Basilar invagination secondary to rheumatoid arthritis

Findings

Axial and sagittal CT images demonstrate severe basilar invagination (Figure 1). The tip of the odontoid process measures 2.3 cm above Chamberlain’s line (yellow line in Figure 2). McGregor's line (red line in Figure 2) is also shown. Incidentally noted are right-sided opacified mastoid air cells (Figure 1).
Once again, severe basilar invagination is evident. On the sagittal T2 image the foramen magnum is narrowed and obliteration of the CSF space is noted at the C2-C3 level (Figure 3). On the axial T2 weighted image increased T2 signal (Figure 4) is seen within the cord at the C2-C3 level indicating edema versus myelomalacia.



Diagnosis: Basilar invagination (impression) secondary to rheumatoid arthritis.


Basilar invagination refers to a condition in which the odontoid process protrudes upward into the intracranial space. Basilar invagination may be classified as primary (congenital) or secondary (acquired). Down syndrome, Klippel-Feil syndrome and Chiari malformations are congenital causes of basilar invagination. Acquired basilar invagination, also known as basilar impression, is associated with softening of the skull base and is often due to rheumatoid arthritis, Paget disease, osteomalacia, hyperparathyroidism and osteogenesis imperfecta. Basilar invagination is probably better described as a radiologic finding rather than a diagnosis. Once the finding is identified, a cause of basilar invagination should be diligently pursued.

Plain lateral radiographs with odontoid views, although not 100% sensitive, are often the initial study used to diagnose basilar invagination. MRI is the optimal study, which also assesses the cervicomedullary junction and cervical cord. Two craniovertebral junction lines are particularly useful in defining basilar invagination. Chamberlain’s line extends between the posterior pole of the hard palate and the posterior edge of the foramen magnum (opisthion). If the dens is >3.0 mm above this line basilar invagination is present. McGregor’s line, a modification of Chamberlain’s line was developed because the opisthion could not always be seen on plain radiographs. This line extends from the posterior pole of the hard palate to the undersurface of the occiput. If the dens extends >4.5 mm above this line basilar invagination is present.

Clinical manifestations of basilar invagination include posterior skull pain, headache, signs and symptoms of brainstem and upper cervical cord compression or disturbances of CSF circulation causing obstructive hydrocephalus. The brainstem may be compressed at the level of the foramen magnum possibly resulting in compromise of the autonomic centers resulting in labile blood pressures, arrhythmias, or sudden death. Neurosurgery is recommended in patients that are symptomatic with concomitant MRI findings indicating compression. Although asymptomatic patients are often followed conservatively, many authors favor surgery even if no symptoms of cord compression are evident in rheumatoid patients.

Although often appearing together, basilar invagination or impression should not be confused with platybasia; which literally means “flattening of the base of the skull”. Platybasia, which can be seen in Klippel-Feil anomalies, cleidocranial dysplasia and achondroplasia, is present when the basal angle formed by intersecting lines from the nasion to the tuberculum sellae and from the tuberculum along the clivus to the anterior aspect of the foramen magnum (basion) is greater than 143 degrees.

Ewing sarcoma of the occipital bone

Findings

Figure 1: Unenhanced CT shows a heterogeneous attenuation mass with cystic spaces in the posterior fossa.
Figure 2: Intense enhancement is noted after contrast administration.
Figure 3: Bone window section showing permeative destruction of the left occipital bone.
Figure 4: Axial T1 weighted image showing extra- axial mass with multiple cystic spaces.
Figure 5: Coronal T2 image showing the extra-axial origin clearly with mass effect on the cerebellum. The cystic spaces appear hyperintense.
Figure 6: Axial T1 weighted image showing intense enhancement of the mass.


Diagnosis: Ewing sarcoma of the occipital bone


Ewing sarcoma is a small round-cell tumor arising from mesenchymal cells. These tumors affect children and young adults in the age group of 5-15 years. The long bones, flat bones like the scapula and the vertebrae are the most common sites. Primary Ewing sarcoma affecting the calvarium is extremely rare, making just 1% of the cases. In the skull, the tumor more often arises from the frontal and parietal bones and less common locations include ethmoid, temporal and occipital bones.

