Brain Imaging(New)
Transcript of Brain Imaging(New)
《內容》
1. CT 和 MRI 上不同灰階所代表的東西2. 生理性鈣化和 CT density 表3. MRI intensity 表4. MRI 基本原理5. Diffusion-weighted image and ADC
6. 各種病灶在 DWI 和 ADC 的表現7. ADC 數值對照表8. Image change in stroke
9. MRS
10.Angiography(carotid artery)
11. Angiography(vertebral artery)
12.Venography
13.Functional Neuroimage
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《Brain Imaging》CT上不同密度所代表的東西
○ 極白,產生假影:金屬。○ 極白:骨頭和鈣化。○ 白色:新鮮凝固血塊。○ 灰白色:纖維組織(韌帶,椎間盤)。○ 灰色:軟組織(如肌肉、腦、肝、腎和大血管)。○ 灰暗色:軟組織水腫、腦組織軟化、膠質化及去髓鞘化。○ 暗:較濃的液體(膿,液化的血腫)和體液(如 CSF、尿液、腹水和膽汁等)。○ 很暗:脂肪。○ 極暗:空氣。
MRI上不同訊號強度所代表的東西
○ 白色:T1WI脂肪,亞急性期的血塊(含 Methemoglobin),骨髓。PDWI亞急性期的血塊(含 Methemoglobin)
T2WICSF,腦水腫,腦組織膠質化及去髓鞘,腦組織壞死(水化),囊腫(含 CSF、水或較多蛋白質),亞急性期的血塊(含 Methemoglobin)
○ 灰白色:PDWI脂肪,腦水腫,腦組織膠質化及去髓鞘,囊腫(含較多蛋白質)和骨髓。○ 灰色:T1WI白質,急性期血塊(含 Deoxyhemoglobin),肌肉。
PDWI灰質,急性期血塊(含 Deoxyhemoglobin),肌肉。T2WI灰質
○ 灰暗色:T1WI灰質,腦水腫,腦組織膠質化及去髓鞘,囊腫(含較多蛋白質)
PDWI白質,腦組織壞死(水化)
T2WI白質,脂肪,骨髓,肌肉
○ 暗色:T1WICSF,腦組織壞死(水化),囊腫(含 CSF 或水),慢性期血塊(含 Hemosiderin),骨皮質。
PDWICSF,囊腫(含 CSF 或水),慢性期血塊,骨皮質。T2WI急性期血塊,慢性期血塊,骨皮質。
○ 暗色(低訊號):T2WI鐵的沈積※生理性鐵的沈積:
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◇ 兒童,測不出◇ 20歲以上成年人:globus pallidus,red nucleus,substantia nigra,dentate nucleus
◇ 70歲以上老年人:putamen, caudate nucleus。
○ 暗色(空訊號):血流。( 血流並非在所有 pulse sequence 皆呈現 signal void 之空訊號 )
○ 沒有訊號或稍暗:鈣化。
Physiological intracranial calcification
Brain parenchyma
Globus pallidus,dentate nucleus,putamen,caudate nucleus,thalamus,大小腦的皮質,皮質下
Others
Pineal gland (60% of adults),Habenular commissure (30%),Petroclinoid (12%) and interclinoid ligaments
Choroid plexus (10%),Falx cerebri (7%) and superior sagittal sinus
Dura mater,Tentorium,Dural plaques (frequently parasagittal),Diaphragm sellae
Pituitary gland (rare)[2]
Carotid arteries (in elderly)
CT number scale(Hounsfield scale; gray scale)
CT number(HU, Hounsfield
unit)
Ordinary window 下之顏色
金屬 大於 3000 極白,產生假影
骨質 600~1000 極白
鈣化 100~300(或更高) 極白
新鮮凝固血塊 60~90 白色
纖維組織(韌帶,椎間盤) 50~70 灰白色
軟組織構造(肌肉、腦、肝、腎臟、大動脈、大靜脈)
35~45 灰色
軟組織水腫(soft tissue edema) 20~30 灰暗色
腦組織軟化(encephalomalacia),膠質化(gliosis),去髓鞘化(demyelination)
10~15 灰暗色
較濃的液體(膿,液化的血液) 10~16 暗
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體液(CSF、尿液、腹水、膽汁) 4~6 暗
水 0 暗
脂肪 -20~-120 很暗
空氣 -1000 極暗
In cases of hyperacute stroke (0-6 h), CT is usually not sensitive in the identification of cerebral infarction.[1] But, it is
quite sensitive in identifying various forms of acute intracranial hemorrhage and other gross lesions that would
preclude the use of thrombolytic therapy. In the first 24 hours, CT signs of infarction are sulcal effacement with loss
of gray-white differentiation in superficial cortical infarction[3] and hypodensity of the basal ganglia
● Acute hematoma:hyperdense,subacute hematoma:isodense,chronic hematoma:hypodense
MRI intensity
T1WI PDWI or FLAIR T2WI
灰質 灰暗 灰 灰白質 灰 灰暗 灰暗CSF 暗 暗 白脂肪,神經 白 灰白 灰暗腦水腫(edema) 灰暗 灰白 白腦組織 gliosis, demyelination 灰暗 灰白 白
腦組織壞死(水化) 暗 灰暗 白囊腫(cyst)
含 CSF、水含較多 protein
暗灰暗
暗灰白
白白
血塊急性期(含 deoxyhemoglobin)
亞急性期(含 methemoglobin)
慢性期(含 hemosiderin)
灰白暗
灰白暗
暗白暗
鈣化 沒有訊號或稍暗 沒有訊號或稍暗 沒有訊號或稍暗鐵的沈積 - - 暗(低訊號)
血流 空訊號(暗) 空訊號(暗) 空訊號(暗)
頭蓋骨骨皮質骨髓
肌肉
暗白灰
暗灰白灰
暗灰暗灰暗
Ischemia(demyelination, pallor, gliosis) Normal Hyperintense Hyperintense
Lacunar infarction Hypointense Hyperintense * Hyperintense
Etat crible(dilated Virchow Robin space) Hypointense Normal (?) Hyperintense
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FLAIR (fluid-attenuated inversion recovery),PDWI(proton density weighted image)
*FLAIR images須視 stage而定。例如剛發生 infarction時,會呈現白色;經過一段時間組織壞死液化後,水的訊號會被壓制而呈現與水相同的黑色(暗)。
(MRI基本原理)
◎本院 MRI 儀器對於使用之 pulse sequences 之不同名稱:Category
Vendor
Regular Imaging Fast Imaging
GE (3.0T) Spin Echo (SE) Gradient Echo (GRE) Fast Spin Echo (FSE) Fast Gradient Echo (FGRE)
Philips (1.5T) Spin Echo (SE) Field Echo (FE) Turbo Spin Echo (TSE) Fast Field Echo(FFE)
《原理》● MR describes the phenomenon whereby the nuclei of certain atoms, when placed in a magnetic field,
absorb and emit energy of a specific frequency. The spectrum of absorbed or emitted energy depends
upon the nucleus under observation and its chemical environment.
