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Cerebrovascular disease

Of the worldDisease burden(WHO, 2019)[1]
Rankingcause of deathDALYs (XNUMX)DALYs (%)DALYs
(Per 10 people)
1Neonatal disease20,182.18.02,618
2Ischemic heart disease18,084.77.12,346
4Lower respiratory tract infection10,565.24.21,371
5diarrheaSexual illness7,931.13.11,029
6Traffic accident7,911.63.11,026
8Diabetes mellitus7,041.12.8913
10Birth defects5,179.72.0672
11Back and neck pain4,653.21.8604
12depressionSexual dysfunction4,635.91.8601
14Trachea, bronchi, lung cancer4,137.81.6537
15Kidney disease4,057.11.6526
16HIV / AIDS4,014.71.6521
20Refractive error of the naked eye3,198.11.3415

Cerebrovascular diseaseWhat is (cerebrovascular disease)?brain OfBlood vesselA general term for diseases caused by disability.

Cerebrovascular accidentcerebral hemorrhage(Bleeding cerebrovascular accident)cerebral infarctionIt is classified into two types (ischemic cerebrovascular accident), and cerebral hemorrhageIntracerebral hemorrhageSubarachnoid hemorrhage, Cerebral infarctionCerebral thrombusandCerebral embolismare categorized.Of these, the ones that developed suddenlystroke(Lie,stroke,apoplexy), Cerebrovascular attack (cerebrovascular attack, CVA),Transient cerebral ischemic attackCalled (TIA).PopularlyStrokeAlso called (chufu, chubu).

Mechanism of onset

Common to cerebrovascular accidents is the occurrence of abnormalities in the blood vessels (blood flow) in the skull that nourish the brain.BleedingbyInflammation·orIschemiaIt is caused by damage to the brain tissue caused by.

Risk factor

In cerebral infarctionArteriosclerosis(Atheroma) is the greatest risk factor and is the cause of arteriosclerosis.high blood pressure,Dyslipidemia(hyperlipidaemia),Diabetes mellitus, Smoking is mentioned.On the other hand, in cerebral hemorrhageIntracerebral hemorrhageThen.High blood pressureBut,Subarachnoid hemorrhageThen.Cerebral aneurysm (Aneurysm) ・Cerebral arteriovenous malformation (AVM) andMoyamoya diseaseIs a major factor.In Japan, the morbidity rate is increasing with the westernization of food culture.prevention,Relapse prevention,リ ハ ビ リ テ ー シ ョ ンBoth are big issues.

High blood pressureIn predicting the onset of stroke,Diastolic blood pressure (Diastolic Blood Pressure: DBP) etc.Systolic blood pressure (Systolic Blood Pressure: SBP) is the most important factor, regardless of gender or racepaper American Journal of Hypertension Was published in the March 2007 issue of.
High blood pressure,smoking, Low waist-hip ratio, unhealthy diet, lack of regular exercise,Diabetes mellitus, Moderate or high alcohol consumption,stressorDepression,ApolipoproteinNine factors, high B / A1 ratios, accounted for 9% of the risk of stroke in various countries.Above allHigh blood pressureWas involved as a single factor in 52% of both ischemic and hemorrhagic cerebrovascular accidents and 74% of hemorrhagic cerebrovascular accidents.[2]

People with chronic sleep deprivationHigh blood pressure,Diabetes mellitus,Hyperlipidemia,Myocardial infarction,AnginaSuch asCoronary artery diseaseAnd are susceptible to lifestyle-related diseases such as cerebrovascular accidents[3].

Cerebrovascular accident caused by trauma

Acute epidural hematoma (AEDH)
Bleeding with a good prognosis.CT The upper part is reflected as a convex lens type high absorption area.The source of bleeding isDura(Middle meningeal artery, Venous sinus) or bone (facet vein).Therefore AEDH is basicallySkull fractureIt is a complication of the disease and is found on the fracture side.There are many cases of damage due to temporal bone fracture and sinus injury due to occipital bone fracture.Hematoma can be removed by craniotomy.
Acute subdural hematoma (ASDH)
Bleeding with a poor prognosis. On CT, it appears as a crescent-shaped high absorption area.Injuries often occur on the other side.ArachnoidIt is said to be caused by damage to the.The arachnoid is not so easily damaged and occurs during severe trauma.Treatment is craniotomy.Brain contusionThen, it can be considered that intracerebral hemorrhage, subarachnoid hemorrhage occurs in pia mater injury, and subdural hematoma occurs in arachnoid injury.
Chronic subdural hematoma
Unlike ASDH, it has a good prognosis. On CT, it appears as a crescent-shaped isosbestic area.Treatment is removal of the hematoma by burr.


