Sialadenitis with sialolithiasis

Findings

Uptake image series: Normal thyroid uptake. Symmetric radiotracer visualized in the sublingual glands. Expected radiopharmaceutical by the bilateral parotid glands and right submandibular gland. Increased uptake in the left submandibular gland. Increased radiopharmaceutical visualized in the oral cavity.
L lat washout and R lat washout image: Unchanged symmetric activity in the thyroid gland. Expected washout and decreased radiopharmaceutical in the parotid glands and right submandibular gland. Decreased washout in the left submandibular gland.
15 min post lemon image: Decreased washout of the radiopharmaceutical in the left submandibular gland with normal washout in the remaining salivary glands.

Differential diagnosis:
- Sialadenitis
- Warthin's tumor
- Oncocytoma
- Oxyphilic adenomas


Diagnosis: Sialadenitis with sialolithiasis

Follow-up: Patient subsequently had her left submandibular gland surgically removed. In the operating room they found a calcified stone in the parenchyma of the gland.



Key Points

Nuclear sialography is used to assess the function of the salivary glands. CT and US are used for structural information. CT and US can be used to differentiate masses from inflammation and benign from malignant. US-guided fine needle biopsy has a high degree of accuracy.
The salivary glands consist of three paired exocrine glands. The parotid glands empty into the oral cavity through Stenson's duct. The submandibular glands empty through Wharton's ducts. The sublingual glands are the third type and connect to the oral cavity through multiple small ducts.
Rinsing the mouth with water before Tc99m-pertechnetate increases retention in the salivary gland and delays its secretion into the oral cavity. Patient is placed in the seated position with the head tilted back to prevent superimposition of the thyroid gland. A dynamic blood flow study should be performed, followed by sequential 1 minute images for 60 minutes. This should demonstrate simultaneous, symmetric uptake of the three paired exocrine glands.
The salivary gland is then subjected to gustatory stimulation with a lemon or with a 1:1 lemon juice to water mix (rinse for 5 seconds and spit). Normally see rapid symmetrical and complete resolution of radiopharmaceutical from the salivary glands. It is useful to obtain lateral views of the head and neck to confirm radiotracer in the saliva of the oral cavity after gustatory stimulation.
Warthin's tumor (papillary cystadenoma) appears as a focal region of increased uptake. Oncocytomas and oxyphilic adenomas are other tumors which may have increased radiopharmaceutical uptake. Increased uptake could also be seen with acute inflammation.
Metastatic lesions appear as focal regions of decreased uptake. Also seen with cysts, enlarged lymph nodes, and chronic inflammatory disease. Could also result from congenital aplasia, obstructive sialolithiasis, trauma, or radiotherapy.
Mixed benign tumors are the most common type of tumor of the salivary glands and may present as focal areas of increased or decreased signal.
With Sjögren's syndrome, there may be asymmetric arrival or delayed accumulation of radiotracer. There may be absent or decreased response to gustatory stimulation, especially the submandibular glands. The presence of high Ga-67 concentration in the lacrimal and salivary glands in pathognomonic for Sjögren's syndrome. A poor response to gustatory stimulation can also be seen with systemic connective tissue disease and viral parotitis or mumps, or following radiotherapy. Failure to excrete radiotracer is seen in stenosis or blockage of the salivary duct.

Vein of Galen malformation

Findings

Figure 1 and Figure 2: Digital subtraction angiography. Left vertebral artery injection (lateral and frontal projections) demonstrating multiple dilated posterior thalamoperforating arteries filling a large sacular structure and early venous sinus enhancement.
Figure 4 and Figure 5: Fluoroscopic lateral and frontal images demonstrating a coil mass in the venous varix.
Figure 6: 3D TOF MRA demonstrating early filling of a dilated falcine vein and dural sinus via enlarged branches of the anterior and posterior cerebral arteries. The previously noted varix has been coiled and is no longer noted.
Figure 7: T1-weighted sagittal image demonstrating susceptibility artifact from coil material within the varix and a dilated falcine vein and dural sinus.