CT scans (bone window) reveal poorly marginated permeative destructive lesion involving both inner and outer tables of the skull. The "onion peel" appearance typical of Ewing sarcoma in long bones is not seen commonly in the calvarium. The extra-dural soft tissue shows intense enhancement on contrast administration.

MR imaging provides better soft tissue delineation of these tumors. The extra dural soft tissue appears hypointense on T1 weighted images while the cystic and necrotic areas appear hyperintense on T2 weighted images. Good contrast enhancement is noted.
The differential diagnosis should include rhabdomyosarcoma, metastatic neuroblastoma and lymphomas.

Treatment is surgery followed by chemotherapy and radiation.

Pott's Puffy Tumor

Findings

Figure 1: The image shows a large collection anterior to the frontal bone and a large epidural abscess with peripheral enhancement.
Figure 2: Erosion of the frontal bone. Sinus tract of the bone into the large anterior collection.
Figure 3: Large collection anterior to the frontal bone.
Figure 4: Large epidural abscess.
Figure 5: Large epidural abscess with peripheral enhancement.
Figure 6: Large collection anterior to the frontal bone. Large epidural abscess. Normal bone marrow signal. Abnormal bone marrow signal in the frontal bone.
Figure 7: Large collection anterior to the frontal bone with peripheral enhancement. Large epidural abscess with peripheral enhancement.
Figure 8: Abnormal bone marrow signal in the frontal bone. There is a lack of enhancement of the frontal bone. The abnormal dark bone marrow signal on T1 images and lack of enhancement on T1 post gad fat sat is consistent with dead necrotic bone from severe osteomyelitis.


Diagnosis: Pott's Puffy Tumor


Pott’s puffy tumor is a subperiosteal abscess of the frontal bone that appears as a localized swelling of the forehead associated with frontal osteomyelitis. Pott’s puffy tumor is a complication of frontal sinusitis or trauma, which is predominatly seen in the adolescent age group. However, there are a few case reports in adults. Pott’s puffy tumor is a rare complication of frontal sinusitis in the post antibiotic era but can be seen in patients with undiagnosed or partially treated sinusitis. Patients will typically present with frontal scalp swelling, headache, fever, nasal drainage, and frontal sinus tenderness. Ocassionally, Pott’s puffy tumor can mimic findings of preseptal or orbital cellulitis. In severe cases, there will be neurologic decompensation. Varying degrees of hemiparesis, obtundation, papillary dilatation or aphasia have been described in case reports.

Imaging is necessary to exclude intracranial complications such as epidural abscess. Pott’s puffy tumor can also be associated with dural sinus thrombosis, meningitis, subdural empyema, epidural abscess, brain abscess, and rarely seizure. Intracranial infection is caused by posterior extension from the frontal sinus while preseptal and orbital cellulitis is caused by downward spread from the frontal sinus to the orbit. Younger children who do not have pneumatized frontal sinuses, are more likely to have ethmoid sinusitis. Orbital cellulitis is a more common complication in patients with ethmoid sinusitis.

Patients must be treated with a combination of surgery and long-term antibiotic therapy.

Infected 4th Branchial apparatus cyst

Findings

Figure 1: Neck CT, contrast enhanced, at level of pyriform sinus. The left pyriform sinus is effaced by an inflammatory mass.
Figure 2: Neck CT, contrast enhanced, at level of subglottic trachea. The image demonstrates continuation of the large inflammatory mass with small areas of necrosis or abscesses. Note displacement of the trachea to the right and lateral displacement of the carotid sheath vessels. Reactive lymphadenopathy is present in the internal jugular chain.
Figure 3: Neck CT, contrast enhanced, at level of the thyroid gland. The image shows a mixed attenuation mass in the enlarged left lobe of the thyroid. This mass arises from extention of the extrinsic anterior and lateral inflammatory mass with phlegmon and abscesses from an infected 4th branchial apparatus cyst.
Figure 4: Neck CT coronal reformation, contrast enhanced. There is extensive phlegmon with multiloculated abscesses, extending from the left lower pharyngeal wall into the left lobe of the thyroid gland. Reactive lymphadenopathy in the left internal jugular lymph node chain is present.


