Clinical Features of Acute Cerebral Infarction Head MRI "Super Interpretation" Phase 2

*Only for medical professionals to read and refer to epic lectures, the content is detailed and recommended for collection! The 2nd Huashan International Forum on Cognitive and Brain Diseases and the 15th China Neurology Forum kick-off meeting was a complete success online from August 5th to 6th, 2021.
The forum was from the First Affiliated Hospital of China Medical University.
Professor Zhiyi He from the Department of Internal Medicine shared a wonderful lecture on the topic of "Clinical Features of Acute Cerebral Infarction Head MRI"
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Due to the large content, the article is divided into multiple issues.
In the last issue, we talked about the infarction of the important branch blood supply area of ​​the internal carotid artery.
This issue brings the second part-the vertebrobasilar artery and its branch blood supply area infarction, one Get up and enjoy! Vertebral-basilar artery and its branch blood supply area infarcted basilar arteries include the median parapontine artery, the anterior inferior cerebellar artery, and the posterior cerebral artery; the vertebral arteries include the posterior inferior cerebellar artery and the anterior spinal artery
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 1.
Basilar artery apex syndrome [Case 1] A 50-year-old male patient was admitted to the hospital with a main complaint of "9 hours of unconsciousness"
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Physical examination: unconsciousness, bilateral pupils of equal size, diameter ≈4.
5mm, loss of light reflection, no response to orbital pressure, immobilization of limbs, Babinski sign (L: +, R: +)
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1~5: CT shows bilateral thalamus and bilateral midbrain symmetrical low-density lesions, MRI shows long T1 and long T2 signal shadows; the lesions are shown by yellow arrows
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6: In this case, the pupils are dilated
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7: A model diagram of typical bilateral thalamus involvement in basilar artery apex syndrome
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[Clinical diagnosis] Cerebral infarction (basal artery tip syndrome)
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[Case 2] A 28-year-old female patient was admitted to the hospital with "dizziness for half a month, aggravated with left-side limb dysfunction for 3 days" as the main complaint
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Half a month ago, the patient had sudden dizziness, tinnitus, and a cold.
He did not get better after taking the cold treatment.
Three days ago, he developed eye crookedness and left limb movement problems.
At the same time, he found that he could not speak.
He has been conscious since the onset of illness
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Physical examination: clear mind, slurred speech, unequal pupils, diameter on the right ≈3.
0mm, diameter on the left ≈2.
0mm, drooping right eyelid, both eyes cannot look up or down, and left eye cannot be abducted at the same time There is nystagmus, the right eye is externally oblique, the right eye cannot be adducted, the left side is facial paralysis, the tongue is in the middle, the right limb muscle strength is grade IV, the left limb muscle strength is grade 0, Babinski sign (L: +, R: -), I feel that the physical examination cannot cooperate
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A plain cranial MRI scan showed multiple long T2 lesions in the right thalamus, left cerebellum, and midbrain, as shown by the yellow arrow
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[Clinical diagnosis] Cerebral infarction (basal artery tip syndrome)
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[Explanation] The top of the basilar syndrome (TOBS) is caused by various causes of the cross of 5 blood vessels (bilateral posterior cerebral arteries, bilateral superior cerebellar arteries, and basilar arteries) centered on the top of the basilar artery A group of clinical syndromes mainly caused by damage to the thalamus, midbrain, cerebellum, and occipitotemporal lobes caused by blood circulation disorders
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When the apex of the basilar artery is occluded, there may be eye movement disorders and pupil abnormalities, transient or continuous disturbance of consciousness for several days, contralateral hemianopia or cortical blindness, and severe memory impairment
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CT or MRI of the brain showed lesions in more than two parts of the occipital lobes, medial temporal lobes, thalamus, cerebellum, and midbrain, suggesting TOBS
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Symmetric butterfly-shaped lesions in the bilateral thalamus and/or lesions near the midbrain midline are more characteristic
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 2.