Differential Diagnosis:
- Vein of Galen malformation
- Childhood dural arteriovenous fistula
- Arteriovenous malformation
- Complex developmental venous anomaly


Diagnosis: Vein of Galen malformation


Vein of Galen malformation (VOGM) can result from
- a pial arteriovenous malformation with deep venous drainage (type 1, choroidal)
- a direct arteriovenous fistula (type 2, mural)
- a combination of both.

VOGM is often a misnomer because the median prosencephalic vein of Markowski is typically involved in the malformation. Arterial supply is usually from the thalamoperforating arteries, anterior cerebral branches, and branches from the posterior cerebral artery, including the posterior choroidal arteries.

The neonatal form of this malformation arises during weeks 6-11 of fetal development when an arteriovenous connection between primitive choroidal vessels and the median prosencephalic vein of Markowski (a temporary drain for the choroids plexus) occurs. The abnormal flow through this connection slows the regression of this embryonic vein, therefore preventing the formation of the vein of Galen. The persistant median vein usually drains into the sagittal sinus via a persistent falcine vein and the straight sinus fails to form.

Children and adults usually present with headaches, seizures, hemorrhage or focal neurologic symptoms. Neonates most commonly present with high output heart failure and seizures, and may have a striking cranial bruit. Mass effect, hydrocephalus, parenchymal loss, intracranial venous stenosis, and steal phenomena leading to ischemia are all sequelae of untreated VOGMs, all increasing morbidity and mortality despite early treatment.

MRA/MRV is as an invaluable imaging tool, helping both to preliminarily map for endovascular procedures and to subsequently monitor for successful therapy. After stabilizing the neonate with medical therapy, endovascular treatment is employed, with embolization options including coils and acrylics. A venous approach is more common due to complications with femoral artery catheterization in neonates; however, an arterial approach appears to be more successful. Multiple endovascular embolizations are often needed. Heart failure responds favorably to embolization. Refractory hydrocephalus may require shunt placement. Endovascular embolization has shown to decrease morbidity and mortality when compared to surgical repair in patients without evidence of cerebral parenchymal damage or multisystem failure.

Dystrophic intracranial calcifications

Findings

Figure 1 and Figure 2: Axial non-contrast enhanced CT images of the brain reveal bilateral symmetric hyperdense areas consistent with calcification involving the basal ganglia, thalami, and dentate nuclei of the cerebellum.


Diagnosis: Dystrophic intracranial calcifications


Most cerebral calcifications are located in the basal ganglia. Additional sites of intracranial calcification include the thalami, dentate nuclei of the cerebellum as well as the subcortical white matter.

The differential diagnostic considerations for basal ganglia calcification are extensive. The most common cause is idiopathic and of no clinical significance, often seen as an incidental finding as in this case. Physiologic calcification occurs with aging and is commonly noted in patients greater than 40 years of age. Thus, biochemical testing is rarely performed unless indicated by additional features. Endocrine disorders such as hypoparathyroidism and hyperparathyroidism also result in intracranial calcification. Other etiologies include metabolic disorders as in Fahr disease (familial cerebral ferrocalcinosis) which is associated with variable neurological manifestations including progressive deterioration of motor function and psychological impairment. Post inflammatory states also account for calcification and may be seen in the setting of infection with neurocysticercosis, tuberculosis or congenital HIV. Traumatic conditions such as birth anoxia, hypoxia, and cardiovascular events may also result in intracranial calcifications. Finally, cases are also seen with toxic poisoning as in chronic lead exposure.

Radiographically, calcification is readily apparent on non-contrast CT examination as high attenuation in the aforementioned structures. As CT easily depicts calcium, this is the preferred modality for localizing and evaluating the extent of calcifications.

Congenital ectopia of the posterior pituitary with anterior pituitary hypoplasia

Findings

Along the tuber cinereum, a 5 mm hyper intensity is noted on precontrast T1 images. The area shows homogenous, hyper intense signal on post contrast sequences. The pituitary infundibulum is threadlike and midline. The anterior pituitary gland is hypoplastic and located in the sella. It shows homogenous enhancement.

