Saturday, 26 May 2012

Effects of Oxygen on FLAIR

A 30 yo pt brought unconscious, required intubation and O2 support. MRI axial FLAIR brain screening show diffusely increased signal in the subarachnoid spaces in the region of cortical sulci and basal cisterns but Csf examination was normal.
An Artifactual high signal in Csf spaces due to para magnetic effect of inhaled Oxygen.
"Pseudo SAH" 
Patients who are intubated and on inhaled oxygen, once the concentration of dissolved oxygen is high enough in the blood, its level will increase in the CSF as well leading to sub optimal suppression of Csf signal on FLAIR due to para magnetic effect of Oxygen and results in diffuse Csf T2 hyper intensity.

Reference: Practical MR Physics and case file of MR artifacts and pitfalls, Alexander C. Mamourian, MD

Friday, 25 May 2012

Neck MR Angiography Pitfall

A young pt with recurrent episodes of TIA advised MR Angiography of neck along with Brain.
Non contrast 2D TOF MRA performed, a MIP image of neck demonstrating of left carotid bifurcation and a row axial image at the level of the ICA origin.
A focal notching in ICA at its origin appears to be:
1. Plaque.
2. External compression.
3. Artifactual.
Answer: it’s an artifact, due to turbulence of flow at the bifurcation as axial sections of contrast enhanced CT Angiography of same patient at the same level are normal. 


Carotid bulb is a normal focal expansion of cervical ICA at its origin is patent and relatively prominent in young patient. Again due to vigorous flow there is formation of an eddy circulation in bulb with reversal of flow. This reversed flow leads to diminished signal on 2D TOF MRA because of the linked saturation band that suppresses all caudal flow, regardless of its nature. 

This problem can be obviated by use of contrast during MR Angiography as in contrast enhanced MRA study, flow related signal by contrast is insensitive to direction of flow and demonstrates the normal contour of the carotid bulb.

Reference: Practical MR Physics and case file of MR artifacts and pitfalls, Alexander C. Mamourian, MD

Monday, 21 May 2012

Truncation Artifact MRI Dorsal Cord

A 40 yo pt with a history of lower limb weakness referred for mri screening of brain and whole spine for cord. MRI sagittal T2 screening of dorsal region shows a faint uniform linear high signal at the center of the cord. The signal abnormality likely to represent:
(1) Cord demyelination.
(2) Syrinx.
(3) Artifact.

Answer : Its an artifact, known as truncation or Gibbs artifact, as axial T2w images planned at right angle to cord at multiple levels are normal including sagittal T2 images repeated with increase in image matrix and lowering FOV.


Interpreting thoracic spinal cord on MR sometimes can be challenging because artifacts due to pulsations of CSF as well as respiratory motion can project over the spinal cord on T2WI. The artifacts from CSF pulsation can be minimized with the addition of flow compensation techniques, and the nearby fat can be suppressed using STIR or saturation bands.
There is, however, one other artifact that can contribute to artifactual high signal in the spinal cord called a Gibbs artifact. This is attributed to the difficulties of replicating the sharp changes in contrast between adjacent structures like cord and CSF using limited frequency information. While large data sets will allow a closer approximation of the edge, with limited time and data there will be some “truncation” of the information. This artifact is most evident where there are sharp contrast borders and a coarse matrix is used for the image acquisition.
It cannot be entirely eliminated, but it can be minimized by using either a smaller FOV ( Field of view) or a larger and finer matrix. It is not seen often today because fast spin echo imaging and high field scanners has allowed the use of a finer matrix without consuming too much time. As the matrix increases and the pixels are therefore smaller, this artifact is minimized because the transition at any high contrast edge is spread over more pixels.
When the Gibbs artifact is visible, it is located in the exact center of the cord as continuous faint high signal intensity line of uniform thickness on sag T2. Dilation of the central canal or a small syrinx generally should not be mistaken for a Gibbs artifact. A syrinx tends to be more sharply defined, more hyper intense and is evident on both T1WI and T2WI axial imaging. In Demyelination or Ischemia, cord involvement will be focal, multi focal or diffuse, axial T2 sections can be used for confirmation.
This artifact was named after the American physicist J. Willard Gibbs, who was called “the greatest mind in American history” by Albert Einstein. He became a professor at Yale in 1871, so his work predated NMR by nearly 100 years. There is some irony in attaching his name to this artifact since his life’s work focused on the mathematics of what is now called thermodynamics.