Cerebrovascular accidents are usually accompanied by hypertension.Since the treatment policy is different for each disease, it is not possible to treat blood pressure and other illnesses without diagnosis.

cerebral infarction
In principle, blood pressure reduction in the acute phase is contraindicated.If there is no bleeding on CT due to cerebrovascular accidentcerebral infarctionThere is a high possibility of.Within 4.5 hours of onsetThrombolytic therapySince the symptoms can be improved, the indication should be evaluated.Based on the medical history, we also diagnose the type of disease such as atherothrombosis.MRI Alternatively, the time of onset will be specified by MRA.Since thrombolytic therapy has indication criteria and careful administration, thrombolytic therapy should be performed after consulting with a specialist.At this time, it is advisable to refrain from inserting the ya because there is an open blood treatment as an act that is out of indication.
Cerebral hemorrhage (cerebral hemorrhage)
In the acute phase, there is no hypotension except for extreme hypertension.In the chronic phase, the blood pressure is lowered to prevent recurrence.What should be done in the emergency room is diagnosis including identification of the bleeding site.hernia,HydrocephalusIt is an evaluation of complications such as.For cerebral hemorrhage that is indicated for emergency surgeryPutamenbleeding,cerebellumBleeding, lower bleeding,ThalamusBleeding can be raised.Hematoma removal is the standard procedure for putamen hemorrhage, cerebral hemorrhage, and subcortical hemorrhage, and ventricular drainage is the standard procedure for thalamic hemorrhage.Surgical indications vary depending on the facility, but in the case of putamen bleeding, when the hematoma volume is 31 ml or more,Consciousness disorderIf there is a strong mass effect on the brain, emergency surgery is required.For cerebral hemorrhage, emergency surgery is required when the hematoma diameter is 3 cm or more and when there is disturbance of consciousness (especially JCS III-100 or more).In the case of subcortical bleeding, emergency surgery is required when the hematoma volume is 30 ml or more, the disturbance of consciousness is more than stupor, the median deviation is 1 cm or more, or the peri-midbrain cistern is deformed.Ventricular bleeding and ventricular bleedingHydrocephalusWhen is found, emergency surgery is performed.
Subarachnoid hemorrhage
Actively control blood pressure.This is to prevent rebleeding.

Neurodiagnosis in the emergency room

NeurodiagnosisNeurodiagnosisBased on the above, the cause diagnosis, anatomical diagnosis, and clinical diagnosis are usually performed in 3 steps.There are many examination items for making an anatomical diagnosis.Such a response is often not possible in the emergency room, and many patients who come to the emergency room with suspected neuropathy often do not.Cerebrovascular diseaseTherefore, a simpler screening method has been developed.Screening examinations are performed only for the purpose of diagnosing the existence of neurological diseases, and although there is less information on local diagnosis and etiology diagnosis than diagnosis based on systematic neurodiagnosis, they are preferred in the emergency room because they can be performed in a short time. Is done.In many cases, screening examination items include consciousness, cranial nerves, motor nerves, sensory nerves, walking, posture, meningism, autonomic nerves, coordinated movements, and deep tendon reflexes (particularly pathological reflexes).

