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A seminar on “Brain Imaging”
Presenter
Dr Ajay Tripathi JR3
Dept of Medicine
Guide
Dr Vimlesh Patidar
Sir
Professor
Dept of Medicine
1
Overview of Talk
•  Orientation of Brain Anatomy
• CT/MRI imaging in different conditions
• Some special Sequences of MR
•  Recent advances
2
3
4
5
6
Imaging of Ischemic Infarct
• NCCT Brain
• Used for quick differentiation of ischemic
stroke from intracranial hemorrhage,
and to rule out other pathological processes,
such as tumors, which may present as stroke.
7
Hyper Acute infarction changes
• In hyper acute stages of infarction, the changes
noticed on CT are the result of cytotoxic edema.
• The latter is seen as reduction in the density of
gray matter in the ischemic tissue and
obliteration of sulci and gray-white matter
differentiation.
8
9
Reduction in the density of gray matter in the ischemic
tissue and obliteration of sulci and gray-white matter
differentiation.
obscuration of lentiform nuclei due to acute ischemia of
lenticulostriate
territory
• In early stages, CT may
also be able to identify
the thrombus in the
affected vessel
• dense MCA sign can be
seen in up to 50% of
all cases.
10
Hyperdense Artery
11
Sub Acute Infarct
3 – 30 days
12
Chronic Infarct
>30 days
13
In chronic stage;
encephalomalacia is
seen as area of low
density with
accompanying loss of
volume in the form of
dilated sulci and
adjacent ventricular
system
• Ultimately, however, the diagnosis of ischemic stroke
is clinical
• Moreover, even with sensitive MRI techniques,
imaging can be negative in cases of true ischemic
stroke, .
•
NCCT findings are time dependent and may be
normal or near normal even in the setting of
established or large infarct, particularly within the first
3 hours of stroke onset (the diagnostic sensitivity for
NCCT is approximately 50% even with modern CT scanners)
and increases by 15% with addition of CTA cuts for vessel and
territory localisation.
14
Exclude Intracranial Hemorrhage
• Any acute Intracranial haemorrhage is contraindication for
reperfusion therapy
• This may be intracerebral hemorrhage, subarachnoid
hemorrhage, and subdural or extradural hematoma
The appearance of ICH on CT depends on the
time elapsed since the hemorrhage.
• Hyper-attenuation 30 to 60 HU
• Hounsfield units (HU) ( Relative and comparable to
chronic infraction attenuation)
• With next few hours as clot retaraction occurs this inc >60 and
mostly upto 100 HU
15
16
• MRI is considered equivalent to
CT for detection of intracranial
hemorrhage.
17
MRI
18
19
20
MRI Brain in suspected Stroke
• More Sn , >80 % infract detected within 24 hours
of insult
• DW Scan , can identify ischemic penumbra, acute
infract looks Bright in DWI
• T2 weighted Images are used as mostly as
Inflammation and Edema looks bright
• With Gandolium contrast T1 weighted images are
used, it enhances blood signal and site of
increased blood supply
• Inferior to CT in detection of bony injury
21
MRI imaging in Stroke
• MRI findings of parenchymal FLAIR
and T2 hyper intensity and swelling
in a topographic distribution
concordant with the clinical symptoms
also confirm the clinical diagnosis of
stroke.
• MRI FLAIR may also be negative in 1st 3 hrs of
ischemic stroke, but detectable in DWI
22
Ischemic Penumbra
• “Ischemic penumbra” a region that is ischemic
but still viable and may infarct if not treated.
• Mismatches between DW and PW images in
hyperacute stroke have been well recognized, and
it has been stated that subtraction of the area of
diffusion abnormality from the area
of perfusion (greater than diffusion) deficit can
provide an estimate of ischemic penumbra.
• DSC area substracted from DWI
23
24
Perfusion is reduced in greater
area in Perfusion weighted
sections while Diffusion weighted
images shows less , diffusion
deficiet
A difference in PWI-DWI shows
ischemic Penumbra at Risk
Perfusion weighted scan- (DSC, DCE,
ASL)
DSC- uses Contrast
Reduction in the density of gray matter in the ischemic tissue and obliteration of
sulci and gray-white matter differentiation.
obscuration of lentiform nuclei due to acute ischemia of lenticulostriate
territory
25
Haemorrhagic Stroke
• Easily differentiated in NCCT and MR
• MR angiography is modality of choice to
identify culprit vessel
• Digital subtraction angiography (DSA) is the
modality of choice to visualize indolent
vascular malformation or aneurysm as the
cause of bleed.
