Knowledge Collection!

1.
Partial enlargement of lateral ventricle1.
Localized brain atrophy

1.
Local enlargement of lateral ventricle 1.
Localized brain atrophy 1.
Localized brain atrophy

Brain atrophy after trauma, brain atrophy after infection, brain atrophy after cerebral infarction, CT shows that the brain parenchyma near the enlarged part of the ventricle is a sheet-like low-density focus.
MR: T1WI shows low signal, T2WI shows high signal
.

At the same time, the sulcus and subarachnoid space widened

Brain atrophy after trauma, brain atrophy after infection, brain atrophy after cerebral infarction, CT shows that the brain parenchyma near the enlarged part of the ventricle is a sheet-like low-density focus.

 

2.
Neuroepithelial cyst of lateral ventricle 2.
Neuroepithelial cyst of lateral ventricle

 

It is usually located in the triangle of the lateral ventricle, with thin cyst wall, usually unclear.
Because the cyst contains cerebrospinal fluid, both CT and MR show signs of cerebrospinal fluid
.

It is usually located in the triangle of the lateral ventricle, with thin cyst wall, usually unclear.
Because the cyst contains cerebrospinal fluid, both CT and MR show signs of cerebrospinal fluid
.

 

 

3.
Anatomical variation 3.
Anatomical variation

 

It is characterized by no lesions in the nearby brain parenchyma, no enlargement of the sulcus and subarachnoid space or abnormal brain structure

It is characterized by no lesions in the nearby brain parenchyma, no enlargement of the sulcus and subarachnoid space or abnormal brain structure

 

 

4.
Isolated temporal (inferior) angle of lateral ventricle 4.
Isolated temporal (inferior) angle of lateral ventricle

 

It is caused by the obstruction of the flow of cerebrospinal fluid in the temporal horn of the lateral brain.
It is often caused by lesions of the lateral ventricle, including intraependymmal hemorrhage, meningioma and choroidal papilloma, etc.
It can also be caused by compression of lesions around the triangle area of ​​the lateral ventricle
.

It is caused by the obstruction of the flow of cerebrospinal fluid in the temporal horn of the lateral brain.
It is often caused by lesions of the lateral ventricle, including intraependymmal hemorrhage, meningioma and choroidal papilloma, etc.
It can also be caused by compression of lesions around the triangle area of ​​the lateral ventricle
.

 

 

2.
Enlargement of one side of the ventricle

 

1.
Normal variation 1.
Normal variation

 

In normal people, a considerable number of bilateral ventricles are inconsistent in size.
One side of the asymmetrical ventricle is obviously larger than the other side
.

Clinically, intelligence and mental development are normal and have no clinical significance

In normal people, a considerable number of bilateral ventricles are inconsistent in size.

 

2.
Atrophy of one cerebral hemisphere 2.
Atrophy of one cerebral hemisphere

 

It can be caused by many reasons, such as cerebral infarction, trauma, hemorrhage and infection
.

The most common cause is a large area of ​​the brain caused by vascular occlusion

It can be caused by many reasons, such as cerebral infarction, trauma, hemorrhage and infection

 

3.
Cerebral trigeminal nerve angiomatosis 3.
Cerebral trigeminal nerve angiomatosis

 

Also known as facial hemangioma syndrome, CT scan is characterized by gyrus-like, orbit-like, arc-like or serrated calcification in the brain parenchyma of one hemisphere
.

Due to the blood supply disorder of the affected side, the brain parenchyma is often atrophy.

Also known as facial hemangioma syndrome, CT scan is characterized by gyrus-like, orbit-like, arc-like or serrated calcification in the brain parenchyma of one hemisphere

 

4.
One side interventricular hole is blocked 4.
One side interventricular hole is blocked

 

Cerebrospinal fluid is mainly produced in the choroidal plexus of the ventricle
.

When one side of the interventricular foramen is blocked, the cerebrospinal fluid produced by the choroidal plexus of the ipsilateral ventricle cannot enter the third ventricle, and the cerebrospinal fluid accumulates in the lateral ventricle.

Cerebrospinal fluid is mainly produced in the choroidal plexus of the ventricle
.
When one side of the interventricular foramen is blocked, the cerebrospinal fluid produced by the choroidal plexus of the ipsilateral ventricle cannot enter the third ventricle, and the cerebrospinal fluid accumulates in the lateral ventricle.
CT and MR examinations show that one side of the lateral ventricle is enlarged.
When the enlargement is obvious, the midline structure may be opposite.
The main causes of lateral displacement are tumors, cysts, cysts and inflammatory adhesions near the interventricular foramen
.
The main points for determining that the enlargement of one side of the lateral ventricle is caused by the obstruction of the interventricular foramen include: one side of the lateral ventricle has obvious expansion and tension .
The transparent septum shifts to the opposite side; the enlarged lateral ventricle does not cause the lateral ventricle to expand.
Other reasons that can be explained
.
tension

 

 

5.
Periventricular Leukomalacia 5.
Periventricular Leukomalacia

 

Mainly related to ischemia, hypoxia and infection.
It is common in premature infants.
It is the main cause of cerebral palsy in premature infants
.
Because the blood supply of the white matter around the ventricle comes from the terminal arteries in the ventricular area and the distal ventricular area respectively
.
The collateral circulation of the deep perforating branches of the terminal arteries in immature babies has not been established, and the periventricular white matter in the late embryo is sensitive to ischemia and hypoxia
.
Therefore, periventricular automalacia is more common in premature infants
.
Because the lesions are often bilateral, the bilateral ventricles often expand at the same time
.
The softening lesions in the white matter showed low-density foci in the white matter on CT scan.
The MR T1-weighted map showed low signal, and the T2-weighted map showed high signal
.

