Colloid cyst

Findings

Head CT: A 7 mm diameter homogeneous hyperdense mass is present at the foramen of Monroe. There is no hydrocephalus or areas of hemorrhage.
Brain MRI: An approximately 7 mm in diameter homogeneous mass is identified within the anterior-superior third ventricle near the foramen of Monroe, slightly lateralizing to the right. It posteriorly displaces the anterior aspect of the internal cerebral veins and superiorly displaces the adjacent anterior septal veins, right more so than left. It demonstrates slight T1 shortening and appears isointense to the brain on FLAIR and fast spin-echo T2-weighted sequences. No definite contrast enhancement is identified. There is no suggestion of obstructive hydrocephalus.

Differential diagnosis:
- Colloid cyst
- Meningioma
- Ependymoma
- Choroid plexus papilloma


Diagnosis: Colloid cyst


Discussion

Colloid cysts are rare brain lesions that account for approximately 1-3% of primary intracranial tumors. The typical location is in the anterior superior third ventricle. Rare cases have been reported in the lateral ventricles, fourth ventricle, and even outside the ventricular system. Diagnoses usually occurs incidentally in adult patients. Very rarely diagnosed in children. Colloid cysts originate during the development of the nervous system from ectopic endodermal elements which migrate into the velum interpositum. These lesions are lined by cuboidal or stratified columnar epithelium and contain proteinaceous components. This lining accounts for the enhancement that is sometimes seen as in this case. The proteinaceous material is derived from the breakdown products and secretions of the epithelial cells.

In many patients, colloid cysts remain clinically silent. They enlarge slowly or stop growing, allowing a balance to develop between the production and absorption of CSF. Even with this slow growth some patients experience signs and symptoms of hydrocephalus due to the obstruction of the foramina of Monro. They experience headache, memory deficits, and nausea/vomiting. The headache is often positional because the foramina of Monro may only become obstructed in certain positions as the cyst is often somewhat mobile. Cases of sudden death have been reported. Although these lesions are benign, they are often surgically managed since the complication of obstructive hydrocephalus may be life threatening.

On CT scans, most are hyperdense to the brain although they are not calcified. Occasionally, they may be hypodense or isodense. The appearance on MRI is variable as well. Most lesions have high signal intensity on T1 and low signal intensity on T2, though they may vary from high to low intensity on both T1 and T2. Thin rim enhancement occasionally is seen as in this case.


Key Points

Typically arise at the anterior superior portion of the third ventricle
Hyperdense on CT and generally have high signal intensity on T1 and low intensity on T2
May obstruct the foramina of Mono, causing hydrocephalus
Associated with acute / severe / positional headache, and may result in sudden death.
Headache worsens by tilting patient's head forward, causing Foramen of Monro obstruction. This is called Brun phenomenon.

Right MCA thrombus leading to acute infarction

Findings

Figure 1: Noncontrast head CT demonstrates high attenuation within the right MCA corresponding to thrombus.
Figure 2, Figure 4, and Figure 6 : T2, FLAIR, and DWI images demonstrate high signal on all sequences, representing high water content (swelling, cytotoxic edema) and restricted diffusion.
Figure 3, Figure 5, and Figure 7 : T2, FLAIR, and DWI images, respectively, demonstrate hyperintensity in the region of infarct.


Diagnosis: Right MCA thrombus leading to acute infarction


Cerebrovascular accident (CVA), or stroke, is caused by disruption of blood flow to an area of the brain as the result of infarction or hemorrhage. Atherosclerosis as the primary cause, early diagnosis and intervention are critical to limit morbidity and mortality. CT can be unremarkable during the first few hours of acute ischemic stroke.

