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😷 | [Type Corona] One person died in Yokohama, 1 people confirmed infected

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[Type Corona] One person died in Yokohama, 1 people confirmed infected

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He said he had high blood pressure, chronic kidney disease, and underlying cerebral infarction.

The city of Yokohama announced on the 7th that a man in his 90s who lives in the city has died over the new coronavirus infection.Also, 10 ... → Continue reading

 Kanagawa Shimbun

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Chronic kidney

cerebral infarction

cerebral infarction(Snow,British: cerebral infarction/stroke), orEncephalomalacia(Let’s go)[Note 1] IsbrainTheNutritionToartery OfOcclusion, Or because of stenosis,Cerebral ischemiaAnd brain tissueoxygen, Or due to lack of nutritionNecrosis, Or a state close to necrosis. In addition, various symptoms caused by it are sometimes called cerebral infarction. Among them, the symptoms were severe (Hemiplegia,Consciousness disorder,AphasiaSudden onset, including those caused by other causes, is generallystrokeCalled. On the other hand, proceed slowlydementiaThere are also forms such as (cerebrovascular dementia).

The number of patients in Japan is about 150 million, and it is said that about 50 people will develop each year,JapaneseOf the most common causes of death indiseaseIs. Also,SequelaeLeavingNursing careIs often needed, about 3% of the causes of bedridden, patient treatment costs account for 1% of Japan's annual medical expenses,welfareIt is a disease that also entails major challenges.


Cerebral infarction is classified into three types, thrombotic, embolic, and hemodynamic, depending on the mechanism of blood vessel occlusion. NIND-III (NINDS: National Institute of Neurological Disorders and Stroke classification by the US National Institute for Neurological Disorders and Strokes) in 3 is well known as a clinical disease type.

In the NIND-III classification, regional cerebral dysfunction is classified into TIA and stroke. Stroke is classified into cerebral hemorrhage, subarachnoid hemorrhage, intracranial hemorrhage associated with cerebral arteriovenous malformation, and cerebral infarction. To be done. NINDS-III, which has different acute treatments and prevention of recurrence depending on the classification, describes the characteristics of clinical type but does not show diagnostic criteria. In clinical trials, TOAST classification and Oxford classification may be used.

In the TOAST classification, large-vessel atherosclerosis (=atherothrombotic cerebral infarction), small vessel occlusion (=lacuna infarction), cardiac embolism (=cardiogenic cerebral embolism), other causes, 5 unexplained diseases Classified into types. Although there are diagnostic criteria, it is possible to make a reliable diagnosis, but it is not possible to make a diagnosis when there are multiple possible causes, such as when there is both a risk of atherothrombotic cerebral infarction and cardiogenic cerebral embolism. Difficult to use. Oxford classification is based on symptoms and imaging findings.

Atherothrombotic cerebral infarction

ArteriosclerosisDeposited on the arterial wall byAtheroma(Athema) that narrows the arterial lumen and cannot maintain sufficient cerebral blood flow. Also, atheroma that falls off the arterial wall and becomes clogged in the periphery is classified as atherothrombogenic. Since atheroma gradually grows and causes blood flow disorders, it grows to some extent during the course of the process.PriceIs possible,NecrosisThe range tends not to be that large. In addition, cerebral ischemic symptoms that do not lead to necrosis before the onset of cerebral infarction (Transient cerebral ischemic attack, TIA), and coping with this TIA is important in the prevention of cerebral infarction[1].. In the TOAST classification, the diagnostic criteria include a stenosis of 50% or more in the responsible blood vessel proximal to the lesion and an infarct size of 1.5 cm or more.

Risk factor

As the underlying diseaseHigh blood pressure,Diabetes mellitus,Dyslipidemia,smokingSuch. Prevention isAntiplatelet drug(aspirin-Ticlopidine(British: Ticlopidine)・Clopidogrel(British: Clopidogrel)・Cilostazol-Dipyridamole(British: Dipyridamole) Etc)AtheromaTo control the growth of the disease, to treat and control the underlying disease, and to keep the blood flow good by drinking water.

Mechanism of onset

TypicallyThrombosisIs obstruction due to arteriosclerosis.Myocardial infarctionIn the case ofcoronary arteryIn most cases, cerebral infarction is known, but several mechanisms are known. First, plaque may break like myocardial infarction.AtheromaIf the plaque is rich and has a thin fibrous cap, it is called vulnerable plaque. These plaques easily break down, causing arterial occlusion due to thrombus. When a blood vessel is occluded or narrowed, the perfusion area of ​​the blood vessel is disrupted to cause cortical branch infarction. When a stenosed part causes a sudden vascular occlusion, a cerebral infarction similar to a cardiogenic cerebral embolism occurs. These things are extracranialInternal carotid arteryAnd mostly in the main brain artery in the skull (see depending on sex).

In addition, the boundary region of the blood supply (watershed, meaning watershed) becomes an ischemic state due to the blockage of blood vessels or a high degree of stenosis, and further infarction occurs due to hemodynamic factors such as a decrease in blood pressure. These are common in the middle cerebral artery and internal carotid artery. If the internal carotid artery has severe stenosis and is accompanied by a decrease in cerebral blood flow in the dominant region,Middle cerebral arteryAt the border of the cortical branch, the border region of the middle cerebral artery/cortex branch in the posterior region is most likely to be in an ischemic state, and thus infarction is likely to occur. In the deep part, it easily occurs in the boundary region between the cortical branch of the middle cerebral artery and the perforator branch. If this mechanism occurs, a stepwise progression and worsening after the onset are seen (progressive stroke). The onset time is high at night and is often noticed when waking up. It is considered that the disease has originally progressed extremely chronically, and patients with such an infarction often have abundant collateral circulation, and clinical symptoms may be poor while compensation is possible.

Due to hemodynamicsIs temporarilyblood pressureIt is a part of the brain that is unable to obtain sufficient blood flow and has become necrotic because of a drop in blood flow. It is characteristic that it develops in the watershed region where necrosis is difficult due to thrombosis or embolism. The watershed area is an area that corresponds to a boundary when the brain is divided according to which artery is nourished. This portion is strong against arterial occlusion because blood flow can be obtained from the other artery even if one artery is occluded. However, since it is far from the main trunk of the artery, it is easy to fall into ischemia when the blood pressure falls. In this case, the diagnosis is atherothrombotic cerebral infarction.

There is also artery to artery embolism (A to A) as a cerebral infarction caused by arteriosclerosis. Internal carotid arteryVertebral arteryA thrombus is released from the atherosclerotic plaque to block peripheral blood vessels. Embolism can occur in both cortical and perforating branches. As with cardiogenic cerebral embolism, sudden onset during activity is likely to be seen.

On the image typically cortical branches,Cerebral cortexToMRIDiffusion weighted image (DWI) shows high-intensity area, and it is easy to take the form of scattered small infarct lesions. Of course, the small size means that it is larger than other atherothrombotic infarctions, and thus the lesion is larger than the lacunar infarction. There is a common site for atherosclerosis. Basically, most Japanese have middle cerebral arteries. However, in recent years, as in Europe and the United States, it is most common at the origin of the carotid internal carotid artery. Other common sites are the siphon of internal carotid artery, the origin of vertebral artery, intracranial vertebral artery, and basilar artery.

Atherosclerotic cerebral infarction is better than lacunar infarctionTransient cerebral ischemic attackIs said to be easy to precede. It is characterized in that it is easy to repeat the symptoms of the dominant region of the occluded artery. Transient amaurosis is famous for internal carotid lesions. This causes ischemia in the ophthalmic artery and central retinal artery region, and the visual acuity on the affected side disappears transiently. Patients complain that the curtains will typically darken in front of you. Dizziness and vomiting in vertebral arteries,DysarthriaIs likely to occur. The frequency of seizures is important, and if they occur frequently in a short period of time, it is called crescendo TIA, which suggests the presence of severe stenosis of the main trunk artery. it is conceivable that.

It is said that cerebral infarction is most likely to occur within 1 month after the first TIA, and especially in recent studies, there are many cases of cerebral infarction within 48 hours after the onset of TIA. About half)[2][3] It is said that hospital scrutiny and treatment are required because[1]. It is recommended to use antiplatelet drugs for atherothrombotic TIA and anticoagulant therapy for cardiogenic or crescendo TIA.

Internal carotid systemVertebral artery system
Movement disorderSymptoms are unilateralMulticolored, alternating hemiplegia, drop attack, paraplegia
Sensory disturbanceUsually unilateralVarious
Visual impairmentTransient black cataractBilateral visual impairment
Visual field impairmentSame name semi-blindCentral avoidance visual field loss, unilateral, bilateralSame name semi-blind
Cerebellar symptomsAbsentAtaxia, swaying gait
Cranial nerve symptomsdiluteArticulation, dysphagia, diplopia
Number of attacksLess, symptoms are the same for each seizureSymptoms vary with each attack
Transition to cerebral infarctionEasy to transitionDifficult to transition

Disorders of the cranial nervous system can also occur in the internal carotid system when upper neuron disorders occur. This is because the central last time is returned to the middle cerebral artery.

Lacunar infarction

Lacunar infarction( British: lacunar infarction ) Originally means a small infarction with a diameter of 1.5 cm or less. It is classically included in the five types shown below, with lesions in the perforator region and the cortex not included. Although a disease called asymptomatic lacunar infarction is also defined in some books, asymptomatic lacunar infarction and chronic ischemic changes are difficult to distinguish and classically, asymptomatic lacunar infarction is not included in lacunar infarction. Lacuna infarction is classified as itself because it is considered that a mechanism different from the above two types is involved. Mainly in the middle and posterior cerebral arteriesGlass degenerationIt is due to the mechanism of causing and blocking. However, among the perforating branches of the middle cerebral artery, the occlusion of may lead to an infarct with a diameter of 20 mm or more called linear internal capsule infarctHemiplegiaOr sensory paralysisSame name semi-blindSymptoms such as may appear. Infarction of the posterior cerebral artery perforator branch may cause slight (red nucleus syndrome). The risk factor is hypertension. Symptoms include hemiplegia and dysarthria, but are often mild or limited and often completely asymptomatic.Consciousness disorderIs almost never accepted,Aphasia,Ignore half space, Neuropsychological symptoms such as agnosia (cortical symptoms) are usually not seen.Multiple cerebral infarctionMost of what is called is a frequent occurrence of this lacunar infarction,dementia-ParkinsonismMay cause (Cerebrovascular Parkinsonism). Whether it is a lacunar infarction or an atherothrombotic cerebral infarction can be easily understood by knowing the type of lacunar infarction. This is because the discrimination may be difficult only if the symptoms are mild and the infarct lesion is small. The feature is that the type in which sensory disturbance and paralysis do not exist at the same time can be lacunar infarction. According to the TOAST classification, the clinical manifestation is lacunar syndrome, a small infarction within 1.5 cm of the perforator branch region, and no stenosis of 50% or more of the responsible blood vessel proximal to the lesion is not recognized.

Lacunar syndromeSymptomsResponsible lesion
Pure motor hemiparesisNo hemiplegia or sensory impairmentOpposite radial crown, inner rear leg, bridge bottom
Pure sensory strokeHalf-sided abnormal sensation or sensory disturbanceContralateral thalamus (retroventral nucleus)
Ataxic hemiparesisStrong hemiparesis and cerebellar ataxia in the unilateral lower limbOpposite bridge bottom, inner rear leg, and coronal crown
Dysarthria-clumsy hand syndromeArticulation disorders and unilateral dyskinesiaOpposite bridge bottom, inner rear leg, and coronal crown
Sensory-motor strokeHemiparesis on the half side and hemiplegia on the same sideThalamus to internal leg

Thalamus infarction is known. There are many lesions outside the thalamus, which cause numbness and abnormal sensation localized on one side of the palm and around the corners of the mouth.ThalamusIt is believed that this occurs because the regions that control the palm and the corners of the mouth are adjacent to each other in the nucleus of. Other than lacunar infarction, often occurs. This is also considered to be a problem of lesion size.

Cerebral embolism (embolism)

Cerebral blood vessel lesions flowed from upstream rather than lesionsthrombusCerebral ischemia caused by clogging of (emboli). The necrotic areas tend to be larger and the symptoms more severe due to sudden obstruction of previously healthy blood flow. Since multiple embolisms may occur, multiple lesions are often present. The most common cause is心 臓Generate withthrombusAnd then leftAtrial fibrillationThere are many cardiogenic cerebral embolisms caused by.About half of all nonvalvular atrial fibrillationAnd other acuteMyocardial infarction, Ventricular aneurysm, rheumatic heart disease, artificial valve,Cardiomyopathy,Sick sinus syndrome,Infective endocarditis, Non-bacterial thrombotic endocarditis, heart tumors and the like. Besides, it was torntumorAnd then it's clogged upFat embolism・Although it is included in this, it is a rare cause. Caused by shunt heart disease (patent foramen ovale), these are referred to as paradoxical cerebral embolisms and will be described later.

High rate of cerebral embolism (30% or more)Hemorrhagic infarctionEasy to cause. This is because a large amount of blood flows into the infarcted area due to reopening of the blood vessel after the occlusion, and the blood vessel breaks down. The reason that antiplatelet therapy and antithrombin therapy are contraindicated during cardiogenic embolism is that they do not occur.

Atrial fibrillationIs often asymptomatic and the heart function does not deteriorate so much, so especially when asymptomaticCerebral embolismPrevention is of paramount importance.AtriumStagnates internally because it does not contract effectivelybloodClots into blood clots, which can cause cerebral embolism if a large blood clot that does not decompose immediately. It is especially contraindicated to carelessly treat atrial fibrillation because it tends to flow out immediately after atrial fibrillation has stopped (returned to normal) (however, it is large within 48 hours after the start of atrial fibrillation. Blood clots are not formed and are considered safe).

To preventAnticoagulantTo use. There is no clear evidence that the prophylactic effect can be increased when used in combination with an antiplatelet drug, and anticoagulant therapy alone is currently being used. Diagnostic criteria include the presence of an infarct size of 1.5 cm or more in the TOAST classification, the presence of high-to-moderate risk embolic heart disease, or the confirmation of acute infarcts that frequently occur in multiple vascular regions. Defines high-risk and moderate-risk sources.

