Imaging in Cerebral Stroke

Cerebral Stroke is classified into two major types - Hemorrhagic and Ischemic.


Hemorrhagic strokes:
Occur due to rupture of a cerebral blood vessel that causes bleeding into or around the brain.
Account for ~ 16% of all strokes.
Further divided into Two major categories, one is Intracerebral hemorrhage is the most common.
Second is Subarachnoid hemorrhage, due to rupture of a cerebral aneurysm.

Ischemic strokes:
Caused by blockage of blood flow in a major cerebral blood vessel due to a blood clot.
Account for ~ 84% of all strokes.
Further divided depending up on their etiology into several different categories including thrombotic strokes, embolic strokes, lacunar strokes and hypoperfusion infarctions.

Both may mimic each other clinically.
Role of imaging is diagnosis as early as possible with as much as close to the etiology.
First of all it is important to mention that these group of pts are highly non co operative so every imaging step should be short and aim oriented. Modifications in imaging protocol and sequences to be done as per the case, most important factors are time with sensitivity n specificity of particular modality or a sequence for that particular condition.

CT is the preferred initial choice.
Non contrast routine CT is sufficient to rule out bleed which is an absolute contraindication for thrombolytic therapy used in ischemic strokes.
A hypertensive bleed is typical for site with history of hypertension / on admission high blood pressure.
If bleed is in non hypertensive or atypical, look for any associated abnormality as a cause of bleed which may require MRI with aim oriented sequences like MRI Brain Angio protocol (Diffusion, FLAIR with non contrast 3D TOF for brain Angio and 2D TOF for neck Angio) to look for any Aneurysm, AVM or MRI Veno protocol (Diffusion, FLAIR, T2*GRE with non contrast 2D TOF for brain venogram) for venous infarct.
Causes of non hypertensive hemorrhagic stroke include hemorrhagic venous infarct, Amyloid angiopathy, Vascular malformation, Coagulopathy, Hemorrhage into a tumor, Drug abuse, etc.

If there is no bleed on CT, go for MR Angio protocol to rule out acute ischemic stroke that was not obvious on CT.

SPIN : STROKE PROTOCOL 
CT Non Contrast
MRI
MR Angio protocol - Diffusion, FLAIR, NC 3D TOF for Brain Angio and 2D TOF for Neck Angio. 
MR Veno protocol - Diffusion, FLAIR, T2*GRE, NC 2D TOF for Brain veno. 


What should raise the suspicion for atypical bleed and encourage for further evaluation ?

1. Non hypertensive pt.
2. Previous clinical and treatment details.
3. Discrepancy in imaging wise age of hematoma and as per history.
4. Site atypical for bleed.
5. Age atypical for bleed.
6. Resolution pattern of hematoma, fluid - fluid level.
7. Perilesional odema disportionate to amount bleed.
8. Any soft tissue density in or adjacent to hematoma.
9. Any vascular malformation in or adjacent to hematoma.

Imaging in Acute Ischemic Stroke

SPIN : STROKE PROTOCOL

Imaging protocols vary among institutions, depending up on the availability of imaging modalities, cost effectiveness and expertise.
In India at least, availability of imaging modality and affordability of patient are the major issue.
And as far as stroke patients are concerned, time is the most important issue.
So the to cut short the time required for imaging without compromising the accuracy of diagnosis the protocol we follow in our institution we believe that is simple, less time consuming and applicable to most institutions.

Role of CT
1. To Rule out bleed: Non contrast CT is sufficient to rule out most important infarct mimic that is bleed which is an absolute contraindication for thrombolytic therapy.
2. Can detect early stage acute ischemia : by depicting features such as the
1) Hyper dense vessel sign,
2) Insular ribbon sign and
3) Reduced parenchymal attenuation with effacement of cortical sulci.

Once bleed is ruled on CT.
MRI is to confirm an infarct with better evaluation.


