One article to clarify: 16 kinds of basal ganglia lesions

*Only for medical professionals to read the reference diagnosis and differential diagnosis, clarify it in one article! Basal ganglia anatomy There are some gray matter masses embedded in the deep white matter of the cerebral hemisphere, called the basal ganglia.

The basal ganglia include caudate nucleus, lenticular nucleus, pleural nucleus and amygdala.

Because the head of the caudate nucleus is connected to the front end of the lenticular nucleus, the gray and white matter is staggered on the cross section, so the caudate nucleus and the lenticular nucleus are also called the striatum.

The basal ganglia are the most sensitive to harmful stimuli such as hypoxia, poisoning, infection, ischemia, and metabolic abnormalities.
Many diseases often cause changes in the basal ganglia first, or basal ganglia lesions are the main manifestations.

Therefore, the diagnosis and differential diagnosis of basal ganglia lesions are very important.

Figure 1: Schematic diagram of the basal ganglia 1.
Basal ganglia degeneration disease 1 Hepatolenticular degeneration (Wilson disease) Hepatolenticular degeneration, also known as Wilson's disease (Wilson), is an autosomal recessive inherited copper metabolism disorder The resulting cirrhosis of the liver and degenerative brain diseases dominated by the basal ganglia.

The clinical manifestations are progressively worsening extrapyramidal symptoms, liver cirrhosis, mental symptoms, renal dysfunction, and corneal pigment ring KF ring.

The imaging showed bilateral symmetry, and most of the head of the lenticular nucleus and caudate nucleus were affected.

The main brain stem is pontine and midbrain lesions, and cerebellar lesions are rare.

Symmetrical abnormal signals in the basal ganglia accompanied by brainstem lesions are Wilson's imaging features.

Figure 2: Hepatolenticular degeneration image 2 Subacute necrotizing encephalomyelopathy (Leigh syndrome) Leigh syndrome is a mitochondrial disease caused by abnormal ATP production in the respiratory chain.
Common symptoms include central hypotonia, eye Muscle paralysis, respiratory and bulbar dysfunction, ataxia.Imaging manifestations of bilateral symmetry T2/FLAIR hyperintensity: striatum (putamen> caudate nucleus> globus pallidus), periaqueductal gray matter, substantia nigra/hypothalamus, dorsal pons, and cerebellum.

Leigh syndrome is often accompanied by microbleeds, and low signal can be shown on the SWI sequence.

Bottom: A.
Axial T2WI shows high signal and slight swelling of the T2 lenticular nucleus on both sides.
Note that there are focal uninvolved tissues in the putamen, and uneven involvement is common.

B.
Cerebral foot T2 hyperintensity, this is another common part of Leigh syndrome involved.

Figure 3: Leigh syndrome image 3 Kearns-Sayre syndrome (KSS) is a type of mitochondrial encephalopathy, and its clinical manifestations include progressive extraocular muscle palsy, retinitis pigmentosa, and heart block.

CT plain scan showed that the bilateral basal ganglia were low-density and T2-weighted high-intensity.

Lesions can also be seen in the thalamus, dentate nucleus, cerebral white matter, and cerebellum.

Often accompanied by mild or severe generalized brain atrophy.

Calcification can occur in the basal ganglia or cerebellar hemisphere in the late stage.

Figure 4: KSS image 4 Nitrogen-containing wastes of liver diseases cause long-term toxic brain damage through the blood-brain barrier.
Acute hyperammonemia can cause bilateral basal ganglia, insular cortex, cingulate gyrus edema, T2WI long signal and DWI diffusion However, the imaging changes after liver transplantation are reversible.

Figure 5: Hyperammonemia brain imaging 5 Hypoglycemia imaging shows bilateral long signals in the cerebral cortex, hippocampus, and basal ganglia on T2WI.
Mild hypoglycemia is manifested as transient white matter abnormalities on MRI, including the corpus callosum pressure and internal Severe patients with cysts and radiation crowns may have diffuse gray matter abnormalities, and involvement of the basal ganglia may indicate a poor prognosis.

Figure 6: Hypoglycemic encephalopathy image 6 Wernicke encephalopathy is caused by vitamin B1 deficiency, or secondary to chronic alcoholism, gastrointestinal or hematological tumors, and the clinical manifestations are triad of changes in consciousness, eyeball dysfunction, and ataxia.

Imaging shows the symmetrical hyperintensity of the paramedian thalamus, the third ventricle, the caudate nucleus, and the putamen.

A hyperintensity area with unclear borders can be seen around the midbrain aqueduct.

Figure 7: Wernicke encephalopathy image 7 Carbon monoxide (CO) poisoning is manifested as acute cognitive impairment or coma after accidental exposure or suicide attempt, and delayed encephalopathy may occur.

Imaging manifestations: There is a tendency for globus pallidus to be involved.
A.
The schematic diagram shows the typical manifestations of CO poisoning encephalopathy.

The most commonly affected site is the bilateral globus pallidus, followed by the white matter of the cerebral hemispheres.

B.
FLAIR symmetrical globus pallidus hyperintensity, which is a typical manifestation of acute CO poisoning.

It is also accompanied by involvement of the posterior temporal cortex and hippocampus.

C.
DWI multifocal diffusion limitation.

D.
FLAIR bilateral hippocampus and symmetrical hyperintensity in the posterior temporal lobe.

Figure 8: CO poisoning image 8 Other poisonings, moldy sugarcane, sulfur dioxide, lead, toluene, cyanide and other poisonings often cause degeneration and necrosis of the basal ganglia as the main manifestations.

