Книги по МРТ КТ на английском языке / Neurosurgery Fundamentals Agarval 1 ed 2019

controversial, intracranial aneurysms are not treated with radiosurgery and is the better answer choice. AVMs and dural AV fistulae are well-described indications for radiosurgery.

3.b.

4.c. During this latency period prior to obliteration, the AVM continues to function as a shunt and there remains a stable chance of hemorrhage.

References

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[33]Vance ML. Treatment of patients with a pituitary adenoma: one clinician’s experience. Neurosurg Focus. 2004; 16(4):E1

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[36]Iyer A, Kano H, Kondziolka D, et al. Stereotactic radiosurgery for intracranial chondrosarcoma. J Neurooncol. 2012; 108(3):535–542

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[38]Pollock BE, Kondziolka D, Flickinger JC, Maitz A, Lunsford LD. Preservation of cranial nerve function after radiosurgery for nonacoustic schwannomas. Neurosurgery. 1993; 33(4):597–601

[39]Pollock BE, Driscoll CL, Foote RL, et al. Patient outcomes after vestibular schwannoma management: a prospective comparison of microsurgical resection and stereotactic radiosurgery. Neurosurgery. 2006; 59(1):77–85, discussion 77–85

[40]Pollock BE, Lunsford LD, Kondziolka D, et al. Outcome analysis of acoustic neuroma management: a comparison of microsurgery and stereotactic radiosurgery. Neurosurgery. 1995; 36(1):215–224, –discussion 224–229

[41]Myrseth E, Møller P, Pedersen PH, Lund-Johansen M. Vestibular schwannoma: surgery or gamma knife radiosurgery? A prospective, nonrandomized study. Neurosurgery. 2009; 64(4):654–661, discussion 661–663

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Divyansh Agarwal, Harvey Rubin, Ali Naji

17.1  Introduction

For centuries, infectious diseases have afflicted humanity, be it in the form of the plague in the mid-1400s, cholera in the 1820s, polio in the early 1900s, or acquired immunodeficiency syndrome (AIDS) in the 1980s. From 1980 through 2014, infectious diseases comprised more than 5% of overall mortality rates in the United States, with a majority of the deaths being due to pneumonia and influenza.1 In this chapter, we will review the framework for microbiological diagnoses of central nervous system (CNS) infections and consider a few important pathogens including flavivirus, meningococcus, and two common para- sites—Taenia solium and Naegleria fowleri— that cause neuroinfectious disease. These organisms, although by no means exhaustive, provide examples of pathogen-­ mediated brain infection. We will further review common postsurgical infections, and the microbiological diagnoses of other CNS infections. Lastly, we include a brief section on the interpreting statistics in the medical literature as it relates to infectious diseases because Big Data analytics will be essential for the next generation of medical researchers, and we believe that infectious diseases provide a good avenue for discussing the basics of ongoing computational work in the field.

17.2  Microbiological Diagnosis

Lumbar puncture (LP) with cerebrospinal fluid (CSF) analysis is essential to diagnose CNS infections ( Fig. 17.1). In adults, the normal CSF opening pressure ranges from 50 to 190 mm H2O, and an elevated opening pressure is suggestive of bacterial

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meningitis. Typical CSF findings in patients with selected infectious causes of meningitis are shown in Table 17.1.2

Two important markers acute-phase reactants are commonly used as markers for inflammation–erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). The ESR corresponds to how much a vertical column of anticoagulated blood falls in 1 hour. If a condition affects red blood cells or fibrinogen levels, the ESR would be affected.3 The ESR rises within 1 to 2 days of the onset of inflammation and falls back slowly. CRP, which is better at measuring acute-phase response, is primarily produced by the liver in response to interleukin-6 (IL-6).4 Another predictive marker of surgical morbidity is impaired perioperative nutritional status, and prealbumin is useful to assess nutritional deficiency.5,​6 Similarly, serum procalcitonin has demonstrated its utility in distinguishing bacterial from viral meningitis, and in conjunction with other inflammatory markers, Procalcitonin levels can be useful in differentiating postoperative infection from inflammation.