MRI  1.5 tesla GE Signa Excite; basic sequences performed are Ax FLAIR, Diffusion, T2*GRE followed by MR Angiography Brain and NECK.


Role of Diffusion:
Most sensitive and relatively specific.
Based on principle of restriction of normal Brownian motion of water molecules in infarcted tissue.
Infarct seen as an abnormal white area and described as an area of restricted diffusion.

Role of FLAIR:
Sensitivity to pick an infarct is arbitrarily comparable to CT.
If an infarct seen on  diffusion and not seen FLAIR called FLAIR / Diffusion Mismatch indicate hyper acute infarct - reversible  ischemic changes and salvageable tissue or  tissue at risk.
If changes are marked on FLAIR indicate already infracted and non salvageable tissue.

Role of T2* GRE:
Sensitive for bleed.
Used to demonstrate hemorrhage or hemorrhagic transformation in the region of infarct as an alternative to CT.
Area of bleed appear dark due to paramagenetic effect of blood degradation products.

MR Angiography of brain and neck: 
To demonstrate any major vessel stenosis or occlusion.
No contrast required.
Accuracy acceptable.  

Case: A 55 yo male, known hypertensive, present with acute onset left side weakness of 5hrs. Clinically there are two possibilities in this case one is hypertensive bleed and second is infarct. On admission CT done first to rule out bleed.

Important findings:

1. No bleed.

2. Faint low attenuation involving right insular cortex and adjacent basal ganglia - 'insular ribbon' sign. Effacement of right hemispheric cortical sulci. 

Immediate MRI Brain with MR Angio performed to confirm infarct and better evaluation.

 

MRI Diffusion show an area abnormal restricted diffusion involving right peri sylvian cereberal cortex, adjacent insular cortex and right basal ganglion suggestive of an infarct. Area of involvement corresponds to right MCA proximal main stem territory. Changes are not marked on FLAIR, except a faint hyper intensity is seen implies to Diffusion - FLAIR mismatch goes in favor of a hyper acute to acute infarct. No marked focal cytotoxic odema to cause significant mass effect.
On MR Angiogram right ICA not visualised from its origin and so the right MCA implies to occlusion. Right ACA filled via contra lateral anterior circulation via Acom. T2*GRE omitted in this case as bleed or hemorrhagic transformation is not excepted and we already have done CT for this, this is how u can do minor modifications in protocol and cut short the number of sequences. 

Imaging in Sub Arachnoid H'rhage

SAH, An extravasation of blood into the subarachnoid space between pia and arachnoid.

Divided as Spontaneous and Post traumatic. 
Spontaneous SAH include Aneurysmal and Non-aneurysmal causes SAH. 
- Aneurysmal SAH 
The most common cause of Spontaneous SAH.
Rupture of a saccular (berry) aneurysm (80%)
Rupture of an arteriovenous malformation (AVM) (10%).
Rarely in the setting of mycotic aneurysms and congenital disorders, including coarctation of the aorta, Marfan's syndrome, Ehlers-Danlos syndrome, fibromuscular dysplasia and polycystic kidney disease.
- Non Aneurysmal SAH: include CVT, amyloid angiopathy, blood dyscrasias, fibromuscular dysplasia, Moyamoya disease, and vasculitis (10%).


Rupture is related to the tension on the aneurysm wall. Tension on the wall is proportional to the diameter. Thus, the rate of rupture is directly related to the size of the aneurysm.

Symptoms and signs:
A sudden onset of severe headache ("thunderclap headache"), often described as the “worst headache of my life" .... most common.
Nuchal pain and rigidity
A sudden loss of consciousness (occurs in half of patients at bleeding onset; it is usually transient)

Location: 
The most common and specific locations of intracranial aneurysms are at the middle cerebral artery bifurcation and along the anterior communicating artery. These 2 locations account for approximately 70% of all intracranial aneurysms.
Other common sites are at the origins of the posterior communicating and ophthalmic arteries.
Approximately 10-20% of aneurysms arise from the vertebral and basilar arteries. The tip of the basilar artery is the most common location of aneurysm formation in the posterior circulation.