Mainly related to ischemia, hypoxia and infection.
It is common in premature infants.
It is the main cause of cerebral palsy in premature infants
.
Because the blood supply of the white matter around the ventricle comes from the terminal arteries in the ventricular area and the distal ventricular area respectively
.
The collateral circulation of the deep perforating branches of the terminal arteries in immature babies has not been established, and the periventricular white matter in the late embryo is sensitive to ischemia and hypoxia
.
Therefore, periventricular automalacia is more common in premature infants
.
Because the lesions are often bilateral, the bilateral ventricles often expand at the same time
.
The softening lesions in the white matter showed low-density foci in the white matter on CT scan.
The MR T1-weighted map showed low signal, and the T2-weighted map showed high signal
.

 

 

3.
Enlarged bilateral ventricles

 

1.
General brain atrophy 1.
General brain atrophy

 

Generalized brain atrophy often involves gray matter and white matter at the same time.
It can be manifested as bilateral lateral ventricle enlargement
.
And it is the most common cause of mild symmetrical enlargement of bilateral ventricles
.
Especially in patients with white matter atrophy
.

Generalized brain atrophy often involves gray matter and white matter at the same time.
It can be manifested as bilateral lateral ventricle enlargement
.
And it is the most common cause of mild symmetrical enlargement of bilateral ventricles
.
Especially in patients with white matter atrophy
.

 

 

The enlargement of the lateral ventricle caused by general brain atrophy is usually symmetrical.
There is no shift in the midline
.
It is characterized by symptoms of cortical atrophy such as brain sulci and brain fissure widening at the same time.

The enlargement of the lateral ventricle caused by general brain atrophy is usually symmetrical.
There is no shift in the midline
.
It is characterized by symptoms of cortical atrophy such as brain sulci and brain fissure widening at the same time.

 

Generalized brain atrophy can be seen in normal elderly

Generalized brain atrophy can be seen in normal elderly

 

The reasons are as follows: ① CT and MR examinations of age-related brain atrophy show that the ventricles and cisterns are slightly enlarged.
The sulci are slightly enlarged.
Often the frontal lobe and the side of the sickle are more obvious
.
②Alzheimer's disease, in addition to the general manifestations of general brain atrophy.
Temporal lobe atrophy is often obvious and early, so the lateral ventricle enlargement is more obvious with the temporal horn
.
The severity of neuronal loss in Alzheimer's disease was hippocampus, posterior temporal lobe, frontal lobe and parietal lobe in order of severity
.
③Huntington's disease (chorea) is an autosomal dominant degeneration of the basal ganglia and cerebral cortex
.
Mainly damage the basal ganglia and cerebral cortex, and the caudate nucleus and putamen are the most obvious
.
Small ganglion cells are severely damaged, large cells are also reduced, Nissl bodies disappear, nuclear pyknosis, amyloid bodies appear, as well as demyelination changes and glial hyperplasia.
The involvement of the basal ganglia is often the most obvious and the earliest
.
The clinic is mainly based on 3 major characteristics: choreography, dementia, and family history
.
④Parkinson's disease, also known as tremor, is a common extrapyramidal disease
.
It is clinically characterized by tremor, muscle rigidity and dyskinesia
.
The first symptom of tremor feeding is obvious when resting and quiet
.
In addition to CT atrophy, sometimes calcification of the basal ganglia can be seen
.
On MR T2WI, there are often multiple high-intensity spots in the basal ganglia and white matter of the brain.
⑤Pick's disease, also known as lobar sclerosis, is more common in women.
The peak incidence is at the age of 50.
The clinical manifestation is progressive dementia
.
CT and MR often focus on atrophy of the frontal and temporal lobes
.
Another feature is that bilateral atrophy is often inconsistent, the left side is more obvious, the front half of the superior temporal gyrus is atrophied, and the back is often normal
.
⑥ Jakob-Creutzfeldt's disease is a kind of encephalopathy characterized by rapidly progressive dementia.
CT and MR manifestations are symmetrical enlargement of the lateral ventricles and widening of the sulci-brain fissure
.
Short-term reexamination showed that the degree of atrophy was significantly worsened, and diffuse white matter demyelination changes may occur in the late stage
.
⑦Other reasons such as hypoxia, poisoning, physical injury, malnutrition, etc. .

The reasons are as follows: ① CT and MR examinations of age-related brain atrophy show that the ventricles and cisterns are slightly enlarged.
The sulci are slightly enlarged.
Often the frontal lobe and the side of the sickle are more obvious
.
②Alzheimer's disease, in addition to the general manifestations of general brain atrophy.
Temporal lobe atrophy is often obvious and early, so the lateral ventricle enlargement is more obvious with the temporal horn
.
The severity of neuronal loss in Alzheimer's disease was hippocampus, posterior temporal lobe, frontal lobe and parietal lobe in order of severity
.
③Huntington's disease (chorea) is an autosomal dominant degeneration of the basal ganglia and cerebral cortex
.
Mainly damage the basal ganglia and cerebral cortex, and the caudate nucleus and putamen are the most obvious
.
Small ganglion cells are severely damaged, large cells are also reduced, Nissl bodies disappear, nuclear pyknosis, amyloid bodies appear, as well as demyelination changes and glial hyperplasia.
The involvement of the basal ganglia is often the most obvious and the earliest
.
The clinic is mainly based on 3 major characteristics: choreography, dementia, and family history
.
④Parkinson's disease, also known as tremor, is a common extrapyramidal disease
.
It is clinically characterized by tremor, muscle rigidity and dyskinesia
.
The first symptom of tremor feeding is obvious when resting and quiet
.
In addition to CT atrophy, sometimes calcification of the basal ganglia can be seen
.
On MR T2WI, there are often multiple high-intensity spots in the basal ganglia and white matter of the brain.
⑤Pick's disease, also known as lobar sclerosis, is more common in women.
The peak incidence is at the age of 50.
The clinical manifestation is progressive dementia
.
CT and MR often focus on atrophy of the frontal and temporal lobes
.
Another feature is that bilateral atrophy is often inconsistent, the left side is more obvious, the front half of the superior temporal gyrus is atrophied, and the back is often normal
.
⑥ Jakob-Creutzfeldt's disease is a kind of encephalopathy characterized by rapidly progressive dementia.
CT and MR manifestations are symmetrical enlargement of the lateral ventricles and widening of the sulci-brain fissure
.
Short-term reexamination showed that the degree of atrophy was significantly worsened, and diffuse white matter demyelination changes may occur in the late stage
.
⑦Other reasons such as hypoxia, poisoning, physical injury, malnutrition, etc. .

