This document discusses several common pathologies seen in the brain: 1. Trauma such as epidural hematomas, subdural hematomas, subarachnoid hemorrhage, and diffuse axonal injury are described along with their imaging appearances on CT and MRI. 2. Strokes including cerebral infarction, intraparenchymal hemorrhage, and subarachnoid hemorrhage are outlined. 3. Infections like meningitis, abscesses, tuberculomas, and neurocysticercosis are covered. 4. Demyelinating diseases like multiple sclerosis are mentioned. 5. Tumors both extra-axial and intra

1. BRAIN : COMMON
PATHOLOGIES
Mr. Sameer Ahmad Ganaie
ASSISTANT PROFESSOR COPMS ADESH
UNIVERSITY, BATHINDA PUNJAB

2. TRAUMA
STROKE
INFECTION
DEMYELINATION
TUMORS
COMMON PATHOLOGIES

3. FINDINGS IN TRAUMA

4. Epidural Subdural Intraparenchymal

5. EPIDURAL HEMATOMA
Etiology – fracture lacerating the middle meningeal artery or venous oozing
Most commonly unilateral and temporoparietal
Cross dural attachment but NOT sutures

6. CT FINDINGS
Biconvex or lentiform
configurations displacing the
gray-white matter interface.
Two thirds are uniformly high
density, one third are mixed
hyper and hypodense.
Secondary herniations are very
common

7. MR FINDINGS
Lentiform mass that strips
the dura from inner table
Acute – Isointense on T1WI,
hyperintense on T2WI
Late Subacute and early
chronic – hyperintense on
both T1 and T2

8. SUBDURAL HEMATOMA
Most lethal of all head injuries
Stretching and tearing of bridging cortical veins at the
site they cross the subdural space to drain into dural
sinus
Cross suture lines but NOT dural attachments
Most commonly unilateral and frontoparietal

9. CT IMAGING
Classically – Crescent shaped,
homogeneously hyperdense
collection with a diffuse spread
Subacute stage – Isointense with
cortex
Chronic stage – encapsulated,
serosanguineous fluid in
subdural space

10. MR IMAGING
Patterns similar to intracerebral
hemorrhage
Exceptions – Chronic subdural hematoma
appears iso or hypointense on T1WI
compared to gray matter

11. SUBARACHNOID HEMORRHAGE
Bleeding within the CSF spaces
Basal cisterns and Sylvian fissures fill first followed by
spread over the cerebral convexities
Appears as high density “feathered” collections along the
interhemispheric fissure
Acute SAH – CT is the investigation of choice

13. DIFFUSE AXONAL INJURY SHEARING
INJURY
Axonal shear-strain deformations induced by sudden
acceleration, deceleration or rotational forces on brain
Disruption of penetrating blood vessels at the grey-white
matter junction, corpus callosum and internal capsule, deep
gray matter and upper brain stem
Grossly produces numerous small hemorrhagic foci
Longer recovery time

14. CT IMAGING
Early imaging – subtle or normal
Late findings –
small hyper densities at the grey-
white matter junction and corpus
callosum
MR IMAGING
 T1WI – unremarkable
 T2WI – multifocal
hyperintense foci at
grey-white interfaces or
in corpus callosum

16. PARENCHYMAL CONTUSIONS
Brain striking an osseous ridge or dural fold
Commonly associated with depressed skull fractures
Location : coup or contre-coup
Non-hemorrhagic : ill defined hypodensities
Hemorrhagic : heterogenous hyperdensities with surrounding ill defined
hypodensities

18. MR FEATURES

19. HYPERACUTE
ISOINTENSE-T1 HYPERINTENSE T2

20. ACUTE
ISOINTENSE T1 HYPOINTENSE T2

21. SUBACUTE (EARLY)
HYPERINTENSE T1 HYPOINTENSE T2

22. SUBACUTE (LATE)
T1 HYPERINTENSE T2 HYPERINTENSE

23. CHRONIC
T2 – mildly hypointense rim GRE – BLOOMING of rim
T1 – hypo to isointense

24. INTRAVENTRICULAR AND CHOROID
PLEXUS HEMORRHAGE
Traumatic IVH reflects severe
injury
Associated with other
manifestations like DAI, deep
cerebral gray matter and
brain stem lesions
CT shows high density
intraventricular blood with or
without a fluid fluid level

