Subdural empyema

Findings

A large left middle cranial fossa subdural empyema is demonstrated, with a relatively thin rim of enhancement. Internally, there is a large quantity of debris. There is mass effect, with a modest midline shift and effacement of the left lateral ventricle. Inflammatory changes are demonstrated in the left temporal bone which is likely the source of the abscess. There is diffusion restriction, not marked, consistent with abscess. There is extensive dural enhancement, along with considerable surrounding edema.

Differential diagnosis:
- Subdural empyema
- Chronic subdural hematoma
- Subdural effusion
- Subdural hygroma
- Dural metastasis


Diagnosis: Large left middle cranial fossa subdural empyema; left mastoiditis


Key points

Loculated collection of pus in subdural space
Best diagnostic clue: Extra-axial collection with contrast enhancing rim
Supratentorial typical
Infratentorial (up to 10%), often associated with mastoiditis
Crescentic typical; may be lens shaped on coronal images
CT demonstrates extra-axial collection, iso-to hyper dense to CSF on noncontrasted CT; shows strong peripheral enhancement with contrast
Best imaging tool: MR with DWI to demonstrate presence, nature, extent and complications
T1W image shows:
Extra-axial collection hyper intense to CSF
Crescentic extra-axial collection
T2WI demonstrates a lesion that is Iso-to hyper intense to CSF,
FLAIR shows a crescentic fluid collection which is hyper intense to CSF, underlying brain may be hyper intense
DWI shows restricted diffusion (increased signal intensity); Differentiates subdural empyema from subdural effusions
T1WI post contrast shows:
Prominent enhancement at margin related to granulomatous tissue and inflammation
Encapsulating membranes enhance strongly, may be loculated with internal fibrous strands
May see enhancement of adjacent brain parenchyma
MRV may show venous thrombosis seen as a lack of flow
CT may miss small collections
Complications include cerebritis and brain abscess, cortical vein and dural sinus thrombosis, and cerebral edema
Subdural empyema is much more common than epidural empyema
In older children, adults: Related to paranasal sinus disease (>2/3), in infants and young children it can be a complication of bacterial meningitis
Most common signs/symptoms include fever, headaches, meningismus, sinusitis, cerebritis
Sinus or ear infection in > 75% of cases
Confused with meningitis which may lead to delayed diagnosis
Can occur at any age
Rare, yet high mortality rate.
If subdural or epidural abscess is discovered, look also for sinusitis, otomastoiditis, dural sinus thrombosis and brain abscess
Progresses rapidly, neurosurgical emergency
Surgical drainage via wide craniotomy is gold standard

Lumbar disc extrusion with a wrapped disc

Findings

There is a left central disc extrusion at L5-S1 that causes mild to moderate left lateral recess narrowing and nerve root displacement without nerve root compression. At this level there is also contrast enhancement traversing the left laminectomy defect and encasing the disc extrusion, consistent with a wrapped disc. There is enhancement in the left lateral recess, suggesting post-operative fibrosis.

Differential diagnosis:
- Wrapped disc
- Peridural fibrosis
- Epidural abscess
- Epidural metastasis
- Nerve sheath tumor
- Disc pseudobulge
- Intervertebral disc protrusion
- Intervertebral disc extrusion
- Recurrent intervertebral disc herniation


Diagnosis: Lumbar disc extrusion with a wrapped disc


Key points: "Wrapped" disc


Disc herniation (protrusion, extrusion, or fragment) may be caused by trauma, repetitive or acute, and are a common source of pain and subsequent back surgery in the general population. In the acute phase, the herniated disc stimulates a fibrovascular response. A "wrapped disc" is the focal herniation (protrusion, extrusion, or fragment) that is encased in vascular scar tissue stimulated by this response and is evident by enhancement on contrast-enhanced T1-weighted images.

Asymptomatic or low back pain and/or radiculopathy are most common in the lumbar spine at L4-L5 and L5-S1. A wrapped disc is a post-surgical sequela, particularly following surgery for spinal stenosis in which the surgical procedure is more extensive, involving a laminectomy and a medial facetectomy.

