Friday 27 January 2012

Neuroglial cyst MRI

Syn: Glioependymal cyst.
An intra parenchymal cyst, follow Csf density on CT or signal intensity on all MRI pulse sequences.
A solitary, uni locular, round to ovoid cyst smooth, thin imperceptible epithelial lined wall.
No calcfication within the cyst or along its wall.
Non enhancing on post contrast.
No restricted diffusion on MRI Diffusion.
Frontal lobe white matter is most common and typical location.  Temporal lobe is second common site.
Size vary from few mm to several cm.
Occur in any age group. No gender preponderance.

Common in pts screened for headache and seizures. Clinical significance in a case is doubtful and needs clinical and EEG correlation. 

Enlarged peri vascular space : usually occur in cluster, common in basal ganglia, less commonly in parietal lobe white matter, rarely mid brain.
Arachonoid cyst : Extra axial.
Ependymal cyst : Intra ventricular.
Porencephalic cyst: Communicate with subarachnoid Csf spaces along cerebral convexity or ventricles.  Being an end result of parenchymal Gliosis usually show a thin hyperintense of rim Gliosis along the adjacent brain parenchyma lining cyst on FLAIR where rest of the cyst show complete signal suppression as that of Csf on FLAIR.

Optic Nerve Atrophy MRI

Coronal and axial T2w images show right side optic nerve atrophy. 

Multiple Sclerosis MRI


Axial T2 images show multiple, bilateral, small, linear to ellipsoid, T2 hyper intensities involving Periventricular white matter, corpus callosum, calloso septal groove, brain stem as well as cerebellar white matter. On Sagittal T2 sections most of the lesions are perpendicular to lateral ventricle - Dawson’s finger.
Sagittal T2 screening of Cervical region spine show small faint patchy intra medullary T2 hyper intensities.

Imaging wise diagnosis: Plaques of Demyelination – Multiple Sclerosis.

A primary demyelinating disease of CNS.
An autoimmune mediated demyelination in genetically susceptible individuals.
In Brain;
Multiple small (~5-10mm), perpendicular, linear to ellipsoid, T2 hyper intensities involving Periventricular white matter (in ~90%) and calloso septal groove (in ~75%). Involvement of cerebellum and brain stem in ~10%.
In spinal cord;
Multiple patchy small ill defined intra medullary T2 hyperintensity.
Most commonly seen in Cervical region cord.
Usually associated with concomitant lesion in brain. Isolated spinal cord involvement in ~15%

Thursday 26 January 2012

Medulloblastoma (Lateral origin)

A 30 yo female with giddiness.

A hyper dense right Cp angle mass with fluid – fluid levels on Non contrast CT.
On  MRI, lesion is iso intense to cortical grey matter on T1 as well as T2 images.
Restricted diffusion on diffusion weighted images.
Faint heterogeneous enhancement on post contrast T1.
Multiple fluid – fluid levels with low signal intensity hemosiderin staining in dependent portions on T2*GRE implies to intra lesional bleed, a faint focus of T1 bright signal in dependent portion of mass attributed to meth Hb – a sub acute stage blood degradation product.
A rim of perilesional edema in adjacent right cerebellar hemisphere.
It is difficult to comment whether lesion is extra axial or intra axial as cerebellum is displaced by mass but there is no clear demarcation between the mass and cerebellum even on post contrast T1.
Single voxel MR Spectroscopy shows significantly reduced NAA at 2ppm, high choline at 3.2ppm  and a lactate peak at 1.3ppm.
Mass effect significant, medulla and Pons compressed. Obstructive hydrocephalus due to fourth ventricle compression evident by mild dilatation of temporal horns of lateral ventricle.

Imagingwise Possible DDs: Medulloblastoma, Meningioma.
Acoustic Schwannoma unlikely as there is no intra canalicular extension or widening of IAC.

Histopathology report : Medulloblastoma – Classic Desmoplastic variant, WHO Grade IV with lateral cerebellar origin – atypical for location. 

Syn: MB, Posterior fossa PNET, PNET – MB,
A highly cellular embryonal cell tumor.
Age group : common in children, ~75% diagnosed by 10 years.
3 times more common in males.

Intraventricular – 4th ventricular roof is a typical and most common location. A most common posterior fossa tumour in children. 
Lateral origin – Cerebellar hemisphere is an atypical location common in older children and adults.