Reference: Practical MR Physics and case file of MR artifacts and pitfalls, Alexander C. Mamourian, MD

Infratentorial insensitivity of FLAIR

Axial FLAIR and T2w images of same patient at the same level show a lacunar infarct in right half of Pons visible only on T2 and not on FLAIR, attributed to relative low sensitivity of FLAIR for Posterior fossa lesions. 
It is common to have conflicting findings on MR from two different sequences of same patient.
The common example is lesions like lacunar infarcts or plaques of multiple sclerosis are visible on the Proton Density / T2w sequence but not on the FLAIR.
In practice, one should put a much higher value on the proton density / T2w sequence in the posterior fossa due to low sensitivity of FLAIR as far as infratentorial lesions are concerned.
It is not entirely clear why lesions like lacunar infarcts or plaques of multiple sclerosis below the tentorium are not well visualized on FLAIR.
This limitation of FLAIR can be dangerous at times when only FLAIR sequence is offered to radiologist for interpretation, the institutions where only axial FLAIR screening of Brain is commonly advised may be to save time or with intention to save patient’s money.

Multiple sclerosis: Case 2

Reference: Practical MR Physics and case file of MR artifacts and pitfalls, Alexander C. Mamourian, MD

MRI Artifacts, Flow void and Signal void

A young pt admitted to casualty with history of trauma. MR study shows two signal voids in the Sylvian fissures on either side on T2 as well as T1w images.
Diagnosis ?  Bilateral MCA Aneurysms ?

Answer : No, as pt's non contrast 3 D TOF MR Angiography of brain normal, the thin axial CT sections in corresponding region nicely demonstrates that the low signal intensity in sylvian fissures on MR is signal voids due to intra cranial air and not flow void of aneurysms. Note the susceptibility Artifact due to air on MR Diffusion. 


Low signal intensity in Sylvain fissures like those on T2WI images could be due to signal void of air or flow void aneurysms. The bright rim evident on the diffusion scan indicates susceptibility Artifact that would not be expected in association with an aneurysm. 

Reference: Practical MR Physics and case file of MR artifacts and pitfalls, Alexander C. Mamourian, MD

Sunday, 20 May 2012

MR Angiography Artifactual flow loss

A 60 yo male for stroke evaluation.
3D TOF MRA, MCA main stem on either side show focal flow loss or narrowing.
Diagnosis ?
1. Stenoses.
2. Artifactual flow loss.

Answer: Artifactual flow loss, common in elderly non co operative patients due to motion.



This case provides a reminder that MRA of the brain using 3D TOF technique is usually acquired as two to five slabs, unlike the 100 or more thin slices acquired during a 2D TOF sequence. This approach is called MOTSA (multiple overlapping thin slab acquisition). To make 3D TOF images of the intracranial vessels, rather than include all the region of interest in a single slab, multiple thin slabs are acquired with an overlap and then knit together to appear as one continuous volume. The image contrast for both 2D and 3D techniques is still the result of entry slice enhancement, i.e. unsaturated spins coming from outside into an imaged volume, and you may recall that the advantage of 3D TOF imaging in the brain is its improved depiction of curving vessels. These multiple thin slabs are necessary because the hydrogen spins become progressively saturated by the repeated 90 degree pulses as they experience as they traverse the slab. As a result, when using a single, thick slab there would be no signal recovered from the most distal portions of a vessel. These slabs are acquired sequentially i.e. one after the other.
The above MR Angiography demonstrates misregistration between slabs due to some head motion that occurred between two adjacent slab acquisitions. Another cause of this artifact is the loss of flow-related enhancement that becomes increasingly evident as the vessel approaches the exit side of each slab. This phenomenon called Venetian blind artifact, common when the slabs are stitched together.
To obviate this artifactual signal loss modify the pulse sequence to “add” vascular signal at the exit side of the slab. This is accomplished by using a variable flip angle on this gradient echo acquisition that changes during each slab acquisition. Since the vascular signal increases with an increase in the flip angle, a modulated or “ramped” flip angle can be used to correct for vascular signal loss. This approach can help to provide a seamless appearance to the vasculature across the multiple slabs.