Preferred examinations:
Non contrast CT
MRI with MRA (Non contrast 3 D TOF)
DSA

Non contrast CT
A preferred initial diagnostic study.

On CT, subarachnoid haemorrhage appears as a high-attenuating, amorphous substance that fills the normally dark, CSF-filled subarachnoid spaces around the brain, appear white in acute haemorrhage, most evident in the largest subarachnoid spaces, such as the supra sellar cistern and Sylvian fissures.
Prediction of site of bleed on CT, is possible. If bleed is marked in anterior inter hemispheric fissure, an Acom aneurysm is possible and if marked only in one side sylvian fissure corresponding MCA aneurysm is possible.

Magnetic Resonance Imaging
Fluid Attenuated Inversion Recovery (FLAIR) is the most sensitive sequence.

On FLAIR images, SAH appears as high signal-intensity (white) in normally low signal-intensity (black) CSF spaces.
MRA for evaluating aneurysms and other vascular lesions that cause SAH. The  sensitivity is low for aneurysms smaller than 5 mm.

DSA (Digital Substraction Angiography)
Considered the standard imaging technique for the detection of intracranial aneurysms.

Detected as focal areas of out pouching or dilatation of the arterial wall, frequently occur at arterial branching points in characteristic locations within or near the circle of Willis.
Gives valuable information about aneurysm location, shape, neck size, and neck-to-maximal diameter ratio  which are crucial in determining whether the aneurysm is better treated with open craniotomy or with an endovascular technique.

Sentinel bleed

Sentinel or "warning" leaks that produce minor blood leakage, reported to occur in 30-50% of cases, precedes the aneurysm rupture and major episode of SAH by a few hours to a few months, so should not be overlooked. MRI FLAIR is the best sequence. Lumbar puncture is confirmatory.

Complications of Subarachnoid Haemorrhage

Hydrocephalus, Communicating and Non-Communicating Hydrocephalus.

Vasospasm.

Communicating Hydrocephalus

SAH with dilatation of the anterior and temporal horns, as well as the third and fourth ventricles. Flow is most likely blocked at the arachnoid granulations resulting in communicating hydrocephalus. 

Requires emergency ventricular shunting.

Non-Communicating Hydrocephalus

Non-communicating (obstructive) hydrocephalus occurs when the ventricular system is not in continuity with the subarachnoid space due to blood clots. Most often, the site of the blockage in non-communicating hydrocephalus is at the cerebral aqueduct, but rarely can occur at the foramen of Monro, the third ventricle, or the outlet of the fourth ventricle.

Important to recognize as it is potentially treatable by shunting.

Vasospasm following Subarachnoid Hemorrhage. 

A known delayed complication of subarachnoid hemorrhage.

Reported to occur in as many as 70% of patients with SAH.

Most commonly occurs 4-14 days after the onset of bleeding.

If severe enough, may lead to progressive ischemia and stroke.
Imp to recognize as typically treated with the calcium channel blocker nimodipine, volume expansion, mild elevation of blood pressure.

Unilateral hydrocephalus

A 5 yo male with delayed mile stones.

CT brain shows:
Marked dilatation of right lateral ventricle.
Left lateral ventricle, third ventricle, and fourth ventricles are normal in size.
There is no peri ventricular ooze of csf.
Adjacent brain parenchyma show normal attenuation. There is no adjacent parenchymal Gliosis.

Imging diagnosis: Unilateral hydrocephalus.

The left foramen of Monro points in the direction of the third ventricle and and incontinuity with third ventricle consistent with normal, unobstructed flow of CSF. Right foramen of Monro ending abruptly, show marked blunting, not pointing towards the third ventricle so the site of obstruction appears to be foramen of Monro and cause appears to be congenital. No obvious adjacent space occupying lesion.

