Monday 26 December 2011

Bilateral Anterior Circulation Stroke

A 70 y o male admitted for stroke evaluation.
Here is MRI Brain diffusion with MR Angio.
MRI Brain Diffusion shows bilateral hemispheric restricted diffusion suggestive of an acute ischemic infarct, involving bilateral peri sylvian cerebral cortex, insular cortex and basal ganglia (bilateral MCA proximal main stem territory), para sagittal fronto parietal cortex (bilateral ACA territories).
Bilateral medial occipital lobes, mesial temporal lobes and thalami (PCA territory) spared.

On Non contrast 3 D TOF brain and 2 D TOF neck angio both the ACAs and MCAs not visualized  Neck angio suboptimal as pt was non coperative.

Diagnosis : Anterior circulation stroke - Simultaneous bilateral hemispheric infarcts / Bilateral ACA - MCA territory. 

Sturge Weber Syndrome

A 15 yo male for epilepsy screening.
Imaging finding on CT brain are very typical of Sturge Weber syndrome.
Unilateral involvement,
Left side cortical atrophy,
Dense gyriform calcification with,
Ipsilateral  mild choroid plexus enlargement,
Ipsilateral bony calvarial thickening, enlargement of para nasal sinuses including left side frontal, sphenoid and mastoid air cells. 

SWS is an encephalo trigeminal angiomatosis, a rare congenital neurological and skin disorder, one of the phakomatoses. Unlike other neurocutaneous disorders (phakomatoses),  Sturge-Weber occurs sporadically without hereditary aetiology.
Characterised by port-wine stains of the face and ipsilateral lepto meningeal angioma.
Port-wine stain as birthmark on the forehead light pink to deep purple in colour, caused by abundance of capillaries around the ophthalmic branch of the trigeminal nerve.
Symptomatic with seizures from birth, mental retardation, glaucoma.

Related posts:

Sturge-weber-syndrome Case 1

Sturge-weber-syndrome Case 2


Sunday 25 December 2011

Multiple intracranial Meningiomas

A19 yo male with history of mild headache.

MRI study shows:
Three meningiomas, largest is falcine meningioma along inter hemispheric fissure, 2nd in left frontal region near orbit, 3rd smaller one in left parietal region.  Signal iso intense to cortical grey matter. Mild perilesional odema.
No vestibular schwannoma on any side.
Clinically no family history or signs of NF2. No family history of meningiomatosis.

Imaging diagnosis : Multiple intracranial meningiomas.

Multiple intracranial meningiomas is a condition where more than one meningioma in several intracranial locations in the same patient without signs of neurofibromatosis.
Incidence varies from 1 to10%.

Multiple intracranial meningiomas do not imply neurofibromatosis.
Despite of multiplicity, multiple meningiomas does not differ in prognosis from benign solitary meningiomas.

Related post : Meningioma MR Spectroscopy

Arterio Venous Malformation (AVM)

A young female consulted in OPD for seizures.
This non contrast CT study of Brain shows mild asymmetry of cerebral hemispheres and lateral ventricles, right side hemisphere is larger in volume than left. 
Right lateral ventricle is smaller than left (Rules out Hemi megaencephaly).
Again multiple nodular densities along the ependymal lining of wall of right lateral ventricle which needed further evaluation.

MRI study of brain with MR Angiography of brain

Ax T2, T2*GRE with Non contrast 3D TOF brain Angio

This MRI study shows:
Multiple serpigenous T2 flow voids clustered in Right temporo parietal lobe suggestive of vascular malformation that to high flow malformation as signals are hyper intense on T2*GRE.
Imaging diagnosis : Arterio venous malformation (AVM).
Right MCA, ACAs and PCAs are the feeder on MR Angio.
Draining channels appears to be superior sagittal sinus and deep cerebral veins.

Related post : AVM 

Secondary Intracerebral Hemorrhage

Young male admitted to casualty for stroke. 
On admission CT 
Follow up CT after a week
Follow up MRI
2 D TOF MR Venogram
Right parietal lobar bleed.
The subependymal venous angioma noted along choroid plexus of right lateral ventricle on follow up CT and T2w images.
Multiple fine T2 flow voids clustured in right temporal lobe adjacent to the hematoma.
Faint dystrophic calcification along the vascular malformation in right temporal region adjacent to the hematoma depicted on CT.
Dilated right side posterior mesencephalic vein, basal vein and vein of Galen noted on MR.
Superior sagittal sinus show absence of normal T2 flow voids. Sinus is not bulky rather smaller in caliber, eccentric dots of T2 flow voids in the region of sinus are partially recanalised channels which show poor flow related signal on 2 D TOF MR Venogram appears to be a chronically thrombosed sinus.