MRA a few days after the onset often shows revascularization phenomenon. There is also a slight increase in BNP and D-dimer within 24 hours of onset. There is also a report of cardiogenic cerebral embolism with sensitivity of 76% and specificity of 0.96% if both BNP>87pg/ml D-dimer>85ng/ml are satisfied.[4].

Summary of 3 types

Cardiogenic cerebral infarctionAtherothrombotic cerebral infarctionLacunar infarction
Proportion30 - 40%30 - 40%30 - 40%
Form of onsetSudden completion, severeStep progressRelatively slow, mild
Medical history, risk factorsAtrial fibrillation and valvular diseaseHypertension, diabetes, hyperlipidemiaHigh blood pressure, diabetes
complicationsheart failureIschemic heart disease, lower limb artery occlusionNothing in particular
Medical treatmentAnticoagulantAntiplatelet drugAntihypertensive drugs, etc. in the chronic phase
Surgical treatmentNoneStent, intimal detachmentNone

The above explanation is often given.

Other strokes

BAD (for other strokes)branch atheromatous disease),Trousseau syndrome(Remote effect of malignant tumor), blood coagulation abnormality, arterial dissection, venous infarction, vasculitis, antiphospholipid antibody syndrome are included.

BAD (branch atheromatous disease

Lacunar infarctionThere is something called BAD as a pathological condition that is intermediate between the two. Proposed by Caplan in 1989. BAD is an infarction in the perforator region that occurs when the perforator branch is occluded near the main trunk artery. Although it is a perforation branch lesion, it does not cause hypertensive vascular necrosis and is caused by atherosclerosis, resulting in an infarction with a major axis of 15 mm or more. Although antiplatelet therapy was performed under the diagnosis of lacunar infarction, it was reported that the symptoms gradually worsened, but this was summarized in the concept of BAD. BAD occurs in the areas of the lateral striatal artery, thalamic geniculate body artery, anterior choroid plexus artery, Heubner recurrent laryngeal artery, perforation of thalamus and paramedian bridge. In particular, the lateral striatal artery and paramedian bridge artery are common sites. Therefore, it is the dominant region of the lateral striatal artery.Basal gangliaConsidering the symptoms and lesions suspected to be lacunar infarction on the ventral side of the pons, which is the dominant area of ​​the paramedian pons artery, the possibility of BAD is considered. In the MRI image of the head, it corresponds to the blood vessel running, and in the lateral striatal artery region, it is up and down long in the paramedian pons artery (there is a lesion on the brain surface, which becomes a fan in the deep, pons covering direction). In the lateral striatal artery region, there is less vascular endothelial damage in the middle cerebral artery, which is the mother artery, and it is considered that the plaque in the proximal part of the perforator branch is predominantly the plaque on the basilar artery wall in the paramedian bridge artery. There is. It is thought that anticoagulant therapy should be performed based on atherothrombotic cerebral infarction, but no cure has been established.Argatroban,Cilostazol,EdaravoneVarious combinations such as combination therapyCocktail therapyHas also been tried.


Damage to the intima of the artery creates a dissociation space between the intima and the media. Occurs with trauma but also naturally.dissociationDue to this, the lumen of the artery is narrowed or occluded, and an aneurysm-like dilation is caused in the adventitia. In recent years, it is more common in the vertebral artery system. Young people without much risk often develop with sudden back neck pain.Wallenberg syndromeIs often present. Cerebral arterial dissection is a concept revealed by the progress of diagnostic imaging and is the largest cause of juvenile cerebral infarction,Subarachnoid hemorrhageIt is also important as a cause. Vertebral artery dissection with subarachnoid hemorrhage requires immediate surgery to prevent fatal rebleeding. Endovascular treatment is the first choice. Confirm the positional relationship between the dissociation cavity and posterior inferior cerebellar artery, anterior spinal artery, perforator branch, and perfusion status of the contralateral vertebral artery, and perform endovascular treatment, craniotomy (including bypass surgery), or a combination of these. When surgical treatment is difficult, conservative treatment is used to prevent rebleeding.

Conservative treatment is the first choice for carotid artery dissection without subarachnoid hemorrhage. Myocardial infarctionAortic dissectionTreatment differs greatly, but in cerebral artery dissection, treatment is similar to cerebral infarction. Treat cerebral infarction to the extent that it does not induce dissociation or bleeding. OrBias pilinSaid that antiplatelet drugs do not increase the bleeding rate in unruptured aneurysmsevidenceTherefore, keep blood pressure from normal to slightly lower and perform antiplatelet therapy. Consider surgical treatment if dissociation progresses. In recent yearsStentSurgical treatment has also been attempted, and it is a good indication especially in chronic obstructive vascular disease.

Internal carotid artery dissection

Symptoms due to dissociation of blood vessels such as headache and headache and cerebral ischemia or bleeding symptoms associated with dissociation are observed. direct findings such as initimal flap, double lumen (two lumens visible), pearl and string sign (arterial dilation with irregular stenosis of a relatively wide range of ribbon), string sign, pearl sign of a relatively wide range of ribbon Indirect findings such as irregular stenosis) and tapered occlusion (tapered occlusion) are known. In the chronic stage, intramural hematoma (intraluminal hematoma T2WI crescent-shaped hyperintensity) may be observed. Occurrence and disappearance of intramural thrombus may be confirmed to diagnose arterial dissection. Causes of head and neck artery dissection are classified into traumatic, iatrogenic, and idiopathic. In idiopathic cases, there may be underlying connective tissue disease. Typically, cystic medial necrosis,Marfan syndrome,Osteogenesis imperfecta, Familial, elastic fibrous xanthoma, etc. For bleeding, surgical treatment for bleeding is performed to prevent the most bleeding, and conservative treatment is the first for ischemia. Caution should be exercised if the patient has a dissecting aneurysm.

Wallenberg syndrome

The medulla oblongata has a cardiovascular center and a respiratory center.arrhythmiaBe careful of sudden death by.

Trousseau syndrome

It is one of the acquired coagulopathy,Malignant tumorCerebral embolism may occur due to abnormal blood coagulation due to the remote effect of. Blood coagulation abnormalities associated with cancer-bearing patients, in a narrow sense cerebral infarction caused by it is called Trousseau syndrome[5]. French physician who first reported this syndromeArmand TrussouBears the name of[5]. The most common malignant tumor that causes Trousseau syndrome is solid cancer, and it is said that there are many adenocarcinomas, especially mucin-producing tumors. In solid cancerBreast cancer,Uterine cancerな どGynecologyMost tumors,Lung cancer,Kidney cancer,Prostate cancerAnd so on[6]. Blood coagulation abnormalities associated with malignant tumorsD dimer,(English editionFibrinolytic markers such as PIC and PIC often show abnormally high values. Thoracoabdominal aortic aneurysms and severe deep vein thrombosis are among those that show abnormally high levels of secondary fibrinolytic markers. In paradoxical cerebral embolism and cardiogenic cerebral embolism, D-dimer is at most about 5.0 mg/dl, and FDP and PIC often remain within the normal range. Most of the causes of cerebral infarction in patients with gallbladder cancer are cardiogenic cerebral embolism due to non-bacterial thrombotic endocarditis (NBTE) complicated with DIC, followed by Trousseau syndrome, bacterial embolism, tumor embolism, cerebral vein. , And sinus thrombosis. Small molecule treatment for Trousseau syndromeHeparinIs effective, but the prognosis is the treatment of the underlying disease.

Cerebral vein/sinus sinus thrombosis (CVT)

Cerebral vein/sinus sinus thrombosis (CVT) is a disease in which cerebral veins or sinuses are occluded and venous return disorders occur, and symptoms such as headache, convulsions, and disturbance of consciousness develop acutely or subacutely. Less than 1% of all strokes are by no means a rare disorder. Symptoms vary, but headache (90%), convulsions (40%), and consciousness disorder (60%) are acute or subacute, and CVT needs to be differentiated.

It is said to be common among women and children under the age of 50. Pregnancy, puerperium, malignant disease adjacent to sinusear,Paranasal sinusInfection of theBacterial meningitisWhen it is spread from the above, it develops on the basis of various pathological conditions such as hypercoagulable state. If D-dimer is normal, CVT is unlikely. MRI including SWI confirms thrombosed vein or sinus, and proves that MRV does not show the same vein as gold standard. No large-scale clinical studies have examined its efficacy, but in the acute phaseHeparinOften treated with continuous infusion. The prognosis is relatively good if diagnosed and treated early. If there is a causative disease, it will be treated together with treatment for convulsions and cerebral edema. Recurrence prophylaxis is treatment of warfarin and causative disease for 3 to 12 months.

Brain amyloid angiopathy (CAA)

To cerebrovascularAmyloidDeposits weaken the blood vessel wall, narrow the lumen, and block the lumen, resulting in cerebral hemorrhage and cerebral infarction. Diagnosis is by Boston criteria.

Fibromuscular dysplasia (FMD)

A large number of cases of juvenile cerebral infarction have been reported in Europe and America, but are rare in Japan.

Remnant primitive blood vessels

Arteriosclerosis may progress due to blood vessel malformation.


The clinical features of suspected cases are: 40 to 50 years of age, relatively young onset, no risk factors for stroke, repeated lacunar infarction attacks, progressive progression of pseudobulbar palsy and dementia symptoms, in families A similar symptom is observed (autosomal dominant inheritance).CADASIL is suspected when trying juvenile cerebral infarction with autosomal inheritance, especially in the case of small vessel lesions. CADASIL is known for three stages of illness.In the first stage, migraine with aura and deep white matter lesions with clear boundaries are observed on MRI.In the second stage, TIA and cerebral infarction occur, and psychiatric symptoms such as depression appear, and deep white matter fused lesions and lacunar infarction lesions are observed by MRI.In the third stage, it progresses like dementia and pseudobulbar palsy, and diffuse deep white matter lesions on MRI. Davous et al. Are known as diagnostic criteria for CADASIL.Pathologically, it is confirmed by degeneration and disappearance of the medial muscularis of the cerebral parenchymal arteriole, fibrous thickening of the adventitia, and non-amyloid acidophilic PAS-positive granule deposition of the vascular wall.For definitive diagnosis, it is necessary to confirm Notch3 mutation (especially hot spot exon1, 2) by gene analysis or confirm GOM (granular osminophilic material) by immunostaining using antibody against Notch3 extracellular domain by skin and muscle biopsy. Is.There is an important similar disease.Leukoencephalopathy caused by arteriosclerosis without hypertension and showing autosomal recessive inheritance.Dementia that progresses from the 3s is similar to CARASIL, but recurrent low back pain, spondylosis deformans, and baldness are characteristic findings of CARASIL. Resulting from loss of function of the HTRA3 geneTGFβInsufficiency of family signaling is involved in arteriosclerosis.Pathologically, the proliferation of vascular endothelium is remarkable, and the expression of extracellular matrix is ​​increased in the endometrium as the expression of TGFβ1 in the media is increased.No effective treatment has been found, and antithrombotic drugs have been used, but their effectiveness has not been confirmed.

Due to vasculitis

VasculitisasAntiphospholipid antibody syndrome,Systemic lupus erythematosusIs due to the cause of juvenile cerebral infarction.

Antiphospholipid antibody syndrome

A primary antiphospholipid antibody syndrome and a secondary antiphospholipid antibody syndrome associated with SLE are known. It is considered that this disease is characterized by thrombus formation in blood vessels throughout the body but thrombus formation in arteries and veins. About 90% of arterial thrombosis is said to occur in cerebral blood vessels. Among anti-phospholipid antibody-positive cases, 20 to 30% are associated with thrombosis, and thrombosis does not occur in most cases. However, it is known that thrombosis occurs repeatedly in more than half of the cases that have developed once. Warfarin is used for venous thrombosis and small doses for arterial thrombosis. In the general examination, antiphospholipid antibody syndrome is suspected if there is evidence of thrombocytopenia (40-50%), APTT prolongation, syphilis thrombotic reaction biological false positive, past history of habitual abortion, thrombosis. .. Even in the absence of these findings, cases of cerebral infarction and risk factors in young people may be tested for anticardiolipin/β2GPI antibody, lupus anticoagulant, antiprothrombin antibody, etc.

Primary cerebrovascular disease (PACNS)

Primary cerebral vasculitis (PACNS) is a vasculitis confined to the central nervous system (CNS), which mainly affects the pial membrane of the brain and spinal cord, and arterioles with a major axis of 200 to 300 μm in the parenchyma to the medium arterial level. R. The cause is not clear,Mycoplasma,VariegThere are cases in which vasculitis is caused by infection with herpes zoster virus, and amyloid deposits are observed in blood vessels, suggesting the involvement of multiple causes. In general, the progression of symptoms often follows a subacute course, but there are also cases where an acute onset such as convulsions or a chronic course of headache persists. Clinical symptoms are cognitive decline 83%, headache 56%, convulsions and fever 30%, cerebral infarction 14%, and cerebral hemorrhage 12%. If spinal cord blood vessels are also damaged, the corresponding symptoms will appear. Many cases are between the ages of 40 and 60, and there is no gender difference. The gold standard for diagnosis is cerebral angiography using a catheter and brain biopsy (small vessel inflammation of the pia mater and cortex). The systemic inflammatory response is poor, but some abnormalities are observed in the cerebrospinal fluid examination. Magnetic resonance imaging (MRI) shows a single or multiple white matter or gray matter cerebral infarction or hemorrhagic lesion after vasculitis, which may appear as a tumor. White matter lesions are also observed as a result of microangiitis. Angiography shows dilation and stenosis of small arteries and is called bead-shaped. Other peripheral blood vessels and blood vessels that have deviated from them are also irregular, and obstruction and disruption are recognized. Treatment may be combined therapy with steroids and cyclophosphamide according to the treatment of polyarteritis nodosa.