17.3  FlavivirusMediated Neurological Disease

Flaviviruses are a family of positive, sin- gle-stranded, enveloped RNA viruses. They are transmitted by ticks and mosquito bites. Viruses in this family, such as yellow fever, dengue fever, and ZKV can cause widespread morbidity and mortality.7 In light of the large outbreak starting in Brazil in 2015 that revealed a strong association between maternal ZKV infection and fetal microcephaly, we will focus on ZKV as an example for neurological infectious agent in the flavivirus family.

•The most common malformations reported in fetuses and newborns with congenital Zika virus (ZKV) infection include agenesis of corpus callosum, macular chorioretinitis, cerebral calcifications, microcephaly, oligohydramnios, intrauterine growth restriction, atrophy of the ventricles, hydrops, and ventriculomegaly.

•ZKV is transmitted through the bite of female Aedes mosquitoes.

•The first trimester of pregnancy is considered the period of major risk for microcephaly.

The World Health Organization (WHO) declared ZKV as a public health emergency of international concern in 2016.8,​9 ZKV infection most commonly presents with initial low-grade fever, arthralgia, myalgia, fatigue, and conjunctival changes.10,​11 Several cases of acute meningoencephalitis and myelitis where ZKV RNA was detected and/or isolated in cell culture from CSF of the patients have also been reported. Definitive diagnosis of acute ZKV infection relies on the use of molecular tests for the direct detection of viral nucleic acids in blood and other biological specimens.12,​13

Although specific antiviral drugs are not available for use in humans to treat any

virus in the flavivirus family, including ZKV, compounds such as mycophenolic acid have been shown to be active against these viruses.

17.4  Meningococcal Disease

Neisseria meningitidis infection was first reported by Vieusseux in 1805, who described it as a “noncontagious malignant cerebral fever.”14 The immunologic reactivity of capsular polysaccharides forms the basis for classification of meningococci into serogroups. Meningococci, best isolated on Thayer–Martin agar medium, change their cytoskeletal structures when they come in contact with cells.15 The α-chain structure of meningococcal lipo-oligosaccharides mimics that of human polysaccharides, which helps the bacteria escapes a host’s immune mechanisms.

•Meningococcal disease is caused by

Neisseria meningitidis, a gram-­ negative, aerobic, oxidase-positive, diplococcus bacterium.

•An important mechanism of virulence that provides sero- group-specific protection is called capsule switching.

•Acute meningitis most commonly presents with headache, neck stiffness, nausea, fever, and altered mental status; in infants, a bulging fontanelle is commonly noticed ( Fig. 17.2).

•Adrenal hemorrhage is a manifestation of fulminant meningococcemia (Waterhouse–Friderichsen syndrome), which also causes diffuse thrombotic lesions or purpura.

•Chemoprophylaxis with rifampin should be given to all household contacts, child care/nursery school contacts, and contacts with exposure to secretions within 7 days of onset.

Fig. 17.2  Diffuse leptomeningeal enhancement seen on a contrast-­ enhanced magnetic resonance image from a 4-month-old girl infant with meningococcal meningitis. (Repro­ duced from Hall W, Kim P, Neuro­ surgical Infectious Disease. Surgical and Nonsurgical Management, 1st edition, ©2013, Thieme Publishers, New York.)

Neisseria meningitides is transmitted by secretions and multiplies in the nasopharynx.16 Meningococcal disease occurs within 2 weeks of exposure.15,​17 A significant proportion of cases of meningococcal disease present with meningococcal­ septicemia, also known as meningococcemia. Abrupt onset of fever, hypotension, disseminated intravascular coagulation (DIC), multiple organ failure, and osteonecrosis due to DIC are some of the consequences of severe meningococcemia. People with deficient terminal complement-mediated immune activity (failure of the C5–C9 membrane attack complex), functional

asplenism, or those living in crowded living conditions, such as college dormitories, are highly susceptible to infection.18

Blood and CSF cultures are commonly used for diagnosis. Management of the systemic circulation, respiration, and intracranial pressure (ICP) is vital for improving the prognosis.17 Third-generation cephalosporins like ceftriaxone are the antimicrobial agents of choice against N. meningitidis. Steroids have also been investigated as an adjunct to antibiotic therapy in bacterial meningitis, and should be considered in patients with irreversible hemodynamic instability. A meningococcal vaccine has been developed and is recommended for entering college freshman, particularly those living in dormitories.