● Nuclei suitable for MRI are those which have an odd number of protons or neutrons and therefore
possess a net charge and have angular momentum.
● 大部份是利用 hydrogen nucleus (or proton),其他可利用的包括 phosphorus (31 P), sodium (23
Na), carbon (13 C), potassium (39 K), exogenous noble gases such as helium (3 He) and xenon (129 Xe)等。《Image parameters》● ρ(proton density):
◇ CSF, urine and other fluids>liver>kidney and spleen>grey matter>white matter>articular
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(A)PDI (B)T2WI (C)FLAIR (D)T1WI
cartilage>fibrocartilage>membranes>cortical bone and air.
◇ Only mobile protons which give an MR signal with conventional techniques. When the protons
are in large molecules or immobilized in solids, they give no detectable signal with most MRI
techniques. Thus cortical bone contains protons, but these do not give a detectable signal.
◇ Proton density increased:oedema, infection, inflammation, acute demyelination, acute
haemorrhage, some tumours, cysts and other conditions.
◇ Proton density decreased:scar formation, fibrosis, some tumours, capsule and membrane
formation as well as with calcification.
● T1(longitudinal relaxation time) & T2(transverse relaxation time):◇ The first of these relaxation times, T1, or the longitudinal relaxation time, represents the time
taken by the system of nuclei to return to thermal equilibrium after the RF pulse.
◇ The second or transverse relaxation time, T2, indicates the characteristic decay time of the FID
(free induction decay) and is due to the irreversible dephasing of the initially coherent precession
of nuclei which follows the RF pulse.
◇ A local change in magnetic field homogeneity, e.g. due to local iron or deoxy-hemoglobin
content, causes a reduction in T2 which is called T2*.
◇ Thus liquids have a very long T1 and T2, soft tissues have shorter values of T1 and T2 and solids
have very long T1s and very short T2s. (肝臟含水量不少,但是因為有 organic iron,所以其T1&T2 下降)
◇ In liquids or systems containing mobile protons, T2/T1 is approximately unity, whereas in solids,
T2/T1 is very small.
◇ 使用 Gd-DTPA(對比劑)會使組織的 T1 和 T2 減少,對 T1 影響的幅度較大。● χ(susceptibility)
◇ 依組織影響 static magnetic field 的方式可分成三類: Diamagnetic materials produce a slight reduction in the field
Paramagnetic materials produce a slight increase
Ferromagnetic materials produce a large and persistent increase
◇ Susceptibility effects may also be seen at air–tissue interfaces as a result of differences in
susceptibility between air and tissue. On transverse images of the brain this can result in artefacts
in the temporal lobes above the mastoid sinuses
《Pulse sequence》● The principal pulse sequences are:
◇ Partial saturation (PS) (also known as gradient echo or field echo)
which typically utilizes a 90° RF pulse but can use a greater or smaller
pulse(角度可以改變) Reducing the flip angle reduces the T1 dependence of the PS sequence. This may be used
in situations in which low T1 dependence and high T2 dependence is being sought such as
with rapid T2-dependent sequences. Typical values of α for low T1 dependence are in the
range of 10–30°
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◇ Spin echo (SE) which utilizes a 90° pulse followed at time TE/2 by a 180°
pulse (where TE is the echo time). At a further time TE/2 an echo of the
original signal is detected.
the spin echo is a two-step process. The first step (longitudinal recovery) determines the
starting intensity for the second step (transverse decay)
TR short時較可以表現出組織 T1的差異性(因為時間長時,組織都 return to thermal
equilibrium,就感覺不出其差異性),TE長時較可以表現出組織 T2的差異性 T1-weighted spin echo sequence:short TR, short TE
T2-weighted spin echo sequence:long TR, long TE
Proton-density-weighted image:long TR, short TE (和組織 T1 和 T2 較無關)
The spin-echo MR signal is greatest when the T1 is short and the T2 and proton
density are high; it is decreased if the T1 is long and the T2 and proton density are
small.