Size vary, average size ranges between 3- 5cm at the time of presentation.
On Non contrast CT, solid 4th ventricle mass, hyperdense, calcifcaiton seen in ~20% cases, small intra tumoural cysts, necrosis in ~50% cases.
On MR signal on T1 iso - hypo intense to cortical grey matter on T1 , iso – hyperintense on T2w and FLAIR. High signal on diffusion attributed to its dense, highly cellular nature.
An associated Obstructive hydrocephalus is common seen in ~ 95% cases.
Usually mild to moderate and homogenous enhancement, may show patchy heterogeneous enhancement due to areas of necrosis.
On MR Spectroscopy, NAA reduced or absent as it’s a non neuronal tumour, raised choline.

Other cases of Medulloblastoma with typical location and drop metastasis.

Sphenoid wing Meningioma MRI

MRI Brain Axial T2, T1 and Post contrast T1.
Axial T1 and T2w MRI sections show an extra axial dura based solid signal intensity mass, overlying lateral sphenoid wing, homogenously iso intense to cortical grey matter on T1 and T2w images, intense homogenous enhancement on post contrast T1 with dural tailing.
Marked peri lesional Odema in adjacent compressed left frontal lobe parenchyma.
An associated adjacent meningeal cyst in left sylvian fissure.

Significant mass effect as mid brain is compressed.

On single voxel MR Spectroscopy,
At 1.3ppm Peaks of Alanine which is very typical for meningioma.
Absence of NAA at 2 ppm implies to Non neuronal neoplasm with high choline at 3.2ppm.

Imagingwise diagnosis : Sphenoid wing Meningioma. 

Histopathological report : Meningioma (Transitional – psammomatous variant).
Gross Appearance : Dull – grey tan tissue with friable appearance.
Microscopy : : Benign neoplasm of probable meningothelial cell origin. It comprise moderately cellular, largely patternless or sheet - like growth 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. Few foci show vague lobularity and occasional mitotic figure. Many scattered foci show psammomatous calcific spherules. The scanty interstitium shows entrapped congested blood vessels. 

Other similar cases : Meningioma

Cavernoma (Cavernous Malformation)

Imaging findings of Cavernoma (Cavernous Malformation) are very typical on MR as in this case.
A focal lesion in right cingulate gyrus faintly hyper dense on Non contrast CT.
On MRI typical "popcorn ball" appearance with low signal intensity hemosiderin rim on T2w images.
T1 bright locules of Meth Hb on T1w images.
Low signal intensity blooming on T2*GRE due to paramagnetic effect of blood degradation product.
Faint enhancement on post contrast T1.
Mild perilesional edema on FLAIR.
No mass effect.

Cavernoma (Cavernous Malformation)

A benign vascular hamartoma, composed of closely packed immature blood vessels with intra lesional micro hemorrhages, without any neuronal tissue.
Best diagnostic clue is "Pop corn ball" like appearance with hemosiderin rim on T2w images.
Occur anywhere in brain. Rare in Spinal cord.
Vary in size from few mms to cms. Average size is between 1 to 5cm.
Usually single solitary, may be multiple, discrete lesions.
MRI is more sensitive and specific for detection of lesion.
Hyper dense on non contrast CT. Calcification seen in ~ 50% cases. No to faint enhancement on post contrast.
On MRI lobulated appearance due to multiple locules which show variable signals, depending up on the blood degradation products. T1 bright locules attributed to Meth Hb - a sub acute stage blood degradation product. Low signal intensity hemosiderin rim on T2 images. Low signal intensity blooming on  T2*GRE images. No to faint enhancement on post contrast T1 images.
No to mild peri lesional odema.
No mass effect.

Clinical presentation:
Seizures 50%
Neuro deficit 25%
Asymptomatic 20%, detected as an incidnetal finding.
No intervention is a rule. But need follow up imaging as it may show progression or regression in size. Rarely show massive bleed.
Can affect any age group.
No gender preponderance.
Familial association in Hispanic Americans - Multiple Cavernoma Syndrome, carries higher risk for bleed and re bleed.

AVM; may see 'pop corn ball'  appearance, but characterised by incomplete hemosiderin rim, flow voids on T2w images, areas of bleed instead of multiple locules of variable signals.

Similar Case :
Cavernoma with bleed

Limbic Encephalitis

A 30 yo male with history of OPP poisoning 5 years back since then mild cognitive decline. 

Axial FLAIR images show faint hyperintensity involving  mesial temporal lobes.
Bilateral symmetrical involvement.
No restricted diffusion on Dw images.
Similar faint T2 hyperintensity involving bilateral para median thalami.

Imaging diagnosis : Limbic Encephalitis - Toxic. 
Closest DD:
Herpes; bilateral symmetrical involvement, without restricted diffusion, para median thalamic involvement with long term history goes less in favor of Herpes. 