26
Angiography
27
Magnetic Resonance Angiography
• MRA allows noninvasive assessment of neck vessels as well
as large intracranial vasculature. The reconstructed
images are similar to those of catheter angiography.
• A number of studies have shown the ability of MRA to
diagnose >70% carotid origin stenosis with a sensitivity of
85–98% and a specificity of 75–96% the spatial resolution
is still not adequate enough to assess small intracranial
vessels on 1.5T, & can be visualized with 3T
28
29
CT Angiography (CTA)
• CT angiography has emerged as the
alternative to the invasive cerebral digital
subtraction angiography (DSA)
• Pitfalls of CT angiography include lack of
visibility of small arteries
30
CT Angiography
• Short scanning time 20-40 s
• Spatial resolution is not comparable to MR
and Catheter Angio but larger intracranial
vessels can be studied
• Extra Cranial vessels can also be studied
31
Cerebral Digital Substraction
Angiography
• Cerebral Digital subtraction Angiography
• Invasive technique by catheter assisted angiography
• Small vessels can also be seen , unmatched resolution
Gold standard .
Identify the cause of bleed, define collateral circulation and assess
vasospasm.
Technically adequate angiography is essential.
Magnification, subtraction and stereoscopic techniques delineate the cause
of bleeding in most cases
Risk- Ischemic events occur in 1.3% of patients in the first 24 hours after
angiography.
Neurological deterioration occurs in 1.8% of patients between 18 and 72
hours of angiography. 32
33
Hypoxic-Ischemic Injury
• Adults, cardiac arrest
with direct reduction
of blood flow to the
brain leads to primary
ischemic injury.
• “bilateral involvement
of gray matter,
in particular the
cortex and deep
nuclei”
34
Venous Ischemia and Stroke
• Venous sinus
or cortical vein
thrombosis
leading to
stroke is rare
compared to
other types of
stroke.
35
• CT Venography has high sensitivity for depicting
the cerebral veins and sinus.
• On CTV, a thrombosed dural sinus is seen as a
filling defect and is often associated with contrast
enhancement of the walls
• But MRV is modality of choice ,do not require
contrast, comparable sensitivity and specificity
• Especially useful when Contrast is Contra-
Indicated
36
37
CNS Infections
38
PYOGENIC MENINGITIS
• In early meningitis, the CT or MR findings may be normal.
• NCCT- Basal Inflammatory exudate and
brain swelling is obliteration of the basal subarachnoid
cisterns, fissures and cerebral and cerebellar sulci.
• On contrast enhanced CT scan, there is enhancement of the
inflammatory exudates
The abnormal leptomeningeal
contrast enhancement is typically more readily apparent and
more intense on MR imaging rather than on CT scanning.
For diagnosis MR+Contrast>CECT>MR>CT
39
• TBM
• Detected more readily in Non Contarst MR
compared to Bacterial Meningitis
• A detection of Meningitis in Non Contrast MR
T1 is highly suggestive of TBM and warrents
early initiation of treatment
• Early detection due to Fibrin Exudates in TBM
40
41
Subdural Abscess (Empyema)
• Ten to fifteen percent of empyemas are due to complication
of meningitis.
• The most common locations of subdural empyema are the
cerebral convexities and the interhemispheric fissure.
• Unenhanced CT scanning reveals a crescentic or
lentiform extra-axial fluid collection that is slightly denser
than cerebrospinal fluid.
• On CT scan, after intravenous contrast administration, an
overlying peripheral rim of enhancement of varying
thickness is identified.
• This rim represents an inflammatory chnages.
• Hypodensity or contrast enhancement of the adjacent brain
parenchyma may also be seen secondary to thrombophlebitis42
43
44
Cerebritis and Brain Abscess
• Cerebritis and abscess formation constitute a
continuum.