Reference: Practical MR Physics and case file of MR artifacts and pitfalls, Alexander C. Mamourian, MD

MR Venography Artifactual flow loss

A 30 y o postpartum woman presents with headaches and drowsiness. The maximum intensity projection (MIP) image from coronal two-dimensional time-of-flight MR venogram (2D TOF MRV) the part of superior Sagittal sinus near torcula show poor flow related signals.
1. Superior sagittal sinus thrombosis.
2. Stenosis.
3. Normal.

Answer: It’s a common finding in 2 D TOF MR Venogram due to inflow artifact, can be passed off as normal.



2 D TOF technique of MR Venogram for demonstration of intra cranial venous system without need for any intravenous contrast. The contrast between the vascular lumen and the background is due to entry slice enhancement of blood flow. Because the image is acquired as a stack of individual slices, every slice represents an entry slice for blood flow. This stack of thin images transformed into MIP reconstructions to demonstrate MR Venogram. The advantages to using a 2D TOF technique over 3D TOF is its sensitivity to relatively slow flow and almost unlimited coverage, there are some artifacts that have to be considered as a result of its single plane of acquisition.
Entry slice enhancement is most effective when the orientation of the acquisition slice is perpendicular
to the direction of flow. For MR Venogram commonly coronal 2D TOF is used because the venous flow in the brain is largely anterior to posterior.
It need to be noticed that the superior sagittal sinus (SSS) is well demonstrated throughout with the exception of the posterior segment at its junction with the straight sinus at the torcula. While this appearance can be readily mistaken for intraluminal thrombus or stenosis, it is important to recognize that this is an artifact of in- plane flow. Since intravascular signal is highest when flow is perpendicular to the slice and lowest when flow is in the same plane as the slice, the signal in the SSS drops off in this vertical segment of the sinus that is in plane on a coronal acquisition.
It is important to know how the source data for the 2D TOF study is acquired coronal or sagittal in order to anticipate these artifacts.
Acquiring two 2D TOF MRV scans in perpendicular directions or using contrast can help resolve some of the problems created by in-plane flow.

Reference: Practical MR Physics and case file of MR artifacts and pitfalls, Alexander C. Mamourian, MD

Facial Colliculus Syndrome MRI Brain

A 50 yo male with recent onset left lateral rectus palsy and left side lower motor neuron facial palsy.
MRI Diffusion shows a punctate focus of recent ischemia with restricted diffusion in dorsal aspect of Pons at the floor of floor ventricle which corresponds to fascial colliculus. 
Facial Colliculus Syndrome

The facial colliculus is an anatomical elevation in the floor of the fourth ventricle located medial to the sulcus limitance.
Not formed by the facial nerve nucleus, but by the abducens nerve and the motor fibres of facial nerve loop dorsal to the 6th CN nucleus before leaving the brainstem known as internal genu of facial nerve resulting a bump at the floor of fourth ventricle called facial colliculus.
There for a nuclear lesion of abducens nerve in pons is frequently associated with an ipsilateral lower motor neuron pattern of facial weakness.

Causes of facial colliculs syndrome vary by age. In young age group tumour, demyelination and viral inection where as in elderly people ischemic lesions are common causes.
Clinical presentation of facial colliculus syndrome is due to a lesion at the facial colliculus Involves
1. Ipsilateral lower motor neuron pattern of Facial nerve palsy. .
2. Abducens nerve (CN VI) nucleus result in ipsilateral lateral rectus palsy.
3. Some times conjugate gase palsy due to an associated contra lateral medial rectus palsy due to involvement of medial longitudinal fasciculus.

Millard Gubler syndrome, a related syndrome to facial colliculus (dorsal pons) resulting in ipsilateral 6th and 7th nerve palsy +/- contra lateral hemiparesis.

Localization in Clinical Neurology,  By Paul W. Brazis
Jacobs DA, Galetta SL. Neuro-ophthalmology for neuroradiologists. AJNR
Sinnatamby CS. Last's Anatomy, Regional and Applied.
Clemente CD. Anatomy, A Regional Atlas of the Human Body.

