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MRI Sequences in Neuroradiology

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C.N.S. MRI Sequences in Neuroradiology
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Page 1: MRI Sequences in Neuroradiology

C.N.S.MRI Sequences in Neuroradiology

Page 2: MRI Sequences in Neuroradiology

Mohamed Zaitoun

Assistant Lecturer-Diagnostic Radiology Department , Zagazig University Hospitals

EgyptFINR (Fellowship of Interventional

Neuroradiology)[email protected]

Page 3: MRI Sequences in Neuroradiology
Page 4: MRI Sequences in Neuroradiology
Page 5: MRI Sequences in Neuroradiology

Knowing as much as possible about your enemy precedes successful battle

and learning about the disease process precedes successful management

Page 6: MRI Sequences in Neuroradiology

MRI Sequences in Neuroradiology1-T12-T23-FLAIR4-PD5-DWI & ADC6-GRE7-MRS8-Perfusion

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1-Conventional Spin-echo T1 :-T1 prolongation is hypointense (dark), T1

shortening is hyperintense (bright)-Most brain tissue are hypointense on T1-The presence of hyperintensity on T1

(caused by T1 shortening) can be an important clue leading to a specific diagnosis

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Normal T1

Page 9: MRI Sequences in Neuroradiology

-Causes of T1 shortening (hyperintensity) include :1-Gadolinium-based contrast agents2-Hemoglobin degradation products (intra- and extra-cellular

methemoglobin)3-Lipid-containing lesions (lipoma, dermoid cyst, implanted

fatty materials, laminar cortical necrosis)4-Substances with high concentration of proteins (colloid

cyst, craniopharyngioma, Rathke’s cleft cyst, ectopic posterior pituitary gland)

5-Melanin (metastatic melanoma)6-Lesions containing mineral substances such as: calcium

(calcifications, Fahr’s disease), copper (Wilson’s disease) and manganese (hepatic encephalopathy, manganese intoxication in intravenous drug abusers)

Page 10: MRI Sequences in Neuroradiology

Phase Time Hemoglobin , Location

T1 T2

1-Hyperacute <6 hrs Oxyhemoglobin, intracellular

Isointense or hypointense

Hyperintense

2-Acute 6-72 hours Deoxyhemoglobin, intracellular

Hypointense

Hypointense

3-Early subacute

3-7 days Methemoglobin, intracellular

Hyperintense

Hypointense

4-Late subacute

1 week-month Methemoglobin, extracellular

Hyperintense

Hyperintense

5-Chronic >1 month Ferritin and hemosiderin, extracellular

Hypointense

Hypointense

Page 11: MRI Sequences in Neuroradiology

Solid/cystic pituitary macroadenoma of prolactinoma type with hemorrhage during therapy with bromocriptine, (A&B) axial unenhanced T1-weighted images show high signal corresponding to methemoglobin, (C) coronal T2 allows for differentiation of methemoglobin types, the lower part of the tumor contains hypointense intracellular methemoglobin and the upper part of a lesion contains hyperintense extracellular methemoglobin

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Left parietal epidural hematoma, (A) T1, (B) T2, hematoma shows high signal on both images, which is consistent with extracellular methemoglobin

Page 13: MRI Sequences in Neuroradiology

Cerebral venous thrombosis, axial T1, (A) left sigmoid sinus thrombosis, (B) superior sagittal sinus thrombosis in the inferior-posterior portion (arrow), (C) superior sagittal sinus thrombosis at the convexity with a thrombosed draining cortical vein, (D) thrombosis of the right vein of Labbe (arrow)

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Quadrigeminal plate cistern lipoma (fat)

Page 15: MRI Sequences in Neuroradiology

Intracranial lipoma, axial T1 shows small hyperintense lipoma located near the midline in the quadrigeminal cistern on the left side

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Non-enhanced CT shows a low-density mass with mural calcifications in the juxtasellar region (A), T1 without contrast reveals high signal of the lesion representing its fatty content (B) and hyperintense droplets in the interpeduncular cistern (B), the frontal horns and sulci (C) after subarachnoid rupture

