Crista galli prominence

A midline thick, triangular process projecting superiorly from the cribriform plate of the ethmoid bone.
The site of attachment for the falx cerebri.
A normal anatomical structure of no clincial significance.
Bright signal on this T1 w image is due to its fatty marrow. 

Coronal Cleft in vertebra

Sagittal MRI T2 images of lumbo sacral region show a low signal intensity representing a coronal cleft of cartilaginous plate in the posterior portion of S1 vertebral body - a normal anatomical variation of no clinical significance.

Coronal cleft in the vertebral body is an anomaly resulting from a failure of fusion of the anterior and posterior ossification centres which remain separated by a cartilage plate.
Represents a delay in normal vertebral maturation.
In most cases clefts disappear by six months after birth. In some cases remains persistent.
Usually seen in the lower thonacic on lumbar vertebral bodies.
Radiographically, a vertical radiolucent band is seen just behind the mid portion of the body on the lateral view.

Spondylolysis

MRI Lumbar spine sagittal T2 right far lateral image, left far lateral image, sagittal T1 right far lateral and left far lateral image, shows non displaced break in L5 pars intercularis on either side. No listhesis.

Non displaced breaks in L5 pars inter articularis on either side confirmed on CT study. 

SPONDYLOLYSIS

Spondylolysis refers to an osseous defect within the pars interarticularis, an isthmus of bone located between the superior and inferior articular processes. 

Spondylolysis most commonly affects the L5 level (in 85  to  95% of cases) with the majority of the remaining cases occurring at L4 (5  to 15% of cases). 

While the exact etiology of spondylolysis is unknown, it is generally believed to represent a stress fracture caused by repetitive loading, although there are hereditary and genetic contributing factors.

Spondyolysis on MRI needs demonstration of an osseous break in pars on sagittal far lateral images which may not be possible every time due to limitations of sagittal plane of imaging. 

Spondyolysis with an associated Spondylolisthesis is readily identified on the midline sagital images. However in most cases of spondyolysis have normal vertebral alignment, several ancillary findings have been described that may aid in the diagnosis of spondylolysis. These include a widened anteroposterior diameter of the spinal canal on sagittal images, reactive marrow changes in the posterior elements and abnormal wedging of the posterior aspect of the vertebral body.

1. Widened anteroposterior diameter of the spinal canal : A ratio of the AP diameter at the L5 level to the AP diameter at the L1 level is used. The canal is measured from the posterior cortex of the vertebral body to the anterior aspect of the lamina on a mid-sagittal image. A ratio of 1.25 is normal. This ratio is increased in patients with spondylolysis due to posterior subluxation of the posterior elements, even in cases where no spondylolisthesis is present. 

A midline sagittal T2 weighted image:  The AP diameter of the canal at L1 measures 1.7cm and the AP diameter of the canal at L5 measures 2.5cm. The ratio of L5:L1 is 1.47, which is above the normal value of 1.25. Even without this calculation, it is clear the canal is enlarged at the L5 level with the posterior elements displaced slightly posterior when compared with the posterior elements of the more cranial vertebral bodies.

2. Reactive marrow changes : Altered marrow signals similar to those observed in patients with degenerative disc disease are identified within the posterior elements adjacent to pars defects in a significant number of patients in ~ 40% of patients with spondylolysis 

3. Abnormal wedging: An abnormal wedging of the posterior aspect of the vertebral body at the level of the pars defect. It is unclear if this finding is an effect of the spondylolisthesis, a predisposing condition, or a combination of both. On sagittal MR images, wedging of the posterior vertebral body is seen both in patients with spondylolisthesis and in those with spondylolysis and no significant subluxation.Therefore, such wedging may suggest the presence of pars defects.

A midline sagittal T2 image lines have been drawn to show the height of the anterior and posterior vertebral body. Posterior wedging of the vertebral body is seen, which is an ancillary finding suggesting the presence of spondylolysis at this level.

Hypoplasia is common in spondylolysis and might mimic spondylolisthesis so careful not to misdiagnose spondylolysis as spondylolisthesis, when hypoplasia is present. 

MRI Second Opinion

Why You Need a Second Opinion

CT and MRI are among the most powerful diagnostic imaging tools available today for detecting many types of illnesses. MRI is considered as the investigation of choice as far as brain and spine are concerned.
In MRI, images of part scanned are captured by the machine. The images obtained then are evaluated by the concerned radiologist. The machine provides images to view inside the body, but it is up to human eyes to interpret the data optimally.  Here lies radiologist’s skill and keen observation to analyze what the machine has recorded.

Many factors can influence the interpretation of an exam in that the radiologist’s experience level, workload and fatigue. Your MRI or CT scan is negative, normal but still you have persistent problem or a problem which is mentioned in your original report based on which your treating physician advises you surgery and in such case to be sure your may need a second opinion. You may be getting conflicting results regarding your scans and to have peace of mind you may need an expert to review your scan.