Best imaging modality: MR (sequences: sagittal and axial T2WI and T1WI, as well as contrast-enhanced axial and sagittal T1WI)
Other imaging modalities: CT, myelography


Imaging findings

MR: Anterior extradural mass contiguous with the disc space extending into the spinal canal
*Contrast-enhanced T1WI: Peripheral enhancement surrounding the disc herniation or fragment with/without central canal, lateral recess, or foraminal stenosis and cord or nerve root impingement. (*most helpful MR sequence)
Non-enhanced T1WI: Isointense to parent disc
T2WI: Iso- to hyper intense to parent disc
General disc hypointensity and height loss at the level of the herniation, as well as postoperative changes (laminectomy defects, etc), degenerative facet disease, and osteophytes, are common associated findings.
CT:
Non-contrast CT: An anterior extradural soft tissue mass that may displace the nerve root / indent the thecal sac
Contrast-enhanced CT: Mild peripheral enhancement of the disc herniation/fragment
Myelography: An extradural mass that indents the thecal sac and nerve root sleeves
Imaging findings of other common differential diagnoses
Peridural fibrosis: Scar within epidural space after lumbar surgery that infiltrates epidural fat, causing homogeneous enhancement that diffusely surrounds the thecal sac and nerve root; increased in T2 signal relative to adjacent disc herniation
Epidural abscess: A distinct fluid collection in the epidural space with peripheral enhancement on post-contrast images, often associated with findings of diskitis
Epidural metastasis: Elongated (cranial-caudal orientation) enhancing mass with osseous involvement and may demonstrate paravertebral extension
Nerve sheath tumor: Avid enhancement surrounding the nerve root, some of which are in a "dumbbell" shape
Disc pseudobulge: Smooth generalized extension of the disc margin without a focal defect due to "uncovering" of disc related to spondylolisthesis
Intervertebral disc protrusion: Anterior extradural mass contiguous with disc space and triangular in shape with broader base than apex; no enhancement
Intervertebral disc extrusion: Anterior extradural mass contiguous with disc space by a "neck," in which this herniated disc material then widens in the epidural space
Recurrent intervertebral disc herniation: Extradural mass contiguous with intervertebral disc margin, demonstrating enhancement peripherally but without central enhancement
Treatment
Conservative: Anti-inflammatory and pain medications, avoid trauma
Surgical: Repeat surgery to remove herniated disc (protrusion, extrusion, fragment)

Intracranial pseudotumor (Tolosa-Hunt syndrome)

Findings

Increased CSF signal demonstrated by T2 hyper intensity within the right optic sheath. Nodular enhancement at the superior aspect of the right optic nerve at the orbital apex, which extends with prominent nodular enhancement posteriorly along the dural reflection of the right cavernous sinus. Asymmetric dilatation of the right superior ophthalmic vein.

Differential diagnosis:
- Meningitis
- Sarcoidosis
- En plaque meningioma
- Meningeal metastases
- Meningeal Non-Hodgkin's lymphoma
- Tolosa-Hunt syndrome


Diagnosis: Intracranial pseudotumor (Tolosa-Hunt syndrome)


Discussion

Intracranial pseudotumor (Tolosa-Hunt syndrome) is a part of a spectrum of "quasineoplastic" lesions that demonstrate orbital, intracranial, or pulmonary involvement, and include such other disorders as plasma cell granuloma and hypertrophic cranial pachymeningitis. It is a chronic granulomatous disease of unknown origin, which has been hypothesized to represent a low grade fibrosarcoma of inflammatory cells versus an autoimmune phenomenon. While Tolosa-Hunt syndrome is rare, orbital pseudotumor is the third most common ophthalmic disorder, and encompasses 5-8% of all orbital masses. Histologically, the lesions of Tolosa-Hunt demonstrate mixed lymphocytic and plasma cell infiltrate, with a variable degree of fibrosis. Lesions favor the cavernous sinus and basal meninges, although falcine and tentorial lesions have been described.

Patients with intracranial lesions are more frequently young adults, who present initially with chronic headaches or cranial nerve palsies. Patients with orbital involvement are more frequently middle-aged, and may present with painful proptosis and vision loss . Symptoms may be intractable, leading to severe disability. Untreated or unresponsive disease may progress to death. First-line treatment is invariably high-dose steroids, with radiotherapy or surgical resection reserved for patients with incomplete response to steroids .


Radiologic Overview of the diagnosis

The imaging hallmarks of Tolosa-Hunt syndrome are characterized by an enhancing, infiltrating meningeal mass, which favors the cavernous sinus or basal meninges, although falcine and tentorial involvement has been described . Focal meningeal thickening may range from just a few millimeters to a greater than 2 cm rind. With intracranial pseudotumor, orbital involvement is spared more than 90% of the time. Tolosa-Hunt remains a diagnosis of exclusion, once meningitis, en plaque meningioma, and meningeal metastases are ruled out.

