Parietal lobe lesion on MRI

A 35 y o male with right side focal seizures.

MRI BRAIN WITH CONTRAST REPORT

Right parietal ~ 20x17mm intra axial lesion with mild peri lesional odema, lesion show thick wall with mild patchy enhancement on post contrast. Restricted diffusion on Dw images. No significant mass effect or mid line shift. On MRS, raised choline, choline / creatinine ratio, markedly reduced NAA, a lactate peak.

DDs:
Abscess was thought in the differential diagnosis during the discussion with neurosurgeon as there is restricted diffusion. But the pattern of restricted diffusion is not typical of an abscess. In abscess the central necrotic core should show restricted diffusion but here if we see carefully the central core is relatively low signal intensity than the thick wall which show restricted diffusion due to its high cellularity and compact architecture.
Superior sagittal sinus show normal T2 flow voids. No obvious thrombosed right parietal cortical vein or focal bleed on GRE, possibility of CVT ruled out.

So Imaging wise the primary diagnosis given was neoplastic primary, Glioma more likely than Metastasis.

Operated with right posterior parietal craniotomy, complete excision of lesion done. No major intra / extra axial bleed on post operative scans.
And here is...

REPORT OF HISTOPATHOLOGICAL EXAMINATION

Specimen         :     Excisional biopsy – Right para-saggital SOL.
Gross Appearance    :     The specimen consists of multiple, irregular pieces of dull grey-tan soft to friable tissue; together measuring 1.0X1.0X0.5 cm. The entire tissue is submitted for processing.

Microscopy        :     Section shows reactive glial tissue, imperceptibly blending with modestly hypercellular zones of neoplastic astrocytes having hyperchromatic nuclei with irregular chromatin density. The cells have scanty to barely discernible cytoplasm. Few nuclei appears elongated or cigar-shaped with irregular condensed chromatin. The background is uniformly fibrillar with numerous microcystic spaces and variable vascular proliferation. No mitosis nor necrosis is seen. No granulomas seen.

Final Diagnosis                   :     Fibrillary Astrocytoma; Grade 1 to 2 of 4 (as per St. Anne - Mayo grading system).

So take home notes is thinking of an Abscess if restricted diffusion is present on MRI is a good attempt but the pattern of restricted diffusion in the lesion is equally important and can be used in cutting down the list of differential diagnosis. 

Frontal lobe SOL on MRI

A 40 y o male with seizures and fall.

Previous CT shows right frontal hypo density, clinical query was right frontal contusion or something else.

MRI BRAIN WITH CONTRAST REPORT

This MRI brain shows an intra axial ~ 74x40mm lesion involving right superior frontal gyrus, adjacent cingulate gyrus and calloso septal groove. Corpus callosum uninvolved. Lesion show ill defined infiltrative margins, mild to moderate heterogeneous enhancement on post contrast due to areas of necrosis, no obvious cystic component. No sub falcine herniation of lesion. ACAs compressed, mid line shift of ~3mm to left.
No e/o bleed in lesion on GRE.
On MR Angiogram of Brain and neck vessels no hemodynamically significant major vessel stenosis or occlusion.
Superior sagittal sinus show normal T2 flow voids. Normal MR Venogram of Brain, CVT ruled out.
Previous CT shows no obvious calcification in lesion.

Imaging wise diagnosis : Glioma  _ Intermediate grade.

REPORT OF HISTOPATHOLOGICAL EXAMINATION

Specimen         :   Biopsy – Right frontal lobe, SOL
Gross Appearance    : The specimen consists  few soft pieces of dull grey white tumourous tissue; together 1.0X1.0X0.5 cm. The entire tissue is submitted for processing.

Microscopy        : Section and additional made serial deeper section a moderately cellular oligodendroglial neoplasm amidst reactive glial tissue. The tumour comprise of fairly uniform appearing intermediate sized, round to oval cells having hyperchromatic nuclei with subtle pleomorphism and finely stippled or coarse nuclear chromatin. The cells have scanty eosinophilic to vacuolated cytoplasm. The interstitium shows short capillaries with angulations. An occasional high power field shows a doubtful mitosis. Also seen are few scattered foci of calcification.

