Labyrinthitis ossificans

Findings

Figure 1: Axial CT image through the left temporal bone shows complete ossification of the left superior semicircular canal.
Figure 3: Axial CT image at the level of the internal auditory canal shows non-erosive soft tissue attenuation lateral to the malleus and incus as well as partial ossification of the lateral semicircular canal.


Diagnosis: Labyrinthitis ossificans


Labyrinthitis ossificans (LO) is the end result of suppurative labyrinthitis where inflammation of the membranous labyrinth progresses to fibrosis and ossification. Suppurative labyrinthitis typically arises following meningitis, although other causes include direct infection from hematogenous sources or trauma.

LO is the most common cause of acquired childhood deafness and can be detected by CT as early as 2 months following an episode of meningitis. Following meningitis, approximately 6% to 30% of children develop some degree of sensorineural hearing loss which is typically bilateral.

On CT, osseous deposition is seen within the membranous labyrinth. On MRI, loss of the normal high signal on T2-weighted images from displacement of the endolymphatic fluid is suggestive of this diagnosis. It is important to the clinician to distinguish between cochlear involvement, non-cochlear involvement, or both as prognosis is determined by response to cochlear implantation. The degree of ossification is important in surgical planning and severe LO may preclude cochlear implantation.

Neurovascular compression syndrome of VII-VIII cranial nerves

Findings

High resolution T2 images at the level of the internal auditory meatus demonstrate the facial and vestibulocochlear cranial nerves entering the internal auditory meatus. The facial nerve lies anterior while the eighth cranial nerves courses posteriorly. With the left side used for reference, a tortuous basilar artery is seen posteriorly displacing the normal course of the right vestibulocochlear/facial nerve complex. The presumed point of symptomatic compression is encountered posteriorly as the nerve complex “bends” over posterior aspect of the internal auditory meatus. Although sometimes seen in asymptomatic individuals, when findings are viewed in the appropriate clinical setting, NVCS should be raised as a diagnostic possibility.


Diagnosis: Dolichoectasia of the basilar artery causing right sided sensorineural hearing loss


Hearing loss can be characterized as either conductive or sensorineural based on clinical exam and audiometry. Conductive hearing loss involves an abnormality of the external auditory canal to the oval window and is best evaluated with high resolution CT as it is able to display the external auditory canal and middle ear structures, particularly the ossicles. Sensorineural deafness implies an abnormality of the inner ear, vestibulocochlear nerve, or its central components which are best evaluated with MRI.

Neurovascular compression syndrome (NVCS) refers to a group of disorders in which an aberrant or tortuous vessel causes nerve compression with subsequent hyperexcitation and neuropathy. Vascular compression syndrome has been described as a causative etiology for cranial nerves III, V, VII, VIII, and IX. Controversy exists, however, because of the normal intimate apposition of nerves and vasculature around the brainstem and the frequency with which it is seen in asymptomatic patients.

Vestibulocochlear NVCS is symptomatic vascular compression of cranial nerve VIII. Clinical symptoms are often non-specific including tinnitus, vertigo, and sensineural hearing loss. A recent article in the American Journal of Neuroradiology failed to reliably determine neurovascular compression as a cause of tinnitus although some authors maintain it may still be considered when presenting with so called "typewriter" tinnitus. In decreasing order of frequency, vessels indicated in NVCS include the anterior inferior cerebellar artery, posterior inferior cerebellar artery, and vertebral artery.

The following MRI classification system for neurovascular compression has been proposed to aid in surgical planning.
- Type I: Point compression where a limited segment of the nerve is in contact with the vessel.
- Type II: Longitudinal compression in which the nerve and vessel traverse parallel to each other.
- Type III: A vascular loop encircling the neve.
- Type IV: The nerve contour is deformed and/or thinned.

Definitive treatment involves retromastoid craniectomy and microvascular decompression in which a small synthetic sponge is interposed between the offending vascular structure and nerve.

