Solitary metastatic lesion of the spine

 70Y old female patient present with low back ache. MRI of the lumbo-sacral spine was performed. 

The whole spine T2 sagittal image is showing an isolated lesion involving the S2 vertebra and superior part of the S3. Lesion is appearing slightly hyperintense in T2, iso to slightly hypointense in T1 and markedly hyperintense in STIR. It is expansile, causing anterior and posterior contour bulge of the involved vertebrae and also the destruction of anterior cortex. 

Lesion is shown in the axial T2 and STIR coronal images here. T2 Axial images is showing near total obliteration of the the sacral spinal canal at the level, with marked compression of the remaining nerve roots. 

Moderate enhancement of the lesion is present with associated restricted diffusion. Features are in favor of an aggressive lesion. Signal intensity is not consistent with chordoma or Giant Cell Tumor.

Biopsy of the lesion was performed, was found out to be metastatic lesion from adenocarcinoma.  

Asymptomatic vascular compression of the cisternal segment of the facial nerve

 40 year of female patient presented with headache. No tinnitus / facial nerve palsy / hemi-facial spasm.

The above CISS 3D Axial image is showing significant anterior displacement of the cisternal segment of the right facial nerve (orange arrow) by the Anterior Inferior Cerebellar Artery (AICA) loop. AICA loop was seen coursing in between the cranial nerves VII and VIII. The focally thickened appearance of the right facial nerve is due to the AICA closely abutting the posterior aspect of the nerve at that site. No compression on the vestibulo-cochlear nerve was seen. 

Sagittal reformats of the CISS images, showing the contact of the AICA loop (orange arrow) and the facial nerve (yellow arrow). Green arrow points to the cranial nerve VIII. 

Interestingly the patient didn't have any symptoms related to the facial nerve compression at the time of the scan.

The Chavda classification of vascular loops in relation to the Internal Acoustic Canal (IAC) is: 

Type I   : Loop is present in the CP angle cistern, but not entering the IAC.

Type II  : Enters the IAC, but <50% of the length of IAC. 

Type III : Occupies > 50% of the IAC. 

Kinking or angulation of the nerve at the site of contact is taken as a sign of vascular compression.

Gorrie et al used a second classification system assessing the relationship of the vascular loop with the VIII cranial nerve. Four different relationships were categorized: 

Class A, no contact; 

Class B, vascular loop lying directly adjacent to nerve; 

Class C, loop running in between VII and VIII nerve ;

Class D, vascular loop displacing the nerve resulting in bowing of the nerve.

Gorrie et al. stated: 'A significant association was demonstrated between the AICA running between the vestibulocochlear and facial nerves. The p value was found to be 0.0162, which demonstrates a statistically significant association between the presence of a Class C loop and hearing loss.'

Studies are yet to conclusively show the significance of these 'compression' as even normal patients with no tinnitus / hearing loss have the type III AICA loop in the IAC.

See a case of of type II vascular loop here.

References

1. McDermott et al. (2003) McDermott AL, Dutt SN, Irving RM, Pahor AL, Chavda SV. Anterior inferior cerebellar artery syndrome: fact or fiction. Clinical Otolaryngology and Allied Sciences. 2003;28:75–80. doi: 10.1046/j.1365-2273.2003.00662.x.

2. Gorrie et al. (2010) Gorrie A, Warren 3rd FM, De la Garza AN, Shelton C, Wiggins 3rd RH. Is there a correlation between vascular loops in the cerebellopontine angle and unexplained unilateral hearing loss? Otology & Neurotology. 2010;31:48–52. doi: 10.1097/MAO.0b013e3181c0e63a.

3. Kim SH, Ju YR, Choi JE, Jung JY, Kim SY, Lee MY. Anatomical location of AICA loop in CPA as a prognostic factor for ISSNHL. PeerJ. 2019 Mar 11;7:e6582. doi: 10.7717/peerj.6582. PMID: 30881768; PMCID: PMC6417406.

Quadrigeminal cistern lipoma

70Y Female patient. Previous history of surgery for ? brain tumor (details not available).  

Sagittal T1 weighted images above are showing a T1 hyperintense lesion in the quadrigeminal cistern. Right parasagittal image is showing a convexity meningioma (green arrow). Blue arrow points to the previous occipital craniectomy defect.

T1 WI axial image shows the hyperintense lesion in the quadrigeminal plate cistern. The Susceptibility Weighted Images (SWI) showed hypointense blooming artifacts, more along the rim of the lesion. 