 

2.
Enlargement of the lateral ventricle of premature infants 2.
Enlargement of the lateral ventricle of premature infants

 

In the early embryonic stage, the lateral ventricle is relatively large.
As the development matures, the lateral ventricle gradually becomes smaller.
It reaches a normal size at 36 weeks of the embryo.
Therefore, preterm infants often show mild symmetrical enlargement of the bilateral lateral ventricles, which is 30 A premature baby born a week ago
.
Can be combined with or without intracranial hemorrhage in premature infants
.

In the early embryonic stage, the lateral ventricle is relatively large.
As the development matures, the lateral ventricle gradually becomes smaller.
It reaches a normal size at 36 weeks of the embryo.
Therefore, preterm infants often show mild symmetrical enlargement of the bilateral lateral ventricles, which is 30 A premature baby born a week ago
.
Can be combined with or without intracranial hemorrhage in premature infants
.

 

 

3.
Giant brain malformation 3.
Giant brain malformation

 

Megacephaly can also be manifested with symmetrical enlargement of both sides of the ventricle.
It is usually mild
.
This kind of giant brain malformation can be a symptom of many diseases: such as Alexander disease, spongiform degeneration, Soto's syndrome and so on
.
The common situation is that many large-headed children have normal clinical mental development and physical development, with no manifestations of increased intracranial pressure, and no signs and symptoms of the nervous system
.

Megacephaly can also be manifested with symmetrical enlargement of both sides of the ventricle.
It is usually mild
.
This kind of giant brain malformation can be a symptom of many diseases: such as Alexander disease, spongiform degeneration, Soto's syndrome and so on
.
The common situation is that many large-headed children have normal clinical mental development and physical development, with no manifestations of increased intracranial pressure, and no signs and symptoms of the nervous system
.
child

 

Soto's syndrome, also known as cerebral gigantism, manifests itself in the neonatal period with a significant increase in body development and birth.
There are also large-head giant brain malformations, mental development and birth delays, and special features, protruding forehead, and palpebral fissure outwards.
Downward tilt.
The eye distance i is too wide, the mandible is thin and prominent, growth hormone and endocrine examinations are normal, and the head CT and MR examinations are mainly manifested as giant brains and lateral ventricles
.
The diagnosis is mainly combined with the above-mentioned clinical conditions
.

Soto's syndrome, also known as cerebral gigantism, manifests itself in the neonatal period with a significant increase in body development and birth.
There are also large-head giant brain malformations, mental development and birth delays, and special features, protruding forehead, and palpebral fissure outwards.
Downward tilt.
The eye distance i is too wide, the mandible is thin and prominent, growth hormone and endocrine examinations are normal, and the head CT and MR examinations are mainly manifested as giant brains and lateral ventricles
.
The diagnosis is mainly combined with the above-mentioned clinical conditions
.
diagnosis

 

 

4.
Abnormal congenital development of the brain 4.
Abnormal congenital development of the brain

 

Many kinds of brain development abnormalities can be manifested at the same time with enlarged lateral ventricles, including forebrain anemia, split brain malformation, anencephaly and giant gyrus
.

Many kinds of brain development abnormalities can be manifested at the same time with enlarged lateral ventricles, including forebrain anemia, split brain malformation, anencephaly and giant gyrus
.

 

(1) Holoprosencephaly: (holoprosencephaly) refers to a series of malformations of varying degrees located in the midline, involving the brain, face, cerebellum and cerebellum.
The forebrain cannot be separated and is incomplete or complete.
The brain cannot distinguish
.
According to the degree of brain and facial deformities, they are divided into leafless type, semi-lobe type and simple lobe type
.

(1) Holoprosencephaly: (holoprosencephaly) refers to a series of malformations of varying degrees located in the midline, involving the brain, face, cerebellum and cerebellum.
The forebrain cannot be separated and is incomplete or complete.
The brain cannot distinguish
.
According to the degree of brain and facial deformities, they are divided into leafless type, semi-lobe type and simple lobe type
.

 

Forebrain without lobules is the most serious.
There are no fissures between the cerebellar hemispheres, and a horseshoe-shaped or crescent-shaped enlarged single ventricle crosses the midline and communicates with the dorsal capsule
.
The thalamus merge with each other, and the facial deformities range from too close to the one-eyed deformity.
They often die in the fetus or neonatal period
.

Forebrain without lobules is the most serious.
There are no fissures between the cerebellar hemispheres, and a horseshoe-shaped or crescent-shaped enlarged single ventricle crosses the midline and communicates with the dorsal capsule
.
The thalamus merge with each other, and the facial deformities range from too close to the one-eyed deformity.
They often die in the fetus or neonatal period
.