17.5  Neurocysticercosis

•Neurocysticercosis (NCC) is caused by the larval form of the pork tapeworm—T. solium.

•Inflammation of the meninges secondary to cysticercosis can present as a combination of visual impairment and several nerve palsies.

•Albendazole, an imidazole that impairs glucose uptake and metabolism in the parasite, is generally considered to be the drug of choice.

NCC is one of the most common parasitic diseases of the human CNS. When food or water contaminate with T. solium eggs is ingested, the eggs hatch in the intestine and spread throughout the body, particularly being avid for the CNS ( Fig. 17.3).19

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NCC can present with signs of increased ICP as well as acute seizures and diffuse cerebral edema. The brain parenchyma is commonly infected, and cysts often deposit at the gray matter–white matter junction.20,​ 21 CSF and blood flow can also be disrupted due to high parasite burden. Spinal NCC should be suspected if the patient presents with motor and sensory dysfunction such as paresthesia and radicular pain along the nerve roots into the lower extremities.21 The diagnosis of NCC can be made by direct visualization of the parasite from brain biopsy. Immunoassays which use targeted antigens to detect antibodies to T. solium in patient serum also provide sensitive and specific diagnostic information.20 In addition to albendazole, praziquantel—an isoquinolone that causes parasite paralysis by disrupting calcium pathways and homeo- stasis—can also be used to treat NCC.

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17.6  Primary Amoebic

Meningoencephalitis

•The CNS infection caused by N. fowleri is mediated by the amoeba’s entry along the olfactory neuroepi­ thelial route via the cribriform plate and nasal mucosa.

•Infection of the olfactory lobes results in alteration of taste, smell, and vision.

•The diagnosis can be made by CSF enzyme-linked immunosorbent assay (ELISA) or immunofluores­ cence studies.

•The Centers for Disease Control and Prevention(CDC)recommendedtreatment regimen includes amphoteri­ cin B, fluconazole, azithromycin, rifampin, and dexamethasone.

Primary amoebic meningoencephalitis (PAM) is a hemorrhagic, necrotizing meningoencephalitis, caused by the thermophilic amoeba N. fowleri.22 The N. fowleri infection is mainly contracted through contaminated water and hot springs. The parasite enters the human body through the nose, and the incubation period between exposure and development of the disease can be days to several weeks.23

The most common presenting symptoms of patients with PAM include headache, fever, nausea, and vomiting, and signs of meningeal irritation, such as confusion, irritability, and seizures.24 The meningoencephalitis can be extremely severe and cause cerebral edema with focal white matter demyelination. In patients who present with neurological changes and have had a recent contact with freshwater or have a history of swimming in hot springs, PAM should be strongly considered on the differential diagnosis. The CSF Gram stain is often negative in these patients, but polymerase chain reaction (PCR) can be used to make the diagnosis of PAM.

17.7  Postsurgical

Infections

•Staphylococci and facultative or aerobic gram-negative bacilli are responsible for majority of the cases of postsurgical meningitis, especially in patients who are hospitalized for a prolonged period after penetrating trauma.

•Careful surgical techniques and an effort to minimize CSF leakage can lower the risk of postoperative meningitis.

•In patients with obstructive hydrocephalus and a lack of communication between ventricular and lumbar CSF; lumbar CSF may not be reflective of ventricular infection.

