Overview.
A watershed cerebral infarction, or watershed infarction (WI), is a cerebral infarction that occurs at the junction of two major arterial regions of the brain, most often in the larger arterial junction of the brain. It is also called marginal zone infarction because it is mainly located in the brain tissue in the marginal zone between the large cortical arteries and the small arteries in the basal nuclei.
Causes
The etiology of cerebral watershed infarction is not well understood, the following factors may be related to cerebral watershed infarction, such as episodic hypotension, carotid artery stenosis or occlusion, vascular microembolism hypoxemia, erythrocytosis, platelet function abnormality, etc. Especially episodic hypotension carotid artery stenosis or occlusion and vascular microembolism are more important, and may be the main causative factors.
Symptoms
Clinical signs and symptoms are more complex in people over 60 years old, and low blood pressure is common at the onset of the disease. General manifestations may include: impaired consciousness, speech disorders, motor aphasia, transcortical motor aphasia, naming aphasia, hemianopsia, motor deficits, sensory deficits, convulsions, mental retardation, psychiatric disorders, personality changes, and positive pyramidal tract signs. Generally, according to the different blood supply areas, it can be divided into 4 types, i.e. anterior watershed cerebral infarction, posterior watershed cerebral infarction, subcortical watershed cerebral infarction and basal nucleus watershed cerebral infarction.
1. Anterior watershed infarction
Anterior cortical infarction refers to the infarct zone located in the superficial area between the anterior cerebral artery and the middle cerebral artery, which is mainly manifested as limb paralysis, tongue and face paralysis is rare, and half of the patients are accompanied by sensory abnormalities. Patients with lesions in the dominant hemisphere are mainly associated with corticomotor aphasia and intellectual disability, while those with lesions in the nondominant hemisphere often have affective disorders.
2. Posterior watershed cerebral infarction
Posterior cortical infarction means that the infarct zone is located in the superficial layer between the middle cerebral artery and the posterior cerebral artery, which is often characterized by hemianopsia, accompanied by macular avoidance phenomenon. In addition, cortical sensory deficits are common, with mild hemiparesis or no dominant hemisphere involvement, manifesting as cortical sensory aphasia, occasional dysarthria, and emotional apathy in nearly half of the patients, or transcortical sensory aphasia-emotional apathy-simple aphasia. Non-dominant hemisphere lesions may present with contralateral spatial neglect and pathosensory deficits.
3. Subcortical watershed cerebral infarction
Subcortical supratentorial infarction refers to the infarction located between the superficial and deep branches of the middle cerebral artery, mostly affecting the parietal ventricles and the white matter of the basal nuclei, and the fibers of the basal nuclei are more centralized. Here, hemiparesis and hemiplegia and hemisensory deficits often occur, and the dominant hemisphere often leads to speech disorders.
4. Cerebral infarction in the basal ganglia subwatershed
Infarction in the subcerebral watershed area is an ischemic infarction between various groups of arterioles in the basal nucleus, and is more common in cerebellar watershed infarction. Clinically, there are often pure hemiplegia and sensory impairment, and pure central facial palsy can also be seen, and the clinical symptoms and signs between different types sometimes do not have obvious characteristics, and diagnosis needs to be based on CT scanning or MRI examination of the brain.
Examination
1. Blood tests and electrocardiograms
Blood tests include routine blood tests, blood rheology, and blood biochemistry (blood lipids, blood sugar, kidney function, and ions). These tests are helpful in detecting risk factors for cerebral infarction.
2. Neuroimaging examination
(1) CT Cranial CT is the most convenient, fast and commonly used imaging means.
(2) MRI can clearly show early ischemic infarction, brainstem, cerebellar infarction, venous sinus thrombosis, etc. The infarction foci show low signal in T1 and high signal in T2.
(3) Angiography DSA, CTA and MRA can detect stenosis, occlusion and other vascular lesions.
3. Lumbar puncture examination
Lumbar puncture is performed only when CT examination is not available and it is difficult to distinguish infarction from cerebral hemorrhage.
4. TCD
It is helpful to evaluate the stenosis, occlusion, spasm or establishment of collateral circulation of intracranial and extracranial blood vessels.
Diagnosis
According to the pathogenesis and etiology of cerebral watershed cerebral infarction patients with hypertension atherosclerosis, high blood lipid coronary artery disease or diabetes mellitus and other factors contributing to cerebral atherosclerosis or a history of heart disease, etc., the sudden emergence of neurological signs such as speech disorders, motor aphasia, naming aphasia, hemiplegia motor disorders, sensory disorders convulsions, intellectual disorders, psychiatric disorders, personality changes and positive pyramidal tract signs, and even consciousness The possibility of cerebrovascular disease should be considered, and brain CT scan and brain MRI are the main diagnostic methods. For watershed cerebral infarction, attention should be paid to finding the cause, such as transcranial Doppler ultrasound, digital subtraction angiography (DSA), magnetic resonance angiography (MRA), electrocardiography, cardiac ultrasound, and blood rheology, in order to clarify the cause of the disease and prevent recurrence.