Pars flaccida cholesteatoma

Findings

There is an 8mm mass in Prussak’s space with erosion of the malleus and scutum.

Differential diagnosis:
- Pars flaccida cholesteatoma
- Cholesterol granuloma
- Paraganglioma
- Pars tensa cholesteatoma


Diagnosis: Pars flaccida cholesteatoma


Key points

A pars flaccida cholesteatoma often occurs when a patient has chronic middle ear inflammation and/or TM perforation. The cholesteatoma forms when there is an accumulation of stratified epithelial cells in Prussak's space. The cholesteatoma can be seen in all age groups, but tend to be more aggressive in children. Patients can present with aural discharge, conductive hearing loss, and otalgia. Early treatment with surgery can preserve hearing.


Radiologic overview of the diagnosis

A pars flaccida cholesteatoma appears as a mass in Prussak's space with erosion of the scutum and/or adjacent ossicle. Ossicle erosion is seen ~70% of the cases. There is no enhancement of the cholesteatoma itself, though surrounding granulation tissue may enhance.

High resolution temporal bone CT is the best modality to evaluate a suspected cholesteatoma. A pars tensa cholesteatoma is far less common and involves the sinus tympanum. A cholesterol granuloma appears blue on otoscopy and may have similar bony erosions as that of a cholesteatoma. A paraganglioma appears as a cherry red mass on otoscopy and usually does not erode bone.

In this case, there is an 8mm mass in Prussak's space with erosion of the malleus and scutum.

Labyrinthine ossificans

Findings

On the left, there is severe ossification and encroachment of the cochlea with extension to the vestibule and semicircular canals, which are also severely involved. The cochlear aqueduct is slightly stenotic. On the right, there is peripheral osseous hyper density of the cochlea with mild encroachment.

Differential diagnosis:
- Labyrinthine ossificans
- Cochlear aplasia
- Intravestibular schwannoma
- Cochlear otosclerosis
- Labyrinthine schwannoma


Diagnosis: Labyrinthine ossificans


Key points

Most common cause of acquired childhood deafness
Most common clinical presentation – bilateral sensorineural hearing loss 2-18 months after meningitis
May also occur after other infectious, inflammatory, trauma, or surgery
After meningitis or hematogenous infection – bilateral
After otitis media – unilateral
Rarely – severe vertigo
Suppurative membranous labyrinthitis starts inflammatory cascade which leads to fibrosis and eventually ossification
Dedicated IAC/temporal bone CT best for detection
Mild – mild increased haziness in the fluid spaces of the membranous labyrinth and prominent modiolus
Severe – complete obliteration of the membranous labyrinth with bony replacement of the fluid spaces
On MR, low signal bone encroaches (mild) or obliterates (severe), high signal fluid spaces of the membranous labyrinth
Importance – must identify cochlear labyrinthitis ossificans before cochlear implant so that it may be surgically treated
Treatment – cochlear implant, or labyrinthectomy for severe vertigo

Squamous cell carcinoma of the external auditory canal

Findings

Figure 1, Figure 2, Figure 4, Figure 5 are axial and coronal T1 and T2 weighted images respectively. Figure 3 and Figure 6 are post contrast T1 weighted fat saturated images. A soft tissue mass is seen in the above images in the external auditory canal appearing isointense on T1 images and hyperintense on T2 images with post contrast enhancement. The middle ear is invaded with no intracranial extension. The internal carotid artery is uninvolved.

Differential Diagnosis:
- Squamous cell carcinoma of the external auditory canal
- Debris in the external auditory canal
- Malignant otitis externa
- External auditory canal cholesteatoma
- Keratosis obturans
- Medial canal fibrosis


Diagnosis: Squamous cell carcinoma of the external auditory canal


Carcinomas of the external auditory canal are rare and form less than 0.2% of head and neck malignancies. Various histological subtypes have been described, the commonest being squamous cell carcinoma followed by adenoid cystic carcinoma.