 

Hemilobular forebrain afissure deformity can be seen in part of the forebrain fissures.
The formation of longitudinal fissures and falx cerebrum of different developmental degrees
.
The two cerebral hemispheres are not completely separated in the anterior part, but the occipital lobe and the bilateral ventricle body are separated, and the thalamus is not completely separated
.
The third ventricle and hippocampus are underdeveloped, and the corpus callosum is only visible in the depressed part, while other parts are absent.
The frontal lobe and the anterior part of the basal ganglia are indistinguishable
.
The clinical manifestations are that the eyes are too close, and facial deformities such as cleft lip and palate, and the lateral ventricles are monotonous and significantly enlarged
.

Hemilobular forebrain afissure deformity can be seen in part of the forebrain fissures.
The formation of longitudinal fissures and falx cerebrum of different developmental degrees
.
The two cerebral hemispheres are not completely separated in the anterior part, but the occipital lobe and the bilateral ventricle body are separated, and the thalamus is not completely separated
.
The third ventricle and hippocampus are underdeveloped, and the corpus callosum is only visible in the depressed part, while other parts are absent.
The frontal lobe and the anterior part of the basal ganglia are indistinguishable
.
The clinical manifestations are that the eyes are too close, and facial deformities such as cleft lip and palate, and the lateral ventricles are monotonous and significantly enlarged
.

 

 

The unilobular acephalic forebrain malformation is only slightly different from the normal developing brain.
For example, the transparent septum is missing or the frontal lobes are not completely separated
.

The unilobular acephalic forebrain malformation is only slightly different from the normal developing brain.
For example, the transparent septum is missing or the frontal lobes are not completely separated
.

 

(2) Split brain malformation: embryonic brain development goes through six main stages: ① dorsal induction stage; ③ ventral induction stage; ③ neuroproliferation stage; ④ neuron migration stage; ⑤ tissue formation stage; ⑥ myelination Stage
.
Split brain malformation occurs in the stage of neuron migration
.
Split brain malformations can affect one or both of the cerebral hemispheres, and the cleft brain malformations are located on the side.
It often involves the central anterior and posterior gyrus and occasionally other parts of the cerebral hemisphere
.
The fissure of cleft brain deformity can be very narrow, and the gray matter on both sides of the fissure closely adheres to each other, which is called closed type
.
The fissure can also be very wide, with cerebrospinal fluid in the middle, separated
.

(2) Split brain malformation: embryonic brain development goes through six main stages: ① dorsal induction stage; ③ ventral induction stage; ③ neuroproliferation stage; ④ neuron migration stage; ⑤ tissue formation stage; ⑥ myelination Stage
.
Split brain malformation occurs in the stage of neuron migration
.
Split brain malformations can affect one or both of the cerebral hemispheres, and the cleft brain malformations are located on the side.
It often involves the central anterior and posterior gyrus and occasionally other parts of the cerebral hemisphere
.
The fissure of cleft brain deformity can be very narrow, and the gray matter on both sides of the fissure closely adheres to each other, which is called closed type
.
The fissure can also be very wide, with cerebrospinal fluid in the middle, separated
.

 

 

Separate split brain malformations need to be distinguished from penetrating malformation cysts.
The fissure of split brain malformation must be surrounded by a gray matter structure on both sides, and there is no brain gray matter surrounding the penetrating malformation cyst
.
Whether there are gray matter structures on both sides of the fissure is a reliable sign to distinguish between a split brain malformation and a penetrating malformation cyst
.
The gray matter on both sides of the fissure may be abnormal and may be multi-cerebellar
.
Split brain malformations can also be associated with heterotopic brain gray matter
.

Separate split brain malformations need to be distinguished from penetrating malformation cysts.
The fissure of split brain malformation must be surrounded by a gray matter structure on both sides, and there is no brain gray matter surrounding the penetrating malformation cyst
.
Whether there are gray matter structures on both sides of the fissure is a reliable sign to distinguish between a split brain malformation and a penetrating malformation cyst
.
The gray matter on both sides of the fissure may be abnormal and may be multi-cerebellar
.
Split brain malformations can also be associated with heterotopic brain gray matter
.

 

The separated type is easy to show on CT.
The closed type is sometimes easily missed.
MRI can easily identify the gray matter structures on both sides of the fissure
.
Split brain malformations are often accompanied by a transparent septum.
Lateral ventricles are enlarged, and the edges of the ventricles are irregular at the split brain malformations.
Fissures or triangular diverticula pointing to the fissures are often seen
.

The separated type is easy to show on CT.
The closed type is sometimes easily missed.
MRI can easily identify the gray matter structures on both sides of the fissure
.
Split brain malformations are often accompanied by a transparent septum.
Lateral ventricles are enlarged, and the edges of the ventricles are irregular at the split brain malformations.
Fissures or triangular diverticula pointing to the fissures are often seen
.

 

Clinically, split brain malformation often manifestsSeizures and other neurological symptoms can range from very mild to very severe.
It mainly depends on the severity of the brain tissue defect caused by the split brain malformation
.
Symptoms of unilateral closed split brain malformation are usually mild, and symptoms of bilateral split brain malformation are more obvious
.

Clinically, split brain malformation often manifestsSeizures and other neurological symptoms can range from very mild to very severe.
It mainly depends on the severity of the brain tissue defect caused by the split brain malformation
.
Symptoms of unilateral closed split brain malformation are usually mild, and symptoms of bilateral split brain malformation are more obvious
.
epilepsy

 

(3) No brain gyrus and giant brain gyrus

(3) No brain gyrus and giant brain gyrus

 

Anencephaly and giant gyrus are a group of gyrus development abnormalities caused by abnormal neuron migration
.
Giant brain gyrus is also called smooth brain
.
The giant gyrus refers to the existence of part of the gyrus, which enlarges and widens abnormally.
The sulci becomes shallow
.
The giant brain gyrus is mainly located in the frontal and temporal regions
.
The upper back of the brainless gyrus should be located at the parietal and occipital areas
.