Limbic encephalitis implies any inflammation in the limbic system.
The brain can be divided into three parts:
1. Brain stem, the most primitive part, plays a vital role in basic attention, arousal and consciousness. All information pass to and fro passes through the brain stem. The brain stem in houses vital centers for respiration, heart , sleep wake cycle, temperature control.
2. Limbic system, is wrapped around the brain stem. It includes the hippocampus, thalamus, hypothalamus and amygdala; involved in memory and much of the behaviour related to sex, hormones, food, fight or flight responses, the perception of pleasure and competition, higher emotions including the protection of the young and feelings such as love, sadness and jealousy.
3. Neocortex, the third and major part of the brain, provides logic and thought,  processes such as speaking, planning and writing.

It is therefore the Limbic Encephalitis is an anatomical diagnosis and not the etiological diagnosis. Not all cases share the same cause or very obvious cause every time.

As per the cause Limbic Encephalitis can divided into 3 main categories:
1. Infectious encephalitis :  usually a virus, number of viruses appear to target this area, mostly but not always include the herpes simplex.  Some people prefer the diagnosis of “limbic encephalitis” whilst others may be given the diagnosis “herpes simplex encephalitis ” for the same finding.
2. Autoimmune encephalitis :  Antibodies are made by all healthy individuals in response to infections or vaccination. The antibodies attack the infectious agent (such as a virus) and help the body’s immune system to get rid of the infection. Unfortunately, a few of these antibodies may “cross-react” with the patient’s healthy tissue proteins, attacking the tissue and causing an autoimmune disease. The antibody binds to the potassium channels, a protein, present in all brain tissue. This causes a reduction in the number of potassium channels, decreasing the control over electrical signals operating in the brain. Potassium channels particularly common in the hippocampus and other limbic areas of the brain explains affection of autoimmune diseases for limbic system.
There are two forms of autoimmune limbic encephalitis; A) paraneoplastic limbic encephalitis (PLE) and B) Non Paraneoplastic limbic encephalitis (NPLE).
A) Paraneoplastic limbic encephalitis (PLE) : occurs in patients with particular cancers like lung, thymus, the breast or testis.
B) Non-paraneoplastic limbic encephalitis (NPLE): recognised in the last five years only,  these patients who had the symptoms of paraneoplastic limbic encephalitis but who did not have any of the marker paraneoplastic antibodies or never developed a tumour. Moreover, some of these patients got better when treated immune suppressant.
3. Toxic and Metabolic. 

HIV Encephalitis – Encephalopathy

Syn: HIV- 1 Encephalitis / Encephalopathy, HIVE.
A syndrome of cognitive, behavioural and motor abnormalities attributed to direct effect of HIV on brain, in absence of opportunistic infection.
Most freqauent neurological manifestation of HIV infection.
Atrophy with bilateral symmetric confluent peri ventricular white matter disease, hypodense on CT and T2 hyperintense on MRI is a diagnostic clue.
Clinical finding should guide imaging finding and not reverse.
Affect any age group and gender.

A 60 yo  male, known Reactive for HIV came for follow up imaging. 
MRI T2w images show bilateral symmetrical confluent peri ventricular T2 white matter hyperintensity. Mild diffuse cerebral cortical atrophy. 

DD is PML (Progressive Multifocal Leukoencephalopathy) , seen in same clinical  setting, characterised by patchy non enhancing white matter lesions, may be unilateral but more often bilateral and asymmetrical. Common in fronto parietal regions.

A case of  

Progressive Multifocal Leukoencephalopathy (PML)

A 30 yo male, known HIV Positive, present with right side weakness. 
Multiple patchy T2 white matter hyperintensities in cerebral white matter in fronto parietal region, basal ganglia, thalami as well as corpus callosum,
Bilateral asymmetrical involvement,
Non enhancing on post contrast T1.
Faint bright signal on diffusion attributed to prolonged T2 effect.
No mass effect.
Mild diffuse cerebral cortical atrophy.

Imaging diagnosis : Progressive Multifocal Leukoencephalopathy (PML)


A sub acute progressive demyelinating disease.
Bad prognosis, even fatal.
Seen in patients with immune disorders particularly impaired cell mediated immune response. Predominantly occurs in patients with AIDS, in ~ 5% of patients with AIDS. Results from JC virus infection - genus Polyomavirus -  family Papovaviridae. Before AIDS epidemic, PML was rare and was associated with other immune compromised conditions like leukemia, lymphoma, organ transplantation and severe combined immunodeficiency (SCID).