Lesion is appearing hyperintense in T2WI, suppressed in T2 FS FLAIR images. 

The patient also has associated absent septum pellucidum.

The right superior parietal convexity meningioma is noted with mass effect on the parietal lobe (Green arrow). Orange arrow points to the absence of septum pellucidum. 

 

Shark face !!! in MRI Prostate 😂

Image from a case of Ca prostate MRI, lower section, resembling a shark eating a fish !!. 😅🙈

Haglund Syndrome

Haglund deformity is the reactive enlargement of the posterior calcaneal tuberosity, better assessed in the sagittal images. Presence of Haglund deformity has a greater prevalence of retrocalcaneal bursitis and insertional Achilles tendinosis.

Haglund deformity doesn't always result in Haglund syndrome. 

Haglund syndrome refers to the presence of Haglund deformity, retrocalcaneal bursitis and insertional Achilles tendinosis.

These images are of a 50yr old male patient who presented with chronic heel pain history. First image shows the small abnormal prominence of the posterosuperior calcaneal tuberosity (Green arrows). 

Associated fluid in the retrocalceal bursa, insertional and non-insertional Achilles tendinosis with associated paratenonitis are also present. Edema and fluid signal in the Kager's fat pad is also present here.

Since this condition is also associated with wearing high heels in females, its sometimes referred to as 'pump-bump'.

Diffuse Idiopathic Skeletal Hyperostosis (DISH)

 

DISH or Diffuse Idiopathic Skeletal Hyperostosis, aka Forestier disease, is a common disorder of unknown etiology, characterized by intermittent pain and stiffness in the involved spine segments. Spinal involvement of DISH characteristically produces flowing type ossifications in the anterolateral margins of the at least 4 contiguous vertebrae. This ossification can be of variable thickness, can measure up to 2cm. 

The above images shows prominent ossifications in relation to the anterior aspects of C3 to C7 levels, with C4 to C7 appearing continuous. This is also causing mass effect on the hypopharyngeal soft tissue / pharyngo-esophageal junction. 

The 'Light bulb sign' of liver hemangioma [MRI]

 Light bulb sign refers to the persistent T2 bright homogeneous signal intensity of a typical liver hemangioma, on increasing the TE  (T2 weightage) of the image. The bright signal is compared to that of a glowing light bulb. This may however also be seen in hypervascular metastases. 

MRI Liver of an young patient with multiple hemangiomas in both lobes. 

On increasing the TE, the signal intensity of hemangioma is well preserved, whereas the signals of other structures such as liver and spleen gets reduced.  

Hemangiomas are T2 homogenously hyperintense, with well defined margins with or without small lobulatations. They appear hypointense in T1WI, hyperintense in DWI. In post Gadolinium images they show peripheral nodular intense enhancement in the arterial phase, with gradual centripetal filling-in of the contrast. In the delayed hepatobiliary phase hemangiomas appear hypointense as they do not contain any hepatocytes. 

Isolated Area Postrema Syndrome (APS) presenting as intractable nausea and vomiting (NMOSD)

 Area Postrema (AP) is an emetic reflex center, one of the circum-ventricular organs that is outside the blood-brain barrier(BBB). It is located in the dorsal aspect of the medulla, at the caudal end of the fourth ventricle. AP along with Nucleus Tractus Solitarius (NTS) and dorsal motor nucleus of Vagus forms the dorsal vagal complex, where most of the vagal afferents terminate. AP by its location outside the BBB is exposed to the toxins in the blood. Activation of the AP brings nausea and vomiting, due to its projections into the NTS. 

AP through its hypothalamic,brainstem connections also regulate fluid balance, immunomodulation etc. It also chemo-sensitive neurons regulating hiccups. 

Neuro Myelitis Optic Spectrum of Disorders (NMOSD) are a group of autoimmune inflammatory demyelinating diseases of the CNS. Most of these show characteristic antibody to aquaporin-4 (AQP-4) water channel. 

 Attacks of intractable nausea, vomiting or hiccups (INVH) in the presence of a dorsal medullary lesion is called as the Area Postrema Syndrome (APS) and upto 30% of NMOSD patients will have APS during their disease course. 

NMOSD lesions in the Area Postrema shows loss of AQP-4 immunoreactivity and inflammation and characteristically lacks necrosis and demyelination which is seen in spinal cord and optic lesions, explaining reversibility of the symptoms. Patients have to tested for Serum and CSF AQP4-IgG antibodies. 