◇ Inversion recovery (IR) which utilizes a 180° pulse followed at time TI (the
inversion time) later by a 90° pulse. Variations in the timing of the RF pulses
in these pulse sequences can produce marked differences in image contrast.
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Mz:longitudinal magnetization,Mxy:transverse magnetization,DC:data collection
T1-weighted spin echo sequence(short TR, short TE)
T2-weighted spin echo sequence(long TR, long TE)
If TI is decreased to 100–150 ms, it is possible to null the signal from fat with the short TI
IR STIR sequence. It is also possible to increase TI in order to null the signal for fluids
(the Fluid Attenuated Inversion Recovery or FLAIR sequence).
● TE(Echo time):Time between center of RF excitation pulse and the center of spin echo formation
(readout period).
● TR(Repetition time):Time between successive excitation of spins. For a gradient echo, it is the
time between successive alpha pulses; for a spin echo it is the time between successive 90° RF pulses.
● Fast pulse sequences:◇ Fast low-angle shot or FLASH sequence:使用 PS,但縮短 TR,而使用小於 90°的 RF 保留
訊號強度◇ Echo-planar imaging (EPI):a train of gradient echoes is obtained after a single 90° RF
excitation,目前最快的成像法,可應用在 fMRI,DWI,PWI,FLAIR 等。(Diffusion-weighted MRI and ADC(apparent diffusion coefficient))
1. 方法:This is achieved by applying a pair of diffusion sensitizing gradients symmetrically around a 180° refocusing RF pulse of a T2-weighted MR sequence.
Mobile molecules acquire phase shifts, which prevent their complete rephasing
and result in signal loss.(因為含 T2 components,所以有些 T2 hyperintense 的lesions 在 DWI 也會 hyperintense,但是 ADC 並不會 hypointense,稱為 T2 shine-
through)
2. Diffusion tension imaging (DTI):new technique(diffusion imaging is done in three(x-y-z)
orthogonal planes and mean diffusion is calculated for each pixel),因為原本是假定 diffusion 在各方向都相同,但是在 in vivo 時卻不是,需要作校正才比較準確。
3. Acute ischemic lesions:cytotoxic oedema , high signal on DWI (‘light bulb sign’) and low signal on ADC
4. Chronic ischemic lesions:low signal on DWI and high signal on ADC
5. Diffusion MRI and ADC 提供大腦組織完整性的資訊,水分子的 diffusion 愈好,ADC 的值愈高。ADC value differences in four conditions(range and mean) x 10-3 mm2/s
Acute infarct(cytotoxic edema) 0.14-0.50(0.32±0.09) low signal
Normal cerebral white matter 0.60-1.05(0.84±0.11) normal signal
Vasogenic edema 1.28-2.20(1.68±0.27) higher signal
CSF 2.40-4.40(3.40±0.45) high signal
6. DWI 對在 6個小時內發生的 early ischemia 和 infarct 的偵測是高度 sensitive 和 specific.
7. Time course of the apparent diffusion coefficient in experimental stroke. 在 cat and rodent
MCAO models 中,動脈阻塞後 2.5 分鐘內會出現 diffusion abnormalities,會表現出 DWI signal
hyperintensity 和↓ADC. ADC↓在 T2 有變化(表示 tissue water content 開始增加)前至少 2~3 小時
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G:grey matter,W:white matter
就會出現. 在接下來 24 小時,ADC 會進一步下降而 DWI 會繼續增加 intensity. 而在 24~28小時的時候,ADC會下降至最低點,約正常值的 50~60%. This is the same level reached after 20
minutes of cardiac arrest and may be the maximum extent to which reduction of the extracellular
volume can occur (50%). A restricted ADC has always preceded the development of infarction.
8. Time course of the ADC in human stroke. 在人類 ischemic stroke, ADC的下降最早在發生後105 minutes出現.. 在接下來48小時 lesions會變得更hyperintense,而ADC會進一步下降. ADC值的下降總是在 infarction發生前出現. The ADC has been found to have a two-phased time course with an
initial decrease that is followed by a return to normal in the subacute to
chronic phases termed pseudonormalization because the tissue is
infarcted. In the chronic phase the ADC subsequently became high due
to increased water diffusion in the residual stroke cavity. The period
during which the ADC remains restricted has varied between
laboratories. In some the ADC had normalized by 48 hours while in
others the ADC pseudonormalized between 4 and 10 days.