25. CEREBRAL EDEMA
Compressed and effaced sulci
Low attenuation brain
parenchyma with loss of WM –
GM interface
Decreased supratentorial
perfusion with preserved infra
tentorial perfusion “White
Cerebellum Sign”

26. STROKE
Clinically defined as acute loss of neurological function secondary to
parenchymal ischemia or hemorrhage
1. Cerebral Infarction (80%)
2. Primary Intraparenchymal Hemorrhage(15%)
3. Subarachnoid Hemorrhage (5%)
4. Venous Occlusions

27. ROLE OF CT / MR IN ACUTE CEREBRAL
INFARCTION
To diagnose or exclude intracerebral hemorrhage
To identify an underlying structural lesion that may mimic stroke clinically :
tumour
vascular malformation
subdural hematoma

28. CT FINDINGS IN CEREBRAL
INFARCTION

29. Obscuration of
lentiform nucleus
Hyperdense MCA
Insular ribbon sign
0 – 12 hours

30. 12 – 24 hours
Loss of grey-white matter interface.

31. Increasing mass effect
Wedge shaped low density area in both grey and white matter
Hemorrhagic transformation
1 – 4 days

32. Hemorrhagic transformation of infarct
Mass effect and edema persist for the next 4-7 days
Resolution of mass effect and edema progresses over 1-8 wks

33. •Encephalomalacic changes
•Volume loss – prominent adjacent sulci,
ipsilateral ventricular enlargement
•Rarely calcification
Months to
Years

34. ACUTE INFARCT CHRONIC INFARCT

35. MR FINDINGS IN CEREBRAL
INFARCTION

36. CONVENTIONAL MRI
T2WI – demonstrate site of parenchymal injury - regions of increased
water content, whether acute or remote hemorrhage
T1WI – provide anatomic definition, detect methemoglobin (hyperintense)
in subacute infarcts
FLAIR images augment T1 and T2 imaging by cancelling CSF signal to
produce a strongly T2 weighted image
Evaluates brain parenchyma immediately adjacent to the ventricular
surfaces and cortical sulci
Also improved conspicuity of lesions in brain stem as compared with spin
echo images

37. MRI IN HYPERACUTE INFARCTS
Identified more often and more accurately
on MR than CT
Within minutes – Absent normal “flow void”
Subtle changes on T1WI – sulcal effacement,
gyral edema , loss of gray-white interface
and cortical hypointensity

38. DIFFUSION WEIGHTED IMAGES
Ultrasensitive to hyperacute ischemic changes
Injured areas appear hyperintense on DWI – representing areas of restricted water
diffusion.
DWI changes are observed in less than 1hr after infarct – before T2 and FLAIR
changes
Improved image localization and detection of the age of the infarct
Pseudonormalization occurs between 4-10 days

40. Hyperintensity on T2W and FLAIR images
Meningeal enhancement adjacent to the infarct
Mass effect
MR Angiography demonstrates vascular occlusion / severe stenosis in major
vessel disease.
MRI in Acute infarcts
(12 – 24 hrs)

41. T2WI FLAIR

42. 1 – 3 days
Edema more obvious - hypointense on T1WI , hyperintense
on T2WI, contrast enhancement
Hemorrhagic transformation –bright on T1WI, dark rim on
T2WI
4 - 7 days
Striking parenchymal contrast enhancement
Mass effect and edema – decrease
MRI in Subacute infarcts

43. Subacute cortical MCA infarct
T1WI
T2WI
Post-contrast enhancement

44. Axial T1WI - partial hemorrhagic transformation

45. MRI IN CHRONIC INFARCTS
Contrast enhancement persists
Mass effect resolves
Decreased abnormal hyperintensity on T2W
Encephalomalacic changes , volume loss
Hemorrhagic residua – hemosiderin / ferritin