Studies have found that not every radiologist will interpret the same MRI picture in exactly the same way.  Your course of treatment depends on the exam results and the patients who want the best healthcare will get extra assurance with an MRI second opinion.

Remember, receiving an MRI second opinion does not mean you do not trust your doctor.  It simply means you are a conscious and motivated patient or patient’s relative ready to play an active role in your own healthcare and most physicians will respect and welcome this.

A second opinion can confirm and validate prior diagnoses or may even present different options for consideration.

Non Hogkin's Lymphoma

A 40 yo male admitted for headache.
Neurological examination normal.
On admission CT shows a hyper dense focal lesion in the region of right basal ganglia with moderate uniform enhancement, marked perilesional vasogenic odema.
Imaging wise possible DDs suggested were Lymphoma and Toxoplasmosis. 

Immune status : Tridot Non reactive.
Csf : Slightly raised protein. Otherwise normal.
CT Chest showed multiple bilateral discrete soft tissue density parenchymal nodules.
CT Abdomen normal.
Neck nodes biopsy and histopathology revealed Non Hogkin's Lymphoma.









The follow up CT after course of radiotherapy shows significant regression in size of lesion, perilesional odema and mass effect support diagnosis of Systemic Non Hogkin's Lymphoma (NHL) with CNS involvement. 

Pilocytic Astrocytoma

A 30 yo male with long standing progressive headache, recently worsened with vomiting.

An intra axial predominantly cystic well circumscribed mass with mural nodule in left frontal lobe.
Marked T2 hyper intense perilesional vasogenic odema.
The fluid content of cystic component is not clear as signal supression on FLAIR is not complete. Cystic component show thin enhancing wall on post contrast T1. The mural nodule is round to ovoid, of soft tissue signal intensity with solid enhancement on post contrast T1.

Histopathology: Pilocytic Astrocytoma with Gemistocytic differentiation and malignant degeneration (Malignant Pilocytic Astrocytoma) 



PILOCYTIC ASTROCYTOMA

Synonym: Polar spongioblastoma.
Astrocytic precursor cell tumor.
Contributes 5-10% of all gliomas.
Most common primary brain tumor in children. More than 80% are under 20 y, Peak incidence: 5-15 years of age, Gender: M = F.

Genetics:
Has syndromic association with NF 1.
15% of NF 1 patients develop PAs, most commonly in optic pathway.
Up to 1/3 of patients with optic pathway PAs have NF 1.

Cystic cerebellar mass with enhancing mural nodule is diagnostic clue.
Overall morphology often determined by cystic Component.
Cerebellum is most common (60%) > optic nerve/chiasm (25-30%) > adjacent to 3rd ventricle > brainstem.

Imaging findings:
Discrete cystic /solid mass, may have little or no surrounding edema.
Solid component variable density on CT and signal intensity on MRI, enhance strongly as enhancing mural nodule in more than 95%.
Non enhancing cyst in ~ 50% cases. Cyst may accumulate contrast on delayed images.
Associated calcification in ~ 20%, hemorrhage rare.
Rarely tumor may spread through subarachnoid space (but is still WHO grade I)
MR Spectroscopy is aggressive appearing metabolite pattern, high choline, low NAA, high lactate

Frequently causes obstructive hydrocephalus, may be a greater clinical management problem than tumor itself.
Most common signs/symptoms are Headache, nausea and vomiting, Ataxia, Cerebellar signs.

Treatment:
Resection.
Adjuvant chemotherapy or radiation only if residual, progressive, unresectable tumor.

DDs:
Medulloblastoma (PNET-MB)
• Hyperdense enhancing midline mass fills 4th ventricle
• Younger patient age (2-6 y)
Ependymoma
• "Plastic" tumor, extends out 4th ventricle foramina

• Ca++, cysts, hemorrhage common; heterogeneous enhancement.
Posted by Dr Balaji Anvekar at 5:06 pm 0 comments

Similar case : http://www.neuroradiologycases.com/2013/12/posterior-fossa-cystic-mass-mri.html

Glioblastoma multiforme

55 yo male with headache and vomiting.

Contrast Enhanced CT and MRI study of brain with MR Spectroscopy shows:
1. An intra axial space occupying lesion in left frontal lobe white matter. T2 iso intense thick enhancing wall with T2 hyper intense central non enhancing necrosis. An enhancing T2 iso intense eccentric nodule. T2 hyper intense Perilesional vasogenic odema. Dw images show high signal along the thick wall. No restricted diffusion in the region of central necrotic core. Faint low signal along the wall on T2*GRE represent hemosiderin staining.
2. Another separate similar signal intensity but smaller fainly enhancing bubbly lesion involving corpus callosum extending in right lateral ventricle.
3. Significant mass effect. Left lateral ventricle compressed, significant mid line shift with mid brain compression.
4. MR Spectroscopy, a 2x2cm voxel placed over the nodular portion of lesion, spectral waveform obtained at short TE of 35 ms. Sharp doublet of lactate at 0.9 to 1.3ppm, short peaks suggestive of markedly reduced NAA at 2.02ppm and creatinine at 3.02ppm. sharp long peak of raised choline at 3.03ppm. raised choline - creatinine ratio.

