Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Aspectos neuroqx de infeccion del snc 2012


Published on

Published in: Health & Medicine
  • Be the first to comment

  • Be the first to like this

Aspectos neuroqx de infeccion del snc 2012

  1. 1. Neurosurgical Aspects ofCentral Nervous SystemInfectionsJason A. Heth, MDInfections of the central nervous system (CNS) canbe severe, life changing, and potentially fatal. Neuro-surgeonsplayacrucialroleinthetreatmentofcertainCNS infections. Imaging is important for appropriatediagnosis, lesion localization, identification of sur-gicalcandidates,andperformanceofsurgicalproce-dures. High-quality imaging is therefore crucial to theneurosurgeon. The knowledge of how neurologicimaging is used by the neurosurgeon may be helpfulto the interpreting neuroradiologist. This articlereviews the most common CNS infections neuro-surgeons encounter. Pathogenesis; microbiology;surgical indications; treatment, including surgicalprocedures; and prognosis are discussed.INTRACEREBRAL ABSCESSBrain abscess has been one of the most fearedCNS infections. This fear arose from the initialpoor outcomes and from the rapid neurologicdeterioration that can occur. Although rapid dete-rioration can still occur, the overall outcomes haveimproved because of improved antibiotics andimaging, which minimize the delay in diagnosisand treatment.The brain parenchyma is not prone to paren-chymal abscess formation, whereas other eventsand risk factors are required to set the stage forabscess formation. Inoculation can occur fromdirect implantation (such as a bullet entering thebrain or after neurosurgery) or contiguous spread(such as from adjacent sinusitis or mastoiditis).1,2Most commonly, however, infection elsewherespreads hematogenously to the CNS.3A classicexample is bacterial endocarditis with septicemboli to the brain resulting in cerebral abscessformation.4,5Other common primary sites includedental abscesses,6cutaneous abscesses, urinarytract infection, pulmonary infection, and soft tissueinfection.3Department of Neurosurgery, University of Michigan, 1500 East Medical Center Drive, Ann Arbor, MI 48103-5338,USAE-mail address: jheth@umich.eduKEYWORDS Cerebral abscess Meningitis Subdural empyema Encephalitis CNS infectionKEY POINTS Intracerebral abscesses can rapidly cause severe neurologic deficits or death and require promptevaluation, imaging, and treatment. Subdural empyema is an uncommon but potentially life-threatening infection that typically requiresprompt surgical decompression, culturing, and antibiotics. The organisms causing meningitis vary by the age of presentation and require prompt treatmentwith differing antibiotics. Herpes simplex encephalitis requires very rapid recognition, diagnosis, and antiviral treatment toprevent severe neurologic deficits or death. Spinal diskitis and spinal epidural abscess are uncommonly a threat to life but may cause para-plegia or quadriplegia without expeditious evaluation, imaging, and treatment.Neuroimag Clin N Am 22 (2012) 791–799doi:10.1016/j.nic.2012.05.0051052-5149/12/$ – see front matter Ó 2012 Elsevier Inc. All rights
  2. 2. Several conditions can predispose to cerebralabscess formation. Systemic immunosuppressionis frequently involved. Immunosuppression canoccur because of intentional immunosuppression(eg, to prevent organ transplant rejection),immune system destruction (eg, with humanimmunodeficiency virus [HIV] and AIDS), or othermedications that affect the immune system (eg,corticosteroids and chemotherapy agents). Pulmo-nary arteriovenous malformations, with or withoutOsler-Weber-Rendu syndrome,7,8and congenitalcyanotic heart malformations9,10are also thoughtto be risk factors.Abscess development occurs in a 3-stepprocess.11The early cerebritis phase is markedby an area of poorly demarcated inflammation.The late cerebritis phase is marked by the migra-tion of fibroblasts, which start depositing reticulin.In addition, necrosis begins to appear centrally.The early capsule (abscess) stage is marked bythe migration of additional fibroblasts and genera-tion of more reticulin in an attempt to wall off anincreasing amount of central necrosis. The latecapsule stage is marked by a mature collagencapsule surrounding the central necrotic zone.The microbiology typically reflects the patho-gens from the primary site that seeded the CNS.Therefore, gram-positive cocci (GPC) predomi-nate after intravascular infection. Infections begin-ning from the urinary tract are more frequentlygram-negative rods (GNR). Postsurgical andpenetrating injuries typically result in skin-relatedpathogens—mostly GPC. Abscesses resultingfrom contiguous sinus spread often may harbormore anaerobic organisms,3whereas dentalabscesses give rise to polymicrobial or anaerobiccerebral abscess pathogens.Patients present with a myriad of possible symp-toms. The most common symptoms are