Saturday, 27 February 2016

Bilateral Mesial Temporal Sclerosis MRI

Coronal high resolution T2 and FLAIR are best to diagnose MTS.
Findings include reduced hippocampal volume that is hippocampal atrophy, increased T2 signal, abnormal morphology that is loss of internal architecture and interdigitations of hippocampus.
Although comparing with opposite is easiest, it must be remembered that up to 10% of cases are bilateral, and thus if symmetry is the only feature being evaluated, many cases may be misinterpreted as normal.
Often mentioned, but probably one of the least specific findings, is enlargement of the temporal horn of the lateral ventricle. If anything, care must be taken to not allow an enlarged horn to trick you to over diagnosis as hippocampal atrophy.

Lateral epipharyngeal cyst MRI

Cystic lesion in the right pharyngeal recess (fossa of Rosenm├╝ller), behind the paryngeal ostium of the Eustachian tube.

Sunday, 21 June 2015

Spinal Epidermoid cyst MRI

Clinically: A 30 y o male with neurogenic bladder. 


This MRI lumbar spine show a spinal intra dural cystic signal intensity well defined lesion hypo intense on T1, hyper intense on T2 with restricted diffusion on Dw images. 
An associated expansion and scalloping of bony spinal canal. 
Lesion is confined to spinal canal and not extending out of neural foramen. 
Lesion is non enhancing on post contrast, except thin rim of enhancement on post contrast T1. 

Imaging diagnosis : Spinal Epidermoid Cyst.

Urinary bladder show diffuse wall thickening, irregularity with trabeculations attributed to associated Neurogenic bladder. 

Spinal Epidermoid Cyst

They are usually extra medullary but rarely can be intra medullary. They may be congenital or acquired.
Spinal epidermoid cysts are uncommon.

Unlike intracranial epidermoid cysts, which are almost always congenital in origin, most of spinal epidermoid cysts are acquired. Although present since birth, congenital epidermoid tumours often do not present until the second to fourth decade of life.
Males are more commonly affected than females.

Spinal epidermoid cysts may asymptomatic and discovered incidentally. If symptomatic, motor disturbances, pain, sensory disturbances, and bowel or bladder dysfunction may be present.
Congenital spinal epidermoids result from anomalous implantation of ectodermal cells during closure of the neural tube between the third and fifth week of embryonic life.
Acquired spinal epidermoids are a late complication of lumbar puncture, resulting from implanted epidermal elements into the spinal canal. The time interval between lumbar puncture and tumour diagnosis ranges from 1 to more than 20 years. Acquired spinal epidermoids are generally extramedullary and situated near a vertebral interspace.

Congenital epidermoids usually occur at the conus or cauda equina. Acquired cysts are found in the lower lumbar region.
Epidermoid cysts are commonly associated with spinal malformations such as spina bifida and hemivertebrae.
On CT, a well circumscribed mass, hypodense (similar to CSF),  minimal to no enhancement on post contrast, calcification is rare. Associated osseous changes include an expanded spinal canal, laminar thinning and vertebral body scalloping. 
On MRI typical signal characteristics include hypointense (similar to CSF) on T1, hyperintense (similar to CSF) on T2 and slightly hyperintense compared to CSF on FLAIR due to incomplete signal suppression. On T1 C+ (Gd) no enhancement or a thin rim of capsular enhancement. Characteristic bright signal on Diffusion with corresponding low intensity on ADC map. Signal intensity may be homogeneous or heterogeneous according to the variable water, lipid and protein composition of the cyst.

Spinal epidermoid cysts are slow growing.
Surgery is the treatment of choice, complete excision.
If the cyst wall is tightly adherent to the cord parenchyma, the wall should be left in place, however this leads to a risk of recurrence.

Differential diagnosis include spinal arachnoid cyst which lacks brightness of restricted diffusion on DWI, complete signal suppression on FLAIR. Vertebral anomalies uncommon.
Spinal dermoid cyst usually contains fatty elements, less likely to demonstrate diffusion restriction on DWI, patients are usually younger than 20 years of age.
Spinal neurenteric cyst common in thoracic and cervical regions, ventral to spinal cord with associated vertebral anomalies. 

AVM with bleed and ischemic complications on MRI

Clinical Details  : Two months ago suffered from a left basal ganglionic bleed. Had to have decompression done. PResently has a power of grade 0 on the right arm and right leg but speech is fairly well preserved. 
Presently on Ecosprin gold, Omnacortil. Pantocard.