46. Chronic infarct
PCA territory
FLAIR
DWI

47. NONTRAUMATIC INTRAPARENCHYMAL
HEMORRHAGE
Most commonly due to hypertension. Other causes:
Amyloid angiopathy
Vascular malformation
Drugs – anticoagulants
Bleeding diathesis
Most commonly located in putamen / internal capsule >
thalamus > pons > cerebellum > subcortical white matter

48. APPEARANCE ON CT
Acute – hyperdense area with mass effect.
Sub acute – isodense with peripheral enhancement.
Chronic – hypodense unless rebleed occurs.

49. Acute parenchymal
hemorrhage – Hyperdense
Chronic parenchymal
hemorrhage – Hypodense

50. SUBARACHNOID HEMORRHAGE
Most common cause is ruptured intracranial
aneurysm
Appears as high attenuation within subarachnoid
cisterns & ventricles
Hemorrhage in interhemispheric fissure and blood
in frontal horn – ACOM aneurysms
Sylvian fissure blood – MCA aneurysms
Fourth ventricle hemorrhage – posterior fossa
aneurysms

51. HIGH DENSITY BLOOD IN THE INTERHEMISPHERIC AND SYLVIAN FISSURES.
POST-CONTRAST CT SCAN SHOWS AN ENHANCING ANEURYSM WITHIN THE
INTERHEMISPHERIC FISSURE

53. INFECTION
1. Meningitis
2. Abcesses
3. Granulomas
 Tuberculoma
 Neurocysticercosis

54. MENINGITIS
 Pathology:
 Purulent exudate in basilar cisterns and sulci
 Perivascular inflammation +/- vasospasm
 Imaging:
 Early : Imaging may be normal
 Effaced sulci with diffuse edema
 Enhancing meninges and exudates

57. ABSCESS
Pathology:
 Focal cerebritis, commonly d/t spread from an extracranial
site – hematogenous or direct
 Necrosis follows with coalescence
 Liquefaction, capsulation, surrounding edema
Imaging:
 Ring enhancing lesion of variable size with edema
 Meningitis, satellite abscesses m/b present

61. RING ENHANCING LESIONS
1. Abcesses
2. Granulomas
 Tuberculoma
 Neurocysticercosis
3. Tumors
4. Resolving hematomas and
infarcts
5. Active lesion of MS

62. TUBERCULOMA
 Pathology:
 Granulomas with central caseous necrosis
 Imaging:
 Ring enhancing lesion(s)
 Thick irregular nodular walls
 Edema
 Calcify on healing

65. NEUROCYSTICERCOSIS
 Pathology:
 Infection by ingestion of Taenia solium eggs
 Imaging:
 Thin regular walls with eccenteric nodule
 Ring enhancement
 Edema in degenerating stage
 Calcify on healing

70. DEMYELINATION
MULTIPLE SCLEROSIS
 Pathology:
 Auto-immune mechanism
 Imaging:
 Flame shaped plaques
 Most commonly at callososeptal interface
 Finger-like extension perpendicular to corpus
callosum & ventricular surface
 Variable enhancement – active stage

73. MASS LESIONS
EXTRA-AXIAL LESIONS:
 Broad based towards calvarium / falx / tentorium
 Displaced grey-white matter interface
 CSF and vascular cleft
 Enlarged ipsilateral CSF space –
CPA cistern or sulcus
 Mass effect on adjacent structures –
Brainstem and Fourth ventricle

74. CP Angle Schwanoma

75. CP Angle Schwanoma

76. Meningioma

77. MASS LESIONS
INTRA-AXIAL LESIONS:
 Epicentre within brain
 Infiltrate adjacent parenchyma
 No CSF and vascular cleft
 Greater degree of edema
 Mass effect +/- infiltration adjacent structures

78. Glioma

79. Pilocytic
Astrocytoma

80. Pilocytic
Astrocytoma

81. Intra-Ventricular Mass

82. …thank you!!!