headache,fever, nausea and vomiting, focal neurologic defi-cits, abnormal sensorium, and decreased level ofconsciousness.Treatment of brain abscess requires accuratemicrobiological diagnosis and appropriate antibi-otic therapy. If a patient is not neurologicallydeteriorating, has no or minimal deficits; and ifa microbiological diagnosis can be obtained fromanother location, antibiotic therapy may beprescribed without a neurosurgical procedure.This strategy does require high quality diagnosticimaging to characterize the lesions initially andduring follow-up. If the lesions respond to antibi-otics by decreasing in size and ultimately resolu-tion, then no neurosurgical procedures arerequired. If the lesions grow, then biopsy anddrainage may be required. Stereotactic biopsyand needle drainage is required when abscess isstrongly suspected but no primary sites can beidentified to culture and when there is a largelesion or lesions causing mass effect and signifi-cant neurologic deficits. Craniotomy for resectionof abscess is another surgical alternative if needledrainage is not successful.The prognosis is related to the initial presentation,response to antibiotic therapy, and any systemicconditions or risk factors that may hinder innateimmunologic attempts to clear the infection. Recentmortality ranges from 5 to 50.3,12–14Patients with norisk factors and stereotactic aspiration had 5%mortality whereas those with several risk factorshad 50% mortality.12Negative prognostic factorsinclude worse functional status at presentation,immunocompromise,12and older age.3SUBDURAL EMPYEMASubdural empyema (SDE) is a very serious butuncommon CNS infection. An empyema is a local-ized purulent infection in an actual cavity ora potential space. In SDE, the empyema occursin the subdural space. Several mechanismsexplain the development of SDE. SDE can occuras a complication of meningitis,15after crani-otomy,16,17and as a result of extension of para-nasal sinus infections1,18or otitis media.Patients with SDE present with headache, signif-icant neurologic deficits, seizures, decreased levelof consciousness, and fever. Empyema cancompress the brain focally to cause focal deficits.SDE can cause significant inflammation in thesubjacent cortex to cause seizures. If the masseffect, inflammation, and edema are significantenough, midline shift, herniation, and global declinecan occur.Therangeofmicrobiologicaldiagnosesisdifferentfrom that of intracerebral abscess and meningitisbecause of the direct extension from the paranasalsinuses or mastoid. Gram-negative organisms areIntracerebral abscesses can rapidly cause severeneurologic deficits or death and require promptevaluation, imaging, and treatment.Subdural empyema is an uncommon but poten-tially life-threatening infection that typicallyrequires prompt surgical decompression,culturing, and antibiotics.Heth792
  3. 3. frequently reported to predominate.19,20In contrast,cultures from postsurgical SDE usually are domi-nated by gram-positive species.16,17,21Surgical treatment must address 3 issues. Thefirst issue is accurate microbiological diagnosis.On occasion this may be obtained from a primarysite such as the paranasal sinuses or mastoid. Ifno other active site is identified, neurosurgical inter-vention is required. The second issue is CNS masseffect. Mass effect, midline shift, and parenchymaldisplacement typically call for surgical intervention.Very significant mass effect and cerebral edemamay require craniotomy or craniectomy for decom-pression and debridement. The third and final issueis the possibility of surgical treatment for purulentloculations that may be too large for antibioticsalone to treat. In such situations, it may be possibleto culture, aspirate purulent material, and irrigatethe subdural space with antibiotic solution throughburr holes.The prognosis is guarded with SDE. Thesepatients are very ill, both systemically and neurolog-ically. They require close multidisciplinary manage-ment among the neurosurgical, infectious disease,and critical care teams. Tsai and colleagues21re-ported 11 of 15 patients having good outcomes(normal to moderate disability) and 4 of 15 patientshaving poor outcomes (severe disability to death).Hlavin and colleagues19reported a mortality rate of18.5% and an additional 18.5% survived withneuro-logic morbidity. They also found advanced age andmore significant encephalopathy at presentation toportend a worse prognosis as well.MENINGITISMeningitis is one of the most common CNS infec-tions, with an incidence of 3.67 to 12.5/100,000patients.22,23Meningitis is an infection of the cere-brospinal fluid (CSF) and the meningeal layersurrounding the brain. The infection can involvethe cerebral ventricles to cause ventriculitis.Meningitis is most frequently treated by neurol-ogists, pediatricians, and infectious diseasespecialists. However, it is crucial for all physiciansto understand and