Infectious Diseases

Parameningeal Infections (other than brain abscess)

OVERVIEW: What every practitioner needs to know

Subdural empyema is a localized collection of pus contained between the dura and arachnoid. Accounting for 15 to 20% of all intracranial infections, subdural empyema is the most common intracranial infection associated with sinusitis. Headache and fever are common early symptoms given the ability of the infection to progress rapidly. Neuroimaging is the diagnostic procedure of choice for subdural empyema given the high degree of sensitivity and for means of planning surgical intervention. The optimal treatment approach to cranial subdural empyema involves surgical drainage by bur hole or open craniotomy and parenteral antibiotic therapy.

Cranial epidural abscess is a collection of pus between the dura mater and the skull. Once the almost exclusive sequelae of sinusitis, otitis media, or mastoiditis, cranial epidural abscesses are now often secondary to neurosurgical complications. An accompanying subdural empyema may be present and the infecting bacterial pathogens are similar. Given the close approximation and essential adherence of the dura to the inner skull, spread of purulence is constrained and the clinical presentation is more indolent than with frank subdural empyema. Similar to subdural empyema, prompt neuroimaging is required for diagnosis and magnetic resonance imaging (MRI) is the preferred modality as a combined medical and surgical approach to therapy is necessary.

Suppurative intracranial thrombophlebitis may arise from the intracranial veins or venous sinuses, or as a consequence of spread from paranasal sinusitis, otitis media, mastoiditis, dental abscess, orbital cellulitis, or infection of the scalp or face. Unique symptomatology, surgical treatment, and prognosis are dependent on the venous sinus affected. Parenteral antibiotic therapy is targeted at the presumed predisposing infection.

Are you sure your patient has a parameningeal infection? What should you expect to find?

Subdural empyema: headache and fever are common early symptoms given the ability of the infection to progress rapidly without marked anatomical constraint. The majority of patients will develop fever and meningismus, approximately 50% will develop altered mental status or seizures, and if left untreated nearly all will develop focal neurologic deficits including hemiparesis, ocular palsies, homonymous hemianopsia, dysphagia, or cerebellar signs. Headache may localize to the infected sinus or ear and vomiting may occur as increased intracranial pressure develops. Though not discussed in detail in this section, spinal subdural empyema may present with radicular pain and multilevel symptoms of spinal cord compression.

Cranial epidural abscess: given the close approximation and essential adherence of the dura to the inner skull, spread of purulence is constrained and the clinical presentation is more indolent than with frank subdural empyema. If secondary to sinusitis or otitis media, the symptoms such as nasal congestion or ear pain may even be more prominent than the dull headache of the cranial epidural abscess. While fever and headache are usually present, patients may often feel well enough to delay seeking medical attention until the epidural abscess has become complicated by subdural empyema, brain abscess, or meningitis. If left untreated with an enlarging abscess confined to the epidural space, a significant amount of mass effect may produce papilledema or other signs of increased intracranial pressure. Uniquely, if an epidural abscess is present near the petrous bone, Gradenigo syndrome may be present with unilateral facial pain, weakness of the lateral rectus muscle, and palsy of cranial nerves V and VI.

Suppurative thrombophlebitis: in addition to the symptomatology of the site of initial infection such as sinusitis or otitis media, a more unique presentation may develop depending on the venous sinus primarily involved (see Table II).

Table II.