Diagnosis: Infected 4th Branchial apparatus cyst


The main differential diagnostic considerations for a cystic neck mass in children include suppurative lymph nodes, abscess, thyroglossal duct cyst, lymphatic malformation, ranula, and branchial apparatus cyst. A branchial apparatus cyst (BAC) results from maldevelopment of an embryonic branchial apparatus (branchial cleft, arch, and pouch). Embryologically, 6 mesodermal branchial arches, separated by 5 external ectodermal branchial grooves (clefts) and 5 internal endodermal branchial pouches are present bilaterally. The majority of branchial apparatus anomalies are cysts that can arise from a remnant of a groove, arch, or pouch. A 2nd BAC is the most common and accounts for >90% all branchial cleft anomalies discovered in teens and adults. It represents 66%-75% of these anomalies discovered in children.

A 1st BAC is typically found as a cystic mass around the pinna or extending from external auditory canal (EAC) to the angle of the mandible. It can communicate with the external auditory canal. The 2nd BAC is typically found at or immediately caudal to the angle of the mandible, lateral to the carotid space and anteromedial to the sternocleidomastoid muscle. An associated fistulous track may extend from the cyst between the external & internal carotid arteries to the palatine tonsil. The cyst can extend to the carotid bifurcation, producing a beaked configuration, which has been called the "notch sign" and which is considered pathognomonic for a 2nd BAC. The 3rd BAC is typically found in the posterior cervical space behind the carotid sheath in the upper neck and along the anterior border of sternocleidomastoid muscle in the lower neck.

A 4th BAC is rare and seen more often in female infants. It can occur anywhere from the apex of pyriform sinus to the ipsilateral thyroid lobe. Involvement with the thyroid can be understood by noting that the thyroid gland arises from the 4th branchial arch. The most typical imaging finding of a non-infected 4th BAC is a unilocular thin-walled cyst found adjacent to or within the superior lateral aspect of the left thyroid lobe. Ninety-four percent of BACs involve the left side of the neck. These cysts normally show minimal or no peripheral contrast enhancement and no calcification. When infected, a thickened cyst wall is seen and often enhances with intravenous contrast media. Infected cysts often develop higher attenuation than noninfected cysts on CT images. Associated thyroiditis/thyroid abscess is not uncommon. An esophagram may demonstrate fistulous communication between the pyriform sinus and a 4th BAC, providing a pathway for spread of infection. Surgical resection of the cyst and its associated sinus or fistulous tract is necessary for complete cure. Medically treated or incompletely resected cysts/tracts are prone to recur.

Adenoid cystic carcinoma with perineural spread of tumor

Findings

There is a large mass centered on the left greater sphenoid wing, extending into the left sphenoid sinus and left pterygopalatine fossa. It also extends into the left middle cranial fossa, left cavernous sinus, and left Meckel's cave. The tumor has involved V3, and foramen ovale is markedly widened on the left. There tumor has extended along the GSPN to the geniculate ganglion, and from there it has involved the tympanic and intracanalicular segments of the 7th nerve. The mass is isointense to brain on T1-weighted images and hypo- to isointense on T2-weighted images, consistent with hypercellularity. There is moderate enhancement of the mass. No macroscopic flow voids are seen to suggest a highly vascular lesion.