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Lipid-containing filling material in the sphenoid sinus, sagittal T1 shows iatrogenic hyperintense lipid-containing filling material in the sphenoid sinus in a patient after transsphenoidal resection of a pituitary tumor

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Cortical laminar necrosis, axial T1 demonstrates segmental necrosis of cerebral cortex visible as linear bands of high signal intensity in the right temporal cortex at the periphery of a chronic ischemic lesion

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Hemorrhagic necrosis of the cortex and basal ganglia, axial T1, hyperintense basal ganglia (A) and cortex along both central sulci (B) consistent with necrosis with petechial hemorrhage in a patient 3 days after cardiopulmonary resuscitation following cardiac arrest

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Colloid cyst, T1 shows an ovoid hyperintense lesion in the typical location near foramina of Monro diagnostic of a colloid cyst (protein)

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A 21-year-old patient with a solid/cystic craniopharyngioma, located in the sellar-suprasellar region, sagittal T1 shows high signal intensity of the cystic portion of the tumor as well as a significant enlargement of sella turcica and compression of the optic chiasm

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Rathke’s cleft cyst, sagittal T1-weighted image demonstrates a hyperintense intrasellar cyst located between anterior and posterior pituitary lobes

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Ectopic posterior pituitary lobe, sagittal (A) and coronal (B) T1 show hyperintense posterior pituitary lobe in the ectopic location within hypothalamus (arrows)

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Metastatic melanoma to the right eyeball, axial unenhanced T1

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Calcifications within oligodendroglioma, unenhanced T1 (A) demonstrates hyperintense foci within the tumor in the right frontal area (arrows) requiring differentiation between hemorrhage and calcifications, unenhanced CT image (B) confirms presence of calcifications (arrows)

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Fahr’s disease, unenhanced T1 (A) reveals high signal intensity of the heads of both caudate nuclei and putamina. Unenhanced CT (B) confirms presence of calcification in the region of basal ganglia

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Wilson’s disease, axial T1 shows bilateral regions of increased signal intensity within globi pallidi (arrows) due to pathological copper accumulation

Page 28: MRI Sequences in Neuroradiology

Hepatic encephalopathy in a 66-years-old man, axial T1 show bilateral symmetrical regions of hyperintensity within globi pallidi (arrows) (A) and substantia nigra in the midbrain (arrows) (B)

Page 29: MRI Sequences in Neuroradiology

Manganese intoxication in a 32-year-old intravenous drug abuser. Axial T1 reveal diffuse brain injury due to abnormal manganese accumulation after 15 years of addiction, significantly increased signal can be noted within the anterior lobe of the pituitary gland (white arrow), superior cerebellar peduncles (black arrows) (A) as well as basal ganglia and hemispheric white matter (B)

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2-Conventional Spin-echo T2 :-T2 prolongation is hyperintense, T2 shortening is

hypointense-Most brain lesions are hyperintense on T2-Water has a very long T2 relaxation constant

(water is very bright on T2), edema is a hallmark of many pathologic processes & causes T2 prolongation

-Since most pathologic lesions are hyperintense on T2, the clue to a specific diagnosis may be obtained when a lesion is hypointense

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Normal T2

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-Causes of hypointensity on T2 :1-Gadolinium-based contrast materials2-Hemoglobin degradation products3-Melanin4-Mucous or protein-containing lesions5-Highly cellular lesions (Due to their high cellularity,

malignant tumors such as medulloblastomas and lymphomas or high-grade gliomas may appear as T2 hypointense lesions, Medulloblastomas and lymphomas are also known as tumors with a very high nuclear to cytoplasmatic ratio)

6-Lesions containing mineral substances such as: calcium, copper and iron

7-Turbulent and rapid blood or CSF flow8-Air-containing spaces

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Midline glioblastoma multiforme, DSC perfusion weighted imaging, (A) Cerebral Blood Volume Map showing malignant hyperperfusion within the tumor core, (B) source T2 image showing hypointense tumor after contrast injection