Stage T2WI DWI ADC
Hyperacute(0-6
hours)
Normal Increased Decreased
Acute(6-96 hours) Normal to
increased
Increased Decreased
Subacute(4-
10days)
Increased Normal to
increased
Decreased/normal
Chronic Increased Decreased to
increased
Increased
9. Abscess:high signal on DWI and low signal on ADC
10.Tumors with central necrosis (both primary and metastatic):low signal on DWI and high
signal on ADC(DWI 可用來 DD ring-enhancing lesion)
11.Abscess 的 ADC 值為 0.21 to 0.34 310-3 mm2/s
An infarct 8 to 24 hours old:0.61 ± 0.14 x 10-3mm2/s
An infarct 1 to 8 days old:0.51 ± 0.18 x 10-3mm2/s
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(MR perfusion imaging)1. 方法:During the first pass of an intravenously injected gadolinium-based
contrast agent, the contrast medium causes a transient signal drop on T2*-
weighted (susceptibility-weighted) MRI. MR perfusion imaging is, however, at
present only semiquantitative and cannot provide absolute values[8] . In the
absence of absolute quantification of the CBF, comparison with the contralateral
hemisphere provides the easiest way to analyse MR perfusion images. This
becomes, however, problematic if the perfusion of the contralateral hemisphere
is not normal, as in the presence of bilateral carotid artery disease.2. PWI may show hypoperfusion in a much larger area of tissue than shown by the DWI. This indicates a much
larger area of tissue is at risk for infarction, a "diffusion-perfusion mismatch", indicating a threatened portion
of the brain that is still salvageable
Relative cerebral blood volume (rCBV), mean transit time (rMTT), and relative cerebral blood flow (rCBF)
DW MR Imaging Characteristics of Various Disease Entities
Disease
MR Signal Intensity
ADC CauseDW
Image
ADC
Image
Acute Stroke High Low Restricted Cytotoxic edema
Chronic Stroke Variable High Elevated Gliosis
Hypertensive encephalopathy Variable High Elevated Vasogenic edema
Cyclosporin toxicity Variable High Elevated Vasogenic edema
Hyperperfusion after carotid
endarterectomy
Variable High Elevated Vasogenic edema
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HIV encephalopathy Variable High Elevated Vasogenic edema
Intraaxial mass
Nectrotic center
Solid tumor
Variable High Elevated Increased free water
Variable Variable Variable Depends on cellularity
Arachnoid cyst Low High Elevated Free water
Epidermoid mass High Low* Restricted* Celluar tumor
Pyogenic infection High Low Restricted Viscosity
Herpes encephalitis High Low Restricted Cytotoxic edema
Creutzfeldt-Jakob syndrome High Low Restricted Unknown
Diffuse axonal injury
Majority of cases
Minority of cases
High Low Restricted Cytotoxic edema
Variable High Elevated Vasogenic edema
Hemorrhage
Oxyhemoglobin(<1d)
Deoxyhemoglobin(1~3d)
Intracelluar methemoglobin(3~7d)
Extracelluar methemoglobin(7~14d)
Hemosiderin(>21d)
High Low Restricted Intracelluar
Low Unknown+ Unknown+ Unknown+
Low Unknown+ Unknown+ Unknown+
High High Elevated Extracellular
Low Unknown+ Unknown+ Unknown+
Multiple sclerosis
Most acute lesions
A few acute lesions
Chronic lesions
Variable High Elevated Vasogenic edema
High Low Restricted Unknown
Variable High Elevated Gliosis, neuronal loss
* Relative to that cerebrospinal fluid(CSF)+The ADC usually cannot be calculated
ADC values(x10-3mm2/s) in the normal brain
ROI ADC value(x10-3mm2/s)
Infants
Unmyelinated white matter 1.64±0.17
Myelinated white matter 0.90±0.12
Paracentral cortices 0.83±0.14
Basal ganglia, thalami 0.98±0.11
Brainstem 1.00±0.10
Cerebellar parenchyma 0.97±0.13
Children and adults
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White matter 0.84±0.11
Corpus callosum 0.75±0.15
Cortex 0.75±0.16
Thalamus 0.83±0.14
Caudate nucleus,putamen 0.82±0.13
Globus pallidus 0.74±0.19
Midbrain 0.76±0.18
Pons 0.84±0.15
Cerebellar parenchyma 0.83±0.17
Hypomyelinated posterior periventricular regions 1.25±0.14
Classification of brain disorders according to ADC values(x 10-3 mm2/s)
Categories Ranges
1.ADC similar to white matter 0.60-1.05
Atrophy
Lipoma
Dermoid
Neuronal migrational disorders
Glutaqric aciduria type I
Nonketotic hyperglycinemia
Pontine myelinolysis due to gluten enteropathy
Calcified giant cell tumor of tuberous sclerosis
Some metastatic tumors with hemorrhage
2.ADC lower than normal white matter Less than 0.60
Ischemia and acute infarct(cytotoxic edema)
Subacute hemorrhage(extracellular methemoglobin)
Venous thrombosis(in superior sagittal sinus)
Metachromatic leukodystrophy(deep white matter)
Epidermoid
Ischemic portions of tumors
Ischemia associated with herpes encephalitis
Normal iron deposition(globus pallidus, red nucleus, substantia nigra)
Localized areas in corpus callosum, and subcortical white matter
3.ADC higher than normal white matter More than 1.05, less than CSF
Vasogenic edema
Enlarged Virchow-Robin spaces
White matter hyperintensities(leukoariasis)
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Transependymal resorption of water
Matrix of tumors
Radiation necrosis
Periventricular leukomalacia
Microcystic encephalomalacia
Hamartomas in tuberous sclerosis and NFI
Rasmussen encephalitis
Herpes infection without ischemia
Multiple sclerosis
Acute disseminated encephalomyelitis
Leigh’s disease
Alexander’s disease
Mucopolysaccharidosis
Metachromatic leukodystrophy(peripheral white matter)
Xanthogranuloma of the choroids plexus
4.ADC similar to CSF 2.40-4.40
Arachnoid cyst
Hydatid cyst
Cystic tumor
Tumor necrosis
Macrocystic encephalomalacia
5.Markedly low or high ADC 0, and 5-10
Low( ADC=0)
Calcification
Hemosiderin
Lipoma(due to a misregistration on ADC maps, actually in category 1)
Large veins(superior sagittal sinus) with normal flow
Air
High(ADC=5.00-1.00 x10-3 mm2/s)
Cystic tumors
Tumor necrosis
Macrocystic encephalomalacia
Enlarged ventricles(5.00x10-3 mm2/s)
Very bright artifacts related with motion, and ADC map creation(10.00x10-3 mm2/s)
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<IMAGE CHANGE IN STROKE>
Acute Infarct
<CT>
1. In cases of hyperacute stroke (0-6 h), CT is usually not sensitive in the identification of cerebral infarction.[1] But,
it is quite sensitive in identifying various forms of acute intracranial hemorrhage and other gross lesions that
would preclude the use of thrombolytic therapy.
