The difference between free water, bound water, and cerebral edema?

Free and bound water

The main object of human MRI is actually water molecules.

Free and bound water

free and bound water free and bound water

The main object of human MRI is actually water molecules.

The main object of human MRI is actually water molecules.

The water in human tissue can be divided into free water and bound water

The so-called free water refers to the water in which the molecules are free and not combined with other tissue molecules.

Some water molecules are also attached to the macromolecular protein to form a hydration layer.

Therefore, the T1 value of free water is very long, while the T1 value of the tissue can be shortened by bound water

Therefore, the T1 value of free water is very long, while the T1 value of the tissue can be shortened by bound water

The increase in the composition of free water in the tissue will manifest as a decrease in signal intensity on T1WI, such as cerebral edema

If the proportion of bound water increases, the signal intensity can be relatively increased on T1WI, or even high signal, such as cysts containing mucous components, viscous pus in abscesses,

Abscess or some tumors such as astrocytoma, because there is bound water in addition to free water in cyst fluid or pus, the signal intensity on T1WI will be higher than that of cerebrospinal fluid basically composed of free water to varying degrees

Cerebral edema Cerebral edema Brain disease is the top priority of clinical MRI examination, and cerebral edema is one of the most common basic pathological changes in brain diseases, which can be seen in a variety of brain tissue diseases

Pathologically, cerebral edema is divided into three types, namely:

• vasogenic edema

• cytotoxic edema

• interstitial edema

vasogenic edema

vasogenic edema

vasogenic edema vascular edema_

cytotoxic edema

cytotoxic edema

cytotoxic edema

interstitial edema

interstitial edema

interstitial edema interstitial edema

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1.

1.

Vasogenic edema is the most common cerebral edema, and the mechanism is mainly the breakdown of the blood-brain barrier, and the leakage of plasma from the blood vessels to the extracellular space

Common in brain tumors, around hematoma, inflammation, cerebral infarction, trauma and other brain diseases

Vasogenic edema is mainly due to the increase of free water, so it appears as low signal on T1WI and high signal on T2WI
.
Interstitial brain edema is more sensitive on T2WI than T1WI
.
Vasogenic edema is mainly due to the increase of free water, so it appears as low signal on T1WI and high signal on T2WI
.
Interstitial brain edema is more sensitive on T2WI than T1WI
.

The diffusion movement of water molecules in the extracellular space is relatively free, so vasogenic cerebral edema does not appear as a high signal on DWI, and the measured ADC value is often higher than that of normal brain tissue
.

The diffusion movement of water molecules in the extracellular space is relatively free, so vasogenic cerebral edema does not appear as a high signal on DWI, and the measured ADC value is often higher than that of normal brain tissue
.

Sometimes on T1WI and T2WI, the tumor is not easy to be completely differentiated from peripheral vascular cerebral edema, and Gd-DTPA-enhanced scanning can be performed
.
Vasogenic edema around tumors and hematomas is generally not enhanced due to the slight damage to the blood-brain barrier
.
Inflammation and cerebral infarction can cause severe blood-brain barrier damage, Gd-DTPA can penetrate, so it is often enhanced, and it is more common in the gray matter area
.

Sometimes on T1WI and T2WI, the tumor is not easy to be completely differentiated from peripheral vascular cerebral edema, and Gd-DTPA-enhanced scanning can be performed
.
Vasogenic edema around tumors and hematomas is generally not enhanced due to the slight damage to the blood-brain barrier
.
Inflammation and cerebral infarction can cause severe blood-brain barrier damage, Gd-DTPA can penetrate, so it is often enhanced, and it is more common in the gray matter area
.

2.
Cytotoxic brain edema

2.
Cytotoxic cerebral edema 2.
Cytotoxic cerebral edema

Cytotoxic edema is mostly caused by cerebral ischemia and hypoxia, and nerve cells cannot undergo anaerobic glycolysis, so they are very sensitive to hypoxia
.
A few minutes after ischemia, the ATP production of nerve cells is significantly reduced, and the sodium and potassium pumps that rely on ATP work will malfunction.
This results in cell swelling and narrowing of the extracellular space, which is cytotoxic edema
.

Cytotoxic edema is mostly caused by cerebral ischemia and hypoxia, and nerve cells cannot undergo anaerobic glycolysis, so they are very sensitive to hypoxia
.
A few minutes after ischemia, the ATP production of nerve cells is significantly reduced, and the sodium and potassium pumps that rely on ATP work will malfunction.
This results in cell swelling and narrowing of the extracellular space, which is cytotoxic edema
.

Common in hyperacute cerebral infarction or acute, subacute cerebral infarction around the lesions
.
In fact, in the process of occurrence and development of cerebral infarction, cytotoxic edema and vasogenic edema often coexist, but some edema is predominant in different stages of the lesion
.

Common in hyperacute cerebral infarction or acute, subacute cerebral infarction around the lesions
.
In fact, in the process of occurrence and development of cerebral infarction, cytotoxic edema and vasogenic edema often coexist, but some edema is predominant in different stages of the lesion
.

In the early stage of cerebral ischemia, cytotoxic edema is often predominant, followed by vasogenic edema.
When cells disintegrate and the blood-brain barrier is severely damaged, vascular edema is predominant, and finally encephalomalacia appears
.

In the early stage of cerebral ischemia, cytotoxic edema is often predominant, followed by vasogenic edema.
When cells disintegrate and the blood-brain barrier is severely damaged, vascular edema is predominant, and finally encephalomalacia appears
.