Differential diagnosis:
- Ectopia of the posterior pituitary
- Craniopharyngioma
- Rathke cleft cyst
- Sarcoid
- Trauma
- Langerhans cell histiocytosis


Diagnosis: Congenital ectopia of the posterior pituitary with anterior pituitary hypoplasia


Discussion

Ectopia of the posterior pituitary is a rare congenital anomaly. The anterior pituitary is often hypoplastic. Patients often will present with panhypopituitarism and short stature secondary to growth hormone deficiency. Those patients with a visible pituitary stalk typically present with isolated growth hormone deficiency. On the other hand, those with absent pituitary stalks will present with multiple hormonal deficiencies. Hypopituitarism has been associated with breech delivery, genital abnormalities, hypoglycemia, single central incisor and jaundice. Even if not initially present, complete anterior pituitary hormone deficiency can develop during a patient's teens or twenties.


Radiologic Overview

MRI is the imaging modality of choice to study the anatomic relationships that exist in the pituitary-hypothalamic region. Both pre and post contrast T1 weighted images should be obtained. The best imaging planes are sagittal and coronal. Fat suppression imaging can also be useful as the bright signal associated with the posterior pituitary will not typically suppress.

Located in midline at the median eminence, the ectopic posterior pituitary gland will either be T1 hyper intense or isointense on precontrast images. It is posterior and inferior to the optic chiasm. On post contrast images, it will appear hyper intense. The sella will either be hypoplastic or completely absent. Similarly, the anterior pituitary will be hypoplastic or absent. As mentioned above, identifying the presence or absence of the pituitary stalk is important as it correlates with the degree/ type of hormonal abnormality.

Cochlear otospongiosis

Findings

There are focal lytic plaques in the pericochlear bony labyrinth bilaterally. The internal auditory canals and vestibular systems appear normal in size and configuration. Each cochlea completes 2.5 turns. Incidental (unrelated) fluid was seen within the right middle ear and right Prussak’s space as well as the right mastoid air cells.

Differential diagnosis:
- Cochlear otospongiosis (AKA otosclerosis)
- Osteogenesis imperfecta tarda
- Paget's disease
- Fibrous dysplasia
- Osteoradionecrosis
- Congenital otosyphilis


Diagnosis: Cochlear otospongiosis


Key points

Cochlear otospongiosisis a primary lytic disease of the endochondral layer of bony labyrinth. Best diagnosed by temporal bone CT.
It is characterized by focal ovoid lytic plaques (aka focal demineralization) in the pericochlear bony labyrinth that can become confluent. The bony labyrinth can have a "halo" appearance with more severe, confluent disease.
As the disease progresses, it can spread to other potions of the labyrinth including the lateral walls of the internal auditory canals.
Cochlear otospongiosis is the less common form (15%). Fenestral otospongiosis far more common (85%).
Fenestral form often coexists with cochlear form but the reverse is not true.
Patients typically present with progressively worsening hearing loss (conductive in fenestral form and mixed conductive and sensorineural in the cochlear form). The cochlear form is bilateral and symmetric in 85% of cases.
The etiology of the disease is unknown as is the exact cause of associated hearing loss. It is postulated that sensorineural hearing loss may result from compromise of the spiral ligament or by protease production that is toxic to cochlear nerve cells.
Early treatment for cochlear form is fluoride. If bilateral and severe disease is present, cochlear implants may be considered.

CNS tuberculosis

Findings

Figure 3, Figure 4, and Figure 5: Post contrast MR images show multiple coalescent ring-enhancing lesions in the left side of the midbrain and pons and in the interpeduncular and suprasellar cisterns.
Figure 1 and Figure 2: These lesions are markedly hypointense on T2-weighted images with surrounding perilesional edema.


Diagnosis: CNS tuberculosis


Tuberculous meningitis is the most common manifestation of CNS tuberculosis across all age groups.
The combination of brain parenchymal lesions and meningeal enhancement is highly suggestive of tuberculosis.
Central areas of hypointensity on T2 WI should suggest tuberculosis or fungal disease.
CNS involvement is seen in 5 % of patients with tuberculosis (TB) but prevalence increases in immunocomprised patients, being seen in up to 15% of cases of AIDS- related TB. Approximately 30 % of TB patients are HIV positive.