Early acute subtle findings include loss of gray/white differentiation (e.g. “insular ribbon” sign), effacement of cortical sulci and a hypodense area (secondary to cytotoxic edema) corresponding to a particular vascular distribution, which is the middle cerebral artery approximately 50% of the time. Less frequently, increased attenutation of an arterial segment indicating presence of thrombus may be identified (as in this case). Similar acute changes representing brain swelling are also noted on MR. Acute stroke manifests as areas of DWI hyperintensity within one to two hours. If contrast enhancement is utilized, intravascular enhancement is commonly seen during the first week. Typically noted at 1 to 3 days, enhancement of the involved vessel is thought to be due to slow flow or vasodilation leading to stasis of gadolinium. Thus, MR intravascular enhancement helps identify early strokes and dates them to less than 11 days old.

On the other hand, parenchymal enhancement typically begins after the first week when intravascular enhancement is waning and indicates a more subacute event.

T1 and DWI changes typically precede changes on T2 and FLAIR sequences which develop within hours of the ischemic event. T2 changes develop 6 to 12 hours postictus and result from increased water content in the infarcted tissue (cytotoxic edema). FLAIR allows heavy T2 weighting, suppressing free water signal from CSF, increasing the conspicuity and hyperintesity from ischemia.

In the chronic phase (> 30 days) further decrease in mass effect and eventual resolution of parenchymal enhancement is seen. Encephalomalacia and loss of enhancement are characteristic.

Toxoplasmosis

Findings

Figure 1: Foci of vasogenic edema are appreciated in the left fronal lobe
Figure 2, Figure 3, Figure 4, and Figure 5: Diffusion, FLAIR, T2, and T1 weighted MR images respectively show vasogenic edema with an underlying ring lesion suspected.
Figure 6 and Figure 7: Post contrast T1 weighted axial and coronal images demonstrate a ring enhancing lesion with a relatively thin rim centered at the grey white junction with surrounding vasogenic edema.
Figure 8: Pulsed arterial spin labeled sequence that provides quantitative cerebral blood flow values shows decreased perfusion in the lesion.
Figure 9: Single voxel MRI spectroscopy obtained with a TE of 35 shows a dominant lipid peak at 1.3 ppm (yellow arrowhead) with depression of the normally expected metabolites including choline at 3.2 ppm, creatine at 3.0 ppm and N-Acetyl aspartate (NAA) at 2.0 ppm. This spectra is characteristic of toxoplasmosis and shows no characteristic features of a neoplastic process.

The patient was treated for toxoplasmosis and showed significant improvement in her mental status as well as interval decrease in the size and edema associated with the ring enhancing lesion.


Diagnosis: Toxoplasmosis


In the patient with HIV, a frequently encountered diagnostic dilemma is the ring enhancing lesion. On conventional MRI sequences in the immunocompromised patient, lymphoma and toxoplasmosis can have similar appearances. Historically nuclear medicine thallium or PET imaging studies have helped differentiate the two entities.

Toxoplasmosis and primary CNS lymphoma, the two most common etiologies of focally destructive brain lesions in AIDS, can share identical presentations clinically [headache, seizures, focal neurologic deficits] and radiologically [ring-enhancing lesion(s) with surrounding vasogenic edema on CT or MR]. Prognosis and treatment vary greatly; toxoplasmosis patients can respond dramatically to antibiotic therapy while lymphoma patients typically survive <1 year even when treated. Serology, polymerase chain reaction, SPECT and PET, response to treatment, and biopsy have been used to differentiate these entities. However, MR perfusion and spectroscopy are fast noninvasive ways to help differentiate these diseases and direct appropriate initial therapy in AIDS patients with acute focal neurologic deficits.

Perfusion analysis in enhancing areas of lymphoma demonstrates an increase in relative cerebral blood volume (CBV) and maximum perfusion, thought to be secondary to greater vascularity in active areas of tumor growth, while enhancing areas of toxoplasmosis demonstrate a decrease in CBV. Central areas of necrosis and surrounding vasogenic edema in both diseases typically show decreased CBV, secondary to avascularity in areas of necrosis and to vasoconstriction in surrounding edematous brain.