This MRI study shows:
Right parietal lobar bleed - a secondary intra parenchymal hemorrhage.
An associated venous Angioma.
Chronic dural sinus thrombosis. 

There is known association of dural venous sinus thrombosis (CVT)  with conditions like venous angioma and av fistulas. Now it is under debate that whether venous angiomas and fistula secondarily result into CVT as a result of altered blood dynamics or chronic CVT is first to occur resulting in  development of alternate abnormal vascular channels.

An intracerebral hemorrhage account for ~15% of all strokes and is the one of the most disabling forms of stroke.
Divided in to two major types primary and secondary.
A. Primary ICH develops in the absence of any underlying vascular malformation or coagulopathy. Primary intracerebral hemorrhage is more common than secondary. Hypertension and Amyloid angiopathy to 2/3 rd of causes primary haemorrhages. Some time it may be difficult to identify the underlying cause.  Hypertension related bleed are more common in basal ganglia along external capsule the reason appears to be high pressure within the Circle of Willis resulting in smooth cell proliferation followed by smooth muscle cell death. Whereas Amyloid angiopathy affects leptomeningeal and intraparenchymal cortical vessels explains the occurrence of large superficial lobar haemorrhages with amyloid angiopathy.
B. Secondary ICH occure secondary to underlying causes like vascular malformation, sinus thrombosis, hemorrhagic conversion of an ischemic stroke, embolic stroke, coagulopathy, intracranial tumor, hemorrhagic metastasis etc. Arteriovenous malformations, aneurysm account for majority of underlying vascular malformations. Venous Angioma are most the time asymptomatic, noted as an incidental finding and is a rare cause of bleed.

Related posts:
Cavernoma with venous-angioma

Pyogenic Abscess MRI

A young male, admitted for recent onset seizures. 
On admission MRI

Description of findings:
A well defined focal lesion in left parietal sub cortical white matter, size ~45x35mm.
Lesion has thin T2 hypointense wall, intensely enhancing on post contrast T1 with a multi locularity, enhancement pattern is peripheral type due to enhancement along its wall, non enhancing necrotic core which is hyper intense T2 and shows restricted diffusion on Diffusion weighted images.
Marked perilesional T2 hyperintense vasogenic odema. Left lateral ventricle is compressed.
No significant mass effect.

Imagingwise Possible DDs: Abscess > Glioma.

Restricted diffusion goes in favor of an Abscess over Glioma.

Histopathology Report : Xanthogranulomatous inflammation, macrophages, granulation tissue with fibroblasts surrounding necrotic core  S/o Pyogenic abscess.

Related post :

Abscess MR Spectroscopy

Wednesday 14 December 2011

MRI 3D Inner Ear

MRI evaluation of internal auditory canal, 7th 8th nerve complexes and inner ear done by means of 3D-FIESTA Sequence.
The 3 D reconstruction of inner ear done with post-processing by maximum intensity projection(MIP) and multi-planar reconstruction(MPR) where as thin axial sections combined with 3 D reconstruction of inner ear by using 3D-FIESTA sequence precisely show IAC with 7th 8th CN Complex, Trigeminal CNs and Inner ear as well as the relationship between lesions and structures in and around IAC.

A case of left facial hemi spasm, MRI Brain axial sections of FIESTA shows tortuous left vertebral causing left side 7th - 8th CN complex compression. 

A case of right side trigeminal neuralgia shows tortuous basilar very close to cisternal portion of right side trigeminal nerve causing mild displacement of nerve. 

Anatomical Variations of Vertebral

Left vertebral arising from arch of aorta near root of left subclavian 
Axial row images of same pt showing origin of left vertebral from arch of aorta near root of left subclavian  
Anatomical Variation of Vertebrals

Right vertebral artery may arise:
from the first part of the subclavian, nearer than normal to the brachiocephalic or to the anterior scalene muscle;
directly from the arch of the aorta;
from the right common carotid, when the right subclavian arises from the aorta beyond the left subclavian;
or from the brachiocephalic trunk. The right artery may pass behind the esophagus.

The left vertebral artery may arise :
directly from the left common carotid;
root of the subclavian, close to the aortic arch.
or from the arch of the aorta.