Squamous cell carcinoma of the external auditory canal is predominantly a disease of the elderly with slight male preponderance. Exposure to radiation therapy for head and neck malignancies, especially nasopharyngeal carcinoma, is a risk factor. The tumor is locally aggressive with a relatively lower tendency to metastasize.

Patients typically present with otorrhea, otalgia, and bloody discharge from the ear. Visible necrotic mass, swelling, tinnitus, hearing loss, facial palsy, otitis externa and otitis media are other presenting features.

Extent, description and staging of the tumor is based primarily on imaging as the region is inaccessible to a complete and satisfactory clinical examination. CT scan of the temporal bone is a routine investigation, and is done to look for bony erosion. Small tumor extent and more outer location of ear malignancy such as the auricle or external ear canal has better prognosis with a higher 5-year survival rate.

Surgical excision is the mainstay of management. There is no consensus over the surgical procedure and approaches vary from en bloc resection to piecemeal removal of the tumor. Invasion of the carotid, middle or posterior fossa renders the tumor inoperable. Any nodal involvement is regarded as advanced disease (stage III and IV) and changes the stage irrespective of the T status of the University of Pittsburgh TNM Classification.

In early stages the tumor is treated by en bloc resection, confirming negative margins, with post operative radiotherapy not offering a documented survival advantage over surgery alone. On the other hand, in advanced stages surgery is routinely followed by radiation and topical chemotherapy (5-FU mostly).

Petrous apex chondrosarcoma

Findings

The head CT (bone windows) demonstrates a region of bony destruction extending from the right petro-occipital fissure into the carotid canal. The axial T2 images demonstrate a hyper intense, extra-axial, right petrous apex mass that extends from the petro-occipital fissure to the cavernous sinus. The margins of the mass are lobulated, and it encases the cavernous internal carotid artery. The axial T1 contrast-enhanced images demonstrate intense enhancement of the mass.


Diagnosis: Petrous apex chondrosarcoma


Key points

Classic MR imaging appearance of petrous apex chondrosarcoma is a mass located at the petro-occipital fissure with high T2 signal intensity that heterogeneously enhances.
The CT shows chondroid mineralization in 50%.
Invasive bone changes at the petro-occipital fissure strongly favors the diagnosis. Greater than 50% will have associated bone destruction.
2/3 located at the petro-occipital fissure, 1/3 located at the anterior basis sphenoid
Usually has lobulated margins
High T2 signal, low to intermediate T1 signal
Heterogeneous enhancement with contrast; whorls of enhancement within tumor matrix are often seen
Often displaces or encases the ICA
Classic presentation is a CN 6 nerve palsy. Other CN palsies can occur less commonly (3, 5, 7, 8—3, 4, and 6 are possible with cavernous sinus invasion)


Differential diagnosis
- Metastatic tumor
- Chondrosarcoma
- Plasmacytoma
- Nasopharyngeal cancer
- Chordoma
- Cholesteatoma
- Calcified meningioma
- Chondromyxoid fibroma

Distinguishing characteristics from other entities in the differential:
- Metastatic tumor – Can have a similar appearance; breast cancer and prostate cancer are two of the most common tumors to metastasize to the petrous apex
- Plasmacytoma - Usually intermediate T1 and T2 signal; usually more midline
- Chordoma - Similar appearance to chondrosarcoma but often see tumor "thumb" indenting the anterior pons; often midline
- Cholesteatoma - Does not enhance but has an otherwise similar appearance
- Calcified meningioma – Not typically destructive; low to intermediate T2 signal
- Chondromyxoid fibroma - Similar MR appearance to chondrosarcoma; areas of ground glass density can be seen on CT

Mondini malformation

Findings

Non-contrast axial CT images through the temporal bones demonstrate incomplete partitioning of the left cochlea and nonvisualization of the modiolus resulting in confluency between the middle and apical segments. Compare this to the right cochlea, which is normal. There is also abnormal dilitation of the left vestibular aqueduct.


