Watch out!

The patient was a 55-year-old female admitted to the hospital with "dizziness and weakness of the right limb for 7 hours". She had a previous history of hypertension. On examination: clear consciousness, slightly small right eye fissure, fluent speech, shallow right nasolabial fold, low angle of the right mouth, tongue extension in the center, right limb muscle strength grade 4, right limb hyperalgesia, right finger-nose test, alternating test, heel-knee-shin test were not stable.

The patient's condition progressed after admission, and 3 days later, the right muscle strength progressed to grade 0. The family was not satisfied with the treatment effect.

Case 2

A 65-year-old male was admitted to the hospital with slurred speech and left-sided limb immobility for 7.5 hours. He was physically fit in the past.

He woke up 7.5 hours ago with slurred speech and left-sided limb dyskinesia without headache and dizziness. He was given Aitongli intravenous thrombolysis in the emergency room, but his symptoms did not improve. He was admitted to the ward. On examination: BP 140/87 mmHg, clear consciousness, poor speech, shallow left nasolabial fold, left limb muscle strength grade 3, low muscle tone, positive left Babinski's sign.

After admission, the patient's symptoms progressed and the muscle strength of the left limb reached grade 0. The family was dissatisfied with the effect of thrombolysis and other treatments and was nagging.

Case 3

A 58-year-old male was admitted to the hospital with slurred speech and right-sided limb immobility for 7 hours. Previous blood pressure and blood glucose were abnormally elevated. On examination: BP 180/93 mmHg, clear consciousness, slurred speech, shallow right nasolabial fold, low right angle of mouth, right tongue extension, right upper limb muscle strength grade 3, right lower limb muscle strength grade 4, right Bartholin's sign (+).

The patient's symptoms also worsened after admission, and the muscle strength of the right limb progressed to grade 0.

Discussion

In the above three patients, the clinical presentation, site of lesion, evolution of disease and degree of disability are very consistent. Is it possible that infarcts in this part of the posterior radiological coronary are all prone to progression! It is indeed the case, see the highlighted font below.

--Posterior radiographic coronary infarction is an independent imaging presentation that predicts stroke progression.

Why are infarcts in this area prone to progression?

1. Responsible vessl - anterior choroidal artery

All three patients involved the posterior limb of the internal capsule and the posterior radiographic coronary. The responsible vessel is probably the anterior choroidal artery (AChA). The typical AChA infarction in the literature looks like this:

The posterior limb of the internal capsule is mostly supplied by the AChA, but sometimes the doublestem artery can also be involved, so that infarction of the posterior limb of the internal capsule alone does not necessarily originate from the AChA. if the posterior limb of the internal capsule is added to the lateral geniculate and medial temporal lobe hippocampal lesions, then the AChA can be identified.

The thin diameter and long stroke of the anterior choroidal artery are most susceptible to changes in cerebral blood flow. No wonder, recurrent stereotype-like TIAs often precede the onset of cerebral infarction, and after repeated episodes, half of the patients progress to internal capsule infarction, a process also known as internal capsule warning syndrome. Symptoms also frequently progress after the formation of cerebral infarction.

2. Mechanism - Hypoperfusion

Let us first review the bead-like lesions of internal watershed infarction and note the lesions in the posterior part of the radiological crown, which are very similar to the lesions in the three patients mentioned above.

It is presumed that the lesions in the three patients may also be associated with hypoperfusion. Look at the following watershed infarction due to occlusion of the left middle cerebral artery:

Again, a posterior radial coronary lesion due to hypoperfusion is seen. It can be assumed that this infarct foci in the posterior part of the radial corona, although not bead-like, are also likely to be due to hypoperfusion.

Based on these factors, the structural characteristics of the anterior choroidal artery, together with hypoperfusion, lead to such a clinical course: repeated stereotyped TIA - cerebral infarction - poor thrombolytic effect - progressive stroke - severe disability.

Therefore, when such a stroke is encountered, the family should be informed of the condition as early as possible, and the symptoms may worsen despite the aggressive treatment given.