Figure 1: A mass lesion involving the skull base and pterygopalatine fossa on the left is shown on this axial FIESTA image. Abnormal soft tissue is seen in the left IAC as compared to fluid in the right IAC. The normal right greater wing of the sphenoid bone is shown. On the left, the greater wing of the sphenoid has been destroyed by the mass.
Figure 2: The soft tissue intensity skull base mass is again shown on the left. Infiltration of fat in the L pterygopalatine fossa is present, as compared with normal bright fatty signal in the R PPF. Asymmetrical signal is again seen in the left vs right IAC.
Figure 3: Following injection of gadolinium, moderate homogeneous enhancement of the mass lesion is shown. Also appreciated is extension into the L sphenoid sinus and displacement of the left cavernous segment of the L internal carotid artery. Meckel’s cave on the L is obliterated. Abnormal enhancement in the left IAC and abnormal thickening and enhancement of the tympanic segment of the facial nerve are also shown. Subtle linear enhancement extends posteriorly from the dominant mass along the greater superficial petrosal nerve on the left.
Figure 4: A more superior post-gadolinium image more discretely defines enhancement and enlargement of V3 on the left, posterior to the main bulk of the tumor mass. Tumor is again seen to extend posteriorly along the GSPN to the geniculate ganglion.
Figure 5: Tumor is seen to involve and expand Meckel’s cave on the left, replacing the normal CSF signal with intermediate signal intensity of a highly cellular tumor. The unaffected Meckel’s cave on the right, filled with CSF, is shown for comparison. The tumor is confined to Meckel’s cave on this image and has not extended through the dura to involve the adjacent temporal lobe.
Figure 6: A more anterior coronal T2-weighted image shows extension of the tumor into the cavernous sinus on the left, adjacent to the flow void of the internal carotid artery. Marked thickening of the third or mandibular division of the trigeminal nerve is shown on the left. The mass has markedly expanded foramen ovale on the left. This image also demonstrates atrophy and mild T2 hyperintensity of the muscles of mastication on the left, due to V3 dysfunction and resultant subacute to chronic denervation change. The masticator muscles on the right have normal bulk.
Figure 7: The enhancing tumor mass involving Meckel’s cave and the cavernous sinus on the left is again shown. This image better demonstrates the unaffected foramen ovale on the right. Also demonstrated on this image is volume loss and diffuse mild enhancement of the left temporalis muscle as compared to the right, consistent with denervation change as previously discussed). Signal drop-off due to dental hardware and inhomogeneity of the magnetic field has resulted in artifact and poor fat suppression in the right masticator space.


Diagnosis: Adenoid cystic carcinoma with perineural spread of tumor


Adenoid cystic carcinomas have a high propensity for perineural invasion and extension.
The facial and trigeminal nerves are the cranial nerves most commonly involved by perineural spread of tumor.
The facial nerve may be invaded directly by tumors of the parotid gland, or the tumor may involve the trigeminal nerve and then extend along the greater superficial petrosal nerve to reach the facial nerve.
A second “five-to-seven” connection is the auriculotemporal nerve, which also provides an important route for perineural spread of tumor.
The proximal greater superficial petrosal nerve, geniculate ganglion, and tympanic segment of the facial nerve often show normal mild enhancement due to investment by a rich vascular plexus in these regions.
Characteristics of perineural extension of tumor include abnormal enhancement and enlargement of nerves, replacement of fat in neural foramina, and widening of neural foramina. Denervation changes in innervated muscles may also be observed.


Adenoid cystic carcinoma (ACC) is the second most common malignant salivary gland tumor after mucoepidermoid carcinoma. It can arise from either the major or minor salivary glands. It is the most common malignancy of the submandibular and sublingual glands. It most commonly presents as a painless enlarging mass, though the initial presentation may be due to perineural extension of tumor (pain or paresthesia, for example) if the tumor is in a deep location. ACC is associated with a high risk of distant metastases (most commonly to the lung), and these can occur 10-20 years after initial diagnosis and treatment of the primary lesion. ACC may spread through local or direct extension of the tumor, hematogenous and lymphatic dissemination, and perineural extension.

ACC has a high propensity for perineural invasion and extension. SCCs also have a high tendency to spread perineurally, and because they are the most common head and neck cancer, one will likely encounter more cases of perineural tumor spread from SCC than from ACC in practice. Other cancers of the head and neck, including melanomas, basal cell carcinomas, and mucoepidermoid carcinomas also extend perineurally, but less commonly. Branches of the facial and trigeminal nerves are most commonly involved as they innervate the cutaneous and mucosal surfaces of the head and neck, where most tumors arise, as well as the salivary glands. The facial nerve can be invaded directly when ACC occurs in the parotid gland, or the tumor may involve the trigeminal nerve and then extend along the greater superficial petrosal nerve to reach the facial nerve. An alternate route for cranial nerve 5 to cranial nerve 7 spread (or vice versa) is the auriculotemporal nerve, which is located posterior to the neck of the mandible.

