema presentation -should suggest the possibility of SDE when - initially it is localized to the side of the associated with significant focal neurologic signs and subdural infection fever. - then becomes more severe and generalized. Contralateral hemiparesis or hemiplegia TREATMENT - most common focal neurologic deficit - can occur from the direct effects of the SDE on -SDE is a medical emergency. the cortex or as a consequence of venous infarction - Seizures begin as partial motor seizures that then Burr-hole drainage or craniotomy become secondarily generalized - definitive step in the management of this infection. Seizures may be due: a. direct irritative effect of the SDE on Empirical antimicrobial therapy should include a the underlying cortex or combination of: b. result from cortical venous infarction a. a third-generation cephalosporin (e.g., cefotaxime or ceftriaxone) - In untreated SDE, the increasing mass effect and b. vancomycin, and increase in ICP cause progressive deterioration in c. metronidazole consciousness, leading ultimately to coma. - Parenteral antibiotic therapy should be continued for a f. Periorbital edema and Potts puffy minimum of 4 weeks. tumor(~40%) reflecting underlying associated -Specific diagnosis of the etiologic organisms is made frontal bone osteomyelitis. based on Gram's stain and culture of fluid obtained via either burr holes or craniotomy - In patients with a recent neurosurgical procedure, wound infection is invariably present, but other symptoms may be subtle and can include: PROGNOSIS a. altered mental status (45%) b. fever (35%), and Prognosis is influenced by: c. headache (20%) a. level of consciousness of the patient at the time of hospital presentation - the diagnosis should also be considered when fever and b. size of the empyema, and headache follow recent head trauma or occur in the c. speed with which therapy is setting of frontal sinusitis, mastoiditis, or otitis media. instituted. DIAGNOSIS - Long-term neurologic sequelae, which include seizures and hemiparesis, occur in up to 50% of cases. - Cranial MRI is the procedure of choice to demonstrate a cranial epidural abscess T2-weighted images - appears as a lentiform or crescent-shaped fluid collection that is hyperintense EPIDURAL ABSCESS compared to CSF T1-weighted images - the fluid collection has a - suppurative infection occurring in the potential space signal intensity that is intermediate between that of brain between the inner skull table and dura tissue and CSF. Gadolinium - a significant enhancement of the dura is seen on T1-weighted images. In distinction to ETIOLOGY AND PATHOPHYSIOLOGY subdural empyema, signs of mass effect or other parenchymal abnormalities are uncommon. - less common than either brain abscess or SDE -accounts for <2% of focal suppurative CNS infections - CT appearance of an epidural empyema is that of a lens or crescent-shaped hypodense extraaxial lesion Develops as: a. a complication of a craniotomy b. compound skull fracture or TREATMENT c. as a result of spread of infection from the frontal sinuses, middle ear, mastoid, or - Immediate neurosurgical drainage is indicated. orbit. - Empirical antimicrobial therapy, pending the results of - Infection in the frontal sinus, middle ear, mastoid, or Gram's stain and culture of the purulent material obtained orbit can reach the epidural space through retrograde at surgery, should include a combination of: spread of infection from septic thrombophlebitis in the a. a third-generation cephalosporin emissary veins that drain these areas or by way of direct b. nafcillin or vancomycin spread of infection through areas of osteomyelitis. c. metronidazole - rarely result from hematogenous spread of infection - Ceftazidime should be substituted for ceftriaxone or from extracranial primary sites. cefotaxime in neurosurgical patients. The bacteriology of a cranial epidural abscess is similar to - Meropenem and vancomycin also provide effective that of SDE empirical therapy in postneurosurgical cases. - etiologic organisms of an epidural abscess that arises -Antibiotics should be continued for at least 3 weeks after from frontal sinusitis, middle ear infections, or mastoiditis surgical drainage. are usually streptococci or anaerobic organisms. - Staphylococci or gram-negative organisms are the usual cause of an epidural abscess that