​Clinical features of acute cerebral infarction MRI, super complete summary

*Only for medical professionals to read, reference and suggest collections! On August 5-6, 2021, at the "Second Huashan International Forum on Cognitive and Brain Diseases and the 15th China Neurology Forum Launching Meeting", Professor Zhiyi He from the Department of Neurology, the First Affiliated Hospital of China Medical University, is for us A wonderful lecture on the topic of "Clinical Features of Acute Cerebral Infarction Head MRI" was shared
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Due to the large content, the article is divided into multiple issues, a total of 8 issues, this is the fifth issue
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Phase 1: The clinical features of acute cerebral infarction head MRI, super interpretation Phase 2: The clinical features of acute cerebral infarction head MRI "Super interpretation" Phase 2: The clinical features of acute cerebral infarction MRI, all Dry goods! Phase 4: MRI clinical features of acute cerebral infarction, super interpretation of this issue, we will bring you cortical watershed infarction, subcortical watershed infarction, cardiogenic cerebral embolism, cortical laminar necrosis, secondary to the pons Wallerian degeneration of the bilateral bridge arms of infarction and the two types of cross-neuronal degeneration, let's not say much, let's learn together! 01 A 56-year-old female patient with cortical watershed infarction was admitted to the hospital with the main complaint of "inoperable left limb for 3 days"
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Three days ago, there was no obvious cause for the patient's left side limbs to be unable to move suddenly, and he could not hold objects and walk strenuously
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In the local hospital, he was diagnosed and treated as "cerebral infarction", but the effect was not good, the symptoms gradually worsened, and he was admitted to the hospital
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Physical examination: Shenqing speaks sharply, the left nasolabial fold becomes shallow, and the tongue sticks out to the left
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The left upper limb muscle strength is grade 0, the left lower limb muscle strength is grade Ⅲ, and the right limb muscle strength is normal
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Pain in the upper and lower limbs on the left side is decreased, Babinski sign (L: +, R: -)
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Past history: 1 year of hypertension, 1 year of cerebral infarction, no sequelae
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Figure 11: Brain CT shows low-density shadows of the right temporal lobe
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2~4: Brain CT showed wedge-shaped low-density foci at the front and back of the body of the right lateral ventricle, with the tip facing the ventricle and the bottom facing the convex surface of the brain
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5: Cerebrovascular CTA showed that the right middle cerebral artery was unclear from the M1 segment, and the distal vascular branches disappeared
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The lesion is shown by the yellow arrow
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▎Explanation: Cerebral watershed infarction (CWI), also known as cerebral watershed infarction, or limbic zone infarction, refers to cerebral infarction that occurs at the junction of two or three major cerebral arteries
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The etiology and pathogenesis of CWI have been controversial
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Traditionally, systemic hypotension, hypovolemia, carotid artery stenosis or occlusion, microembolism, abnormal hemorheology, and anatomical variation of the posterior communicating artery are the main causes
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The subcortical type can involve the basal nucleus, internal capsule and lateral ventricle, etc.
, mainly hemiplegia and hemisensory disturbance
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The cerebellar type is mostly manifested as mild ataxia and disturbance of consciousness
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The diagnosis of this disease is not difficult.
The treatment is mainly based on volume expansion, anti-platelet aggregation, brain protection agents or thrombolysis, but it does not advocate lowering intracranial pressure and lowering blood pressure
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The prognosis is generally good
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02 A 74-year-old female patient with subcortical watershed infarction was admitted to the hospital with the main complaint of "inoperable right limbs for 3 days"
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Three days ago, the patient had no obvious cause for sudden inability to move right limbs and strenuous walking.
The above symptoms were progressively aggravated, with slurred speech, drooling, no headaches, no fascination, no coughing with drinking water, and no dysphagia
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Past history of hypertension
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Physical examination: Consciousness, poor dysarthria, double pupils with a large perfect circle, diameter ≈3.
0mm, sensitive light response, muscle strength of the right limb Ⅳ, Babinski sign (L: -, R: +)
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Figure 21, 2: Brain DWI: The center of the left half-oval is scattered with high-intensity restricted diffusion (shown by the yellow arrow), showing a "bead-like" lesion
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3: CTA of the cephalic vessel shows segmental stenosis of the left middle cerebral artery (shown by the yellow arrow), and occlusion of the right anterior cerebral artery (shown by the red arrow)
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▎Explanation: Subcortical watershed infarction is also called internal watershed infarction.
The infarct area is mainly located at the junction of the superficial perforating branch of the middle cerebral artery and the blood supply area of ​​the deep perforating branch of the middle cerebral artery, or the superficial perforating branch of the middle cerebral artery and The superficial perforating artery blood supply junction area of ​​the anterior cerebral artery, the infarction is located at the radial crown or semi-oval center near the lateral ventricle or the outer upper part of the lateral ventricle.
It is a cigar-shaped fusion lesion, or a chain or bead-like partial fusion lesion
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The main clinical manifestations are hemiplegia and cognitive impairment.
