Cerebral infarction, also known as ischemic stroke, is a limited hypoxic-ischemic necrosis of brain tissue due to impaired blood supply to the brain and ischemia and hypoxia, with corresponding neurological deficits.
According to the evolution of symptoms and signs, they are classified as
1.Completed ischemic stroke: The symptoms of neurological deficit are heavy and complete after the onset of stroke, often reaching a peak within 6 hours.
2. progressive ischemic stroke: the symptoms of neurological deficit are still progressively worse from 6 hours to 2 weeks after the onset of stroke.
3.reversible ischemic neurologic deficit (RIND): refers to a mild neurologic deficit that lasts for more than 24 hours after onset, but can recover within 3 weeks.
Causes of cerebral blood flow disruption include arterial thrombosis, embolism, extra-arterial wall compression and hemodynamic alterations. According to the pathological mechanism, cerebral infarction is further divided into the following types: cerebral thrombosis, lacunar cerebral infarction and cerebral embolism. Cerebral thrombosis and cerebral embolism are described as follows.
Cerebral thrombosis is a common type of stroke, accounting for about 30% of all types of strokes, due to narrowing or even occlusion of the lumen of the cerebral artery trunk or its cortical branches caused by atherosclerosis or other reasons, resulting in ischemia, hypoxia, softening and necrosis of the brain tissue and corresponding neurological symptoms and signs. A large number of studies have shown that hypertension, hyperlipidemia and diabetes are risk factors for cerebral thrombosis.
It belongs to the category of “stroke” in Chinese medicine. Stroke is usually caused by anger and worry, poor diet, alcohol indulgence, overexertion or climate change, resulting in imbalance of yin and yang, internal organs and Qi, and disorder of Qi and blood.
I. Diagnosis
1.1 Clinical manifestations
1.1.1 Symptoms and signs
The symptoms and signs of cerebral thrombosis depend mainly on the site and size of the infarct. It usually develops when the blood flow is slow in the quiet state, and the symptoms can progress for several hours or even reach the peak in several days. The clinical manifestations according to the location of the infarct are as follows.
(I) Internal carotid artery system
1. Severe luminal stenosis or occlusion of the main trunk of the internal carotid artery can cause severe cerebral edema due to ischemia in one cerebral hemisphere. Patients often have varying degrees of impaired consciousness, hemiparesis and sensory loss on the contralateral side of the lesion, sometimes accompanied by visual loss, pupil dilation and loss of light reflex on the ipsilateral side of the lesion, suggesting impaired blood supply to the ophthalmic artery. In severe cases, hippocampal sulcus herniation may occur, which is characterized by small eye fissure, dilated pupil, and extraocular booth on the ipsilateral side of the lesion, paralysis of the upper and lower limbs on the contralateral side of the lesion, and patients often fall into deep coma and respiratory impairment.
2. Middle cerebral artery stenosis or occlusion: cortical branch occlusion may manifest as contralateral hemiparesis, including central facial palsy and tongue palsy, with the upper limbs often heavier than the lower limbs, gaze paralysis or spatial neglect to the opposite side, and hemianesthesia. Motor aphasia or sensory aphasia may occur if the lesion is located in the dominant hemisphere. Central branch occlusion presents with contralateral hemiparesis and hemianesthesia without symptoms of cortical deficits. If the middle cerebral artery is occluded at the beginning of the middle cerebral artery and the lateral branch circulation is poorly compensated, clinical manifestations of both cortical branch and central branch occlusion can be seen.
3. Anterior cerebral artery stenosis or occlusion is manifested as contralateral hemiparesis, with the lower limbs heavier than the upper limbs, and may be accompanied by sensory loss. Due to the damage of the paracentral lobule, there may be incontinence of urine and feces. In right-sided patients, if the hemiplegia is on the right side, there is left-sided loss of use. Psychiatric symptoms are sometimes present.
(II) Vertebrobasilar system
The severity of symptoms in vertebrobasilar artery stenosis or occlusion depends on the site of occlusion and the degree of perfection of collateral circulation. The clinical manifestations are complex, and the common signs are characterized by.
(1) Crossed paralysis or sensory disturbance.
(2) Bilateral limb motor and sensory impairment.