• The majority of patients with brain abscess
demonstrate a contiguous focus of infection
usually sinusitis or otitis media
45
• Cerebral abscesses as a result of dental sepsis often
containmixed mouth flora with a predominance of anaerobic
bacteria.
• Hematogenous brain abscesses have the following
characteristics
• (i) a distant focus of infection (ii) location in the
distribution of the middle cerebral artery (iii) initial location at
the gray-white matter junction (iv) poor encapsulation (v)
high mortality.
• These abscesses are more commonly multiple
and multiloculated as compared to those that have an origin
in foci of contiguous infection.
46
47
Typically the center of a mature abscess contains necrotic
material hypointense on T1-weighted images and
hyperintense to brain on T2-weighted images.
Edema surrounding an abscess may be greater in volume
than the abscess itself and causes much of the associated
mass effect
48
NEUROCYSTICERCOSIS
• Cysticercosis is a disease transmitted by the ingestion
of the eggs of the worm Taenia solium.
• The initial host is the pig.
• Cysticercosis may involve any tissue and any
organ in the body, most symptoms are due to invasion
of the central nervous system (CNS)
• Clinical presentations include seizures,
headaches, syncope, focal neurological deficits
•
49
• Parenchymal cysticercosis 4 stages
• A) Vesicular- In the vesicular stage, a clearly marginated cyst with
thin cyst wall that is usually not identifiable is seen. The cyst
fluid is similar to cerebrospinal fluid in signal intensity.
• A discrete, eccentrically located scolex completes the image
of a parenchymal cyst in the vesicular stage.
• No contrast enhancement of the cyst wall is seen in this stage
because the cyst is alive; there is no immune response by the host
at this stage and no surrounding edema is seen.
50
51
Contrast Enhanced Axial CT
• b) In the next stage (colloidal vesicular stage), the larva
begins to degenerate .
• There is associated surrounding white matter edema The
capsule becomes visible on T1-weighted or FLAIR
• The cyst fluid is slightly hyperintense on T1-weighted
images and markedly hyperintense on T2-weighted
• Contrast enhancement is seen involving the cyst wall which
is a result of an inflammatory reaction caused by the
degenerating
parasite.
52
53
• In the third stage (granular nodular stage),
the cyst undergoes retraction, the wall of the
cyst thickens and the scolex is transformed
into a coarse mineralized granule.
•
Surrounding edema regresses gradually.
• nodular or a thick, small, ring-like
enhancement
54
55
56
CENTRAL NERVOUS SYSTEM
TOXOPLASMOSIS
• Toxoplasma gondii is a parasite
• The definitive host is the cat
• H/o of contact with Cats, or unwashed salad/vegetable
consumption
• Most toxoplasmosis infections in immunocompetent
individuals are subclinical or mildly symptomatic.
57
Imaging Findings
• On noncontrast CT, toxoplasma encephalitis characteristically
appears as multiple areas of hypodensity.
• There is a predilection for the basal ganglia (in 75–88%) and
the corticomedullary junction and lesions may involve the
posterior fossa.
•
• Lesions vary in size from less than 1 cm to over 3 cm and there
is surrounding mass effect and edema of variable degree.
Postcontrast CT demonstrates ring or nodularenhancement.
• Ring enhancement is more common with central hypodensity.
• The rings are usually thin and smooth 58
• On MRI T2-weighted images, depict active lesions as
variable signal intensity
• Godolinium reveals ring or nodular enhancement
in active lesions are clearly distinguishable from the
surrounding edema
• Magnetic resonance has a greater sensitivity than CT
59
60
T2W and T1W image Post contrast
Target sign
Surrounding Edema
FLAIR hyperintensity due to local edema
HYDATID DISEASE
• Hydatid disease is caused by Echinococcus
granulosus and less frequently by
Echinococcus multilocularis.
• H/o contacts with Dogs and Sheep, or
unwashed salad/vegetable consumption
•
61
Imaging
• Imaging Findings
• T2-weighted MR images, the better of the two
sequences for imaging these lesions, shows a
thin low signal intensity rim representing the
capsule surrounding a hyperintense lesion.
• Rim enhancement or edema is uncommon
unless the cyst becomes superinfected
.