Spectroscopy in lymphoma demonstrates a markedly elevated choline peak in enhancing solid areas of tumor, with less pronounced increases in lactate and lipid. In contrast, spectroscopy in toxoplasmosis demonstrates marked elevation of lactate and lipid peaks with significant depression of normal brain metabolites. As with perfusion, necrotic areas of lymphoma and toxoplasmosis may demonstrate similar spectral patterns.

Historically, SPECT and PET have helped differentiate toxoplasmosis and lymphoma, demonstrating hypometabolic activity in the former and hypermetabolic activity in the latter. However, MR perfusion and spectroscopy have demonstrated congruent results with the capability of evaluating the entire brain at once with higher spatial resolution, avoiding additional contrast and radioactivity, and adding only a few minutes to the MR acquisition time.

Multiple myeloma with extramedullary plasmacytomas

Findings

Figure 1: Axial section from a non-contrast head CT at the level of the orbits shows an oval-shaped soft tissue mass involving the right lateral rectus muscle consistent with an extramedullary plasmocytoma.
Figure 3, Figure 4, and Figure 5: There are bifrontal lytic bone lesions with soft tissue components consistent with plasmacytomas as well as additional lytic lesions in the calvarium.
Single AP view of the CXR (not showed) shows a Mediport in place. There are multiple old rib fractures as well as an old fracture of the right clavicle.


Diagnosis: Multiple myeloma with extramedullary plasmacytomas


Multiple myeloma is characterized by malignant single clone of plasma cells with a wide spectrum of manifestations. The malignant clone of plasma cells secretes malignant paraprotein (heavy and/or light chain immunoglobulin) which in turn leads to a variety of clinical consequences. The peak incidence of multiple myeloma is between 50-60 years of age. The pathophysiology of myeloma is diverse. Over proliferation of plasma cells may hinder production of normal marrow elements resulting in anemia, thrombocytopenia and leukopenia. There is impaired humoral immunity secondary to an inadequate complement of antibodies. Overproduction of clonal antibodies leads to hyperviscosity, amyloidosis and renal failure. Plasma cell proliferation may result in soft tissue tumors (plasmacytomas) or lytic lesions within bone producing pain, pathologic fractures and hypercalcemia.

The diagnosis of multiple myeloma rests on three clinical criteria: (1) M-protein in the serum and/or urine. Electrophoresis of the serum and/or urine reveals increased monoclonal immunoglobulin in the blood or light chains in the urine. Paraprotein levels directly correlate to tumor burden (2) Clonal bone marrow plasma cells or plasmacytoma (3) Related organ or tissue impairment (hypercalcemia, renal insufficiency, anemia, or lytic bone lesions). Myeloma may have a variety of presentations in the skeleton: a permeative pattern, purely lytic lesions (as seen in this case), or as a bubbly lytic lesion i.e. medullary plasmacytoma. Because the solitary bony lesions of myeloma are purely lytic, they may not be conspicuous on bone scan. Skeletal lesions in myeloma involve the hematopoetic axial skeleton i.e. skull, spine and pelvis.

Plasmacytomas are masses of clonal plasma cells involving the bone (medullary) or soft tissue (extramedullary). These entities can be found independent of myeloma, however, medullary plasmacytomas progress to myeloma in 50-60% of patients while the extramedullary variety progresses to myeloma in 11-30% of patients. Plasmacytomas may precede clinical evidence of myeloma by 3-5 years. Medullary plasmacytomas arise from the bone marrow. The most common presentation of medullary plasmacytomas is pain related to bony destruction. Medullary plasmacytomas may present as solitary lytic lesions with a narrow zone of transition on plain radiographs. Rarely, they present as a lucent lesion of bone resembling aneurysmal bone cyst or giant cell tumor. Sclerotic appearing plasmacytomas are associated with POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes). On magnetic resonance imaging, medullary plasmacytomas are low in signal on T1 and high in signal on T2 weighted-images.

