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1. DR. SUNIL KUMAR SHARMA
SENIOR RESIDENT,DEPT. OF NEUROLOGY
G.M.C. & M.B.S. HOSPITAL, KOTA
2. INTRACEREBRAL HEMORRHAGE
(ICH)
Intracerebral hemorrhage (ICH) accounts for
approximately 10-15% of strokes. Its clinical
importance derives from its high frequency and 30-day
mortality, which is close to approx. 50%.
3. Mechanisms of Intracerebral
Hemorrhage
Hypertension
Vascular Malformations
Intracranial Tumors
Bleeding Disorders, Anticoagulants, and Fibrinolytic
Treatment.
4. Mechanisms of Intracerebral
Hemorrhage...
Cerebral Amyloid Angiopathy
Granulomatous Angiitis of the Central Nervous System
and Other Vasculitides
Sympathomimetic Agents
Hemorrhagic Infarction
Head Trauma
5. Imaging Modalities for ICH
Conventional-
CT scan
MRI
New imaging techniques-
Positron emission tomography (PET)
Single photon emission computed tomography
(SPECT)
MR perfusion, and CT perfusion. (These newer
techniques have demonstrated perihematomal regions of
hypoperfusion and bioenergetic compromise).
6. Imaging Modalities for ICH…
Near infrared spectroscopy- (can potentially identify
subdural and epidural hematomas in patients with
head trauma)
Diffusion tensor imaging, ( by utilizing its property
of visualizing white matter tracts.)
CT angiography
MR angiography
7. CT appearance in ICH
The CT scan has traditionally been used in the
diagnostic workup of ICH.
There is a linear relationship between CT attenuation
(hyperdensity) and hematocrit values,hemoglobin
conc.
Fresh intracerebral blood clot typically appear
hyperdense on CT independent of its location.
8. Stages of brain hemorrhage in CT
Hyperacute(0-24hr.):
hyperdense
Acute(1-2 days) : hyperdense
Sub acute(3 days - 28 days) :
isodense
Chronic(>month) : hypodense
9. Hyperacute and Acute ICH…
In hyperacute (<24 hours after onset) and acute
hemorrhage (24 to 48 hours), the patient’s hematocrit
largely determines the lesion’s degree of density on CT.
With a normal hematocrit, both retracted and
unretracted clots exhibit hyperdensity .
In cases of anemia, however, small hemorrhagic
lesions may potentially be overlooked .
The surrounding edema is seen as hypodensity.
11. Hyperacute and Acute ICH…
If the pt. has normal
coagulation but the blood is
accumulating very
rapidly,unretracted semiliquid
clot may be present.This result
in hypodense area within the
generally hyperdense acute
hematoma,the so called
“SWIRL sign”
12. Subacute ICH
The attenuation of
uncomplicated hematoma
decreases with time at an
avg. rate of 1.5 HU/day.
CT performed 7 days later
, the periphery of the
hematoma is now
isodense to the brain
while the center of the
hematoma has
hyperdensity.
13. Subacute ICH…
(C) CT performed 13 days later
,shows continued evolution of
the hematoma with decreasing
attenuation.
14. Subacute ICH…
The initially distinct border of the hematoma changes
within days to a few weeks after onset and becomes
irregular and “moth-eaten” due to the phagocytic
activity of macrophages.
Small hematomas may disappear on CT within 1 week
15. Chronic ICH
Unless rebleeding has
occurred chronic
hematomas are
hypodense compared
to adjacent brain.
Target sign in post
contrast CT scan can
be seen if rebleeding
occur within an
organizing hematoma.
16. Chronic ICH
(D) CT performed 5 months
later , shows a small area of
encephalomalacia in Rt.
Thalamus.
17. MR appearance of ICH
Hyperacute(0-24 hr.)
Acute(1-2 days)
Early Subacute(3-7 days)
Late subacute(1-4 weeks)
Early chronic(months)
Late chronic(months to years)
18. Hyperacute ICH (0 to 24 Hours)
In the early (hyperacute) phase of intraparenchymal
hemorrhage (<24 hours) the red blood cells are intact,
and a mixture of oxy- and deoxyhemoglobin is
present).
Signal on T1-weighted images is isointense to the
brain.
On T2-weighted images, the oxyhemoglobin
portion is hyperintense and deoxyhemoglobin is
hypointense.
19. Hyperacute ICH (0 to 24 Hours)…
On gradient echo images, hyperacute hemorrhage
will exhibit heterogeneously isointense to markedly
hypointense signal, the latter corresponding to
deoxyhemoglobin content in more peripheral portions
of the clot.