Imaging findings:

MRI is the preferred imaging modality over CT.
Usually bilateral and asymmetrical involvement. Patchy and multifocal. Unilateral involvement uncommon.
Predominantly involve fronto parietal white matter; may involve periventricular white matte or sub cortical white matter or both.
On CT, ill defined patcy areas of low attenuation. No enhancement on post contrast.
On MR, ill defined patchy areas of T2 hyperintensity. May show high signal on diffusion due to prolonged T2 effect. No enhancement on post contrast T1.

An associated atrophy,  increase in confluence of lesions, increase in hypo intensity of lesion on T1,  involvement of corpus callosum are poor prognostic indicators.

Faint enhancement seen on post contrast T1 in follow up MRI of PML pts treated with Anti Retroviral Therapy is associated with increase in their CD4+ count, may indicate favourable prognosis.

HIV Encephalitis / Leukoencephalopathy : Usually characterised by bilateral symmetrical Periventricular T2 white matter hyperintensity, an associated diffuse cortical atrophy and ventricular dilatation which are not predominant findings of PML. Clinically PML is associated progressive focal motor and sensory deficits, whereas HIV leukoencephalopathy pt present with altered cognition.

Case of Hiv-encephalitis-encephalopathy
Hiv-encephalitis-vs- PML

Monday 23 January 2012

Platybasia with Basilar invagination

MRI Mid sagittal section of CV junction shows:
  • Platybasia (abnormal flattening of the skull base) evident by wide NTB (Nasion – Tuberculum – Basion) angle,
  • Forward folding of the Clivus – Axis Angle (Angle of Wackenheim) causing lordotic tilt at CV junction, Elevated plane of the foramen magnum with retroflexed dens. 
  • Basilar invagination evident by violation of Chamberlain’s (Hard palate - Ophisthion) line by the Dens. 
  • Among two types of basilar invaginnation (Ventral and Paramesial), this is a Ventral variety of Basilar Invagination characterized by shortening of basiocciput due to short and horizontally placed clivus leading to forward facing plane of foramen magnum. 
  • Abnormal sharp Clivus – Odontoid Angle causing exteme indentation over cervico medullary junction. However signal abnormality not very obvious in compressed medulla or cervico medullary junction.
  • Normal Atlanto- Odontoid Distance. No obvious Atlanto Dental subluxation or dislocation. 
Imaging diagnosis : Platybasia with Basilar invagination.
Basal angle or NTB (Nasion – Tuberculum – Basion) angle. 

Chamberlain's line (Hard plate to Ophisthion)

Clivus – Axis Angle or ‘ Angle of Wackenheim’

Similar Post : Basilar-impression

Sunday 22 January 2012

Central Pontine Myelinolysis

A 60 y o female brought unconscious to casualty.
On Admission MRI T2w images show T2 hyperintensity confined to centre of Pons. No abnormal restricted diffusion on Dw images. Changes of small vessel disease. Brain Angio show no significant major vessel stenosis or occlusion; Normal basilar.
Pathology reports mentioning normal Na+. Slightly raised Cl-

Imaging diagnosis: Central Pontine Myelinolysis.

Syn : Osmotic Demyelination Syndrome, ODMS.

An acute demyelination caused by rapid shift in serum osmolarity.
Classic setting is rapid correction of hyponatremia.
ODMS may occur in Normonatremic patients (Reports with normal Na+ levels).

CT; may be normal. May show faint hypodensity confined to center of Pons. Non enhancing on post contrast.
MRI; T2 hyperintensity confined to center of Pons seen in ~50% of cases. Diffusion may be normal or may show faint high signal.
May involve basal ganglia and cerebral white matter without Pontine involvement is called Extra Pontine Myelinolysis. Pontine and Extra Pontine involvement together is pathognomic for ODMS. 

Infarct: Usually off midline and unilateral as commonly occur due to occlusion of perforators arising from basilar. May affect centre of Pons and extending to periphery if there is complete basilar occlusion, restricted diffusion on Dw images, an associated basilar occlusion on MR Angio.
Neoplasm: Imaging Pontine Glioma may confuse with CPM. Clinically CPM has acute debilating course. Pontine Glioma pt will be young, clinically stable with slow progressive symptoms, without any history of hospital admission or osmotic corrections.

Global Cerebral Hypoxia

Cerebral hypoxia refers to reduced oxygen supply to the brain.
Cerebral anoxia refers to complete lack of oxygen to the brain.
Hypoxic Ischemic Encephalopathy (HIE) is a condition result when the entire brain is deprived of an adequate oxygen supply, but the deprivation isn't total. HIE is often seen in the neonate as a part of birth asphyxia, but it can occur in all age groups and often seen as a complication of cardiac arrest.