recognize meningitis becausemeningitis is generally very treatable whenpromptly diagnosed and treated, whereas menin-gitis can be devastating if diagnosis and treatmentare delayed.Meningitis presents most commonly with head-ache, fever, and nuchal rigidity. Other symptomsinclude seizures and cranial nerve deficits. Lossof consciousness can occur from seizures, inflam-mation and cerebral edema, or hydrocephalus.Herniation can occur and cause coma and death.The pathogenesis and range of responsiblemicrobes differ with age groups. Neonatal menin-gitis occurs due to exposure to pathogens duringdelivery, particularly with vaginal delivery.24Patho-gensinclude Escherichiacoli,groupBstreptococci,and Listeria. Children aged 3 months to 5 years arepredominantly affected by Streptococcus pneumo-niae and Neisseria meningitidis (meningococcus).Pneumococcus is a colonizer of the nasopharynxthat is transmitted via respiratory droplets andsecretions. From the nasopharynx, it can spreadto cause meningitis. A 7-valent pneumococcalvaccine was licensed for use in the United Stateswhich resulted in a decrease in childhood pneumo-coccal meningitis incidence and mortality.15Menin-gococci are gram-negative commensal bacteriathat colonize the nasopharynx. Transmission alsooccurs through respiratory droplets and secretions.Once colonization has occurred, meningococcican then progress to meningitis, which has a veryfulminant and rapid course. This fact makes vacci-nation strategies much more attractive to preventmeningococcal meningitis.25A quadrivalent menin-gococcal vaccine was licensed for use in 2005, andmonitoring is ongoing to assess the decrease inmeningococcal meningitis incidence. Haemophilusinfluenzae type b previously was an importantspecies in this age group; however, routine child-hood immunization (Hib) begun in the early 1990’shas reduced the incidence of H influenzae menin-gitis nearly to 0. Patients aged 5 years–50 yearscontinue to experience meningitis caused predom-inantly by S pneumoniae and meningococci.24Spread is facilitated among people living in closequarters, such as dormitories. Patients older than50 years experience S pneumoniae and meningo-coccal infections; however, Listeria and gram-negative entericorganisms can also be causative.24The treatment of meningitis requires promptdiagnosis and antibiotic administration. If there isany suspicion about the possible presence ofmeningitis, especially if a patient is experiencingsignificant symptoms, a first dose of broad-spectrum antibiotics should be given. The mainstayof diagnosis is the lumbar puncture (LP). Gram’sstain and cell count with differential, total protein,and glucose are recommended. Again, antibioticadministration is begun without waiting for theseresults if concern of meningitis is present.Neurosurgical intervention is required if hydro-cephalus is present. In the setting of meningitis,The organisms causing meningitis vary by theage of presentation and require prompt treat-ment with differing antibiotics.Central Nervous System Infections 793
  4. 4. a ventriculostomy would be placed for ventriculardrainage while the infection is treated. Oncetreated, it may be possible to wean the drainage ifthe normal CSF outflow can resume. If the normalCSF outflow does not re-establish itself, ventriculo-peritoneal shunt placement is likely required.Heroic measures such as craniectomies, eithersupratentorially or in the posterior fossa in thecase of trans-foramen magnum herniation aresometimes recommended in severe cases.26,27These procedures are more likely to be consideredwhen the deterioration has been very abrupt,observed, brought rapidly to medical attention,and the patient is already in the hospital so thatsurgery can be rapidly undertaken. When rapiddevastating deficits develop before the patientpresents in hospital, the time involved in transport,evaluation, transport to operating room, set-up,and start, even when rapidly undertaken, rarelyoccurs quickly enough to reverse neurologicdevastation.Prognosis for patients with meningitis is variable.Rapid diagnosis and initiation of antibiotics iscrucial to improving outcomes; Køster-Rasmussenand colleagues28demonstrated a 30% increase inodds of unfavorable outcome per hour of delaybefore antibiotic administration. Recent mortalityranges from 13% to 18.7%.13,22Neonates, theelderly, the immunocompromised, and thosepresenting with significant neurologic deficitssuffer higher mortality rates. Major morbiditiesoccurred in 12.8% of cases and minor morbiditiesoccurred in 8.6% of cases.29The most commonmorbidities were hearing loss (33.6%), seizures(12.6%), and motor deficits (11.6%).29VIRAL, FUNGAL, AND PARASITIC INFECTIONSViral and fungal infections can also cause verysignificant neurologic dysfunction and imagingabnormalities. Antiviral and antifungal agents arethe main treatments for these infections; however,neurosurgical