The amount of edema is mild in this stage.
21. Acute ICH (1-2 days)
During this stage, hemoglobin is transformed to
deoxyhemoglobin, but the membranes of the
erythrocytes are still intact .
The hematoma becomes slightly hypointense on T1
and strikingly hypointense on T2-weighted images.
Edema surrounding the clot is prominent at this stage
and is hypointense on T1 and hyperintense on T2
23. Early subacute(3-7 days)
As blood degradation evolves, deoxyhemoglobin is
converted to methemoglobin.
At this stage, the blood degradation products are still
intracellular.
Intracellular methemoglobin is hyperintense on T1 and
hypointense on T2-weighted images.
During this stage, the amount of edema starts to
decrease.
25. Late subacute(1-4 weeks)
In the late subacute phase, the membranes of the red
blood cells disintegrate, and methemoglobin becomes
extracellular.
Extracellular methemoglobin, contrary to intracellular
methemoglobin, causes hyperintense signal change on
both T1- and T2-weighted images.
The amount of edema around the hematoma
continues to decrease gradually.
27. Chronic ICH
In the chronic stage ,the core of larger hematomas
turns into a slitlike or linear cavity with CSF signal
characteristics, being hypointense on T1 and FLAIR
and hyperintense on T2-weighted images.
At the periphery of the lesion hemosiderin and ferritin
are deposited in their lysosomes, resulting in a rim of
hypointense signal on T2-weighted and GRE images.
30. I Bleed
T1 Isointense
T2 Bright
hyperacute < 24 hrs
I Die
T1 Isointense
T2 Dark
acute 1 to 3 days
Bleed Die
T1 Bright
T2 Dark
early subacute 2 to 7 days
Bleed Bleed
T1 Bright
T2 Bright
late subacute 7 -28 day
Die Die
T1 Dark
T2 Dark
chronic > 28 days
31. Hypertension
The main cause of ICH is
hypertension.
72%-81% of pt. have history
of hypertension.
Putamen is the commonest
site.
32. AVM
These lesions are often documented by MRI, by pathological
examination of specimens obtained at the time of surgical
drainage of ICHs, or at autopsy.
ICHs caused by small AVMs or cavernous angiomas are
frequently located in the subcortical white matter and in pons .
characteristic pattern on T2-weighted images, with a central
nidus of irregular bright signal intensity mixed with mottled
hypointensity (the “popcorn” pattern), surrounded by a
peripheral hypointense ring corresponding to hemosiderin
deposits
cerebral angiography also plays an important role in the
diagnosis of these lesions.
Smaller, and symptoms develop more slowly than with
hypertensive ICH.
34. Intracranial Tumors
Bleeding into an underlying brain tumor is relatively
rare in series of patients presenting with ICH,
accounting for less than 10% of the cases.
The tumor types most likely to lead ICH are-
Glioblastoma multiforme .
Metastases from melanoma,
Bronchogenic carcinoma,
Choriocarcinoma,
Renal cell carcinoma
35. imaging characteristics that should suggest an underlying brain tumor,
including:
(1) the presence of papilledema on presentation,
(2) the location of ICH in sites that are rarely affected in
hypertensive ICH, such as the corpus callosum, which
in turn is commonly involved in malignant gliomas,
(3) The presence of ICH in multiple sites simultaneously,
(4) A CT scan characterized by a ring of high-density
hemorrhage surrounding a low-density center in a
noncontrast study,
(5) Enhancing nodules adjacent to the hemorrhage on contrast
CT or MRI,
(6) A disproportionate amount of surrounding edema and mass
effect associated with the acute hematoma
36.
37. Bleeding Disorders, Anticoagulants, and
Fibrinolytic Treatment
Rare causes of ICH.
Generally younger than age 18.
Mortality is high, about 10% for subdural hematomas and 65% for ICH
Treatment with oral anticoagulants increases the risk of ICH by 8- to 11-
fold,(Account for 9% to 11% of ICH).
These hemorrhages tend to present with a slowly progressive course, at
times over periods as long as 48 to 72 hours, in contrast with the
usually more rapidly evolving presentation of hypertensive ICH
Volumes larger than those occurring in hypertensive ICH.
Recombinant tPA for the treatment of acute ischemic stroke was
complicated by ICH in 6.4% of cases and 11% in case of Intraarterial
thrombolysis by Prourokinase.