Suppurative intracranial thrombophlebitis: predisposition, common microbiology, and presenting signs and symptoms by infected sinus.
Sinus involved Predisposition Microbiology Signs/symptoms
Cavernous sinus SinusitisSoft tissue infections of middle third of face (orbital cellulitis)Dental abscesses Staphylococcus aureus (60–70%)StreptococciAnaerobes Periorbital edema, headache, photophobia, diplopia, proptosis, chemosis, extraocular muscle weakness, papilledemaFindings spread to contralateral side in 24–48 hours
Lateral (transverse) sinus Otitis mediaMastoiditis Gram-negative bacilli (Escherichiacoli)Anaerobes including Fusobacterium and Bacteroides speciesStreptococciHaemophilus influenzaeStaphylococci Headache, otalgia, high fever, and occiput swelling and tenderness (Griesinger sign)Less common photophobia, diplopia, or unilateral nuchal rigidity
Superior sagittal sinus Scalp traumaUpper face infectionPost-bacterial meningitis or subdural and epidural space infection Staphylococci StreptococciAnaerobes Altered mental status, papilledema, nuchal rigidity, seizures, motor weakness
Inferior petrosal sinus Otitis mediaMastoiditis Gram-negative bacilli Anaerobes StreptococciHaemophilus influenzaeStaphylococci Gradenigo syndrome of ipsilateral facial pain and lateral rectus weakness
  • Cavernous sinus thrombosis: the majority of patients experience fever and periorbital edema, and headache is common. Vision loss, diplopia, proptosis, and chemosis may develop. Papilledema is present in 65% of cases and drowsiness or change in mental status may accompany increased intracranial pressure. Cranial nerve VI traverses the lumen of the cavernous sinus and a lateral gaze palsy may be present as an early diagnostic clue. If left untreated, within 48 hours of the initial periorbitial edema, infection may spread to the contralateral sinus.

  • Lateral sinus thrombosis: symptom onset may be more gradual than cavernous sinus thrombosis and is marked by headache, otalgia, high fever, and mastoid swelling and tenderness. The posterior auricular swelling and pain, present in 50% of cases, has been termed Griesinger sign. Photophobia, nuchal rigidity, vomiting, and vertigo are not uncommon. Of note, the nuchal rigidity tends to be unilateral with negative Kernig and Brudzinski signs. In a case series of children with lateral sinus thrombosis, 54% had diplopia.

  • Superior sagittal sinus thrombosis: abnormal mental status, nuchal rigidity, and papilledema predominate and given that most cases are secondary to bacterial meningitis, the onset may be rapid. Seizures can be observed.

  • Inferior petrosal sinus thrombosis: may present with Gradenigo syndrome of ipsilateral facial pain and lateral rectus weakness.

How did the patient develop a parameningeal infection? What was the primary source from which the infection spread?

  • Subdural empyema: infection of the subdural space occurs following sinusitis by spread through valveless emissary veins with or without associated thrombophlebitis, or by extension of an epidural abscess nearby a site of osteomyelitis of the skull. When secondary to meningitis the initial predisposition is likely a sterile subdural effusion that becomes secondarily infected. Following widespread vaccination for Haemophilus influenza type b, incidence of subdural empyema secondary to bacterial meningitis in infants and children has decreased dramatically.

  • Cranial epidural abscess: once the almost exclusive sequelae of sinusitis, otitis media, or mastoiditis, cranial epidural abscesses are now often secondary to neurosurgical complications. Less invasive procedures, such as fetal scalp monitoring and halo pin placement have also been reported as etiologies. An accompanying subdural empyema may be present.

  • Suppurative intracranial thrombophlebitis: may arise from the intracranial veins or venous sinuses, or as a consequence of spread from paranasal sinusitis, otitis media, mastoiditis, dental abscess, orbital cellulitis, or infection of the scalp or face. Conditions that may predispose to a suppurative thrombosis of the venous sinuses are those associated with hyperviscosity or hypercoagulability such as pregnancy, intravascular volume depletion, oral contraceptive use, malignancy, systemic lupus erythematosus or the more specific presence of antiphospholipid antibodies or deficiencies in antithrombin III, and protein C or S.

Which individuals are of greater risk of developing a parameningeal infection?

  • Subdural empyema: accounting for 15 to 20% of all intracranial infections, subdural empyema is the most common intracranial infection associated with sinusitis. Concomitant brain abscess is present in 9 to 17% of cases of subdural empyema. While initial infection of the paranasal sinuses is present in up to 80% of cases, additional causes include meningitis, otitis media, postneurosurgery, or in other posttraumatic settings of penetrating head trauma or pre-existing subdural hematoma.

  • Cranial epidural abscess: patients with untreated sinusitis, otitis media, or mastoiditis are at risk for cranial epidural abscesses, as well as those having had neurosurgery or other less invasive procedures such as fetal scalp monitoring and halo pin placement. Concomitant brain abscess is present in 6 to 22% of patients who have an epidural abscess.