Anencephaly and giant gyrus are a group of gyrus development abnormalities caused by abnormal neuron migration
.
Giant brain gyrus is also called smooth brain
.
The giant gyrus refers to the existence of part of the gyrus, which enlarges and widens abnormally.
The sulci becomes shallow
.
The giant brain gyrus is mainly located in the frontal and temporal regions
.
The upper back of the brainless gyrus should be located at the parietal and occipital areas
.

 

 

Clinically, children with anencephaly and giant gyrus both show microcephaly and slight facial abnormalities.
Complete anencephaly and often die before the age of two.
Incomplete gyrus can often survive for a long time
.

Clinically, children with anencephaly and giant gyrus both show microcephaly and slight facial abnormalities.
Complete anencephaly and often die before the age of two.
Incomplete gyrus can often survive for a long time
.

 

Both CT and MR can well show anencephaly and giant gyrus.
The surface of the cerebral hemisphere is almost smooth.
Only a few broad, thick and flat gyrus can be seen.
The sulci is absent.
The gray matter of the brain is thickened and the brain The white matter becomes thinner, the gray-white matter interface is abnormally smooth, and no white matter extends into the gray matter
.
The common transparent septum is present.
The lateral ventricle is enlarged and the subarachnoid space is widened
.

Both CT and MR can well show anencephaly and giant gyrus.
The surface of the cerebral hemisphere is almost smooth.
Only a few broad, thick and flat gyrus can be seen.
The sulci is absent.
The gray matter of the brain is thickened and the brain The white matter becomes thinner, the gray-white matter interface is abnormally smooth, and no white matter extends into the gray matter
.
The common transparent septum is present.
The lateral ventricle is enlarged and the subarachnoid space is widened
.

 

5.
Obstruction of bilateral interventricular orifice 5.
Obstruction of bilateral interventricular orifice

 

Same as obstruction of one side interventricular foramen, after obstruction of bilateral interventricular foramen, it can be manifested as symmetrical or asymmetrical enlargement of bilateral ventricles.
The enlargement of ventricles is usually significant.
There are usually interstitial cerebral edema around the ventricles.
The reason for the blockage of the interventricular hole is the same as that of the interventricular hole on one side
.
May also be accompanied by narrow aqueduct
.

Same as obstruction of one side interventricular foramen, after obstruction of bilateral interventricular foramen, it can be manifested as symmetrical or asymmetrical enlargement of bilateral ventricles.
The enlargement of ventricles is usually significant.
There are usually interstitial cerebral edema around the ventricles.
The reason for the blockage of the interventricular hole is the same as that of the interventricular hole on one side
.
May also be accompanied by narrow aqueduct
.

 

Diagnosis points: The bilateral lateral ventricles are enlarged and the third ventricles are normal in size
.

Diagnosis points: The bilateral lateral ventricles are enlarged and the third ventricles are normal in size
.

 

 

6.
Periventricular Leukomalacia 6.
Periventricular Leukomalacia

 

Mainly related to ischemia, hypoxia and infection
.

Mainly related to ischemia, hypoxia and infection
.

 

It is common in premature babies
.
The common cause in premature infants is related to the time when brain damage occurs in the embryonic stage.
Brain damage in the early and mid embryonic stage mainly causes developmental malformations, and the later stage mainly causes cerebrovascular changes
.

It is common in premature babies
.
The common cause in premature infants is related to the time when brain damage occurs in the embryonic stage.
Brain damage in the early and mid embryonic stage mainly causes developmental malformations, and the later stage mainly causes cerebrovascular changes
.

 

Since the blood supply of the white matter around the ventricle comes from the terminal arteries in the ventricular area and the distal ventricular area, the collateral circulation of the deep perforating branch of the terminal artery in immature babies has not been established, and the white matter around the ventricle is sensitive to ischemia and hypoxia in the late embryonic stage
.
Therefore, periventricular leukomalacia is more common in premature infants
.

Since the blood supply of the white matter around the ventricle comes from the terminal arteries in the ventricular area and the distal ventricular area, the collateral circulation of the deep perforating branch of the terminal artery in immature babies has not been established, and the white matter around the ventricle is sensitive to ischemia and hypoxia in the late embryonic stage
.
Therefore, periventricular leukomalacia is more common in premature infants
.

 

Due to the softening and atrophy around the lateral ventricle, the enlarged lateral ventricular rim is often irregular and not smooth.
This irregularity and unevenness are the characteristics of the disease causing the enlargement of the ventricle.
In addition, the disease is characterized by decreased white brain mass and Patchy softening lesions in the white matter of the brain.
When the white matter reduction is severe, the white matter disappears in some areas, and the cerebral cortex is close to or even connected to the lateral edge of the ventricle
.
CT showed patchy low-density foci
.
MR showed low signal on T1WI and high signal on T2WI
.

Due to the softening and atrophy around the lateral ventricle, the enlarged lateral ventricular rim is often irregular and not smooth.
This irregularity and unevenness are the characteristics of the disease causing the enlargement of the ventricle.
In addition, the disease is characterized by decreased white brain mass and Patchy softening lesions in the white matter of the brain.
When the white matter reduction is severe, the white matter disappears in some areas, and the cerebral cortex is close to or even connected to the lateral edge of the ventricle
.
CT showed patchy low-density foci
.
MR showed low signal on T1WI and high signal on T2WI
.