Diagnosis: Mondini malformation


Case points

Mondini malformation occurs when there is abnormal development of the cochlea resulting in less than 2.5 turns and incomplete formation of the modiolus.
It is a cause of sensorineural hearing loss.


Discussion

Mondini malformation refers to an anomaly of the cochlea in which the modiolus fails to develop properly in the seventh week of fetal life, resulting in a cochlea with only 1.5 turns instead of the normal 2.5 turns. In addition, the interscalar septum between the middle and apical segments fails to form leading to a confluent, sac-like cochlea. There is an association with an enlarged vestibular aqueduct and anomalies of the vestibules and semicircular canals. In some cases, Mondini malformation may also be associated with Pendred Syndrome (bilateral sensorineural hearing loss and goiter)

Patients present with gradual or sudden sensorineural hearing loss with preservation of high-frequency hearing because the basal turn of the cochlea is usually preserved. These patients are also at increased risk for developing meningitis or perilymphatic fistula.

Treatment revolves around clinical presentation. Cochlear implants may be used to enhance hearing while middle ear infections are treated aggressively due to the increased risk for meningitis.

Endolymphatic Sac Tumor

Findings

CT images showing an erosive lesion of the right petrous bone, centered at the right vestibular aqueduct opening (endolymphatic sac). The lesion is eroding the posteriolateral wall of the jugular fossa. There is also erosion of the posterior wall of the right IAC, however the right IAC itself is still intact. There are scattered bony spicules seen within the lesion.
Axial T1 and axial T2 precontrast images, respectively, at the level of cerebellopontine angle. There is a hyperintense multilobulated lesion occupying the right endolymphatic sac space. There is also a central area of low signal intensity which enhances post-gadolinium.
T1-weighted post-gadolinium axial and coronal images, respectively. There is a central area of enhancement indicating hypervascularity. Low-signal intensities within the lesion represent intratumoral bony spicules.

Differential Diagnosis:
- Paraganglioma (glomus jugulare)
- Cystic and papillary adenocarcinoma
- Chondroid lesions
- Cholesterol granuloma
- Metastasis
- Cystic schwannoma


Diagnosis: Endolymphatic Sac Tumor (Papillary Adenomatous Tumor of the Temporal Bone)


The endolymphatic sac is part of the membranous labyrinth derived from the neuroectoderm and located within the petrous portion of the temporal bone where it also contacts the dura. Endolymphatic sac tumors (ELST) were described in 1989 by Heffner as a unique pathologic entity originating from the epithelium of the endolymphatic sac, specifically the rugose or middle portion of the sac. ELST histology is benign and exhibits two patterns; mixed type and papillary adenomatous type. The former is generally confined while the latter demonstrates a more aggressive nature by locally invading the temporal bone. Patients most often present with sensorineural hearing loss and may also present with tinnitus, facial nerve palsy or vestibular dysfunction. ELST is a rare skull base lesion and most lesions are sporadic. However, there is an increased incidence seen in patients with von Hippel-Lindau disease (vHL), 7% of whom are diagnosed with this lesion. If ELST is seen bilaterally, vHL becomes a likely diagnosis.

ELST is a slow growing lesion which erodes the temporal bone and often presents with intratumoral bony spicules. In addition, due to the tumor’s slow growth, the petrous bone cortex expands and surrounds the lesion with a thin shell of reactive bone. The lesion may also exhibit hypervascularization, usually from a branch of the external carotid artery.

CT may show a soft tissue mass in the endolymphatic sac between the sigmoid sinus and internal auditory meatus. On MR imaging, this lesion exhibits a hyperintense focus on T1WI with an inhomogeneous signal on T2WI. Focal low signal intensities within the lesion represent bony fragments. Tumor foci may enhance on T1WI with gadolinium due to hypervascularity. Advanced lesions may spread far, making it difficult to identify the origin of the tumor and expanding the differential. Treatment is surgical resection.