Diagnosis         :  Biopsy – Right frontal lobe, SOL :   Oligodendroglioma.

(Adv. Immunohistochemical ancillary studies for confirmation and definite lineage typing).

Multiple enhancing lesions in frontal lobe, basal ganglia and posterior fossa

A 60 y o female, referred for further management with known multiple lesions in brain on previous CT and MRIs. 

MRI study of brain reveals multiple lesions with nodular and multi locular enhancement on post contrast, lesions clustered in right fronto parietal region along sulci and sub cortical white matter, marked peri lesional vasogenic odema, a similar right temporal white matter lesion. Similar right basal ganglia, bilateral thalamic and bilateral dentate nuclei lesions, with odema.
Few were new lesions compared to previous MRI.
On MR Spectroscopy there is raised choline and choline creatinine ratio.
Absent NAA peak.
Clinically : HIV negative. 

Imaging wise DDs given:
Granulomatous lesion_ Tuberculomas.
Toxoplasmosis. 
Lymphoma
Metastasis.

Histopathology report

Specimen         :  Biopsy -? Tumour tissue, frontal lobe (multicentric SOL’s in brain).
Gross Appearance    : The specimen was received in two containers – bearing patient’s name. Both the containers consists of soft-friable fragments of dull grey-tan tissue; each measuring 1.0X0.5X0.3 cm. and 1.0X0.5X0.5 cm. Both the tissues are submitted as entire specimen for processing.  Codes : A and B.
Microscopy        : Sections A and B both show fragmented bits of neoplastic tissue comprising sheets or rather cohesive aggregates of fairly monotonous appearing intermediate sized, round to oval neoplastic lymphoid cells with stippled – vesicular chromatin and scanty eosinophilic cytoplasm. In few foci the neoplastic lymphoid cells show angiotropism with perivascular clustering. Couple of foci show scattered mitosis. No evidence of glial differentiation seen. No granulomas seen.

Diagnosis         : 
Histo pathological features are consistent with “Primary Central Nervous System, Malignant Non-Hodgkin’s Lymphoma – of probable B lineage”

Advsed Immunohistochemical ancillary studies for confirmation and definite lineage typing.

Anaplastic Astrocytoma MRI

A 37 y o male  with right side focal seizures, left side weakness.

Previous MRI shows right insular and adjacent opercular lesion.

No change compared to previous MRIs.

MR study of brain reveals abnormal intra axial lesion as an area of T2 hyper intensity with focal parenchymal swelling involving right basal ganglia, adjacent opercular and insular cortex, non enhancing on post contrast, no restricted diffusion.
Imaging wise primary diagnosis : Infiltrative Glioma_ Anaplastic Astrocytoma.
Differential diagnosis: Nil.

REPORT OF HISTOPATHOLOGICAL EXAMINATION

Specimen         : Biopsy – Insular SOL.
Gross Appearance    : The specimen consists of irregular soft pieces of dull greyish white tissue; together measuring 2.2X1.8X1.0 cm. The entire tissue is submitted for processing.
Codes : A and B.

Microscopy        : Sections A and B both show reactive glial tissue amidst which is seen embedded fragments of astrocytic neoplasm. The tumour consists of hypercellular zones of neoplastic astrocytes displaying nuclear hyperchromasia, subtle pleomorphism, coarse chromatin and irregular nuclear membranes. The cells have scanty eosinophilic cytoplasm. The background is fibrillary with variable microvascular proliferation. No microcysts nor necrosis nor increased mitosis is seen. No granulomas seen.

Final Diagnosis : Anaplastic ( Fibrillary ) Astrocytoma ; Grade 2 to 3 of 4 (as per st. Anne - Mayo system).     

Orbital lesion on MRI with histopathology

Clinically: 60 y o male with right side painful eye movement, ptosis.

MRI Brain with MR Angiography was normal.