62
63
HERPES SIMPLEX VIRUS
• Herpes simplex virus (HSV) types 1 and 2 most
commonly manifest as reactivated latent
infections.
• HSV-1 is nonsexually transmitted and
commonly produces skin lesions and
encephalitis.
• HSV-2 is sexually transmitted and is associated
with genital lesions
64
• CT scan and MR imaging findings are nonspecific early in
the course of CNS HSV infection and scans may even appear
normal
• Initial CT scans show subtle hypodense lesions in the
periventricular white matter with relative sparing of the
basal ganglia, thalami and posterior fossa structures
• Finger-like areas of increased
attenuation within the cortical gray matter
65
66
• MR imaging can demonstrate the early
edematous changes of herpes encephalitis
seen as
• hyperintensity on T2-weighted images with
characteristic involvement of the temporal
lobes and inferior frontal lobes
67
68
DWI and FLAIR sequences
White Matter disease
• Multiple sclerosis
69
• Diagnostic criteria proposed for establishing the
diagnosis of MS, have been based on three main
principles:
•
Demonstration of demyelinating lesions disseminated
in space (DIS)
Demonstration of demyelinating lesion demonstrated
in time (DIT)
Exclusion of alternative explanation for the clinical
presentation.
70
• The MR appearance of MS is widely variable depending on the
acuity and extent of the disease.
• The characteristic lesion is a T2 hyperintense lesion that
occurs throughout the CNS. It shows a typical distribution
in the PV (touching ventricle surface) location more so than
the peripheral white matter .
• Within the white matter, the lesion may be discrete or juxtacortical.
• Rarely the lesion may lie entirely within the gray matter (cortical)
71
72
73
74
Corpus callosum lesions are frequent and lie within the
inner or deep surfaces.18 The corpus callosum is a region that
is especially vulnerable to demyelination in MS,
fMRI
• Functional MRI
• Based on BOLD technique
• Blood oxygenation level dependent (BOLD)
imaging is the standard technique used to
generate images in functional MRI (fMRI) studies,
and relies on regional differences in cerebral
blood flow to delineate regional activity.
• “specific region of the cortex increases its activity
in response to a task”
75
Recent Advances
• MRI sequence developed that can aid in
identification of Neoplastic tissue in body
• (Alexander wong et al March 2022 )
• MR sequence “synthetic correlated diffusion
imaging (CDIss)”
• DWI concept , restricted diffusion coefficient due
to abnormal microstructure of Neoplasm
76
References
1) AIIMS-MAMC-PGI
diagnostic book of Radiology
2) CT-MRI of Whole Body 6th
Ed Jhon s. Hagga et all
3) Radiopedia.org
4) Internet
Thank you
77

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Brain Imaging.pptx

  • 1. A seminar on “Brain Imaging” Presenter Dr Ajay Tripathi JR3 Dept of Medicine Guide Dr Vimlesh Patidar Sir Professor Dept of Medicine 1
  • 2. Overview of Talk •  Orientation of Brain Anatomy • CT/MRI imaging in different conditions • Some special Sequences of MR •  Recent advances 2
  • 3. 3
  • 4. 4
  • 5. 5
  • 6. 6
  • 7. Imaging of Ischemic Infarct • NCCT Brain • Used for quick differentiation of ischemic stroke from intracranial hemorrhage, and to rule out other pathological processes, such as tumors, which may present as stroke. 7
  • 8. Hyper Acute infarction changes • In hyper acute stages of infarction, the changes noticed on CT are the result of cytotoxic edema. • The latter is seen as reduction in the density of gray matter in the ischemic tissue and obliteration of sulci and gray-white matter differentiation. 8
  • 9. 9 Reduction in the density of gray matter in the ischemic tissue and obliteration of sulci and gray-white matter differentiation. obscuration of lentiform nuclei due to acute ischemia of lenticulostriate territory
  • 10. • In early stages, CT may also be able to identify the thrombus in the affected vessel • dense MCA sign can be seen in up to 50% of all cases. 10
  • 12. Sub Acute Infarct 3 – 30 days 12
  • 13. Chronic Infarct >30 days 13 In chronic stage; encephalomalacia is seen as area of low density with accompanying loss of volume in the form of dilated sulci and adjacent ventricular system