  • Suppurative thrombophlebitis: most commonly, cavernous sinus thrombosis is secondary to infection of the frontal, ethmoid, or sphenoid sinuses, but can be observed with dental abscesses, orbital cellulitis, or infections of the middle third of the face. Lateral sinus thrombosis can be observed in the presence of both acute and chronic otitis media, whereas infection of the inferior and superior petrosal sinuses may arise from otitis media or mastoiditis. Lateral sinus thrombosis is more common in children and can be a devastating complication. The superior sagittal sinus may become infected following trauma to the scalp, after another infection of the subdural or epidural space, or after bacterial meningitis.

Beware: there are other diseases that can mimic parameningeal infection:

The following diseases can mimic parameningeal infection:

  • brain abscess

  • bacterial meningitis

  • intracranial bleed

  • ischemic stroke

  • noninfectious space occupying lesion (e.g. tumor, particularly in an immunocompromised host)

What laboratory studies should you order and what should you expect to find?

Results consistent with the diagnosis

  • Subural empyema/cranial epidural abscess: lumbar puncture is contraindicated given the risk of cerebral herniation, and cerebrospinal fluid (CSF) cultures are routinely negative unless complicated by bacterial meningitis.

  • Suppurative thrombophlebitis: laboratory findings may be nonspecific. Lumbar puncture results are more characteristic of a parameningeal focus with mild pleocytosis that can be neutrophilic or mixed, and elevated CSF protein. In superior sagittal thrombophlebitis secondary to bacterial meningitis, CSF Gram stain and culture can be diagnostic. Blood cultures should be drawn prior to administration of broad spectrum antibiotics in all cases of suspected suppurative venous thrombosis and may be positive in patients with a more fulminant presentation.

Results that confirm the diagnosis

  • Abscess/drainage culture:material obtained at the time of surgery that was cultured for aerobic/anaerobic bacteria and fungi is diagnostic. Histopathologic staining of infected tissue may be additionally confirmatory.

What imaging studies will be helpful in making or excluding the diagnosis of parameningeal infection?

Neuroimaging is the diagnostic modality of choice for suspected parameningeal infection

  • Subdural empyema: neuroimaging is the diagnostic procedure of choice for subdural empyema given the high degree of sensitivity and for means of planning surgical intervention. Contrast-enhanced computed tomography (CT) or MRI can identify a crescent-shaped or elliptical area of hypodensity adjacent to the falx cerebri or beneath the cranial vault. Imaging may reveal loculations within the hypodensity or associated mass effect. Edema related mass effect includes displacement of midline structures, effacement of basilar cisterns, and flattening of cortical sulci. MRI has greater sensitivity for smaller subdural empyema, and for locations at the base of the brain, the posterior fossa and along the falx cerebri. Both imaging modalities will detect sinusitis and otitis, but MRI is preferred if spinal subdural empyema is a consideration. $$$–$$$$

  • Cranial epidural abscess: similar to subdural epyema, a contrast-enhanced CT scan or MRI are essential to the diagnosis of cranial epidural abscess and MRI is the preferred modality. MRI can distinguish lentiform or crescentic collections overlying the cerebral convexity or within the interhemispheric fissure. Compared with CT scans, MRI can better differentiate sterile postsurgical effusions and hematomas. $$$$

  • Suppurative thrombophlebitis: a contrast-enhanced CT scan may demonstrate an empty delta sign of darkened thrombus in the vessel lumen surrounded by enhancement of the surrounding wall. MRI may demonstrate adjacent areas of cerebral edema, and an acute thrombus appears isointense on T1-weighted images and hypointense on T2-weighted images with absence of the flow void signal. Magnetic resonance venography (MRV) is more sensitive than contrast-enhanced CT or MRI and can demonstrate loss of signal followed by absence of flow within the thrombosed sinus. However, MRV is usually performed in conjunction with contrast-enhanced CT or MRI in order to better visualize the paranasal sinuses, and evaluate for subdural or epidural infection and cerebral infarction. $$$–$$$$

    Approximate cost ($ = 60–125, $$ 125–500, $$$ 500–1,000, $$$$ >1,000)

What consult service or services would be helpful for making the diagnosis and assisting with treatment?

If you decide the patient has a parameningeal infection, what therapies should you initiate immediately?