Infarction of the blood supply area of ​​the posterior cerebral artery [Case 1] A 72-year-old female patient was admitted to the hospital with a chief complaint of "headache for 5 days, aggravated with left limb inactivity for 14 hours"
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History of present illness: The patient had headache, nausea but did not vomit, fecal incontinence, unconsciousness, and limb dysfunction 5 days ago
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The left side limb was not able to move well 14 hours ago
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Physical examination: clear mind, slurred speech, large perfect circle with double pupils, diameter 2.
5mm, sensitive light response
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The movement of the eyes in all directions is limited, and there is no nystagmus
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The nasolabial fold on the left is shallow and the tongue is in the middle
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The muscle tone of the left limb is reduced and the muscle strength is normal
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BCR (L: +, R: +), PSR (L+, R: +), Babinski sign (L: +, R: -)
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The left face and limbs have decreased superficial sensation, and deep sensory disturbance
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Cranial MRI showed the temporal and occipital T2 hyperintensity lesions in the blood supply area of ​​the right posterior cerebral artery, as shown by the yellow arrow
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[Clinical diagnosis] Infarction of the blood supply area of ​​the posterior cerebral artery
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[Case 2] A 34-year-old male patient was admitted to the hospital with "intermittent headache, head obsessed for 3 months, and paroxysmal convulsions for 3 days" as the main complaint
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The
patient has experienced headaches, head obsessive and other non-specific symptoms since December 2012, 2013 Poor sleep started in January of 2008.
From February 15th, his family complained of slow response.
CT of the brain showed lesions in the anterior horn of the right lateral ventricle
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Fatigue and limb weakness appeared in mid-March, and the above symptoms gradually aggravated.
Brain MRI was performed It shows long T1 and long T2 signal shadows in the right frontal lobe
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On March 23, the patient's fatigue and weakness of the limbs increased.
MRS on the brain showed that the space-occupying lesions of the anterior horn of the right lateral ventricle could not be excluded.
The electroencephalogram showed mild abnormalities.
EEG
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When the patient went to the toilet on March 27.
There was a sudden twitch, and his consciousness became clear after 20 seconds
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He convulsed again on March 29 and was admitted to the hospital for systematic diagnosis and treatment
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Past history: Denies the history of hypertension, coronary heart disease, diabetes and other diseases
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Admission to the hospital for physical examination: drowsiness, cooperative physical examination, double pupils are equal in size, diameter ≈3.
0mm, and sensitive to light
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Speech and pronunciation are normal
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The cranial nerve examination showed no obvious abnormalities
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Extremities muscle strength is V grade, muscle tension and tendon reflex are normal, Babinski sign (L:-, R:-)
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There was no definite abnormality in the physical examination of deep and shallow sensation and mutual aid movement
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The patient had several seizures on the second day of admission, and each time lasted for a few seconds to relieve.
After the seizures on the third day, she was unconscious, and the muscle strength of both lower limbs and left upper limb was grade Ⅱ, and the muscle strength of right upper limb was grade Ⅰ
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The pupil is equal to a perfect circle, with a diameter of ≈3.
0mm, a light response is present, and the Babinski sign (L:-, R:-)
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On April 1, the patient suddenly had pupils of unequal size, with a diameter of ≈4.
0mm on the left side and ≈2.
5mm on the right side.
The photoreaction was slow, and brain herniation was considered
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Re-examination of the cranial CT showed that the ventricular system was enlarged
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On the same day, he was transferred to neurosurgery for lateral ventricle drainage, which elicited colorless and clarified cerebrospinal fluid
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On the second day after the operation, the patient regained consciousness and could complete instructions such as tongue extension and handshake.
His pupils recovered to a perfect circle with a diameter of ≈3.
5mm.
The light response was present.
The distal muscle strength of the right upper limb was Ⅲ.