  • 14. • Ultimately, however, the diagnosis of ischemic stroke is clinical • Moreover, even with sensitive MRI techniques, imaging can be negative in cases of true ischemic stroke, . • NCCT findings are time dependent and may be normal or near normal even in the setting of established or large infarct, particularly within the first 3 hours of stroke onset (the diagnostic sensitivity for NCCT is approximately 50% even with modern CT scanners) and increases by 15% with addition of CTA cuts for vessel and territory localisation. 14
  • 15. Exclude Intracranial Hemorrhage • Any acute Intracranial haemorrhage is contraindication for reperfusion therapy • This may be intracerebral hemorrhage, subarachnoid hemorrhage, and subdural or extradural hematoma The appearance of ICH on CT depends on the time elapsed since the hemorrhage. • Hyper-attenuation 30 to 60 HU • Hounsfield units (HU) ( Relative and comparable to chronic infraction attenuation) • With next few hours as clot retaraction occurs this inc >60 and mostly upto 100 HU 15
  • 16. 16
  • 17. • MRI is considered equivalent to CT for detection of intracranial hemorrhage. 17
  • 19. 19
  • 20. 20
  • 21. MRI Brain in suspected Stroke • More Sn , >80 % infract detected within 24 hours of insult • DW Scan , can identify ischemic penumbra, acute infract looks Bright in DWI • T2 weighted Images are used as mostly as Inflammation and Edema looks bright • With Gandolium contrast T1 weighted images are used, it enhances blood signal and site of increased blood supply • Inferior to CT in detection of bony injury 21
  • 22. MRI imaging in Stroke • MRI findings of parenchymal FLAIR and T2 hyper intensity and swelling in a topographic distribution concordant with the clinical symptoms also confirm the clinical diagnosis of stroke. • MRI FLAIR may also be negative in 1st 3 hrs of ischemic stroke, but detectable in DWI 22
  • 23. Ischemic Penumbra • “Ischemic penumbra” a region that is ischemic but still viable and may infarct if not treated. • Mismatches between DW and PW images in hyperacute stroke have been well recognized, and it has been stated that subtraction of the area of diffusion abnormality from the area of perfusion (greater than diffusion) deficit can provide an estimate of ischemic penumbra. • DSC area substracted from DWI 23
  • 24. 24 Perfusion is reduced in greater area in Perfusion weighted sections while Diffusion weighted images shows less , diffusion deficiet A difference in PWI-DWI shows ischemic Penumbra at Risk Perfusion weighted scan- (DSC, DCE, ASL) DSC- uses Contrast
  • 25. Reduction in the density of gray matter in the ischemic tissue and obliteration of sulci and gray-white matter differentiation. obscuration of lentiform nuclei due to acute ischemia of lenticulostriate territory 25
  • 26. Haemorrhagic Stroke • Easily differentiated in NCCT and MR • MR angiography is modality of choice to identify culprit vessel • Digital subtraction angiography (DSA) is the modality of choice to visualize indolent vascular malformation or aneurysm as the cause of bleed. 26
  • 28. Magnetic Resonance Angiography • MRA allows noninvasive assessment of neck vessels as well as large intracranial vasculature. The reconstructed images are similar to those of catheter angiography. • A number of studies have shown the ability of MRA to diagnose >70% carotid origin stenosis with a sensitivity of 85–98% and a specificity of 75–96% the spatial resolution is still not adequate enough to assess small intracranial vessels on 1.5T, & can be visualized with 3T 28
  • 29. 29
  • 30. CT Angiography (CTA) • CT angiography has emerged as the alternative to the invasive cerebral digital subtraction angiography (DSA) • Pitfalls of CT angiography include lack of visibility of small arteries 30
  • 31. CT Angiography • Short scanning time 20-40 s • Spatial resolution is not comparable to MR and Catheter Angio but larger intracranial vessels can be studied • Extra Cranial vessels can also be studied 31
  • 32. Cerebral Digital Substraction Angiography • Cerebral Digital subtraction Angiography • Invasive technique by catheter assisted angiography • Small vessels can also be seen , unmatched resolution Gold standard . Identify the cause of bleed, define collateral circulation and assess vasospasm. Technically adequate angiography is essential. Magnification, subtraction and stereoscopic techniques delineate the cause of bleeding in most cases Risk- Ischemic events occur in 1.3% of patients in the first 24 hours after angiography. Neurological deterioration occurs in 1.8% of patients between 18 and 72 hours of angiography. 32