There are occasionally two left vertebral arteries. In such case, one may from the arch of the aorta, the other from the left subclavian artery in the normal position.
The origin of the left vertebral artery from the aortic arch is a very common variation, but the origin of the vertebral artery from the right side of the arch is very rare.
The left and right vertebrals may be doubled with each vessel entering a different transverse foramen. In rare occasion either vertebral artery may arise from the thyrocervical trunk or from the costocervical trunk.

The two vertebrals are usually unequal in size, the right being smaller than the left. The dominant continues as basilar. Intra cranial portion of contra lateral vertebral may be hypoplastic or completely absent.

Very rarely the two vertebrals fail to unite to form the median basilar artey, hence the basilar may appear to be doubled. The two longitudinal trunks may be united by anastomoses between them.
The vertebral artey may exist as several vessels that eventually unite, or it may form an arterial ring traversed by the hypoglossal nerve.

Related post:
Duplication of vertebral 

On left side there are 2 separate origins of the vertebral artery from the corresponding subclavian, the duplicated vessels join together before continuing as one vessel in the foramina transversaria

Tuesday 13 December 2011

Post traumatic Subdural Hygroma

Syn: Subdural Effusion.
Widening of subdural space filled with a Csf density collection.

The most common cause.
Arachnoid tears and Arachnoid - dura separations which commonly occur near sylvian fissure appears to be the possible mechanism which results in CSF escape into subdural space.
Reported in approximately 10% of head injuries, provided it is moderate to severe type. Associated fractures in approximately 35% cases.
Usually appears after a week on follow up imaging as a new finding.
When associated with other intracranial post traumatic lesions like subdural hematoma, epidural hematoma, intracerebral hemorrhage termed as complex hygroma.
Other uncommon causes are meningitis, Post ventricular shunting or lumbar puncture over drainage.

A post trauma pt, 1st is on admission CT. 2nd is follow up CT after 5days showing bilateral subdural hygroma, widening of subdural space with density same as that of Csf.
Crescent-shaped extra axial collection with CSF density on CT or signal intensity on MRI.
Usually bilateral often more or less symmetrical.
Displaces cerebral cortex and cortical veins. Gyri are significantly displaced away from calvaria.
No widening of cortical sulci, rather sulci may be obliterated with flattening of gyri due to mass effect.
A new finding  on follow up imaging.

Imagingwise DDs: 
1. Chronic subdural hematoma: the closest differential which is usually unilateral and asymmetrical if bilateral.
2. Cerebral cortical atrophy: In atrophy, subarachnoid space is widened, the cortical veins traversing widened CSF spaces over cerebral convexities favours atrophy best seen on post contrast T1 MRI. In hygroma cerebral cortex and cortical veins are displaced away from calvaria. Cortical veins seen only along the margin of displaced cortex and do not traverse fluid collections over cerebral convexities.
Definitive diagnosis is possible only by trephine openings in bone calvarium. Chronic subdural hematoma contains dark "motor oil" fluid which does not clot and devoid of pre albumin. Hygroma is a clear fluid and under pressure contains pre albumin.

Course on follow up imaging: 
Both spontaneous regression with cerebral expansion as well as progression of hygroma with further complication is known. Progression of hygroma can occur due to transudation or further CSF accumulation due to flap-valve mechanism. Widening of sub dural space causing stretching and rupture of bridging veins, bleeding in the same or newly formed sub dural space.

Monday 12 December 2011

Wernicke's Encephalopathy MRI

Axial FLAIR shows an abnormal T2 hyperintensity involving mammillary bodies and hypothalamus support changes of Wernicke's Encephalopathy.
In WE, CT Brain is often normal.
MRI is investigation of choice.

Signal abnormality in peri aqueductal grey matter of mid brain, mammillary bodies, hypothalamus > para median portion of thalami is an imaging wise diagnostic clue.

T2 hyperintensity on FLAIR and T2w images, may show restricted diffusion and contrast enhancement in corresponding region in acute stage.

Clinically WE characterised by triad of Ataxia, Ophthalmoplegia (especially VI CN palsy) and Altered sensorium, all the three component may not be present every time in every patient depends on stage of the disease. Considered as a medical emergency. If left untreated coma and death may ensue. Respond very quickly and completely to thiamine supplementation.

Thiamine deficiency impairs thamine dependent enzymes resulting in accumulation of Glutamate and cell damage. On microscopy there is axonal degeneration, demyelination and neuronal loss in affected areas.
Thiamine deficiency commonly seen in alcoholics which contributes ~50 % of cases. Can occur in Non alcoholics even in children and causes include severe malnutrition, hyperalimentation.