Extramedullary plasmacytomas arise from submucosal plasma cells. Eighty percent of extramedullary plasmacytomas occur in the head and neck. Involvement of the nasophayrnx and paranasal sinuses is common with most symptoms related to tumor size and location. Extramedullary plasmacytomas appear as nonspecific soft tissue density on imaging studies. Because of submucosal growth, deep biopsy, open biopsy or excision is necessary for histopathologic examination. Other clinical features of myeloma must be excluded before making the diagnosis of solitary extramedullary plasmacytoma. There are three clinical stages of extramedullary plasmacytoma. Stage I is local disease. Stage II disease is characterized by regional lymph node spread or bony erosion. Stage III represents disseminated disease (including bony metastases) which carries a better prognosis then multiple myeloma. Primary treatment of symptomatic plasmacytomas is radiotherapy. Recurrence is common for which additional treatment with surgery or chemotherapy may be considered.

Floor of the mouth abscess causing early symptoms of Ludwig angina

Findings

Figure 1: Contrast enhanced axial CT at the level of the hyoid bone demonstrates complex cystic mass with peripheral rim enhancement and adjacent soft tissue reticulation.
Figure 2: Axial CT in bone window demonstrating the left mandibular molar dental extraction site.

Differential diagnosis:
- Branchial cleft cyst
- Neoplasm (squamous cell carcinoma)
- Cystic hygroma
- Dermoid
- Thyroglossal duct cyst
- Laryngocele
- Abscess
- Necrotic node (metastasis)
- Ranula


Diagnosis: Floor of the mouth abscess causing early symptoms of Ludwig angina


In a case of suspected oral cavity infection, the role of imaging is to evaluate the integrity of the airway and to document the presence of gas forming organisms, underlying dental infection, and possibly drainable neck abscess. Reactive or suppurative adenopathy involving the submandibular and submental nodes is commonly seen in association with oral cavity infections. As these nodes receive drainage from the chin, floor of the mouth, and the tongue, foci of infection within these regions should be sought.

Before the antibiotic era, infections at the floor of the mouth dissected inferiorly along the fascial planes into the mediastinum. Ludwig angina is a feared complication of abscess at the floor of the mouth. Ludwig angina is characterized by swelling from a rapidly spreading cellulitis of the sublingual, submental, and submandibular spaces with elevation and edema of the tongue, drooling, potentially leading to airway obstruction. The condition is odontogenic in 90% of cases and arises from the second and third mandibular molars in 75% of cases.

In this case, the patient had undergone left mandibular molar extraction two weeks prior to this presentation. She presented to the ED with mild intermittent airway discomfort and was admitted following the CT. During the incision and drainage in the operating room, the abscess was found to be in direct connection with the mandibular extraction site as the surgeon was able to express pus in the mouth by compressing the neck abscess from outside. Although this case presented early and was treated successfully, airway compromise is the leading cause of death in Ludwig angina.

Baastrup’s disease

Findings

Pseudo-articulation and close approximation of multiple hypertrophic lumbar spinous processes. Associated sclerosis and degenerative spurring. Vertebral compression deformities and vaccuum disks with prior L1 and L4 vertebroplasty.


Diagnosis: Baastrup’s disease


Key points

Baastrup's sign, aka "Kissing Spine", and many other synonyms including: Arthrosis interspinosa, diarthrosis interspinosa, kissing osteophytes, kissing spinous disease, osteoarthrosis processus spinosi vertebrarum lumbalum, osteoarthrosis interspinalis.
Hypertrophy of spinous processes of adjacent vertebral bodies in close approximation or actual contact; i.e., arthritic joints between the spinous processes.
Joints undergo reactive sclerosis/degenerative change, including formation of degenerative cysts as seen in this case.
Etiology uncertain, may be related to excessive lordosis with degeneration of intervening ligaments.
Can cause low back pain; originally described as "pain in the back when standing erect which is relieved by bending forward".
Can be associated with interspinous bursal fluid, which can extend into posterocentral epidural space and cause posterior compression of the thecal sac.
Named for Danish radiologist Christian Baastrup (1885-1950).