The dominant hemisphere disease may have language impairment
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In clinical work, if chain-like fusion lesions or bead-like partial fusion lesions are found near or above the lateral ventricle, the possibility of internal watershed infarction should be considered, and vascular examination should be performed as soon as possible
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Vascular examinations often indicate stenosis or occlusion of the internal carotid artery or middle cerebral artery
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03 A 55-year-old male patient with cardiogenic cerebral embolism was admitted to the hospital with the main complaint of "inoperable left limbs for 1 day"
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There was no obvious cause for the patient's left-side limb dysfunction 1 day ago, and he fell down on the stairs and was found by his family.
With slurred speech, his eyes were staring to the right without convulsions.

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No headaches, nausea, vomiting, unconscious disturbance
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No hemorrhagic foci were found in the CT scan of the brain at the local hospital
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Past history: More than 10 years of atrial fibrillation, self-administered Betaloc to control heart rhythm
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He had a history of hypertension for more than 10 years, his systolic blood pressure was up to 180mmHg, and he did not take antihypertensive drugs regularly
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Physical examination: Consciousness, slurred speech, eyes staring to the right
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The tongue is stretched to the right, left upper limb muscle strength is 0, left lower limb muscle strength is Ⅰ, right limb muscle strength is V, Babinski sign (L: +, R: -), left deep and shallow sensation is decreased
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Figure 3 Craniocerebral MRI T2WI right semi-oval center, paraventricular, right basal ganglia area and right temporal lobe light flaky and slightly longer T2 signal changes
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FLAIR showed hyperintensity changes in the center of the right half oval, paraventricular, right basal ganglia and right temporal lobe
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The lesion on the right side of the middle cerebral artery blood supply area on DWI showed high signal intensity with limited diffusion
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▎Explanation: The main points of diagnosis and treatment of cerebral embolism: 1) Most patients suddenly onset, focal neurological dysfunction quickly reaches a peak, which is the fastest onset and severe symptoms of stroke; 2) The source of emboli is divided into cardiogenic And non-cardiogenic, confirmed by physical examination, electrocardiogram, echocardiogram, etc.
; 3) Cerebral infarction is confirmed by cranial CT and MRI
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04 Cortical lamellar necrosis, a 56-year-old male patient, was admitted to the hospital with a chief complaint of "headache and blurred vision for 10 days"
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The patient had a sudden headache 10 days ago without any precipitating cause, which was a persistent right occipital pain, accompanied by blurred vision, nausea, and no vomiting
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There is no limb movement and fever due to illness
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Physical examination: clear and clear, double pupils are equal in size, diameter ≈3.
0mm, light response is sensitive
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The cranial nerve examination showed no abnormalities
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Extremity muscle strength is grade V, BCR (L: ++, R: ++), PSR (L: ++, R: ++), Babinski sign (L: -, R: -)
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There were no obvious abnormalities in the depth sensation and the physical examination of mutual aid movement
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Figure 4 "Three highs", 1, 2: MRI scan of the brain shows a short layered T1 signal in the right occipital lobe, and FLAIR shows a high signal (shown by the yellow arrow)
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3: Magnetic sensitivity (SWI) sequence shows the right occipital leaf-shaped high signal shadow (as shown by the yellow arrow)
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▎Explanation: Cortical laminar necrosis (CLN) can occur at different ages and can be seen in the central nervous system oxygen and (or) glucose uptake disorder caused by various reasons and genetic or acquired defects in brain energy metabolism
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The brain MRI features of lamellar cortical necrosis are T1 lamellar gyrus-like hyperintensity changes
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Due to the high signal on the T1 sequence, it needs to be distinguished from hemorrhagic cerebral infarction.
If it is difficult to distinguish clinically, the MRI SWI sequence can be perfected.
If the SWI shows increased cortical signal, cortical laminar necrosis can be considered
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05 A 52-year-old male patient with bilateral wallerian degeneration (WD) secondary to pontine infarction was admitted to the hospital with a main complaint of "slurred speech and unsteady walking for 1 week"
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One week ago, the patient developed slurred speech, unsteady walking, choking on drinking water, dizziness, nausea but no vomiting, no diplopia, and no tinnitus
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8 years of previous hypertension
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Physical examination: clear mind, slurred speech (articulation disorder), normal movement of both eyes in all directions, no nystagmus, bilateral eyelash signs (+), middle tongue extension, limb muscle strength grade IV, pain and positional examination Normal
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BCR (L: +++, R: +++), PSR (L: ++, R: ++), Hoffmann sign (L: -, R: -), Babinski sign (L: +, R: + ), the left finger nose, rotation is slightly awkward
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Figure 51~3: MRI of the brain shows the left pons long T1 and long T2 signals, without enhancement effect, it is an infarct (shown by the yellow arrow)
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4-9: Cranial MRI showed bilateral cerebellar midfoot long T1 and long T2 signals, FLAIR showed high signal, and it was a WD lesion (shown by the yellow arrow)
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10, 11: No enhancement effect is seen in the enhanced cranial MRI scan; 12: The left pontine infarct on the coronal T1-weighted image of the cranial MRI shows a deep low signal (old lesion), which is related to the bilateral midfoot of the cerebellum.