 

 

7.
Optic-septal dysplasia 7.
Optic-septal dysplasia

 

It is a rare congenital malformation, which mainly includes: 1.
Absence or hypoplasia of the transparent septum, 2.
Dysplasia of the optic nerve, optic chiasm and funnel 3.
Various degrees of hypothalamic-pituitary dysfunction
.
The imaging findings may be mild, including the absence of a transparent septum, thinning of the optic nerve and optic chiasma, small optic canal, enlargement of the three ventricle optic recesses, enlarged bilateral lateral ventricles, and a square anterior horn of the lateral ventricles
.
It is more common in women and may manifest as diabetes insipidus, visual impairment and subthalamic dysfunction
.

It is a rare congenital malformation, which mainly includes: 1.
Absence or hypoplasia of the transparent septum, 2.
Dysplasia of the optic nerve, optic chiasm and funnel 3.
Various degrees of hypothalamic-pituitary dysfunction
.
The imaging findings may be mild, including the absence of a transparent septum, thinning of the optic nerve and optic chiasma, small optic canal, enlargement of the three ventricle optic recesses, enlarged bilateral lateral ventricles, and a square anterior horn of the lateral ventricles
.
It is more common in women and may manifest as diabetes insipidus, visual impairment and subthalamic dysfunction
.

 

 

8.
Dysplasia of the corpus callosum 8.
Dysplasia of the corpus callosum

 

At the late stage of ventral induction of brain development, the dorsal part of the newly formed side wall of the cerebellum is thickened and inverted, and extends backward along the not fully developed cerebral interhemispheric fissure
.
Two months later, a commissural cell frame of the corpus callosum fibers is formed, and the corresponding part of the corpus callosum develops immediately after the cell frame is formed
.
The knees develop first
.
Then there are the body and pressure.
The mouth of the corpus callosum, which is located behind the knees of the corpus callosum, develops finally
.
If harmful factors occur during the development of the corpus callosum, it may lead to dysplasia of the corpus callosum, which is completely absent or partly absent
.
Often manifested as the presence of the knee or the presence of the knee and body
.
The pressure part and the corpus callosum mouth are missing
.

At the late stage of ventral induction of brain development, the dorsal part of the newly formed side wall of the cerebellum is thickened and inverted, and extends backward along the not fully developed cerebral interhemispheric fissure
.
Two months later, a commissural cell frame of the corpus callosum fibers is formed, and the corresponding part of the corpus callosum develops immediately after the cell frame is formed
.
The knees develop first
.
Then there are the body and pressure.
The mouth of the corpus callosum, which is located behind the knees of the corpus callosum, develops finally
.
If harmful factors occur during the development of the corpus callosum, it may lead to dysplasia of the corpus callosum, which is completely absent or partly absent
.
Often manifested as the presence of the knee or the presence of the knee and body
.
The pressure part and the corpus callosum mouth are missing
.

 

The dysplasia of the corpus callosum can be seen alone, but it is more common to be accompanied by other malformations of the central extension system, including lipoma around the corpus callosum, encephalocele, communicating hydrocephalus Chaarii malformation, Dandy-Walker cyst, cleft cerebral malformation and so on
.
Clinically, it can be asymptomatic or only mild clinical symptoms.
Clinical examination shows that the eye distance is too wide, macrocephaly, and mental retardation
.
In the absence of the corpus callosum, the anterior horn of the upper lateral ventricle in the coronal position of MR appears crescent-shaped, and the body of the lateral ventricle is separated and runs vertically and parallel
.

The dysplasia of the corpus callosum can be seen alone, but it is more common to be accompanied by other malformations of the central extension system, including lipoma around the corpus callosum, encephalocele, communicating hydrocephalus Chaarii malformation, Dandy-Walker cyst, cleft cerebral malformation and so on
.
Clinically, it can be asymptomatic or only mild clinical symptoms.
Clinical examination shows that the eye distance is too wide, macrocephaly, and mental retardation
.
In the absence of the corpus callosum, the anterior horn of the upper lateral ventricle in the coronal position of MR appears crescent-shaped, and the body of the lateral ventricle is separated and runs vertically and parallel
.

 

 

4.
Simultaneous enlargement of the third ventricle and the lateral ventricle

 

1.
Narrow aqueduct: 1.
Narrow aqueduct:

 

The midbrain aqueduct is the narrowest passage in the ventricular system and the most common site where the circulation of cerebrospinal fluid is blocked
.

The midbrain aqueduct is the narrowest passage in the ventricular system and the most common site where the circulation of cerebrospinal fluid is blocked
.

 

The etiology of aqueduct stenosis is more complicated, mainly including: ① congenital developmental stenosis ② gel-like changes around the aqueduct ③ aqueduct adhesion and so on
.
Congenital developmental stenosis can be linear stenosis, bifurcated stenosis, or diaphragm formation
.
Glue around the aqueduct is mostly caused by inflammation, which is mainly seen after congenital intrauterine infection, especially toxoplasma infection
.

The etiology of aqueduct stenosis is more complicated, mainly including: ① congenital developmental stenosis ② gel-like changes around the aqueduct ③ aqueduct adhesion and so on
.
Congenital developmental stenosis can be linear stenosis, bifurcated stenosis, or diaphragm formation
.
Glue around the aqueduct is mostly caused by inflammation, which is mainly seen after congenital intrauterine infection, especially toxoplasma infection
.

 

Aqueduct adhesions are mainly seen after intracranial infection and hemorrhage, can occur in the embryonic period, and can also be seen at any age after birth
.
The stenosis caused by adhesion of the aqueduct is mostly located at the distal end of the aqueduct
.
The length of the stenosis is usually 2 to 5mm, and the different aqueous tube at the proximal end of the stenosis can be expanded like a bell mouth
.

Aqueduct adhesions are mainly seen after intracranial infection and hemorrhage, can occur in the embryonic period, and can also be seen at any age after birth
.
The stenosis caused by adhesion of the aqueduct is mostly located at the distal end of the aqueduct
.
The length of the stenosis is usually 2 to 5mm, and the different aqueous tube at the proximal end of the stenosis can be expanded like a bell mouth
.

