Image acquisition protocols:
Routine head CT often requires additional spiral aquisitions in trauma,
or when angio-CT is employed (detection of cerebral aneurysms or vascular malformations).
- Recommended acquisition parameters for routine head CT on a Siemens Somatom 16: sequential (axial) scan: 120 kV,
effective mAs 400,
rotation time = 1s,
detector acqusition/collimation : 8x1,2,
slice thickness 4,8 mm (recon: 2,4 mm),
Kernel H31s.
- Spiral (helical) scan using fine detectors (16x0.6),
rotation time = 1s,
pitch = 0.85 slice thickness up to 1 mm for trauma/Angio-CT
The routine MRI protocol for the brain includes,
on a GE Signa 1.5 T machine:
- Axial T2,
Ax/Cor FLAIR,
Axial T1 SE,
3D T1 FSPGR,
DWI
- Selected cases benefit from SWI,
T2 gradient recalled echo sequences,
arterial and/or venous MRA (3D TOF/2D TOF),
and if necesary,
gadolinium administration.
CT appearance of bleeding (Fig. 6):
–Hyperacute: extravasated blood has a slightly heterogeneous appearance with specific densities between 45-60 HU (similar to normal cerebral parenchyme areas)
–Acute and early subacute: blood clot retraction with increased density of the accumulation (80 HU) surrounded by an area of edema
–Late subacute: hematoma is isodense to normal cerebral parenchyme areas
–Chronic: hypodense appearance as the hematoma is progressively resorbed,
and can associate atrophy of surrounding parenchyme and ventriculomegaly
MRI appearance of bleeding (Fig. 7) :
–Hyperacute: long T1 and T2 relaxation times: hypo-/ or isointense on T1-weigthed images and high signal intensity on T2-weighted images = protein containing fluid [6]
–Acute: preferential T2 proton relaxation enhancement shortens T2 but not T1: slightly hypo-/ or isointense on T1-weigthed images and low signal intensity on T2-weighted images (Fig. 8)
–Early subacute: proton-electron dipole-dipole interaction shortens T1 as well as T2; accentuated T2 relaxation (T2 proton relaxation enhancement) leading to high signal intensity on T1-weigthed images and low signal intensity on T2-weighted images (Fig. 9)
–Late subacute: loss of T2 proton relaxation enhancement; proton-electron dipole-dipole relaxation enhancement leading to a decrease of T1.
Remaining high signal intensity on T1-weigthed images .
T2 shortening leading to high signal on T2-weighted images = protein containing fluid (Fig. 10)
–Chronic: no dipole-dipole interaction occurs; hemosiderin is slightly hypointense on T1-weigthed images,
and very hypointense on T2-weighted images,
especially due to the inhomogenous distribution which leads to T2 proton relaxation enhancement. (Fig. 11)
Compartments of intracranial bleeding (Fig. 12) :
The location of the bleeding is important,
as it brings information relevent for the cause of the hemorrhage,
as follows:
A.
Intraaxial (=Intraparenchymal) hemorrhage occurs most frequently dur to hypertensive damage to blood vessel walls (hypertension,
eclampsia,
drug abuse),
altered hemostasis,
hemorrhagic transformation or other. (Fig. 2)
B.
Extraaxial:
- Subdural or epidural - Subdural hematomas occur between the skull and the outer endosteal layer of the dura mater,
involve meningeal or ethmoidal arteries or venous sinuses and have a typical biconvex lens appearance (Fig. 13). Epidural hematomas occur between the dura and the arachnoid,
involve bridging veins and have a typical crescent shape appearance (Fig. 14).
- Subarachnoid - occurs most commonly in head trauma; non-traumatic appears in the setting of a ruptured cerebral aneurysm or arteriovenous malformation (AVM) (Fig. 15).
- Intraventricular - is uncommon without parenchymal involvement; primary intraventricular hemorrhage has been noted in hypertension,
anterior comunicating artery aneurysm,
anticoagulation,
moyamoya disease and intraventricular neoplasia (Fig. 16).
What is important to report?
- Location and etiology of the hemorrhagic lesion
- Signes of gravity: mass effect,
hydrocephaly
- Prognostic-evolution in time