Multiple Cavernomas in Brain

Young male patient with recurrent brain hemorrhages, due to multiple Cavernomas.

Cavum Septum Pellucidum

Cavum Vergae

The main lesion - which is heterogenously hyperdense. Lesion also showed CSF density areas - possibly sequelae to old hemorrhages. Characteristic MRI appearance is described in T2WI as 'Popcorn Appearance'.

Tiny lesion in right high frontal lobe.

This patient had previously undergone MRI Brain, which showed multiple cavernomas (SWI blooming) - much more than that in present CT.

'Popcorn Appearance' of Cavernoma in T2 WI MRI.

Bilateral thalamic and cerebellar hypodensity

These are the CT Brain images of a young male patient, who had h/o fever & Status Epilepticus 

(? for 1 hour),became unresponsive and was intubated.

Left Centrum Semi Ovale showed two calcific foci.

Left frontal lobe showed a round, relatively well defined hypodensity - ? Focal Infarct. Smaller scattered hypodensities were also present bilaterally.

Bilateral symmetrical parieto-occipital, basal ganglia and thalamic hypodensities were noted. See following images.

Thalami are sort of expanded ? Edematous.

Temporal horns and sulci show effeacement -( brain edema)

The patient unfortunately expired after 2 days of the CT.

Hypodensities due to severe Ischemia or Hypoxia usually spares the Cerebellum and the Central structures - which is called as the White Cerebellum Sign or the Dense Cerebellum Sign or Reversal Sign.

See Radiopaedia Article  http://radiopaedia.org/articles/white-cerebellum-sign

But in this case there is Symmetrical involvement of bilateral thalami and cerebellar white matter ! - point against Hypoxic etiology.

Symmetrical cerebellar involvement also !

So this case would be Atypical for Hypoxia/Ischemia alone. One thing here to be noted is, majority of the cerebral parenchyma is not showing much decreased attenuation and the grey-white differentiation is preserved.

These findings 1. Diffuse brain edema +/- Thalamic +/- Cerebellar hypodensities , infarcts has been described in Cerebral Malaria !!

For further data on Imaging in Cerebral Malaria : 

1. Adult Cerebral Malaria: Prognostic Importance of Imaging Findings and Correlation with Postmortem Findings - Radiology 2002, September by Patankar et al.
Cerebral Malaria Imaging @ Radiology RSNA, Patankar et al.

2. http://radiopaedia.org/articles/cerebral-malarial-infection

Patankar et al describes 4 patterns in cases of Cerebral Malaria
1. Normal Imaging 2. Diffuse brain edema 3. Diffuse brain edema with bilateral thalamic hypoattenuation and 4. Diffuse cerebral edema with thalamic and cerebellar hypoattenuation.

"These areas of hypoattenuation represent infarction in the territories supplied by the thalamoperforating and cerebellar vessels as a result of microvascular occlusion.  "

4th pattern is the most severe and survival is rare, as in our case. 

Normal imaging is the most common pattern. (2nd pattern was the MC in Patankar et al Study). 


"Focal hemorrhagic or nonhemorrhagic infarcts in the cortex, basal ganglia, thalamus, pons, and cerebellum in patients with cerebral malaria occasionally have been described in isolated case reports." The left frontal lesion may represent a focal infarct.


"Bilateral, symmetric infarction of the thalami has been seen in internal cerebral vein thrombosis, Japanese encephalitis, and occlusion of both paramedian thalamic and mesencephalic arteries caused by atherosclerosis or tuberculous meningitis."

"Hypoglycemia, which occurs in 8%–32% of patients with cerebral malaria , may also cause serious cerebral damage. The cortex, hippocampus, basal ganglia, and the substantia nigra (but not the thalamus or cerebellum) are particularly vulnerable to this."


So our possible diagnosis for this case would be CEREBRAL MALARIA.


Whats your opinion on this case?

Case Of Ca Lung

A Case of Carcinoma Lung

50year old male patient, smoker, admitted with fever & sepsis.

CT Chest lung window shows a spiculated mass lesion
 in right upper lobe with multiple pleural tails/tags.

Lesion shows heterogenous, peripheral enhancement, indicating a necrotic lesion. 

Enlarged rim enhancing (necrotic) 3cm mediastinal lymph node is also seen.

In same patient liver showed a well-defined, but irregularly marginated hypodense (20-30HU) lesion with minimal peripheral enhancement. ?Liver Abscess !.