MRI Orbit shows an abnormal ill defined enhancing soft tissue at right orbital apex, obliterating superior orbital fissure, involving superior rectus muscle which is bulky show high signal on STIR. Mild right orbital proptosis.
No obvious osseous destruction of CT at orbital apex.
Minimal adjacent sphenoid sinus mucosal thickening.

DDs suggested:
Inflammatory Pseudo tumor ( most likely)
Sinus disease, fungal.
Lymphoma, Metastasis.

REPORT OF HISTOPATHOLOGICAL EXAMINATION

Specimen         :    Right orbital mass.
Gross Appearance    :    The specimen consists of dull grey soft to firm pieces together measuring 0.3X0.3X0.3 cm. The entire specimen is submitted for processing.

Microscopy        :    The section shows striated muscle and fibrofatty tissue along with a couple of pieces of (undecalcified) bone. The fibrofatty tissue shows minimal lymphocytic infiltration. The muscle shows considerable degenerative changes however, and consists of fragmented fibers, sarcolemmal nuclear proliferation with mild fibrosis and lymphocytic infiltration. There are no granulomas seen. Deeper sections show similar appearance.

Final Diagnosis                   :    Chronic inflammation with degenerative changes in muscle ? inflammatory pseudotumor.

Frontal SOL, Guess Histopathology

A known case of Left frontal lesion referred for further management.

MRI BRAIN WITH CONTRAST REPORT

Left frontal well defined mixed signal intensity lesion, major portion of lesion is cystic measures ~ 75x45mm with thin enhancing wall, an ~ 23x25mm eccentric avidly enhancing mural nodule within the lesion, marked perilesional vasogenic odema. Mass effect, mid line shift of ~ 15 mm to right, sub falcine herniation, mild mid brain compression.

Imaging wise diagnosis given was Neoplastic Primary Glioma, Metastasis.

Any other guess ? 
Ok.. here is ...

REPORT OF HISTOPATHOLOGICAL EXAMINATION

Specimen         : Excisional biopsy – Left frontal lobe SOL.
Gross Appearance    : The specimen consists of multiple, irregular, soft to friable pieces of dull grey – tan tissue; together measuring 4.0X3.3X2.0 cm. The cut section shows dull grey tan appearance. Representative sections are submitted for processing.  Codes : A and B.

Microscopy        : Sections A and B both show cellular meningothelial neoplasm. It comprise lobules and sheets of intermediate sized, round to oval cells having modestly hyperchromatic nuclei with round to oval configuration and having delicate - peripherally condensed chromatin and many cells having small nucleoli. Overall scattered cells show nucleoli - cytoplasmic invaginations. The cells have faint eosinophilic cytoplasm with indistinct margins. The interstitium shows prominent congested vasculature with scattered few lymphocytes. Overall the entire tumour shows 0 – 2 mitosis per 10 HPF. There is no evidence of frank cytological anaplasia nor of brain invasion.

Diagnosis  :  Meningioma; grade I of III.

Even surgeon was also surprised with histopathology report.

Retrospectively review of case shows enhancing dural thickening in left frontal region. Meningioma is known to be associated with meningeal cysts which varies in size and can be large enough as in this case giving appearance of a predominantly cystic lesion with mural nodule. 

Bilateral symmetric medial temporal calcification

Clinical Details  : First of two sibs born of non consanguineous marriage, full term cesarean birth
Reportedly had meconium aspiration, neck holding about 9 month sitting somewhat at the age of one year, started walking with difficulty at one and half years and even now there is no speech
Suffered a febrile seizure at the age of one year.
Presently on phenytoin 3.5ml BID
Can walk independently but very clumsily.
No abnormal posturing.
Previous CT reports multiple areas of calcification, evaluated for TORCH infection.
EEG was reported normal.

CT brain shows bilateral symmetric medial temporal horn like calcification.
Bilateral parietal white matter hypo density due to abnormal myelination.