Takayasu arteritis (aortitis syndrome)

Takayasu arteritis(Former name: Aortitis Syndrome) is a large vasculitis that occurs in the aorta and its trunk, coronary and pulmonary arteries. It is characterized by low-grade fever, dizziness, high inflammatory response, and vascular murmur in young women. There is no blood or biochemical test specific to this disease, and the activity of Takayasu's arteritis is evaluated based on the presence or absence of CRP, blood sedimentation, white blood cell count, gamma globulin, and anemia. To do. Cure is a steroid, and antiplatelet drugs are sometimes used to prevent organ infarction.

Nerve Behcet's disease

Nerve behcet's diseaseBehcet's diseaseIt is found in about 10 to 20% of.About 2 to 5 times more common in men. 20-40 years old is the most common.Neurological symptoms often appear 3 to 6 years after the onset (after Behcet's disease diagnosis), but neurological symptoms may be the first onset.The classification of neuro-Bechett's disease is divided into parenchymal lesions (brain stem, cerebrum, spinal cord lesions) 80% and non-parenchymal lesions (vascular lesions, aneurysms, etc.) 20%, and parenchymal lesions are further divided into acute type and chronic type.The acute type shows meningitis and local symptoms, and has good steroid response.In the chronic type, neuropathy and psychiatric symptoms progress after the course of the acute type.With atrophy of the brain stem, cerebrum, and cerebellum, cerebrospinal fluid IL-6> 20 pg / ml (which also increases with SLE, etc.) is a characteristic laboratory finding.It is steroid-resistant and MTX low-dose pulse therapy (7.5 to 15 mg / week) is effective.Cyclosporine, used with eye Behcet's disease, exacerbates and induces neuro-Behcet's disease.The acute form is considered to be vasculitis.

Hypertrophic dural inflammation

Is a syndrome in which the dura of the brain and spinal cord is thickened due to various causes, and various symptoms such as headache, cranial nerve palsy, convulsions and spinal cord compression symptoms occur depending on the lesion site. Contrast-enhanced CT and contrast-enhanced MRI show thickening of the dura with contrast effect. The cause is a series of infectious diseasesANCAThere are reports of related vasculitis syndrome, IgG4-related multiple organ lymphoproliferative syndrome (IgG4+MOLPS), etc. The main treatment is steroids.

Disease classificationdisease
Infectious diseaseTuberculosis, bacteria, fungus, syphilis, HTLV-1
Collagen disease-relatedRheumatoid arthritis, polymyositis, MCTD, Sjogren's syndrome, SLE, polyarteritis nodosa, ANCA-related vasculitis, MOLPS
OtherIdiopathic, malignant tumor, sarcoidosis, intrathecal administration of contrast agent, sinus thrombosis, dialysis, trauma, drug

Cerebral infarction of unknown cause

A cerebral infarction whose apparent cause could not be identified even after close examination. Biaspyrine is routinely used to prevent recurrence, but it is considered that long-term follow-up cases include cardiogenic cerebral embolism in which atrial fibrillation etc. could not be detected by holter ECG.

Not important but important concept of cerebral infarction

Juvenile cerebral infarction

The type and etiology of cerebral infarction in young people are significantly different from those in middle-aged and older people. In middle-aged and elderly people, cardiovascular diseases and atrial fibrillation are associated with arteriosclerosis, whereas juvenile cerebral infarction under 40 years of age has little effect of arteriosclerosis and atrial fibrillation, and often has a specific cause. Antiphospholipid antibody syndrome, Circle of Willis artery occlusion (Moyamoya disease),VasculitisIt is well known to be caused by abnormal coagulation, paradoxical brain embolism, etc.Paradoxical cerebral embolismIs a condition in which a thrombus generated in a vein flows into the left heart system from the right heart system via the right heart system left heart shunt and develops cerebral embolism. Known shunt diseases include patent foramen ovale (PFO), pulmonary arteriovenous fistula (PAVF), and atrial septal defect (ASD). The frequency is about 5% in the case of continuous cerebral infarction. In the PFO in Cryptogenic stroke Study (PICSS), warfarin and aspirin have the same therapeutic effect in patients with cerebral infarction who have PFO but no deep vein thrombosis or embolic heart disease. It is said that the risk of recurrence is increased in the presence of atrial septal aneurysm (ASA, a condition in which the atrial septum alternates between the left and right atriums), but no conclusion has been reached regarding its recurrence prevention. .. In addition, there is no indication of long-term prognosis or post-closure antithrombotic therapy regarding catheter closure of the shunt.

Striatal capsule infarction

This is a concept that partially overlaps with BAD. BAD must be a cerebral infarction of unknown origin in the TOAST classification, but striatal capsule infarction may include cases such as internal carotid artery stenosis and atrial fibrillation. According to the classification of Donnan et al., intrastriatal infarction is classified into cardiogenic cerebral embolism, internal carotid artery occlusion group, middle cerebral artery proximal anomaly group, and 4 unknown etiology. The abnormal group in the middle cerebral artery proximal region corresponds to BAD. It forms a large infarct that contains several perforated areas, the cortical area escapes the infarction, but does not normally occur in lacunar infarction, such as aphasia, visual field loss, apraxia, agnosia.Cortical symptomsOften occur.

Binswanger disease

Known as cerebrovascular dementia characterized by white matter lesions. It accounts for about half of Japan's cerebrovascular dementia with multiple lacunar infarct dementia. It is classified as subcortical vascular dementia and is mainly caused by cerebral small blood vessel lesions.

Multiple cerebral infarction

When multiple cerebral infarctions or multiple infarctions are observed in the whole body, treatment is started with cardiogenic cerebral embolism in mind, and in parallel with that, search for heart diseases that may be an embolization source. Non-valvular atrial fibrillation is the most prominent disease, and rheumatic heart diseaseMitral stenosis,acuteMyocardial infarction,Ventricular aneurysm,Artificial valve, Left atrial myxoma, paradoxical cerebral embolism, etc. As a cause of non-cardiogenic cerebral embolism, thrombus released from arteriosclerotic lesions of the intracranial and external main trunk arteries such as the aortic arch and the common carotid artery is a frequent source of embolism. Congenital coagulation disorders such asAntiphospholipid antibody syndrome, Disseminated intravascular coagulation syndrome, acquired coagulopathy such as remote effect of malignant tumor.

Brainstem infarction

Cerebral infarction and confusing pathology

In differentiating cerebral infarction in the emergency roomHypoglycemia,痉挛However, cerebral infarction and the like associated with aortic dissection are important differential diseases because of different treatment methods. In addition, mention rare but important diseases.

Transient Amnesia (TGA)

(TGA) is a characteristic of being unable to understand my situation due to marked recent memory deficits or sudden retrograde amnesia that suddenly occurs when cognition and intelligence are maintained, and the same question is repeated many times. is there. The seizure persists for about 6 to 7 hours and improves after shortening of retrograde amnesia. Caplan diagnostic criteria and Hodge diagnostic criteria are known. Information on seizure witnesses is obtained. Neurological symptoms are anterograde or retrograde amnesia, transient memory impairment only, seizures disappear within 24 hours, recent trauma or within 2 yearsEpilepsyThere are four important features. According to Hodge et al., the annual incidence rate is 4, the average age is 3 years, the recurrence rate is 10%, and the seizure duration is 62 minutes to 13 hours. Mental and physical stress (15%), cold water bath (12%), emotional changes, sexual intercourse, angiography, driving, and karaoke have been reported as incentives. The pathological condition of TGA is considered to be a transient metabolic disorder of the hippocampus and limbic system including the memory circuit of Papes.


Characterized by juvenile diabetes with a family history, hearing loss, etc.Mitochondrial encephalomyopathyOne of them is MELAS. MELAS repeats seizures due to dysfunction of vascular wall mitochondria and stroke-like attacks such as hemiparesis and hemiblindness. Stroke-like attacksOccipital lobe,Parietal lobeIt is often seen in stroke and is referred to as a stroke-like seizure because the distribution of lesions does not match the dominant region.


RPLS is a concept advocated by Henchey et al. in 1996.headacheOr visual impairment,Consciousness disorderShows symptoms such as. The lesion is reversible. ,Uremia,Eclampsia,Collagen disease,chemical treatment,ImmunosuppressantIt is known that the cause is administration. Usually, systolic blood pressure is 200 to 220 mmHg or more, and diastolic blood pressure is 120 mmHg or more. In young people, systolic blood pressure may occur at about 150 mmHg. In the case of immunosuppressive drugs, it is considered that the drug is caused by endothelial cell damage. It is said that the basic pathological condition is that BBB is disrupted due to an increase in blood pressure that exceeds the upper limit of blood pressure autoregulation, and angioedema occurs due to increased vascular permeability (breakthrough theory). Since acute hypotension is likely to cause cerebral ischemia, the goal is to use an intravenous drug whose volume can be adjusted easily within 1% of the average blood pressure within 25 hour of starting and 2/6-160 mmHg within the next 100-110 hours. May be used together. As another treatment, if you have a convulsionAntiepileptic drugIs the administration of.

Transient cerebral ischemic attack (TIA)

TIAConfusion of definition is admitted about. According to the Ministry of Health and Welfare standards of 1990, “local neurological symptoms due to cerebral ischemia appear, but disappear completely within 24 hours (mostly within 1 hour) and head CT shows an organic lesion that corresponds to the responsible lesion. However, due to the widespread use of MRI after that, there were very many cases in which a high-intensity area was observed in diffusion-weighted images even if the above definition was satisfied, and some patients had a cerebral infarction. Therefore, in 2002, the TIA working group stated that “TIA is a symptom of a short-term neurological symptom caused by focal cerebral ischemia or retinal ischemia, and usually the symptom disappears within 1 hour and is accompanied by the findings of acute cerebral infarction. There is no such thing." In any case, the diagnosis name will change depending on whether emergency MRI can be performed. The ABCDD score can be used to predict the progression of cerebral infarction. There are also reports that accuracy is improved by including diffusion-reduced lesions in MRI and arteriosclerotic changes in MRA.

A (age)Over 60 years old1 points
B (blood pressure)Systolic blood pressure ≧140 mmHg or diastolic blood pressure ≧90 mmHg1 points
C (clinical features)Weakness on one side2 points
Speech disorders without weakness1 points
D (duration of symptoms)60 minute or more2 points
10 minutes or more and less than 60 minutes1 points
D (diabetes)Have diabetes1 points

The risk of stroke within 2 days after the onset of TIA is 3% at 1.0 points or less, 5% at 4.1 points or less, and 6% at 8.1 points or more. The ABCD score excluding diabetes is evaluated for the risk of stroke within one week, with 1 points at 4-2%, 4 points at 5-12%, and 28 points at 6-28%. As the concept of TIA spreads, all transient neurological symptoms tend to be diagnosed with TIA. The symptoms that are not characteristic of TIA and the symptoms that are unlikely to be TIA are summarized below. In NINDS-Ⅲ, focal cerebral dysfunction = TIA + stroke. Focal brain dysfunction is a neurological deficient condition that can be explained by functional localization of the brain.syncopeIs a global transient ischemia of the brain, not focal stroke, which is focal cerebral dysfunction.. A stroke may cause disturbance of consciousness, but in a case of widespread cerebral infarction. TIA is not suspected unless it is a transient disturbance of consciousness and is accompanied by localized neuropathy.

Symptoms not characteristic of TIAImpaired consciousness without other symptoms of the vertebral basilar artery system
Tonic seizures, tonic-clonic seizures, clonic seizures
Symptoms of persistent progression across several areas of the body
Flashing scotoma
Symptoms that are unlikely to be TIAProgression of sensory disorders
Vertigo only
Upset (floating) dizziness only
Dysphagia only
Dysarthria only
Double vision only
Stool or urinary incontinence
Visual impairment due to changes in consciousness level
Local symptoms associated with migraine
Only confusion
Amnesia only
drop attack only

However, cerebral infarction with only vertigo, which is extremely rare, is also known, and exclusion should be carefully performed.

TSI (Transient symptoms associated infarction)[Note 2]

It is TIA that diffusion reduction is not observed on MRI images, but the time course and TIA of which diffusion reduction is observed on the image may be distinguished from TSI. This is considered to correspond to unstable angina in ischemic heart disease. In the hyperacute phase, DWI shows a high signal but ADC-MAP does not show a low signal, which is considered to be a penumbra in many cases. This image finding needs to be distinguished from the pseudo-normalization of cerebral infarction.


Cerebral infarction develops in a necrotic area (a symptom due to a loss of brain function in that area), and therefore exhibits various symptoms depending on the case. The responsible lesion can be determined from the symptoms (Neurodiagnosis).AHA(American Heart Assocition;American Heart Association), the general public states the following symptoms and symptoms as a trigger for suspecting stroke.

Paralysis on one side
Usually presents with unilateral weakness, clumsiness, or heavy feeling.paralysisIs:motionThe most common symptom is paralysis.Middle cerebral arteryBy the blockage ofFrontal lobeOr is it necrotic?BrainstemIn the infarctCone pathIt develops depending on the necrosis.
In most cases, one upper limb, lower limb, or face is weak or weakHemiplegiaTake the form of[Note 3]. However, in brainstem infarction, the paralyzed side may differ between the face and extremities.
Numbness on one side
Usually, bluntness on one side of the body, abnormal sensation. It appears by necrosis of sensory fibers or sensory centers in the parietal lobe. In addition to blunting or loss of sensation, in the chronic phasepainMay appearQOLHas a large effect on.
Language disorder
Language comprehension and speech disorder (Aphasia) Or ambiguous language (Dysarthria). Larynx/pharynx/tongueThe paralysis and sensory deficits also affect the movements of the animals, resulting in impairment of swallowing and vocalization functions. Articulation disorders are different from the aphasia described later,言语Although the processing function is maintained, communication is insufficient due to an obstacle at the vocalization stage. Dysphagia causes inadequate eating and makes it difficult to return to society.aspirationBypneumoniaIt has a great effect on the cause of.
Disorders of pharyngeal and laryngeal functions that cause swallowing and dysarthriaMedulla oblongataFrom the failure ofBulbar paralysisIs called (medullary bulb is spherical), but from the upper part to the medulla oblongataNerveIt is called because there are similar symptoms in fibrotic disorders.
Blindness on one side
Painless loss of sight of the single eye, often described as "curtain hanging".
It feels like it's spinning around when it rests. Dizziness alone is a common symptom of nonvascular disease. Therefore, it is necessary that at least another transient cerebral ischemic attack or cerebral infarction be present.
Deterioration of balance function, stumbling during walking, staggering, and unilateral coordination disorder.cerebellumorBrainstemAppear in the infarction ofwalking, Utterance,Sense of balanceThe obstacle appears. In this connectiondizzyMay appear.