The imaging modality of choice for imaging patients with Tolosa-Hunt remains MRI, although useful information may be gleaned from other modalities. On non-contrast enhanced CT (NECT), there are no specific findings to suggest the diagnosis; however, this modality may be of some value in differentiating the lesion from en plaque meningioma. On contrast enhanced CT (CECT), salient imaging findings include enhancing, thickened meninges or a curvilinear appearance of a single meningeal region. As aforementioned, MRI remains the primary modality for diagnosis of Tolosa-Hunt syndrome, and each sequence may provide critical information required to make the diagnosis. On T1WI, one may find focal thickening of the meninges that is isointense to gray matter. On T2WI, lesions are characterized as iso- to hypo intense regions of focal meningeal thickening, which may be more hypo intense as they become more fibrotic. FLAIR is of little help in making the diagnosis, but it is unlikely to demonstrate focal brain edema underlying the lesion . Contrast enhanced T1WI is the single most valuable sequence for evaluation of Tolosa-Hunt syndrome, and is characterized by diffusely enhancing region of meningeal thickening, which may range from a few millimeters to greater than 2 cm in some cases. Diffuse boney infiltrates may be appreciated on fat saturated contrast enhanced T1 sequence. While angiography is not considered a primary modality, severe disease may result in carotid artery narrowing, thus MRA may be a useful adjunct in the appropriate clinical setting.

The appropriate differential diagnosis of Tolosa-Hunt syndrome includes meningitis, sarcoidosis, en plaque meningioma, meningeal metastases, and meningeal Non-Hodgkin's lymphoma.

Hypertensive intracranial hemorrhage

Findings

Axial CT of the head shows a large hyper dense focus with peripheral hypo density in the left frontal lobe, causing sulcal effacement at the frontal cortex but no significant midline shift. Surrounding rim of low density represents edema (image 1). Unenhanced MRI of the brain shows an the same mass-like focus in the left frontal lobe, which has an isointense center with a hyper intense rim (image 2). Post gadolinium-enhanced T1 image of the brain shows no internal enhancement of this lesion (image 3).


Differential diagnosis:
- Hypertensive intracranial hemorrhage
- Ruptured arteriovenous malformation (AVM)
- Hemorrhagic intracranial mass
- Posttraumatic cerebral contusion


Diagnosis: Hypertensive intracranial hemorrhage


Acute blood appears hyper dense of unenhanced head CT.
Without a history of trauma, intraparenchymal brain hemorrhage on head CT could represent a hemorrhagic mass, a ruptured AVM, or a hemorrhagic brain tumor (primary or metastatic).
MRI with and without contrast is the best diagnostic tool for determining if a mass lesion is present, and for evaluating the age of the intracranial hemorrhage.
Acute blood products on T1 appear hypo intense to isointense (image 2), whereas subacute and chronic hematoma are hyper intense.
Neoplasms should enhance on post contrast T1. The lack of enhancement in this patient on post contrast T1 excludes neoplasm (image 3).

Sequestered disk

Findings

There is an non- enhancing ovoid mass slightly hyper intense to muscle on both T1 and T2 sequences, in the anterior epidural space at the L3 level, measuring approximatelyl 12 x 8 x 12 mm. This is not contiguous with any adjacent disks. No signal dropout on fat-saturated sequences. The mass causes severe stenosis of the left half of the spinal canal at the L3 level, compressing the left descending nerve roots. T1 and T2 hyper intensity at the endplates abutting L2-L3 disc space representing Modic Type II changes. There is intervertebral disk space height loss at L2-L3 with severe disk desiccation changes.


Differential diagnosis:
- Sequestered disk
- Extruded disk
- Failed back surgery
- Epidermoid
- Epidural abscess
- Epidural hematoma
- Lipoma


