1. Basics of Brain hemorrhage
Dr.R.Rengarajan

2. • Intracranial haemorrhage is a collective term
encompassing many different conditions
characterised by the extravascular accumulation of
blood within different intracranial spaces.

3. • Extra-axial hemorrhage
– extradural haemorrhage (EDH)
– subdural haemorrhage (SDH)
– subarachnoid haemorrhage (SAH)
• Intra-axial hemorrhage
– intracerebral haemorrhage - basal ganglia, lobar,
pontine and cerebellar
– intraventricular haemorrhage (IVH)

4. • CT scan is almost always the first imaging modality used to
assess patients with suspected intracranial haemorrhage.
• Acute blood is markedly hyperdense compared to brain
parenchyma.
• CT angiography is increasingly used to assess for a vascular
underlying cause, where location/appearance of bleed
make a primary haemorrhage less likely.
• CT venogram can be used to reliably assess for patency of
the dural venous sinuses.

5. • MRI is typically requested when an underlying abnormality
is being sought, particularly when an underlying tumour is
suspected.
• MRI of haemorrhage can pose some challenges in that the
appearance of blood changes depending on the sequence
and the time since the haemorrhage and the size and
location of the bleed.
• Cerebral angiography is usually performed when a vascular
abnormality is suspected and the CT angiogram is either
normal (and index of suspicion is high) or equivocal.

6. Extra-axial hemorrhage

7. Lining layers
• Dura is a thick tough membrane.
• The inner surface of dura is lined by a transparent
flimsy membrane called the arachnoid membrane.
• The third layer is the pia mater which tightly hugs the
brain going into every sulcus and gyrus on the brain
surface.

9. Spaces
• Extradural or epidural – between the skull and the dura
• Subdural – potential space between the dura and
arachnoid membrane
• Subarachnoid space – relatively large space which is
filled with CSF
• Blood clots within the pia mater are called as intraaxial

11. Characteristics

12. Characteristics
• Site
• Size
• Side
• Shifts
• Symptoms and signs

13. Site

14. Size

15. Side

16. Shifts

19. • The mass effect may produce compression of the
ventricles and shift of the 3rd ventricle and septum
pellucidum to the opposite side.
• Such displacement can produce severe brain or
vascular damage.
• These displacements are called herniations. Patients
with sufficient mass effect are at risk
for transtentorial and subfalcine brain herniation and
death.

20. TYPES OF BRAIN HERNIATION
Subfalcine herniation
The supratentorial brain, along with the lateral ventricle
and septum pellucidum, herniates beneath the falx and
shifts across the midline toward the opposite side.
Transtentorial herniation
Usually, the cerebral hemispheres are displaced
downward through the incisura beneath the tentorium
compressing the ipsilateral temporal horn and
causing dilatation of the contralateral temporal horn.

21. Foramen magnum/tonsillar herniation
Infratentorial brain is displaced downward through the
foramen magnum.
Sphenoid herniation
Supratentorial brain slides over the sphenoid bone either
anteriorly (in the case of the temporal lobe) or posteriorly
(for the frontal lobe).
Extracranial herniation
Displacement of brain through a defect in the cranium.

22. Epidural hemorrhage
• Epidural haematomas do not normally cross suture
lines as the dura insertion is tough thereby restricting
the enlarging clot to the confines of the sutures of
that particular bone.
• Hence they compress the brain and appear biconvex.

23. • Typically extradural hematomas are seen in young patients
who have sustained head trauma, usually with an
associated skull fracture.
• The source of bleeding is typically from a torn meningeal
artery, usually the middle meningeal artery.
• An associated skull fracture is present in about 80% of cases.

25. Subdural hemorrhage
• Subdural hematomas are crescent shaped in comparison to
extradural hematomas.
• Subdural haemorrhages are believed to be due to stretching
and tearing of bridging cortical veins as they cross the
subdural space to drain into an adjacent dural sinus.
• These veins rupture due of shearing forces when there is a
sudden change in the velocity of the head.

27. • They are usually more extensive than extradural hematomas.
• In contrast to extradural haemorrhage, SDH is not limited by
sutures, but are limited by dural reflections, such as the falx
cerebri, tentorium, and falx cerebelli.
• Overall 85% of subdural haematomas are unilateral.
• Common sites for subdural hematomas are fronto-parietal
convexities and the middle cranial fossa.