 

When the aqueduct is narrowed, the third ventricle is often enlarged.
The anterior optic and infundibular crypts of the third ventricle expand or disappear, and the pineal and suprapineal crypts in the posterior part of the third ventricle are obviously protruding to the cerebellum.
The pool herniated
.
In severe cases, it can oppress the cerebellum
.

When the aqueduct is narrowed, the third ventricle is often enlarged.
The anterior optic and infundibular crypts of the third ventricle expand or disappear, and the pineal and suprapineal crypts in the posterior part of the third ventricle are obviously protruding to the cerebellum.
The pool herniated
.
In severe cases, it can oppress the cerebellum
.

 

 

2.
Inferior cerebellar tonsillar hernia 2.
Inferior cerebellar tonsil hernia deformity

 

Also known as Chiari's malformation, the cerebellar tonsils move down into the spinal canal, and the medulla oblongata and the fourth ventricle are elongated and partly shifted down
.
Can be divided into 3 types
.
All types often have hydrocephalus
.
The third ventricle and the lateral ventricle are enlarged
.
Type I: If only the cerebellar tonsils move down
.
Tonsil below the lower edge of the foramen magnum connection than 5mm, no brain stem and to the fourth ventricle changer type Ⅰ
.
Type Ⅱ: In addition to the downward shift of the cerebellar tonsils, part or all of the fourth ventricle descends below the foramen magnum
.
Type Ⅲ: Type Ⅲ if the whole cerebellum and four brains herniate into the foramen magnum below
.

Also known as Chiari's malformation, the cerebellar tonsils move down into the spinal canal, and the medulla oblongata and the fourth ventricle are elongated and partly shifted down
.
Can be divided into 3 types
.
All types often have hydrocephalus
.
The third ventricle and the lateral ventricle are enlarged
.
Type I: If only the cerebellar tonsils move down
.
Tonsil below the lower edge of the foramen magnum connection than 5mm, no brain stem and to the fourth ventricle changer type Ⅰ
.
Type Ⅱ: In addition to the downward shift of the cerebellar tonsils, part or all of the fourth ventricle descends below the foramen magnum
.
Type Ⅲ: Type Ⅲ if the whole cerebellum and four brains herniate into the foramen magnum below
.

 

 

5.
Enlargement of all ventricles

 

1.
Communication hydrocephalus 1.
Communication hydrocephalus

 

Also known as ventricular obstructive hydrocephalus, it is hydrocephalus caused by cerebrospinal fluid circulation after the exit of the fourth ventricle
.
It is often located in the subarachnoid space, with the basal cistern the most common
.
The main causes include meningitis, subarachnoid hemorrhage, meningeal metastasis, trauma, venous sinus thrombosis , post-cranial surgery and cerebrospinal fluid absorption dysfunction
.
The clinical manifestations are mainly caused by increased intracranial pressure.
Headaches, vomiting, diplopia and papilledema can be manifested
.
When communicating hydrocephalus, the expansion of the fourth ventricle usually appears later, so in the early stage, only the lateral ventricle and the third ventricle may be enlarged
.
It should be distinguished from obstructive hydrocephalus caused by aqueduct stenosis
.
MR sagittal T1-weighted image is the best way to directly observe whether the aqueduct has stenosis
.
In addition, it needs to be distinguished from general brain atrophy.
When the brain is atrophy, the sulci-brain is widened, and when the hydrocephalus, the sulci is narrowed and disappears or is normal
.
In addition, the expansion of the third ventricle is not obvious
.
The expansion of the ventricle is more obvious .
The third ventricle enlarges more obviously when the brain shrinks
.
In the late stage, communicating hydrocephalus appears and the entire ventricular system is generally enlarged and the sulci is normal or narrowed and disappeared
.

Also known as ventricular obstructive hydrocephalus, it is hydrocephalus caused by cerebrospinal fluid circulation after the exit of the fourth ventricle
.
It is often located in the subarachnoid space, with the basal cistern the most common
.
The main causes include meningitis, subarachnoid hemorrhage, meningeal metastasis, trauma, venous sinus thrombosis , post-cranial surgery and cerebrospinal fluid absorption dysfunction
.
The clinical manifestations are mainly caused by increased intracranial pressure.
Headaches, vomiting, diplopia and papilledema can be manifested
.
When communicating hydrocephalus, the expansion of the fourth ventricle usually appears later, so in the early stage, only the lateral ventricle and the third ventricle may be enlarged
.
It should be distinguished from obstructive hydrocephalus caused by aqueduct stenosis
.
MR sagittal T1-weighted image is the best way to directly observe whether the aqueduct has stenosis
.
In addition, it needs to be distinguished from general brain atrophy.
When the brain is atrophy, the sulci-brain is widened, and when the hydrocephalus, the sulci is narrowed and disappears or is normal
.
In addition, the expansion of the third ventricle is not obvious
.
The expansion of the ventricle is more obvious .
The third ventricle enlarges more obviously when the brain shrinks
.
In the late stage, communicating hydrocephalus appears and the entire ventricular system is generally enlarged and the sulci is normal or narrowed and disappeared
.
thrombus

 

 

2.
Normal pressure hydrocephalus 2.
Normal pressure hydrocephalus

 