Impression:

Lipoid proteinosis is a rare diagnosis suggested imaging wise, though there is no associated blephritis at present on clinical examination.
This can not be TORCH sequel as medial temporal horn like calcification is bilateral and symmetric.

Similar Case of Lipoid Proteinosis : Click here

Lipoid proteinosis

Syn : Urbach-Wiethe disease, initially described by Urbach and Wiethe in 1929 as “hyalinosis cutis et mucosae”.
A rare genodermatosis characterized by multisystem involvement due to intracellular deposition of an amorphous hyaline material.
Caused by mutations in the ECM1 gene on chromosome 1q21.
Normally EMC1 gene is expressed in the dermis, basal keratinocytes, endothelial cells and developing bones and is linked to keratinocyte differentiation, basement membrane regulation, collagen composition, and growth-factor binding. The mutated ECM1 gene gives rise to hyaline material deposition in the dermis and thickening of the skin and mucous basement membrane around blood vessels and adnexal epithelia.
The patient may present with abnormal scarring and wound healing. Premature skin aging, skin and mucosal thickening usually the first clinical manifestation. Moniliform blepharosis is considered a pathognomonic finding present in 50% of patients.

Associated hoarseness is present at birth or in the early infancy in two-thirds of patients, due to early hyaline material larynx infiltration, progressing with time.

When CNS is affected, a wide variety of neurologic abnormalities may be present. The hallmark findings are calcifications, mostly occurring in the amygdalae, hippocampus, parahippocampal gyrus, or even the striatum.
CNS infiltration occurs predominantly around the hippocampal capillaries, resulting in wall thickening, which later progresses to perivascular calcium deposition.
Neurologic manifestations range from migraine, variable degrees of mental retardation, seizures, depression, anxiety, and panic attacks to disturbances in decision making, memory, and abnormal social interaction patterns.

In half of cases imaging assist in the diagnosis and gives clue to the diagnosis because there are few diseases that can manifest such a typical pattern of bilateral and symmetrical calcification occurring in the medial temporal lobes. Amygdalae involvement is considered pathognomonic.
The other commonly affected sites are the amygdalae, hippocampus, parahippocampal gyrus, or even the striatum. The calcification pattern described is dense curvilinear horn-shaped well depicted by CT in the amygdaloid bodies. In MR imaging, such lesions are hypointense in all pulse sequences, especially in GRE T2*

Reference : American journal of Neuroradiology, Amygdalae and Striatum Calcification in Lipoid Proteinosis F.G. Gonçalvesa,b, M.B. de Meloa,  V. de L. Matosa, F.R. Barraa and R.E. Figueroac.

A focal Vermian bleed on MRI

 

MRI BRAIN WITH CONTRAST REPORT

This MRI study of brain reveals an ~ 12x13mm well defined round to ovoid nodular lesion in cerebellar vermis at the roof of fourth ventricle. Lesion is bright on T1 with high signal on T2 suggestive of blood degradation product with low signal on GRE. No marked peri lesional odema. No significant mass effect or mid line shift.

Imaging wise diagnosis suggested was Tumor nodule with bleed, however possibility of underlying vascular malformation can not be ruled out on imaging.

Operated with posterior fossa craniotomy. E/o complete excision of lesion on post operative scans. No major extra / intra axial bleed.

REPORT OF HISTO PATHOLOGICAL EXAMINATION

Specimen         : Excisional biopsy – SOL in base of skull (cerebellar vermis). 
Gross Appearance    : The specimen consists of few irregular soft pieces of dull greyish white tissue; together measuring 0.3X0.3X0.2 cm. The entire tissue is submitted for processing.    

Microscopy        : Section and additional made serial deeper section shows fragmented bits of reactive cerebellar tissue with the central portion showing ectatic vascular channel with undulating wall, devoid of smooth muscle and elastic lamellae. Also seen are couple of fragments with microhaemorrhage and scattered haemosiderophages along with prominent perivascular lymphocytic cuffing. There is no evidence of malignancy. 

Final Diagnosis  : Bleed secondary to Cavernous Angioma (Cavernoma).