Imagingwise diagnosis : Multicentric Glioma and Abscess.
Absence of restricted diffusion, thick enhancing wall with eccentric nodule goes more in favour of Glioma over abscess.
Histopathology report : Glioblastoma Multiforme.

GBM, a grade iv glioma, most common primary brain tumor, ~12-15% of all intracranial neoplasms, ~50-60 % of astrocytoma, multifocal in upto 20% cases. 

Craniopharyngioma

A 35 yo male with headache and visual field defect.

MRI Brain

Axial T2 T1 and FLAIR with sagittal post contrast T1 images.

Findings: 

A multi lobulated, well circumscribed, sellar supra sellar mass with solid cystic component.

The solid component seen as profuse enhancing nodule anteriorly. 

Cystic component is hyper intense on FLAIR due to absence of complete signal suppression as fluid content is not clear. Thin rim of enhancement along its wall. 

Mild T2 hyper intense peri lesional odema in the adjacent frontal and medial temporal lobes. 

Mild dilatation of lateral ventricles appears to be due to trapping possible at the level of foramen monro secondary distortion of supra sellar anatomy. Splaying of mid brain. Both the ICA is displaced laterally. 

Flattened normal enhancing Pituitary seen separately at the floor of hypophyseal fossa. 

Imagingwise diagnosis : Craniopharyngioma. 

DD : Cystic macro adenoma. 

Histopathology proven: Craniopharyngioma.

Craniopharyngioma 

Syn : Craniopharygeal duct tumor, Rathke pouch tumor, Admantinoma. 

A benign dysontogenetic epithelial tumor derived from Rathke pouch epithelium.

Most common pediatric intra cranial tumor of non glial origin. 

Histologically two types : Adamantinomatous and Papillary.

A supra sellar multi lobulated mass with solid cystic component and calcifications in a young patient is a diagnostic clue. Cystic component may not be clear, often hyper intense on FLAIR even on T1w images  depending up on its proteinaceous content.  

Imagingwise locations of CPs.

Supra sellar ~ 75%

Supra + Intra sellar ~21%

Intra sellar  ~4%

Rare ectopical locations are Optic chiasma, third ventricle, Nasopharynx, pineal region.

For surgical interest divided into three groups as par location into sellar, pre chiasmatic and retro chiasmatic.

Size is variable, often large at the time of presentation more than 5cm.

Presentation is common with visual field defect with headache due to optic chiasma compression. Hydrocephalus.         

Central Neurocytoma

Non contrast CT study of brain of a 40 yo male.

Findings:

A well circumscribed intra ventricular lobulated mass lesion.

Centred to septum pellucidum.

Extending in third ventricle, pineal region and upto fourth ventricle.

Density is mixed, heterogeneous due to solid and cystic necrotic areas.

Moderate hydrocephalus.

Imaging diagnosis : Findings are typical of Central Neurocytoma.

Steriotectic biopsy performed.

Histo pathology report : Central Neurocytoma.

Central Neurocytoma

Syn : Neurocytoma.

An intra ventricular neuro epithelial tumour.

Extra ventricular Neurocytoma is known but rare.

Bubbly lobulated well circumscribed mass.

Location is typically lateral ventricles attached to septum pellucidum.

May extend up to third ventricle. Extension in fourth ventricle is extremely rare as in this case.            

Calcification is common in ~ 60%.

Hydrocephalus is common.                     

Fusion and adjacent segment degeneration

Sagittal MRI cervical spine shows:
C5-6 Congenital fusion, as the intervening C5-6 disc is rudimentary with concavity of combined anterior surfaces of C5 and C6 - 'wasp waist' sign.
Absent normal cervical lordosis.
Marked degenerative changes at adjacent levels particularly C4-5 and C6-7.
No significant canal stenosis or cord compression.

In this case I've tried to focus on the relation between fusion of vertebral bodies let it be congenital or post discectomy and the advancement of degenerative changes at adjacent levels.

Development of adjacent segment degeneration (ASD) secondary to fusion :
The mechanical and shearing motion exerted by the lever moment at adjacent levels.
Increased intra discal pressures at adjacent levels which is proved in vitro during normal load testing.
Combination of these two mechanisms is postulated as being responsible for hypermobility and accelerating degenerative changes in the pathogenesis of ASD.