Thursday 8 December 2011

Role of MRI Diffusion

Diffusion-weighted imaging (DWI) is based on principle of Brownian movement of water molecules, a microscopic random motion of the water molecule protons across cell membranes, a physiological phenomenon.
The diffusion of water molecules in brain tissue like other tissues, is guarded by biologic barriers like cell membranes and cellular organelles, which are blessed with sodium/potassium pumps for this. The quantification of this diffusion is known as the apparent diffusion coefficient (ADC), and is done by this type of imaging.

From the clinical experience at our institute, we have enlisted the following conditions showing bright signal on diffusion (I'am not saying Restricted diffusion):
- Acute and sub acute ischemic stroke - Usually takes 7-14 days for hyperintensity to subside.
- Hemorrhagic stroke.
- Trauma, Diffuse Axonal Injury.
- Acute demyelination, Marchiafava Bignami disease.
Hypoglycemic Encephalopathy. 
- Encephalitis – Herpes, CJD, Influenza like encephalitis.
- Focal cerebritis, Ac cerebellitis, Brain Abscess and Empyema.
- Choroid plexus cyst.
- Epidermoid cyst.
- Cholesteatoma.
- Medulloblastoma.
- Atypical Meningioma. 
- Thrombus dural venous sinuses.
- Near mastoid and roof of orbit, an  Air-bone interface artefact.

In ischemic insult, altered intra celluar energy metabolism results in sodium/potassium pump failure which in turn affect intracellular and extracellular water molecule movement and is the presumed explanation for cytotoxic odema, result in increase in brain tissue water in the region of infarct. Occurs within minutes of the onset of ischemia.
When magnetic field is applied, the water molecules move in the direction of the magnetic field gradient; these water protons accumulate a phase shift in their transverse magnetization relative to that of a stationary one, and this phase shift is directly related to the signal attenuation of the image. Provides image contrast that is different from that provided by conventional MR techniques. Region of ischemia appears intensely bright described as an area of restricted diffusion and is confined to particular vascular territory involved.
In trauma, rotational acceleration and deceleration forces produces shear-strain in brain tissue common sites are gray-white junction,  corpus callosum and mid brain. Altered calcium and potassium homeostasis, release of excitotoxic amino acids ,free radicals, and tissue acidosis affects ADC values. Other possible explanation is presence of microscopic hemorrhage and ruptured axons with membrane fragmentations, increasing the barriers to the free movement of water molecules.
In brain abscess, bright signal at the periphery or at core is secondary to increased viscosity of pus which in addition contains large molecules such as fibrinogen that bind with water molecules and add to the effect of restricted diffusion.
In bleed, the appearance of bleed on Dw images is complex and is affected by many factors, including age of hematoma, relative amounts of different hemorrhagic products and the pulse sequence used.
Oxyhemoglobin and Extracellular methemoglobin are bright on diffusion. Oxyhemoglobin is hyperintense on DW images due to relative restriction of water movement inside the red blood cell. Extracellular methemoglobin has a higher ADC than does normal brain tissue, indicates high mobility of water molecules in the extracellular space. This prolongation of the T2 component of fluid with extracellular methemoglobin results in hyperintensity on DW images. Hemorrhage containing deoxyhemoglobin, intracellular methemoglobin, and hemosiderin are hypointense on DW as well as T2w images because of magnetic susceptibility effects.
In demyelination, Multiple sclerosis and Acute disseminated encephalomyelitis; Acute plaques have significantly higher ADCs, this elevated diffusion result from an increase in the size of the extracellular space due to edema and demyelination. In rare instances, acute plaques have restricted diffusion may result from increased inflammatory cellular infiltration with extracellular odema.

In Hypoglycemic Encephalopathy, splenium of corpus calloum and bilateral posterior limb of internal capsules are the commonly affected areas. Pathogenetic mechanisms for diffusion restriction in HE include energy failure, excitotoxic edema, and asymmetric cerebral blood flow.  Glucose deprivation leads to arrest of protein synthesis, incomplete energy failure and loss of ion homeostasis, cellular calcium influx and intracellular alkalosis.  Excitotoxic edema in contrast to cytotoxic edema, does not imply neuronal damage, this is the reason signal changes on MRI diffusion in HE are usually transitory and completely reversible after glucose infusion.