Discussion:
Unilateral hydrocephalus (UH) is an uncommon type of hydrocephalus, often congenital.
In congenital hydrocephalus, vast majority of cases are bilateral, symmetric hydrocephalus with high rate of association with CNS and extra-CNS anomalies and a mortality rate up to 85%.
In contrast, unilateral hydrocephalus is less frequently associated with other anomalies, and if no other anomalies are present, the survival rate is 70%.
UL first described by Von Mohr (1842), usually due to obstruction at FM.
In congenital, cause is atretic, stenotic FM or occluded by a membrane. Can be seen in conjunction with corpus callosal anomalies.
In Acquired, etiologies for obstruction at FM include thalamic and intraventricular neoplasm, colloid cysts, tuberculoma, post tb ependymal adhesions, ventriculitis, vascular malformations, and non-specific inflammatory conditions.

Related Posts:
Mild-asymmetry-of-lateral-ventricles
Post-shunt-lateral-ventricle-asymmetry

Medulloblastoma MR Spectroscopy

An 14 yo male with persistent headache, nausea and vomiting.

Description:
A well circumscribed ovoid intra ventricular space occupying mass completely occupying and expanding fourth ventricle, leading to obstructive hydrocephalus.
Signals of mass corresponds to dense soft tissue, isointense to cortical grey matter on T1 and Flair, slightly hyperintense on T2.
No cystic component or marked areas of necrosis.
Restricted diffusion on Dw images.
Lobulated mild enhancement on post contrast T1.
On single voxel MR Spectroscopy at short TE of 35 ms, no peak of NAA at 2.01ppm, no peak of creatine at 3.02 with peak of raised choline at 3.2ppm.

Imaging and MR Spectrocsopy findings are very typical for a Medulloblastoma.

Diagnostic clues:
Dense 4th ventricular mass,
Hyper dense (~90%) on CT with spotty calcification (~20%) ,
Nearly isointense to cortical grey matter on MRI with restricted diffusion on Dw images.
Markedly reduced or no peak of NAA with high choline on MRS implies to non neuronal / Non Glial neoplasm.
May see drop metastasis.
Age group ~75% < 10 years; M > F.

Similar posts:
Medulloblastoma with drop metastasis
Lateral origin medullobastoma

MEDULLOBLASTOMA

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.

Location:
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.

Post TBM Vasculitis induced infarcts

A 40 y o male, known case of Tubercular Meningitis as per previous discharge summery and lab report containing Csf profile and IGg levels. 

Now re admission with left sided recent onset weakness and altered sensorium.

On Admission;
CT Brain Plain + Contrast

MRI Brain Axial FLAIR, Diffusion and 3 D TOF Non contrast MR Angio Brain

Findings:
CT Brain shows effacement of cortical sulci in right peri sylvian region with sulcal hyperdensity.
Multiple non enhancing punctate hypodensities involving right insular cortex and adjacent right parietal cortex.
MRI Brain Axial FLAIR and Diffusion show:
Multiple T2 hyper intensities involving right peri sylvian cerebral cortex and adjacent insular cortex with restricted diffusion.
MR Angiogram shows:
Right MCA distal main stem stenosis, marked sparsity of its cortical branches.

Impression : Vasculitis and vasculitis induced infarcts in a known case of tubercular meningitis.

"IVY" sign : Axial Flair image no 1 show a serpigenous hyperintensity in right temporal cortical sulcus represent a cortical branch of right MCA with abnormal sluggish flow - IVY sign, reported in Moya Moya disease and Vasculopathies.
Similar posts for IVY sign:
IVY sign in early infarction
IVY sign Moya Moya disease

Diffuse low marrow signal on T1

An 18 y o male, MRI cervical spine c/o of neck pain.
No radiculopathy.
No neurological signs.

Previous 2 year old lab reports mentions, macrocytes with anisocytosis and poikilocytosis. Low RBS count and Hb.
Increased MCV ( mean corpuscular volume) and MCH ( mean corpuscular hemoglobin).
Normal MCHC (mean corpuscular hemoglobin concentration- 34 g/dL).
Low reticulocyte count.
Platelet count Normal.
Senile neutrophils.
Lab findings are suggestive of megaloblastic anemia.

