Causes and clinical features of stroke

Stroke is a clinically defined syndrome

Stroke is not a single disease, but is caused

Transient ischemic attack (TIA) and stroke are defined

TIA is traditionally defined as a transient episode of focal neurologic deficits unrelated to permanent cerebral infarction lasting less than 24 hours

However, these definitions now have little significance in clinical practice for the following reasons: First, the treatment of stroke is time-sensitive and needs to be started as soon as possible after diagnosis; Second, the 24-hour time boundary is arbitrary

Classification of strokes

According to the TOAST classification system, stroke can be defined as 5 subtypes, including:

(1) Aortherosclerotic type;

(2) Cardiogenic embolic type;

(3) Small blood vessel occlusive type;

(4) Other stroke types that determine the cause;

(5) Stroke type with unknown etiology

Risk factors for stroke

Unchangeable risk factors:

This includes age, sex, ethnicity, and genetic factors

➤ Age: The most important factor

➤ Gender: Premenopausal women have the same or higher

Modifiable risk factors:

➤ High blood pressure: This is the most important modifiable risk factor

➤ Diabetes: an independent risk factor

➤ Cardiogenic factors: Myocardial infarction (mainly from atrial fibrillation (AF)) is the most severe subtype of ischemic stroke, with a high disability rate and mortality

➤ Smoking: Double

➤ Hyperlipidemia: The relationship between dyslipidemia and stroke is complex

➤ Alcohol consumption and substance abuse: Mild and moderate alcohol consumption (< 4 U/day) has been reported to be associated with a reduced risk of ischemic stroke, while larger amounts of alcohol consumption are significantly associated

➤ Obesity and sedentary behavior: Much of the effect of BMI on stroke risk is mediated by blood pressure, cholesterol and glucose concentrations

➤ Inflammation: Elevated inflammatory biomarkers are associated with an increased risk of arteriosclerosis and stroke

Pathogenesis of stroke

➤ Youth stroke: About 10%-15% of strokes occur in
adults aged 25-49 years.
Extracranial carotid or vertebral artery dissection is a common and important cause
.

➤ Ischemic stroke: Approximately 85% of strokes are ischemic strokes, mainly caused
by cerebral small vessel disease (CSVD), cardiac embolism, and aortic disease (atherosclerosis).

➤ Cerebral small angiopathy: CSVD includes deep perforated branch artery disease (also known as arteriolosclerosis or hypertensive arterial disease) and cerebral amyloid vascular disease (CAA
).
Deep penetrating branched arteriopathy affects the structure and function of the small blood vessels supplying the basal ganglia and brainstem, resulting in approximately 25% of ischemic strokes, 80% of non-traumatic intracranial hemorrhages, and about 45% of dementia (see Figure 1a
).
CSVD is diagnosed on the basis of imaging, including: recent small infarction under the cortex, white matter hyperintensity, cavity space, cerebral microhemorrhage, enlargement of the perivascular space, and brain atrophy on MRI; or white matter low density and CT-shown cavities
.
Its prevalence increases with age, there is no difference between sexes, and it may be higher
in Asian populations.
The most important risk factor for CSVD is high blood pressure
.

➤ Cardiogenic stroke: 25% of ischemic strokes are caused by cardioembolism (mainly AF), the risk of which increases
with age.
Paroxysmal AF is more common
than persistent AF in stroke patients.

➤ Aortic disease: About 20% of ischemic strokes are caused by narrowing or occlusion of the aorta cerebral arteries (mainly extracranial carotid arteries) (see Figure 1b).

Arteriosclerosis plaque rupture leads to in situ thrombosis and distal embolism
.
In addition, rupture of carotid artery plaques leads to extensive activation of platelets and recurrent events are very common
.

➤ Cryptogenic stroke: In 20% to 30% of patients with ischemic stroke, no cause
is found.
These strokes may be associated
with undiagnosed cardioembolic disease, hypercoagulable state, abnormal embolism due to aperture ovale, substenosis atherosclerotic disease, nonatherosclerotic arterial disease, insidious recreational drug use, or undiagnosed genetic disorders or risks.

Figure 1(a) Axial diffusion-weighted MRI shows acute subcortical microinfarction of white matter in the center of the right hemisphere with small-vessel occlusion (red arrow).

(b) CT angiography shows carotid artery stenosis (red arrows)
≥ 95%.
(c) Non-enhanced axial CT of the brain shows acute thrombosis of the right middle cerebral artery ("high-density MCA sign", red arrow).

(d) Causes acute infarction, showing a high signal on the brain axial diffusion weighted MRI, indicating limited
diffusion.

➤ Intracerebral hemorrhage (ICH): Spontaneous (non-traumatic) ICH can be anatomically divided into deep cerebral hemorrhage and lobar hemorrhage (see Figure 2
).
Deep cerebral hemorrhage accounts for about 2/3 of ICH cases, mostly in basal ganglia and inner capsule (35% to 70%) or brainstem (5% to 10%)
.
Approximately 5% to 10% of the ICH is located in the cerebellum and the rest is lobe cortico-inferior cortex, often approaching or reaching the convex surface of the
brain.
Hypertension (deep puncture) arterial disease (CSVD) is the most important cause of deep cerebral hemorrhage, but it also causes lobar hemorrhage
.

Figure 2(a) shows deep cerebral bleeding
in the basal ganglion region.
(b) Shows venous hemorrhagic infarction in the right temporomopex-parietal region
.
(c) Shows lobar hemorrhage, superficial hemosiderin staining in and around the sulcus (superficial hemosiderosis cortex, blue arrow), and strictly lobar parenchymal microhemorrhage (red arrow), consistent
with CAA.