Advised MRI for better evaluation


MRI Brain with MR Angiography of Brain Report

Sequences planned are FLAIR, T2w*GRE and DW images.
Non Contrast Enhanced intracranial Angio performed with 3D TOF and Neck Angio performed with 2D TOF sequence. The study viewed in row as well as 3D reconstructed images.

A focal Gliosis  with hemosiderin staining on GRE involving left thalamus, adjacent basal ganglia, insula and temporal lobe_ Chronic resolved hematoma with areas of chronic ischemic infarcts in left MCA cortical branches territory. 
An associated changes of distal wallerian degeneration on left side. 
An obvious high flow vascular malformation _ AVM noted, left pcom appears to be the feeder. 
Sparisty of cortical branches of left MCA. 

Rest of the both intra cranial as well as extra cranial vessels show normal flow related signals on 3D reconstructed images of Non Enhanced 3D TOF and 2D TOF sequences.


Chronic resolved hematoma with chronic infarcts in left MCA cortical branches territory.
An obvious high flow vascular malformation / AVM noted, left pcom appears to be the feeder. 
Sparisty of cortical branches of left MCA compared to right.

Needs DSA for better evaluation / confirmation. 

Tuesday, 16 June 2015

Atypical Trigeminal Neuralgia MRI

Clinical details: right side trigeminal neuralgia.


Multi planner multi echo MRI study of brain has been performed. Sequences planned are FSE T1W, FSE T2W, FLAIR, T2w *GRE and DW images. FIESTA for cranial nerves.
Pc t1

This MRI Brain shows:
Abnormal T2 hyper intensity in right half of Pons at the entry point of right side trigemninal nerve, and adjacent right side trigeminal nerve_ significant for patients clinical complaints.
There is faint high signal on DW images in corresponding region.
No abnormal enhancement on post contrast T1.

Possibilities given were Demyelination, Ischemia.

He was prescribed
Amytryptiline 25 mg HS
Wyselon 20mg daily for 5 days, 10 mg for next 5 day and then stop
Gabapentine 300mg BD

During follow up after 2 weeks
He was clinically improved by 75 % which goes in favor of Demyelination.
During this follow up, MRI imaging shows lesion is same in size without any significant change on T2w images. The faint hyper intensity which was seen in previous MRI was reduced.
Advised further follow up imaging.

Current clinical status after 2 months, 100% improved.

There are persuasive evidences that trigeminal neuralgia is usually caused by demyelination of trigeminal sensory fibres within either the nerve root or, less commonly, the brainstem at the entry point of nerve. However in most cases, the trigeminal nerve root demyelination involves the proximal, CNS part of the root and results from compression by an overlying artery or vein.

Tuesday, 2 June 2015

Unilateral Optic Nerve Aplasia

Clinically a premature baby, Ophthamological evaluation revealed abnormally small Optic disc on right side. Advised MRI for further evaluation. 
MRI brain shows absent right side optic nerve, its intra cranial as well as intra orbital portion.
Left side optic nerve normal in caliber and signals, left half of optic chiasm and bilateral optic tracts normal. No associated anomalies of corpus callosum or septum pellucidum. Pituitary gland normal, no posterior lobe ectopia.

Impression: Congenital Unilateral Optic Nerve Aplasia.

Optic Nerve Aplasia 

A rare developmental anomaly characterized by the congenital absence of the optic nerve, central retinal vessels and retinal ganglion cells.
Aplasia is often unilateral, generally associated with otherwise normal brain development while bilateral optic nerve aplasia is usually accompanied by severe and widespread CNS malformations.
The pathogenesis of optic nerve aplasia may be due to defective formation of the embryonal fissure, failure of the mesenchymal anlage of the hyaloid system to enter the embryonal fissure, or primary agenesis of the retinal ganglion cells.

Optic nerve hypoplasia is seen ophthalmoscopically as an abnormally small optic nerve head. A peripapillary ring around a small optic disc is the hallmark, but is not always present. ONH may be associated with tortuosity of the retinal vasculature. A relative afferent pupil defect adds weight to the diagnosis.

ONH is commonly asymptomatic and may first be detected by identification of visual field loss or observation of the optic nerve head.

1. Isolated ONH.
2. Absent septum pellucidum.
3. Posterior pituitary ectopia (commonly associated with endocrine dysfunction).
4. Migrational anomalies in the cerebral hemispheres (for example, thinning of the corpus callosum, which is predictive of neurodevelopmental problems). Other associated brain abnormalities include porencephaly, schizencephaly, intracranial arachnoid cyst, and intracranial epidermoid cyst.