The distal muscle strength of the left upper limb Grade II, muscle strength of both lower limbs, Babinski sign (L: +, R: +)
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Re-examination of the brain MRI on April 3 showed that bilateral parieto-occipital cortex swelling showed large symmetrical long T1 and long T2 signals
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Craniocerebral MRA was performed on April 7: The distal lumen of the P2 segment of the bilateral posterior cerebral artery was significantly narrowed, and the beginning of the A3 segment of the bilateral anterior cerebral artery was significantly narrowed
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Craniocerebral MRV: The lumen of the transition between the left transverse sinus and the confluence of the sinus becomes thinner
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1~3: Brain CT (February 15) showed lesions in the anterior horn of the right lateral ventricle
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4~6: Brain MRI showed the right frontal lobe with long T1 and long T2 signal lesions, and DWI showed high signal with limited diffusion
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7~9: Brain CT (April 1) showed enlarged ventricular system
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10~12: Brain MRI (April 3) showed large symmetrical long T1 and long T2 signals in the bilateral parieto-occipital cortex; the lesion is shown by the yellow arrow
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13~15: Sudden brain MRI (April 3) showed bilateral occipital lobe and parietal FLAIR with hyperintensity, DWI showed diffusion-limited hyperintensity
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16: Craniocerebral MRV (April 7) showed that the lumen of the transitional part of the left transverse sinus and the confluence of the sinus became thinner
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17, 18: Craniocerebral MRA (April 7) showed obvious stenosis at the beginning of the A3 segment of the bilateral anterior cerebral artery, and obvious stenosis of the distal lumen of the P2 segment of the bilateral posterior cerebral artery
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19: Craniocerebral MRI+ enhancement (April 3): After enhancement, a patchy uneven light enhancement signal can be seen above the anterior horn of the right lateral ventricle
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20: Craniocerebral MRS (March 23) showed an increase in the CHO peak and a decrease in the NAA peak, and CHO/NAA suggested space-occupying lesions
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The lesion is shown by the yellow arrow
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[Clinical diagnosis] bilateral posterior cerebral artery infarction (bilateral occipital lobe infarction after tentorium notch hernia), hydrocephalus, and lesions in the anterior horn of the right lateral ventricle (high tumor possibility)
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[Explanation] The posterior cerebral artery (PCA) is the terminal branch of the basilar artery.
Later, the communicating artery is demarcated at the anastomosis point.
The posterior cerebral artery is divided into proximal and distal segments, but it gradually separates during the journey: (1) Central artery (including Thalamus perforation and thalamic genicular artery); (2) posterior choroidal artery; (3) posterior cerebral artery cortical branch, hippocampal branch, anterior inferior temporal artery, middle inferior temporal artery, posterior inferior temporal artery, talar artery and parietooccipital Arteries
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Clinical features: (1) Headache: It is often described as "severe", "burst-like" and "pulsating" headaches
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About 70% of headaches are located in the occipital, orbital or forehead
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(2) Visual symptoms: Co-directional visual field defect is the most common and characteristic symptom of PCA ischemia, and most hemianopia is complete.
Even upper quadrant blindness, isolated lower quadrant blindness is rare
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(3) Sensory and motor symptoms: sensory symptoms are second only to visual symptoms, manifested as paresthesias, and sometimes only appear on the hands and face
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Dyskinesia is mostly manifested as transient hemiplegia.
When it involves the thalamus, internal capsule, cerebral peduncle, and the midbrain area, persistent hemiplegia may occur
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Eye movement disorders are also more common
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(4) Sensory aphasia or named aphasia, aphasia and memory impairment without agraphia
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Summary of PCA blood supply schematic diagram The infarction of the posterior cerebral artery supply area is relatively rare in clinical practice.
Most patients have mild or even asymptomatic symptoms.
The common symptoms are headache and visual field defects.
The infarcts are often found in imaging examinations
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Clinically, patients with headache and visual symptoms as their main symptoms should consider the possibility of infarction in the blood supply area of ​​the posterior cerebral artery
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It is worth noting that tentorium cerebellar notch hernia can cause bilateral occipital lobe infarction.
Therefore, in clinical work, if you encounter patients with bilateral occipital lobe lesions after brain herniation, you should think that this is due to tentorium cerebellar notch.
Bilateral occipital infarction caused by hernia compressing bilateral posterior cerebral arteries
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Due to space limitations, the second issue ends here.
In the next issue, we will continue to talk about the other contents of the second part, including the two major mesencephalic infarction syndromes (Claude syndrome and Wernekink syndrome) and two types of pontine infarction As well as the infarction of the blood supply area of ​​the anterior and posterior inferior cerebellar arteries, the exciting continues, so stay tuned!