Isolated APS is easily mistaken clinically and is often attributed initially to other causes like gastritis including H.Pylori, GERD, Cholecystitis, Pancreatitis, food poisoning, gastroparesis etc. 

Immunotherapy usually results in rapid relief of symptoms usually within 2-3 days, responding to Methyl Prednisolone or Immunotherapy in most cases. Refractory cases may need drugs like Azathioprine, MMF, Rituximab.   

Below are the MRI images of a young female with intractable nausea and vomiting. 

T2 and T2 FLAIR hyperintensity noted in the region of the Area Postrema, called the Inverted-V sign.

Bilateral symmetrical normal optic nerves.

No restricted diffusion seen in the abnormal signal areas of Area Postrema.

Corresponding sagittal T2 FLAIR image showing the level of Area Postrema.
Abnormal signal intensity is also seen in the inferior colliculi of midbrain in the sagittal image. 

Diagram showing the location of AP, NTS in the dorsal medulla.

Hepatocellular Adenomas

Hepatic / Hepatocellular adenomas are uncommon benign tumor commonly seen in young to middle aged women, with history of oral contraceptive use. 

👉 Hepatic adenomatosis:  >10 adenomas. Adenomas in hepatic adenomatosis is not related to the hormonal or other risk factors. They tend to be multiple, progressive, symptomatic, more likely to lead to hepatic dysfunction and possible malignant transformation. 

HCAs are now classified based on the genetic and pathologic subtypes as :

1. Inflammatory hepatocellular adenoma.
2. Hepatocyte-nuclear-factor-1-alpha (HNF-1α-mutated) hepatocellular adenoma. 
3. β-catenin-mutated hepatocellular adenomas.
4. Unclassified subtype (includes HCAs without any genetic abnormalities).

Typical hepatic adenomas show moderate arterial phase enhancement with washout in portal venous and delayed, appears isointense to rest of liver. Chemical shift imaging can produce loss of signal of the adenoma in out of phase images due to the presence of fat within.


Name two hepatocyte specific contrast agents?

1. Gd-BOPTA / Gadobenate Dimeglumine
2. Gadoxetate Sodium.

What will happen in case of HCA with hepatocyte specific contrast agents?
Ans : Will appear darker than rest of liver, as the hepatocytes in HCA are non-functional.

Easy to remember Hepatic Adenoma better as ‘Hepatocyte’ Adenoma, as it lacks biliary epithelium, portal vein and even Kupffer cells.

Incidence Ratio in Female to Male is 9:1, Why 

Ans: OCP use. (Anabolic steroids also increase the risk, common with young men).

Surgery is recommended irrespective of size, why?

1. Risk of rupture and shock.
2. Transformation into HCC.

Below MRI images are of a 25yr old female patient who presented with pain related to cholecystolithiasis. Three incidental slightly echogenic lesions are seen in both lobes during USG, for which MRI was suggested.

T2 weighted images showing slightly T2 hyperintense lesion in the superior subcapular portion of the left lobe, lateral segment. 

Another similar signal intensity lesion in right lobe, segment VII/VIII

The main lesion showing the signal intensity loss in the Out-phase images, suggesting intralesional microscopic fat content. No restricted diffusion were seen in these lesions. 

Subtlest of three in the superior portion of segment VII of right lobe, again showing the loss of signal intensity. 

Increasing the TE of T2 WI reduces the signal intensity of the lesion in addition to that of rest of the structures. (c.f. hemangioma shows similar signal on increasing TE). See this article to see how a hemangioma looks like on increasing TE ('The Light Bulb Sign')

  Dynamic post contrast images shows prompt arterial phase enhancement of the lesion (yellow arrow), and appearing someehat isointense to rest of liver in the further images.

References:

1. Luigi Grazioli, Lucio Olivetti, Giancarlo Mazza, Maria Pia Bondioni, "MR Imaging of Hepatocellular Adenomas and Differential Diagnosis Dilemma", International Journal of 
   Hepatology, vol. 2013, Article ID 374170, 20 pages, 2013.
2. Hepatocellular Adenomas: Correlation of MR Imaging Findings with Pathologic Subtype Classification, Radiology.
3. Hepatic Adenomas: Imaging and Pathologic Findings. Luigi Grazioli, Michael P. Federle, Giuseppe Brancatelli, Tomoaki Ichikawa, Lucio Olivetti, Arye Blachar, Radiographics.