On CT scan, the bilateral basal ganglia showed low density and T2-weighted high signal.

It is more symmetrical, usually with globus pallidus changing.
In severe cases, the caudate nucleus can also be affected.

Diagnosis is mainly based on medical history.

2.
Basal ganglia inflammation disease 1 Creutzfeldt-Jakob disease prion-related diseases, manifested as rapidly progressive dementia, myoclonus and multifocal neurological dysfunction.

Imaging findings: T2 progressive hyperintensity in the basal ganglia, thalamus, and cerebral cortex.
Gray matter is significantly affected.
The caudate nucleus and putamen are more affected than the globus pallidus.

If the thalamus occipitalis is also affected, it will show a typical "hockey stick sign.
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Figure 9: CJD image 2 Viral encephalitis Viral encephalitis that invades the basal ganglia is often bilateral, but the shape of the bilateral lesions is often not symmetrical, and a few can be more symmetrical.

The lesions are often not limited to the basal ganglia, and often involve the basal ganglia and surrounding brain tissue at the same time.

Bottom: CT plain scan shows large slices, asymmetrical low density in the basal ganglia on both sides, with a space-occupying effect, and narrowing of the frontal angle of the lateral ventricle.

Figure 10: Viral encephalitis image 3 Hypoxic-ischemic encephalopathy Hypoxic-ischemic encephalopathy causes damage to most of the activation domains in the deep brain nuclei, brain stem, and cerebral cortex.

DWI can detect abnormal image changes at the earliest stage.

A.
DWI axis shows extensive hyperintensity related to cytotoxic edema of the entire cortex, subcortical white matter, and outer capsule.

B.
T2WI axis shows high signal intensity in the entire cortex, subcortical white matter and external capsule.

The gyri swells and the sulcus disappears.

Figure 11: Image of ischemic hypoxic encephalopathy III.
Basal ganglia vascular disease 1 Basal ganglia infarction The basal ganglia is the most common site of cerebrovascular diseases such as lacunar cerebral infarction, subcortical arteriosclerotic encephalopathy, multi-infarct dementia, etc.
.

In these diseases, the basal ganglia lesions are often relatively small, often appearing as multiple spots or patches, involving one or both sides of the basal ganglia and the surrounding white matter, and occasionally only one side of the caudate nucleus head and bean-shaped All or most of the nucleus.

Figure 12: Basal ganglia infarction image 2 Deep cerebral venous thrombosis Patients with deep venous thrombosis often have hypercoagulable factors, which are manifested as bilateral thalamus, internal capsule, basal ganglia and deep white matter involvement.
Hemorrhage transformation is more common.

A.
Axial schematic diagram showing bilateral internal cerebral vein (ICV) and rectal sinus thrombosis, and bleeding in the choroid plexus and thalamus.

Thalamus, basal ganglia, and deep white matter edema are common manifestations.

Linear white matter medullary veins may fill and strengthen.

B.
CT plain scan showed high density of ICV, compared with the surrounding white matter, bilateral thalamic edema, showing symmetrical isodense (normally high density).

Figure 13: Image of deep cerebral venous thrombosis IV.
Basal ganglia calcification Symmetrical calcification of the basal ganglia is more common, especially globus pallidus calcification.

Calcification can also be seen in the caudate nucleus, tunic and lateral thalamus.

Rarely, the cerebellar dentate nucleus and internal capsule are also affected.

1 Fahr’s disease Fahr’s disease is the most common basal ganglia calcification disease.
Due to hypoparathyroidism, calcium and other minerals are deposited in the basal ganglia, thalamus, dentate nucleus, and semi-oval center.
The symptoms are non-specific, including headaches, Dizziness, dyskinesia, syncope, seizures, etc.

Imaging findings: A.
T1 hyperintensity on the lateral occipital side of the thalamus is a characteristic sign of Fabry disease.

B.
CT plain scan showed calcification of the right caudate nucleus, bilateral putamen, and lateral thalamus.

Figure 14: Fahr disease image 2 Other calcifications Other basal ganglia calcification diseases can be seen in idiopathic calcification, familial calcification, some special white matter lesions, Down syndrome, etc.

5.
Increased iron deposits in the basal ganglia.
Neurodegenerative disease of iron deposits in brain tissue (NBIA) is a group of neurodegenerative diseases characterized by dystonia, paralysis agitans and spasticity.

Including pantothenate kinase-related neurodegenerative disease (PKAN) and infantile axon dystrophy (INAD).

1 Pantothenic acid kinase-related neurodegenerative disease (PKAN) axial T2WI lipid pressure MR showed typical PKAN imaging findings.

The low signal caused by the deposition of globular iron, accompanied by high signal in the center, the "tiger eye sign", is highly specific to PANK2 mutations.

Figure 15: PKNA image 2 Other NBIA axis T2WI showed bilateral hyposymmetry of globus pallidus, no "tiger eye sign".

Therefore it is other NBIA.

Figure 16: Other NBIA imaging references: 1.
"Central Nervous System CT and MRI Image Interpretation", edited by Quanguan Democracy, People's Medical Publishing House 2.
Lou Xin compiled "Neuroimaging", Peking University Medical Press 3.
Yubo "Central Nervous System CT and MR Differential Diagnosis" edited by Lang, Shaanxi Science and Technology Press