  • 33. 33
  • 34. Hypoxic-Ischemic Injury • Adults, cardiac arrest with direct reduction of blood flow to the brain leads to primary ischemic injury. • “bilateral involvement of gray matter, in particular the cortex and deep nuclei” 34
  • 35. Venous Ischemia and Stroke • Venous sinus or cortical vein thrombosis leading to stroke is rare compared to other types of stroke. 35
  • 36. • CT Venography has high sensitivity for depicting the cerebral veins and sinus. • On CTV, a thrombosed dural sinus is seen as a filling defect and is often associated with contrast enhancement of the walls • But MRV is modality of choice ,do not require contrast, comparable sensitivity and specificity • Especially useful when Contrast is Contra- Indicated 36
  • 37. 37
  • 39. PYOGENIC MENINGITIS • In early meningitis, the CT or MR findings may be normal. • NCCT- Basal Inflammatory exudate and brain swelling is obliteration of the basal subarachnoid cisterns, fissures and cerebral and cerebellar sulci. • On contrast enhanced CT scan, there is enhancement of the inflammatory exudates The abnormal leptomeningeal contrast enhancement is typically more readily apparent and more intense on MR imaging rather than on CT scanning. For diagnosis MR+Contrast>CECT>MR>CT 39
  • 40. • TBM • Detected more readily in Non Contarst MR compared to Bacterial Meningitis • A detection of Meningitis in Non Contrast MR T1 is highly suggestive of TBM and warrents early initiation of treatment • Early detection due to Fibrin Exudates in TBM 40
  • 41. 41
  • 42. Subdural Abscess (Empyema) • Ten to fifteen percent of empyemas are due to complication of meningitis. • The most common locations of subdural empyema are the cerebral convexities and the interhemispheric fissure. • Unenhanced CT scanning reveals a crescentic or lentiform extra-axial fluid collection that is slightly denser than cerebrospinal fluid. • On CT scan, after intravenous contrast administration, an overlying peripheral rim of enhancement of varying thickness is identified. • This rim represents an inflammatory chnages. • Hypodensity or contrast enhancement of the adjacent brain parenchyma may also be seen secondary to thrombophlebitis42
  • 43. 43
  • 44. 44
  • 45. Cerebritis and Brain Abscess • Cerebritis and abscess formation constitute a continuum. • The majority of patients with brain abscess demonstrate a contiguous focus of infection usually sinusitis or otitis media 45
  • 46. • Cerebral abscesses as a result of dental sepsis often containmixed mouth flora with a predominance of anaerobic bacteria. • Hematogenous brain abscesses have the following characteristics • (i) a distant focus of infection (ii) location in the distribution of the middle cerebral artery (iii) initial location at the gray-white matter junction (iv) poor encapsulation (v) high mortality. • These abscesses are more commonly multiple and multiloculated as compared to those that have an origin in foci of contiguous infection. 46
  • 47. 47 Typically the center of a mature abscess contains necrotic material hypointense on T1-weighted images and hyperintense to brain on T2-weighted images. Edema surrounding an abscess may be greater in volume than the abscess itself and causes much of the associated mass effect
  • 48. 48
  • 49. NEUROCYSTICERCOSIS • Cysticercosis is a disease transmitted by the ingestion of the eggs of the worm Taenia solium. • The initial host is the pig. • Cysticercosis may involve any tissue and any organ in the body, most symptoms are due to invasion of the central nervous system (CNS) • Clinical presentations include seizures, headaches, syncope, focal neurological deficits • 49
  • 50. • Parenchymal cysticercosis 4 stages • A) Vesicular- In the vesicular stage, a clearly marginated cyst with thin cyst wall that is usually not identifiable is seen. The cyst fluid is similar to cerebrospinal fluid in signal intensity. • A discrete, eccentrically located scolex completes the image of a parenchymal cyst in the vesicular stage. • No contrast enhancement of the cyst wall is seen in this stage because the cyst is alive; there is no immune response by the host at this stage and no surrounding edema is seen. 50