Septo-optic dysplasia comprise any combination of ONH, pituitary gland hypoplasia, and midline abnormalities of the brain. Recent studies have shown that in SOD, key mutations have been identified in Hesx-1, a protein that is involved in the mediation of normal development of the forebrain and the eyes during embryogenesis.

Sunday, 31 May 2015

Brain Stem Lesion MRI



Multi planner multi echo MRI study of brain has been performed. Sequences planned are FSE T1W, FSE T2W, FLAIR, T2w *GRE and DW images. Pc T1 

This MRI study of Brain with whole spine shows:
1. An ~ 25x27mm intral axial cystic lesion with an avidly enhancing eccentric nodule, lesion causing marked expansion of medulla, marked peri lesional odema extending in adjacent Pons. Obstruction at the level of outlet foramen of fourth ventricle causing mild communicating hydrocephalus. 
2. An associated severe cervico dorsal cord syrinx.
3. Avidly enhancing nodule of spinal drop metastasis at D7-8 and D11.

Imaging wise Possible DDs given were Neoplastic_ like Medullary Pilocystic Astrocytoma, Hemangioblastoma. 


Posterior fossa craniotomy with excision of lesion.

Histopathology report

Gross : The specimen consist of single nodular piece of gray white tissue, measuring 2x2x2cm. 


Sections shows moderately vascular neoplasm of both cellular and reticular areas comprising numerus proliferating vascular channels of varying caliber few of them appear to congested. The interstitium shows scattered round to oval cells having modestly hyperchromatic nuclei with coarse chromatin and abundant eosiophillic to vacuolated cytoplasm. These cells have indinct cytoplasmic margins. No atypical mitosis nor tumor necrosis seen. 

Impression :

Histopathological diagnosis : Hemangioblastoma. 

Posterior Fossa Mass MRI

Clinical Details  : About four to five months history of headaches over the vertex and the occipito-nuchal region, constant, not associated with any vomiting or blurring of vision. She has also been complaining of some blurring of vision. Examination shows papilloedema in the right eye. No other signs. 
Previous CT shows mild ventriculomegaly and an enhancing posterior fossa lesion behind right cerebellum with some degree of compression over 4th ventricle.
Advised MRI for better evaluation.



Multi planner multi echo MRI study of brain has been performed. Sequences planned are FSE T1W, FSE T2W, FLAIR, and DW images. PC T1. 
Single voxel MR Spectroscopy. 

An extra axial dural based ~ 60x30mm well-demarcated mass at the floor of posterior cranial fossa extending beyond foramen magnum in spinal canal, compressing cerebellar hemispheres , medulla and vertebrals at foramen magnum. Obstructive hydrocephalus due to fourth ventricle compression, peri ventricular ooze of Csf. 
No marked perilesional odema. Lesion is homogenously iso intense on cortical gray matter on T1 and iso intense on T2 images with homogeneous enhancement on post contrast T1.
On MRS, No NAA peak, significantly reduced Creatinine. High choline and choline -creatinine ratio. 

Impression: Imaging wise diagnosis given was Meningioma.


Posterior fossa craniotomy done with complete excision of lesion.

Histopathology report

A high grade extra medullary myeloid cell tumor without any lineage differentiation.
The tumor cells express LCA, Mic 2 Weak , CD 3, TdT few cells and CD10 and are CD 33, 7, 68, 61 and Glycophorin C.
The Mib 1 labeling index is approximately 50%

Impression : High grade extra medullary myeloid cell tumor without any lineage differentiation - LYMPHOMA.

" This is second time that Lymphoma has surprised me". 

Sunday, 24 May 2015

Ulegyria MRI

Ulegyria refers to shrunken cortical gyri due to ischaemic damage in the neonatal period.
The main method of detecting ulegyria is MRI will reveal a focal gliosis of affected gyri. In addition, unaffected gyri are also present especially in watershed regions indicating delayed effects of perinatal hypoxic damage.
There are three main criteria for diagnosing ulegyria using MRI. The presence of a poorly demarcated lesion, atrophy and thinning of the cortex resulting in the characteristic “mushroom” like shape of ulegyria and presence of white matter signal abnormalities on FLAIR.
Ulegyria must be differentiated from polymicrogyria, which is a neuronal migration disorder, characterized by excessive folding of the surface gyri and a thickening of the cerebral cortex, rather than the sulcal scarring that is typical of ulegyria.
The period in which polmicrogyria and ulegyria emerge is also different. Polymicrogyria typically forms while the embryo's central nervous system is maturing. Ulegyria is acquired later in development during the perinatal period after neuronal migration has already occurred. It is also suspected that polymicrogyra is genetically linked, whereas ulegyria is caused by environmental factors like ischemia.
Polymicrogyria can lead to similar conditions that are linked to ulegyria such as mental retardation, cerebral palsy, and epilepsy. It has been observed that patients with polymicrogyria are not receptive to epilepsy surgery. However, responses of patients with ulegyria to similar surgeries are still not fully known, which makes distinction of these two disorders significant. 

