This cerebral infarction is characteristic: a case of acute symmetric cerebellar mid-foot infarction

Case review

A 61-year-old man was admitted to the hospital for "slurred speech and weakness of the
left limb for more than 20 days".
Patients present with deafness, slurred speech, and dizziness that prevents them from opening their eyes
.
History of hypertension, diabetes, atrial fibrillation, and heavy smoking and drinking
.

physical examination

Blood pressure 134/95mmHg
.
Clear consciousness, poor spirit; Lack of clarity and fluency in speech; The bilateral pupils are not equal in size, with a diameter of about 3mm on the left side and a diameter of about 4mm on the right, with sensitive direct and indirect light reflections, no drooping eyelids, flexible movement of bilateral eyeballs in all directions, and no nystagmus in both eyes; Bilateral nasolabial folds are symmetrical, tongue extension, teeth, gills, etc.
cannot cooperate; Hearing loss
in both ears is marked.
Sensory system checks are uncooperative
.

Right limb muscle strength grade IV.
, left limb muscle strength grade III.
, normal muscle tone, limb tendon reflexes (+++), bilateral Babinski sign, Chaddock sign (+), meningeal irritation sign (-), inability to cooperate with the rest of the nervous system physical examination
.

Imaging tests

Diffusion-weighted imaging (DWI) of head MRI 2 weeks before admission showed symmetrical hyperintensity in the feet of the bilateral cerebellum (Figure 1a); MR angiography (MRA) showed no visualization of the right vertebral artery, severe stenosis or occlusion from the distal left vertebral artery to the beginning of the basilar artery, bilateral inferior cerebellar anterior artery and bilateral posterior cerebral artery, but the left posterior cerebral artery was significantly slender (Figure 1b).

On the 6th day of admission, the whole brain DSA showed complete occlusion of the right vertebral artery, diffuse severe stenosis from the V4 segment of the left vertebral artery to the proximal end of the basilar artery, good visualization of bilateral inferior anterior cerebellar artery, moderate stenosis at the beginning of the right inferior cerebellar artery, and no obvious abnormalities in the bilateral superior cerebellar artery and posterior cerebral artery (Fig.
1c).

The course of treatment

After the onset of the disease, patients were given risk factor control, oral bispecific antibody (aspirin 100mg + clopidogrel 75mg, once / day), antiplatelet aggregation therapy (edaravone 30mg intravenous drip, once / day), oxygen free radical scavenging and symptomatic supportive therapy
.

After the condition is stabilized, stenting of stenosis arteries is performed, the stenosis is basically relieved after the stent is released, the intracranial vascular imaging is better than before, and after 20 minutes of observation, the stenosis is basically gone, the stent placement position is ideal, the adhesion is good, and the distal blood flow is smooth (Figure 1d).

After surgery, tilofiban sodium chloride hydrochloride injection (100ml, 10ml/min pumped)
was given.
The patient's condition improved, and he still had symptoms of ataxia such as deafness and restlessness at the time of discharge
.
Patients were discharged from hospital with oral bispecific antibodies (aspirin 100 mg + clopidogrel 75 mg once daily) and rosuvastatin (10 mg once daily).

After 6 months, the patient was admitted to the hospital for reexamination of the whole brain DSA, and the patient's hearing, ataxia, and limb weakness improved significantly compared with before, but there was still hearing loss in both ears and bilateral ataxia, and it was difficult to close his eyes, and there were no obvious abnormalities
in the other nervous system physical examination.
Whole brain DSA was re-examined 6 months after stent placement, showing no obvious abnormalities at the stent placement site and other cerebral vessels (Figure 1e).

discuss

The middle cerebellar peduncle (MCP), also known as the pontine arm, is an important structure connecting the cerebellum and the pons, and the blood supply comes mainly from the anterior inferior cerebellar artery (AICA) and partly from the superior cerebellar artery
.
Therefore, MCP belongs to the watershed region
between AICA and the superior cerebellar artery.

AICA usually begins distal to the basilar artery, about 75% of patients start in the lower 1/3 of the basilar artery, and then divide into proximal and lateral branches, the proximal branch supplies the lateral pons, and then divides into two branches, one along the surface of the middle of the cerebellar hemisphere and anastomoses with the posterior inferior cerebellar artery, supplying the anterior lower part of the cerebellar hemisphere, including the pom-pom and its adjacent tissues; The other arteriole supplies MCP and the anterior inferior pontine.

Therefore, the blood supply range for AICA is MCP, lateral pons, and anterior inferior cerebellum
.

It has been suggested that MCP infarction is the core area of infarction in the AICA blood supply area, which is a characteristic manifestation
on the image.
Adams described the first isolated case of AICA infarction in 1943 as rotational dizziness, vomiting, tinnitus, and dysarthria, ipsilateral dysreparation of infarction, facial paralysis, sensory disturbance in the trigeminal nerve distribution, Horner syndrome, and pain and temperature disturbance on the contralateral side of the infarction
.
This description later became known as the classic AICA syndrome
.

Some scholars divide it into complete and incomplete AICA syndrome
according to symptoms.
The presence of vertigo, ataxia, peripheral facial paralysis, and ipsilateral hearing loss (with or without other symptoms) suggests complete AICA syndrome
.

This patient has vertigo, nausea, vomiting, ataxia, dysarthria, and bilateral hearing impairment, consistent with complete AICA syndrome
.
Patients develop severe deafness, which may be due to cranial nerve VIII injury, which may be caused by the fact that most of the internal auditory arteries originate from AICA, and as the only artery supplying the inner ear, there is a lack of collateral circulation, and when AICA is affected, deafness and tinnitus symptoms
occur.

MCP infarction is mostly caused
by basilar atherosclerosis or thrombosis based on atherosclerosis.
The mechanisms that cause bilateral MCP infarction may be:

(1) Occlusion of one vertebral artery with severe stenosis of the other vertebral artery, bilateral vertebral artery blockage or severe stenosis; Low perfusion in the watershed zone may also be the mechanism
leading to MCP infarction.

(2) Arterial-derived emboli coincidentally enter bilateral AICA at the same time, resulting in bilateral MCP infarction
.

The patient had a pons pointate infarction and a history of atrial fibrillation, and the possibility of MCP infarction due to cardiogenic embolism could not be ruled out, unfortunately cardiac ultrasound was not performed on this patient
.
Symmetric MCP lesions can also be seen in other diseases, such as neurodegeneration, metabolic diseases, demyelinating and inflammatory diseases, tumors, extrapontine myelinolysis, Waller degeneration, toluene poisoning, etc
.

Most symmetric MCP infarcts occur on the basis of vertebrobasilar artery stenosis, and their treatment is mainly anticoagulation, antiplatelet aggregation therapy and risk factor
control.
With the development of endovascular interventional therapy, intra-arterial stenting has become an important treatment method
to solve arterial stenosis from the vascular morphology.

In this case, the patient underwent stenting of a stent after exclusion of contraindications to intervention
.
After half a year of admission, the patient's condition improved significantly, the symptoms of ataxia and hearing impairment recovered significantly, and there was no obvious stenosis
on cerebral angiography.
Therefore, for patients with conditions and no obvious contraindications, stent placement can significantly improve the prognosis
of patients.