Cerebral watershed infarct (CWSI) is an infarct that occurs at the junction of two arterial blood supply areas in the brain and accounts for approximately 10% of all cerebral infarcts.
I. Typing
Precortical type: it is a watershed infarct in the blood supply area of the anterior and middle cerebral arteries; postcortical type: the lesion is located in the parietal, occipital and temporal junction area, and it is a watershed infarct between the middle and posterior cerebral arteries, or the cortical branches of the anterior, middle and posterior cerebral arteries; subcortical type: it is a watershed infarct between the cortical branches of the anterior, middle and posterior cerebral arteries and the deep penetrating branches, or the return branch of the anterior cerebral artery (Heubner artery) and the doublestem artery of the middle cerebral artery. The lesion is located in the deep white matter of the brain, the nucleus accumbens, and the caudate nucleus.
Etiology and pathogenesis
(I) Hemodynamic factors
Various causes of hypotension and reduced cardiac output can cause cerebral watershed infarction. Insufficient blood volume and severe episodic hypotension lead to a decrease in cerebral perfusion area, and the more distal the perfusion is, the lower it becomes, which eventually leads to ischemic necrosis of brain tissue in the cortical junctional area of peripheral blood supply, mostly bilateral infarction. The causes are syncope, shock, arrhythmia, cardiac arrest, cardiac surgery, and improper use of antihypertensive and paralytic drugs.
(II) Vascular wall factors
Watershed infarction can also occur when the cerebral vessels have pre-existing atherosclerotic stenosis or obstruction, and when the systemic blood pressure is too low. Mechanism: arterial stenosis and occlusion, when the arterial stenosis reaches 50% or more, if there is sufficient cerebral perfusion pressure and sufficient blood volume, ischemia may not occur. When the systemic blood pressure decreases, resulting in a decrease in the cerebral perfusion area, the blood supply barely maintained by the narrowed artery will be rapidly reduced, coupled with the hardening of the arterial wall auto-regulation mechanism and the infarction of the marginal zone of the blood supply area.
(C) Blood rheological factors
Erythrocytosis, patients with sickle cell aplasia, hyperfibrinogenemia, and thrombocytosis can all lead to watershed infarction.
III. Pathology
Watershed infarcts are superficial in the brain, mainly in the cortex, mostly involving the frontoparietal junction area or parieto-occipitotemporal junction area and subcortex. Typical watershed infarcts are triangular or wedge-shaped with the tip pointing toward the lateral ventricles and the low side facing the soft meninges, and some are striped parallel to the cortex.
Microscopically, neuronal cell loss was seen, especially in the third layer of the cortex, and fibrous tissue filling was seen in the vessels of fresh lesions, with occasional phagocytosis. Glial hyperplasia was seen at the margins. Granular brain atrophy is seen in advanced stages.
Typical lesions are wedge-shaped or striped parallel to the cortex, and mildly impaired lesions may be clustered, sometimes coexisting with old and new lesions.
IV. Clinical manifestations
Most of them occur in 50-69 years old, slightly more males than females, mostly with a history of recurrent hypotension or hypertensive patients with acute drug hypotension and blood pressure drop greater than 25%, some patients have a history of heart disease and cardiac insufficiency, and there may be a history of transient ischemic attack before the onset of the disease.
(A) Pre-cortical type lesion between the anterior and middle cerebral artery cortical branch blood supply area, involving the frontoparietal lobe
1. Motor disorders In addition to the face, contralateral hemiplegia is present, with the upper limbs predominant.
2. Sensory impairment About 50% of the patients have hemiplegia.
3.Language disorder The dominant hemisphere lesion can appear transcortical motor aphasia, which shows good repetition, telegraphic language, and poor fluency.
4.Intelligence and emotion disorder: the performance of calculation, comprehension, judgment and memory is reduced, and the emotion is indifferent and unmotivated.
5, syncope and seizures Epilepsy is mostly partial seizures, or manifested as Jacksow seizures.
6. Bilateral lesions manifest as quadriplegia (no facial palsy).
(II) Postcortical type
1, typical manifestation is hemianopsia, which can be quadrant, the lower quadrant is the most obvious, with macular avoidance phenomenon.
2. Sensory impairment Cortical hemianopsia, two-point discrimination, graphic perception, form perception and weight perception impairment.
3.Speech disorder The dominant hemisphere is damaged with transcortical sensory aphasia, naming aphasia, dysarthria, emotional euphoria, hyperphonia, hyperactivity.
4.Cerstmann syndrome Damage to the superior gyrus and adjacent areas of the angular gyrus of the dominant hemisphere, manifesting as left-right loss of recognition, finger loss of recognition, loss of writing and inability to calculate.
5.Body image disorder Non-dominant hemisphere damage may have spatial orientation disorder and disease sense deficit.
6. Light hemiparesis of the contralateral limb.
7. Bilateral lesions may manifest as mental gaze paralysis, spatial attention deficit and visual loss.
(C) Subcortical type
1.Mild hemiparesis
2. About 5% of the patients have hemianesthesia.
3. Damage to the dominant hemisphere may lead to motor aphasia.
V. Auxiliary examinations
(I) Cranial CT
Typical posterior cortical watershed infarcts are wedge-shaped with the tip facing the lateral ventricles, and anterior cortical watershed infarcts are distributed in the frontoparietal lobe. The subcortical infarcts appear as strips of hypodense areas parallel to the cortex, located in the parietal ventricular radiocoronal area, and sometimes the hypodense foci in the basal ganglia may be patchy or irregular.
(II) MRI
MRI can show typical long T1 and long T2 abnormal signal areas within 3 hours of onset.
(C) Angiography
It can clearly show occlusion or obvious stenosis at the end of two adjacent vessels, and the infarcted area is not visualized, but emboli rarely occur.
(iv)Other examinations
EEG may have limited slow waves. SPECT and PET may reveal a decrease in local blood flow (rCBF) and an increase in oxygen consumption (CMRO2). Cerebrospinal fluid examination often has no abnormal findings.
VI. Diagnosis
Acute onset, history of episodic hypotension or long-term hypertensive patients with blood pressure dropping more than 25% in a short period of time, or aphasia, dyscognition, loss of use, mild paraplegia, and sensory impairment after a drastic decrease in blood volume. typical wedge or strip-shaped hypointense area on cranial CT, wedge-shaped area or strip-shaped shadow with long T1 low signal and long T2 high signal on MRI. no shadow in the infarcted area on DSA. SPECT and PET can reveal a local decrease in rCBF and an increase in CMRO2 to make the diagnosis.
VII. Prognosis and prevention
Prognosis: Most of the watershed infarcts have a good prognosis after timely treatment, and the motor function of the limbs is often recovered quickly and completely.
Prevention: treatment of heart disease and arrhythmia, prevention of episodic hypotension, slow and moderate antihypertensive treatment for hypertension; timely hemostasis and blood volume replenishment, active treatment of atherosclerosis and primary diseases such as diabetes, hyperlipidemia, hyperviscosity, hyperlipidemia, etc.; surgical treatment is feasible for severe stenosis of the extracranial segment of the internal carotid artery or the beginning segment of the vertebral artery.
VIII. Treatment
The principle of treatment for watershed infarction is roughly the same as that for thrombotic cerebral infarction. At the same time, attention should be paid to etiological treatment, such as correction of hypotension, treatment of shock, replenishment of blood volume, and treatment of cardiac disorders and internal carotid artery lesions.