Superficial Siderosis MRI T2*GRE Brain

Axial T2 *GRE images of brain reveals low signal intensity hemosiderin staining on surface of parietal lobes marked on right side suggestive of Superficial siderosis, not at all obvious on any other sequence. Axial FLAIR images in corresponding region normal. 
Superficial Siderosis

A rare condition characterised by abnormal hemosiderin staining of sub arachonid space, may be diffuse or focal, commonly overlying cerebral and cerebellar convexity, basal cisterns, ventral surface of brain stem on T2*GRE, results from excessive and repetitive subarachonid bleed.
An associated staining along cranial nerves particularly i, ii and viii CNs.
May see an associated atrophy of cerebellar hemispheres and vermis, lepto meningeal thickening with enhancement.
CT usually normal may show faint hyperdense layering.
Differential diagnosis is none, it has a pathognomonic appearace on T2*GRE.

Superficial siderosis is not a final diagnosis but an important finding indicating a remote or recurrent intra cranial bleed in subarachnoid space. Further imaging evaluation should be directed towards source of bleeding like MR Angiography to rule out aneurysm or any other vascular malformation.
The issue is cause of bleed. In ~25% cases cause in not found.

Clinically common symptoms are ataxia, hearing loss, anosmia, dementia; in long standing cases adjacent brain parenchymal atrophy ensues with altered cognition.
Treatment directed towards finding and removing cause of bleeding. Iron chelating agents.

Reference: Teaching atlas of brain imaging: By Nancy J. Fischbein, William P. Dillon, A. James Barkovich : Dural and lepto meningeal processes, Case 65, page  231.

To see another case of Superficial siderosis :
Case 1 : Click here
Case 2 : Click here

Wednesday, 16 May 2012

Hallervorden Spatz Syndrome

A 14 yo male under psychiatric treatment for cognitive decline, speech and gait disturbance since 2years. Report of previous CT study of brain normal. Films not available.
MRI study of Brain shows bilateral symmetrical involvement of Globus pallidi. Focal hyper intensity surrounded by low signal intensity on T2 and T2*GRE images.

Imaging wise Diagnosis: Hallervorden Spatz Syndrome.

Hallervorden Spatz Syndrome
Rare condition.
Syn: HSS; Pantothenate Kinase- Associated Neurodegeneration (PKAN); neurodegeneration with
brain iron accumulation type 1 (NBIA type 1). Neurodegeneration with brain iron accumulation

(NBIA) is a new umbrella term for disorders of focal brain iron accumulation, includes former HSS, aceruloplasminemia, neuroferritinopathy and others.
HSS is a progressive neurodegenerative disorder characterized brain iron accumulation.

Imaging wise the diagnostic clue is "Eye-of-the-tiger" sign is a bilateral, symmetric foci T2 hyperintensity in globus pallidus surrounded by hypointensity. The ferritine bound iron deposition is responsible for T2 hypo intensity.

CT Findings: Normal or Hyperdense Globus Pallidi.

MRI (The best imaging tool) Findings:
• Tl WI: Variable (ferritin-bound iron has greater Tl shortening than hemosiderin-bound)
• T2WI and FLAIR : Eye-of the tiger appearance in Globus pallidi.
• T2* GRE: Low signal intensity "bloom" due to paramagnetic effect iron
• T1 C+: No abnormal enhancement
• MRS:  reduced NAA in GP implies to neuronal loss.

Lab findings: Normal serum and CSF iron levels.

o Autosomal recessive (50% sporadic)
o PKAN: PANK2 mutation on chromosome 20p12.3-p13.
Theory is PANK2 mutation > CoA deficiency > energy and lipid dyshomeostasis > production oxygen free radicals > phospholipid membrane destruction. Basal ganglia in that GB is esp more prone to oxidative damage because of high metabolic demands. Cysteine accumulation in GP secondary to decreased phosphopantothenate causes iron chelation and peroxidative cell membrane damage is a contributing factor.

Clinical presentation: 
Dystonia (most common), other extrapyramidal signs/symptoms are dysarthria, rigidity, choreoathetosis.
Cognitive decline is frequent, dementia.
Pigmentary retinopathy 66%
Psychiatric and speech disturbances
Teenager with speech, psychiatric disturbance is classical. Majority present before age of 6 yrs.