treatment is also sometimesrequired. Such infections include herpes encepha-litis (HSE), viral encephalitis, toxoplasmosis, andneurocysticercosis.HSEHerpes encephalitis (HSE) is a very serious condi-tion, which is the most common and likely mostsevere viral encephalitis and therefore will be dis-cussed separately. The herpes virus reactivatesand generates a very significant inflammatoryreaction that occurs predominantly in the temporallobes. Viral reactivation sets off a chain of eventsresulting in necrosis (frequently hemorrhagic) inthe temporal lobes. Although a high percentageof the population harbors the herpes virus, HSEis uncommon, occurring in approximately 1 in250,000 to 500,000 patients per year.30Patients may present with altered mentation,decreasing consciousness, focal neurologic find-ings, headache, seizures, and fever. HSE occursin all age ranges.30Effective treatment of HSE depends on rapidrecognition and treatment. The presentation,physical examination, imaging, and laboratoryresults from peripheral blood typically suggestthe diagnosis to begin intravenous acyclovir. Earlyadministration of antiviral medication is crucial inhalting the process. LP may also be recommendedas long as the basal cisterns are patent, and therisk of herniation after LP is thus minimized. CSFis examined to rule out bacterial infection. CSFanalysis typically demonstrates a cellular pleocy-tosis and high protein with normal glucose values.Detection of HSV DNA by polymerase chain reac-tion (PCR) has a sensitivity of 94% and a specificityof 98%31and is now the gold standard of clinicaldiagnosis of HSV encephalitis.The primary treatment is the rapid use ofacyclovir as first-line therapy.32Seizures areaggressively treated. Attentive supportive care isprovided. Surgical intervention is rarely undertakenwith the possible exception of fulminant HSE withsignificant mass effect on the brainstem. In thissetting, craniectomy may be considered.33,34The prognosis for HSE depends on early diag-nosis. Without effective treatment, mortality rateis greater than 70% with only 9% of survivorsreturning to normal function30With acyclovir, the6-month mortality is 19%.30The rate of return tonormal function in the setting of acyclovir treat-ment is 38%.30Viral EncephalitisViral encephalitis is a diffuse viral infection, particu-larly of the cerebrum and cortex. Patients with viralencephalitis present with a range of symptoms,including headaches, behavioral changes, fever,seizures, and altered sensorium.32,35Viral patho-gens include Varicella; Enteroviruses; Measles;Rubella; Mumps; arthropod-borne viruses, suchas West Nile Virus and Japanese encephalitis;rabies; and human herpes virus 6 amongst manyothers.36Diagnosis typically, includes history,Herpes simplex encephalitis requires very rapidrecognition, diagnosis, and antiviral treatmentto prevent severe neurologic deficits or death.Heth794
  5. 5. physical examination, laboratory studies, imaging,and LP. LP is notable for lack of bacterial growth,normal glucose, high protein, and possibly a highwhite blood cell count. Frequently, CSF leukocy-tosis shows a predominance of lymphocytes.CSF from LP can also be subjected to PCR testingto assay for herpes simplex virus (HSV), Varicellazoster virus (VZV), human herpes virus (HHV) 6and 7, cytomegalovirus (CMV), Epstein-Barr virus(EBV), enteroviruses, and HIV amongst others.32Serologic testing for antibodies to HSV, VZV,CMV, HHV6 and HHV7, EBV, HIV, influenza A andB, respiratory syncytial virus, rotavirus, coxsackieB5 and parainfluenza 1 viruses32is also available.The minimum treatment of viral encephalitis isattentive supportive care. Seizures are aggres-sively treated. Depending on the causative agent,antiviral therapy may be available. For VZV,acyclovir may also be used. Foscarnet or ganciclo-vir can be used for HHV6. Ganciclovir, foscarnet,cidofovir can be tried for CMV. Corticosteroidtreatment is controversial and no definitiverecommendations are made for their use in viralencephalitis.The prognosis is generally variable and dependson the patient’s age, systemic condition, and thecausative virus. In adults, West Nile Virus encepha-litis resulted in death in 13% of cases and 38% dis-charged to a long-term care facility.37Wong andYeung38reported mortality of 28%. Of the survi-vors, 24% had neurologic sequelae. Wang andcolleagues39reported 26% mortality in culture-proven enterovirus cases. As these representativereports demonstrate, mortality and morbidity ratescan be considerable for viral encephalitis.ToxoplasmosisToxoplasma gondii is an obligate intracellular para-site that is the causative agent of CNS toxoplas-mosis. T gondii is typically acquired by ingestionof oocysts from contaminated soil or food, orbradyzoites in undercooked meat.40In im-munocompetent adults, the parasites is typicallycontrolled; however, it can reactivate in the settingof immunosuppression. Two