The disease is found primarily in children and young adults. A history of previous extracranial TB is elicited in 60%, but only 30% have concomitant manifestations of TB outside the CNS at presentation.

CNS tuberculosis usually results from hematogenous spread, often from a pulmonary source. However, it may result from direct rupture or extension of a subependymal or subpial focus (Rich focus) and may be located in the meninges, brain, or spinal cord.

CNS tuberculosis can manifest in a variety of forms, including:
- tuberculous meningitis
- tuberculomas
- tuberculous abscesses
- osteomyelitis of the skull or spine, often with associated epidural abscess

Tuberculous meningitis is the most common manifestation of CNS tuberculosis across all age groups. The typical radiographic finding is abnormal meningeal enhancement, usually most pronounced in the basal cisterns. This is best seen at gadolinium-enhanced MR imaging. Appearances usually resolve relatively quickly with adequate treatment; however, radiographic resolution is delayed if there are thickened exudates. The common complications of tuberculous meningitis are communicating hydrocephalus, ischemic infarcts or cranial nerve involvement, most commonly affecting the second, third, fourth, and seventh cranial nerves.

The acid-fast bacilli disseminate hematogeneously and lodge at the gray- white matter junction and form tuberculous granulomas. Tuberculous abscess formation with central liquefaction is rare and reflects a poor host immune response.

There are 4 stages in the evolution of tuberculomas:
- 1. Cerebritis stage: non specific edema, ill-defined enhancement
- 2. Solid, granulomatous stage: enhancing nodules with surrounding edema
- 3. Central caseation stage: central hypointensity on T2- peripheral enhancement
- 4. Involution stage- multiple calcified lesions

CNS tuberculosis has a mortality rate as high as 30 %; in HIV positive patients, it is up to 80 %. Serial imaging is useful to assess response to therapy.

Vertebral artery dissection and basilar artery thrombosis

Findings

Figure 1: Hyperdense basilar artery and edema involving the brainstem, left cerebellum with partial effacement of the fourth ventricle.
Figure 2: Hyperdense basilar artery and edema involving the brainstem, left cerebellum and left occipital lobe with near complete effacement of the fourth ventricle.
Figure 3: Edema in the left occipital lobe. Effacement of the quadrigeminal plate and right ambient cistern. Dilation of the temporal sweeps of the lateral ventricles. Normal vascular attenuation of the left posterior cerebral artery.
Figure 4 and Figure 5: DWI and ADC map shows restricted diffusion in the brainstem, bilateral superior cerebelli, and left occipital lobe.
Figure 6: 3D MIP MRA shows normal flow related signal in the normal right vertebral artery and complete lack of flow in the contralateral left vertebral artery.
Figure 7: 3D MIP MRA: Lack of normal flow signal in segment IV of the left vertebral artery and left PICA. Abrupt loss of signal in basilar artery. Normal signal in right VA and right PICA.


Diagnosis: Vertebral artery dissection and basilar artery thrombosis


Although once thought to be a rare occurrence, spontaneous dissection of the verterbral artery has become increasingly recognized as a cause of posterior circulation infarction, largely due to the advent of MR angiography. In recent literature, VAD has been shown to be the underlying etiology in up to 40 percent of posterior fossa ischemic strokes. VAD is seen 3 times more commonly in females. Predisposing factors include hypertension, and collagen vascular disease such as Ehlers-Danlos disease and Marfan syndrome, but is not uncommonly seen in completely healthy individuals, often in the setting of minor neck trauma. The most studied association is chiropractic spinal manipulation, but VAD has been described in various other minor traumas such as: yoga, ceiling painting, nose blowing, and judo.

The underlying abnormality in spontaneous VAD is thought to be an expanding hematoma within the vessel wall and, as a result, on CT angiogram an intimal flap is not always seen (unlike larger artery dissection where contrast commonly tracks into the false lumen). Patients with VAD often present with occipital headaches and nuchal pain, and when ischemia occurs, typically have vertebrobasilar symptoms. The dreaded consequence of VAD is hemodynamically significant vertebral artery stenosis/thrombosis, distal thomboembolism and subsequent ischemia. VAD carries a 10% mortality rate in the acute phase.