Cerebral hypoxic – ischemic brain damage can be grouped as follow.
Global cerebral hypoxia (Diffuse Hypoxic ischemic brain damage): Brain damage resulting from low oxygen levels in the blood.
Cerebral ischemia or infarction:  Focal when particular vascular territory is involved, as a result of thrombotic or embolic event. Global when a complete stoppage of blood flow to the brain occurs.
Brain is most sensitive organ to oxygen deprivation, Hypoxic – ischemic brain damage follows a typical pattern on CT or MR Imaginng depending upon the selective vulnerability of different areas of brain.

On CT; Diffuse cerebral odema, loss of the normal cortical gray white matter differentiation, blurring of the insular ribbon are the best known signs of global hypoxia. In severe cases, reversal of the gray -white matter densities with relatively increased density of the thalami, brainstem and cerebellum so called “reversal sign on CT” and is associated with bad prognosis. Some time these findings may be subtle and difficult to recognize .
On left side CT of a 7 day old with history of perinatal asphyxia, shows diffuse low attenuating supratentorial brain parenchyma with relatively hyperdense Cerebellum - "CT Reversal sign" of Global hypoxia.

MRI is much more superior over CT in these regard, in that diffusion-weighted imaging (DWI) is most sensitive and specific sequence, earliest to pick up the ischemic changes.
On MR, the involved area shows abnormal bright signal on diffusion described as restricted diffusion results from cytotoxic odema in response to ischemia.

Different patterns seen in Diffuse Hypoxic brain damage are as follow
1. Cortical involvement :
2. Deep grey nuclei involvement.
3. Border zone involvement.

Cortical involvement:
Cortical grey matter is involved result in cortical laminar necrosis, occurs because of the selective vulnerability of cortical layers 3, 4, and 5 to anoxia and ischemia. The selective vulnerability of gray matter may be due to higher metabolic demand and higher concentration of excitatory amino acids receptors that are released after the anoxic ischemic event, precipitating the excitotoxicity. In addition to neurons Glial cells are also damaged. The area of involvement show thin band of high signal in the region of cortical grey matter on DW images.  Sometimes hyper intense signal observed on T1 is believed to be caused by the accumulation of denatured proteins in dying cells and does not represent Meth Hb from haemorrhage.
In a patient with cardiac arrest, cortical abnormalities are associated with poor outcome.
In very severe cases of cortical necrosis can be visualized on CT scan, as a gyriform high attenuation.

A 35yo female brought unconscious to casualty with low pulse and blood pressure. On admission MRI Diffusion shows bilateral cerebral cortical involvement with involvement of bilateral basal ganglia and thalami.
Cortical laminar necrosis seen as high signal intensity confined to cortical grey matter.

Basal Ganglia Involvement:
Changes in the deep gray nuclei are seen in most cases of anoxic-ischemic brain damage.
Involvement is usually bilateral and often symmetrical, seen in isolation or in association with cortical involvement.
Thalami, lenticular nuclei, and caudate nuclei involved in various combinations even in same patient the distribution of lesions may change over period of time.

Border zone involvement: 
Border zone infarcts are seen along the Watershed between major cortical branches or between cortical and deep perforator branches of intra cranial vessels.
Between cortical branches of ACA , MCA and PCA called cortical border zone and between cortical branches and deep branches called internal border zone.
I would like to add that watershed infarcts are not typically seen in conjunction with laminar necrosis as hypoxic ischemic damage is seen in both of these but mechanism of injury is different. It is hypothesized that watershed infarcts occur in cases of severe hypo perfusion without anoxia as happens when they are caused by carotid occlusion, systemic hypotension or severe blood loss; whereas laminar necrosis results from Global hypoxic or anoxic injury where cerebral perfusion is often normal.

A 60 yo male brought unconscious to casualty with possible cardiac event. On admission MRI Diffusion show bilateral fronto parietal and parieto occipital cortical restricted diffusion. Similar restricted diffusion in caudate nuclei. Area of involvement corresponds to cortical as well as internal border zone infarcts.
Imaging wise : Bilateral border infarcts.

Vulnerable Cortical Areas: 
Perirolandic and Occipital Cortex are often involved to a greater extent than other cortical areas.
The medial occipital cortex is most commonly affected after anoxic-ischemic brain injury.
The intense baseline metabolic demand of these regions explains their selective vulnerability.
Although it is commonly held that the hippocampi in the mesial temporal lobes are the cortical areas most susceptible to anoxia, evidence of damage to these structures on imaging is seen much less commonly seen after cardiac arrest than the lesions in the medial occipital lobes and perirolandic regions.
A 14yo with delayed milestones showing bilateral peri rolandic cortical and occipital cortical Gliosis suggestive of Perinatal Hypoxic Ischemic injury. 