populations may beaffected by this parasite: neonates and the immu-nosuppressed patients (particularly patients withAIDS and transplant patients).41,42Risk factorsfor acquiring T gondii include working with meat;having 3 or more cats; eating locally producedcured, dried, or smoked meat; eating rare lambor raw ground beef; and drinking unpasteurizedgoat’s milk.43Neonates may be infected by in ute-ro transplacental transmission of the parasite,which can cause fetal death, CNS calcifications,chorioretinitis, and hydrocephalus. Adult patientsagain may present with varying symptoms andsigns, including headache, fever, seizures, focalneurologic deficits, and more severely diminishedsensorium. PCR and quantitative real time PCRcan also be done for the DNA of Toxoplasma inthe CSF with sensitivity of 79% to 100% and spec-ificity of 92% to 97%.44,45In some occasions,when all attempts at diagnosis have failed, stereo-tactic biopsy of a representative lesion can beperformed. This procedure has been an issue inthe management of patients with AIDS withabnormal ring-enhancing lesions. The differentialdiagnosis in this setting includes lymphoma. Onestrategy to obtain the diagnosis is to treat fortoxoplasmosis and assess the response.46,47Apositive response favors a toxoplasmosis diag-nosis whereas no response still leaves a diagnosticdilemma that may require surgical biopsy toresolve.Toxoplasmosis is treated with antitoxoplasmo-sis agents. The prognosis is good if treatment isstarted expeditiously and the immunosuppressioncan be minimized.NeurocysticercosisNeurocysticercosis is a parasitic disease causedby Taenia solium. Humans are the definitive hostsin whom the parasite develops into an adult tape-worm, reproduces, and sheds eggs. The eggs canthen be ingested by several intermediate hosts.Pigs are the prototypical intermediate host. Thecysticerci lodge in the skeletal muscle of pigs; ifthe meat from infected pigs is not cooked appro-priately, the cysts from the ingested meat allowthe parasite to complete its life cycle by devel-oping into adult tapeworms,48resulting in taeni-asis. When a human ingests the parasite eggs,they treat the human host as an intermediatehost. The eggs hatch and migrate throughout thebody to lodge and develop into cystic larval forms.These cysts can occur in the skeletal muscle,brain, eye, and subcutaneous tissue.49,50Neuro-cysticercosis is endemic in the developing worldand is a leading cause of epilepsy worldwide.49Patients with neurocysticercosis may present indifferent manners based on lesion location. Symp-toms depend on cyst location, the number ofcysts, and the degree of immune response to thedisease.49Cysts can occur in the brain paren-chyma, the ventricular system, the subarachnoidspace, and the spinal cord. Seizures can occurwhen cysts cause cortical dysfunction. Hydro-cephalus can be caused by cysts occluding theCSF outflow pathways and can be symptomaticwith headaches, somnolence, or loss of con-sciousness. Focal neurologic deficits can ariseCentral Nervous System Infections 795
  6. 6. from loss of function caused by a cortical or spinalcyst. Patients may also present with dementia.51The clinical setting and imaging can stronglysuggest the diagnosis. Serologic testing on CSFand peripheral blood are very specific and quitesensitive for T solium infection.49,50Diagnosticbiopsy may be obtained from cysts in other loca-tions, such as skeletal muscle. Patients in whomthese evaluations cannot solidify the diagnosis,a diagnostic CNS biopsy may be required.Treatment is directed at the presenting symp-toms as well as the parasite itself. Seizures areaggressively treated. Seizure control is very highwith appropriate anticonvulsant managementalthough lifelong anticonvulsants may be required.Hydrocephalus must be aggressively treated.Endoscopic treatment can include cyst removal,third ventriculostomy, and septum pellucidumfenestration.52,53If endoscopic treatment fails oris not an option, shunt placement can be per-formed although there is a concern for high rateof failure with neurocysticercosis. If a cyst is largeand causing mass effect and neurologic deficits,a cyst resection could be considered. Cysticidaltreatment is recommended to treat the parasitesthemselves.The prognosis depends on the manner ofpresentation. Seizures can be readily controlledwith good outcomes. Hydrocephalus can also beeffectively treated. Intracranial hypertension re-sulting from mass effect from the cysts or froman aggressive immune response to the cysts canbe life threatening.SPINAL DISKITIS AND SPINAL EPIDURALABSCESSVertebral diskitis and spinal epidural abscess (SEA)are CNS infections that can affect the spine andspinal cord. They are discussed here, becausethey are readily treated with good outcomes ifpromptly recognized and treated. If not promptlyrecognized and treated, they can cause rapid onsetparaplegia and quadriplegia. Diskitis