The vertebral artery is divided into 4 segments:
- Segment I begins at the vertebral artery origin, at the craniodorsal aspect of the subclavian artery, and extends to the transverse foramen of cervical vertebra (typically at C6 or C5)
- Segment II of this artery is defined as the segment that lies entirely within the transverse foramina from C5/C6 extending to the C2 level
- Segment III is the tortuous segment which exits the C2 transverse foramen, courses around the posterior arch of C1 and passes between the atlas and occiput
- Segment IV is the intracranial segment; it begins as the artery that pierces the dura and then continues until it joins the contralateral vertebral artery at the vertebrobasilar junction


Segment III is the most common site for spontaneous VAD.

Imaging findings in VAD include abrupt narrowing of the vessel lumen, as commonly seen on CTA. A hyperintense intramural hematoma may sometimes be seen on noncontrast axial T1 weighted imaging with fat-saturation, when blood products are in the subacute phase (methemoglobin). On occasion, it may also be termed the “crescent sign” because of its morphology. Signs of posterior fossa infarction can perhaps be seen on CT and MR even at the time of initial presentation. Mass effect from acute infarcts may lead to brain herniation, as in the patient presented herein.

Otospongiosis

Findings

Figure 1 and Figure 2: Axial CT images of the bilateral temporal bones show marginal thickening of the stapes footplate and prominent focus of loss of normal bone at the fissula ante fenestrum.
Figure 3 and Figure 4: Axial CT images of the bilateral temporal bones show prominent focus of loss of normal bone at the fissula ante fenestrum.
Figure 5: Coronal CT image of the left temporal bone shows prominent focus of low attenuation at the fissula ante fenestrum.


Diagnosis: Otospongiosis


Otospongiosis is the disease responsible for most adult cases of conductive hearing loss.
Initially starts at the anterior margin of the oval window (fissula ante fenestrum, site of predilection).
The “Schwartze sign” is a vascular hue behind the tympanic membrane seen on otoscopy

Otospongiosis is a primary focal spongifying disease limited to the temporal bones of humans that occurs when the dense, ivorylike endochondral bone is replaced by spongy, highly vascular irregular foci of haversian bone tissue. Lesions can arise in almost any region of the labyrinthine capsule, but about 90% of the time develops in the fissula ante fenestrum. This so-called “area of predilection” is a cleft of fibrocartilaginous tissue just anterior to the oval window.

Otospongiosis is the disease responsible for most adult cases of conductive hearing loss. Clinically, patients present with unexplained bilateral, progressive hearing loss. On otoscopy, clinicians can see a vascular hue behind the tympanic membrane, termed the “Schwartze sign”. Fenestral otospongiosis is limited to the margins of the oval and round windows, causing conductive hearing loss. In rare instances, the disease is diffuse and spreads to the inner ear otic capsule, termed cochlear otospongiosis and causes progressive sensorineural hearing loss. Otospongiosis may be difficult to distinguish from Paget’s disease on histology, however Paget’s disease demonstrates diffuse skull base involvement. Otospongiosis, which describes the active disease process, is a better term than otosclerosis which is the chronic (sclerotic), healing phase.

Noncontrast CT is the primary diagnostic tool and findings include a radiolucent focus seen at the anterior margin of the oval window which spreads through the otic capsule and thickening of the stapes footplate. Treatment includes stapedectomy followed by prosthesis insertion. As the disease progresses to cochlear otosclerosis, rates of success decline.