Persistent Trigeminal Artery (PTA), Tau sign

Persistent Primitive Trigeminal Artery is one of the persistent carotid-vertebro-basilar anastomoses. PTA arises from petrous-cavernous junction, runs posterolaterally along the trigeminal nerve, crosses over or through dorsum sella.  

Two types of PTA have been described. 

Saltzman Type I : PTA supplies the distal basilar artery. PComs are usually absent. The distal basilar artery is absent or hypoplastic. Distal vertebral arteries are also hypoplastic. 

Saltzman Type II : PTA supplies the Superior Cerebellar Arteries, with PCAs supplied by the PCom. 

TOF MRA images showed Saltzman type I PPTA, where the PTA is seen replacing the distal basilar artery. 

Sagittal MIP MRA image showing the distal basilar artery completely supplied by the PTA. 

The Tau sign, resembling a 'T' is classically described in the sagittal images. 

Eosinophilic Gastroenteritis

Case: 40Y Male patient presented with abdominal pain and diarrhoea. 

Plain CT image shows thickened appearing colon (orange arrows) with surrounding fat stranding. Thickening of anterior pararenal fascia is also seen bilaterally (blue arrows). 

Contrast CT images showed edematous thickening of the terminal ileum (not shown) and large bowel upto distal descending colon. Peri-colonic inflammatory fat stranding is noted. The SMA-SMV, IMA-IMV showed normal contrast opacification. 

Contrast CT images showing mild right pleural effusion (yellow arrow) and ascites (green arrows). 

Differential Leukocyte count revealed Eosinophil count of 18% initially and rose upto 68% within 3 days. Peripheral smear showed normocytic normochromic picture with marked eosinophilia. 

Colonic biopsy showed dense chronic inflammation with predominance of eosinophils - features compatible with Eosinophilic enterocolitis.

Patient was treated with Steroids and Azathioprine, improved and was asymptomatic with normalized lab parameters in the last visit.  

Eosinophilic gastroenteritis  is a rare inflammatory disorder of the gastrointestinal tract, characterized by focal or diffuse eosinophilic infiltration of the gastrointestinal tract. Clinical features and radiological findings are non-specific, so a high index of suspicion is needed, in cases of peripheral eosinophilia (seen in >60%). This usually presents with dyspepsia and diarrhoea. It may rarely cause GOO / SBO and pancreatitis. This disease was first described by Kaijser in 1937.

Although any age group can be affected, majority of patients are in the 3rd to 5th decades, with a slight male preponderance. Most patients have history of seasonal allergies, asthma, food sensitivity, eczema, elevated IgE levels. 

EG is a self-limiting disorder in most cases and usually responds well to steroids. 

Three types of EG have been mentioned, 

1. Mucosal EG (most common) : presents with fecal blood loss, anemia, weight loss due to malabsorption or protein losing enteropathy.
2. Muscularis EG : presents with obstruction (GOO/SBO).
3. Subserosal EG : manifests as eosinophilic ascites. 

Definitive diagnosis of EG requires bowel biopsy correlation demonstrating the eosinophil infiltration. In cases of the subserosal EG, high eosinophil count in a sterile ascitic fluid by paracentesis can also be demonstrated. 

Major DD would be a intestinal parasites, which necessitates stool examination to look for ova and parasites. 

Hypereosinophilic syndrome (HES) is an idiopathic condition associated with marked peripheral eosinophilia (>1500/uL for >6months) and gastroenteritis. Heart, lungs, brain and kidneys are also affected in HES. 

Imaging features are non-specific, can show edematous wall thickening. Ascites and pleural effusion can be seen. Esophagus, stomach, small bowel and also colon can be affected. 

References:

• A Review of Eosinophilic Gastroenteritis.
• Radiopaedia. 

Thanks to Dr. GP. 

Radiation enteritis

Below are the CT images of a 60y female patient, post surgery, post chemo-radiotherapy for Ca Rectum 3 months before the CT. 

CT images show 'long segment, contiguous, mild circumferential wall thickening of distal and terminal ileum, measuring length of ~30cm and maximum wall thickness of ~6mm. No peri-enteric fat stranding or lymph node enlargement seen'.  There were no sinuses or fistulae or any features of bowel stricture or obstruction.  

The blue arrows point to the thickened ileal loops. 