The greater superficial petrosal nerve emerges from the geniculate ganglion of cranial nerve VII carrying sensory (from the soft palate mucosa) and parasympathetic fibers. It courses anteromedially through the temporal bone and emerges through the facial hiatus. It then travels underneath Meckel’s cave and combines with the deep petrosal nerve (carrying sympathetic fibers) to form the vidian nerve. The vidian nerve travels anteriorly to the pterygopalatine ganglion, where the parasympathetic fibers synapse before being distributed to the lacrimal gland and mucosal glands of the nasal and oral cavities. This nerve pathway is vulnerable to tumor infiltration and is a common pathway for perineural extension of tumor.

Portions of the facial nerve that are invested with a rich vascular plexus may normally enhance on MRI. These normally enhancing regions are the proximal greater superficial petrosal nerve, geniculate ganglion, and tympanic segment of the facial nerve; the labyrinthine and descending mastoid segments of the facial nerve may also show mild enhancement under normal circumstances. The more distal and anterior portions of the greater superficial petrosal nerve, however, are not invested by a vascular plexus and should not enhance with contrast on MRI. Similarly, the facial nerve in the IAC does not demonstrate any enhancement under normal conditions at 1.5T. Characteristics of perineural spread to the facial nerve include thickening and abnormally intense enhancement of nerve segments, as well as replacement of fat in neural foramina by tumor. Denervation changes in the muscles of facial expression may be observed, but these are often extremely subtle due the small size of the affected muscles. Due to ACC’s high propensity for perineural spread and high tendency to recur, it is important to regularly assess for perineural extension of these tumors when MR images are being interpreted.

Sialadenitis with an obstructing sialolith in the right submandibular gland duct

Findings

Coronal and axial post contrast CT images show a swollen right submandibular gland with dilatation of the intraglandular ducts and an obstructing stone.


Diagnosis: Sialadenitis with an obstructing sialolith in the right submandibular gland duct


The most common cause of sialadenitis of the SMG is an obstructing calculus with subsequent suppurative sialadenitis. Less common causes are suppurative sialadenitis leading to duct stenosis and chronic sialadenitis. Rare etiologies include include Sjogren syndrome, AIDS and bacterial/viral infection.

SMG accounts for 10% of sialadenitis of all major salivary glands. Other diagnostic considerations in SM space include reactive submandibular lymph node, mandibular osteomyelitis, benign mixed tumor, submandibular carcinoma and metastases.

Calculi are more common in the SMG duct. Compared to the parotid gland, the saliva in the SMG is thicker, much more mucinous and more alkaline. The SMG duct courses superiorly which makes it more prone to stasis. SMG duct is larger in diameter.

When sialadenitis is present therapy may depend on stone location. If the stone is in the anterior portion of the duct, the stone can be removed and gland salvaged. If stone is in the posterior duct, the duct and gland will likely be removed with the stone.

Tornwaldt cyst

Findings

There is no intracranial hemorrhage, calvarial fracture or transtentorial herniation. On the lower images of the brain, there is a cystic hypoattenuating lesion at the posterior wall of the nasopharynx measuring 1.4 x 1.2 cm.


Diagnosis: Tornwaldt cyst


A Tornwaldt cyst is a benign proteinaceous cyst that is located in the midline of the posterior nasopharynx, superficial to the superior constrictor muscle of the pharynx. It is surrounded by adenoid tissue and arises from notochordal remnants in the pharyngeal bursa (pouch of Luschka). They are seen in up to 4% of the population (equally in males and females) and are usually asymptomatic unless they become infected. If infected, they can cause a variety of symptoms including purulent drainage, sore throat, prevertebral muscle spasms, halitosis and Eustachian tube obstruction.

These fluid-filled cysts are usually discovered on imaging (both CT and MRI) as incidental findings. The cyst is well-circumscribed and located in the midline in the posterior nasopharynx (between the longus coli muscles). On CT, it is hypo-attenuating and appears cystic. It will almost invariably appear bright on T2-weighted images. The T1 signal will vary from CSF signal to very bright hyperintensity depending on the amount of protein, fat, hemorrhage and mucus within the cyst. A thin rim of peripheral enhancement may be seen with gadolinium administration. Nasopharyngoscopy, although not necessary for asymptomatic cases, can help supplement the diagnosis.

Treatment is not necessary in most cases. For the rare symptomatic cases treatment options include surgical excision, electrocoagulation or marsupialization.