The lower signal is related, so it is called WD lesion
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▎Explanation: Brain neurons are composed of cell bodies, dendrites and axons
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When the cell body or axon is broken or hypoxic necrosis, the axon below the necrotic end will eccentrically collapse to the end.
This process of change is called WD
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After cerebral infarction occurs, the cortex or subcortical white matter in this part is necrotic due to ischemia, the connection between the pyramidal cells and their axons is severed, and the pyramidal tract loses its source of nutrition, and WD occurs
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After brain damage, there will be a pyramidal tract WD on the same side as the primary focus, and the clinical manifestations need to be distinguished from the weakness of the limbs caused by cerebral infarction
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Craniocerebral MRI is the first choice for the diagnosis of pyramidal tract WD.
For patients with a history of recurrent cerebral infarction, attention should be paid to distinguish new infarcts and pyramidal tract WD
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06 Trans-neuronal degeneration■ Case 1 of secondary hypertrophic degeneration of the olive nucleus after pons hemorrhage, a 44-year-old male, was admitted to the hospital with a complaint of "tremor of the limbs with head tremor for 2 months"
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The patient gradually developed limb tremor and head tremor since 2 months ago, as well as mouth numbness, limb numbness, awkward speech, unstable walking, and difficulty in controlling balance
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Physical examination: Clear, clumsy speech
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The left eyeball has poor adduction and abduction, and the right eye has poor adduction.
The vertical nystagmus of both eyes is obvious, the tongue is slightly deviated to the right, the limbs and head tremor are obvious when speaking, the muscle strength of the limbs is Ⅳ, and the muscle tension is normal
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Bilateral fingers and nose are not stable, rotation is awkward, bilateral heel knee and shin test is not stable, closed eyes are difficult to stand and cannot cooperate, the right side of the body acupuncture pain is reduced, and the right lower extremity has deep sensory disturbance
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Past history: 7 months ago, hemorrhage of the pons, poor muscle strength of the remaining limbs, ataxia, clumsy speech, and diplopia
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Figure 61, 2: Brain MRI pons long T1 and long T2 signals.
This lesion is an old lesion of pons hemorrhage 7 months before the onset
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3: The long T2 signal in the olive nucleus of the medulla oblongata is visible on both sides
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Case 2 is a 48-year-old male patient.
He was admitted to the hospital with the main complaint of "head fascination, double vision, and left limb shaking for more than 20 days"
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The patient developed head fascination, left limb shaking, and headache more than 20 days ago
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He did not dare to open his eyes because of the swaying vision .

Physical examination: insufficient adduction and abduction of the right eye, insufficient abduction of the left eye, floating eyes downward, central facial paralysis on the left side, middle tongue extension, muscle strength of the left limb Ⅲ, BCR (L: ++, R:++), PSR (L:++, R:++), Hoffmann’s sign (L:-, R:-), Babinski’s sign (L:-, R:-), pain and positional examination See exception
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Anamnesis: Hemorrhage in the pons 6 months ago, and the left side limb has poor muscle strength
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Figure 71: Brain CT shows the pons hemorrhage lesions in case 2 patients 6 months before the onset
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2, 3: Craniocerebral MR showed that the patient with this form showed a long 2 signal in the right medulla oblongata after the onset of this disease
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■ Case 3 female, 67 years old, with secondary hypertrophic olive degeneration after basal ganglia infarction
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He was admitted to the hospital with the main complaint of "walking instability for 2 years"
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Two years ago, the patient had unsteady walking without obvious inducement, and gradually worsened.
He did not dare to go up and downstairs, struggled to start, turn around, and sit down
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Physical examination: clear, clear language, physical examination cooperation
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The pupils are of equal size, D≈3.
0mm, and the light response is sensitive.
The eyes move fully in all directions without nystagmus
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Bilateral frontal lines and nasolabial folds are symmetrical, soft palate and uvula are in the center, uvula twitching (mandibular spasm) can be seen when opening the mouth, pharyngeal reflex is normal, and tongue extension is in the center
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Extremities muscle strength is V grade, extremities muscle tension is normal; extremities reflexes are normal
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Babinski sign (L:-, R:-)
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The finger-nose test was not stable bilaterally, and the knee-shin test was not stable bilaterally
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Figure 8 shows multiple spots around the left lateral ventricle with short T1 and long T2 signal shadows, and high signal on the FLATR sequence.
Figure 9 shows the long T2 signal in the medulla oblongata and the high signal in the Flair sequence (such as yellow arrows).
(Shown)▎Explanation: Hypertrophic lower olive nucleus degeneration is a trans-synaptic neuronal degeneration caused by damage to the dentate-red nucleus-olive nucleus circuit, and often secondary to brain stem or cerebellar injury Patients often have clinical manifestations such as palatine myocardial degeneration, nystagmus, diplopia, ataxia, and limb clonus.
Brain MRI can show T2-weighted high signal and T1-weighted low or other signals in the lower olive nucleus area
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At this point, this issue is over, and the next issue is even more exciting.
It will describe in detail the cerebral infarction caused by the embryonic posterior cerebral artery, so stay tuned!