Again, the left adrenal showed a macroscopic fat containing lesion. (Adrenal Adenoma)

TSTCs - Too Small To Characterize

TSTCs or ' Too Small To Characterize' Lesions

• Hepatic lesions 1.5 cm in diameter or smaller are frequently difficult to characterize at CT and are often reported as being “too small to characterize” (TSTC) by the interpreting radiologist.
• Most of the TSTCs are hypodense.
• In a patient without a known malignancy, TSTCs should be considered benign.
• Single TSTC in patient with malignancy are considered benign.
• If >1 TSTCs in a Oncology patient, they are mostly benign, especially if they are homogenous and sharply defined.
• Of cancers Ca. Breast TSTCs are more likely to be a metastatic lesion, than others (Ca Breast > Colorectal > Lymphoma).
• TSTCs are followed up, to look for change in size.

References
1. Hepatic lesions deemed too small to characterize at CT: prevalence and importance in women with breast cancer. Radiology 2005.
2. Liver Incidentalomas http://www.radiologyassistant.nl/en/p45a5e818c709d


 

Incidental CP Angle Meningioma

Patient here is a middle aged female, with headache. CT Brain was asked to r/o SAH.

Small hyperdense non-calcified lesion was noted in the left Porus Acousticus of IAC, with minimal intracanalicular extension.

Lesion shows minimal intracanalicular extension. No widening of IAC was noted. No bone sclerosis or lysis was present.

Tentorial Hemorrhage !

And Bilateral SDH !!  ??

Gartner Duct Cyst (Vaginal Cysts)

The Vaginal and perivaginal cysts include

 1. Vaginal Cysts

  a) Gartner Duct Cysts
  b) Bartholin Gland Cysts

 2. Perivaginal Cysts

  a) Skene Gland Cysts (Periurethral gland Cysts)
  b) Nabothian Cysts of Cervix.

Gartner Duct Cysts

'Gartner duct cysts result from incomplete regression of the wolffian ducts. These cysts most commonly develop in the anterolateral wall of the upper vagina, above the inferior border of the pubic symphysis. Gartner duct cysts are lined with nonmucinous cuboidal or columnar epithelium. When Gartner duct cysts are located at the level of the urethra, they can cause mass effect on the urethra, giving rise to urinary tract symptoms.'

(Ref - Overlooked Diseases of the Vagina: A Directed Anatomic-Pathologic Approach for Imaging Assessment October 2011 RadioGraphics, 31, 1583-1598.)



Gartner Duct Cysts as mentioned occur on the upper anterolateral vagina, whereas Batholin Gland Cysts occur in the posterolateral aspect of the lower vagina.Bartholin Cyst's location at or below the level of the pubic symphysis helps to differentiate them from Gartner duct cysts.

As name suggests the Peri-urethral gland(Skene Gland) cysts do occur in the lower periurethral region, anterior to the vagina.The Skene glands are paired structures located near the external urethral meatus, with ducts draining directly into the urethral lumen.

Urethral diverticula, which comes as a DD for Skene Gland Cyst tend to be midurethral in location

Intra Uterine Gestation with IU Contraceptive device in-situ

Simultaneous IUGS and IUCD(Cu-T)

TAS showing an Intra Uterine Gestational Sac with a fetal pole. Cardiac activity was present.

The IU Contraceptive device (Cu-T) is in-situ here.

Occurrence of an IUGS with a Cu-T in-situ is rare.

The risk of Ectopic Gestation is lower than those who use no contraceptive method.

However if a gestation occur in IUCD in-situ, there is a 3-4% chance of it being an ectopic one.

Did u know in PTE

1. D-dimer has a sensitivity and negative predictive value of 97 -100%.
2. Hampton's hump in CXR is seen in <10%.
3. Westermark's sign is seen in less than 2%.

Low grade vs High grade Brain Neoplasms

- Some benign intracranial tumors like Pilocytic Astrocytoma, Pleomorphic Xanthoastrocytoma(PXA), GanglioGlioma(GG) can have cystic areas and PXA and GG can have enhancement.

Approximate Normal ADC Values

Gray matter  - 0.85 +/- 0.13 x 10 e-3 mm2 / s

White Matter - 0.80 +/- 0.13 x 10 e -3 mm2/s

CSF   - 3.63 +/- 0.30

DIffusion Restriction Areas ~ 0.60 - 0.65

Proton MR Spectroscopy - ppm of Minor Metabolites

Metabolite                PPM

Valine
Leucine                         --->      0.9 ppm
Isoleucine

Alanine                          --->     1.48 ppm

Acetate                          --->     1.9 ppm

Succinate                      ---->     2.4 ppm

Lipid / Lactate              ---->     0.8 to 1.3 ppm


PS: To differentiate Lipids vs Lactate which occur at the 1.3ppm in the short TE acquisition, and additional TE = 135ms imaging is done in which the lipids do not invert.