Melanotic Neuroectodermal Tumor of Infancy (MNTI)

Findings

Large mass involving left side of face with invasion, mass effect, and extensive bony involvement. The mass does not appear to cross the midline. Enhancing focus on MR adjacent to the superior aspect of the falx and superior sagittal sinus. FDG-avid spine lesions.


Diagnosis: Pathology-proven melanotic neuroectodermal tumor of infancy (MNTI)


Discussion

MNTI is a rare osteolytic, pigmented neoplasm that typically affects the head and neck, predominantly the maxilla, of infants. It is typically considered a benign lesion, with only a few reported cases of metastatic disease reported in the literature. It usually presents in the first year of life. It may appear as a rapidly expanding, non-ulcerated, lightly pigmented, blue or black lesion on the anterior aspect of the maxilla. It may extend intraorally, cause bone destruction and dislodgement of teeth.

MNTI is considered to be of neural crest origin, and some patients will high urinary excretion of vanillylmandelic acid (VMA). The tumor is typically non-encapsulated, showing local invasion of bone. The histologic appearance is similar to other cells of neural crest origin, demonstrating small, round blue cells, as well as containing a moderately vascular fibrous background. Part of the lesion may contain large polygonal cells arranged in sheets that contain melanin. Immunohistochemistry and electron microscopy can aid in the final diagnosis. The few reported cases of malignant disease have noted increased numbers of mitoses per high-powered field.

Conventional radiography may demonstrate a well-circumscribed or ill-defined radiolucency, with destruction of bone as the lesion progresses. CT can delineate the extent of soft tissue involvement and osteolysis. Contrast-enhanced MRI can demonstrate soft tissue tumors with nonenhancing, heterogeneous tissue density and can also demonstrate osseous involvement. There may be foci of T1-hyper/T2-hypointensity secondary to melanin.

Surgical excision with partial maxillectomy and 5 mm margins are typically curative, with 10-15% recurrence rates. There are no standards of care for malignant disease.

Initial biopsy of this patient's facial lesion demonstrated a high mitotic index. After 2 surgical excisions and recurrence, the patient developed intracranial and spinal column metastases. The patient underwent multiple cycles of radiotherapy and chemotherapy. The intracranial lesion was never biopsied due to the precarious location, however it has regressed, and there appears to be a slight interval decrease in size of the soft tissue component of the maxillary lesion.

Florid Cemento Osseous Dysplasia

Findings

Figure 1, Figure 2, Figure 3, and Figure 4: Mandibular and maxillary cystic lesions with central calcification, bony expansion and selective involvement of the periapical regions are noted.


Diagnosis: Florid Cemento Osseous Dysplasia


Florid cemento-osseous dysplasia is a slow growing benign lesion which is extremely aggressive and infiltrative. It involves the periapical regions of both the maxilla and mandible with a diffuse distribution of mixed lucent-opaque osseous changes. The lesions are benign fibro-osseous lesions, which histologically, represent normal bone replaced by highly cellular fibrous connective tissue and cementum. Cemento-osseous dysplasia predominantly affects females greater than males (10-14:1) with a predilection for African American patients. Treatment of these lesions should be further radiographic follow-up without surgery unless the lesions become symptomatic, necrotic, or super-infected. Odontoma would also be in the differential as it is a hamartomatous malformation composed of odontogenic tissues. These lesions are usually discovered in the 2nd decade of life and can cause impaction, malpositioning or resorption of adjacent teeth. Ameloblastoma is the most common odontogenic tumor arising from follicular epithelium, dental lamina or enamel. It is a benign lesion but extremely aggressive and infiltrative. It most commonly occurs as an expansile lesion in the posterior mandible in the region of the third molar within the 3rd to 5th decades of life. The unicystic variant occurs in adolescents and has a soap bubble like appearance and involves the ramus and posterior body of the mandible. Large tumors may erode the bony cortex and infiltrate adjacent soft tissues. More malignant processes such as osteosarcoma exhibit a more pronounced periosteal reaction, bone destruction and the presence of a soft tissue mass. Multifocal osteosarcoma is rare. Also, chronic diffuse osteomyelitis is less likely, as it is usually unilateral, associated with pain and fever, exhibits poorly defined borders and would not be exclusively confined to tooth bearing areas.