Role of MR Csf flow study in NPH

By definition NPH is Ventriculomegaly on MRI with normal CSF pressure, altered CSF dynamics.

Of course NPH is a clinical diagnosis.
The classical clinical triad of NPH is
1) urinary incontinence
2 ) deterioration in cognition (dementia) and
3 ) Ataxia i.e. Gait disturbances.
As the name suggests mean CSF opening pressure in patients with NPH is within the normal range with a classic neurological sign is magnetic gait.

Best diagnostic clue on MRI is ventricles and Sylvian fissures symmetrically dilated out of proportion to sulcal enlargement, with normal hippocampus which distinguishes NPH from atrophy.
Ventriculomegaly is prominent in all 3 horns of lateral ventricles and 3rd ventricle, with relative sparing of 4th ventricle.

Role of MRI is now not confined only to support the clinical diagnosis of NPH but is to identify shunt-responsive NPH pts from non responsive by calculating aqueductal stroke volume non invasively.
This is because studies have shown that aqueductal stroke volume in patients of NPH decreases later in the disease process despite clinical progression and classifcal findings on MRI this has been theorized to be caused by cerebral atrophy, which indicates that the patient is unlikely to respond to shunt surgery.

Normal CSF flow and its dynamics

The stroke volume across aqueduct is the average CSF volume flowing through the aqueduct in one cardiac cycle, craniocaudad during systole OR caudocraniad during diastole.
Normal values of stroke volume is < .04 ml/cycle
It is assumed that the net flow over 1 cardiac cycle is [negligible enough to be considered as] zero
Aqueductal velocity (caudal): 3-8mm/s
The peak velocity was determined from the maximum value of the measured velocities of each cardiac phase.

CSF flow study findings in NPH
In NPH actually there is lack of flow from the cisternal and subarachnoid spaces with significant increase in amount of ventricular csf flow.
There increased flow void across aqueduct with increase stroke volume.
1) Increased aqueductal stroke volume is the average volume of CSF moving through the cerebral aqueduct calculated by summing the absolute values of stroke volume in systole and diastole and dividing by 2
i.e   Forward stroke volume +  Reverse stroke volume   /   2
2) Increased aqueductal peak velocity.

Various publications have set various normal and abnormal ranges.
Flow rate of > 24.5mL/min 95% specific for NPH.
Stroke volume of > 42 microL shown on one paper to predict good response from shunting was statistically significant (P < .05).Studies have shown that aqueductal stroke volume decreases later in the disease process despite clinical progression.
Sroke volume upper limit is now suggested to be variable between institutions due to intrinsic scanner differences, thus each centre should obtain their own "normal values", with the upper limit being suggested as two times the normal value.
There was no statistically significant relationship between aqueductal CSF flow void score and responsiveness to shunting.

Case 1

With clinical diagnosis of NPH

MR brain reveals diffuse cerebral and cerebellar cortical atrophy.
The ventricular dilatation is disproportionate to the amount of cortical atrophy, scalloping of inferior margin of corpus callosum and prominent flow void in posterior portion of third ventricle, across cerebral aqueduct and superior portion of fourth ventricle consistant with clinical diagnosis of NPH.
Csf flow study report :
Gated cine phase contrast study was performed to evaluate the CSF flow.
The diastolic phases are equal in number to the systolic.
The stroke volume is 41 microliters per cycle consistent with shunt responsive status (Reference : Patients with stroke volume more than 40 microliters respond well to VP shunt _ Bradley et al)

Case 2 

Atrophy Vs NPH clinically

MRI brain reveals moderate cerebral and cerebellar atrophy. The ventricular dilatation is mildly disproportionate to the amount of cortical atrophy.

Csf flow study report :
Gated cine phase contrast study was performed to evaluate the CSF flow.
The diastolic phases are equal in number to the systolic. The stroke volume is 30 microliters per cycle consistent with non-shunt responsive status. ( Reference : Patients with stroke volume more than 40 microliters respond well to VP shunt _ Bradley et al).

Dr Deepak Patkar (HOD, Nanawati Superspeciality Hospital, Vile Parle, Mumbai)
Dr Balaji Anvekar (Short visiting Fellowship in Neuroradiology and Recent Advances in Neuroimaging)