Brain death due to subarachnoid hemorrhage

Findings

Figure 1: Noncontrast cranial CT with high density material in the subarachnoid spaces and fourth ventricle compatible with hemorrhage. Loss of the gray matter/white matter differentiation consistent with diffuse cerebral edema is also identified.
Figure 2: Noncontrast cranial CT with high density material in the subarachnoid space and layering dependently in the occipital horns of the lateral ventricles compatible with hemorrhage. Loss of the gray matter/white matter differentiation consistent with severe cerebral edema is again identified.
Figure 3: This coronal image from a CT angiogram demonstrates absent intracranial arterial blood flow compatible with brain death. The superficial temporal arteries (branches of the external carotid arteries) are patent. High density material can be seen in the subarachnoid spaces compatible with hemorrhage.
Figure 4: This static image obtained following the administration of 99mtechnetium-ECD demonstrates absent intracranial radiotracer accumulation compatible with brain death. Note dense accumulation of tracer at the level of the midface, consistent with the "hot nose" sign.


Diagnosis: Brain death


The diagnosis of brain death is predominantly a clinical diagnosis made at the bed side. The criteria require that certain clinical conditions be met, such as a core temperature above 32°C, as well as a neurologic examination demonstrating the absence of brain function. In cases where these criteria cannot be met other means of diagnosis may be employed. These methods include an electroencephalogram (EEG), cerebral angiography, magnetic resonance angiography (MRA), computed tomographic angiography (CTA), and brain scintigraphy.

Documentation of the absence of cerebral perfusion is one method of diagnosing brain demise when clinical criteria are not met. This can be accomplished in several ways including, conventional angiography, CTA, and brain scintigraphy. The pathophysiology behind the findings demonstrated on these studies has to do with the cerebral edema associated with brain demise. This edema causes an elevation in intracranial pressure (ICP) such that it exceeds the mean arterial pressure (MAP), and thus cerebral blood flow is impeded. This finding is well demonstrated in the following equation: cerebral perfusion pressure = MAP - ICP. False negatives may occur with either examination in the presence of a ventricular shunt, trauma, a recent surgical procedure to lower ICP, and open cranial sutures. Each of these lower ICP and thus allow cerebral perfusion.

Images obtained from a CTA will demonstrate absent blood flow beyond the extracranial internal carotid and vertebral arteries; the external carotid arteries and its branches should remain patent. Likewise, brain scintigraphy may also be performed to confirm the diagnosis. Technetium 99m-labeled hexamethylpropyleneaminoxime (99mTc-HMPAO) or 99mTc-labeled ethylene L-cysteinate dimer (99mTc-ECD) are two perfusion agents that made be used. As their names imply, these perfusion agents demonstrate uptake in perfused tissues. In the presence of cerebral demise, the dynamic and static images will demonstrate the absence of radiotracer above the skull base. The bolus of radiotracer will fail to perfuse the intracranial internal carotid and cerebral arteries. Relatively increased flow through the maxillary branch of the external carotid artery will cause relatively increased radiotracer accumulation in the nasal region, resulting in the “hot nose” sign, which is best seen on the anterior static images. While this finding has been observed in as many as 52% of patients diagnosed with brain death, it cannot in itself indicate brain death.

In conclusion the diagnosis of brain demise is important in the care of patients and their families. While this diagnosis is primarily one made clinically, imaging studies can allow for accurate diagnosis when clinical criteria cannot be met.

Scheuermann’s disease (adolescent kyphosis)

Findings

Sagittal T1 and T2 weighted, and STIR MRI images of the thoracic spine demonstrate exaggerated thoracic kyphosis, with multiple levels of mild anterior vertebral body wedging, anterior disc space loss (with anterior disc bulging), disc desiccation, endplate irregularity, and Schmorl’s nodes. Axial image demonstrates increased AP diameter of the vertebral body. Coronal images show a mild thoracic dextroscoliosis.

Differential diagnosis:
- Scheuermann’s disease (adolescent kyphosis)
- Osteochondrodystrophy
- Developmental notching of anterior vertebrae


Diagnosis: Scheuermann’s disease (adolescent kyphosis)


Key Points

Vertebral osteochondrosis.
Kyphotic deformity of the thoracic (75%) or thoracolumbar (25%) spine in teenagers (onset at puberty).
Disorder consisting of vertebral wedging, endplate irregularity, and narrowing of intervertebral disk space.
Anterior wedging of vertebral body > 5 degrees.
Increased AP diameter of vertebral body.
Kyphosis of > 40 degrees. Loss of lordosis. Scoliosis.
Schmorl's nodes (intravertebral herniation of nucleus pulposus into vertebral body.
Anterior wedging of at least 1 vertebral body; usually 3-5 vertebral bodies involved.
Prevalence – 31% of male, 21% of female patients with back pain.