If these symptoms are observed, it is advisable to see a medical institution as soon as possible. In addition, the following symptoms are also typical.

Consciousness disorder
When the arousal system of the brainstem is disturbed, etc.ConsciousnessLevel drops and widespreadCerebral cortexAlso seen in the destruction of. Even without it, in the acute phasebrainBrain activity is suppressed by swelling of theAwareness levelMay go down. Lacuna infarction is less likely to cause disturbance of consciousness because the infarct area is small and swelling and other effects on the entire brain are small.
Higher brain dysfunction
Aphasia,DisapprovalAnd a variety ofHigher dysfunctionMay appear.Ignore half space(空间Of these, either the left or right is out of consciousness). This is the cerebrumParietal lobeYou can see it in右 利 き95% of humans have inferior hemispheresrightMost of the "right-handed left hemiplegia"patientIt can be said that this is a symptom. Aphasia, on the other hand, is a disorder of, and is often seen in patients with "right-handed right paralysis".

The severity of the above-mentioned symptoms is often evaluated by NIHSS in Japanese medical institutions and KPSS (Kurashiki Prehospital Stroke Scale) in prehospital.


Symptoms of cerebral infarction vary from progressively increasing to suddenly completing. However, embolic ones often complete suddenly.
The most common onset time is from night to early morning. This is associated with a tendency to dehydrate during sleep because it does not drain water. Throughout the yearSummer: Winter:There are many. Dehydration in the summer and immobility in the winter are associated with the onset. In particular, elderly people are more afraid of nocturia and often refrain from drinking water, which is one of the causes of the increased incidence.
Paralysis is the most noticeable symptom. For complaints such as "the body is leaning" and "I can't stand up"hospitalOften come to the. On the other hand, a seemingly bizarre symptom such as aphasia may not be recognized as a cerebral infarction and delays the visit to a medical institution.
Acute period
The symptoms of cerebral infarction are strongest in the acute phase, and gradually improve thereafter. This is because the brain tissue that has fallen into necrosis is swollen, and the surrounding brain tissue is also compressed and damaged. As the swelling subsides, the surrounding tissues recover their functions and the symptoms are fixed. However, swelling and release from necrotic tissueFree radicalsHas a function of necrotizing surrounding tissues, and suppressing them leads to improvement of functional prognosis.
In the acute phaseblood pressureBecomes higher. In some cases (systolic blood pressure), it may exceed 200 mmHg. This is a physiological reaction of sending blood flow to the ischemic site, and do not attempt to reduce blood pressure. (If the blood pressure is lowered too much, the infarct area may be widened.)
Antihypertensive drugs and careless elevation of the head worsen cerebral blood flow, causing recurrence and exacerbation of symptoms. Rest on bed for at least 24 hours until symptoms stabilize.
Subacute phase
In mild to moderate cases, brain swelling and hypertension subside within a few days, and in some cases almost all of the symptoms disappear and disappear. However, if a large aftereffect remains,リ ハ ビ リ テ ー シ ョ ンIt is very difficult to recover the function to the same level as before the onset even after continuing the treatment.
Chronic phase
Although it depends on the cause, the recurrence rate of cerebral infarction in persons with a history of cerebral infarction is very high. Therefore, it is necessary to continue to take medication to prevent recurrence. Also, as a long-term aftereffectEpilepsy,ParkinsonismMay develop.

Confirmation method

There is a confirmation method called FAST that you and your family can do[7][8][9].America-MassachusettsPublic awareness campaign (en) Has also produced a video animation [10].

  • Face: Confirmation of facial paralysis.The side of the mouth is called the corner of the mouth, but try to pull up the corners of the mouth on both sides and say "yes".SmileI will make. If nothing happened until then, but one of the corners of the mouth suddenly disappears, you are paralyzed[7].
  • Arm: wristCheck for paralysis. With your eyes closed, palms up and your arms stick out straight ahead. If there is paralysis, the arm on the paralyzed side will rotate inward and lower[7].
  • Speech: Confirmation of verbal paralysis.Actually pronounce some short simple sentences and check them.For example, it is easy to understand if you say a sentence with many "La lines" such as "Taro gave Hanako an apple".[7].. If you can't remember, say any number of sentences, any sentence[7].. If you can't say it clearly, you have paralysis of language.
  • Time: Check the above three (FAS), and if any of them is clearly applicable, go to the hospital because it is "Time", that is, it is time to see a doctor.Have your family take you by car or call 3 to tell them what the FAST confirmation was and ask them to come to the ambulance.Perform an examination at the hospital.


neurologyorNeurosurgeryHowever, prompt response is required in the hyperacute phase within 3 hours after onset,Emergency departmentThere are many things to do.

Physical findings (neurological findings)

In addition to the above-mentioned nest symptoms, suggests upper central disordersPyramidal sign(Tendon reflexIncrease inBabinski reflectionCan be inferred from the appearance) and abnormalities. Several scales have been proposed as a method of describing the objective severity of cerebral infarction (stroke) from neurological findings. The easiest and most clinically usedNIHSS(National Institute of Health Stroke Scale)[11].. This is an essential item when performing thrombolytic therapy in the hyperacute phase.

Inspection findings

Although there are no characteristic findings on a general blood test, thrombosis may be enhanced when platelet function is examined. However, it is significant to evaluate basic diseases such as hyperlipidemia and diabetes from blood tests. When performing thrombolytic therapy in the hyperacute phaseHigh blood sugar,HypoglycemiaBlood tests are mandatory because there are absolutely contraindicated items such as.

Image findings

X-rayCTThen,cerebral hemorrhageDistinction with a median structure deviation,Early (early) ischemic changes(Early CT sign) can be confirmed. In the case of cerebral hemorrhage, hematoma can be confirmed as a clearly high absorption region from the hyperacute phase unless it is very small. Since it is difficult to determine the early CT sign depending on the CT imaging conditions, the CT imaging conditions are standardized in the “rt-PA (alteplase) intravenous therapy appropriate treatment guideline”. Early CT signs are known to indicate cerebral ischemia and occluded blood vessels. Cellular edema is often seen around 1 hour after onset and angiogenic edema is often seen around 3 hours after onset.
early CT signFindingsSignificancePathology
Obscuring the lens nucleusThe boundary between the lens nucleus and the internal capsule is unclear, but the boundary with the island cortex is clearIschemia in the middle cerebral arteryCellular edema
Loss of the island cortexBlurring the border between the island cortex and the subcortexIschemia in the middle cerebral arteryCellular edema
Obscuring the border of the pulpThe boundary between the cortex and the subcortex becomes unclearIschemia in the middle cerebral arteryCellular edema
Loss of sulciThe sulci are narrowedIschemia in the middle cerebral arteryAngiogenic edema
hyperdense MCA signMiddle cerebral artery M1 shows high absorptionOcclusion of middle cerebral artery M1Vascular occlusion
MCA dot signMiddle cerebral artery M2 shows high absorptionOcclusion of middle cerebral artery M2Vascular occlusion
When cerebral ischemia exceeds 1/3 of MCA area (1/3MCA area), thrombolytic therapy is out of therapeutic indication, and thus it is important to judge the presence or absence of initial ischemic change in recent years. The area of ​​MCA is calculated by the ASPECT method. In the ASPECT method, scoring is performed by the deduction method using two slices of the basal ganglia thalamus level and the lateral ventricle level. If there is no early CT sign, the score is 2, and if all are recognized, the score is 10. The best indication is an example of ASPECT with a score of 0 or higher, and ASPECT of 8 or lower has a risk of bleeding more than 2 times higher than that of 3 or higher.
Over time, necrotic brain swelling may occur. Then, the necrotic tissue softens within a few days of onset and becomes dark on CT, but none of these findings are clear in the acute stage of onset.
MRIThen, it is possible to catch the findings earlier.T2-weighted imageThe lesion becomes a high signal at (細胞Swelling) is seen about 6 hours after onset,Diffusion weighted image (DWI)It is said that the high signal can be recognized after about 3 hours. Conceptually, it is considered that the site showing high signal intensity in DWI already shows irreversible change, and it is a reversible site around it.PenumbraAre believed to exist. However, it is known that most of DWI's high-intensity areas correspond to infarct lesions, but reversible lesions may be included in pale lesions. On the contrary, it is often observed that DWI shows false negatives in the very early stage. About 24% of false negatives are known within 5 hours of onset. In particular, 6% of false negatives are observed in the vertebral artery perfusion area within 20 hours of onset. Especially, it is said that there are many medullary lesions. On the contrary, false negatives in the cerebral cortex are low and about 2%. It is advisable to take another 24 hours after the first DWI, even when no high signal is observed, and when cerebral infarction is strongly suspected from the symptoms. In that case, the detection rate becomes higher when the slice is thinned to about 3 mm and the b value is 2000 or more.
Immediately after onset (0-1 hour)Perfusion abnormality immediately after occlusionDisregardDisregardDisregardDisregard
Hyperacute (1-24 hours)Cellular edemaHigh signalLow signalDisregardearly CT sign
Acute period (1-7 days)Cellular edema and angioedemaHigh signalLow signalHigh signalLow absorption
Subacute (1-3 weeks)Gradually reduce edema from inflammatory reaction due to cell necrosisHigh signal gradually to low signalFrom low signal to high signal graduallyHigh signalFrom low absorption to low absorption via FE
Chronic period (1 month -)Necrosis, absorption, scarringLow signalHigh signalHigh signalCSF concentration
The above table is a typical time course of MRI in cerebral infarction. In the hyperacute phase, the diffusion coefficient decreases due to cellular edema, which is expressed as high signal in DWI and low signal in ADC-MAP. In the acute phase, disruption of the BBB of capillaries causes angioedema. Since the amount of water per unit tissue increases due to angioedema, T2WI shows a high signal. In the acute phase, reperfusion exacerbates angioedema, causing marked cerebral edema andHemorrhagic infarctionMay cause. In the subacute phase, the diffusion coefficient increases due to cell necrosis and vascular necrosis, so that the pseudonormalization occurs for a period of time. In the diffusion-weighted image, the high signal continues until the latter half of the subacute period under the influence of T2 shine through. Because of this phenomenon, even if the signal is high in the diffusion-weighted image, it cannot be said that the diffusion coefficient is low or the stroke is cerebral infarction hyperacute phase. Therefore, ADC-MAP is also used for evaluation. Approximately 2 weeks after the onset, CT even temporarily reduces lesions due to the reduction of angioedema. However, it is obscured and is called FE (fogging effect). In the subacute stage, bleeding within a small infarct may be observed due to the development of collateral circulation due to pial meningeal anastomosis and compensatory perfusion increase, and a low signal is shown at T2*. Unlike acute hemorrhagic infarction, this does not lead to aggravation of serious neurological symptoms, but in the case of lacunar infarction, it is considered safe not to administer antiplatelet drugs if these findings are present. .. After that, T2WI hyperintensity is seen as a chronic phase finding, but depending on the degree of tissue deficiency, the FLAIR image may be hypointensified. This is due to the opening of the extracellular fluid space.
It is known that in the cerebrovascular disorder, secondaryness occurs in the remote area. A representative example is shown.
Secondary changeFindings
Wallerian degeneration of the corticospinal tractCorticospinal tractIf there is a disorder in T4, T2 will be shortened from 10 weeks later and T2 will be extended from 2 weeks later. In DWI, signal changes are observed in 8 to XNUMX days.
Thalamic degenerationWhen the middle cerebral artery area including the lateral striatal artery is impaired, T3 is prolonged 2 months after the onset of ipsilateral thalamus via corticothalamic tract. It often originates from the dorsomedial nucleus.
Degeneration of the substantia nigraStriatumT10 prolongation was observed about 2 days after the onset of ipsilateral midbrain substantia nigra, and disappeared in about 1 month.
Lower olive nuclear pseudohypertrophyIn the cerebellar dentate nucleus lesion, degeneration occurs on the contralateral inferior olive nucleus and on the ipsilateral side of the dorsal central tegmental tract. T2 prolongs in a few months and then enlarges.
Crossed cerebellar atrophyWhen the pontine nucleus is damaged, Wallerian degeneration occurs in the contralateral midcerebellar peduncle. When the vicinity of the pontine nucleus is disturbed, similar degeneration occurs on the contralateral side, and thus it is often bilateral.
Other famous findingsCortical layered necrosis(Cortical laminar necrosis), which means that the vertebral body cell layer (third layer) selectively falls into ischemia.High signal area along the cortex at T3WI about 1 weeks after onsetIs recognized. Regarding the blockage of blood vesselsintra-arterial sign(IA sign) is known.Normally, the blood vessel lumen becomes a flow void in the FLAIR image, but when blood stasis is observed, the blood vessel can be visualized in the FLAIR image in the acute phase.
Stenosis and occlusion of the main brain artery may be revealed by TOF-MRA or MIP. Occlusion of the main artery can be detected by confirming the disappearance of flow voids, but it becomes easier to understand by performing MRA. The flow void means the disappearance of the signal generated due to the flow of blood and cerebrospinal fluid. In addition, contrast MRA of the carotid artery is often used together with CTA in transarterial evaluation. A point of caution with MIP images is that it is easy to overestimate stenosis. Stenosis is overestimated when turbulence is observed. Due to this effect, it may appear as a blockage at first glance (flow gap). If the periphery is visualized to the same extent as the contralateral side, it is likely that turbulent flow is being observed instead of severe stenosis. In 3T MRA, plaque properties can be evaluated by using the imaging method called 3D black blood imaging.
PlaqueTOFT1WIProton density weighted imageT2WI
Lipid core (no bleeding)Equal signal to mild high signalEqual signal to mild high signalEqual signal to mild high signalEqual signal to mild high signal
Lipid core (fresh bleeding)High signalHigh signalLow signal to equal signalLow signal to equal signal
Lipid core (with bleeding)High signalHigh signalHigh signalHigh signal
Fibrous capLow signalEqual signal to mild high signalEqual signal to mild high signalEqual signal to mild high signal
CalcificationLow signalLow signalLow signalLow signal
Fibrous tissueEquivalent to low signalEqual signal to mild high signalEqual signal to mild high signalEqual signal to mild high signal
BPAS (basiparallel anatomic scanning)
It is said to be effective in detecting arterial dissection and distinguishing between chronic obstruction and acute obstruction. MRA signals the flow of blood, whereas BPAS gives an indication of the appearance of blood vessels.
Carotid echo
If thrombotic, cervical blood vesselsechoIn some cases, narrowing due to atheroma (plaque) on the inner wall of the blood vessel can be confirmed (subject to surgical resection in advanced cases). Echoes may also show microemboli (HITS) flowing through intracranial blood vessels.
Echo brightness, surface quality, uniformity, and mobility are often evaluated as properties of plaque. Echo brightness is said to be in contrast to pathological tissue, low brightness corresponds to atheroma or hematoma, equal brightness to fibrous tissue, and high brightness to calcified lesion. When the brightness is low, it is vulnerable and the risk of cerebral infarction is high. As a surface texture, irregularities in the wall are said to be at risk of cerebral infarction even without plaque. Also, a depression of 2 mm or more, that is, an ulcer is at high risk of cerebral infarction. In addition, it is said that the risk of cerebral infarction is higher when the plaque is uneven in character than when it is uniform. It is also thought that there is a high risk of high speed when mobile thrombus is attached to the plaque, but the frequency is low.
Non-valvularAtrial fibrillationIs the most risk of cardiogenic cerebral embolism,EchocardiographyFurther detailed evaluation can be performed by performing. Important findings as embolic sources include left atrial appendage thrombosis, patent foramen ovale (PFO), atrial septal aneurysm, heart tumor, and aortic arch compound atheroma lesions, which are detected by transesophageal echocardiography The rate is high. About 20% of patent foramen ovale (PFO) is observed in general autopsy, and it becomes a right-left shunt, and thrombosis formed in the vein flows out into the left ventricle system, causing cerebral infarction. This is referred to as paradoxical cerebral embolism, and is frequently seen in younger people and cerebral infarction of unknown cause. If the onset pattern is suspected to be embolism but there is no atrial fibrillation and no significant lesion is found in the internal carotid artery, suspect aortic cerebral embolism and search for aortic arch compound atheroma lesion.