Cholesteatoma

Findings

Non contrasted temporal bone CT reveals a soft tissue mass of the right tympanic membrane and Prussak’s space with associated erosions of the scutum, epitympanum walls, lateral semicircular canal, tegmen tympani and middle ear ossicles.

Differential diagnosis:
- Chronic otomastoiditis
- Acquired cholesteatoma
- Middle ear cholesterol granuloma
- Glomus tympanicum paraganglioma


Diagnosis: Cholesteatoma


Key points

An acquired cholesteatoma is a collection of exfoliated squamous epithelium and debris.
Cholesteatomas often begin at the pars flaccida of the tympanic membrane and grow in Prussak's space of the temporal bone and produce inflammatory reaction.
Cholesteatomas typically occur in the setting of chronic dysfunction of the Eustachian tubes and recurrent otitis media.
Cholesteatomas can be as small as a couple of millimeters in size or can grow to fill the entire middle ear.
Erosions of the scutum and ossicles are commonly seen.
The presence of bony erosions or expansion are strong support of cholesteatoma over chronic otomastoiditis.
Acquired cholesteatomas occur in children and adults.
Most common presenting symptoms include ear discharge, hearing loss, ear pain and vertigo.
Without treatment cholesteatomas will progressively increase in size.
Complications include: Hearing loss, CN 7 palsy, venous sinus thrombosis, semicircular canal fistulas, and intracranial invasion.
Early surgical intervention usually results in complete eradication and preservation of hearing.

Superior semicircular canal dehiscence

Findings

Figure 1: On the left, there is dehiscence of the superior semicircular canal.
Figure 2: Oblique view through the plane of the superior semicircular canal shows bone dehiscence on the left.


Diagnosis: Superior semicircular canal dehiscence


Superior semicircular canal dehiscence refers to absence of the bony roof over the superior semicircular canal. Dehiscence of the lateral and posterior canals may also occur, but is much less common. Although this may be asymptomatic, it can result in Tullio phenomenon as in this case, conductive hearing loss, or chronic disequlibrium. When symptomatic, it is often referred to as superior semicircular canal dehiscence syndrome (SCDS). Thinning of the bone over the canal is thought to predispose patients to this entity, which has been demonstrated in 2% of persons at autopsy.

Normally, the semicircular canals are a closed hydraulic system. With dehiscence of the semicircular canal, a "third window" is created. When this occurs, movement of the oval window and stapes in response to sound can result in slight movement of the covering of this third window and subsequent unphysiologic motion of endolymph in the semicircular canal.

Imaging is critical in the diagnosis of semicircular canal dehiscence, and it is only with the advancements in thin section MDCT and multiplanar reconstructions that have made effective evaluation possible. Non contrast temporal bone CT is the examination of choice. Oblique coronal reconstructions are often the most useful. MR imaging cannot be used to diagnose semicircular canal dehiscence but may be of benefit in ruling out other pathology.

Semicircular canal dehiscence is fortunately a treatable form of vestibular disturbance. A conservative approach with earplug use and avoidance of provoking stimuli may be appropriate in certain circumstances. Surgical correction varies from middle fossa craniotomy and covering of the defect with bone wax, cement, or fascia to less invasive approaches involving reinforcement of the oval and round windows to decrease their movement. Techniques are still evolving.

Nasal dermoid sinus with cyst

Findings

CT show a hyper dense mass within the lower anterior interhemispheric fissure. MR confirms the extra-axial mass within interhemispheric fissure. The mass is isointense on T1, hyper intense on T2 and does not exhibit restricted effusion. There is a tract identified extending from the bridge of the nose to the lesion, best seen on sagittal images. Mild peripheral enhancement of the lesion is noted following the administration of intravenous contrast.