Corpus callosal Hypoplasia

MRI Brain Axial T2w sections shows inter hemispheric fissure is not a straight mid line with inter digitating gyri.

Sagittal T1w mid line section show a relatively smaller thickness body portion of Corpus callosal stripe. All portions of corpus callosum visualized. No any particular portion missing.
Normal anterior lobe of pituitary.

Imaging diagnosis: Hypoplasia of Corpus callosum.

Hypoplasia refers to a thin but morphologically intact corpus callosum, not a normal variant of development but rather an abnormality of cerebral development.
Associated with development delay, autism, congnitive disorders and Hereditary Spasitc Paraplegia. 

Corpus callosal Agenesis

Agenesis of CC may be complete (all segment of CC absent) or Partial (usually body remains rest of the CC may be absent)
Imaging findings in complete CC Agenesis:
1. Parallel non converging widely separated lateral ventricles on axial sections,the most striking feature.
2. Occipital horn dilated – Colpocephaly.
3. Pointed or trident shaped frontal horns on coronal sections.
4. Non visualisation of normal stripe of CC on mid sagittal section, gyri and sulci directly radiating from roof of third ventricle.
5. High riding third ventricle.
6. Absent cingulate gyrus on sagittal section which is normally seen parallel and cranial to CC.
7. Vertically originated hippocampi with key hole appearance of temporal horns on coronal sections.
8. Probst bundles, the abnormal longitudinally orientated band of white matter track medial to lateral ventricles seen on coronal sections.

Related posts :
Corpus callosal agenesis with heterotrophia
interhemispheric-cyst-without-copus callosal anomaly

Sunday 15 January 2012

Miliary Tuberculosis of CNS

CNS Tuberculosis is still prevalent in many developing countries like india, can present in many radiological patterns, in that disseminated or miliary brain tuberculomas are very rare.
I'm describing a case of a 17 y o female, clinically a known case of Tubercular meningitis, now presented with progressive headache and unsteady gait. Immunocompetent as her TRI DOT reports mentions Non reactive.
MRI study of brain revealed multiple discrete punctate and ring enhancing focal lesions in supra tentorium as well as posterior fossa suggestive of Miliary Tuberculomas.

Her Chest radiograph was normal. Other investigations and clinical examination failed to reveal any evidence of TB outside the CNS.
Started on Anti TB drugs showed clinical as well as radiological improvement.
In conclusion miliary brain tuberculomas are rare and unique radiological entity, may affect immunocompetent individuals without any evidence of TB outside the CNS.

Multiple sclerotic lesions skull

A 65 yo female with a breast nodule under evaluation. Brought in casualty with recent onset seizures.
Her CT study of brain shows Multiple Sclerotic focal lesions in bony calvarium.
Possibility suggested was Osteoblastic metastasis to bony calvarium in view of the Breast nodule.
Brain brain parenchyma show normal attenuation. Even Axial FLAIR images of brain done to rule out any parenchymal metastasis, revealed no significant signal abnormality in brain parenchyma.

Follow up :
Breast nodule biopsy and histopathology revealed no obvious malignancy.
Blood reports revealed Hyper calcemia, which evaluated further with radionucleid study revealed a Parathyroid Adenoma and Hyperparathyroidism.

In addition to multiple Sclerotic focal lesions there is diffuse thickening of bony calvarium.
Apart from Osteoblastic metastasis one should try to add Hyper parathyroidism in the list of DDs though uncommon to present with these kind of isolated multiple sclerotic lesions. 

Multiple Myeloma MRI Spine

A 60 yo female with low backache.

MRI sag T2 screening of whole spine show:
Heterogeneous marrow signal through out whole spine.
Collapsed D7 with posterior bowing of cortex causing mild to moderate bony canal stenosis. Cord compression not significant.
Imaging wise : Neoplastic marrow infiltrative / proliferative disorders like Metastasis and Multiple Myeloma were suggested.
Bone marrow biopsy and histopathology revealed Multiple Myeloma.

MRI is superior to radiography for both, focal as well as diffuse involvement of neoplastic marrow infiltrative / proliferative disorders.
Five different infiltration patterns can be differentiated.
(1) Normal appearance despite minor microscopic plasma cell infiltration,
(2) Focal involvement,
(3) Homogeneous diffuse infiltration,
(4) Combined diffuse and focal infiltration,
(5) Heterogeneous bone marrow due to punctuate infiltration with interposition of fat islands “Salt-and-pepper”-pattern.