(3) Cerebellar dysfunction: vertigo, vomiting, nystagmus, etc.
(4) Ocular synkinesis disorder.
(5) Hemianopsia or cortical blindness. Occlusion of the main basilar artery is often severe, and death may even occur due to tetraplegia and deep coma.
1. Occlusion of the posterior inferior cerebellar artery can affect the blood supply to the dorsolateral part of the medulla oblongata, and its manifest clinical symptoms are also known as Wallenberg syndrome (Wallenberg syndrome). The typical presentation is severe vertigo, nausea, vomiting, nystagmus, but clear consciousness. The examination reveals ipsilateral facial pain, loss of warmth, ataxia of upper and lower extremities, soft palate and vocal cord paralysis causing choking and coughing, dysphagia, hoarseness, Horner syndrome and contralateral hemianesthesia and loss of warmth.
2. Unilateral median pontocerebellar artery thrombosis with Foville syndrome: lateral visual motor deficits and contralateral hemiparesis of the eyes to the side of the lesion are seen bilaterally. However, some only see contralateral hemiparesis; bilateral median artery thrombosis: typical atresia syndrome, see quadriplegia, bilateral pseudobulbar palsy, bilateral lateral palsy, bilateral abduction palsy, lateral visual palsy, visual, hearing, consciousness, sensory and vertical eye movement disorders.
3, Paracentral pontocerebral artery thrombosis: Millard-Gubler syndrome, see ipsilateral ocular abduction palsy and peripheral facial palsy, contralateral limb hemiparesis.
4. Midbrain penetrating artery thrombosis: Weber syndrome: ipsilateral arteriovenous nerve palsy, contralateral limb paralysis, damage to the reticular formation, and impaired consciousness. Red nucleus syndrome: ipsilateral oculomotor nerve palsy and involuntary movement of the contralateral limb.
5, cerebellar infarction Less common, often with acute cerebellar damage: ataxia of the lateral limb, reduced muscle tone, balance disorder and unsteadiness, nystagmus, vertigo, vomiting, headache and impaired consciousness due to secondary cerebral edema and cranial hypertension.
6, posterior cerebral artery thrombosis: cortical branch occlusion, seen as contralateral hemianopia, macular evasion; there may also be other visual impairment. Central branch occlusion manifests as thalamic syndrome: contralateral hemianesthesia, abnormalities, thalamic pain and extravertebral symptoms.
1.2 Ancillary examinations
1.2.1 Cranial CT scan The focal area shows hypointense shadow. However, there is often no positive finding on CT scan when the softening of brain tissue is mild within 24 hours of onset, or when the lesion is too small or located in the brainstem or cerebellum. CT scans performed 48-72 hours after the onset of the disease can increase the positive rate.
1.2.2 Magnetic resonance imaging (MRI) shows abnormal signal in the focal area, with low signal in the T1-weighted phase and high signal in the T2-weighted phase. Compared with CT, MRI has the ability to show lesions early and clearly show small lesions and posterior cranial fossa infarcts, and MRI diffusion-weighted images (DWI) and perfusion-weighted images (PWI) can detect lesions in the early 20-30 minutes of ischemia, which can guide the significance of thrombolysis.
1.2.3 Angiography: DSA or MRA can detect the site of stenosis and occlusion, and can show arteritis and arteriosclerosis.
1.2.4 Doppler ultrasonography Doppler ultrasonography of intracranial and external arteries can sometimes show arterial lumen narrowing and increased blood flow velocity, which can provide a basis for cerebral infarction.
1.3 Diagnostic criteria (refer to “Neurology”)
1.3.1 There may be antecedent symptoms.
1.3.2 Onset is more frequent during quiet time, often after waking up from morning sleep.
1.3.3 Symptoms often worsen gradually over several hours or over a longer period of time, in a worsening stroke pattern.
1.3.4 Consciousness often remains conscious, while focal neurological deficits are more pronounced in terms of hemiplegia and aphasia.