Page 34: MRI Sequences in Neuroradiology

Phase Time Hemoglobin , Location

T1 T2

1-Hyperacute <6 hrs Oxyhemoglobin, intracellular

Isointense or hypointense

Hyperintense

2-Acute 6-72 hours Deoxyhemoglobin, intracellular

Hypointense

Hypointense

3-Early subacute

3-7 days Methemoglobin, intracellular

Hyperintense

Hypointense

4-Late subacute

1 week-month Methemoglobin, extracellular

Hyperintense

Hyperintense

5-Chronic >1 month Ferritin and hemosiderin, extracellular

Hypointense

Hypointense

Page 35: MRI Sequences in Neuroradiology

Intracerebral active bleeding from an arteriovenous malformation located parasagitally (black arrows) within the left hemisphere, (A) T2 and (B) T1, central area of low signal on T2 (A) is consistent with acute bleeding and deoxyhemoglobin (white arrows) which is surrounded by a large hyperacute hematoma with T2 and T1 signal characteristic of oxyhemoglobin

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Early subacute hematoma within the right cerebellar hemisphere 72 hours after the onset of bleeding, (A) T1, (B) T2, (C) unenhanced CT, low signal on T2 and high signal on T1 indicate intracellular methemoglobin

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Chronic intracerebral hematomas in both frontal and left temporal lobes, T2 shows hyperintense hematomas with hypointense margins indicating hemosiderin

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Chronic hemorrhagic infarction within the right hemisphere, T2 (A) shows a diffuse hypointense area indicating hemosiderin which is better visualized on a susceptibility-weighted image (B)

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Cavernoma in the left parasagittal location, T2 shows typical salt and pepper appearance with central high signal and peripheral hypointense rim

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Cavernoma and developmental venous anomaly within the left cerebellar hemisphere, T2 (A) shows hypointense oval cavernoma and bands of superficial hemosiderosis due to chronic bleeding which are better depicted on SWI (B), T1+C (C) reveals coexisting developmental venous anomaly

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Diffuse axonal injury, axial susceptibility weighted images show multiple small hypointense foci of hemorrhage within the right temporal lobe and midbrain (A), splenium of the corpus callosum (B) and right parietal lobe (C), which are usually hardly visible on other MR sequences

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Metastatic melanoma to the right eyeball, axial T2 shows low signal characteristic of melanin

Page 43: MRI Sequences in Neuroradiology

Colloid cyst, T2 shows a hypointense ovoid lesion in a typical location within the third ventricle close to the foramina of Monro (arrow)

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Rathke’s cleft cyst, sagittal T2 shows low signal within the cyst which is typically located between the anterior and posterior pituitary lobes

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Primary central nervous system lymphoma, MRI show two homogeneously hypointense tumors on T2 (A) with strong contrast enhancement on T1+C (B), DWI reveals almost homogenous diffusion restriction with high signal on DW image (C) and low signal on the ADC map (D)

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Aging brain, T2 (A) shows low signal of both globi pallidi due to iron accumulation in a 75-year-old female patient, iron overload may be better visualized on T2* (B)

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Fahr’s disease, unenhanced CT image (A) shows typical bilateral calcifications in the region of basal ganglia, T2 (B) shows hypointense both globi pallidi, while T2* image (C) reveals larger areas of hypointensity due to a susceptibility artifact and a “blooming effect”

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Calcified meningioma in the left frontal location with a very low signal on T2

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Vascular malformations, sagittal T2 (A) shows small pericallosal aneurysm (arrow), axial T2 (B) shows multiple flow voids within a large arteriovenous malformation in the left hemisphere

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High-pressure hydrocephalus due to a tumor located at the cranio-cervical junction, sagittal T2 shows enlarged ventricles and a hypointense jet through an aqueduct indicating very fast flow of the CSF

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T2 shows a large amount of hypointense air within the lateral ventricles after a neurosurgical procedure

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3-Fluid Attenuation Inversion Recovery (FLAIR):

-FLAIR sequence is a T2 with suppression of water signal based on water’s T1 characteristics

-A normal FLAIR image may appear similar to T1 since the CSF is dark on both, however, the signal intensities of the gray & white matter are different :

*T1 : normal white matter is brighter than gray matter

*FLAIR : white matter is darker than gray matter

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Page 54: MRI Sequences in Neuroradiology

4-Conventional Spin-echo Proton Density (PD):