2. In the first 24 hours, CT signs of infarction are sulcal effacement with loss of gray-white differentiation in
superficial cortical infarction[3] and hypodensity of the basal ganglia.
3. A clot in a large cerebral vessel appropriate to clinical symptoms may be seen in 20–50% of ischemic acute
stroke patients. When observed in the middle cerebral artery, the so-called ‘hyperdense middle cerebral
artery sign’documents the cause of the ischemic event and suggests the most likely stroke etiology [13].
4. The other hyperacute CT changes, early parenchymal changes, reflect likely severe ischemic injury in
various portions of the ischemic territory. These early parenchymal changes on CT include attenuation of the
lentiform nuclei, loss of the insular ribbon, hemispheric sulcal effacement and hemispheric hypodensity.
<MRI>
1. Hyperintensity of the ischemic brain in acute strokes is seen on FLAIR as early as 4 to 6 hours after ictus at a
time when T1-weighted images (T1WI) and T2-weighted images (T2WI) are usually normal
2. FLAIR may detect slow flow in the arterial bed in the hyperacute phase of stroke. These slow-flowing arteries
are depicted by FLAIR as hyperintensities against darker brain tissue, leading to the "hyperintense vessels
sign" (HVS). HVS is a reversible sign most commonly associated with hypoperfusion without infarction
3. At this time point (6-24 h), tissue ischemia/infarction is well developed on FLAIR images and begins to show on
T2WI (hyperintensity) and T1WI (hypointensity).
4. Hyperintensity develops on T2WI as early as 8 hours after infarction due to cytotoxic and vasogenic edema.
5. Hypointensity on noncontrast T1WI is usually seen 16 to 24 hours after ictus and, again, is related to both
cytotoxic and vasogenic edema. The intravascular enhancement sign peaks at this stage due to sluggish
intravascular flow. This is the counterpart of HVS but is not specific for stroke
<Thrombolysis 的選擇>
1. DWI/PWI mismatch(PWI>DWI):表示非 completed stroke,mismatch 的部份稱為 penumbra
2. Infarction <1/3 of arterial territory:太大出血機率較高3. 可考慮做 CTA 看 thrombus 的位置,也可以考慮用 Xenon CT(可看 cerebral blood
flow),SPECT,PET,MRS(acute infarct 時 lactate 會增加,而 NAA 會減少,mismatch between elevated
lactate and reduced NAA 表示 ischemic penumbra 的區域),and MRA,Diffusion tensor imaging 來看penumbra 的區域,和分辨 stroke 的原因。
Subacute Infarct
1. After the first 24 hours, T1W1, T2W1, FLAIR, and contrast-enhanced images are most useful in subacute and
chronic stroke, where the focus shifts from identifying the presence and extent of infarct and ischemic
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penumbra to identifying the underlying pathophysiology.
2. As the infarct evolves during the first week, the edema and mass effect increases, and both the morphologic
and signal changes seen in the magnetic resonance sequences become more prominent and well demarcated.
Infarctions continue to appear as areas of hypointensity on T1WI and hyperintensity on T2WI.
3. Edema is generally maximal at 48 to 72 hours beyond ictus, although there is considerable variability. In
general, mass effect is best appreciated on T1WI. The intravascular enhancement sign may persist well into
the subacute stage but is typically absent after 1 week.
4. Gyriform parenchymal enhancement, similar to the enhancement seen in postcontrast CT scans, is typically
seen approximately 5 to 7 days beyond stroke onset and remains for a few weeks in cases of complete
infarction.
5. As reperfusion of infarcted tissue occurs, both petechial hemorrhage and frank hematomas may be seen,
especially at 24 to 48 hours after stroke onse. Petechial hemorrhage within infarctions may give rise to a
"fogging" phenomenon in which hemoglobin degradation products, extravasated proteins, or both generate
signal changes within infarcted tissue, which mask the infarction on T1WI and T2WI.
Chronic Infarct
1. By the chronic stage, edema has resolved and volume loss occurs in the area of infarction, beginning 1 month
postictus.
2. Tissue loss leads to ipsilateral ex vacuo ventricular enlargement and widening of cortical gyri and fissures in
the area of the infarct. Parenchymal signal in the area of chronic infarction continues to show CSF-like
hypointensity on T1WI and hyperintensity on T2WI. The core of the chronic infarction is also CSF-like on FLAIR
images, but surrounding gliosis appears hyperintense.