In the early stage of cytotoxic edema, the total water in the brain tissue was only slightly increased, and there was no obvious change in signal intensity on T1WI and T2WI
.
Sometimes the signal intensity of acute cerebral infarction changes only slightly, and conventional MRI methods are helpful for the detection of lesions in two ways:

In the early stage of cytotoxic edema, the total water in the brain tissue was only slightly increased, and there was no obvious change in signal intensity on T1WI and T2WI
.
Sometimes the signal intensity of acute cerebral infarction changes only slightly, and conventional MRI methods are helpful for the detection of lesions in two ways:

(1) Although T1WI is not as sensitive as T2WI in response to signal changes, it shows better structural changes than T2WI.
In acute cortical infarction, morphological changes such as sulcus narrowing, swollen and blurred gyri may appear on T1WI before signal abnormalities appear;

(1) Although T1WI is not as sensitive as T2WI in response to signal changes, it shows better structural changes than T2WI.
In acute cortical infarction, morphological changes such as sulcus narrowing, swollen and blurred gyri may appear on T1WI before signal abnormalities appear;

(2) T2WI is more sensitive to signal changes caused by edema than T1WI, but the slight increase in gray matter signal in the early infarcted brain is easily masked by higher signal cerebrospinal fluid.
At this time, if the FLAIR sequence is used to suppress the cerebrospinal fluid signal, it is conducive to the display of abnormal cortical signals.

.

(2) T2WI is more sensitive to signal changes caused by edema than T1WI, but the slight increase in gray matter signal in the early infarcted brain is easily masked by higher signal cerebrospinal fluid.
At this time, if the FLAIR sequence is used to suppress the cerebrospinal fluid signal, it is conducive to the display of abnormal cortical signals.

.

In recent years, diffusion-weighted imaging (DWI) of water molecules, which has been launched clinically, is the most sensitive method for detecting cytotoxic edema
.

In recent years, diffusion-weighted imaging (DWI) of water molecules, which has been launched clinically, is the most sensitive method for detecting cytotoxic edema
.

Cytotoxic edema is due to the entry of extracellular water into the cell, and the intracellular water molecules are bound by the cell membrane and other structures, and the diffusion movement is significantly limited; at the same time, the extracellular space is narrowed due to cell swelling.
Compared with normal tissue, the water in it Molecular diffusion is also more restricted to varying degrees
.
Due to the limited diffusion of water molecules in DWI, the signal attenuation of cytotoxic edema is significantly lower than that of normal brain tissue, so it presents a high signal and the ADC value is significantly reduced
.

Cytotoxic edema is due to the entry of extracellular water into the cell, and the intracellular water molecules are bound by the cell membrane and other structures, and the diffusion movement is significantly limited; at the same time, the extracellular space is narrowed due to cell swelling.
Compared with normal tissue, the water in it Molecular diffusion is also more restricted to varying degrees
.
Due to the limited diffusion of water molecules in DWI, the signal attenuation of cytotoxic edema is significantly lower than that of normal brain tissue, so it presents a high signal and the ADC value is significantly reduced
.
Cytotoxic edema is due to the entry of extracellular water into the cell, and the intracellular water molecules are bound by the cell membrane and other structures, and the diffusion movement is significantly limited; at the same time, the extracellular space is narrowed due to cell swelling.
Compared with normal tissue, the water in it Molecular diffusion is also more restricted to varying degrees
.
Due to the limited diffusion of water molecules in DWI, the signal attenuation of cytotoxic edema is significantly lower than that of normal brain tissue, so it presents a high signal and the ADC value is significantly reduced
.

 

At present, DWI technology has been widely used in the early diagnosis of acute cerebral ischemia
.
It should be pointed out that some other lesions, such as some tumors, hematomas, active multiple sclerosis, and some abscesses, can also show hyperintensity on DWI, which should be identified by combining medical history with conventional MRI and enhanced scans
.

At present, DWI technology has been widely used in the early diagnosis of acute cerebral ischemia
.
It should be pointed out that some other lesions, such as some tumors, hematomas, active multiple sclerosis, and some abscesses, can also show hyperintensity on DWI, which should be identified by combining medical history with conventional MRI and enhanced scans
.

3.
Interstitial cerebral edema

3.
Interstitial cerebral edema 3.
Interstitial cerebral edema

Interstitial cerebral edema is mainly secondary to hydrocephalus caused by various causes
.
Due to increased intraventricular pressure, cerebrospinal fluid passes through the ependyma into the white matter surrounding the ventricle
.

Interstitial cerebral edema is mainly secondary to hydrocephalus caused by various causes
.
Due to increased intraventricular pressure, cerebrospinal fluid passes through the ependyma into the white matter surrounding the ventricle
.

Interstitial cerebral edema is often distributed in the white matter around the lateral ventricle, and free water and bound water are increased at the same time.
The signal on T1WI is lower than that of normal white matter, but slightly higher than that of cerebrospinal fluid, and the signal on T2WI is significantly higher than that of normal brain.
white matter, but slightly below the cerebrospinal fluid
.

Interstitial cerebral edema is often distributed in the white matter around the lateral ventricle, and free water and bound water are increased at the same time.
The signal on T1WI is lower than that of normal white matter, but slightly higher than that of cerebrospinal fluid, and the signal on T2WI is significantly higher than that of normal brain.
white matter, but slightly below the cerebrospinal fluid
.
Free water and bound water increased at the same time, the signal on T1WI was lower than that of normal white matter, but slightly higher than that of cerebrospinal fluid, and the signal on T2WI was significantly higher than that of normal white matter, but slightly lower than that of cerebrospinal fluid
.

Interstitial cerebral edema does not show hyperintensity on DWI, and the ADC value in the lesion area is often slightly to moderately elevated
.

Interstitial cerebral edema does not show hyperintensity on DWI, and the ADC value in the lesion area is often slightly to moderately elevated
.

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