-PD images aren’t used in many Neuroradiology MRI protocols, but they do have the highest signal to noise ratio of any MRI sequence

-PD sequences are useful in the evaluation of multiple sclerosis (MS), especially for visualization of demyelinating plaques in the posterior fossa

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Axial brain MR images of a patient with MS, obtained before the onset of clinical symptoms, on the proton density-weighted image (A), many periventricular and discrete white matter lesions are visible. Two of them enhance on T1+C (B)

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5-Diffusion Weighted Images (DWI) & Apparent Diffusion Coefficient (ADC) :

-Diffusion MRI is based on the principal that the Brownian motion of water protons can be imaged

-Signal is lost with increasing Brownian motion -Free water (CSF) experiences the most signal

attenuation, while many pathologic processes (primarily ischemia) cause reduced diffusivity & less signal loss

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-Diffusion MRI consists of two separate sequences, DWI & ADC, which are interpreted together to evaluate the diffusion characteristics of tissue

-Diffusion is 95 % sensitive & specific for infarct within minutes of symptom onset

-DWI is an inherently T2 weighted sequence (obtained with an echo-planar technique), on DWI, reduced or restricted diffusivity will be hyperintense (less Brownian motion << less loss of signal) & lesions are very conspicuous

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-The ADC map shows pure diffusion information without any T2 weighting, in contrast to DWI, reduced diffusivity is hypointense on the ADC map

-An important pitfall to be aware of it is the phenomenon of T2 shine through, because DWI images are T2 weighted, lesions that are inherently hyperintense on T2 may also be hyperintense on DWI even without diffusion restriction, this phenomenon is called T2 shine through, correlation with ADC map for a corresponding dark spot is essential before concluding that diffusion is restricted

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-In the brain, diffusion images are obtained in three orthogonal gradient planes to account for the inherent anisotropy of large white matter tracts, anisotropy is the tendency of water molecules to diffuse directionally along white matter tracts

-The b-value is an important concept that affects the sensitivity for detecting diffusion abnormalities, the higher the b-value, the more contrast the image will provide for detecting reduced diffusivity

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-Although diffusion MRI is most commonly used to evaluate for infarct, the differential diagnosis for reduced diffusion includes :

1-Acute Stroke2-Bacterial Abscess3-Cellular Tumors (Lymphoma &

Medulloblastoma)4-Epidermoid Cyst5-Herpes Encephalitis6-Creutzfeldt-Jakob Disease

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Acute Stroke

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Acute Stroke

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Bacterial Abscess

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Bacterial Abscess

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CNS Lymphoma

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CNS Lymphoma

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CNS Lymphoma

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Medulloblastoma

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Medulloblastoma

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Epidermoid Cyst

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Epidermoid Cyst

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Herpes Encephalitis

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Herpes Encephalitis

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Creutzfeldt-Jakob Disease

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Creutzfeldt-Jakob Disease

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6-Gradient Recall Echo (GRE) :-GRE captures the T2* signal, because the 180-degree

rephasing pulse is omitted, GRE images are susceptible to signal loss from magnetic field inhomogeneites

-Hemosiderin & calcium produce inhomogeneites in the magnetic field, which creates blooming artifacts on GRE & makes even small lesions conspicuous

-Susceptibility-weighted imaging (SWI) is a rapidly evolving technique that utilizes both the magnitude and phase information to obtain valuable information about susceptibility changes between tissues

-SWI is very sensitive to the paramagnetic effects of deoxyhemoglobin

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-The D.D. of multiple dark spots on GRE includes :

1-Hypertensive microbleeds (dark spots are primarily in the basal ganglia, thalami, cerebellum & pons)

2-Cerebral amyloid angiopathy (dark spots are in the subcortical white matter, most commonly the parietal & occipital lobes)

3-Familial cerebral cavernous malformations (an inherited form of multiple cavernous malformations)

4-Axonal shear injury5-Multiple hemorrhagic metastases

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Page 79: MRI Sequences in Neuroradiology

Hypertensive Microbleeds

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Hypertensive Microbleeds

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Amyloid Angiopathy

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Amyloid Angiopathy

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Amyloid Angiopathy Hypertensive Microbleeds

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Multiple Cavernous Malformations