対 応

If cerebral infarction is within 8 hours in the hyperacute phase, thrombolysis is the first choice, and if it is not possible, physical elimination removes the thrombus. At this point, no necrosis has occurred,Penumbra(penumbra), at the stage of cells that are still alive but have ischemic symptomshealingThere is a possibility. Especially, thrombolytic therapy has an extremely short time limit (rt-PAWithin 4.5 hours (4 hours 30 minutes)), the situation fought for seconds. For the treatment in the hyperacute phase, new therapies have appeared one after another since the end of the 20th century, but the confirmation of safety etc. is still insufficient.

In the acute phase of 8-24 hours, swelling andFree radicalsThe first is to prevent the necrosis from progressing. It is also necessary to prevent reinfarction. Therefore, if it seems to be thrombotic, use an anticoagulantGlycerinIncrease plasma osmolality with (Glyceol ™) or mannitolBrain edemaWithin 24 hours of onsetEdaravone(Radicut ™) suppresses free radical production.In addition, blood flow is maintained at the boundary between the infarct and the penumbra.

Thrombolytic therapy

DrugPoints to remember
rt-PA (tissue plasminogen activator, alteplase)It is indicated for all disease types within 4.5 hours of onset.Evidence-based medicineClassification byRecommended Grade A(Highest priority)[12].. However, there are items such as contraindications and careful administration, so caution is required. A rapid intravenous injection of 0.6% of 60 mg/kg (up to 10 mg) is given, and the rest is infused over 1 hour.AlteplaseOther t-PAs are not approved in Japan and are recommended grade C2 (not recommended because there is no scientific basis)[12].
Urokinase (arterial catheter)Within 6 hours of onset. Indicated for embolic occlusion of middle cerebral artery. Recommended grade B (recommended). For all other types, it is recommended Grade C1 (though it may be considered to be done, but there is insufficient scientific evidence). Urokinase acts more systemically than rt-PA and is more likely to cause side effects. Therefore, this therapy in which an arterial catheter is inserted close to the thrombus and is directly administered to the thrombus is desirable.

In the case of atherothrombosis or embolism, immediately after the onset (Within 4.5 hours (4 hours 30 minutes)), and if you have a well-equipped medical institutionrt-PA(Tissue plasminogen activator, Alteplase) can be administered locally intravenously. This is the main component of thrombusFibrinMeltPlasminHas the effect of activating. At the Japan Stroke Society rt-PA (Alteplase) Intravenous Therapy Appropriate Treatment Guideline Second Edition October 2012 (Partially revised in September 10) Has been published. Also,UrokinaseArterial catheters are adaptable within 6 hours of onset[13].. However, urokinase has a weaker thrombolytic effect than rt-PA, and the side effect of blood loss is likely to occur, so rt-PA is the first choice in an environment where both can be used. UrokinaseIntravenous injectionCan be done after 6 hours, but the effect is even worse.

Activacin and glutopa are mainly used as alteplase.A good example of thrombolytic therapy is that treatment can be started within 3 hours of onset.If the symptoms are too serious, the drug should be administered with caution. In NIHSS, around 5 to 15 points is a positive adaptation. Do not perform if CT shows lesions in more than 1/3 of the MCA area (MRI does not need to be performed).In addition, as an evaluation of the risk of bleeding, the medical history, platelet count, and PT-INR <1.7 are used as indicators.Hypertension poses a risk of bleeding, but it is considered that there is no problem if it can be controlled to 185/110 or less at the time of intravenous injection.According to the management guidelines, neurological evaluation such as NIHSS is to be performed every 1 minutes for 15 hour during rt-PA administration, every 7 minutes for 30 hours after the start of administration, and every hour for up to 24 hours thereafter. Antithrombotic therapy is contraindicated within 1 hours when intravenous rt-PA is given.Therefore, rt-PA and urokinase arterial catheter cannot be used together.However, after 24 hours, antithrombotic therapy is also commonly used.

rt-PA (Alteplase) Intravenous Therapy Appropriate Treatment Guideline Second Edition October 2012 (Partially revised in September 10) According to the study, treatment indications are evaluated in three groups: confirmation, contraindications, and careful administration. The revision in September 2016 partially relaxed. The outline is summarized below.

Items to check
The confirmation rule is an item that must be evaluated for all, specifically, the onset time (final non-onset confirmation time) and the severity. It is said that if the symptom is mild, it is not indicated, but it is often NIHSS 4 or less. In addition, the rapid improvement of symptoms is often an improvement of NIHSS 4 or higher.
Exceeding the time limit, recurrence of non-traumatic intracranial hemorrhage, recurrence of cerebral infarction within 1 month, subarachnoid hemorrhage (including suspicion), hypertension (when systole 185 mmHg/diastole 110 mmHg or more after antihypertensive therapy), severe Liver disorders, abnormal blood sugar, etc. If any of these apply, it will be out of the indication (Recommended Grade D: It is recommended not to do it). If you have a convulsion,EpilepsyIt is contraindicated when it is judged that there is a high possibility of (because it is a careful item unless epilepsy). Intracranial hemorrhage is intracerebral hemorrhage and subarachnoid hemorrhage, and does not include traumatic epidural hematoma over 3 months.
Cautious items
81 years or older[14], Uncontrolled diabetes mellitus, previous cerebral infarction (before 1 month), intracranial tumor[15][16],aneurysm[15], Moyamoya disease[15], Intracranial hemorrhage[15] Etc. are included. The indication for this patient is recommended grade C1. The treatment can be performed only when the doctor judges that the benefit of the treatment outweighs the disadvantage and obtains the consent from the patient or the legal representative with sufficient explanation.

According to a 1995 US report, 31% recovered almost asymptomatic andplacebo) Was better than 20%. The mortality rate was 17%, which was superior to the control 21%. on the other hand,cerebral hemorrhageSide effects were 6.4%, which was significantly higher than the control 0.6%[17].. 2002-2004, clinical trial in Japan (J-ACT) was done. The subjects were 3 patients with cerebral infarction within 103 hours after the onset, who received 1 mg/kg body weight, which is 0.6/2 of the overseas dose. Three months later, the recovery was 3% (3/36.9 cases) and death was 38% (103/9.7 cases) without disability. In addition, cerebral hemorrhage within 10 hours was 103% (36/5.8 cases). From this result, it was reported that the same effect could be obtained at the dose of 6/103 overseas.[18].

As a result of these clinical trials, even in Japan, since October 2005, the treatment of hyperacute ischemic cerebrovascular disease by intravenous administration of alteplase (genetical recombination) in rt-PA was covered by health insurance. Initially, the indication was within 10 hours of onset.

When using rt-PA for the treatment of myocardial infarction, 1.76% (7/398 cases) before approval and 14 cases (14,360 times of administration) after marketing were reported. It may be a treatment method that can be carefully selected in a well-established institution such as a cerebral infarction ward, with sufficient explanation and consent. Also, in order to meet the condition of "starting treatment within 4.5 hours", other than the patient's own condition, where there are hospitals that can be treated with rt-PA is shared among the ambulance crew, hospitals, and local governments. Must work together. According to the guidelines of AHA (American Heart Association), if an acute stroke is suspected, rt-PA treatment may be considered and it should be transported by ambulance. With the revision of medical fees in 2008, "hyperacute stroke addition" (12,000 points), which can be calculated when medical treatment using rt-PA was given to a medical institution designated by the Minister of Health, Labor and Welfare, was set. In the future, it will be necessary to take measures at the administrative level.

On August 2012, 8, the rt-PA indication was expanded from within 31 hours to 3 hours after onset.[19].

Vascular treatment (thrombus recovery therapy, mechanical recanalization therapy)

#Vascular treatment (vasodilation)See also

Next to the thrombolytic therapy was a treatment in which the thrombus itself was entangled with a wire or the like, or aspirated with a pump to remove it (thrombus recovery therapy, mechanical recanalization therapy). Indications for thrombus recovery therapyWithin 8 hours of onsetLimited to[20].Within 6 hours of onsetIn addition, the recommended grade A of this therapy in combination with rt-PA[21].. If rt-PA is ineffective or non-adaptive and the main cerebral artery is occluded within 8 hours of onset, this therapy may be considered (recommended grade C1[20]). In middle cerebral artery embolic occlusion with neurologic deficient symptoms, if local symptom at admission is moderate or less and no infarct lesion on CT or slight infarction remains, selective local thrombolytic therapy should be used instead of this therapy. (Urokinase arterial catheter) is prioritized (Recommended Grade B)[20].

Initially, it was only indicated when the treatment with rt-PA could not be used or was ineffective.[22], April 2015, the Japanese Society for Stroke, Japanese Society for Neurosurgery, and Japanese Society for Endovascular Neurotherapy show that rt- for ``acute cerebral infarction due to main artery occlusion within 4 hours of onset''. It was concluded that the effect of adding this therapy to medical treatment including PA is scientifically supported. On the other hand, for the main trunk artery occlusion of the posterior circulatory system, and 6 to 6 hours after the onset, and the case after that, it is said that the knowledge of efficacy has not been accumulated yet.[23].. No significant side effects were reported in any of them. Although it was pointed out that his condition worsened when he failed, he has rapidly established himself as a treatment method.

In 2015, there was also a report saying that the treatment result exceeded that of rt-PA.[24].. Sadayoshi Watanabe, Director of General Tokyo Hospital, said that the revascularization rate with the "Solitaire FR clot removal device" has increased to around 9%.[25].. Also, on February 2015, 2,カナダ,University of CalgaryMayank Goyar, et al., reported in the "The New England Journal of Medicine," a study group of 300 patients with cerebral infarction comparing the effects of endovascular and conventional treatments. The patients involved were relatively mild and treatment was initiated within 12 hours of onset. As a result, in the group receiving the endovascular treatment, the average time from the first confirmation of the blood vessel condition by CT to the restoration of blood flow was 84 minutes. After endovascular treatment, the rate of recovery to independence was 53.0%, which was higher than the control rate of 29.3%. The mortality rate was 10.4%, which was superior to the control 19.0%. On the other hand, cerebral hemorrhage with symptoms was 3.6%, which was higher than that of the control, 2.7%. However, the probability of intracerebral hemorrhage is statisticallySignificant differenceWas not said[26].

The following are all distinguished by product name,common name TheCentral circulatory system embolus removal catheter.. Contraindications vary depending on the product, so care must be taken when treating.

“Merci Retriever” has been approved by the Ministry of Health, Labor and Welfare on April 2010, 4.[22][27].. In October of the same year, insurance was applied. A catheter is inserted into a blood vessel, and a thrombus is directly collected with a wire and a thread.
As of June 2011, 6, the approval of the Ministry of Health, Labor and Welfare was "PenumbraSystem (Penumbra System)". In October of the same year, insurance was applied[28].. This is the same up to the point of inserting the catheter into the blood vessel, but there is a difference in sucking a thrombus with a pump.
Approved by the Ministry of Health, Labor and Welfare as of December 2013 is the "Solitaire FR blood clot removal device"[29].. In July 2014, it was covered by insurance. A mechanism in which a catheter is inserted into a blood vessel and a blood clot is directly collected with a wire, but only the wire portion collects a blood clot.
As of March 2014, the “Trevo ProVue Retriever” was approved by the Ministry of Health, Labor and Welfare.[30].. In July 2014, it was covered by insurance. A catheter is inserted into the blood vessel and the thrombus is directly retrieved with a wire. Real-time X-ray fluoroscopy is possible, and you can proceed with the treatment visually.