28. • Isolated inter-hemispheric/ parafalcine subdural
hematomas are seen more frequently in children,
and are common in cases of non-accidental trauma.
• In the vast majority of cases, CT scans are sufficient
to make the diagnosis and manage these patients.

29. • Hyper-acute
Relatively iso-dense to the adjacent cortex, with a swirled appearance
do to mixture of clot, serum and ongoing unclotted blood.
• Acute
Homogeneously hyperdense extra-axial collection that spreads
diffusely over the affected hemisphere.
• Subacute
Iso-dense to the adjacent cortex.
• Chronic
Hypodense and can be iso-dense to CSF, and mimic subdural
hygromas.
• Acute on chronic
Hypodense collection with a haematocrit level (located posteriorly).

31. Chronic subdural hematoma

32. Acute on chronic sub-dural haematoma

33. Acute on chronic SDH

34. Indirect signs of SDH
• CSF filled sulci do not reach the skull but rather fade
out into the subdural
• Mass effect including sulcal distortion and midline
shift
• Apparent thickening of the cortex

35. Huge isodense subdural haematoma causing gross
compression to the left hemisphere including
subfalcine herniation of the cingulate gyrus

36. Subarachnoid hemorrhage
• The distinction between SAH and intracerebral hemorrhage is
important because spontaneous subarachnoid haemorrhage is
most frequently caused by aneurysm rupture, which is fatal in one
third of cases.
• The majority of aneurysms occur around the circle of Willis, hence
aneurysmal subarachnoid haemorrhage tends to appear mainly in
the basal cisterns and sylvian fissure on CT scan.
• The main blood vessels in the brain travel in the subarachnoid
space, hence when an aneurysm ruptures, it bleeds into the
subarachnoid space where there is very little to tamponade the
bleed.

39. Usual locations
• The Interhemispheric Fissure
The interhemispheric fissure is the home of the anterior
communicating artery and anterior cerebral artery aneurysms, the
commonest site of aneurysms. Subarachnoid haemorrhage here is
characterized by interhemispheric blood or haematoma and not
infrequently it ruptures into the ventricle.
• The Sylvian Fissures
The sylvian fissures are home to middle cerebral artery aneurysms. It is
important to note that the sylvian fissures communicate freely with
the central sulcus and other sulci that run to the convexity of the
brain.

43. • The Ambient Cisterns
The ambient cisterns surround the midbrain and communicate with
the interpeduncular fossa where the circle of Willis is located.
Bleeding into this space could come from several places and is easily
recognized by the ‘loss’ of the dark CSF density around the
midbrain.
So that even if they (the ambient cisterns which are normally
hypodense) were to appear isodense with brain, then a focused
scrutiny is required to look for other evidence of SAH.

45. • Prepontine Cisterns
The prepontine cistern is a very important location to
scrutinize for SAH because basilar tip aneurysms make
their home here and hyperdense blood from SAH could
be easily obscured by the surrounding bone, which
forms the anterior boundary of this space.

48. Associated features
• Hydrocephalus
• Infarction
• Giant aneurysm
• Hematoma

49. Hydrocephalus
• Hydrocephalus (often transient) is a frequent
accompaniment of SAH.
• The brain CT scan may show only early hydrocephalus
characterized by dilatation of the temporal horns of the
lateral ventricles.
• This should be taken as a strong clue of recent SAH
because in the normal brain scan the temporal horns
are usually not visible or barely seen.

51. Infarction
• Low densities in the brain parenchyma associated with a
recent (≥3–10 days) history of SAH when present implies
established or imminent infarction or oedema of the brain.
• The hypodensities in SAH tend to cross vascular boundaries
and be more pronounced in the watershed areas.
• This complication which represents vasospasm with
ischemia usually occurs after the third day.

53. Giant aneurysms
• Giant or large aneurysms may be visible on brain CT scan.
• They exert a lot of mass effect and may precipitate
hydrocephalus.
• Aneurysms generally have a more smooth and rounded
outline compared to tumours and are often located in the
areas where aneurysms are usually found – the suprasellar
cistern and the sylvian fissures.
• In addition, SAH associated with tumours like gliomas,
meningioma or pituitary tumors for example, is a very rare
occurrence.