Differential diagnosis
1. Cerebral hemorrhage
Most of them have a history of hypertension and large fluctuation of blood pressure, with rapid onset, headache, vomiting, impaired consciousness, and high-density hemorrhagic foci visible on CT scan of the brain.
2. Brain tumor
Slowly progressive cerebral infarction should be distinguished from brain tumor. Primary brain tumor has slow onset, metastatic tumor sometimes has similar onset with acute cerebrovascular disease, CT scan should be done in time, and if brain tumor and cerebral infarction can’t be distinguished, it is better to do brain MRI to make a clear diagnosis.
Complications
Since patients often have a history of hypertension, diabetes mellitus, heart disease, etc., the clinical manifestations of the original disease are often combined.
Treatment
1. General treatment
In the acute stage, bed rest should be given as much as possible, and attention should be paid to the balance of water and electrolytes. If the patient still cannot eat after 48～72 hours, nasal feeding should be given to ensure the nutritional supply. Strengthen the skin, oral cavity, respiratory tract and urinary and fecal care.
2. Treatment of etiology
Actively treat the causes of cerebral infarction in the watershed area, such as carotid artery disease and heart disease, medical hypotension, water and electrolyte imbalance, hypoxemia, erythrocytosis and platelet function abnormality.
3. Treatment of cerebral edema
Reasonable application of dehydration and cranial pressure-lowering drugs, because some patients with cerebral infarction in the watershed area have a history of hypertension, and recently there may be irrational blood pressure lowering leading to low blood pressure, and the relative insufficiency of cerebral blood supply, such as over-application of dehydration and cranial pressure-lowering drugs can easily reduce the blood volume, and aggravate the condition, so it should be applied reasonably according to the condition, and generally use osmotic diuretics, 20% mannitol hypertonic solution, which is effective in the treatment of cerebral edema in the large cerebral infarction area and with Mannitol is generally used as an osmotic diuretic, 20% mannitol hypertonic solution, which has better efficacy in cerebral infarction with a large range of cerebral edema around the foci, while mannitol also has strong free radical scavenging effect. According to the condition, 20% mannitol can be used for rapid static injection, and the dosage should be controlled for elderly patients, patients with long-term hypertension, patients with renal impairment or patients with poor renal function.
4. Thrombolytic therapy
Because the most important causes of cerebral infarction in the watershed area are low blood pressure in body circulation, narrowing or occlusion of large arteries in the brain, heart disease, etc., of which atherosclerosis is an important underlying cause, so thrombolytic therapy is generally not carried out, but according to the blood test indexes, it can be used to apply a more moderate treatment of snake venomous drugs, such as defibrillin (defibrillinase) injections, a course of 5 days to reduce the blood viscosity, inhibit the red blood cells, enhance the vascularization of the red blood cells through the blood vessels. A course of 5 days can reduce blood viscosity, inhibit red blood cell aggregation, enhance the vascular permeability and deformation ability of red blood cells, reduce vascular resistance and improve microcirculation.
5. Anticoagulation therapy
Reasonable application can prevent further formation or aggravation of cerebral infarction, commonly used enteric-coated aspirin, and other drugs such as warfarin (warfarin), vinblastine (new anticoagulant tablets) and so on.
6. Regulation of blood pressure in acute stage
Since the pathogenesis of cerebral infarction in the watershed area is mostly related to hypotension in the body circulation, blood pressure must be taken seriously. For the regulation of blood pressure in cerebral infarction in the watershed area, there is no uniform standard at present, and it is mostly advocated that the principle of prudence and moderation should be followed. When the blood pressure is not high or slightly low in the acute stage, appropriate antihypertensive drugs or timely supplementation of fluids can be considered to ensure the blood supply to the brain and prevent the aggravation of the condition. For those whose blood pressure is slightly increased, most of the patients do not need to undergo blood pressure lowering treatment urgently, and changes in the condition should be closely observed.
The lowering of blood pressure should be carried out slowly, generally the first 24 hours to reduce the average blood pressure by 10% to 20% is appropriate. If the rapid and drastic lowering of blood pressure is bound to aggravate the cerebral ischemic damage, a small dose of dopamine or sensitized wheat injection and other drugs can be used for treatment. The regulation of blood pressure should be carried out on an individualized basis.
Prognosis
The prognosis of this disease is good, and the mortality rate is extremely low. Clinical symptoms are relatively mild, and the effect of drug treatment is relatively satisfactory. Most of the symptoms will disappear gradually, and some patients can even return to the pre-morbid level.
Prevention
Treatment of hypertension, atherosclerosis, hyperlipidemia, diabetes, heart disease and carotid stenosis should be strengthened. Attention should be paid to changing bad life habits and moderate physical activities. Avoid bad habits such as smoking, alcoholism, overeating. To low-fat, low-calorie, low-salt diet, and to have enough high-quality protein, vitamins, fiber and trace elements. When the temperature suddenly changes, middle-aged and elderly people, especially the frail and sickly, most often do not adapt to and fall ill, especially when the cold and summer, the elderly adaptability is poor, the immune system is reduced, morbidity and mortality are higher than usual.