Conservative treatment

If there is atherothrombotic infarction or lacunar infarction that has not been applied after the onset of time, ozagrel sodium (Antiplatelet agent) ・Administer argatroban (antithrombin drug, thronon HI, etc.) at an early stage of onset. However, in cardiogenic embolism these are contraindicatedHeparinAre used. In the presence of two-vessel lesions (such as extensive infarction extending to the anterior cerebral artery region and middle cerebral artery) and infective endocarditis, bleeding risk is high and antithrombotic therapy is generally absent. A combination therapy with aspirin and clopidogrel sulphate is common.Combination within 3 months of onsetWas effective in preventing recurrence without increasing bleeding (Recommended Grade B)[31].. The combination of aspirin and warfarin has a high risk of bleeding and is uncommon. Also, concomitant use of antiplatelet drugs for more than 1 year has not been demonstrated to have a recurrence-suppressing effect, and it is recommended not to use it because it increases the risk of bleeding (recommended grade D). On the other hand, adding cilostazol to either aspirin or clopidogrel has no difference in safety, and it has been reported that the addition of cilostazol is more effective in preventing cerebral infarction recurrence.[32].

DrugPoints to remember
EdaravoneIs a brain protectantEdaravone(Edaravone) (Radicut(Radicut), etc.) are indicated for all disease types within 24 hours after onset. Recommended grade B[33].. Contraindicated when renal dysfunction is observed.
Free radicalsIt is considered that the elimination effect has the effect of reducing cellular edema. Dissolve 1 mg once in physiological saline etc. and infuse twice a day for 30 minutes. It can be administered for 1 days.
In recent years, it is often used together with t-PA. Consider the case of short-term termination depending on the symptoms.
Edema 1 to 4 days after onset is angioedema with edema and etalabone is not effective and glyceol (glyceleb) may be used.
Ozagrel sodiumSodium (cataclot, xanthone), a thromboxane A2 synthase inhibitor (antiplatelet drug), is contraindicated in cardiogenic cerebral embolism, but in acute phase (within 5 days of onset) atherothrombotic cerebral infarction and lacunar infarction There are adaptations. Recommended grade B for indication cases[34].
Dissolve 80 mg of this drug in 200 mg of maintenance solution, and infuse twice a day for 1 hours. Administration is possible for up to 2 weeks.
Especially in the acute stage of lacunar infarction, etc.Ozagrel) And aspirin are often used together.
ArgatrobanIs a selective thrombin inhibitorArgatroban(Argatroban) (Suronnon HI and Novastan HI) are contraindicated in cardiogenic cerebral embolism but are often used in atherothrombotic cerebral infarction and lacunar infarction. There is no indication for lacunar infarction in terms of insurance treatment.
Recommended Grade B for the indication type[35].. Be careful of hemorrhagic complications immediately after administration and consider adding antiplatelet drugs or changing to heparin if cerebral infarction is suspected to worsen from day 3 onward. In the acute phase of atherothrombotic cerebral embolism, argatroban and aspirin are often used together.
The half-life is 15 to 30 minutes, and it is considered that the effect decreases after the end of continuous infusion.
Heparin sodiumAnticoagulantIsHeparinHow to treat depends on the type of disease.
In case of cardiogenic cerebral embolism, bleeding (hematoma formation) occurs within 24 hours after onset,Hemorrhagic infarctionMay be
Therefore, head CT is performed 24 hours after the onset, and if there is no hematoma formation, heparin is given as a low-dose continuous infusion of 1 to 1 units/day to prevent recurrence in the acute phase. Switch to anticoagulation therapy.
In the case of progressive cerebral infarction in the case of lacunar infarction and atherothrombotic cerebral infarction, low dose continuous infusion of 1 to 1 units/day and APTT are controlled to 5 to 1.5 times the standard value. All are recommended grade C2.
Warfarin potassiumIs an anticoagulantWarfarin(Warfarin) is often used for chronic management, following the use of heparin in the acute phase.
If severe stenotic lesions are observed in atherothrombotic cerebral infarction, argatroban and heparin will be continuously administered.
In cardiogenic cerebral embolism, control PT-INR to 2.0-3.0 (1.6-2.6 in elderly and low risk). It is also used in paradoxical cerebral embolism with deep vein thrombosis. Recommended grade A for cardiogenic cerebral embolism in chronic phase[36].
aspirinIt is also preferred in the acute phase because of its rapid onset of action. The dose differs between the acute and chronic phases, and the acute phase is 160 to 300 mg/day, and the dose is reduced to 2 to 75 mg in about 150 weeks.
Even if the cause is unknownaspirinIs often selected.
If aspirin intolerance, such as aspirin asthma, or symptoms occur during oral aspirin, consider switching to other antiplatelet agents or concomitant use. Recommended grade A for all disease types in acute phase within 48 hours[34].. Recommended grade A for non-cardiogenic cerebral infarction in the chronic stage. Since warfarin is the first choice for cardiogenic cerebral embolism, warfarin will be the recommended grade B only for those contraindicated[36][37].
Ticlopidine hydrochloridehydrochloric acidTiclopidine(Ticlopidine) (Such as Panaldine) may be administered at 200 to 300 mg/day in the acute phase. 200 mg/day in the chronic phase. Recommended grade B for non-cardiogenic cerebral infarction in the chronic stage[37].. Although the efficacy is similar to that of the generic drug clopidogrel sulfate, the application of this drug is decreasing due to the strong side effects.
CilostazolCilostazol(Cilostazol) (Pletal, etc.) is administered at 200 mg / day in the acute phase.It is contraindicated in congestive heart failure and should be administered with caution in ischemic heart disease.Indications for noncardiogenic cerebral infarction in the chronic phase, recommended grade A[38].
Clopidogrel sulfateClopidogrel(Clopidogrel) (Plavix, etc.) is administered at 50 to 75 mg/day in the acute phase. Non-cardiogenic cerebral infarction in the chronic phase, 75 mg/day is recommended Grade A[37].
UrokinaseThrombolytic drugsIsUrokinaseIntravenous injection is generally contraindicated for cardiogenic cerebral embolism.
However, in the case of basilar artery occlusion, intracatheter infusion may be performed.
In the case of lacunar infarction and atherothrombotic cerebral infarction, 5 units/day of intravenous injection or hyperacute arterial infusion is given within 6 days of onset. Recommended grade C1.
DextranPlasma expander.DextranThe best indication for is atherothrombotic cerebral embolism, which is suspected to involve hemodynamic mechanisms. It may also be used in high-Ht lacunar infarction.
Use for 500 days at 5ml/5hr. Use may be considered in all cases, but efficacy is not well-founded and recommended grade C1[38].
GlyceolAtherosclerotic cerebral infarctionGlyceolAdminister 200 ml twice a day for 1 hours once. For cardiogenic cerebral embolism and cerebral hemorrhage, administer 2 to 1 times daily. If cerebral edema is prominent, it may be used about 2 times. Recommended Grade B for the indication type[39].
In heart failure, it becomes Na-loading, so careful administration is necessary. Stronger brain pressure effect than glyceolMannitolThe use of (manninigen, mannitol, etc.) is poorly evidenced. Recommended grade C1.
Atherothrombotic cerebral infarction
In the case of atherothrombotic cerebral infarction, either antiplatelet therapy or anticoagulant therapy may be an option. As antiplatelet therapy, ozacrel sodium (cataclot, xanthone) 160mg/day will be instilled or aspirin 160-300mg/day will be orally administered. On the other hand, as anticoagulant therapy,HeparinIntravenous administration (adjusted by APTT) and selective thrombin inhibitor argatroban (thronnon HI and novastan HI). Argatroban is often selected for severe cases and advanced cases, while ozacrel sodium tends to be selected for mild cases and stable cases. Combinations of argatroban with aspirin and heparin with aspirin are often used.
If the onset is within 24 hours, edaravone (such as Radicut), which is a brain protectant, may be used.Free radicalsIt is believed that the elimination action has the effect of reducing cellular edema. In recent years, it is often used together with t-PA.
If divided by the time it takes to start treatment after onset, rt-PA within 3 hours, within 24 hoursEdaravone(Radio cut, etc.) within 48 hoursArgatroban(Surongnon HI and Novastan HI), and within 7 days, there is also a proper use such as ozacrel sodium (cataclot, xanthone).
Edema 1 to 4 days after onset is angioedema in edema and etalabone is not effective and glyceol (glyceleb) may be used. Atherosclerotic cerebral infarctionGlyceolAdminister 200 ml twice a day for 1 hours once. For cardiogenic cerebral embolism and cerebral hemorrhage, administer 2 to 1 times daily. Stronger brain pressure effect than glyceolMannitolThe use of (manninigen, mannitol, etc.) is poorly evidenced.
Lacunar infarction
For lacunar infarction, aspirin or (cataclot, xanthone) is recommended. When BAD (branch atheromatous disease) is suspected, treatment with the thromboxane synthase inhibitor ozagrel sodium (cataclot or xanthone) is often performed under the diagnosis of lacunar infarction. Dissolve 80 mg of this drug in 200 mg of maintenance solution, and infuse twice a day for 1 hours (up to about 2 weeks). Immediately after the start of administration, attention should be paid to physical findings suggesting hemorrhagic complications, and if cerebral infarction symptoms worsen, it is common to consider changing to argatroban or heparin or concomitant use. Or from the beginning in the treatment of atherothrombotic cerebral infarction, argatroban (such as Suronnon HI and Novastan HI) may be used. Immediately after administration, be careful of hemorrhagic complications, and if cerebral infarction is suspected to worsen on the third day or later, consider adding an antiplatelet drug or changing to heparin.
Cardiogenic cerebral embolism
In the case of cardiogenic cerebral embolism, there is no indication for treatment with antiplatelet therapy, and heparin administration is started if 24 hours or more have passed after the onset, not for rt-PA. The use of heparin depends on the presence or absence of bleeding, but it is often used at low doses of 5000-10000 units/day.

Other therapies

A therapy that lowers the body temperature to 32-34 degrees and protects the brain. The efficacy has not been thoroughly examined (recommended grade C1). The same applies to normal fever therapy with antipyretic drugs.[40].
Hyperbaric oxygen therapy
A therapy in which high concentrations of oxygen are inhaled in a hyperbaric environment, and oxygen is replenished to the brain cells whose blood flow is disrupted due to infarction.RCTThere are few studies on the effectiveness of the drug, and there is no sufficient scientific basis (recommended grade C1).[41].
Craniotomy decompression
Progressive in patients under 70 yearsConsciousness disorderOn CTBrainstemIn the case of unilateral cerebral hemisphere infarction including the middle cerebral artery perfusion region with compression findings, it is difficult to control the cerebral pressure with drugs, and external decompression surgery by craniotomy is necessary. In case of extensive cerebral infarction, marked cerebral edema, hydrocephalus due to occlusion of the 4th ventricle, etc.Brain herniaThe idea is that decompression is necessary because pressure on the respiratory center can occur. According to the stroke treatment guideline 2009, patients aged 18 to 60 years with infarcts of 50% or more of the middle cerebral artery region within 48 hours after the appearance of symptoms.NIHSSIf the score is 15 or higher, improvement in survival rate and mRS after 1 year with external decompression accompanied by dura formation is shown. Recommended Grade A for the indication type[42].. If cerebellar infarction is accompanied by hydrocephalus, ventricular drainage may be considered, and if cerebellar infarction has brainstem compression and thus coma, decompressive craniotomy may be considered. All are recommended grade C1.
Vascular treatment (vasodilation)
In the 21st century,Endovascular treatmentWith the advance of micro with ballooncatheterVasodilation to expand the blood vessel or stent placement to place a stent (recommended grade C1[43]), cerebral intravascular treatment such as vasodilation which injects a drug that advances a catheter to a clogged place to inflate a blood vessel and thrombolytic therapy which injects a drug that dissolves a thrombus at the site are performed.
Blood vessel/cranial nerve regeneration
Clinical in JapanClinical trialThis is a stage, not insurance coverage.
Conventionally, it was believed that adult brain cells did not proliferate, and once dead brain cells could never be regenerated. this isSantiago Ramon i CajalArgued for a long time. However, it was found that brain cells of other animals such as monkeys have a regenerative ability, and in 1998 it was found that human brain cells also have a regenerative ability.[44].. However, the ability to reproduce was limited. This is around the affected areaNeural stem cellThis is because the nutrients and oxygen do not spread to them and almost die. So the patientBone marrowIt is inHematopoietic stem cellsBy culturing and returning it to the body by drip, the regeneration of blood vessels around the affected area is first promoted. Then, research began to promote regeneration of neural stem cells by distributing nutrients and oxygen from blood vessels. Since it's own cells, there are few side effects[45].
Since 2009Clinical trialBegins, andSapporo Medical University HospitalIs proceeding with a clinical trial. In the first clinical trial at an advanced medical center hospital, it was conducted in 1 patients with cardiogenic cerebral infarction, and 12 patients recovered their gait function. Patients with atherothrombotic cerebral infarction within 9 days after onset at the Advanced Medical Center Hospital and within 10 days after onset at Sapporo Medical University Hospital[46] Are targeting clinical trials[47]. Also,Free medical careThere is a place where the doctor has begun implementation.NiproWas acquired by Sapporo Medical CollegePatentBased on, and aims to put to practical use as a pharmaceutical in the prospect of the 2018[48].
Also, instead of autologous culture, hematopoietic stem cells from healthy individuals should be used.Genetic recombinationClinical trials are being conducted by culturing in and injecting into the brain.[49]. The sales rights in Japan for "SB623" scheduled to be released by SanBio areTeijin[50] But the United StatesカナダThe sales rights ofSumitomo Dainippon Pharma[51] But each has acquired. Aiming for 2020 sales in the United States[52]. However, it took place in the United States on January 2019, 1Phase 2b (Late Phase II) clinical trialAnnounced that it failed to meet the primary endpoint of chronic cerebral infarction[53].
Similarly,JCR PharmaIs developing a method of culturing the dental pulp-derived stem cells (DPC) of healthy individuals and injecting them intravenously. 2017May 7, Signed joint development agreement with Teijin and sales rights in Japan[54][55]. Treatment with other stem cells is targeted at the chronic phase, but JCR Pharma is developing "JTR-161" for the acute phase.
OverseasabortionFetusAlthough the drug development using the neural stem cells is being conducted, it has not been conducted in Japan, including clinical trials and practical use.
Carotid artery lesion
For cervical internal carotid artery stenosis, it is said that surgery has a significant effect of preventing the next seizure in both symptomatic and asymptomatic cases in comparison with drug treatment (antiplatelet drug). Famous cases are NASCET and ECST for symptomatic cases, and ACAS and ACST for asymptomatic cases. In patients with stenosis of 70% or more and severe ulcer lesions,General anesthesiaSurgery should be considered in patients who tolerate and survive for more than 5 years. It is a case-by-case for the elderly (75 years old or older), those who are at high risk of surgery, and those who have coronary artery disease. Bypass surgery may be performed in patients with hemodynamic TIA or cerebral infarction due to internal carotid artery occlusion, but the most common surgery for carotid lesions is carotid endarterectomy (CEA). Cases where CEA is difficult are performed (CAS). Specifically, the elderly (75 years old or older), cardiopulmonary disease, post-CEA stenosis, high-grade lesion, contralateral occlusion, irradiation, etc. are good indications. Insurance will be applied from April 2008.
Middle cerebral artery lesion
A bypass operation known as superficial temporal artery-middle cerebral artery anastomosis (STA-MCA) is known.