Postoperative meningitis, although rare, is a serious complication of neurosurgery. The use of devices for therapeutic drainage of CSF or for ICP monitoring, such as external ventricular drains (EVD), external spinal drains (ESD), and shunts, correlates with a relatively high rate of postoperative meningitis.25 Nosocomial meningitis can also be seen secondary to a complicated head trauma, and metastatic infection in the setting of hospital-acquired bacteremia. Bacterial meningitis occurs in 1 to 2% of patients who undergo craniotomy. Two important risk factors that increase the risk of postsurgical meningitis are (1) a duration of surgery of more than 4 hours, and (2) a concomitant infection at the site of the incision.26

Patients who require the use of foreign bodies, for example, internal ventricular drains, are susceptible to infections from cutaneous organisms such as Staphylococcus epidermidis.27Streptococcus pneumoniae is associated with complications after a basilar skull fracture or after head, neck, and/or ear surgery.26 Infections associated with an internal ventricular catheter are best addressed by a combination of antimicrobial therapy, removal of all components of the infected catheter, and placement of an external drain as they are successful measures to address the underlying infection.26 In the case of shunt infections caused by

Staphylococcus aureus or gram-negative bacilli, multiple negative cultures and a 10-day course of antimicrobial therapy are recommended before placing a new shunt.28 Common clinical findings in patients with postsurgical meningitis include fever, malaise, and a decreased level of consciousness. The clinician should use neuroimaging modalities to evaluate ventricular size and possible CSF leaks. In patients who undergo neurosurgery, a lactate concentration of 4 mmol/L or more in the CSF has also been shown to have an excellent sensitivity and specificity, a positive predictive value of 96%, and a negative

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predictive value of 94% for diagnosing bacterial meningitis.29

The pathogenesis of infection guides a clinician’s choice of empirical antimicrobial therapy. For patients who are hospitalized for an extended period after penetrating head trauma, the most frequently used regimen consists of vancomycin in combination with either meropenem, cefepime, or ceftazidime.30 Therapy should be optimized once a specific pathogen has been isolated. Antimicrobials are directly infused into the ventricles through a catheter if infections are difficult to eradicate with parenteral antimicrobial therapy alone. Treatment should be withdrawn after 72 hours if the results of CSF cultures are negative. This recommendation has been shown to be effective in a prospective study,31 and is in accordance with the British Society for Antimicrobial Chemotherapy.

17.8  Additional

Neurological Infections

17.8.1  Subdural Empyema

A subdural empyema (SDE) is a rare, suppurative infection that forms in the subdural space. It most often occurs due to the direct extension of local infection. Spread of the intracranial compartment may occur through the diploic veins and is associated with thrombophlebitis. SDE is often associated with paranasal sinusitis and chronic otitis media. Consider SDE on your differential diagnosis in a patient with fever, meningismus, hemiparesis, speech difficulty, papilledema, seizures, altered mental status, nausea, and sinus tenderness or swelling.32 Common organisms that cause SDE include aerobic Streptococcus, Staphylococci, aerobic gram-negative rods, and other anaerobes. Treatment involves emergent

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surgical drainage and broad-spectrum antibiotics.

17.8.2  HIV and AIDS

Half the patients with AIDS develop neurological symptoms. Toxoplasmosis, primary CNS lymphoma (associated with Epstein– Barr virus), progressive multifocal leukoencephalopathy (PML), and cryptococcal abscess are the most common conditions that produce focal CNS lesions in AIDS. CNS toxoplasmosis usually occurs when CD4 counts are fewer than 200, and can present as a mass lesion, meningoencephalitis, and encephalopathy. PML is caused by a polyomavirus, called the JC virus, and leads to focal myelin loss which results in mental status changes, blindness, aphasia, and ultimately coma.32 Magnetic resonance imaging (MRI) with gadolinium is the preferred screening modality for AIDS patients with CNS symptoms because of lower false-negative rate compared with computed tomography (CT) ( Fig. 17.4).

17.8.3  Creutzfeldt–Jakob

When a normal prion protein becomes misshapen into an infectious prion, it can build up in the brain and disrupt normal brain function ( Fig. 17.5). Creutzfeldt– Jakob disease (CJD) is a rare disorder that is fatal, usually within 6 months of diagnosis. About 300 new cases per year are reported in the United States. There are three main forms of prion disease—sporadic, genetic, and acquired—categorized by how the disease occurs. Rapid neurocognitive decline in the form of memory loss, confusion, difficulty with coordination, and balance and personality changes are hallmark of CJD. Electroencephalography (EEG) recordings commonly show periodic sharp wave complexes. The 14–3–3 protein, which appears after neuronal destruction, is a useful surrogate CSF marker. There is no known