The screening items alone can provide considerable information on cerebrovascular accidents.This is assumed because most cerebrovascular accidents have hemiplegia as the main complaint.First, below the neck where there is no paralysis on the faceHemiplegiaIfSpinal cordIt can be thought of as a level of angiopathy.If you have hemiplegia and contralateral facial paralysis, that is, alternating paralysisBrainstemIt is an obstacle.Brainstem disorderEndotracheal intubationThe need for is high.Loss of pharyngeal reflex, etc.Bulbar paralysisBoth symptoms and alternating paralysis are conditions in which endotracheal intubation is actively considered.It is necessary to perform head CT urgently (as for the management of the emergency room, even if localization diagnosis is performed when cerebral hemorrhage is diagnosed, it does not affect the treatment policy).The nerve diagnosis to be performed now is the examination of the cranial nerves.Cranial nerve I --IV If paralyzedmidbrain, Cranial nerves V --VIII If paralyzedbridge, Cranial nerves IX --XII If paralyzedMedulla oblongataIs likely to be the responsible lesion.If facial paralysis is found on the ipsilateral side of hemiplegia, it is a subcortical or cortical level disorder.In this case, since it is a supratent lesion, if there is a corectopia, it is a disorder at the cortical level in the direction of deviation (corectopia faces the diseased side in the supratent lesion and the healthy side in the subtent lesion). ..If no corectopia is present, distinguish whether cortical symptoms are present or not.If there is cortical symptom, it is a disorder at the cortical level, and if there is no cortical symptom, or if there is no sensory disorder, it is a subcortical level, that is, lacunar infarction.Cortical symptomsAs a cortical sign of the dominant hemisphereAphasiaIs famous, and other as a guideline for impaired blood vessels as an inferior hemispherical cortical symptomHigher dysfunction,Disapproval,Abusive,Ignore half spaceCan be given.Also on both sidesCerebral cortexAs a function ofComplex sensationThis is also a cortical symptom.As a widespread cortical symptomConsciousness disorderCan also be given.Regarding impaired blood vessels, in the case of cortical level disorders, disorders of the anterior cerebral circulatory system are suspected.If the lower limbs are severely impaired, the area, if the facial or upper limbs are severely impaired,Middle cerebral arteryregion,Same name semi-blind,visionIf is found, the area is doubtful.Subcortical, especiallyInclusion,Thalamus,Basal gangliaBecause is predominantly perfused by the penetrating branches, lacunar infarction is suspected in the absence of cortical symptoms, motor paralysis without sensory paralysis, or sensory paralysis without motor paralysis.

Summarize very useful findings in the localization diagnosis of cerebrovascular accidents.

Alternate hemiplegia is a very important finding as a sign of the brainstem.Brainstem disorders cause ipsilateral cranial neuropathy and paralysis of the upper and lower limbs on the opposite side.Cerebral disorders can be easily distinguished because they cause hemiplegia that swells the opposite face.In short, it can be predicted that the lesion of the brain stem is caused by the opposite side of the cranial nerve symptoms and the hemiplegia of the upper and lower limbs. This is the alternating hemiplegia.The cranial nerve symptoms that appear are related to the location of the nucleus.That is, if alternating paralysis with left oculomotor nerve palsy is observed, it is a disorder of the left midbrain.It is the lesion inside the medulla oblongata that causes alternate hemiplegia due to the disorder of the medulla oblongata.Lateral medullary, i.e.Wallenberg syndromeThen.Pyramidal disordersDoes not happen.
Dissociative sensory deficits are a sign of spinal cord lesions.
  • Anterior disability type: Decreased warm pain below the disability level
  • Posterior disability type: below the disability levelDeep sense,Tactile senseIs seen to decrease.
  • Central disorder type: Warm pain sensation decreases when suspended in the air.
  • Brown Sequar Syndrome: Contralateral hypothermia and ipsilateral other sensations, pyramidal tract disorders occur.

Imaging findings of typical cerebrovascular accidents

Diagnostic imaging in the emergency room

imageHyperacute cerebral hemorrhageHyperacute cerebral infarction
Findings immediately after onsetSignal changes are observed on T2WI and DWI immediately after the onsetNo findings were found immediately after the onset.
T2WIModerate hyperintensity in central hematoma and hypointensity in margin, surrounding edematous changes in T2WIIn T2WI, no signal change due to angioedema is observed until several hours after the onset.
DWIHigh signal in the center of the hematoma and low signal in the marginFindings may appear 30 minutes after onset, but are still localized compared to the final infarction.

In the emergency room, it is often sufficient to distinguish between the name of the disease and the presence or absence of hernia and hydrocephalus based on the findings from the hyperacute stage to the acute stage, and evaluation is generally performed based on the above table.With the widespread use of thrombolytic therapy, CT imaging is performed first, and if there is no bleeding and there is a symptom suspected to be a clear cerebrovascular disorder, or if there is a medical history, it is often considered as a cerebral infarction and treated.CT and MRI are equivalent in detecting intracerebral hemorrhage in the acute phase, but CT is preferred because of its simplicity.

cerebral infarction

cerebral infarctionThe image findings of.