General treatment approach

  • Subdural empyema: optimal approach involves surgical drainage by bur hole or open craniotomy and empiric parenteral antibiotic therapy. Drainage allows relief of mass effect and the ability to obtain aerobic and anerobic bacterial cultures of purulent material that will ultimately guide antibiotic choice.

  • Cranial epidural abscess: as with subdural empyema, a combined medical and surgical approach is necessary for the treatment of cranial epidural abscess. Given the more indolent nature of cranial epidural abscesses and the likelihood of encountering a more thickened and tenacious purulence, open craniotomy or craniectomy is preferred over bur hole placement.

  • Suppurative thrombophlebitis: surgery is often required and targeted at draining the initial source and this is particularly the case for cavernous sinus thrombosis secondary to paranasal sinusitis. Mastoidectomy is often performed for suppurative lateral sinus thrombosis if mastoiditis is present. Anticoagulation is recommended if central venous thrombosis is truly aseptic but remains controversial in suppurative thrombophlebitis with greatest risk being intracranial hemorrhage.

Principles of anti-infective therapy: initial Gram stain and culture of the aspirated pus will guide final antibiotic choice. Parenteral antibiotics are continued for 3 to 6 weeks depending upon clinical resolution and the need for repeat surgical drainage or exploration. Given the increase in methicillin-resistant Staphylococcus aureus and the finding of coagulase negative staphylococci in up to 5% of cases of subdural empyema, vancomycin is typically added to the combination of a third generation cephalosporin and metronidazole for community acquired subdural empyema and cranial epidural abscess. In the postneurosurgery setting, a cephalosporin with coverage of Pseudomonas aeruginosa or meropenem is preferred. Given the spectrum of anaerobic activity of meropenem when used, metronidazole is not required. Empiric regimens are detailed below.

1. Anti-infective agents

If I am not sure what pathogen is causing the infection what anti-infective should I order?

  • Community acquired subdural empyema or cranial epidural abscess: we recommend a third generation cephalosporin such as cefotaxime 3 to 4g every 8 hours, or ceftriaxone 2g every 12 hours plus metronidazole at 7.5mg/kg (usually 500mg) every 6 hours plus vancomycin at 15 to 20mg every 12 hours.

  • Postneurosurgery or penetrating trauma: we recommend an anti-pseudomonal cephalosporin such as cefepime at 2g every 8 hours or ceftazidime at 2g every 8 hours plus metronidazole at 7.5mg/kg (usually 500mg) every 6 hours plus vancomycin at 15 to 20mg/kg every 12 hours. Alternatively, meropenem at 2g every 8 hours can be substituted for the anti-pseudomonal cephalosporin and metronidazole.

  • Suppurative thrombophlebitis: bacterial pathogens are similar to those observed with community acquired subdural empyema and cranial epidural abscess, but overall staphyloccoci are more prevalent and particularly so for suppurative cavernous sinus thrombosis; therefore, empiric therapy should always include vancomycin. We recommend a third generation cephalosporin such as cefotaxime 3 to 4g every 8 hours, or ceftriaxone 2g every 12 hours plus metronidazole at 7.5mg/kg (usually 500mg) every 6 hours plus vancomycin at 15 to 20mg every 12 hours, until cultures and susceptibility can guide therapy.

Pathogen-specific treatments for intracranial infection are summarized in Table I. Certain species are unlikely to be involved in isolated subdural empyema or cranial epidural abscess, but rather may be observed with associated brain abscess.

Table I.