Differential diagnosis for extra-axial mass in the interhemispheric fissure:
- Nasal dermal sinus with epidermoid/dermoid
- Fatty marrow in cristi galli
- Nasofrontal cephalocele
- Meningioma

Findings are most compatible with a nasal dermal sinus tract with a cyst within the interhemispheric fissure. The mass is felt to be more compatible with a cyst rather than a dermoid or epidermoid because it does not have signal characteristics of fat as seen with with a dermoid, or exhibit increased signal intensity on diffusion like an epidermoid. There is no evidence surrounding edema.


Diagnosis: Nasal dermoid sinus with cyst (presumed diagnosis).


Key points

Nasal dermoid sinus is a result of defective embryology of the anterior neuropore resulting in any combination of sinus tract with epidermoid/dermoid.
Typical presentation is a young child with pit on the skin of nasal bridge.
Other clues to the diagnosis is a bifid cristi galli and enlarged foramen cecum.
Predisposes to recurrent meningitis if left untreated.
Treatment is surgical excision.

Right petrous apicitis (Gradenigo's syndrome clinically)

Findings

CT shows an expansile, destructive lesion in the right petrous apex, which is bright on T2 weighted MR images, and has an enhancing soft tissue component on post contrast T1 weighted-images.

Differential diagnosis:
- Petrous apicitis
- Cholesterol granuloma
- Trapped fluid
- Chondrosarcoma
- Cholesteotoma
- Lymphoma


Diagnosis: Right petrous apicitis (Gradenigo's syndrome clinically)


Key points

Synonyms for petrous apicitis include apical petrositis and confluent apical petrositis.
Petrous apicitis typically occurs via spread of infection from mastoids through air cells into petrous apex.
Clinical presentation is variable; most have otorrhea and pain. Patients can have cranial neurophaties.
In kids, petrous apicitis is often a sequelae of acute otomastoiditis. In adults, it is more often due to chronic infection.
Gradenigo's syndrome is acute otomastoiditis, trigeminal (CN 5) nerve neuritis, and Abducens (CN 6) palsy (CN 6 controls the lateral rectus muscle).
Temporal bone CT and MRI are the best imaging modalities for making the diagnosis.
On CT, findings of petrous apicitis include a destructive lesion with both cortical and trabecular loss in the petrous apex.
The best clue to diagnosis is trabecular destruction in an opacified petrous apex, which is best appreciated on CT.
On MR, findings of petrous apicitis are a thick walled, enhancing area of soft tissue with fluid in the petrous apex.
Nuclear medicine Gallium-67 scan with SPECT can improve the sensitivity for disease detection and can be used to monitor response to treatment.
Petrous apicitis was a common, severe and life-threatening infection in the pre-antibiotic era. It is now relatively uncommon.
Inflammation/infection from the petrous apex can spread to meninges and cause meningitis or can lead to cavernous thrombosis.
Treatment requires antibiotics and often surgical drainage.

Gas producing otogenic brain abscess with cerebral edema and pseudosubarachnoid hemorrhage sign

Findings

Figure 1: Soft tissue windows demonstrate generalized cerebral edema with loss of grey-white differentiation and near total obliteration of the CSF spaces. An ill-defined hypodense gas containing region is present within the left temporal lobe consistent with abscess formation. The subarachnoid spaces are hyperdense especially in the suprasellar region representing pseudosubarchnoid hemorrhage associated with cerebral edema and/or pyogenic leptomeningitis, not true hemorrhage.
Figure 2: Nondependently layering air is present within the anterior horn of the left lateral ventricle indicating communication between the left temporal lobe abscess and the left lateral ventricle and CSF spaces. On soft tissue windows, normal subcutaneous fat is seen confirming that this is intraventricular air, not fat.
Figure 3 and Figure 4: Bone windows demonstrate total opacification of the middle ear cavity and mastoid air cells consistent with otitis media and mastoiditis. There is subtle bony sclerosis and remodeling which along with the patient’s history is consistent with chronic otitis media with mastoiditis. Also note that there is no evidence of fracture to suggest penetrating trauma as an etiology for these findings. Bone window confirms the presence of air, not fat, in the frontal horn of the right lateral ventricle.


