《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

12347910121518222528

《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：

1

◇ 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

2

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

3

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

4

(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°

5

◇ 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.

6

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

7

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

8

（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

9

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

10

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)

11

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)

12

<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

13

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)