Cerebral infarctionprognosisIt is,リ ハ ビ リ テ ー シ ョ ンIt depends largely on how aggressively they were able to implement. It is important to make the rest period in the hospital bed as short as possible and aim for an everyday life from the early stage. Rehabilitation from the day of onset, called hyperacute rehabilitation, has been shown to be most effective. It is known that in the process of recovery from paralysis, a phenomenon called joint exercise is observed in which multiple muscles move when trying to move some muscles.

There are several reports on the recovery process of hemiplegia. It is said that if the Brunnstrom stage is IV or higher at the time of onset, almost complete recovery will be achieved within 6 months. It is said that if Brunnstrom stage recovers to IV or higher within 2 weeks after the onset, it will recover to stage VI in almost 8%. It is said that the more prominent the paralysis at the onset and the more mild the paralysis recovers at the early stage of the onset, the better the prognosis. It takes about two months to improve the paralysisplateauAlthough it reaches the plateau and plateau, it may recover gradually up to about a year. The degree of paralysis recovery depends on the age and severity of the paralysis, and it is said that it is less likely to recover in complete paralysis (stage I or II) and older people. A plateau of 1 months to 6 year is the exercise capacity. On the other hand, in the repeated facilitation therapy (Kawahira method) developed by, it is said that it is effective for patients who have passed more than 1 year by the therapy such as pinpoint stimulation of the part where paralysis is desired to be recovered.[56][57].

Higher brain dysfunctionAccording to the "Evidence Based Review of Stroke Rehabilitation", 2/3 of patients develop some kind of disorder.Attention disorderIs the easiest to recover,Memory disorderIs hard to recover. Also,dementiaThe risk of is up to 10 times. 16-20% of patients improve. The effect of rehabilitation is slightly inferior to physical ability (recommended grade B to C1[58][59]). Most recovery occurs within 3 months of onset, but recovery may continue for at least 1 year. The prevalence of memory impairment was 3-23% at 55 months and 1-11% at 31 year. Rehabilitation (memory, diary, pager, computer memory, etc.) may be effective in memory disorders. IsAbusiveIs effective against. The medicineGalantamine, (Unapproved), (Unapproved), (Unapproved), etc. have been reported.AphasiaIs expected to recover with sufficient rehabilitation. Recovery is greatest within 1-3 months of onset and continues for 1 year. After that, the recovery will be very mild or will never reach a plateau[60].

Acute rehabilitation
Rehabilitation within 2 weeks to 1 month after onset. It is said that even in healthy muscles, resting for 2-3 weeks causes 20-25% of muscle atrophy. The muscles that show paralysis are atrophied more quickly, and prevention of disuse syndrome is important. Passive passive range-of-motion exercises, postural changes, and maintenance of good limb positions can be performed as basic care in the acute phase, paying attention even when the onset of symptoms or when symptoms are unstable. The basic idea is that exercise training is possible after 12 to 24 hours have passed since the neurological symptoms have stabilized and there is no possibility of infarct development. As for the timing of starting the sitting position, JCS is a single digit, and if the general condition is stable and there is no exacerbation of paralysis, it can be done under careful observation. As a guideline, if it is a lacunar infarction, the neurological symptom is exacerbated from 3 days to 5 days after the onset, since it may shift to the advanced type if stenosis or occlusion of the main artery is confirmed in atherothrombotic cerebral infarction from the day after the diagnosis. Check that there is no sitting position and start getting out of bed. Treatment with rehabilitation as soon as possible with adequate risk management is recommended Grade A[61]. In addition, it is necessary to pay sufficient attention to complications (recommended grade B).
Convalescent rehabilitation
Rehabilitation within 180 days after onset. When recovery of physical function reaches a peak. If the obstacle does not remain, it is not necessary to do it. In cases where disability remains in multiple areas such as mobility, self-care, swallowing, communication, and cognition, more specialized focused convalescent rehabilitation is required (Recommended Grade B[62]).
Maintenance phase rehabilitation
Life support is the main focus. It is recommended to maintain/improve muscle strength, physical strength, walking ability, etc. (Recommended Grade A[63]). Therefore, consider home-visit rehabilitation, outpatient rehabilitation, and regional rehabilitation (Recommended Grade B). Intermittent hospital rehabilitation does not have sufficient scientific evidence (recommended grade C1). If you wish to return to work, consider vocational rehabilitation if there is an adaptation to work ability (recommended grade C1).
2006 yearsMedical system reformSo, the rehabilitation fee for cerebral vascular disease such as cerebral infarction is 180 days after the start of treatment.Medical feeIt was excluded from the target (within 180 days, 1 point 20 minutes, up to 1 points per day are subject to medical treatment remuneration. Regarding acute phase rehabilitation, it was thicker than before). This is maintenance phase rehabilitationHealth insurancenot,Long-term care insuranceThis is to be done by. However, exceptions were made when it was judged that recovery could be expected due to aphasia, agnosia and apraxia, and higher brain dysfunction. However, it was supposed as a saucernursing homeIs poor, and especially for the poor, it often happened that the rehabilitation had to end in 180 days. In response to criticism from patients and various groups, the restrictions were slightly relaxed from April 2008, and "when the doctor judges that improvement can be expected" is up to 4 points a day, and in other cases "required" rehabilitation If you continue the procedure, you will be granted medical fees up to 1 points per month.[64][65].

Chronic management

The problem with using anticoagulant/antiplatelet drugs to prevent recurrence isHemorrhagic infarctionIs. This is because the blood vessel wall is torn by the blood flow reflowing into the necrotic blood vessel,cerebral hemorrhageIt is a state that has reached. This is especially a problem with extensive cerebral infarction. Therefore, in a wide range of cases such as embolism, it is indispensable to carefully check the infarction progression and then to follow up with CT for bleeding.

Identification of the cause of infarction is very important in the subsequent recurrence prevention plan. First of all, in addition to collecting risk factors by listening to medical history and lifestyle,EchocardiographyWhether there is a thrombus in the atrium,Holter ECGWhether there is arrhythmia, carotid arteryechoIt is necessary to evaluate the presence or absence of plaque byHigh blood pressureAnd nonValvular diseaseSexualAtrial fibrillationIf so, that control is especially important.

Atherothrombotic cerebral infarction
Antiplatelet therapy is well known for preventing recurrence of atherothrombotic cerebral infarction. If the cause is intracranial stenosisaspirin(Biaspyrin, etc.),Cilostazol(Pletal etc.),Clopidogrel(Plavix, etc.),Ticlopidine(Panarudine, etc.) are known. It is standard to use cilostazol or clopidogrel around aspirin. In middle cerebral artery lesions, clopidogrel (Plavix, etc.) is considered to be highly effective in preventing recurrence. In the acute phase, clopidogrel 75 mg (such as plavix) and aspirin 100 mg (such as biaspyrin) are used in combination, and switching to a single agent within a few months is a common method. In addition, improvement of stenosis may be observed when aspirin 100 mg is combined with cilostazol 200 mg.
Lacunar infarction
There is much debate about the use of antiplatelet drugs in the chronic treatment of lacunar infarction. It goes without saying that the elimination of risk factors such as hypertension is important, but there is clear evidence for the prevention of recurrence of lacunar infarction.Cilostazol(Pletar, etc.) only. It is customary to be treated with aspirin. The presence of microcerebral hemorrhage (CMB) tends to be avoided by the administration of antiplatelet drugs because it risks bleeding. MRI T2* is often used to detect microcerebral hemorrhage.
Cardiogenic cerebral embolism
It is common to treat with t-PA or heparin in the acute phase and use warfarin to prevent recurrence.
Response of aftereffects
Chronicdizzy,NumbnessIs used for such symptoms.Amantadine(Symmetry)Nicergoline(Samion),Ifenprodil(), (Ketas), etc. are known.Use ifenprodil (seroclar) for improvement of subjective symptoms of cerebral infarction, especially for dizziness and numbness, nicergoline () for decreased spontaneity, amantadine (symmetry) and ibushilast (ketas) for decreased spontaneity. It may be done.In the psychiatric fieldSSRIAs paxil,Cheap priadeThe grammar reel is used as. Gramarille is effective in reducing cognitive function. Dementia progression is often vascular dementia progression, but normal pressureHydrocephalusMay be a merger of. It is not common to use Aricept for suspected Alzheimer's disease.
Central pain
Centrality after cerebral infarctionpainForAmitriptyline(Tryptanol),Lamotrigine(Lamictal), (Mexitil), etc. are considered effective.Carbamazepine(Tegretol) may be effective but not effective on EBM.


The pathological image of cerebral infarction consists of a series of biological reactions involved in the process of lesion repair of ischemic necrosis. Pathologically, it is classified into anemic infarction that appears macroscopically and hemorrhagic infarction with bleeding.

Anemia and hemorrhagic infarction

Anemia infarction
It is difficult to identify macroscopic abnormal findings in the acute phase. Histologically, minute vacuolar changes appear in neuropil 1 to 3 hours after onset. Due to the spongy change and edema, it seems that the transparency increased.gray matterWhite matterThe boundary of is unclear. Histologically, the staining of the lesion is markedly reduced. From day 3 into the infarct nestMacrophageBegins to infiltrate the necrotic tissue and becomes foamy macrophages. Macrophages are said to be present for about 3 months, but may be seen for several years if the infarct lesion is large. Axonal swelling (or spheroids) is observed in the white matter around the infarct lesion. The same site shows eosin preference and argyrophilicity, and AFP () is accumulated. AFP-positive images may also be found in part of the white matter fiber bundles. One week after the onset, hypertrophy of reactive astrocytes and neocapillaries are observed at the margin of the infarction. Reactive astrocytes at this time are fertilized astrocytes. Eosinophil with wide vesicles like glass and short projections. At 1 to 3 months, the necrotic tissue is phagocytosed by macrophages and becomes hollow,Cerebrospinal fluidIs filled with. In the tissue surrounding the cavity, the reactive astrocytes become fibrous astrocytes with elongated protrusions and become a state of fibrotic gliosis. Fibrous astrocytes leave the glial fibrils in the endoplasmic reticulum, and the cells themselves gradually disappear to form a glial scar. If the infarct is small, only the scar is left. 1 cm3It takes 3 months for the cerebral infarction to completely hollow out.
Hemorrhagic infarction
It is accompanied by petechiae in the gray matter that has fallen into infarction. It is a secondary change in anemia infarction. Histologically, it is recognized as leaky hemorrhage around capillaries and venules. Even if it is macroscopically anemic infarction, microscopicallyHemorrhagic infarctionSometimes.

Background lesion of cerebral infarction

Hypertensive vasculopathy
Moyamoya disease
Arterial dissection
Intracranial vasculitis
Cerebral amyloid angiopathy
Venous thrombosis


Microbleeding (MBs) shows an almost circular uniform low-intensity region observed in the basal ganglia region, brain stem, and subcortical region at T2*WI. Physiological calcification and intravascular thrombus can be distinguished on the image. Although it is intracerebral microbleeding (CMB), it is not included in the exclusion items of rt-PA, and is not involved in the treatment policy in acute treatment. Many are found in brain amyloid angiopathy. Consider discontinuation of antithrombotic therapy during the chronic phase if there are 5 or more CMBs, as there is a risk of bleeding. However, if the number is less than 5, the presence of CMB itself is a risk of cerebral infarction, so antithrombotic drugs are often not stopped. As of 2010, they do not have sufficient evidence.

Cerebral infarction complications

early seizure

Within 1-2 weeks after stroke onset痉挛It is a seizure. It is thought to be caused by changes in brain metabolism. The seizure type is often a partial seizure or a direct-onset seizure due to generalization of the partial seizure. In rare cases, there is an inhibitory seizure that shows neurological deficits without convulsions. Hemorrhagic stroke is common, especially in lesions involving the cortex. Early seizure has few recurrences in the chronic phase and continuous prescription of antiepileptic drug is not always necessary.

About asymptomatic lesions

Brain MRI of the elderly has asymptomatic cerebral infarction, asymptomatic cerebral white matter lesions, and enlarged perivascular space, and there is considerable confusion in these judgments. Summarize the discrimination criteria in Japan Brain Dock Guideline 2008.