and SEAoccur through similar mechanisms. Diskitis canalso occur through direct inoculation (even withproper antisepsis), such as LP, diskogram, surgicalexposure, and epidural anesthesia.The disk spacecan be seeded from a primary infection elsewhere,such as a soft tissue infection or endocarditis.SEA can arise from untreated diskitis as well asdirect exposure54,55as previously mentioned. Inone report, as many as 52.6% of SEA cases wereassociated with neurosurgical procedures or spinalblocks.56SEA can also occur from contiguousspread. An example is cervical soft tissue abscessthat erodes into the cervical spinal canal.The main complaint of patients with diskitis ispain appropriate to the spinal level. Diskitis isa very painful condition and responds poorly tofirst-line medications used to treat degenerativespine disease. Fever can also occur.56,57Diskitisin the lumbosacral region can cause radicularsymptoms with leg pain and radicular deficits.Stenosis can also occur and cause leg pain thatworsens with ambulation. Diskitis in the cervicaland thoracic regions can cause radicular symp-toms, but most importantly cervicothoracic diskitiscan cause spinal cord compression, myelopathy,and quadriparesis/plegia or paraparesis/plegia,respectively. Incontinence can also occur.57Risk factors for diskitis and SEA are similar topreviousinfectiousconditionsdiscussedandincludediabetes mellitus, end-stage renal disease, endocar-ditis, immunosuppression, hepatic cirrhosis, andillicit intravenous drug use.57,58Patients with SEA also can have pain55although itis not as uniformly and exquisitely painful as diskitis.The same range of neurologic deficits can occur.The microbiological species involved vary.56,57Staphylococci are the species most commonly iso-lated.56–58If seeding occurs from a primary site, themicrobiology of the primary site will dictate thediagnosis. Direct spread from cervical, abdominal,or pelvic abscess increases the possibility of GNR,anaerobic, and polymicrobial infections. Individ-uals in whom diskitis and SEA occur from directmanipulation, skin flora and GPC dominate. Fungaland candidal diskitis can also occur.59Diagnosis and treatment of diskitis and SEAmust address 3 issues. The first issue is microbio-logical diagnosis, which allows prescription ofmaximally effective antibiotics.Diagnosis froma primary site may be possible. With diskitis,computed tomography–guided needle biopsyyields the diagnosis in 90% of cases.59In somecases, open biopsy may be required if all otherdiagnostic attempts have failed. The second issuethat must be addressed is neural compression. Inspinal cord compression with cervical or thoracicmyelopathy, emergent decompression is indi-cated and usually requires laminectomy. If caudaequina symptoms develop from lumbar diskitis orSEA, emergent decompression, usually laminec-tomy, is required. In cases of radicular symptomsonly, nerve root decompression may be consid-ered. The third issue that must be considered isSpinal diskitis and spinal epidural abscess areuncommonly a threat to life but may causeparaplegia or quadriplegia without expeditiousevaluation, imaging, and treatment.Heth796
  7. 7. spinal stability. If the infection has destroyed crit-ical spinal elements, then spinal stabilization maybe also be required.The prognosis for diskitis is generally good ifpromptly diagnosed and the treatment is rapidlybegun. Eighty percent of cases can experiencea good outcome.59Mortality is uncommon anddepends more on systemic infection. Similarly,prompt diagnosis is important to overall prognosisin SEA.56The prognosis in SEA has been variable inthe literature. One group reported 10 of 21 casesdeteriorating,58whereas another reported 67% to75% of patients improving after treatment57and5% worsening neurologically. Mortality rate inSEA can be up to 23% and can occur secondaryto systemic sepsis or resulting from systemicconditions that predispose to SEA, such as end-stage renal disease.57SUMMARYCNS infections are very serious conditions, whichcause rapidly progressive symptoms and loss offunction. Rapid deterioration can also lead todeath, which is particularly true of cerebralabscess, SDE, meningitis, and herpes simplexencephalitis. Although perhaps not as frequentlylife threatening, diskitis and SEA can cause rapidonset of very severe neurologic deficits. In all ofthese conditions, rapid diagnosis and treatment iscrucial. Imaging is important for appropriate locali-zation, diagnosis, and surveillance once treatmenthas begun. Viral encephalitis, toxoplasmosis, andneurocysticercosis can also cause a myriad ofsymptoms and disability. Again, imaging playsa crucial role in diagnosis and in treatment of theseconditions as well.REFERENCES1. Germiller JA, Monin DL, Sparano AM, et al. Intracra-nial complications of sinusitis in children and adoles-cents and their outcomes. Arch Otolaryngol HeadNeck Surg 