For the fast and complete assessment of all patterns a combination of a FSE T1 and STIR can be employed for whole spine screening with enough sensitivity and specificity.

Saturday 14 January 2012

Multiple Myeloma X Ray Skull

The skull x-ray lateral and AP view reveals multiple oil droplet like punched out lytic defects throughout bony calvarium. The appearance is highly suggestive of, but not completely diagnostic for, multiple myeloma.
Bone marrow biopsy and histopathology confirmed the diagnosis of Multiple Myeloma.

Leptomeningeal Enhancement

A young male, known case of tubercular meningitis came for follow up imaging.
Contrast Enhanced CT study of brain show abnormal lepto meningeal entrancement along inter hemispheric fissure.

Contrast enhancement on cross-sectional imaging divided into Extra axial and Intra axial (Parenchymal) Enhancement. Extra axial enhancement can be further classified into Pachy meningeal (Dura-Arachnoid Enhancement) or Lepto meningeal (Pia-Arachnoid Enhancement).

Leptomeningeal enhancement is the enhancement pattern, which follows the pial surface of brain and fills the subarachnoid spaces of the sulci and cisterns.
Usually associated with meningitis; bacterial, viral, or fungal.
Mechanism of this enhancement is breakdown of the blood-brain barrier. Pathogens release Glycoproteins which cause breakdown of the blood-brain barrier and allow contrast material to leak from vessels into the cerebrospinal fluid. The subarachnoid space is infiltrated with inflammatory cells which also retain contrast. The permeability in the meninges itself increase in response to inflammation.

Friday 13 January 2012

Subdural Empyema - Abscess

35 y o male with severe left temporal headache.
On Admission CT study of brain shows:
A focal low density collection with peripheral enhancement along tentorium near left mastoid.
No odema in adjacent brain parenchyma obvious on CT.
No significant mass effect.
Left side mastoid poorly pneumatised and sclerotic. E/o left side mastoidectomy.

The collection show restricted diffusion on Diffusion weighted images with focal vasogenic odema in adjacent left temporal lobe white matter on FLAIR.

Imagingwise diagnosis given was Subdural Empyema - Abscess. 

Left temporal craniotomy with dural patching and grafting done.
Histopatholgy report : ‘Empyema - Pyogenic Abscess’; Microscopy shows few fragmented bits of largely necrosed brain parenchyma with evidence of central coagulative - ischaemic necrosis; partially flanked by inflammatory granulation tissue with dense mixed acute on chronic inflammatory infiltrate. Congested thrombosed blood vessels. No granulomas nor fungi seen. Towards the periphery are seen fragments of reactive glial tissue with reactive astrocytic proliferation. There is no evidence of tuberculosis or malignancy.

Related post : Subdural-empyema

Syn: Subdural (SDE) or Epidural (EDE) Abscess. 
An extra axial localised collection of pus in sudural or epidural space or both.
SDE is more common than EDE.
SDE more common in Supra tenotrium ( Cerebral convexity > interhemispheric fissure > tentorium) than Infratentorium (Cp angle > Cerebellar convexity) 
EDE Supra tentorium (Frontal region). 
Collection is extra axial cresentic shaped if SD and bi convex shaped if ED.
Density on CT and signal intensity on MR vary depending up on its density and protein content. 
Strong peripheral enhancement on post contrast is must. Restricted diffusion on MRI Diffusion is typical and is helpful to rule out other DDs like hygroma and effusion. 
Clinical issues:
Can occur at any age, No gender predominence. 
Often present with headache and fever. May show signs of meningitis. 
An associated mastoid or sinus infection present in more than 75%.
Can be a complication of trauma or neurosurgical procedure. 
Progress rapidly, fulminant course, a neurosurgical emergency.
Complications and bad prognosis more common in SDE than EDE are CVT, focal cerebritis, Parenchymal abscess, meningitis, Hydrocephalus. Reason is in EDE the tough dura limits the collection and act as barrier between infection and brain. 
Mortality is 10-15%. 
Diagnosis solely based on imaging.
Lumbar puncture can be fatal. Csf examination can be normal. 
Treatment is mainly surgical drainage by wide craniotomy followed by patching. IV Antibiotics. 

Hyperintensity along cortical sulci

Case : A 40 yo male with severe recent onset headache. On admission Plain CT study show hardly any obvious abnormality, except marginal fullness of lateral ventricles - a subjective finding.
MR Axial FLAIR study of brain performed immediately after that shows abnormal hyperintensities in the region of hemispheric cortical sulci. 
T2*GRE and Diffusion normal. MR Angiography and Venography of Brain normal.
So the final Impression was "Diffuse sulcal hyperintensity on FLAIR" as the only important positive finding in the study. Possible DDs suggested were SAH and Exudates of Meningitis. 
Csf evaluation strongly supported SAH. 
DSA performed 4 days after also could not reveal any obvious cause of SAH. 