Pathogen specific treatment for intracranial infection.
Organism Medication Dose Alternative
Streptococci* Penicillin GCeftriaxoneCefotaxime 20–24 million units/day (divided every 4 hours)2–4g/day (divided every 12 hours)12g/day (divided every 6 hours) Vancomycin 15–20 mg/kg (divided every 12 hours)
Methicillin-sensitive Staphylococcus aureusMethicillin-resistant S. aureus Nafcillin or oxacillinVancomycin Nafcillin 9–12g/day (divided every 12 hours)Vancomycin 15–20mg/kg (divided every 12 hours) VancomycinTrimethoprim-sulfamethoxazole (if sensitive); 15–20mg/kg trimethroprim (divided every 6 hours) (if sensitive)
Fusobacterium spp. Penicillin G 20–24 million units/day (divided every 4 hours) Clindamycin 2.4–4.8g/day (divided every 6 hours)
Prevotella spp. Metronidazole 30mg/kg (divided every 6 hours) Clindamycin 2.4–4.8g/day (divided every 6 hours)
Listeria monocytogenes Ampicillin 12g/day (divided every 4 hours) Trimethoprim-sulfamethoxazole; 15–20mg/kg trimethroprim (divided every 6 hours)
Haemophilus influenzae CeftriaxoneCefotaxime 2–4g/day (divided every 12 hours)12g/day (divided every 6 hours) Aztreonam 6–8g/day (divided every 6 to 8 hours)Trimethoprim-sulfamethoxazole; 15–20mg/kg trimethroprim (divided every 6 hours)
Enterobacteriaceae CeftriaxoneCefotaxime 2–4g/day (divided every 12 hours)12g/day (divided every 6 hours) Aztreonam 6–8g/d (divided every 6 to 8 hours)Trimethoprim-sulfamethaxazole; 15–20mg/kg trimethroprim (divided every 6 hours) (if sensitive)
Pseudomonas aeruginosa CeftazidimeCefepime 6g/day (divided every 8 hours)6g/day (divided every 8 hours) Meropenem 6g/day (divided every 8 hours)Aztreonam 6–8g/day (divided every 6 to 8 hours)
Actinomyces spp. Penicillin G 20–24 million units/day (divided every 4 hours) Clindamycin 2.4–4.8g/day (divided every 6 hours)
Nocardia spp. Trimethoprim-sulfamethoxazole 15–20mg/kg trimethroprim (divided every 6 hours) Meropenem 6g/day (divided every 8 hours) or imipenemAmikacin 15mg/kg (divided every 8 hours)Ceftriaxone or cefotaximeMinocycline
Mycobacterium tuberculosis Isoniazid +Rifampicin +Pyrazinamide +Ethambutol 300mg (every 24 hours) +600–900mg (every 24 hours) +15–30mg/kg (every 24 hours) +15mg/kg (every 24 hours)
Candida spp. Amphotericin B deoxycholateLiposomal amphotericin B 0.6–1.0mg/kg (every 24 hours)5mg/kg (every 24 hours) Fluconazole 800mg (every 24 hours)
Aspergillus spp. Voriconazole 8mg/kg (divided every 12 hours) Amphotericin B deoxycholate 1.0mg/kg (every 24 hours)Liposomal amphotericin B 5mg/kg (every 24 hours)
Mucorales (Zygomycetes) spp. Amphotericin B deoxycholateLiposomal amphotericin B 1.0mg/kg (every 24 hours)5mg/kg (every 24 hours) Posaconazole 800mg (divided every 6 to 8 hours)
Scedosporium spp. Voriconazole 8mg/kg (divided every 12 hours) Posaconazole 800mg (divided every 6 to 8 hours)
Cryptococcus neoformans Amphotericin B deoxycholateLiposomal amphotericin B 0.6–1.0mg/kg (every 24 hours)5mg/kg (every 24 hours) Fluconazole 800mg (every 24 hours)
Toxoplasma gondii Pyrimethamine +Sulfadiazine 25–75g (every 24 hours) +4–6g (divided every 6 hours) Pyrimethamine 25–75g (every 24 hours) + Clindamycin 2.4–4.8g/day (divided every 6 hours)Pyrimethamine 25–75g (every 24 hours) + Atovaquone or Dapsone; Trimethoprim-sulfamethoxazole; 15–20mg/kg trimethroprim (divided every 6 hours)

Surgery and other therapeutic modalities

  • Subdural empyema: the decision between bur hole or open craniotomy must be individualized to patient presentation and anatomic location of the abscess. Early subdural empyema when pus is more liquefied and less tenacious may be adequately treated with bur hole drainage or limited craniectomy, but this stage can be difficult to predict based on neuroimaging. Patients with a high risk of surgical mortality, such as those presenting in septic shock, may only safely be treated with bur hole drainage, but may require multiple bur holes. In contrast, craniotomy may be the only option for patients with posterior fossa subdural empyema. Many patients, regardless of initial approach with bur hole or craniotomy, will require reoperation. Once stabilized, the otorhinologic source may also require surgical correction.