Prognosis: Fatal; mean duration disease after symptom onset = 11 yrs

Treatment: No curative treatment.
Iron chelation ineffective.
Palliative treatment with Baclofen, trihexyphenidyl, stereotactic pallidotomy, Pantothenate (vit B5).

Reference: Diagnostic Imaging Brain, Anne G. Osborn.

Hallervorden Spatz Syndrome Another Case

Tuesday, 15 May 2012

Hypoglycemic Encephalopathy MRI Diffusion

A 55 yo male brought to casualty with history of 3.5hr sudden onset left side hemi paresis. Referred to neuro interventional unit with a suspicion of recent onset stroke in window period. 
MRI brain Diffusion done immediately. Mean while blood sample sent for sugar level evaluation.  
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. 
Hypoglycemia is decrease in serum glucose level less than 50 mg/dL, commonly induced by overuse of insulin or oral hypoglycemic agents.
Glucose is the main energy substrate and profound hypoglycaemia known to cause neuronal death in pathologic studies however the vulnerability of different brain regions to neuronal damage in hypoglycaemia is different.
Presentation of HE is variable depends on the area affected as per its vulnerability and severity of hypoglyemia. Neurologic symptoms include giddiness, focal neuro deficits, coma and death in ~3%. May present with hemi paresis and mimic acute stroke.

MRI Diffusion imaging demonstrates alteration of the diffusion of water within the extracellular space and between intracellular and extracellular spaces, may demonstrate changes suggestive of hypoglycemia by the restricted diffusion in the affected area.
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.

Recent seizures episode, drug toxicity, viral encephalitis, and metabolic encephalopathy may show similar reversible signal abnormality on diffusion should be considered in imaging wise DDs.

Diagnosing Hypoglyemic encephalopathy requires clinical suspicious and its confirmation with blood glucose which is easly available, cost effective and should be the first step in diagnosis of HE and not the MRI. 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.

The time necessary for hyperintense lesions on DWI to disappear after glucose infusion in humans is not completely clear.

References :
Diffusion MR Imaging of Hypoglycemic Encephalopathy, E.G. Kang AJNR.
Diffusion-Weighted MR Imaging in Early Diagnosis and Prognosis of Hypoglycemia, L. Loa AJNR.
Rapid improvement of diffusion‐weighted imaging abnormalities after glucose infusion in hypoglycaemic coma, J Maruya, H Endoh, H Watanabe, H Motoyama, J Neurol Neurosurg Psychiatry 2007

Friday, 11 May 2012

Unilateral Basal Ganglionic T1 hyperintensity

MRI sagittal and axial T1w images of brain show faint T1 hyperintensity in left basal ganglia.
Clinically pt was drowsy. Relatives complaining of repeated involuntary movement of right half of face and right upper limb. When insisted relative forwarded all previous lab investigations, in that pt’s blood sugar level were abnormal.
Fasting blood sugar 142 mg/dl (N 70-110 mg /dl)
Postprandial 276 mg/dl (80-150mg/dl)
Fasting urine sugar Nill.
Postprandial urine sugar 0.5%

Considering above clinical details and report of abnormal blood sugar level,
Imaging wise diagnosis: Hyperglycaemic Hemichorea – Hemiballismus.

Hyperglycemic Hemichorea-Hemiballismus
Syn: HCHB, Hemiballismus-hemichorea, Chorea-ballismus with nonketotic hyperglycemia, Nonketotic hyperglycemia,
Triple H of Hyperglycemic Hemichorea-Hemiballismus are 1. Unilateral basal ganglionic T1 Hyper intensity, 2. Hyper glycemia / Hyper glycemic coma and 3. Hemi chorea / Hemi ballismus.

It is a syndrome associated with nonketotic hyperglycemia in patients with poorly controlled diabetes mellitus, characterized by sudden onset hemiballismus or hemichorea.
The most common cause of hemichoreahemiballism in adults is a vascular lesion in the basal ganglia. Rarely, it can also be the first clinical manifestation of non-ketotic hyperglycemia, associated with unique radiological features.

Imaging findings of Hyperglycemic Hemichorea-Hemiballismus:
CT may be normal. May show faint unilateral basal ganglionic hyperdensity.
MRI is most sensitive. May show typical unilateral T1 hyperintensity in basal ganglia.