Lacunar infarction (without cavitation)Perivascular spaceCerebral white matter lesions
T1WILow signalLow signalEtc-gray matter
T2WIClear high signalClear high signalPale high signal
Proton density weighted imageClear high signal (+ low signal in the center)Low signalPale high signal
FLAIR imageEtc-High signal (low signal in the center)Low signalPale high signal
大 き さ≧ 3mm<3 mm (may exceed 1 cm in 3/1 below the basal ganglia)Various
ShapeIrregular shapeOrthopedic, linear in white matterVarious
Common siteBasal ganglia (upper 2/3), white matter, thalamus, brain stemWhite matter,Hippocampus,midbrainCerebral white matter, bottom of bridge

As shown by the image course of cerebral infarction, it is difficult to distinguish only by images, but in the case of asymptomatic, low signal with T1WI and FLAIR indicates lacunar infarction and enlargement of perivascular space. It is common. In addition to the linear shape and position of the perivascular space and the lacunar infarction, it is common to suspect the lacunar infarction with a high signal in the surrounding FLAIR and the perivascular space without it. This is considered to be a finding after a tissue defect or cavitation due to lacunar infarction. The internal signal is characteristically similar to CSF. The concept of asymptomatic lacunar infarction itself may not be recognized depending on the book, but it takes a position to exist in diagnostic imaging.

Perivascular space
Perivascular space (Virchow Robin space) is found around perforating arteries and medullary arteries and veins. Since the lateral striatal artery is the preferred site, the lower third of the basal ganglia is the preferred site. It was once thought to be a continuation of the subarachnoid space, but as of 1, it is thought to be a continuation of the voids in the pia mater. Is rarely seen in young adults,High blood pressureEnlarge with patient. It is a normal age-related change and is not a risk factor for stroke or other neurological symptoms.Basal gangliaWhen there are many enlarged perivascular spaces, it is sometimes called etat crible.
Asymptomatic white matter lesions
In the Brain Dock Guideline 2008, periventricular lesions (PVH) and deep white matter lesions (DWMH) are generally evaluated separately.
 Fazekas classificationBrain Dock Society Classification
PVHgrade 0abcenceNone or rim only
grade Icap or pencil-thin lininglocalized lesions like cap
grade IIsmooth halloLesions that spread slightly thickly around the ventricles
grade IIIirregular PVH extending into the deep wahite matterIrregular lesions extending to deep white matter
grade IV Deep-wide lesions that extend to the subcortical white matter
DWMHgrade 0abcenceNone
grade 1punctate fociPunctate lesions <3 mm or enlarged perivascular space
grade 2beginning confluence of fociSpotty and diffuse lesions of 3 mm or more
grade 3large confluent areaLesions showing a fusion tendency with unclear boundaries
grade 4 Lesions that coalesce and are widely distributed in most of the white matter

pathologyFrom the perspective of PVH and DWMHMyelin sheathIt is considered to be the clearing and dilatation of the perivascular space. PVH is often accompanied by enlargement of extracellular space, and DWMH is often accompanied by microinfarction. Both are considered to be chronic ischemic changes associated with arteriosclerosis. Advanced is similar to subclinical cerebral infarctionstrokePowerful ofRisk factorIt is also strongly related to cognitive impairment and depression. Active indication of antihypertensive therapy is recommended. On the other hand, in mild cases, it is considered to have no pathological significance. Differentiating from lacunar infarction is a problem for mild DWMH.

Mechanism of exacerbation of cerebral infarction

Keio UniversityThe medical school groupPeroxiredoxinThe mechanism of exacerbation of symptoms by (peroxiredxin) was discovered[66].. Peroxiredoxin activated inflammatory cells and was involved in the worsening of neurological symptoms such as enlargement of the infarcted area, paralysis, and numbness.[67].


  1. ^ The name "encephalomalacia" comes from the fact that brain cells melt when necrotic ("melting necrosis").
  2. ^ Please note that there is no definitive translation yet, so it is a provisional translation.
  3. ^ According to an experiment by Prof. Junichi Nabekura (Neurophysiology) and others, hemiplegia due to cerebral infarction is recovered by recombination of the other neural circuit of the affected brain.


  1. ^ a b Yukito Shinohara et al. (2009) pp.78-83
  2. ^ Johnston SC, Gress DR, Browner WS, Sidney S. (Dec 13 2000). “Short-term prognosis after emergency department diagnosis of TIA.”. JAMA. 284 (22): 2901-6. PMID 11147987. http://jama.ama-assn.org/cgi/content/full/284/22/2901 2010th of February 8Browse.. 
  3. ^ Lisabeth LD, Ireland JK, Risser JM, Brown DL, Smith MA, Garcia NM, Morgenstern LB. (Aug 2004). “Stroke risk after transient ischemic attack in a population-based setting.”. Stroke. 35 (8): 1842-6. PMID 15192239. http://stroke.ahajournals.org/cgi/reprint/35/8/1842 2010th of February 8Browse.. 
  4. ^ Stroke. 2008 Aug; 39 (8): 2280-2287 PMID 18535284
  5. ^ a b Nogawa, Shigeru "Special Feature 1: Platelets and Malignant Tumors-Cancer and Cerebral Infarction-Clinic of Trusseau Syndrome"Journal of the Japanese Society for Thrombosis and Hemostasis," Vol. 27, No. 1, Japan Society for Thrombosis and Hemostasis, 2016, pp. 18-28,2019th of February 12Browse.
  6. ^ Uchiyama, Shinichiro, "I. Clinical types depending on the site of injury and pathology 7. Trousseau syndrome," The Japanese Society of Internal Medicine, Vol. 97, No. 8, 2008, pp. 1805-1808, two:10.2169 / naika.97.1805, ISSN 1883-2083,2019th of February 12Browse.
  7. ^ a b c d e NHK Asaichi Cerebral Infarction Special Broadcast on March 2013, 3, St. Marianna University School of Medicine Dr. Hatakawa Hatahiro commentary
  8. ^ Japan Stroke Association Fukuoka Branch and Fukuoka City Fire Department Brochure on ACT-FAST pdf... Retrieved August 2013, 3
  9. ^ The United KingdomNational Health Service (NHS) ACT-FAST commentary page [1].. Retrieved August 2013, 3
  10. ^ Massachusetts Public Health Site [2].Retrieved January 2013, 3
  11. ^ http://melt.umin.ac.jp/nihss/nihssj-table.htm NIHSS judgment table
  12. ^ a b Stroke Treatment Guidelines 2015 [Supplement 2017] 1-3 Thrombolytic Therapy -Japanese Stroke Society
  13. ^ Stroke Treatment Guidelines 2009 1-2. Thrombolytic therapy (intra-arterial administration) -Japanese Stroke Society
  14. ^ Before the revision in September 2016, it was "9 years old or older".
  15. ^ a b c d With the revision in September 2016, contraindications have been changed to careful items.
  16. ^ from before,Meningioma,Rathke's cystThere was an opinion that calcified tumors are not contraindicated because of the low risk of bleeding.
  17. ^ [63] New treatment for cerebral infarction -Cardiovascular disease information service National Cardiovascular Research Center,
  18. ^ Alteplase at 0.6 mg / kg for Acute Ischemic Stroke Within 3 Hours of Onset Japan Alteplase Clinical Trial (J-ACT) -Stroke Japan Alteplase Clinical Trial (J-ACT) Takenori Yamaguchi, Etsuro Mori, Kazuo Minematsu, Joji Nakagawara, Kazuo Hata, Isamu Saito, Yukito Shinohara(English)
  19. ^ Cerebrovascular Medicine/Cranial Neurology -
  20. ^ a b c Stroke Treatment Guidelines 2015 [Supplement 2017] 1-8 Cerebral arteries: Intravascular recanalization therapy (mechanical thrombus recovery therapy, local fibrinolytic therapy, etc.) -Japanese Stroke Society
  21. ^ In the 2017 supplement, upgraded from C1.
  22. ^ a b May 22 Japanese Society of Stroke Members Members Merci Retriever Users -Japanese Society of Stroke Akira Ogawa, Kazuo Minematsu
  23. ^ Percutaneous transluminal cerebral thrombus collection device proper use guideline 2nd edition April 2015 -Japanese Society of Stroke, Japanese Society of Neurosurgery, Japanese Society of Endovascular Therapy
  24. ^ [February 2015, 2] "Impact on Stroke Treatment in the World", International Stroke Society showing the effectiveness of endovascular treatment by three RCTs --MTPro (Full text is membership system, only doctors and medical personnel can register)
  25. ^ 2015.2.3 08:30 updated "Solitaire FR" attracting attention Cerebral infarction, recanalization rate improved with new equipment -"Sankei Shimbun] Kanematsu
  26. ^ February 2015, 2 28:3 PM For cerebral infarction, rapid “intravascular treatment” is carried out within 30 hours to clear and relieve vascular clogging Compared with standard treatment for about 12 people -Med Edge
  27. ^ 2011 pages of Asahi Shimbun on March 3, 10
  28. ^ Regarding the results of the business of collecting safety use information immediately after marketing of medical devices 23 report on the collection of safety use information immediately after market (fixed point observation business) -Ministry of Health, Labor and Welfare
  29. ^ Solitaire FR clot removal device - Independent administrative agencyPharmaceuticals and Medical Devices Agency
  30. ^ Trevo Pro Clot Retriever -Pharmaceuticals and Medical Devices Agency
  31. ^ Stroke Treatment Guidelines 2015 [Supplement 2017] 1-4 Acute antiplatelet therapy -Japanese Stroke Society
  32. ^ Lancet Neurol. 2019 Jun; 18 (6): 539-548. PMID 31122494
  33. ^ Stroke Treatment Guidelines 2009 1-5. Brain protectant -Japanese Stroke Society
  34. ^ a b Stroke Treatment Guidelines 2009 1-4. Acute antiplatelet therapy -Japanese Stroke Society
  35. ^ Guidelines for stroke treatment 2009 1-3. Acute anticoagulation therapy -Japanese Stroke Society
  36. ^ a b Stroke Treatment Guidelines 2009 4-2. (2) Cardiogenic cerebral embolism -Japanese Stroke Society
  37. ^ a b c Stroke Treatment Guidelines 2009 4-2. (1) Non-cardiogenic cerebral infarction (atherothrombotic cerebral infarction, lacunar infarction, etc.) -Japanese Stroke Society
  38. ^ a b Stroke Treatment Guidelines 2015 [Supplement 2017] 1-11 Hemodilution therapy -Japanese Stroke Society
  39. ^ Stroke Treatment Guidelines 2009 1-6. Brain edema management -Japanese Stroke Society
  40. ^ Stroke Treatment Guidelines 2015 [Supplement 2017] 1-14 Hypothermia Therapy -Japanese Stroke Society
  41. ^ Stroke Treatment Guidelines 2015 [Supplement 2017] 1-15 Hyperbaric oxygen therapy -Japanese Stroke Society
  42. ^ Stroke Treatment Guidelines 2009 1-13. Extracranial decompression therapy -Japanese Stroke Society
  43. ^ Stroke Treatment Guidelines 2009 1-15. Acute cervical carotid artery revascularization (angioplasty/stent placement) -Japanese Stroke Society
  44. ^ Brain cells are reborn in adults -"Nikkei Science" G. Kempelman/FH Gauge
  45. ^ Current status and future prospects of regenerative medicine using autologous bone marrow stem cells for cerebral infarction patients -
  46. ^ From February 2015, 2, cardiogenic embolism was also added to the target.
  47. ^ Announcement of clinical trial of regenerative medicine at Sapporo Medical University Hospital -Sapporo Medical University Hospital
  48. ^ April 2014, 4 Nipro Co., Ltd. (code number: 28) Announcement of a patent license agreement for the commercialization of "the first cell drug in the regenerative medicine field in Japan" -Nipro
  49. ^ Challenging Diseases Part 4: Front Lines of Cerebral Infarction (Middle) Overturn "Unhealed" -"Nikkei Sangyo Shimbun] June 2014, 6 issue / Sanbio
  50. ^ February 2010, 2 New stroke treatment license agreement signed for full-scale entry into regenerative medicine market -Teijin
  51. ^ Announcement of joint development and license agreement in North America for SB623, a therapeutic agent for cerebral infarction, September 2014, 9 -Sumitomo Dainippon Pharma
  52. ^ Joint development of cerebral infarction drug in the US Aiming to sell for 20 years such as Sumitomo Dainippon 2015/10/2 23:39 -"Nihon Keizai Shimbun"
  53. ^ Q & A regarding the press release dated January 2019, 29, "Breaking news of analysis results of Phase 623b clinical trials in the United States for regenerative cell medicine" SB2 "for chronic cerebral infarction" -Sanbio
  54. ^ Announcement of Joint Development Agreement for Human Dental Pulp-Derived Stem Cells to Expand Regenerative Medicine -JCR Pharma
  55. ^ July 2017, 7 Signed a joint development contract for human dental pulp-derived stem cells to expand the field of regenerative medicine -Teijin
  56. ^ "Boomeran" Vol.27 "Repetitive therapy for facilitation" that brings light to the rehabilitation of strokes The key to strengthening the neural circuit is the key! - Shimadzu
  57. ^ Kagoshima University Hospital Kirishima Rehabilitation Center
  58. ^ Guidelines for stroke treatment 2009 2-9. Rehabilitation for language disorders -Japanese Stroke Society
  59. ^ Stroke Treatment Guidelines 2009 2-10. Rehabilitation for cognitive impairment -Japanese Stroke Society
  60. ^ Evidence Based Review of Stroke Rehabilitation Japanese version -Robert Teasell and others /Kio University(I translated)
  61. ^ Stroke Treatment Guidelines 2009 1-4. Acute rehabilitation -Japanese Stroke Society
  62. ^ Stroke Treatment Guidelines 2009 1-6. Convalescent rehabilitation -Japanese Stroke Society
  63. ^ Stroke Treatment Guidelines 2009 1-7. Maintenance phase rehabilitation -Japanese Stroke Society
  64. ^ Interview survey with related organizations regarding the standard number of days for rehabilitation (report) -Ministry of Health, Labor and Welfare
  65. ^ Part 7 Rehabilitation -Ministry of Health, Labor and Welfare
  66. ^ Discovery of a mechanism for exacerbation of cerebral infarction New target treatment with protein target 47 NEWSDiscovery of a novel mechanism that exacerbates cerebral infarction Keio University School of Medicine(Retrieved September 2012, 7)
  67. ^ Elucidation of the mechanism of inflammation that exacerbates cerebral infarction - Keio University Hospital Article created: March 2014, 3 Last updated: March 1, 2014


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