Normal pressure hydrocephalus

Findings

Substantial enlargement of the 3rd, 4th, and lateral ventricles. Relative normal appearance of sulci for age. No evidence of substantial vascular pathology.

Differential diagnosis:
- Normal pressure hydrocephalus
- Obstructive communicating hydrocephalus
- Acute lacunar infarct
- Vitamin B12 deficiency
- Atrophic ventriculomegaly
- Multi-infarct dementia


Diagnosis: Normal pressure hydrocephalus


Key points

Classical clinical triad of dementia, gait disturbance, and urinary incontinence is seen with normal pressure hydrocephalus.
Symptoms result from distortion of white matter by distended ventricles.
Patients commonly have a history of prior SAH or meningeal infection.
Gradient between ventricular system and subarachnoid space due to incomplete subarachnoid block.
Radiographic key: Diffuse ventriculomegaly out of proportion to sulcal prominence.
Not a radiographic diagnosis. Diagnosis made by improvement of symptoms after shunting.
Radioisotope cisternogram shows early entry into the lateral ventricles with persistence at 24-48 hours and delayed ascent to parasagittal regions.
Flow void can be seen through the aqueduct of Sylvius on MR due to increased flow velocity.

Spinal epidural lipomatosis

Findings

Figure 1 and Figure 2: Sagittal T1 FLAIR and T2 FSE with fat saturation demonstrate an abnormal amount of epidural fat which suppresses on the T2 weighted images following the signal characteristics of the subcutaneous fat.
Figure 3 and Figure 4: Axial T1 FLAIR sequences demonstrate an abnormal amount of epidural fat which is deforming the dural sac in the characteristic geometric “Y-shaped” configuration seen with spinal epidural lipomatosis.
Figure 5 and Figure 6: Axial T2 FSE sequences again demonstrate an abnormal amount of epidural fat deforming the dural sac in the characteristic “Y-shaped” configuration.


Diagnosis: Spinal epidural lipomatosis


Spinal epidural lipomatosis is a disorder characterized by an abnormal accumulation of unencapsulated adipose tissue in the extradural space of the spinal canal. The distal lumbar spine and the mid and distal thoracic spine are the most commonly involved sites, with rare involvement of the cervical spine. Most cases have been attributed to long standing exogenous steroid administration, however idiopathic and non exogenous steroid related causes have been reported including: Cushing disease, Cushing syndrome, hypothyroidism, pituitary prolactinoma and obesity.

Patients often will present with back pain, lower extremity weakness and radiculopathy resembling a herniated disk. However, symptoms will be dependent on the level of the cord or nerve root involvement. Bowel and bladder incontinence have been reported, but are felt to be rare complications.

Men have been reported to be involved more frequently than women, comprising 75% of the reported cases. The mean age in the reported literature is 43 years, with the youngest reported case involving a 6-year-old boy.

Radiographic examination may demonstrate thinning of the pedicles and lamina as well as widening of the spinal canal, indicating the possibility of increased spinal pressure. Myelography will demonstrate constriction of the dural sac from an epidural structure over several segments. CT manifestations can include an excess or increased amount of fat attenuation tissue in the spinal canal, most often posterior in the thoracic canal with anterior displacement of the thecal sac and spinal cord, while it often involves the ventral, dorsal and lateral aspects of the lumbar spinal canal. MRI examination displays the increased epidural soft tissue with signal characteristic of fat on T1 and T2 weighted sequences. The dural sac will often have a characteristic geometric “Y-shaped,” polygonal spiculated or stellar deformation resulting from the presence of the meningovertebral ligaments.

Therapeutic options include conservative or surgical interventions. Conservative therapy includes weaning of patients form exogenous steroids, treatment of endogenous corticosteroid overproduction or weight loss. Surgical intervention would include laminectomy with resection of the excessive epidural adipose tissue.