Clinical Application of diffusion:
Ischemia: A major clinical implication of Dw imaging is in acute ischemic stroke, a most important sequence in stroke protocols.
Fast, because Dw imaging uses fast echo-planar  technique, it is highly resistant to patient motion and imaging time ranges from a few seconds to 2 minutes suits the situation.
Most easy sequence to interpret, as its provides image contrast that is different from that provided by conventional MR techniques. Ischemic area with restricted diffusion seen white area stands out over the adjacent normal non ischemic parenchyma.
Most sensitive for acute ischemia, restricted diffusion associated with acute ischemia has been detected as early as 30 minutes after a witnessed ictus making Dwi very sensitive and relatively specific. The detection of ischemia as hypo attenuation on CT scans and hyperintensity on T2-weighted MR images requires a substantial increase in tissue water. Dw imaging is totally based on different principle which occurs within minutes of the onset of ischemia.  For infarctions imaged within 24 hours, reported a sensitivity of 58% for CT and 82% for MR imaging. For the detection of hyperacute and acute infarctions, with a sensitivity of 88%–100% and a specificity of 86%–100%.
FLAIR – Diffusion mismatch, if an infarct is seen on diffusion and not seen on FLAIR interpretated as FLAIR – Diffusion mismatch indicate salvageable tissue or tissue at risk.
Acute on Chronic infarcts, on T2 images both appear bright. Foci of recent ischemia obscured in the background of marked focal cytotoxic odema of relatively older infarcts. In that case foci of recent ischemia characterised by restricted diffusion stands out on the background of rest of the T2 hyper intensity without restricted diffusion.
Transient ischemic attacks, nearly 50% of patients with transient ischemic attacks have lesions characterized by restricted diffusion; lesions usually are smaller less than 1cm.
> Trauma: to rule out DAI in patient with normal CT brain with poor glass glow coma scale.
> Epidermoid vs Arachnoid cyst: Both follow near same signal on conventional sequences. Restricted diffusion is a characteristic of Epidermoid and rules out Arachnoid.
> Posterior Reversible Encehalopathy Vs ischemia : Ischemia in the territory of posterior circulation or along posterior cortical border zone is closest differential for PRESS. Absence of restricted diffusion is very typical of PRESS.
> Cholestatoma: show typical restricted diffusion in the back ground of T2 hyper intense CSOM and mastoiditis.
> Encephalitis : Herpes,  show restricted diffusion with bilateral asymmetrical involvement of Mesial temporal lobes. CJD, characterized by atrophy with insular and cingulate gyral involvement.  Influenza like encephalitis, show restricted diffusion common in splenium of corpus callosum.
> Marchiafava bignami disease in chronic alcoholics show restricted diffusion splenium of corpus callosum.
> Abscess vs Glioma. Restricted diffusion along its wall or core is more common in abscess than glioma.
> Empyema vs subdural effusions: Empyema is characterized by restricted diffusion.
> AEDs: A transient restricted diffusion in splenium of corpus callosum in pts on long Anti Epileptic Drugs, a debatable issue that whether its drug induced toxicity and demyelination or a reversible post ictal change. Certain studies hav reported this transient finding reversing on discontinuation of drugs.
> Hypoglycemic Encephalopathy : Role of MRI Brain Diffusion in HE to evaluate topographic distribution of signal abnormality of hypoglycaemia which decides severity and prognosis of HE.  If signal abnormality is confined to WM such as the CC, IC, or CR and the signal abnormality regresses on follow-up imaging carries good recovery without a neurologic deficit. If lesions are detected in the cerebral cortex, BG, or hippocampus and the lesions do not regress on follow up imaging is associated with poor outcome.

Image Gallery:
CT study of Brain shows faint low attenuation involving right insular cortex and adjacent basal ganglia - insular ribbon sign. Faint T2 hyperintensity seen on FLAIR. DW images show an obvious infarct with restricted diffusion, seems to be an acute infarct as changes are not marked on FLAIR and CT study. Area of involvement is larger on Dw compared to FLAIR, a FLAIR - Diffusion Mismatch.

A sub acute stage Hematoma with restricted diffusion 

A pt with h/o RTA, brought unconscious, on admission CT nearly normal except mild subjective diffuse cerebral odema. MRI Diffusion show restricted diffusion in corpus callosum an example of axonal injury and typical for site.

Tumefactive Demyelination; A known case of demyelination responding well to steroid. Skipped doses for some other reason. 

A Epidermoid cyst in prepontine cistern with typical restricted diffusion, rules out Arachnoid cyst.    