X-ray CT Well, first and foremostcerebral hemorrhageIt is important to distinguish it from.This is because hematoma can be confirmed as a clear high absorption region from the hyperacute stage unless it is very small in cerebral hemorrhage.Furthermore, in cerebral infarctionEarly (early) ischemic changesFindings called (early CT sign) may be seen. As an early CT signLens nucleusObscuring shadows,Island cortexObscure, dermal border (cortex andWhite matterBoundary) obscuration,SulcusIs famous for its disappearance (narrowing).When these changes exceed 1/3 of the MCA region (1/3 MCA region), thrombolytic therapy is not indicated, so it has become important to determine the presence or absence of initial ischemic changes in recent years.Over time, necrotic brain swelling may be seen.The necrotic tissue softens and darkens on CT a few days after onset, but none of these findings are clear during the acute onset.
MRI Then, 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, the part showing high signal in DWI is considered to already show irreversible change, and it is a reversible part around it.PenumbraIs believed to exist.However, it is known that most of the hyperintensity of DWI coincides with the infarct lesion, but reversible lesions may be included in the pale lesions.On the contrary, it is often observed that DWI also shows false negatives in the very early stage.About 24% of false negatives are known even within 5 hours of onset.In particular, false negatives are common in the vertebral artery perfusion area within 6 hours of onset, and as many as 20% are observed.It is said to be especially common in medulla oblongata lesions.On the contrary, false negatives in the cerebral cortex are low, about 2%.Even if no high signal is observed on the first DWI, if cerebral infarction is strongly suspected from the symptoms, it is desirable to take another picture 24 hours later.In that case, the detection rate will be higher if a thin slice of about 3 mm is used with a b value of 2000 or higher.
Immediately after the onset(0-1 hour)Perfusion abnormality immediately after occlusionDisregardDisregardDisregardDisregard
Hyperacute phase(1-24 hour)Cellular edemaHigh signalLow signalDisregardearly CT sign
Acute period(1-7 days)Cellular edema and angioedemaHigh signalLow signalHigh signalLow absorption
Subacute phase(1-3 weeks)Gradually reduce edema from macrophage infiltration and angiogenesis due to cell necrosisHigh signal gradually to low signalFrom low signal to high signal graduallyHigh signalFrom low absorption to low absorption via FE
Chronic phase(1 month - )Necrosis, absorption, scarringLow signalHigh signalHigh signalCSF concentration

The above table shows typical changes over time in MRI in cerebral infarction.In the hyperacute phase, the diffusion coefficient decreases due to cellular edema, which is expressed in the form of high signal on DWI and low signal on ADC-MAP.In the acute phase, angioedema occurs due to the rupture of the BBB of the capillaries.Since angioedema increases the amount of water per unit tissue, T2WI shows a high signal.Reperfusion exacerbates angioedema in the acute phase, markedlyBrain edema,Hemorrhagic infarctionMay cause.In the subacute phase, cell necrosis and vascular necrosis increase the diffusion coefficient, resulting in apparent normalization for a period of time.Diffusion-weighted images are affected by T2 shine through and the high signal persists until the latter half of the subacute phase.Due to this phenomenon, it cannot be said that the diffusion coefficient is lowered or the cerebral infarction is in the hyperacute stage even with a high signal in the diffusion-weighted image, and ADC-MAP is also used for evaluation.About 2 weeks after the onset, the lesion is temporarily isosbestic due to the reduction of angioedema even on CT.However, it is obscured and is called FE (fogging effect).In the subacute phase, bleeding in a relatively small infarct may be observed due to the development of collateral circulation and compensatory perfusion increase due to pial meningeal anastomosis, and a low signal is shown at T2 *.Unlike hemorrhagic infarction in the acute phase, this does not lead to serious exacerbation of neurological symptoms, but in the case of lacunar infarction, it is safer not to administer antiplatelet drugs if these findings are present. ..After that, the T2WI signal becomes high as a chronic finding, but it may become low in the FLAIR image depending on the degree of tissue defect.This is due to the dilation of the extracellular fluid cavity.