MRI Cervical spine Sag T1 and T2w images

This MRI cervical spine show diffuse low marrow signal, iso intense to skeletal muscle. 
Signal abnormality is diffuse and homogenous. 
Vertebral bodies as well as posterior elements are equally involved. 
Inter vertebral discs are spared. 
No abnormal T2 hyperintensity on STIR to suggest any marrow odema.

The lab findings of long standing megaloblastic anemia with diffuse low marrow signal on T1 supports hyperplastic marrow on MR imaging.

The similar signal abnormality involving clivus again goes in favour of a benign reconversion process rather than a more serious neoplastic marrow infiltrative or proliferative disorders.
Hyperplastic marrow is a hemopoetic marrow.
Hyperplasia also called marrow reconversion, from fatty to hemopoetic marrow.

Normal physiology is, in the neonate, all is hematopoietic marrow. Normal conversion from red (hematopoietic - T1 low) to yellow (fatty - T1 bright) marrow begins few weeks after birth, a gradual and progressive process, involving distal ends of distal most long bones first, exend towards axial skeletal. The adult pattern of bone marrow attained by approximately 25 year, where hemopoetic marrow is confined to only the axial skeleton (pelvis, vertebrae, sternum, ribs, and skull) and the proximal shafts of the femora and humeri while the remainder of the skeleton show fatty marrow.
The location and extent of the relative amounts of hematopoietic and fatty marrow depends primarily on age and the bone.
In marrow hyperplasia or reconversion, this hemopoetic marrow is increased. The numerous disease processes cause this “reconversion” , chronic anaemia is common and important cause.

Apart from hyperplastic marrow other differential diagnosis for such diffuse low marrow signal intensity on T1 and T2 MRI is fluorosis, myelofibrosis, mastocytosis, lymphoma, osteopetrosis, osteoblastic metastasis, and Paget’s disease.

Bone Marrow MR Imaging

MRI is ideal for bone marrow screening because of its high-resolution images with great soft-tissue contrast. Protocol for screening of bone marrow should must include FSE T1 and STIR and if possible FSE T2.

• FSE T1w : A routine T1-weighted image without fat suppression is one of the most important sequences for distinguishing between normal and abnormal marrow.  Normal bone marrow is composed of both fatty and hematopoietic elements. Although fatty marrow contains more fat cells than hematopoietic marrow, both types of marrow appear hyperintense relative to skeletal muscle on T1-weighted imaging because they contain a higher proportion of fat cells relative to skeletal muscle. Abnormal marrow is iso - hypointense to skeletal muscle on T1-weighted imaging because the replacement of fatty marrow elements by the pathologic process causes loss of the normal fat signal.

• STIR: are extremely sensitive for detecting fluid and so areas with bone marrow oedema appear as hyperintense relative to the background of normal signal suppressed fatty marrow.

• FSE T2w: Not primarily used for assessing bone marrow abnormality because both fat and fluid appear bright on T2w sequence. Thus, a pathologic marrow lesion could potentially be overlooked against the background of normal bright fatty marrow.  Use of T2 is confined to evaluation of an associated neural element compression.

Mesial Temporal Sclerosis MRI

A 23 yo male came for MRI Epilepsy screening.

MRI BRAIN EPILEPSY PROTOCOL
Oblique coronal T1w SPGR and T2w used for medial temporal lobes.
Coronal T1w SPGR used for comparison of size and T2w images for signal abnormality.

 Subjective evaluation of size and signal of hippocampi show right hippocampus is smaller in volume compared to left implies to atrophy with abnormal T2  hyper intensity.

Hippocampal sclerosis (Mesial temporal Sclerosis - MTS) needs consideraton with clinical and EEG correlation.