1.3.5 The age of onset is high.
1.3.6 There is often cerebral atherosclerosis and atherosclerosis of other organs.
1.3.7 Often associated with hypertension and diabetes mellitus.
1.3.8 Cranial CT scan The lesion area shows hypodense shadow. However, there is often no positive finding on CT scan when the softening of brain tissue is mild within 24 hours of onset, or when the lesion is too small or located in the brainstem or cerebellum. CT scans performed 48-72 hours after the onset of the disease can increase the positive rate.
1.3.9 Magnetic resonance imaging shows abnormal signal in the focal area, with low signal in the T1-weighted phase and high signal in the T2-weighted phase.
1.4 Differential diagnosis
1.4.1 Cerebral hemorrhage Cerebral hemorrhage has a faster onset than cerebral thrombosis, with symptoms usually peaking within minutes. However, a small amount of cerebral hemorrhage may not show symptoms of increased intracranial pressure, which can be easily misdiagnosed as cerebral infarction. Cranial CT scan shows high-density hemorrhagic foci, which can be differentiated.
1.4.2 Chronic subdural hematoma Patients often do not remember the history of head trauma, or the trauma is not serious, or even some elderly people do not have a history of head trauma but spontaneous subdural hematoma occurs. If cerebral angiography or cranial CT scan is not performed in time, the condition can be easily delayed and even cause death.
1.4.3 Intracranial tumor or abscess The former generally progresses slowly, while the latter has the manifestation of infection, and can be differentiated by cerebrospinal fluid or CT or MRI.
II. Identification
2.1 Middle meridians
2.1.1 Liver and kidney yin deficiency, wind and yang upward disturbance: dizziness and headache, tinnitus and dizziness, soreness and weakness of the waist and knees, sudden hemiplegia of one limb, numbness, distortion of the mouth and eyes, which may be accompanied by language speech, red tongue, thin white or thin yellow coating, and thin or slippery pulse.
2.1.2 Phlegm-heat and internal organs: sudden hemiplegia, numbness of one side of the body, distortion of the mouth and eyes, constipation, or dizziness, or excessive phlegm, speech is abrupt, tongue is red, moss is yellow and slippery pulse.
2.1.3 Phlegm stasis obstructing the ligaments: sudden hemiplegia, numbness of the deviated body, distortion of the mouth and eyes, dizziness, dull tongue, white greasy coating, slippery or string pulse.
2.1.4 Qi deficiency and blood stasis: hemiplegia, partial numbness, accompanied by swelling of the limbs, aversion to cold, unfavorable flexion and extension of the limbs, or weakness, with a pale or dark purple tongue, greasy moss, and a sunken or slippery pulse.
2.2. Central viscera
2.2.1 Closed evidence
2.2.1.1 Yang closed: sudden fainting, teeth closed, mouth silent, hands clenched, urination and defecation closed, strong spasm of limbs, red face and body heat, thick breath and bad breath, restlessness, yellowish moss, slippery and numbered pulse.
2.2.1.2 Yin closed: sudden fainting, teeth closed, mouth silent, hands clenched, urine and stool closed, strong spasm of the limbs, white face and lips dark, restless, limbs not warm, phlegm and saliva congestion, white and greasy coating, sunken and slippery pulse or slow.
2.2.2 Desiccation: sudden fainting, unconsciousness, eyes closed and mouth open, snoring, cold hands and limbs, sweating, urination and defecation, limbs limp, tongue atrophied, pulse weak and dying.
Treatment
3.1 Traditional Chinese medicine treatment
3.1.1 Acupuncture treatment
According to the depth of the disease and the severity of the disease, the clinical classification of stroke is divided into two categories: middle meridian and middle viscera. In the middle meridian, the disease is lighter, the disease is in the meridian, not in the internal organs, or the function of the internal organs is gradually restored, while the meridian qi and blood are still blocked, generally no mental changes, or the mental will turns clear, only manifested as hemiplegia, strong tongue and aphasia, swallowing disorders, incontinence, facial paralysis, etc.; in the internal organs, the disease is deep in the internal organs, the disease is more serious, manifested as different degrees of consciousness disorders, and see hemiplegia, aphasia and other symptoms in the meridian. Acupuncture treatment of stroke in the meridians is certainly effective.