56. Hematoma
• Subarachnoid haemorrhage associated with intracerebral
haematoma also signifies large volume of haemorrhage and the
location is often in the temporal lobe (middle cerebral artery
aneurysm) or the frontal lobes – interhemispheric haematoma from
anterior communicating artery aneurysm.
• The typical appearance consists of subarachnoid haemorrhage in
the usual locations associated with a large hyperdense clot inside
the brain proper.
• The important differential diagnosis here is hypertensive
intracerebral haemorrhage, which can be distinguished from
aneurysmal haemorrhage with haematoma by the classic basal
ganglia location of the former as well as the lack of a significant
SAH.

58. SAH epilogue

59. Intra-axial hemorrhage

60. Intracerebral hematoma
• Intracerebral haematomas are clots located entirely within the
substance of the brain or the larger part of it is in the substance of
the brain
• But they may track into the ventricles or into the subdural space.
• Contusions are small intracerebral haemorrhages that often occur
in areas where the brain comes in contact with the very rough floor
of the skull like the floor of the frontal lobe and the temporal lobe.
• They also occur in deeper brain structures from shear injury and
larger contusions form intracerebral haematomas.

61. • The principal concern in intracerebral haematoma is the
mass effect and functional damage.
• Spontaneous intracerebral haematoma is often the result
of uncontrolled hypertension or amyloid angiopathy.
• The lenticulostriate vessels arise from the middle cerebral
artery bringing relatively high hydrostatic pressure from the
carotid to the internal capsule, basal ganglia and thalamus.
• These areas are therefore prone to hypertensive
haemorrhage and are the usual locations although a large
haemorrhage could rupture into the ventricles.

63. Basal ganglial haemorrhage
• A basal ganglial haemorrhage is a common form
of intracerebral haemorrhage.
• Usually as a result of poorly controlled long standing
hypertension, and the stigmata of chronic hypertensive
encephalopathy are often present.
• Other sites of hypertensive haemorrhages are the
pons, and the cerebellum.

67. Lobar haemorrhage
• Primary lobar haemorrhages (usually due to cerebral amyloid
angiopathy) are typically seen in elderly.
• Younger patients may also develop lobar haemorrhages, but in such
cases they usually have an underlying lesion (e.g. cerebral AVM).
• CT is usually the modality first obtained, and demonstrates
hypderdense collection of blood, located superficially within the
lobes of the brain
• Extension into the subdural or subarachnoid and even
intraventricular space (the later is far more common in basal ganglia
haemorrhages) may be seen.

69. Pontine haemorrhage
• Most commonly due to long standing poorly controlled chronic
hypertension.
• Primary pontine haemorrhages account for approximately 10% of
all intracranial haemorrhages.
• Typically patients are elderly with a long history of poorly controlled
hypertension.
• Pontine hemorrhages can also be due to vascular malformations,
tumours, downward herniation (duret haemorrhages) and
supratentorial surgery (remote haemorrhage).

70. Cerebellar haemorrhage
• Most frequently seen in the setting of poorly controlled
hypertension.
• Although the can of course also be secondary to an underlying
lesion (e.g. tumour or vascular malformation) or due to
supratentorial surgery .
• Larger bleeds can impair consciousness and obstruct
the fourth ventricle resulting in obstructive hydrocephalus.

72. Intraventricular haemorrhage
• Intraventricular haemorrhage (IVH) merely denotes the present of
blood within the ventricular system of the brain, and is responsible
for significant morbidity due to the development of obstructive
hydrocephalus in many of these patients.
Some of the more common causes of primary intraventricular
haemorrhage in adults include :
• intraventricular tumours
• vascular malformations
Secondary causes of intraventricular haemorrhage include:
• intracerebral haemorrhage hypertensive haemorrhage,
especially basal ganglia haemorrhage (common)
• subarachnoid haemorrhage

74. Role of MRI in bleeds

75. • Neuroradiological semeiology is based on the time elapsed since
the onset of the intraaxial bleeding.
• The temporal evolution of the MR characteristics of blood is caused
both by alterations of the erythrocytes as well as the haemoglobin
present under several differing conditions.
• Haemoglobin alterations are influenced by various factors,
including: pH, conditions of osmolarity, temperature, partial oxgen
pressure (pO2) and the metabolic microenvironment along with the
concentration of the oxidizable sublayers.