In fact, it is a special type of communicating hydrocephalus.
Also known as occult hydrocephalus, low-position hydrocephalus or chronic communicating hydrocephalus
.
The reason for normal cerebrospinal fluid pressure may be due to the decrease in the compensatory secretion of cerebrospinal fluid and the strengthening of absorption, which makes the pressure of cerebrospinal fluid in a relatively normal state; ②the absorption of cerebrospinal fluid through the ependyma
.
Keep the cerebrospinal fluid pressure constant; ③The tension of the brain parenchyma is reduced
.
Normal pressure hydrocephalus may be caused by occult subarachnoid hemorrhage or infection.
It may also be secondary to other brain diseases
.
Including subarachnoid hemorrhage, traumatic brain injury, inflammation, adhesions after brain surgery
.
Normal pressure hydrocephalus is common after 50 years of age
.
The clinical manifestations are actually the manifestations of chronic communicating hydrocephalus plus brain atrophy.
Its typical clinical manifestations are dementia, abnormal gait and incontinence, which are progressively worsening
.
A few cases also have limbs and transient disturbance of consciousness
.
CT and MR examination showed general ventricle enlargement, but the sulci did not narrow or disappear
.
Or it may show widening of sulci and brain fissure, which is difficult to distinguish from brain atrophy
.
Normal pressure hydrocephalus can also only show brain atrophy without ventricular enlargement.
Therefore, when the clinical symptoms are typical, only brain atrophy can not exclude the diagnosis of normal pressure hydrocephalus

In fact, it is a special type of communicating hydrocephalus.
Also known as occult hydrocephalus, low-position hydrocephalus or chronic communicating hydrocephalus
.
The reason for normal cerebrospinal fluid pressure may be due to the decrease in the compensatory secretion of cerebrospinal fluid and the strengthening of absorption, which makes the pressure of cerebrospinal fluid in a relatively normal state; ②the absorption of cerebrospinal fluid through the ependyma
.
Keep the cerebrospinal fluid pressure constant; ③The tension of the brain parenchyma is reduced
.
Normal pressure hydrocephalus may be caused by occult subarachnoid hemorrhage or infection.
It may also be secondary to other brain diseases
.
Including subarachnoid hemorrhage, traumatic brain injury, inflammation, adhesions after brain surgery
.
Normal pressure hydrocephalus is common after 50 years of age
.
The clinical manifestations are actually the manifestations of chronic communicating hydrocephalus plus brain atrophy.
Its typical clinical manifestations are dementia, abnormal gait and incontinence, which are progressively worsening
.
A few cases also have limbs and transient disturbance of consciousness
.
CT and MR examination showed general ventricle enlargement, but the sulci did not narrow or disappear
.
Or it may show widening of sulci and brain fissure, which is difficult to distinguish from brain atrophy
.
Normal pressure hydrocephalus can also only show brain atrophy without ventricular enlargement.
Therefore, when the clinical symptoms are typical, only brain atrophy can not exclude the diagnosis of normal pressure hydrocephalus

 

 

3.
Obstruction of the outlet of the fourth ventricle 3.
Obstruction of the outlet of the fourth ventricle

 

The simple fourth ventricle outlet obstruction is mostly caused by adhesions
.
It is clinically rare
.
After adhesion, obstructive hydrocephalus is caused, and all ventricles are enlarged, but the enlargement of the fourth ventricle is usually the most significant, and it is often difficult to distinguish from a cyst in the fourth ventricle
.
The most effective way to identify is to perform an anaphoric CT examination of the ventricle.
If it is a cyst, it appears as a round filling defect in the fourth ventricle.
When the outlet of the fourth ventricle is blocked, the fourth ventricle is filled with cerebrospinal fluid.

The simple fourth ventricle outlet obstruction is mostly caused by adhesions
.
It is clinically rare
.
After adhesion, obstructive hydrocephalus is caused, and all ventricles are enlarged, but the enlargement of the fourth ventricle is usually the most significant, and it is often difficult to distinguish from a cyst in the fourth ventricle
.
The most effective way to identify is to perform an anaphoric CT examination of the ventricle.
If it is a cyst, it appears as a round filling defect in the fourth ventricle.
When the outlet of the fourth ventricle is blocked, the fourth ventricle is filled with cerebrospinal fluid.

 

 

4.
Dandy-Walker's syndrome 4.
Dandy-Walker's syndrome

 

Also known as congenital atresia of the lateral foramen in the fourth ventricle
.
In the early embryonic stage, the median foramen and lateral foramen of the fourth ventricle are blocked, resulting in cystic expansion of the fourth ventricle, accompanied by dysplasia of the cerebellar vermis and hemisphere.
The expanded fourth ventricle develops backward and connects with the cistern major The posterior fossa is enlarged and the tentorium is raised
.
Hydrocephalus in this disease is usually seen in infancy, or exists after birth, but does not develop until adulthood
.

Also known as congenital atresia of the lateral foramen in the fourth ventricle
.
In the early embryonic stage, the median foramen and lateral foramen of the fourth ventricle are blocked, resulting in cystic expansion of the fourth ventricle, accompanied by dysplasia of the cerebellar vermis and hemisphere.
The expanded fourth ventricle develops backward and connects with the cistern major The posterior fossa is enlarged and the tentorium is raised
.
Hydrocephalus in this disease is usually seen in infancy, or exists after birth, but does not develop until adulthood
.

 

 

5.
Cysts in the fourth ventricle 5.
Cysts in the fourth ventricle

 

Fourth ventricle cyst can cause obstruction and enlargement of the entire ventricular system
.

Fourth ventricle cyst can cause obstruction and enlargement of the entire ventricular system
.

 

 

6.
Isolated fourth ventricle 6.
Isolated fourth ventricle

 

When the aqueduct and the fourth ventricle outlet are severely narrowed or completely blocked, the fourth ventricle is isolated.
This situation is called isolated fourth ventricle
.

When the aqueduct and the fourth ventricle outlet are severely narrowed or completely blocked, the fourth ventricle is isolated.
This situation is called isolated fourth ventricle
.

 

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