Orbital cellulitis and abscess secondary to dacryocystitis

Findings

Right sided preseptal soft tissue inflammation with rim enhancing preseptal and extraconal fluid collections. No definitive evidence of intraconal spread of infection, extension to the orbital apex or adjacent bony erosion.

Differential Diagnosis:
- Cellulitis with abscess
- Subperiosteal abscess
- Ethmoid mucocele
- Dacryocystocele
- Congenital/Developmental lesions: lymphangioma, dermoid cyst
- Subperiosteal hematoma
- Orbital pseudotumor
- Orbital rhabdomyosarcoma


Diagnosis: Orbital cellulitis and abscess secondary to dacryocystitis


Key points

Dacryocystitis occurs secondary to stagnation of fluid within the lacrimal sac resulting in bacterial overgrowth.
Acute dacryocystitis commonly presents as tender preseptal cellulitis and is treated with antibiotics while chronic cases usually present as painless purulent reflux from the lacrimal sac and is treated with definitive dacryocystorhinostomy.
Acute dacryocystitis most often results in preseptal cellulitis; however, orbital extension with abscess is also a known complication which can result in severe visual compromise.


Key radiologic features

MRI and CT are imaging modalities of choice, with MRI preferred when evaluating for possible intra-cranial extension.
Edema of the orbital soft tissues.
Low density fluid collection with rim enhancement.
Associated myositis represented by swelling and/or abnormal enhancement of the extra-ocular musculature.

Nasopharyngeal teratoma

Findings

Figure 1 and Figure 2: Centered within the nasopharynx, there is a large heterogeneous, soft tissue mass with associated calcifications. There is no associated bony destruction or intra-cranial extension.
Figure 3, Figure 4, and Figure 5: MRI of the brain reveals a large complex mass with sold and fatty areas centered within the nasopharynx. Areas of low signal within the mass correspond to calcifications visualized on CT images. There in no intracranial extension or visualized intracranial abnormality. A normal pituitary gland and sella turcica can be appreciated on the sagittal image (Figure 3).


Diagnosis: Nasopharyngeal teratoma


Neonatal teratomas are very rare congenital tumors which are formed from cells derived from all three embryonic germ cell layers. The incidence of neonatal teratomas is between 1:20,000 and 1:80,000 live births. Most occur in the sacrococcygeal region and only 5% are found in the head and neck region, specifically the cervical region followed by the nasopharynx. They can be associated with a cleft palate, intracranial abnormalities including hemicrania and anencephaly, other head and neck anomalies, diaphragmatic hernia and renal and vertebral anomalies.

Nasopharyngeal teratomas most commonly present with difficulties in swallowing and obstructive respiratory distress. The size and location serve as the major causes of morbidity and mortality. Rapid airway stabilization, including endotracheal intubation, cricothyrotomy or tracheotomy, is crucial in the management of these patients. After securing the airway, imaging is very useful to help differentiate this tumor from other masses. Ultimately surgical excision is the mode of treatment. These tumors are often encapsulated or pseudoencapsulated which yields excellent surgical prognosis.

The differential diagnosis for neonatal nasopharyngeal lesions is extensive and includes: teratoma, dermoid, craniopharyngioma, encephalocele, cystic hygroma, rhabdomyoscarcoma, hemangioma, lipoma, chordoma, neurofibroma, Rathke’s pouch and sarcoma botryoides.

Prenatal ultrasound can be useful in identifying a nasopharyngeal teratoma when there are signs of polyhydramnios secondary to pharyngeal obstruction. On CT and MR, these tumors are heterogeneous masses with cystic and solid components and in some cases associated calcifications. CT and MR are also important in helping to identify vascularity and intracranial extension. There may be signs of a long-standing lesion with mass effect on adjacent structures, especially distortion of the ipsilateral hemimandible and pterygoid plates.

Routine follow up is necessary for complete management. Patients should be evaluated for recurrence by physical examination and flexible nasopharyngoscopy, CT or MRI when indicated.

Dural metastasis

Additional clinical history: The patient has a history of breast cancer.