77. • In the hyperacute phase (in the first 12 hours from onset )
• Intraparenchymal haemorrhagic foci are composed of intact red
blood cells with high oxygen saturation and therefore containing
oxyhaemoglobin.
• The MR relaxation times are longer than those of the surrounding
tissue due to the local alteration in free water content and protein
concentration.
• isointensity on the T1-weighted images,
• minor hyperintensity on PD-weighted images, and
• isointensity on the T2-weighted images

79. • In the oxygen-dependent acute phase (12 hours - 2 days),
• The pO2 within the extravasated blood starts to drop fairly quickly,
and consequently there is a reduction in the haemoglobin’s oxygen
saturation, with the eventual formation of deoxyhaemoglobin.
• The presence of deoxyhaemoglobin in the haemorrhagic lesion
translates into
• relative hypo-isointensity on T1-weighted images,
• iso-hypointensity on PD-weighted images and
• rather marked hypointensity on T2- weighted images.

81. • The subacute, glucose-dependent phase (2- 14 days) is
characterized by two events that occur in parallel but
slightly out of phase with one another, partly sharing
the same pathogenic mechanisms:
– the formation of metahaemoglobin (methaemoglobin: 2-7
days) and
– erythrocyte lysis (7-14 days).

82. • Methaemoglobin causes a reduction in T1 relaxation due to
the dipole-dipole interaction between the external shell
electrons of the methaemoglobin and water protons.
• relative hyperintensity on T1-weighted images,
• hyperintensity on PD-weighted images and
• hypointensity on T2-weighted images.

83. • Once erythrocyte lysis has taken place, a loss of T2 relaxation
enhancement occurs, as methaemoglobin assumes a
homogeneous distribution, which translates into
hyperintensity of the MR signal on T2-weighted images.
• relative hyperintensity on T1- weighted images,
• hyperintensity on PD-dependent images and
• hyperintensity on T2- weighted images.

84. • The chronic phase of haematoma evolution is characterized by the
phagocytosis of erythrocyte lysis products by microphages around
periphery of the haemorrhagic collection.
• Within the macrophages heme iron accumulates primarily within
lysosome vacuoles in the form of haemosiderin.
• The presence of haemosiderin causes increased T2 relaxation and
therefore hypointensity on T2-weighted images within the
peripheral rim of the haemorrhagic lesion that persists indefinitely.
• In the meantime, methaemoglobin within the haemorrhagic
collection continues to cause MR signal hyperintensity on the T1-
and T2- weighted images.
• Subsequently, as months pass, methaemoglobin breaks down into
derivatives that do not have T1 relaxation effects.

89. • MRI can also sometimes provide information that
indicates the underlying cause of the bleeding.
• Apart from arterial hypertension, and excluding
trauma, intracerebral bleeding typically is caused by
vascular malformations or richly vascularized
intracerebral neoplasias.

90. Site
• Nucleo-capsular haemorrhages (between the
basal ganglia nuclei and the internal capsule:
50%) - capsulo-lenticular, capsulo-thalamic and
capsulocaudate.
• Lobar haemorrhages (35%)
• Infratentorial haemorrhages (10%)
• Intraventricular haemorrhages (5%)

91. Morphology and structure
• Intraaxial haematomas can be round or oval, with well-
defined margins, or alternatively irregular with dendritic
margins or even with completely irregular boundaries having
a somewhat map-like appearance.
• Haematoma morphology can be linked to either a vascular
malformation/ aneurysm or a spontaneous aetiology,
however, haematomas with irregular margins are more
commonly encountered in patients with blood dyscrasias.

92. Number
• Intraaxial blood collections tend to be single in number.
• The finding of multiple haemorrhagic foci, usually in a
superficial lobar position (excluding those of traumatic
origin), point in the direction of a diagnosis of a
– blood disorder (including iatrogenic anticoagulation),
– multiple haemorrhagic neoplastic metastases (including
melanoma) or
– dural venous sinus thrombosis with venous
infarcts/haemorrhages.

94. Thank you