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Multiple Cavernous Malformations

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Multiple Cavernous Malformations

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Axonal Shear Injury

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Axonal Shear Injury

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Multiple hemorrhagic metastases

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Multiple hemorrhagic metastases

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7-Magnetic Resonance Spectroscopy (MRS) :-MRS describes the chemical composition of a brain region-The ratio of specific compounds may be altered in various

disease states :1-Choline : is a marker of cellular membrane turnover and

is therefore elevated in neoplasms , demyelination and gliosis

2-Creatine : provides information about cellular energy stores , reduces in high grade gliomas

3-N-acetylaspartate (NAA) : is a normal marker of neuronal viability , it is therefore reduced in any process that destroys neurons , such as high grade tumors,  radionecrosis , non-neuronal tumors (e.g. cerebral metastases and primary CNS lymphoma)

4-Lactate : is a marker of anaerobic metabolism (no peak is seen in normal spectra) , it is therefore elevated in necrotic areas (e.g. higher grade tumors) and infections (cerebral abscess)

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Patient with glioblastoma with oligodendroglioma component , (a) MRS spectrum from region of brain not affected by the tumor , (b) Spectrum from a voxel within the tumor showing elevated choline , decreased NAA & Creatine

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MRS shows decreased NAA peak & elevated lactate in infarction

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5-Lipid : is a marker of severe tissue damage with liberation of membrane lipids, as is seen in cerebral infarction or cerebral abscesses

6-Alanine : elevated in meningioma7-Gamma-aminobutyric acid (GABA) : is the principle

inhibitory neurotransmitter of the central nervous system, decreases in epilepsy & schizophrenia

8-Glutamate-Glutamine (Glx) peak :  It overlaps with the GABA peak and cannot be routinely separated from each other

9-Citrate : decreased in prostate cancer10-Myo-inositol : elevated in low grade astrocytoma, PML,

Alzheimer disease, regions of gliosis & congenital CMV infection

Decreases hepatic encephalopathy & Glioblastoma

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-The peaks of the three principle compounds analyzed occur in alphabetical order :

Choline, Creatine & NAA-Canavan disease is a dysmyelinating disorder

known for being one of the few disorders with elevated NAA

-Hunter’s angle is a quick way to see if the spectrum is close to normal, a line connecting the tallest peaks should point up like a plane taking off

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MRS in Canavan disease , the NAA peak is abnormally high due to the inability to catabolize NAA

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(a) Normal spectrum , Hunter’s angle (yellow arrow) is pointing up as a plane at take off , (b) Abnormal spectrum due to oligoastrocytoma , with elevated choline & decreased NAA , a line connecting the tallest peaks would point down , which is a clue that the spectrum is abnormal

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-In some circumstances, Spectroscopy may help distinguish :

1-Recurrent tumor from Radiation necrosis :-Recurrent tumor : choline will be elevated-Radiation change : NAA, Choline and Creatine will all

be low2-Glioblastoma & Metastases :-Glioblastoma : is an infiltrative tumor that features a

gradual transition from abnormal to normal spectroscopy

-Metastases : would be expected to have a more abrupt transition

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3-Lymphoma From Toxoplasmosis in AIDS :-Lymphoma shows high choline peak-Toxoplasmosis shows high lipid peak4-Brain Abscess From Necrotic Brain Tumor :-Increased lipid/lactate is noted in both tumors and

abscess-BUT only abscess spectrum shows amino acids,

acetate, aspartate and succinate peaks

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MRS in brain abscess

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8-Perfusion :-Advanced technique where the brain is imaged

repeatedly as a bolus of gadolinium contrast is injected-The principle of perfusion MRI is based on the theory

that gadolinium causes a magnetic field disturbance which (counterintuitively) transiently the image intensity

-Perfusion images are echo-planar T2* images which can be acquired very quickly

-Perfusion MRI may be used for evaluation of stroke & tumors

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Acute Stroke

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Acute Stroke

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Biopsy-proven glioblastoma multiforme, (A) T1+C shows a heterogeneous enhancing lesion within the posterior right frontal and parietal lobes, (B) Increased blood volume in the region of the tumor is shown on the relative cerebral blood volume map

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