Related Posts: Mesial Temporal (Hippocampal) Sclerosis


Mesial temporal sclerosis 

Syn : MTS, hippocampal sclerosis (HS), Ammon horn sclerosis.
A seizure associated neuronal loss and gliosis in hippocampus.

CT is typically normal as is insensitive to MTS. MRI is investigation of choice.
Hippocampal atrophy with abnormal T2 hyperintenssity is a diagnostic clue.
Atrophy of fornix mamillary body, enlarged ipsilateral temporal horn of lateral ventricle, loss of hippocampal head digitations, atrophy of white matter in parahippocampal gyrus, increased T2 signal in anterior temporal white matter may be the additional associated findings.

In Mesial temporal lobe, Hippocampus is most commonly involved followed by amygdala > fornix > mamillary bodies. Involvement is bilateral in 20% of cases.

Etiology is controversial, may be acquired or developmental. Likely that MTS represents a common outcome of both acquired and developmental processes. Acquired causes related to changes after prolonged febrile seizures, status epilepticus, complicated delivery and ischemia.Familial cases of mesial temporal lobe epilepsy have been reported.

Microscopic features are decrease in hippocampal neurons and gliosis.
Chronic astrogliosis with a fine fibrillary background containing bland nuclei of astrocytes and few remaining neurons.
CA1, CA4, and CA3 are most affected. May involve entire cornu ammonis and dentate gyrus.

Dual pathology occurs in 15% of cases of MTS . Cortical dysplasia is most common dual pathology.

Clinical presentation: Complex partial seizure is the most common signs/symptoms, may progress to tonic-clonic seizures. Disease of childhood, young adults with no gender predominance.

EEG often helpful for lesion localization in 60-90%.

Medical treatment successful in only 25%.
Anterior temporal lobe resection for medically intractable disease.
Anterior temporal lobectomy successful in 70-95% patients with MR findings of MTS
If MR is normal, success of anterior temporal lobectomy is 40-55%
If amygdala involved, decreased success of surgery,approximately 50%
Resection includes anterior temporal lobe, majority of hippocampus, variable portions of amygdala.

Reference : Diagnostic imaging Osborn.

Sequel of CNS Rickettsia MRI Brain

A 14 yo female pt came for follow up imaging.
Here is her MRI Brain T2w image.

MRI Brain shows:

T2 hyperintense lacunes in bilateral thalami.
Rest of the brain parenchyma unremarkable. 

Previous history was significant.

History of hospital admission 5years back, for fever, headache and altered sensorium.

Lab reports mentions 

Weil felix : positive

Anti Ox 19 nil

Anti Ox 2  1:16

Anti Ox k  1:40

Csf pro 48 mg %

Sugar 75mg%

Cells 8 per mm3

Chlorides 119 mcf per L

Imaging wise: Bilateral thalamic chronic lacunes, considering lab reports appears to be the sequel of previous Rikettisial infection and represent vasculitis induced changes and ischemia due to small vessel involvement.

Vertebral Osteomyelitis MRI

MRI Cervical spine Sagittal T1 and Post contrast T1

This MRI Cervical spine shows:
Multiple and contiguous involvement of cervical vertebrae (C2 to C6); vertebral bodies as well as there posterior elements show diffuse low marrow signal on T1 due to abnormal replacement of normal T1 bright fatty marrow.
An associated anterior epidural soft tissue extending from C2-3 to C7-D1 disc levels causing bony canal stenosis and cord compression. Encasement of exiting nerve roots in neural foramen.
The epidural soft tissue is in continuity with pre vertebral space, pre vertebral soft tissue extending from C1-2 to C7-D1 level with erosions of adjacent anterior surfaces of vertebral bodies.
Areas of abnormal marrow signals, the anterior epidural and pre vertebral soft tissue show homogeneous enhancement on post contrast T1.
Intervening inter vertebral discs are relatively spared.
Loss of normal cervical lordosis.

Imaging wise : Vertebral Osteomyelitis with an associated anterior epidural and prevertebral Abscess.