Aneurysm of the right cervical internal carotid artery causing vocal cord paralysis

Findings

CT imaging through the neck demonstrates findings suggestive of right vocal cord paralysis.
Figure 1 shows dilation of the right pyriform sinus.
Figure 2 shows thickening and medial positioning of right aryepiglottic fold.
Figure 3 shows dilation of the laryngeal ventricle.
Figure 4: CT through the skull base reveals a rounded well defined brightly enhancing mass in the right carotid space displacing the carotid and internal jugular vein.
Figure 5: MR images demonstrate flow void on T2 weighted images.
Conventional angiography confirms an aneurysm of right internal carotid artery.


Diagnosis: Aneurysm of the right cervical internal carotid artery causing vocal cord paralysis


Unilateral vocal fold paralysis (UVFP) occurs from a dysfunction of the recurrent laryngeal or vagus nerve innervating the larynx. Clinical presentation includes characteristic hoarseness often accompanied by swallowing disabilty, weak cough, and sometimes shortness of breath. Its is important to note that a high vagal lesion results in both a recurrent laryngeal nerve and superior laryngeal nerve palsy with the latter resulting in significant anesthesia of the pharynx and increasing the risk for aspiration

CT scanning or MRI should be performed as part of a workup for a unilateral vocal fold paralysis (UVFP) of unknown etiology. The imaging should include the entire path of the vagus/recurrent laryngeal nerve involved. For left unilateral vocal fold paralysis (UVFP), imaging should extend from the base of skull to the mid chest (arch of the aorta) with right sided vocal fold paralysis including the base of the skull to the clavicle.

Unilateral vocal cord paralysis can be reliably identified on cross sectional imaging. Characteristic findings include:
1. Medial positioning and thickening of the ipsilateral aryepiglottic fold.
2. Ipsilateral pyriform sinus dilatation.
3. Ipsilateral laryngeal ventricle dilatation.
4. Fullness of the ipsilateral true vocal cord.
5. Anteromedial positioning of the ipsilateral arytenoid cartilage.

Causes of vocal cord paralysis are varied with nearly 25% classified as toxic or idopathic. Post-surgical cord paralysis is another important consideration often without specific imaging findings. Identifiable causes include mass compression and or malignant invasion. Although rare, aneurysm or pseudoaneurysm of the cervical internal carotid artery should be considered in the differential diagnosis of a carotid space mass. Because of the intimate proximity of structures within the carotid space, it is sometimes difficult to definitively determine the epicenter of an enhancing lesion. However, as the resolution of cross-sectional imaging improves, preoperative characterization is increasingly possible. A demonstrable arterial connection, arterial enhancement, peripheral calcification, and flow void on MR imaging is suggestive of the diagnosis.

Pleomorphic Adenoma of the lacrimal gland

Findings

Completely ossified left lacrimal gland with no soft tissue mass, associated superficial inflammatory change or proptosis.


Diagnosis: Pleomorphic Adenoma of the lacrimal gland


Pleomorphic adenomas (benign mixed tumors) are the most common major salivary gland tumor often found in the parotid glands. When seen in minor salivary glands, the hard palate and the upper lip are the most common locations. It is, however, the most common epithelial tumor of the lacrimal gland. Approximately 50% of lacrimal masses are secondary to epithelial tumors; the other 50% are due to lymphoid and inflammatory causes. It will usually present as a palpable lacrimal fossa mass or proptosis. Other lacrimal gland tumors include: germ cell (dermoid and epidermoid), lymphoma/leukemia, metastasis, and sarcoma.

Pleomorphic adenomas are composed of epithelial and connective tissue components. Lesions may have a variable histology with growth patterns in sheets, strands, or islands of spindle and stellate cells with a myxoid configuration occasionally predominating. Cystic degeneration, squamous metaplasia, calcification or ossification may be observed in lacrimal gland pleomorphic adenomas. There may or may not be lytic remodeling or erosion of adjacent bone depending upon the chronicity of the tumor; adjacent bone abnormality does not necessarily confer malignancy. A small percentage of pleomorphic adenomas may undergo malignant transformation.