Diagnosis: Gas producing otogenic brain abscess with cerebral edema and pseudosubarachnoid hemorrhage sign


Complications of chronic supurative otitis media include (in order of decreasing frequency):
- mastoid abscess
- meningitis
- postauricular fistula
- lateral dural venous sinus thrombosis
- facial palsy
- cerebellar abscess
- Bezold’s abscess (involving sternocleidomastoid muscle)
- internal jugular vein thrombosis
- epidural abscess
- perisinus abscess
- Gradenigo’s syndrome (due to petrous apicitis)
- interhemispheric abscess
- temporal lobe abscess
- subdural abscess
- serous labyrinthitis
- Luc’s abscess (subperiosteal temporal bone without mastoiditis)

Otitic meningitis is the most common intracranial complication and can occur as a result of direct disease extension from the mastoid through a cortical defect or due to retrograde thrombophlebitis despite an intact appearance of the bone. Otogenic brain abscesses usually occur in the temporal lobe and cerebellum (2:1). Nearly all otogenic brain abscesses have underlying chronic suppurative otorrhea. More than half of all otogenic brain abscesses have an associated cholesteatoma.

Although the relative incidence of complications related to chronic otitis media is debated within the literature, many authors agree that the most dangerous complication is intracranial abscess formation which carries a 40-50% mortality rate. According to Nunez et al, 1.5 % of adults have active chronic otitis media and in an adult with active chronic otitis media, the annual risk of developing an intracranial abscess is about 1:10,000 with a male to female risk ratio of approximately 3:1. Though at first glance this risk appears relatively low, the lifetime expectancy of a 30 year old person with active chronic otitis media developing an abscess is 1:200. Intracranial complications in patients with active chronic otitis media are also more prevalent in adolescents and young adults.

Radiologic evaluation of a patient suspected of having intracranial complications related to active chronic otitis media is crucial to diagnosis and management. Axial CT with contrast is the usual modality of choice preferably with thin cuts, which can demonstrate the presence or absence of an abscess as well as details regarding its size and location. An intraparenchymal mass may show parenchymal low density with mass effect with or without an enhancing capsule. CT may be limited in the setting of acute infections. MRI may improve diagnostic accuracy, with increased sensitivity and specificity.

Etiologic agents usually include anaerobes, Proteus mirabilis, Pseudomonas aeruginosa, Streptococcus, and Staphylococcus. Anaerobic and gram negative bacteria appear to be the most common causes. Consequently, in addition to surgical management, initial treatment should include broad spectrum antibiotics with good cerebrospinal fluid penetration as well as anaerobic coverage. A team approach including an otolaryngologist, radiologist, anesthesiologist, and an infectious disease specialist among others is recommended for optimal outcome.


Pseudosubarachnoid Hemorrhage Sign

A pseudosubarachnoid hemorrhage sign is an unusual neuroradiologic finding which may be present in cases of diffuse cerebral edema and/or pyogenic leptomeningitis. In addition to increased attenuation of the otherwise normal subarachnoid spaces, the falx and tentorium can also appear dense. The etiology of this presentation is unknown. Current theories include: 1) blood-brain-barrier breakdown from microorganism toxins in pyogenic meningitis allowing leakage of dense proteinaceous material into the subarachnoid spaces; 2) cerebral edema causes displacement of CSF from the subarachnoid spaces with engorgement of the superficial pial structures creating a predominantly vascular space with relatively dense intravascular blood. Since management of the causes of subarachnoid and pseudosubarachnoid hemorrhage is quite different, it is important to be able to recognize this relatively rare sentinel neuroradiologic sign.