3. After several months, Wallerian degeneration occurs.
4. After several years, dystrophic calcification may appear bright on T1WI
14
ICH(intracerebral hematoma)
時間 CT形狀 MRI形狀T1WI T2WI
Hyperacute(<4hr) liquid liquid
Acute stage(4hr~8天)
Subacute stage
(吸收期)(8~20天)
完全吸收期(20~60天)
後遺症期(2個月至數年)
● MRI
T1WI T2WI
Deoxyhemoglobin(hours
to days)
Intermediate to dark Dark
Intracelluar Intermediate to bright Dark
15
血塊
血塊
Perifocal edema Deoxyhemoglobin4hr~3天 3~8天
Perifocal edema已吸收血塊
殘存血塊
Hemosiderin Edema
已吸收血塊殘存血塊
Methemoglobin
Methemoglobin Hemosiderin
Cavity Split
Hemosiderin
Cavity
Split
5~15天
15~50天
4hr~5天Edema
methemoglobin
Methemoglobin(extracellu
lar*)
Bright Bright
Hemosiderin Intermediate to dark Dark
*After red cell lysis
(Magnetic resonance spectroscopy(MRS))※Proton spectroscopy(一般會將water 和 fat[extracerebral]的訊號抑制):可半定量的測量大腦的許多成分 0.90 p.p.m:pyruvate and a complex peak, indicating
amino acids valine, leucine, and isoleucine
不會出現在 necrotic/cystic tumor,而所有 abscess
都會出現,來自 proteolytic activity of
polymorphonucleocytes
1.33 p.p.m:Lac(lactate),依條件的不同,peak 可能向上也可能向下(inverted doublet)
代表 anaerobic metabolism
1.50 p.p.m:alanine
1.92 p.p.m:acetate
metabolic end products arising from microorganisms
,不會出現在 necrotic tumor
2.01 p.p.m:NAA(N-acetylaspartate)
Neuronal marker(主要在 neurons 的 axons 和 nerve processes 出現)
在 neuronal loss or damage, e.g., degenerative disorders,stroke 和 multiple sclerosis 時會降低。.
2.40 p.p.m:succinate
metabolic end products arising from microorganisms,不會出現在 necrotic tumor
3.03 p.p.m:Cr/PCr (creatine peak)
phosphocreatine- and creatine-containing substances in the cell
一般是穩定不變的,可充當 standard
3.22 p.p.m:Cho (choline)
cholinecontaining substances in the cell membrane
16
在 demyelinating lesions 或 tumor 時會增加 3.6 p.p.m:Ins(myo-inositol)
4.7 p.p.m:residual water proton (H2O).
※ Phosphorus spectroscopy(可用來測量參與能量代謝的分子,如 ATP,ADP,以及 neuronal
membranes 的成分,像是 phosphomonoesters(PMEs)和 phosphodiesters(PDEs)
※ Lithium MRS:可測量 brain lithium levels
※ Fluorine MRS:可測量 fluorinated compounds(如 fluoxetine)
Stroke
Cerebral edema associated with tumors and ischemic stroke
Increased Lac/Cr
Decreased NAA/Cr
Abscess
Decreased choline and Cr
Increased succinate or acetate
Increased lactate
出現 0.90 p.p.m:pyruvate and
a complex peak
Tumor
Decreased NAA and Cr
Increased choline
Decreased Cr/Cho, NAA/Cho ratio
17
Normal brain MRS
Ins (3.60 ppm) Glc (3.43 ppm) Cho (3.2 ppm) Cr (3 ppm) Glu (2.35 ppm) GABA (2.25 Gln (2.15 ppm) NAA (2.02 ppm) Lac (1.3 ppm)
1H MRS 31P MRS
Meningioma:會有 Ala(Alanine) peak
GBM:會有 LA(lactate)和 Lipid peakMultiple sclerosis
Low NAA in plaques of MS and in normal-appearing white matter
Early plaque:Large increases in the Cho,Moderate increases in LA
Hyperacute phase:a transient decrease in Cr
Lipids 和 myoinositol 會增加 Subacute and chronic plaques:normal Cr signal
Epilepsy
Acidosis
Decreased CrP,CrP/Pi
Elevated Pi,lactate Constant ATP
Reduced NAA
Increased FFA(free fatty acid)
Dementia
Neuronal(NAA),glial(myo-inositol)
markers,energies(PME(phosphomonoester) and
PDE(phosphodiester)),osmolytes, neurotransmitter(glutamate,GABA) Increased myo-inositol/Cr
Decreased NAA/Cr
18
(Angiography)19
《 Carotid artery 》
20
CM(Callosomarginal a.)
Peric(Pericallosal a.)
FP(Frontopolar a.)
A.Ch.(Anterior choroidal a.)
Sy.P(Sylvian point)
L.S.(Lenticulostriate a.)
M1,M2,M3 segments of middle cerebral a.
ICA(Internal carotid a.)
C.Siph(Carotid siphon)
A.Com(Anterior communicating a.)
A1,A2,A3 segments of anterior cerebral a.
FP(Frontopolar a.)
ICA(Internal carotid a.)
Oph(Ophthalmic a.)
PC(posterior cerebral a.)
P.com(posterior communicating a.)
C.Siph(Carotid siphon)
21
Table 37C-2. Segments of the internal carotid artery and associated branchesFischer segment
Boundary Branches and vascular territory
C5 "gasserian segment"
Endocranial opening of carotid canal to the beginning of the first (posterior) ICA genu
Meningohypophyseal artery (posterior trunk) (near C4 and C5) Inferior hypophyseal (pituitary gland) Marginal tentorial or Bernasconi and Cassinari (tentorium) Clival dural branch (cavernous sinus, cranial nerves III through VI)
C4 "cavernous segment"
End of ascending portion and beginning of the horizontal segment
Inferolateral trunk-ILT (lateral mainstem artery) supplies cranial nerves III, IV, VI, and gasserian ganglion (cranial nerve V) and cavernous sinus dura, foramen of rotundum
C3 "carotid knee"
Posterior 90-degree bend to anterior 90-degree bend
Capsular branches (distal C3) supplies pituitary gland
C2 "cisternal segment"
End of horizontal segment to end of cavernous segment C1
Capsular branches (proximal C2) supplies pituitary gland
C1 "terminal segment": supraclinoid
Superior hypophyseal, perforating, ophthalmic, PComA, AChA
AChA = anterior choroidal artery; AVM = arteriovenous malformation; ICA = internal carotid artery; ILT = inferolateral trunk; PComA = posterior communicating artery.