Posterior Reversible Encephalopathy, Bilateral asymmetrical involvement of parieto occipital cortex, T2 hyperintensity without restricted diffusion. 
Bilateral cholesteatoma with typical restricted diffusion

Herpes encephalitis with bilateral asymmetrical involvement of mesial temporal lobes and adjacent insular cortex with restricted diffusion on dw images. 

CJD, A 30 yo female with progressive dementia and altered cognition. MRI show diffuse cerebral cortical atrophy significant for age with restricted diffusion involving cigulate gyri and insular cortex.

Encephalitis, a 13yo male brought unconscious, history of low grade fever since 3 days. On admission MRI show restricted diffusion in splenium of corpus callosum consistent with viral (influenza like) encephalitis further supported by Csf examination.

Focal cerebritis / Encephalitis; bilateral asymmetrical involvement, fronto parietal cortical restricted diffusion with T2 hyperintensity and focal parenchymal swelling.

Acute cerebellitis, a young male with history mild fever since last 3days, now complaining of giddiness. On neurological examination revealed profund ataxia. 

Tubercular Abscess with restricted diffusion and multilocular peripheral enhancement, peri lesional odema. 

Sub dural empyema with restricted diffusion. A known case of bilateral mastoiditis. 

Pt on AEDs, a known case of GTCS under treatment of anti epileptic drugs. Conscious and well oriented came for routine follow up MRI screening show a focal restricted diffusion in splenium of corpus callosum. rest of the brain parenchyma unremarkable. 

A thrombus in cortical vein showing bright signal on diffusion. 
A thrombus in superior sagittal sinus showing bright signal on diffusion. 

Bilateral high signal near mastoid and roof of orbit is artifactual due to Air bone inter phase.

Leigh syndrome


An Olfactory groove meningioma, bright on diffusion implies to atypical variety of meningioma.
A 55 yo male brought to casualty with focal neuro deficit period. MRI Brain Diffusion shows Restricted Diffusion along posterior limb of bilateral internal capsules with Blood sugar level 45 mg/dL suggestive of Hypoglycemia induced reversible signal abnormality on MRI diffusion. HE known to present with focal neurological deficit and may mimic stroke. 
Conclusion: Apart from infarct there are many other conditions and lesions which are bright on diffusion. In infarct restricted diffusion is the exact mechanism behind brightness on dw images where as in other lesions cellularity, compact arrangement of cells, protein content and water binding property contributes to brightness on diffusion. So the more accurate way in such cases is just describe the high signal intensity of such region or lesion instead of using term restricted diffusion. 

Saturday 3 December 2011

T1 Hyperintense Globus pallidi

A 30 yo male with walking imbalance. On admission MRI Brain T1w images shows bilateral symmetrical hyperintensity in the region of Globus pallidi. Rest of the brain parenchyma unremarkable.  
T1 hyperintense Globus pallidi on MRI Brain.  
In further evaluation : Blood sugar levels, Serum Bilirubin levels, Liver function test and Usg abdomen for liver cirrhosis was advised.

Blood sugar Random 210mg/dl (Normal 60-140).. high.
SGPT 46 IU/L (Normal 5-35).. high
S Bilirubin
Total 1 mg/dl
Direct 0.7 mg/dl  .. High
Indirect 0.3 mg/dl
Platelet count 89x10^3/microL (Normal 150-450).. Low

Usg abdomen showed normal sized liver with normal echotexture.
No obvious changes of liver cirrhosis. pt is Non Alcoholic.
Marked increase in echogenicity around portal vein and its intra hepatic branches.
Spleen 15mm along long axis with rounding of inferior pole .. Moderate spleenomegaly.
Marked dilatation and tortuousity of splenic vein.
Possibility of ? Non Cirrhotic Portal Fibrosis with Portal Hypertension suggested.
An associated Hyperspleenism possible as platelet count is low.

Causes of T1 Hyperintense Globus pallidi in this case appears to be either Hepatic Encephalopathy secondary to Non Cirrhotic Portal Fibrosis and Portal Hypertension or Hyperglycemia.

DDs of T1 hyperintense Globus pallidi : 
- Hepatic / Bilirubin Encephalopathy. 
- Hyperglycemia. 
- Long term total parenteral nutrition.
- Manganese toxicity. 

The mechanism behind signal abnormality is not known but various hypotheses involving the deposition of proteins, myelin breakdown products, blood or calcium or other minerals have been proposed.