2006;32(9):969–76.2. Isaacson B, Mirabal C, Kutz JW, et al. Pediatric oto-genic intracranial abscesses. Otolaryngol HeadNeck Surg 2010;142(3):434–7.3. Chun CH, Johnson JD, Hofstetter M, et al. Brainabscess. A study of 45 consecutive cases. Medicine(Baltimore) 1986;65:415–31.4. Bitsch A, Nau R, Hilgers RA, et al. Focal neurologicdeficits in infective endocarditis and other septicdiseases. Acta Neurol Scand 1996;94(4):279–86.5. Kieran SM, Cahill RA, Sheehan SJ. Mycotic periph-eral aneurysms and intracerebral abscessessecondary to infective endocarditis. Eur J Vasc En-dovasc Surg 2004;28(5):565–6.6. Ewald C, Kuhn S, Kalff R. Pyogenic infections of thecentral nervous system secondary to dental affec-tions–a report of six cases. Neurosurg Rev 2006;29(2):163–6 [discussion: 166–7].7. Brydon HL, Akinwunmi J, Selway R, et al. Brainabscesses associated with pulmonary arteriove-nous malformations. Br J Neurosurg 1999;13(3):265–9.8. Kawano H, Hirano T, Ikeno K, et al. Brain abscesscaused by pulmonary arteriovenous fistulas withoutRendu-Osler-Weber disease. Intern Med 2009;48(6):485–7.9. Ciurea AV, Stoica F, Vasilescu G, et al. Neurosurgicalmanagement of brain abscesses in children. ChildsNerv Syst 1999;15(6-7):309–17.10. Takeshita M, Kagawa M, Izawa M, et al. Currenttreatment strategies and factors influencingoutcome in patients with bacterial brain abscess.Acta Neurochir (Wien) 1998;140:1263–70.11. Britt RH, Enzmann DR. Clinical stages of humanbrain abscesses on serial CT scans after contrastinfusion. Computerized tomographic, neuropatho-logical, and clinical correlations. J Neurosurg 1983;59(6):972–89.12. Kondziolka D, Duma CM, Lunsford LD. Factors thatenhance the likelihood of successful stereotactictreatment of brain abscesses. Acta Neurochir(Wien) 1994;127(1-2):85–90.13. Pfister HW, Feiden W, Einha¨upl KM. Spectrum ofcomplications during bacterial meningitis in adults.Results of a prospective clinical study. Arch Neurol1993;50(6):575–81.14. Yang SY, Zhao CS. Review of 140 patients with brainabscess. Surg Neurol 1993;39(4):290–6.15. Tsai CJ, Griffin MR, Nuorti JP, et al. Changing epide-miology of pneumococcal meningitis after the intro-duction of pneumococcal conjugate vaccine in theUnited States. Clin Infect Dis 2008;46(11):1664–72.16. Dashti SR, Baharvahdat H, Spetzler RF, et al. Oper-ative intracranial infection following craniotomy. Neu-rosurg Focus 2008;24(6):E10.17. McClelland S, Hall WA. Postoperative centralnervous system infection: incidence and associatedfactors in 2111 neurosurgical procedures. Clin InfectDis 2007;45(1):55–9.18. Tsai BY, Lin KL, Lin TY, et al. Pott’s puffy tumor in chil-dren. Childs Nerv Syst 2010;26(1):53–60.19. Hlavin ML, Kaminski HJ, Fenstermaker RA, et al. Intra-cranial suppuration: a modern decade of postopera-tive subdural empyema and epidural abscess.Neurosurgery1994;34(6):974–80[discussion:980–1].20. Penido Nd O, Borin A, Iha LCN, et al. Intracranialcomplications of otitis media: 15 years of experiencein 33 patients. Otolaryngol Head Neck Surg 2005;132(1):37–42.21. Tsai YD, Chang WN, Shen CC, et al. Intracranialsuppuration: a clinical comparison of subduralCentral Nervous System Infections 797
  8. 8. empyemas and epidural abscesses. Surg Neurol2003;59:191–6 [discussion: 196].22. Giorgi Rossi P, Mantovani J, Ferroni E, et al. Inci-dence of bacterial meningitis (2001–2005) in Lazio,Italy: the results of a integrated surveillance system.BMC Infect Dis 2009;9:13.23. Loughlin AM, Marchant CD, Lett SM. The changingepidemiology of invasive bacterial infections inMassachusetts children, 1984 through 1991. Am JPublic Health 1995;85(3):392–4.24. Williams AJ, Nadel S. Bacterial meningitis: currentcontroversies in approaches to treatment. CNSDrugs 2001;15(12):909–19.25. Stephens DS. Biology and pathogenesis of theevolutionarily successful, obligate human bacteriumNeisseria meningitidis. Vaccine 2009;27(Suppl 2):B71–7.26. Baussart B, Cheisson G, Compain M, et al. Multi-modal cerebral monitoring and decompressivesurgery for the treatment of severe bacterial menin-gitis with increased intracranial pressure. ActaAnaesthesiol Scand 2006;50:762–5.27. Di Rienzo A, Iacoangeli M, Rychlicki F, et al. Decom-pressive craniectomy for medically refractory intra-cranial hypertension due to meningoencephalitis:report of three patients. Acta Neurochir (Wien)2008;150(10):1057–65 [discussion: 1065].28. Køster-Rasmussen R, Korshin A, Meyer CN. Antibi-otic treatment delay and outcome in acute bacterialmeningitis. J Infect 2008;57(6):449–54.29. Edmond K, Clark A, Korczak VS, et al. Global andregional risk of disabling sequelae from bacterialmeningitis: a systematic review and meta-analysis.Lancet Infect Dis 2010;10(5):317–28.30. Whitley RJ. Herpes simplex encephalitis: adoles-cents and adults. Antiviral Res 2006;71(2-3):141–8.31. Lakeman FD, Whitley RJ. Diagnosis of herpessimplex encephalitis: application of polymerasechain reaction to