3.1.1.1 Hemiplegia
Floppy phase: Features: limb impotence and weakness, low muscle tone, and diminished or absent tendon reflexes. It usually occurs within 2 weeks after the disease, and the period of upper limb flaccidity can last for 1 – 3 months.
Treatment: transportation of yin and yang meridians, Zong Luo Tian Yi method, acupuncture of the twelve well points as the main treatment.
Acupuncture points: twelve well points, Renying, Feng Qi, Baihui.
Pre-rigid paralysis: partial recovery of limb strength, gradual increase in muscle tone and joint movement. This period usually lasts from the soft palsy period to 1–3 months after the disease.
Treatment: Activate blood circulation, remove blood stasis and activate the meridians.
Acupuncture points: Hegu, Tai Chong, Bai Lao, Tian Zong, Arm Zhong, Wai Guan, Da Yin Yu, Cheng Shan, Wei Zhong, Eight Evil, Eight Wind, Bai Hui, Feng Chi, Feng Qi, Da Zhi.
Scleroparesis stage: the affected limb has high muscle tone, although there is muscle strength, but flexion and extension difficulties, and even spasticity and stiffness, showing the typical flexor spasm of the upper limb and extensor spasm pattern of the lower limb. Usually occurs 3 months after the disease – more than six months.
Acupuncture points: Dazhi, Baihui, Bailao, Sidu, Hegu through Houxi, Daoyu, Yinmen, Zhizhong, Chengzhi, Qiuhui through Zhaoxi, Shenhu through Zhaoxi, Eight Evil, Eight Wind. The acupuncture points are taken from the affected side and needled once a day for 1 month to 3 months.
3.1.1.2 Strong tongue aphasia
Includes dysarthria and aphasia.
Features of the disease mechanism: phlegm clouding the orifice and stasis of the tongue ligament.
Treatment: remove phlegm and eliminate stasis, and clear the tongue.
Acupuncture points: Gongsun, Tongli, Yumen, Lianquan, Renying, Fengfu, Baihui.
Acupuncture is performed once a day for 1 month to 3 months for 1 course of treatment. Aphasia treatment generally takes a long time and should not be given up easily.
3.1.1.3 Swallowing disorder
Treatment: Invigorate blood and open the orifice.
Acupuncture points formula: Renying, Lianquan, Bailao, Fengfu.
Acupuncture day 1 – 2 times, cure as degree.
Acupuncture is very effective in treating swallowing disorders. Mild cases can be effective in 1 – 2 times, while severe cases require about 20 – 30 times to be cured.
3.1.1.4 Incontinence
Treatment: To facilitate the flow of qi through the bladder.
Acupuncture points: secondary s, Huiyang.
Both points are electro-acupunctured with low-frequency electrical stimulation for 20 minutes. Electroacupuncture once a day, 5 – 10 times a course of treatment.
Electroacupuncture for stroke diaphoretic incontinence efficacy is precise, the milder 3 – 5 times can be cured, the more severe must be treated half – 1 month.
3.1.1.5 Mental disorders
Post-stroke mental disorders are more common, mainly depression, anxiety, and a few manifestations of manic excitement.
Acupuncture points: Baihui, Fengfu, Fengchi, Dazhi, Sun, and Shangin Tang.
Operation method: all bilateral points, high-frequency electroacupuncture for 20 minutes, once a day, 10 – 30 times for a course of treatment.
3.1.1.6 Middle viscera – closed evidence.
Treatment: pacify the liver and quench the wind, clear the heart and expel phlegm, open and close the orifice, and release blood by acupuncture.
Selected points: Shuigou, 12 well points, Tai Chong, Laogong, Fenglong.
3.1.1.7 Middle visceral organs – detachment.
Treatment: Returning Yang and fixing detachment, relying on moxibustion.
Selected points: Guan Yuan, Shen Que.
3.1.2 Identification and treatment
Liver and kidney yin deficiency, wind and yang upward disturbance
Treatment: Calming the liver and quenching the wind, nourishing the liver and kidney.
Addition and subtraction of Liver and Wind Extinguishing Soup: 15 grams of tian dong, 20 grams of each raw dragon and peony, 15 grams of dai ochre, 15 grams of turtle board, 15 grams of white peony, 15 grams of xuan shen, 6 grams of neem, 10 grams of raw wheat sprout, 15 grams of white hyssop, 10 grams of yin chen, 10 grams of licorice.