  • Cranial epidural abscess: given the more indolent nature of cranial epidural abscesses and the likelihood of encountering a more thickened and tenacious purulence, open craniotomy or craniectomy is preferred over bur hole placement.

  • Suppurative thrombophlebitis:

    • Surgery: surgical drainage or removal of the infected source is often necessary, but it is highly dependent on the affected sinus and the original site of the infection. For instance, mastoidectomy is often performed for suppurative lateral sinus thrombosis if mastoiditis is present.

    • Anticoagulation: early anticoagulation with unfractionated heparin may be beneficial with broad spectrum antibiotics for isolated cavernous sinus thrombosis, in order to prevent the spread of thrombus to other sinuses. Pre-existing intracranial hemorrhage is a contraindication. Duration of anticoagulation has varied from 2 weeks to as long as thrombus resolution with transition to oral anticoagulant. Anticoagulation has proven ineffective for lateral sinus thrombosis.

What complications could arise as a consequence of a parameningeal infection?

What should you tell the family about the patient's prognosis?

  • Subdural empyema and cranial epidural abscess: survival rates among patients with subdural empyema are more than 90% if the patient is not comatose at presentation. Regardless of presentation, 10 to 45% of patients will have long-term neurological sequelae.

  • Suppurative thrombophlebitis: prior to antibiotic therapy, the mortality rate from suppurative intracranial thrombophlebitis approached 100%. More recent series have placed mortality rates at 0 to 15% for septic lateral sinus thrombosis and 10 to 30% for septic cavernous sinus thrombosis. However, individual outcomes vary considerably depending on the extent of the predisposing infection. Outcomes remain poor for suppurative sagittal sinus thrombosis, with the mortality rate reported as high as 78% in one series.

What pathogens are responsible for this disease?

  • Subdural empyema and cranial epidural abscess: polymicrobial infections are common with both aerobic and anaerobic streptococci predominating. Staphylococci are less frequently cultured (10–15% of cases) and followed in prevalence by aerobic gram-negative bacilli, and non-streptococcal anaerobes. For instance, Propionibacterium acnes has been increasingly reported following penetrating head trauma and after neurosurgery with the use of dural allograft material. It is important to note that no organism is isolated in up to 30% of cases and organisms cultured from the paranasal sinuses do not correlate with those isolated from subdural cultures. Rare cases of cranial subdural empyema have been reported secondary to Mycobacterium tuberculosis.

  • Suppurative thrombophlebitis:

    • Bacterial pathogens: the likely pathogens are dependent upon the source of the initial infection. Staphylococcus aureus is isolated in the majority of cases of suppurative cavernous sinus thrombosis. Streptococci, anaerobes including Fusobacterium necrophorum, and gram-negative bacilli are most commonly associated with lateral sinus thrombosis. Polymicrobial infections are frequently encountered [see Table II].

    • Fungal pathogens: suppurative venous sinus thrombosis has been observed in the neutropenic host with rhinocerebral mucormycosis or invasive aspergillosis.

How do these pathogens cause parameningeal infection?

Subdural epyema/cranial epidural abscess: infection of the subdural space occurs following sinusitis by spread through valveless emissary veins with or without associated thrombophlebitis, or by extension of an epidural abscess nearby a site of osteomyelitis of the skull. In contrast to the epidural space in which the dura is tightly opposed to the cranium, once infection has penetrated the subdural space it may proceed unimpeded over large portions of the brain. When secondary to meningitis the initial predisposition is likely a sterile subdural effusion that becomes secondarily infected, which then may involve the epidural space.

Suppurative thrombophlebitis: the dural venous sinuses and cranial veins do not contain valves, and flow is determined by pressure gradients. For instance, bacteria entering the facial veins must traverse the cavernous sinuses and the petrosal sinuses before entering the internal jugular vein. Most commonly, cavernous sinus thrombosis is secondary to infection of the frontal, ethmoid, or sphenoid sinuses, but can be observed with dental abscesses, orbital cellulitis, or infections of the middle third of the face. Lateral sinus thrombosis can be observed in the presence of both acute and chronic otitis media, whereas infection of the inferior and superior petrosal sinuses may arise from otitis media or mastoiditis. The superior sagittal sinus may become infected following trauma to the scalp, after another infection of the subdural or epidural space, or after bacterial meningitis.