Elderly diabetic patients with non-ketotic hyperglycemia presenting with hemichorea-hemiballism, hyperdensity in contralateral basal ganglia on CT scan and high signal intensity in corresponding areas on T1 weighted MRI have been already reported.
But there was much controversy regarding the cause of these imaging changes.
Initially it was thought to  be due to calcification.
Chang and colleagues postulated petechial haemorrhage to be the cause.
Stereotactic biopsy and histopathology from the striatum revealed gliotic brain tissue with abundant gemistocytes suggesting that the hyperintensities in T1 could be due to the protein hydration layer inside the cytoplasm of the swollen gemistocytes.
These gemistocytes abundantly present in the basal ganglia and cause excessive neuronal activity especially in the GABA-ergic projections and thus may be responsible for generating hemichorea-hemiballism.
The basal ganglia hyperintensity generally resolves within a few months rarely reported to remain for several years.
So it may be concluded that hemichorea -hemiballism occurring in diabetes mellitus owing to non-ketotic hyperglycemia is a rather benign condition with a good prognostic outcome provided the syndrome is recognized early and corrected.

Other causes of basal ganglioinic T1 hyperintensity:
There are many causes of basal ganglionic T1 hyperintensity, majority are related to deposition of T1 intense elements within the basal ganglia.
Methaemoglobin in intracranial hemorrhage or hemorrhagic transformation of infarct.
Idiopathic calcification.
Hepatic failure.
Hamartoma in neurofibromatosis type 1.
Hyperalimentation or long term parenteral nutrition, manganese toxicity.
Carbon monoxide.
Wilson's disease (copper),  acquired non-Wilson's hepatocerebral degeneration
Japanese encephalitis,
global hypoxia,
Hyperglycemia associated chorea-ballism /  non ketotic hyperglycaemic hemichorea,

Causes of unilateral basal ganglioinic T1 hyperintensity are very uncommon than bilateral and are unique. Unilateral basal ganglionic / putaminal CT or MR signal abnormality of nonketotic hyperglycemia to be recognized and distinguished from acute ischemic stroke in patients with acute neurologic symptoms. Although nonketotic hyperglycemia may mimic stroke in clinical presentation and imaging findings, the pathophysiologic mechanisms of this entity are not clearly ischemic, so recognisation of this syndrome is important as it can affect the treatment options. Physicians and radiologists needs to be aware of non-ketotic hyperglycemia and its imaging findings as a cause for a potentially reversible hemichoreahemiballism syndrome.

Similar case : hemichorea-hemiballismus : Unilateral basal ganglionic hyperdensity CT Brain

Neurology Asia 2010; 15(1) : 89 – 91, Diabetic non-ketotic hyperglycemia and the hemichorea-hemiballism syndrome: B Shalini , W Salmah.
 Lai PH, Chen C, Liang HL et-al. Hyperintense basal ganglia on T1-weighted MR imaging. AJR Am J Roentgenol. 1999;172 (4): 1109-15. AJR Am J Roentgenol (citation)
 Lai PH, Tien RD, Chang MH et-al. Chorea-ballismus with nonketotic hyperglycemia in primary diabetes mellitus. AJNR Am J Neuroradiol. 17 (6): 1057-64.

Monday, 7 May 2012

Vein of Trolard MR Venogram of Brain

Vein of Trolard on right side
Vein of Trolard on either side
Syn:  Superior Anastamotic Vein.
The vein of Trolard, is a part of the superficial venous system of the brain, often located in post central sulcus, connects superficial middle cerebral vein of Sylvius to superior sagittal sinus.

Also important know here about vein of Labbé, the inferior anastomotic vein crosses the temporal lobe, connects the superficial middle cerebral vein of Sylvius to the ipsilateral lateral sinus.
The dominance of these anastomotic veins is dictated by the relative size of the superficial middle cerebral vein and the other anastomotic vein. There is inverse relationship between the size of these three, the superficial middle cerebral vein, the anastomotic vein of Trolard and the vein of Labbé, as all three shares a same drainage area.