Radiation induced enteritis, especially of the small bowel is less often seen even though small bowel is very radiosensitive, because of its relatively increased mobility. Among small bowel the terminal ileum is the most sensitive, as it is more or less fixed. Fixation due to adhesions from a previous surgery or previous inflammation (including PID) can increase the risk of radiation induced bowel damage. Thin habitus, diabetes and hypertension can also influence the post radiation injury. 

Radiation doses >50Gy administered over 6 weeks can produce radiation induced bowel injury, which in 10% of cases might require surgical intervention. ~5-15% patients receiving >45Gy develop chronic radiation enteropathy.

The three stages of radiation enteritis are acute, subacute (2-12 months) and late phase. Acute phase is usually the mucosal inflammation, crypt abscesses, superficial ulcerations. Subacute phase, is a phase of regeneration, arteriolar sclerosis. Late phase is usually due to fibrosis. This phase can result in strictures, obstruction, fistula and sinus formation. 

👉  Point to remember : Keep in mind the differential of radiation induced bowel injury, in cases of bowel wall thickening. Especially in a post op patient, ask for history of radiotherapy. 

Perineural cysts (Tarlov cysts) of the cervical spine

Calyceal Diverticulum

Calyceal diverticula are outpouchings of renal calyces or even renal pelvis (pelvi-calyceal diverticula) into the renal cortex connected by narrow neck. These are lined by non-secreting urothelium (transitional cell epithelium).

Incidence: 0.2-0.6% of patients undergoing renal imaging.

Usually these are incidental findings and are mostly asymptomatic. Due to stagnation of urine within the diverticulum, these are prone for stone formation. Stones can be found in upto 50% of the calyceal diverticula.

Exact etiology of the formation of calyceal diverticula are not known, may be congenital or acquired due to infections, VUR, or rupture of a cortical cyst.

These are subdivided into two types:¹
Type 1 communicating with a calyx, usually found in upper pole.
Type 2 communicating with renal pelvis, larger, usually found in mid-pole (also called pyelo-calyceal diverticula). Radiopaedia adopts a slightly varied types, with type 1 from minor calyx and type 2 from major calyx or renal pelvis.²

There may be internal calcifications, either in the form of stones or of milk of calcium. In one small ultrasound series, 7 of 11 cases of calyceal diverticula demonstrated mobile echogenic material. It is suggested that the presence of mobile hyperechogenic material within a cystic structure is diagnostic of a calyceal diverticulum. ³

Differential considerations of a calyceal diverticulum would include complex cyst, dilated calyx, cystic renal neoplasm and abscess. Unless an excretory (or urogram) phase is acquired diagnosis of calyceal diverticulum is not possible. Dilated calyx can be due to obstructing stone, tumor or due to infundibular stenosis in TB.



The following plain and contrast CT images are of a 40 year old male patient who was evaluated for left lumbar pain and tenderness.

Plain CT Axial sections showing calcific focus within a subtle hypodense area in the bilateral renal parenchyma. 

Type I Bosniak cyst is noted medially (not marked).

The above three images shows the Plain CT, venous phase and excretory phase axial sections of both kidneys, which shows contrast filling of the cystic appearing area in the venous phase - consistent with the diagnosis of Calyceal Diverticulum of both kidneys. Calculus formation is noted in both these calyceal diverticulum. 

Oblique coronal MIP image showing the contrast filled bilateral calyceal diverticulum (Green arrows). The yellow arrow points to the pathology for which the patient underwent the CT examination (colitis). As in most cases, this case of bilateral calyceal diverticulum was also asymptomatic.  

3D VRT image demonstrating the calyceal diverticula. 

References
1. Mullett, Rebecca et al. “Calyceal diverticulum - a mimic of different pathologies on multiple imaging modalities.” Journal of radiology case reports vol. 6,9 (2012): 10-7. doi:10.3941/jrcr.v6i9.1123

2. Stunell, H et al. “The imaging appearances of calyceal diverticula complicated by uroliathasis.” The British journal of radiology vol. 83,994 (2010): 888-94. doi:10.1259/bjr/22591022

3. Reynard J, Brewster S, Biers S. Oxford Handbook of Urology. Oxford: Oxford University Press; 2006. p. 328.

4. Leveillee RJ, Bird VG. Treatment of Caliceal Diverticula and Infundibular Stenosis. In: Smith AD, Badlani G, Bagley D, et al., editors. Smith’s Textbook of Endourology. 2nd ed. Ontario: BC Decker; 2007. pp. 171–185.