  • 52. • b) In the next stage (colloidal vesicular stage), the larva begins to degenerate . • There is associated surrounding white matter edema The capsule becomes visible on T1-weighted or FLAIR • The cyst fluid is slightly hyperintense on T1-weighted images and markedly hyperintense on T2-weighted • Contrast enhancement is seen involving the cyst wall which is a result of an inflammatory reaction caused by the degenerating parasite. 52
  • 53. 53
  • 54. • In the third stage (granular nodular stage), the cyst undergoes retraction, the wall of the cyst thickens and the scolex is transformed into a coarse mineralized granule. • Surrounding edema regresses gradually. • nodular or a thick, small, ring-like enhancement 54
  • 55. 55
  • 56. 56
  • 57. CENTRAL NERVOUS SYSTEM TOXOPLASMOSIS • Toxoplasma gondii is a parasite • The definitive host is the cat • H/o of contact with Cats, or unwashed salad/vegetable consumption • Most toxoplasmosis infections in immunocompetent individuals are subclinical or mildly symptomatic. 57
  • 58. Imaging Findings • On noncontrast CT, toxoplasma encephalitis characteristically appears as multiple areas of hypodensity. • There is a predilection for the basal ganglia (in 75–88%) and the corticomedullary junction and lesions may involve the posterior fossa. • • Lesions vary in size from less than 1 cm to over 3 cm and there is surrounding mass effect and edema of variable degree. Postcontrast CT demonstrates ring or nodularenhancement. • Ring enhancement is more common with central hypodensity. • The rings are usually thin and smooth 58
  • 59. • On MRI T2-weighted images, depict active lesions as variable signal intensity • Godolinium reveals ring or nodular enhancement in active lesions are clearly distinguishable from the surrounding edema • Magnetic resonance has a greater sensitivity than CT 59
  • 60. 60 T2W and T1W image Post contrast Target sign Surrounding Edema FLAIR hyperintensity due to local edema
  • 61. HYDATID DISEASE • Hydatid disease is caused by Echinococcus granulosus and less frequently by Echinococcus multilocularis. • H/o contacts with Dogs and Sheep, or unwashed salad/vegetable consumption • 61
  • 62. Imaging • Imaging Findings • T2-weighted MR images, the better of the two sequences for imaging these lesions, shows a thin low signal intensity rim representing the capsule surrounding a hyperintense lesion. • Rim enhancement or edema is uncommon unless the cyst becomes superinfected . 62
  • 63. 63
  • 64. HERPES SIMPLEX VIRUS • Herpes simplex virus (HSV) types 1 and 2 most commonly manifest as reactivated latent infections. • HSV-1 is nonsexually transmitted and commonly produces skin lesions and encephalitis. • HSV-2 is sexually transmitted and is associated with genital lesions 64
  • 65. • CT scan and MR imaging findings are nonspecific early in the course of CNS HSV infection and scans may even appear normal • Initial CT scans show subtle hypodense lesions in the periventricular white matter with relative sparing of the basal ganglia, thalami and posterior fossa structures • Finger-like areas of increased attenuation within the cortical gray matter 65
  • 66. 66
  • 67. • MR imaging can demonstrate the early edematous changes of herpes encephalitis seen as • hyperintensity on T2-weighted images with characteristic involvement of the temporal lobes and inferior frontal lobes 67
  • 68. 68 DWI and FLAIR sequences
  • 69. White Matter disease • Multiple sclerosis 69
  • 70. • Diagnostic criteria proposed for establishing the diagnosis of MS, have been based on three main principles: • Demonstration of demyelinating lesions disseminated in space (DIS) Demonstration of demyelinating lesion demonstrated in time (DIT) Exclusion of alternative explanation for the clinical presentation. 70
  • 71. • The MR appearance of MS is widely variable depending on the acuity and extent of the disease. • The characteristic lesion is a T2 hyperintense lesion that occurs throughout the CNS. It shows a typical distribution in the PV (touching ventricle surface) location more so than the peripheral white matter . • Within the white matter, the lesion may be discrete or juxtacortical. • Rarely the lesion may lie entirely within the gray matter (cortical) 71