WHAT'S THE EVIDENCE for specific management and treatment recommendations?

Osborn, MK, Steinberg, JP. "Subdural empyema and other suppurative complications of paranasal sinusitis". Lancet Infect Dis. vol. 7. 2007. pp. 63-7.

(An exemplary case is presented with review of the suppurative complications of sinusitis.)

Tunkel, AR, Mandell, GL, Bennett, JE, Dolin, R. "Subdural empyema, epidural abscess and suppurative intracranial thrombophlebitis". Principles and Practices of Infectious Diseases. Churchill Livingstone. 2010.

(A comprehensive review of epidemiology, pathophysiology, clinical manifestations, diagnosis, and treatment.)

Wispelwey, B, Petersen, KM, Schlossberg, D. "Intracranial suppuration". Clinical Infectious Diseases. Cambridge University Press. 2008.

(An accessible review also covering brain abscess.)

Southwick, FS, Richardson, EP, Swartz, MN. "Septic thrombosis of the dural venous sinuses". Medicine (Baltimore). vol. 65. 1985. pp. 82-106.

(An excellent review of clinical manifestations based on involved sinus.)

Bales, CB, Sobol, S, Wetmore, R, Elden, LM. "Lateral sinus thrombosis as complications of otitis media: 10-year experience at the Children’s Hospital of Philadelphia". Pediatrics. vol. 123. 2009. pp. 709-13.

(Case series of pediatric lateral sinus thrombosis, highlighting cranial neuropathy as presenting sign and recent otitis media as historical feature.)

Hartman, BJ, Helfgott, DC, Weingarten, K, Scheld, WM, Whitley, RJ, Marra, CM. "Subdural empyema and suppurative intracranial phlebitis". Infections of the Central Nervous System. Lippincott Williams & Wilkins. 2004.

(A comprehensive review of epidemiology, pathophysiology, clinical manifestations, diagnosis, and treatment.)

Ebright, JR, Pace, MT, Niazi, AF. "Septic thrombosis of the cavernous sinuses". Arch Intern Med. vol. 161. 2001. pp. 2671-6.

(An accessible review focusing on the cavernous sinuses.)

Weon, Y-C, Marsot-Dupuch, K, Ducreux, D, Lasjaunias, P. "Septic thrombosis of the transverse and sigmoid sinuses: imaging findings". Neuroradiology. vol. 47. 2005. pp. 197-203.

(A case series of neuroradiographic findings including representative images.)

Manolidis, S, Kutz, JW. "Diagnosis and management of lateral sinus thrombosis". Otol Neurotol. vol. 26. 2005. pp. 1045-51.

(A case series describing the current management of septic otogenic lateral sinus thrombosis.

Fillippidis, A, Kapsalaki, E, Patramani, g, Fountas, KN. "Cerebral venous sinus thrombosis: review of the demographics, pathophysiology, current diagnosis, and treatment". Neurosurg Focus. vol. 27. 2009. pp. 1-10.

(A review encompassing septic and noninfectious thrombosis with focus on management.)

Nathoo, N, Nadvi, SS, Gouws, E, van Dellen, JR. "Craniotomy improved outcomes for cranial subdural empyemas: computed tomography-era experience with 699 patients". Neurosurgery. vol. 49. 2001. pp. 872-8.

(A large, retrospective case series demonstrating improved outcome with craniotomy for subdural empyema.)

Dill, SR, Cobbs, CG, McDonald, CK. "Subdural empyema: analysis of 32 cases and review". Clin Infect Dis. vol. 20. 1995. pp. 372-86.

(A case series highlighting clinical presentation, treatment, and outcome.)

Chu, RM, Tummala, RP, Hall, WA. "Focal intracranial infections due to Propionibacterium acnes: report of three cases". Neurosurgery. vol. 49. 2001. pp. 717-20.

(A small case series describing association of P. acnes with neurosurgical procedures and an indolent and delayed presentation.)
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