cerebrospinal fluid from brain-biopsied patients and correlation with disease.National Institute of Allergy and Infectious DiseasesCollaborative Antiviral Study Group. J Infect Dis1995;171(4):857–63.32. Steiner I, Budka H, Chaudhuri A, et al. Viral menin-goencephalitis: a review of diagnostic methodsand guidelines for management. Eur J Neurol2010;17(8):999–e57.33. Adamo MA, Deshaies EM. Emergency decompres-sive craniectomy for fulminating infectious encepha-litis. J Neurosurg 2008;174–6.34. Gonza´lez Rabelino GA, Fons C, Rey A, et al. Cra-niectomy in herpetic encephalitis. Pediatr Neurol2008;39(3):201–3.35. Michael BD, Sidhu M, Stoeter D, et al. Acute centralnervous system infections in adults–a retrospectivecohort study in the NHS North West region. QJM2010;103(10):749–58.36. Huppatz C, Durrheim D, Levi C, et al. Etiology ofEncephalitis in Australia, 1990–2007. Emerg InfectDis 2009;15(9):1359.37. Tyler KL, Pape J, Goody RJ, et al. CSF findings in 250patients with serologically confirmed West Nile virusmeningitis and encephalitis. Neurology 2006;66(3):361–5.38. Wong V, Yeung CY. Acute viral encephalitis in chil-dren. Aust Paediatr J 1987;23(6):339–42.39. Wang SM, Liu CC, Tseng HW, et al. Clinical spec-trum of enterovirus 71 infection in children insouthern Taiwan, with an emphasis on neurologicalcomplications. Clin Infect Dis 1999;29(1):184–90.40. Walker M, Zunt JR. Parasitic central nervous systeminfections in immunocompromised hosts. Clin InfectDis 2005;40(7):1005–15.41. Denier C, Bourhis JH, Lacroix C, et al. Spectrum andprognosis of neurologic complications after hemato-poietic transplantation. Neurology 2006;67(11):1990–7.42. Weber C, Schaper J, Tibussek D, et al. Diagnostic andtherapeutic implications of neurological complicationsfollowing paediatric haematopoietic stem cell trans-plantation. BoneMarrowTransplant 2008;41(3):253–9.43. Jones JL, Dargelas V, Roberts J, et al. Risk factorsfor Toxoplasma gondii infection in the United States.Clin Infect Dis 2009;49(6):878–84.44. Alfonso Y, Fraga J, Fonseca C, et al. Molecular diag-nosis of Toxoplasma gondii infection in cerebro-spinal fluid from AIDS patients. Cerebrospinal FluidRes 2009;6:2.45. MesquitaRT, ZieglerAP, HiramotoRM,et al. Real-timequantitative PCR in cerebral toxoplasmosis diagnosisof Brazilian human immunodeficiency virus-infectedpatients. J Med Microbiol 2010;59(Pt 6):641–7.46. Portegies P, Solod L, Cinque P, et al. Guidelines forthe diagnosis and management of neurologicalcomplications of HIV infection. Eur J Neurol 2004;11(5):297–304.47. Smego RA, Orlovic D, Wadula J. An algorithmicapproach to intracranial mass lesions in HIV/AIDS.Int J STD AIDS 2006;17(4):271–6.48. Fleury A, Escobar A, Fragoso G, et al. Clinicalheterogeneity of human neurocysticercosis resultsfrom complex interactions among parasite, hostand environmental factors. Trans R Soc Trop MedHyg 2010;104(4):243–50.49. Garcia HH, Del Brutto OH, Cysticercosis WorkingGroup in Peru. Neurocysticercosis: updated con-cepts about an old disease. Lancet Neurol 2005;4(10):653–61.50. Mahanty S, Garcia HH, Cysticercosis WorkingGroup in Peru. Cysticercosis and neurocysticercosisas pathogens affecting the nervous system. ProgNeurobiol 2010;91(2):172–84.51. Ciampi de Andrade D, Rodrigues CL, Abraham R,et al. Cognitive impairment and dementia inHeth798
  9. 9. neurocysticercosis: a cross-sectional controlledstudy. Neurology 2010;74(16):1288–95.52. Proan˜o JV, Torres-Corzo J, Rodrı´guez-DellaVecchia R, et al. Intraventricular and subarachnoidbasal cisterns neurocysticercosis: a comparativestudy between traditional treatment versus neuroen-doscopic surgery. Childs Nerv Syst 2009;25(11):1467–75.53. Torres-Corzo JG, Tapia-Pe´rez JH, Vecchia RR, et al.Endoscopic management of hydrocephalus due toneurocysticercosis. Clin Neurol Neurosurg 2010;112(1):11–6.54. Green LK, Paech MJ. Obstetric epidural catheter-related infections at a major teaching hospital:a retrospective case series. Int J Obstet Anesth2010;19(1):38–43.55. Sethna NF, Clendenin D, Athiraman U, et al. Inci-dence of epidural catheter-associated infectionsafter continuous epidural analgesia in children.Anesthesiology 2010;113(1):224–32.56. Gonza´lez-Lo´pez JJ, Go´rgolas M, Mun˜iz J, et al.Spontaneous epidural abscess: analysis of 15 caseswith emphasis on diagnostic and prognostic factors.Eur J Intern Med 2009;20(5):514–7.57. Karikari IO, Powers CJ, Reynolds RM, et al. Manage-ment of a spontaneous spinal epidural abscess:a single-center 10-year experience. Neurosurgery2009;65(5):919–23 [discussion: 923–4.58. Wang TC, Lu MS, Yang JT, et al. Motor functionimprovement in patients undergoing surgery forspinal epidural abscess. Neurosurgery 2010;66(5):910–6.59. D’Agostino C, Scorzolini L, Massetti AP, et al.A seven-year prospective study on spondylodisci-tis: epidemiological and microbiological features.Infection 2010;38(2):102–7.Central Nervous System Infections 799