Diagnosis: Sequestered disk


A focal disk protrusion is an extension of intervertebral disc material (nucleus pulposus) beyond the vertebral margin (AP diameter < mediolateral diameter). An extruded disk is one in which the nucleus pulposus has herniated through a rent in the annulus fibrosis. The AP diameter > ML diameter, and the disk may migrate craniocaudally, but maintains attachment to the parent disk (frequently symptomatic).
When extruded disk material loses its attachment to the parent disk, it is referred to as a sequestered disk. Sequestered discs usually lodge in the anterior epidural space (AES), just anterior to the posterior longitudinal ligament, and migrate either cephalad or caudad (with equal frequency). Because there is a midline septum associated with the PLL in the AES, the fragment is usually just off midline (to the right or left). Rarely, the sequestered fragment may migrate beyond the PLL into the posterior epidural space, through the dural ( intrathecal location), or into the paraspinal muscles.
They usually resemble the parent disk on MR, with T1 hypo intense and T2 iso- / hypo intense. There may be surrounding T2 hyper intensity and a rim of enhancement from inflammatory changes.
This is a crucial diagnosis to make, as a sequestered disk is a contraindication to limited disk procedures (e.g. Percutaneous discectomy) and may result in failed back surgery.

Methotrexate neurotoxicity

Additional clinical history: Patient was diagnosed with acute lymphocytic leukemia 2 months previously. He is status post induction therapy with a negative bone marrow biopsy, and is currently receiving consolidation chemotherapy with methotrexate, and presents with right upper extremity weakness.


Findings

MR images of the brain demonstrate a focal area of diffusion restriction involving the left frontoparietal white matter. There is minimal associated T2/FLAIR hyperintensity. No associated enhancement. Remainder of the brain was within normal limits.
Imaging done four months later shows lesion has nearly resolved.


Diagnosis: Methotrexate neurotoxicity


Discussion

Methotrexate is a folic acid analogue. Its cytotoxic effects are carried out through inhibition of the enzyme dihydrofolate reductase, which reduces tetrahydrofolic acid levels, ultimately inhibiting cell division.

From bone marrow cell precursors to the quickly dividing cells of the intestinal tract, methotrexate exerts its effects on all dividing cells in the body. One of its rare side effects is CNS toxicity. The decreased folate levels achieved with methotrexate have implications on metabolism of adenosine, homocysteine, and biopterin. Low folate levels lead to a subsequent decrease in S-adenosyl-methionine(SAM) concentrations. This eventually leads to chronic demyelination and neurologic symptoms.

An additional side effect of MTX is the elevated levels of adenosine in the CSF. Adenosine is a vasodilator, which causes dilatation of cerebral vasculature resulting in neurotoxicity. The increased homocysteine levels caused by MTX have been shown to damage vascular endothelium and lead to subsequent strokes and thromboemboli. Methotrexate has also been found to cause cytotoxic edema, which is the most common cause of lesions that enhance on MRI DWI.

The neurotoxicity caused by MTX can be immediate, acute to subacute, or delayed. Symptoms of the disease can range from headache, nausea, vomiting, and fever, to transient or permanent focal neurologic symptoms. The immediate form occurs within a day of MTX administration and presents as a chemical meningitis. The acute to subacute form presents from days to weeks after administration of MTX, and presents with seizures or focal neurologic symptoms. The delayed form presents as leukoencephalopathy and a generalized decrease in higher cognitive function.


Radiological findings

A case series containing nine cases of MTX neurotoxicity revealed that lesions found in this disease tend to be focal and show up on DWI as well as T2 and FLAIR imaging. These abnormalities can continue to persist on imaging long after the symptoms have resolved. The DWI shows diffusion restriction with T2/FLAIR hyperintensity being less conspicuous.

In another independent case study on MTX neurotoxicity, MRI demonstrated restriction diffusion with no significant T2 or FLAIR signal abnormality. Based on a combination of these imaging findings, it was determined that cytotoxic edema was likely the cause of focal neurologic symptoms on the patient, and demyelination was a less likely cause based on the MRI findings.

A different case study had MRI findings showing subtle signal changes in the left centrum semiovale, with an obviously abnormal area of restricted diffusion, indicating the presence of increased fluid. The authors of this case also mentioned a relation between elevated choline levels in lesion areas with myelin breakdown.

The lesion in this disease is similar in appearance to ischemic stroke, but differs in distribution. The lesions in MTX neurotoxicity can show up in many different patterns, whereas ischemic strokes often follow a vascular distribution, helping differentiate the two.


Radiology

MRI:
MRI with DWI is the gold standard for diagnosis
Will show focal areas of demyelination and/or edema throughout the brain
Can be normal, even in the presence of symptoms
Must perform early to avoid unnecessary workup


CT:
Can be used to rule out other etiologies that may cause focal symptoms, but is not a sensitive test for demyelination and edema found with MTX neurotoxicity
Ultimately need MRI to make diagnosis as CT is often negative
Angiography
Not very useful as it is usually normal