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.

Another well-known finding is cortical laminar necrosis, in which the pyramidal cell layer (third layer) is selectively ischemic, and the cortex is detected by T3WI about 3 weeks after the onset. A high signal range along the line is recognized.

Intracerebral hemorrhage

Intracerebral hemorrhageThe image findings of.

Head CT
When blood flows out of the blood vessel, it coagulates and the plasma component is absorbed, resulting in an increase in hemoglobin concentration.Therefore, CT shows a high absorption range and diagnosis is relatively easy.
Head MRI
In the hyperacute phase, MRI can also be used to distinguish between cerebral hemorrhage and cerebral infarction.However, it is said that the detection ability of cerebral hemorrhage is almost the same even with CT.
imageHyperacute cerebral hemorrhageHyperacute cerebral infarction
Findings immediately after onsetSignal changes are observed on T2WI and DWI immediately after the onsetNo findings were found immediately after the onset.
T2WIModerate hyperintensity in central hematoma and hypointensity in margin, surrounding edematous changes in T2WIIn T2WI, no signal change due to angioedema is observed until several hours after the onset.
DWIHigh signal in the center of the hematoma and low signal in the marginFindings may appear 30 minutes after onset, but are still localized compared to the final infarction.

The significance of MRI is that it can distinguish the biochemical state of hemoglobin.

StageProperties of heme ironmagneticLocalizationT2WIT1WICT
Hyperacute phase(within 3hours)OxyhemoglobinFe2 + / diamagnetismIn red blood cellsMild high signalMild low signalHigh absorption range
Acute period(Within 3 days)Deoxy hemoglobinFe2 + / paramagnetismIn red blood cellsLow signalMild low signalHigh absorption range
Acute period(Within 7 days)MethemoglobinFe3 + / paramagnetismIn red blood cellsLow signalHigh signalHigh absorption range
Subacute phase(Within 2 weeks)Free methemoglobinFe3 + / paramagnetismOutside red blood cellsHigh signalHigh signalLower from the edge
Chronic phase(After 1 month)HemosiderinFe3 + / paramagnetismOutside red blood cellsLow signalLow signalLow absorption range

Immediately after the onset of intracerebral hemorrhage, the erythrocyte membrane in the hematoma is normal and insidehemoglobinMost of them are oxygenated oxyhemoglobin.Since oxyhemoglobin is a diamagnetic substance, it does not affect the T1 relaxation time and T2 relaxation time, but since blood clots contain water, they generally show a mild T2 prolongation.Oxyhemoglobin becomes deoxyhemoglobin within a few hours.Deoxyhemoglobin is a paramagnetic substance and shows a marked low signal at T2WI.It is the gradient echo method T2 * weighted image that is sensitive to the magnetic susceptibility effect.In this image, acute hematoma shows a marked hypointensity.However, it is difficult to distinguish between acute and chronic hematomas on T2 * -weighted images.From the acute phase to the subacute phase, deoxyhemoglobin is oxidized from the margin and converted to methemoglobin.Methemoglobin is a paramagnetic substance and exhibits a remarkable T1 shortening effect, so the signal is increased by T1WI.At this time, hematoma melting begins at the same time.The signal is increased by T2WI due to the outflow of methemoglobin from the blood cells due to the destruction of the erythrocyte membrane and the edematous change.At this time, the margin of the hematoma becomes a low absorption area on CT, so MRI can more accurately determine the boundary of the hematoma and edematous changes.In the chronic phase, methemoglobin becomes hemosiderin, edema subsides, and both T1WI and T2WI have low signals. The T2 * weighted image also shows a low signal.

Subarachnoid hemorrhage

The most famous CT finding of subarachnoid hemorrhage is known to be bleeding to the so-called pentagon, which is common in cases of intracranial internal carotid artery aneurysm rupture, and the subarachnoid hemorrhage due to other aneurysm ruptures. Lower bleeding does not result in such an image.It is said that about 30% of ruptured aneurysms are complicated by intracerebral hemorrhage.Cerebral aneurysmThe most common sites of the anterior communicating artery (Acom), the first branch of the middle cerebral artery, and the internal carotid-posterior communicating artery (IC-PC).Medial and medial anterior cerebral artery in anterior communicating artery aneurysm, temporal lobe in IC-PC, outer capsule and temporal lobe in middle cerebral artery aneurysm, distal anterior cerebral artery aneurysmCorpus callosumからGyrusForm an intracerebral hematoma.The distribution is clearly different from that of hypertensive intracerebral hemorrhage, and in principle, it is in the vicinity.Subarachnoid hemorrhageIs accompanied by.Subacute bacterial endocarditisIt is known that aneurysms are complicated with subarachnoid hemorrhage and intracerebral hemorrhage in patients with villous cancer.The method for estimating the responsible aneurysm from the bleeding site is summarized below.