  • 72. 72
  • 73. 73
  • 74. 74 Corpus callosum lesions are frequent and lie within the inner or deep surfaces.18 The corpus callosum is a region that is especially vulnerable to demyelination in MS,
  • 75. fMRI • Functional MRI • Based on BOLD technique • Blood oxygenation level dependent (BOLD) imaging is the standard technique used to generate images in functional MRI (fMRI) studies, and relies on regional differences in cerebral blood flow to delineate regional activity. • “specific region of the cortex increases its activity in response to a task” 75
  • 76. Recent Advances • MRI sequence developed that can aid in identification of Neoplastic tissue in body • (Alexander wong et al March 2022 ) • MR sequence “synthetic correlated diffusion imaging (CDIss)” • DWI concept , restricted diffusion coefficient due to abnormal microstructure of Neoplasm 76
  • 77. References 1) AIIMS-MAMC-PGI diagnostic book of Radiology 2) CT-MRI of Whole Body 6th Ed Jhon s. Hagga et all 3) Radiopedia.org 4) Internet Thank you 77

Editor's Notes

  1. Mid Brain
  2. 20 HounsFiled Unit approx is hypoattenuation of density seen in Hyperacute infraction on NCCT
  3. Lenticulostriate artery – Small perforating artery from Circle of Willis , to Basal ganglia
  4. CT diff Acute Ischemic stroke from Intra Cranial Hemorrage & Mass
  5. SO in hyperacute phase <6hrs a CT can miss a Hemorrage which shall look like a Chronic infraction , Hyperattenuation- White , Hypoattenuation - Dark
  6. DSA is a Fluroscopic technique Its based on Xrays and Contrast flow , orientation and use of computers to digitally substract noise in the film
  7. The evolution from cerebritis to abscess has been categorized into four stages: Early cerebritis, late cerebritis, early capsule formation and late capsule formation.17 In the early cerebritis (the first 4–5 days) stage, the organism grows in the parenchyma. Acute inflammatory cells, particularly polymorphonuclear leukocytes, migrate into the parenchyma to ingest or destroy bacteria. Opening of the blood-brain barrier produces edema (Figs 7A to C). Microscopic hemorrhage may be seen during the acute cerebritis stage but is unusual later. In the late cerebritis stage (7–10 days), the small areas of necrosis coalesce into one large focus filled with necrotic debris. Granulation tissue forms at its margins containing macrophages. Edema and small foci of cerebritis are seen surrounding this area. These small foci form satellite lesions adjacent to the large abscess. In the early capsule stage (10–14 days), the body attempts to wall off the infection by forming a fibrous capsule. Formation of a collagenous capsule by fibroblasts is seen.18 The central necrotic area is liquefied and the surrounding edema persists. The late capsule stage (>14 days) is characterized by a decrease in the surrounding edema. A gliotic reaction develops at the outer margin of the abscess capsule. Thus, pathologically the abscess capsule consists of three layers: an inner layer of granulation tissue, a relatively thick middle layer of collagen and an outer layer of reactive glial tissue. The time that is required to progress from cerebritis to mature abscess is highly variable from 2 weeks to several months. The rate of progression depends on several factors including the aggressiveness of the organism and status of the host’s immune system.
  8. The appearance of the contrast-enhancing rim of an abscess capsule on postcontrast MR images is similar to that seen with postcontrast CT scans. Postgadolinium T1-weighted images are a key in the diagnosis of the brain abscess (Figs 10A to C). The enhancing rim is usually thin, measuring 5 mm or less, often with thinner ventricular margin.
  9. the larva is seen as a small marginal nodule projecting into a small cyst containing clear fluid. The parasites are viable and elicit little or no inflammatory response in the surrounding tissue. The parasite may remain in this stage for years or may undergo a process of degeneration as a result of the host’s immune response that leads the parasite to the next stage of pathologic changes.
  10. Similar findings are seen with slight alteration in prediclination of involvemnet in Varicella Zoster encephalitis and Japanease Encephalitis
  11. PV- Periventicular