       Pic F - Short TE                                           Pic G - Intermediate TE

Distinguishing the Amino acid peaks of Valine, Leucine and Isoleucine at the 0.9ppm and the lactate/lipid at 0.8-1.3ppm is important in distinguishing between Cystic Tumors (Both primary and mets) from Brain Abscesses - by doing the Intermediate TE (135ms) Spectroscopy, which causes the inversion of Aminoacids and lactate peak, but not of lipid.

Image showing the inversion of lipid in intermediate TE..

Fibrodysplasia Ossificans Progressiva

1. Bilateral Hallux Valgus - with malformed first metatarsal and phalanges.

2. Medial cortical thickening with formation of Pseudo-exostosis ( Calcification of Gracilis / Semitendinosus tendons).

3. Shortened first metacarpals

4. Usually the hetrotopic ossification begins in the soft tissues of neck, even after trivial trauma.

5. FNAC is contraindicated as it can result in permanent deforming ossification.

6. F.O.P is an AD disease with complete penetrance,, but with variable expressivity.

7. Can be diagnosed by the HALLUX VALGUS. Genetic testing is available.

8. Small vertebral bodies, enlarged pedicles, small spinal canal may be seen.

9. Starts by 2-5yrs, Death by 3rd decade by recurrent pulmonary infections due to prevention of expansion of thoracic cage (Impairing Respiration).

Causes of CT Bowel Fat Halo Sign

CT Bowel Fat Halo Sign

Seen in 

1. Chronic Inflammatory Bowel Disease

2. Cytoreductive therapy

3. GVHD.

4. Normal patients ~20% of normal, with increased BMI can have this sign positive.

"When seen in both the small and large bowel, the halo sign has been considered specific evidence of Crohn’s disease. When only the colon is affected, the degree and geographic distribution

of bowel wall thickness are signs used to distinguish ulcerative colitis from Crohn’s disease. '

(Gore RM, Balthazar EJ, Ghahremani GG, MillerFH. CT features of ulcerative colitis and Crohn's, AJR, 1996)

Fluid-blood levels in Intracranial Hemorrhage

Excerpt from the Stroke Article
ref: http://stroke.ahajournals.org/content/24/4/554.full.pdf

"The cause of lobar hemorrhage after fibrinolytic treatment remains puzzling. We speculate, but have
proof in only one patient, that the presence of amyloid angiopathy may be an important risk factor. We cannot exclude the possibility, however, of hemorrhage into a prior silent infarction as the mechanism in some of these patients. Long-standing hypertension has been specifically implicated as a risk factor for cerebral
hemorrhage.
However, the site of hemorrhage associated with hypertension is usually in the distribution of perforating vessels, not lobar.
Patients with hypertension alone usually have bleeding into sites such as basal ganglionic, posterior lateral thalamus, pons, and cerebellar hemispheres.
Patients with hypertension and lobar hemorrhages may have amyloid angiopathy as well.

One recent study of surgically treated patients with lobar hematomas indeed suggested that amyloid angiopathy is a major contributing factor. 

In two series of patients with lobar hemorrhage but without anticoagulant or fibrinolytic treatment, hypertension was found in only one third of the patients. Although hemorrhage into the cerebellum has traditionally been linked to hypertension, blood pressure was normal in our one patient with a massive vermis hemorrhage. Furthermore, one study claimed that vermis hemorrhages were relatively frequent in anticoagulated patients."

" We suspect, therefore, that cerebral amyloid angiopathy may be a contributing, if not crucial, factor in

fibrinolysis-associated hemorrhages. Intracerebral lobar hemorrhage is frequently associated with cerebral amyloid angiopathy in patients in the sixth or seventh decade of life. It encompasses multiple, usually superficially located, areas of hemorrhage on CT scans. Frontal or parietal lobe hemorrhages are common, but cerebellar and putaminal locations have been described in association with amyloid angiopathy. Recently, it was also noted that cerebral amyloid angiopathy associated with lobar intracerebral hemorrhage resulted in good outcome in the vast majority of patients."