Findings

Axial FLAIR, axial T1 W pre- and post-contrast and coronal T1 W post-contrast images through the posterior fossa demonstrate an enhancing primarily extra axial mass which appears dural-based with possible extension into the underlyingcerebellar parenchyma. There was also regional mass effect resulting in acute hydrocephalic changes, inferior tonsillar herniation and effacement of the pontomedullary junction.

Differential Diagnosis:
- Meningioma
- Schwannoma
- Sarcoidosis
- Primary meningeal lymphoma
- Leptomeningeal metastases
- Acute cerebellitis
- Dysplastic cerebellar gangliocytoma


Diagnosis: Metastatic breast cancer


Key points (Posterior fossa extra-axial metastatic disease)

Adult population.
Clinical presentation may include headache, 7th and 8th nerve palsies, polycranial neuropathy, vertigo.
Most common tumors to metastasize to this area include breast, lung and melanoma.
Diagnosed with increasing frequency due to improved cancer survival.
Poor prognosis.


Key radiologic features

Enhancing lesion with meningeal and/or calvarial destruction.
Smooth thickening, nodularity, loculation, lobulation, fungating masses.
May extend into the IAC resembling acoustic tumor.

Cavum velum interpositum

Findings

There is a fluid density structure between the bodies of the lateral ventricles. The septum pellucidum is intact. This structure splays the fornices laterally.

Differential Diagnosis:
- Cavum velum interpositum (CVI)
- Cavum septum pellucidum (CSP)
- Cavum vergae (CV)
- Arachnoid cyst
- Epidermoid cyst


Diagnosis: Cavum velum interpositum


Key points

CVI is a cystic dilation of the cistern of the velum interpositum (usually a potential space)
M=F, prevalence decreases with age.
Not associated with other anomalies if found prenatally.
Usually incidentally detected. Rarely, large ones may cause obstructive hydrocephalus.
On axial images, it is a triangular shaped CSF collection between the bodies of the lateral ventricles that is below the fornices. It contains the internal cerebral veins.
Does not extend anterior to the foramina of Monro. (Distinguishes from CSP and CV).
On MR, no contrast enhancement, follows CSF on all sequences, suppresses on FLAIR and no diffusion restriction (distinguishes from epidermoid cyst).
May be indistinguishable from arachnoid cyst.
Usually no treatment needed unless symptomatic. In these cases, may be fenestrated or shunted.

Papillary thyroid carcinoma

Findings

Incidental finding on follow-up MR examination: In the left lower lobe of the thyroid, there is a hyperintense lesion on T2 STIR which was not seen on the previous exam. Ultrasound shows an irregular heterogeneous spiculated mass in the gland.

Differential Diagnosis:
- Adenoma 5-10% of nodules
- Colloid nodule
- Neoplasm
Papillary 75%
Follicular 10%
Medullary 5%
Anaplastic <5%
Hürthle cell
Metastasis (renal cell, lung, breast)


Diagnosis: Papillary thyroid carcinoma, biopsy proven


Key Points

Papillary cell is most common thyroid malignancy.
75% of thyroid malignancy.
Treated with subtotal thyroidectomy and I-131 ablation.
Typically age less than 40.
90-95% survival at 20 years.
Distant mets rare.
Local lymph node involvement does not effect prognosis.
Ultrasound is very sensitive for nodules but is not specific.

Benign US feature
- Cysts
- Solid nodule with significant cystic component
- Hyperechoic
- Peripheral hypoechoic halo
- Well defined margin
- Peripheral egg shell calcification
- Multiplicity

Suspicious US features.
- Single, solid nodule without a cystic component
- Hypoechoic
- Micro calcifications: Can be confused with inspissated colloid
- Thick peripheral halo
- Associated enlarged lymph nodes

Thyroid is very radiosensitive. As little as 10cGy may cause excess cancers.
Linear dose response curve with no evidence of a threshold at low doses.
Radiation causes an increase in all types and sizes of nodules.