Clinical significance:
Surgery : Important to know about these vein , to preserve the vein during lobectomy or Decompressive craniecotmy.
Thrombosis : isolated thrombosis of this vein is known where MR Venogram may show controversial findings like normal superior sagittal sinus with an adjacent hemorrhagic venous infarct which may be otherwise mistaken for a hemorrhagic contusion if there is history of trauma. T2*GRE sections in high parietal region can be of great help in such situation, may demonstrate low signal intensity thrombus in the vein.

Sunday, 6 May 2012

Microphthalmia MRI

Microphthalmia ( microphthalmos) is a congenital underdevelopment or acquired diminution in size of eye ball.
Congenital Microphthalmia is a part of a spectrum of that begins with Anophathalmia result when there insult to embryo after outgrowth of optic vesicle. The condition may be associated with orbital cyst.
Microphthalmia may be unilateral or bilateral, can occur as an isolated disorder or associated with other ocular, craniofacial or systemic anomalies.
In older age group patient this disorder may result from surgery, trauma, inflammation, radiation and process that result in disorganisation of eye ball (phthiasis bulbi). In these patient small eye ball often associated with intra orbital calcification.
An eye with axial length less than 21mm in adult or less than 19mm in a year old child defined as Microphthalmia. In full term infants size of globe axial length measures 17.3mm. In a 2 year old child size of the globe is 90% of the adult (20-22mm)
On CT / MRI congenital Microphthalmia seen as small eye balls with poorly developed orbits.

The principle conditions in which Microphthalmia may be seen as an associated finding are:
Isolated Microphthalmia.
Microphthalmia with orbital cyst.
Persistent hyperplasic primary vitreous.
Retinopathy of prematurity.
Congenital rubella.
Congenital toxoplasmosis.
Congenital syphilis.
Post traumatic.
Post inflammatory herpes, cmv.
Post radiation.
MIDAS syndrome (Microphthalmia, Dermal Aplasia, Sclerocornea)
Lowe syndrome.
Norrie syndrome.
Warburg syndrome.
Meckel syndrome.
Trisomy 13 and 18 syndrome.

Intraventricular hemorrhage in Moyamoya

A  30 years old male brought to casually with a CT showing intra ventricular bleed for further evaluation and management.
MRI  Axial T1w images of brain shows an intra ventricular bleed in left lateral ventricle (yellow arrow), T1 bright meth Hb – a sub acute stage blood degradation product.

3 D TOF MR Angiography of Brain shows non visualization of intracranial portion of both the ICA. Both the MCA show poor flow related signal with marked sparsity of cortical branches of MCA on either side. Lateral and oblique view showing collaterals from PCA giving puff of smoke appearance (Red arrow). 
Diagnosis: Intraventricular hemorrhage in Moyamoya disease.

Moyamoya disease is a bilateral steno occlusive disease of the intra cranial internal carotid artery. Moyamoya is a Japanese word for a "puff" or "cloud of smoke" , and it has been used to refer to an extensive basal cerebral network of small anastomotic vessels at the base of the brain around and distal to the circle of Willis secondary to segmental stenosis or occlusion of the terminal parts of both internal carotid arteries.  The basal vascular network is contributed by lenticulostriate, chorioidal, thalamoperforating, premammilary and thalamogeniculate arteries, as well by to unnamed branches arising directly from the circle of Willis.
Pseudo aneurysms and micro aneurysm are well reported along these collaterals and circle of Willis. Pathogenesis of MD is not well understood.
Various theories of inflammatory and immunologic mechanisms remain unproven. Very high concentration of basic fibroblast growth factor (bFGF) with high angiogenic activity in Csf samples of patients typical imaging findings of Moyamoya disease.
There are strong evidences to support hereditary and familial factors especially among the Japanese.

Clinical manifestation of MD include ischemic symptoms common in children where as intracranial bleed in the form of subarachnoid bleed,  intra parenchymal or intraventricular bleed common in adults.

Causes of intracranial haemorrhage in MD are rupture of dilated fragile collaterals or rupture of aneurysms along the circle of Willis and basal cerebral network of collaterals.

Reference: MOYAMOYA DISEASE: CLINICAL AND ANGIOGRAPHIC FEATURES Dragan Stojanov ,  Petar Bošnjaković,  Zoran Milenković, Nebojša Stojanović CLINICAL FEATURES OF MOYAMOYA DISEASE yong seung Hwang,