Anterior view
22
Lateral view
○ MCA:most of the lateral surface of the hemisphere,insula 和 anterior and lateral aspects of the temporal lobe M1 or sphenoidal segment(origin to limen insulae)
Lateral lenticulostriate arteries:basal ganglia(caudate nucleus) and the anterior limb of the internal capsule
Anterior temporal branches(有時從 proximal M2 分出):temporal tip cortex M2 or insular segment(runs along the insula)
Anterior cortical branches:Lateral orbitofrontal,operculofrontal(ascending frontal or
candelabra branch)和 central sulcus arteries(precentral or prerolandic 和 central or rolandic branches)
Posterior cortical branches:anterior and posterior parietal,angular,和 posterior temporal arteries
M3 or opercular segment(operculum superior to the insula) M4 or terminal segment(convex surfaces)
M4 superior:orbitofrontal,prefrontal,precentral,postcentral,anterior and posterior
parietal,和 angular arteries
M4 inferior:temporal lobe and part of the occipital lobe,包括temporopolar,anterotemporal,middle temporal,posterotemporal 和 temporo-occipital arteries.
23
Lateral view
○ ACA:anterior two thirds of the medial portions of the cerebral hemispheres and 約 1cm of the superolateral surface of the brain convexity A1 or horizontal segment(origin to AComA)
Medial lenticulostriate arteries(head of the caudate nucleus and the anterior limb ofthe internal capsule,hypothalamus,optic chiasm 和 infundibulum)
AComA(Anterior communicating artery):lamina terminalis and hypothalamus, anterior commissure, fornix, septum pellucidum, paraolfactory gyrus, the subcallosal region, the anterior part of the cingulated gyrus, the head of the caudate nucleus(basal ganglia)
A2 segment(AComA to its bifurcation into pericallosal and callosomarginal arteries)recurrent artery of Heubner(50%在 A2,44%在 A1,不常在 AComA):caudate
nucleus,the rostral putamen 和 anterior limb of the internal capsuleOrbitofrontal and frontopolar arteries
A3 segment(cortical suppliers)Callosomarginal a.Anterior,middle,posterior(internal) frontal 和 paracentral a.
Pericallosal a.parietal(internal) superior and inferior 和 splenial arteries
《 Vertebral artery 》
24
AICA(anterior inferior cerebellar a.)
BA(basilar a.)
BT(basilar tip)
DCC(dosal a. of the corpus callosum)
PC(posterior cerebral a.)
P.com(posterior communicating a.)
P.Ch(posterior choroidal a.)
PICA(posterior inferior cerebellar a.)
POB(parieto-occipital branch of PC)
P. Th(posterior thalamoperforating a.)
TB(temporal branch of PC)
SCA(superior cerebellar a.)
Tent(tentorium cerebelli)
VA(vertebral a.)Tent(tentorium cerebelli)
PICA(posterior inferior cerebellar a.)
VA(vertebral a.)
BA(basilar a.)
BT(basilar tip)
AICA(anterior inferior cerebellar a.)
POB(parieto-occipital branch of PC)
TB(temporal branch of PC)
PC(posterior cerebral a.)
25
○ VA(Vertebral artery):posterior meningeal artery(falx cerebelli),anterior spinal artery(cervical
anterior spinal cord),posterior spinal artery(rare and may arise from PICA),PICA(posterior
inferior cerebellar artery),which runs around the medulla and over the tonsil and supplies the
inferior vermis,the choroid plexus of the fourth ventricle 和 inferior surface of the cerebellum.