develops as a complication of craniotomy or compound skull fracture. PROGNOSIS CLINICAL PRESENTATION -Mortality is <5% in modern series -full recovery is the rule in most survivors. Patients present with: a. fever (60%) b. headache (40%) c. nuchal rigidity (35%) Suppurative Thrombophlebitis d. seizures (10%), and Septic venous thrombosis of cortical veins and e. focal deficits (5%) sinuses. May occur as a complication of: - Bacteria in the sphenoid and ethmoid sinuses a. bacterial meningitis can spread to the cavernous sinuses via the small emissary b. SDE veins. c. epidural abscess; or d. infection in the skin of the face, paranasal Sphenoid and ethmoid sinuses sinuses, middle ear, or mastoid. -most common sites of primary infection resulting in septic cavernous sinus thrombosis. A. Anatomy & Pathophysiology Cerebral veins and venous sinuses have no valves; CLINICAL MANIFESTATIONS therefore, blood within them can flow in either direction. Septic thrombosis of the superior sagittal sinus presents with: Superior sagittal sinus a. headache - largest of the venous sinuses b. fever - receives blood from the frontal, parietal, and c. nausea and vomiting occipital superior cerebral veins and the diploic veins, d. confusion, and which communicate with the meningeal veins. e. focal or generalized seizures. Bacterial meningitis - There may be a rapid development of stupor and coma. - a common predisposing condition for septic thrombosis of the superior sagittal sinus - Weakness of the lower extremities with bilateral Babinski signs or hemiparesis is often present. Diploic veins - drain into the superior sagittal sinus - When superior sagittal sinus thrombosis occurs as a - provide a route for the spread of infection from complication of bacterial meningitis, nuchal rigidity and the meninges, especially in cases where there is purulent Kernig's and Brudzinski's signs may be present. exudate near areas of the superior sagittal sinus. Structures that pass throuth the cavernous sinus: - Infection can also spread to the superior sagittal sinus a. oculomotor nerve from nearby SDE195 or epidural abscess. b. trochlear nerve c. abducens nerve Contributory to cerebral venous sinus thrombosis d. ophthalmic and maxillary branches of the a. Dehydration from vomiting trigeminal nerve, and b. hypercoagulable states, and e. internal carotid artery c. immunologic abnormalities, including the presence of circulating antiphospholipid The symptoms of septic cavernous sinus thrombosis are: antibodies a. fever b. headache - Thrombosis may extend from one sinus to another, and c. frontal and retroorbital pain, and often at autopsy thrombi of different histologic ages can d. diplopia. T be detected in several sinuses. The classic signs (due to deficits of CN III, IV, and VI) -Thrombosis of the superior sagittal sinus is often a. ptosis associated with thrombosis of superior cortical veins and b. proptosis small parenchymal hemorrhages. c. chemosis, and d. extraocular dysmotility Transverse sinuses - drainage of the Superior Sagittal Sinus - hyperesthesia of the ophthalmic and maxillary divisions - also receive venous drainage from small veins of the fifth cranial nerve and a decreased corneal reflex from both the middle ear and mastoid cells. may be detected. - becomes the sigmoid sinus before draining into - There may be evidence of dilated, tortuous retinal veins the internal jugular vein. and papilledema. Septic transverse/sigmoid sinus thrombosis - can be a complication of acute and chronic Headache and earache otitis media or mastoiditis -most frequent symptoms of transverse sinus - Infection spreads from the mastoid air cells to thrombosis. the transverse sinus via the emissary veins or by direct - may also present with otitis media, sixth nerve invasion. palsy, and retroorbital or facial pain (Gradinego's syndrome). Cavernous sinuses - inferior to the superior sagittal sinus at the - Sigmoid sinus and internal jugular vein thrombosis may base of the skull present with neck pain. - receive blood from the facial veins via the superior and inferior ophthalmic veins. DIAGNOSIS - Bacteria in the facial veins enter the cavernous sinus via these veins. - 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 the efficacy of these therapies in septic venous sinus thrombosis is unknown.
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