Stands for 'Fluid Attenuated Inversion Recovery' Sequence sequence has become a routine part of MRI studies of the brain; rather it has become the most commonly used sequence in MRI brain studies. In some institution like ours it is performed as a screening study for brain in cases of emergencies and non affordable patient.
An inversion recovery pulse to null the signal from CSF and a long echo time to produce a heavily T2-weighted sequence. Produces images highly sensitive to T2-weighted prolongation in tissue but minus the Csf. Improves detection of lesions within the subarachnoid space and brain parenchyma, particularly the lesions located near the brain–CSF interface.
When disease occurs within the subarachnoid space, the relaxation time of CSF is altered, result in hyperintensity of the CSF or subarachnoid space during the FLAIR sequence. Commonly seen in dependent portions of brain in parieto occipital region with effacement of cortical sulci, an alternative term cerebral odema can be used to describe this associated finding. 
Common causes of such non specific diffuse hyperintensity along sulcal space is Meningitis and Subarachnoid hemorrhage. 
In meningitis and SAH both the  higher protein content and cellular concentrations causes an offset in the null point of CSF inversion times, resulting in increased T2-weighted prolongation.
In massive SAH or obvious Meningitis with exudates and hydrocephalus diagnosis may not be a problem but in subtle cases, results of both in vivo and in vitro studies have suggested that FLAIR imaging is more sensitive than CT in the evaluation of these milder and subtle form of acute SAH and meningeal inflammation in which cases where CT may show only mild effacement of cortical sulci. T2*GRE has not role in cases of milder forms of sub arachnoid hemorrhages, may be normal as in above case. Differentiation between the two is difficult most of time and is out of imaging consecus. Contrast enhanced T1 or Flair may help out by demonstrating leptomeningeal enhancement in meningitis.
Always keep in mind other, less common cause of subarachnoid space FLAIR hyperintensity is artifact. In my institution one patient was advised brain axial FLAIR and sagittal T2 cervical spine screening. First brain screening was performed, which was showing similar abnormal diffuse non specific hyperintensity along sulci spaces and basal cisterns. Cervical spine screening performed and axial Flair repeated again. It is strange to mention that this time axial flair screening was absolutely normal. I had two such incidences. After discussion with my technician i came to conclusion that this was artifactual as some changes were done by him in hurry in TR TE during the study.
Patient intubated and on inhaled O2 can show similarPatient intubated and on inhaled O2 can show similar abnormal diffuse hyper intensity in the region of cortical sulci and basal cisterns due to para magnetic effect of dissolved oxygen. 

Conclusion: Most of the time an associated finding may suggest the cause of the subarachnoid space hyperintensity on FLAIR. But in cases of milder form, diffuse distribution and a lack of ancillary findings often make this finding nonspecific and may require clinical correlation and CSF analysis. It’s better to mention the finding and suggest csf analysis. Commonest causes of diffuse sulcal hyperintensity on FLAIR include Meningitis and SAH. 

Intubated patient on inhaled O2 can show similar picture due to para magnetic effect of dissolved oxygen.
To read more about effect of inhaled oxygen on FLAIR Click here 

Wednesday 11 January 2012

Viral Encephalitis MRI

A 15yo male brought unconscious, history of fever and drowsiness since 2wks.
On admission MRI Ax FLAIR and Diffusion shows bilateral parieto occipital cortical T2 hyper intensity with restricted diffusion. Area of involvement does not corresponds to any particular vascular territory.
Imaging findings are consistent with clinical diagnosis of Acute Viral Encephalitis.

Acute cerebellitis MRI

A 18 yo male with fever, giddiness and ataxia since 3wks. Now complaining vomiting and headache. On admission MRI Brain and Diffusion show diffuse T2 high signals involving cerebellar hemispheres with marked parenchymal swelling, causing compression over Pons and Mid brain with obstructive hydrocephalus. 

Imaging diagnosis : Acute cerebellitis
Csf evaluation revealed pleocytosis to support the diagnosis.

Acute cerebellitis also known as acute cerebellar ataxia, an inflammatory syndrome of cerebellar dysfunction.
Can be Infectious, post-infectious, or post-vaccination.
Typically seen in children, adult cases are also known. 
Outcome of cerebellitis in young adults is considered quite favourable compared to children.