○ BA(Basilar artery): AICA(anterior inferior cerebellar arteries) that course around the pons and toward the
cerebellopontine angle and the internal auditory canal meatus to supply the anterior cerebellar hemispheres,CN VII 和 VIII,和 lateral pontine structures
Labyrinthine artery(15%會從 basilar artery直接分出) Small pontine perforators SCA(superior cerebellar artery) that runs around the brainstem in the pontomesencephalic
groove in the perimesencephalic cistern below the oculomotor and trochlear nerves and above the trigeminal nerve to supply the superolateral surface of the cerebellar hemisphere 和 lateral pontine structures
Anteriorview
26
○ PCA(Posterior cerebral artery):basilar artery 在 pontomesencephalic junction, which is superior to
the oculomotor nerve and the tentorium,分出 2條 PCA,供應diencephalon,midbrain,posterior one third of the medial hemisphere surface 和 occipital lobe
P1 or peduncular segment(basilar top to the PComA):Thalamoperforating arteries:diencephalon 和 midbrain
P2 or ambient segment(runs in the ambient cistern from the PComA to the posterior aspect of the midbrain):Posterior thalamoperforating and thalamogeniculate arteries:thalamus,geniculate
body,posterior limb of internal capsule 和 optic tract
Medial PChAs(posterior choroidal arteries):colliculi,posterior thalamus,pineal
gland,part of the midbrain
Lateral PChAs:chroid plexus of the lateral ventricle,和 AChA 有 anastomoses
P3 or quadrigeminal segment:inferior temporal arteries(anterior,middle 和 posterior
temporal arteries),parieto-occipital artery(most of the posterior one third of the brain’s
medial surface and a small area of the lateral surface),calcarine artery,splenial artery(和distal ipsilateral pericallosal 有 anastomoses)
Lateral view
(Venography)
27
BVR(basilar vein of Rosenthal)
C(cavernous sinus)
ICV(internal cerebral vein)
IS(inferior sagittal sinus)
O(occipital sinus)
Sig(sigmoid sinus)
SP(superior petrous sinus)
SR(sinus rectus, straight sinus)
SS(superior sagittal sinus)
SV(septal vein)
T(transverse sinus)
VG(vein of Galen)
VL(vein of Labbe)
VT(vein of Trolard)
MCV(middle cerebral vein)
TSV(thalamostriate vein)
VA(venous angle)
SS(superior sagittal sinus)
IS(inferior sagittal sinus)
VT(vein of Trolard)
SV(septal vein)
C(cavernous sinus)
SP(superior petrous sinus) Sig(sigmoid sinus)
BVR(basilar vein of Rosenthal) T(transverse sinus)
VG(vein of Galen)
SR(sinus rectus, straight sinus)ICV(internal cerebral vein)
28
Anteriorview
○ The cerebral venous system由 dural sinuses,superficial cortical veins,deep cerebral 和transmedullary veins 組成。
○ Venous system of the brain 基本上可以分成 supratentorial 和 infratentorial systems
29
Lateral view
Table 37C-9. Major vessels of the venous circulation
Dural sinuses
Superior sagittal sinus,Inferior sagittal sinus,Straight sinus,Torcular
herophili (sinus confluens),Transverse sinus,Sigmoid sinus,Occipital
sinus,Inferior petrous sinus,Superior petrous sinus,Cavernous sinus
Superficial cortical
Sylvian veins,Veins of Trolard and Labbé,Frontal ascending/descending
cortical veins,Occipital cortical veins,Sphenoparietal vein
Deep cerebral vein
Subependymal veins,Thalamostriate veins,Septal veins,Internal cerebral
veins,Basal vein of Rosenthal,Vein of Galen,Anterior pontomesencephalic
veins,Precentral cerebellar vein,Superior and inferior vermian veins
Dural veins Meningeal vein,Emissary veins (connection between sinus and scalp)
Scalp veins Occipital vein,Temporal vein
Cervical veins
Jugular bulb,Internal/external jugular veins
(Functional Neuroimage)Table 37E-1. Representative radiotracers
Radiotracer What it measures
Single-photon emission computed tomography
99mTc-HMPAO Blood flow
99mTc-ECD Blood flow
123I-IMP Blood flow
123I-altropane Dopamine transporter
123I-βCIT Dopamine transporter/serotonin transporter
123I-epidipride Type 2 dopamine (D2) receptor
123I-IBZM Type 2 dopamine (D2) receptor
99mTc-TRODAT-1 TRODAT-1:cocaine analog that can bind to the
dopamine transporter (DAT) sites at presynaptic neuron
membrane
Positron emission tomography
C15O2, H215O Blood flow
18F-fluorodeoxyglucose Glucose metabolism
11C-altropane Dopamine transporter
11C-SCH 23,390 Type 1 dopamine (D1) receptor
11C-raclopride Type 2 dopamine 2 (D2) receptor
11C-WAY 100635 Type 1A serotonin (5-HT1A) receptor
18F-setoperone Type 2 serotonin (5-HT2) receptor
11C-flumazenil Benzodiazepine receptor
11C-diprenorphine Opioid receptor (nonselective)
11C-carfentanil Opioid receptor (mu selective)
<Single photon emission computed tomography(SPECT) and positron emission tomography(PET)>
Normal Tc-99m HMPAO brain SPECT: Patients without central nervous system disease and with normal X-Ray/ CT examination
demonstrate bilaterally symmetrical activity on the SPECT perfusion images.
Activity is greatest along the convexity of the frontal, temporal, parietal and occipital lobes
-corresponding anatomically to cortical gray matter. Activity is also high in the regions
corresponding to the basal ganglia and thalamus. Regions between the basal ganglia
and the convexity corresponding anatomically to cortical white matter and the ventricles
have less activity.
Dementia
The characteristic “earmuff”(禦寒耳罩)
pattern of decreased metabolism or
30
Fluorodeoxyglucose PET of a patient with advanced Alzheimer’s disease
blood flow in bilateral temporoparietal
and frontal regions with sparing of the
somatosensory cortex is associated
with the diagnosis fo advanced
Alzheimer’s disease.
Seizures
Seizure foci demonstrate increased metabolism or blood flow during a seizure and
decreased metabolism or blood flow during the interictal period
Parkinson’s disease
Number of intact dopaminergic neurons in the striatum 會減少 Cerebral Ischemia
可以 detect hypoperfusion following an acute ischemic event almost immediately
Neoplasms
Neoplasms typically demonstrate greater metabolism or blood flow than surrounding
tissue.
Tumor metabolism is thought to be proportional to tumor cell proliferation.因此 PET and
SPECT studies 可能可以用來作為 tumor classification.
PET and SPECT 可用來分辨 radionecrosis from tumor recurrence.
31
Fluorodeoxyglucose PET of a patient of temporal lobe epilepsy(interictal period)