Rupture siteSpread of bleeding
Anterior communicating arteryLongitudinal fissureFrom the front, chiasmatic cistern, interpeduncular cistern, etc.Sylvian fissureIt exists symmetrically up to, and is characterized by hematoma in the septum pellucidum.
Middle cerebral arteryCentered around the ipsilateral Sylvian fissure
Intracranial internal carotid artery regionIt exists asymmetrically bilaterally around the upper cistern of the saddle.The so-called Pentagon.
Vertebral basilar artery regionIt exists symmetrically around the detour tank, interpeduncular cistern, and pontine cistern.


According to the percentage and ranking of deaths by causative disease in Japan, cerebrovascular disease1951 から1980 1st place,1981 から1984 2st place,1985 から1994 3st place,1995 から1996 2st place,1997 から2010 3st place,2011 から2015 4th place[6][7][8][9][10][11][12]In 2015, of the 129 deaths, the death toll from cerebrovascular disease was 0428.[11][12], The ratio to the total number of deaths is 8.7%.


As a sequela of stroke, spasticity (tension) of the muscles of the limbs may be seen.For this sequelae, the latest treatment methods including botulinum treatment are being tried in clinical practice.


  1. ^ (Excel) Global health estimates: Leading causes of DALYs (Report). who(2020-12). Download the data> GLOBAL AND BY REGION> DALY estimates, 2000–2019> WHO regions. https://www.who.int/data/gho/data/themes/mortality-and-global-health-estimates/global-health-estimates-leading-causes-of-dalys 2021/3/27Browse.. 
  2. ^ O'Donnell MJ et al. Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): A case-control study. Lancet 2010 Jul 10; 376: 112.
  3. ^ "Deep relationship between sleep and lifestyle-related diseases". 2015/11/23Browse.
  4. ^ "Death and DALY estimates for 2004 by cause for WHO Member States (xls) ”. World Health Organization (2004). 2011/12/20Browse.
  5. ^ "WHO Disease and injury country estimates". World Health Organization (2009). 2009/11/11Browse.
  6. ^ Ministry of Health, Labor and Welfare > Statistical information / white paper > Various statistical surveys > List of welfare labor statistics > Vital statistics survey > Overview of vital statistics (fixed number) > 22 (2010) Overview of vital statistics (fixed number) > Vital statistics Annual report Main statistical table (latest data, annual transition)> Page 14 Table 7 Annual transition of the number of deaths and mortality rate (per 5 population) by mortality ranking (up to 10th place)
  7. ^ Ministry of Health, Labor and Welfare> Vital Statistics> FY23> Table 6 Number of deaths / mortality rate (per 10 population), by simple classification of causes of death
  8. ^ Ministry of Health, Labor and Welfare > Vital Statistics > 23 > Table 7 Deaths by cause of death (1st to 5th) Number of deaths / mortality rate (per 10 population), gender / age (5 years old)
  9. ^ Ministry of Health, Labor and Welfare> Vital Statistics> FY25> Table 6 Number of deaths / mortality rate (per 10 population), by simple classification of causes of death
  10. ^ Ministry of Health, Labor and Welfare > Vital Statistics > 25 > Table 7 Deaths by cause of death (1st to 5th) Number of deaths / mortality rate (per 10 population), gender / age (5 years old)
  11. ^ a b Ministry of Health, Labor and Welfare > Vital Statistics > FY6 > Table 10 Number of deaths / mortality rate (per XNUMX population), by simple classification of causes of death
  12. ^ a b Ministry of Health, Labor and Welfare > Vital Statistics > 27 > Table 7 Deaths by cause of death (1st to 5th) Number of deaths / mortality rate (per 10 population), gender / age (5 years old)


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