Phlegm-heat in the internal organs
Treatment: Removal of phlegm and clearing the internal organs.
Xingguo Chengqi Tang: Bile Nanxing grams, whole Guahuo grams, raw rhubarb 10 grams, mannitol grams.
Phlegm stasis blocking the ligaments
Treatment: resolving phlegm and clearing ligaments.
Er Chen Tang and Blood Mansion and Blood Stasis Soup with addition and subtraction: 10 grams of Radix Panax notoginseng, 10 grams of Chen Pi, 12 grams of Poria, 12 grams of Calamus, 12 grams of Yuan Zhi, 6 grams of Bamboo Roo, 8 grams of Angelica Sinensis, 10 grams of Red Peony, 10 grams of Chuan Dou, 10 grams of Niu Knee.
Qi deficiency and blood stasis
Treatment: Benefit Qi and invigorate Blood.
Tonic Yang Returning Five Soup: Astragalus membranaceus 20g, Angelica sinensis 10g, Chuan Dou 8g, Tao Ren 10g, Safflower 10g, Di Long 6g, Radix Paeonia lactiflora 10g.
3.2 Western medicine treatment
3.2.2 Ultra-early thrombolytic therapy: It should be performed within 6 hours of onset. Urokinase, streptokinase, and recombinant tissue-type fibrinogen activator are commonly used in China. Urokinase, for example, is commonly used in the amount of 25-1 million u, added to 5% glucose intravenous drip for 30 minutes-2 hours, and interventional arterial thrombolysis is also an option.
3.2.1 General treatment
Monitoring and controlling body temperature, blood pressure, blood gas and blood glucose play an important role in reducing ischemic brain damage.
Adjustment of blood pressure: when blood pressure is higher than 200/120 mmHg or may impair cardiac function, it should be cautious to use antihypertensive methods that can easily control the amount of medication, and excessive speed of blood pressure lowering should be avoided to aggravate cerebral ischemia.
Control blood sugar: hyperglycemia will aggravate cerebral infarction and should be actively dealt with. When blood sugar is greater than 9.0mmol/L, appropriate amount of insulin can be added during rehydration.
During the progressive stage of disease, bed rest is the main treatment, and oxygen therapy can be given if there is delirium, and gastric tube and urinary catheter can be left in place.
Prevention of complications: For patients with limb paralysis or coma, turn them over on time and carry out rehabilitation activities as early as possible to prevent pulmonary embolism, lower limb deep vein thrombosis, decubitus ulcers, muscle spasm and joint ankylosis, etc. Pay attention to oral care and keep bowel and stool unobstructed.
3.2.2 Ultra-early thrombolytic therapy: It should be performed within 6 hours of onset. Urokinase, streptokinase, and recombinant tissue-type fibrinogen activator are commonly used in China. Urokinase, for example, is commonly used in the amount of 25-1 million u, added to 5% glucose intravenous drip, and finished in 30-2 hours. Interventional arterial thrombolysis is also an option for symptomatic treatment.
3.2.3 Fibrin-lowering therapy: mainly used for combined hyperfibrinogenemia, but also for early thrombolytic therapy. Generally, the first dose of 10 Bu of fibrin-lowering enzyme is used, and 5 Bu is injected intravenously every other day, and 3 times is a course of treatment.
3.2.4 Anticoagulation and anti-platelet aggregation drugs have no direct thrombolytic effect on formed thrombus, but are used as adjuvant therapy after thrombolysis. Anticoagulation is indicated for progressive stroke, especially vertebrobasilar thrombosis.
3.2.5 Vasodilator therapy: small infarct foci without significant cerebral oedema are available; red infarcts or hypotension are contraindicated.
3.2.6 Dehydration and cranial pressure reduction: dehydrating agents or surgical treatment should be applied promptly to large infarct foci to reduce cerebral edema.
3.2.7 Cerebral protection therapy: commonly used are calcium channel antagonists, cytidylcholine, etc.
Early standardized, comprehensive and individualized rehabilitation treatment, including physical, language, cognitive and psychological aspects.