Lacunar infarction in the elderly
Introduction
Introduction to lacunar infarction in the elderly Lacunarinfarction is a concept of pathology-CT-clinical integration. It is a common disease in the elderly. The high-risk age group is 60-70 years old. Fisher outlined it as an ischemic microinfarction (or softening foci) that occurs in the deep penetrating artery (or other tiny arteries) and an irregular cavity that develops after chronic healing. The diameter of the tiny artery involved in the lesion is about 200m, and the pathological change is a cavity or infarction of 2-20mm. The CT scan of the skull shows a density reduction zone of 2-20mm (generally should not exceed 15mm). Diagnose more than 20 lacunar syndromes. basic knowledge The proportion of illness: 0.005-0.01% Susceptible people: good for 60 to 70 years old Mode of infection: non-infectious Complications:
Cause
The cause of lacunar infarction in the elderly
High blood pressure (30%):
Hypertension is the most direct cause of this disease, especially when chronic hypertension exceeds 21.3/12.7 kPa (160/95 mmHg). The incidence of hypertension in patients with lacunar infarction is 45% to 90%. And the effect of increased diastolic blood pressure on the disease is more obvious.
Hypertension leads to two possible mechanisms for lacunar infarction:
1 persistent hypertension acts on the deep penetrating artery or other tiny arterial wall of the brain, which increases vascular permeability, coagulation function and anticoagulant function, leading to segmental fat hyaline degeneration of microvascular wall, fibrin necrosis and arteriole Tumors and the like change, causing obstruction of small arteries and formation of microemboli.
2 persistent hypertension causes the basilar artery of the brain to elongate, the deep perforating artery is displaced, the blood vessel is twisted, and the lateral blood flow is further reduced to cause ischemic microinfarction.
Arteriosclerosis (20%):
Lacunar infarction is closely related to arteriosclerosis. Fisher used continuous sectioning to confirm the basal ganglia. The feeding artery of the cystic lesion in the internal capsule area has severe cerebral arteriosclerosis, ie segmental arterial structural destruction, cellulose-like Necrosis or vascular necrosis, other scholars have also found that the obvious change in the medullary artery is the thickening of the wall of the tube, and the narrowing of the lumen of the vessel. The frequency of lacunar infarction in each brain is directly proportional to the degree of arteriosclerosis.
Diabetes (10%):
It is well known that diabetes can cause small infarct lesions in the distal limbs, kidneys, retina, peripheral nerves and cranial nerves, but the role of diabetes in small vessel lesions of the brain has not been clearly defined. Epidemiological findings indicate that diabetes is a stroke. One of the risk factors, but there is still no evidence of association between diabetes and lacunar infarction. Mast et al have only confirmed that diabetes is associated with multiple lacunar infarction, but not with single-shot, but diabetes. Increased blood coagulation and viscosity, enhanced platelet adhesion, can undoubtedly increase the blood flow supply of the deep penetrating artery of the brain plays an important role in the formation of lacunar infarction.
Embol (10%):
(1) Cardiac emboli: the attachment of the wall embolus for rheumatic heart disease or non-rheumatic heart disease.
(2) Arterial emboli: including atherosclerosis with or without ulceration, fibromuscular vascular disease, thrombus detachment of dissecting aneurysms, especially the ascending aorta, embossed by atherosclerotic plaque in the carotid artery It is one of the important causes of lacunar infarction and has attracted more and more attention.
Other factors (10%):
Factors such as hyperlipidemia, hyperviscosity, smoking, drinking and changes in brain blood flow also have an effect on the occurrence of lacunar infarction.
Pathogenesis
The pathological cavity is a small cavity containing water in the brain parenchyma, which is caused by lacunar infarction and non-lacvular cerebral infarction. According to Fisher et al., lacunar infarction should be ischemic infarction. It is mainly found in the basal ganglia and the basal part of the pons, such as the lenticular nucleus, the caudate nucleus, the thalamus, the radioactive crown, the internal capsule, the white matter of the brain, the pons, etc., and recent data indicate that in addition to the above-mentioned sites, Other parts such as the cerebellum, cerebral cortex, midbrain, and cerebral peduncle can also occur, especially in the cerebral cortex, with the most parietal lobe, followed by the temporal and frontal lobes, and the occipital lobe.
The size of lacunar infarction is related to the size of the affected vessels. It is most common in blood vessels with a diameter of 2 to 5 mm. Most of the reported lacunar infarctions have a diameter of 3 to 15 mm and a maximum of 20 mm. Or multiple, the lesion wall is irregular, there are other shapes such as a circle, and there are fine connective tissue cords in the cavity. Some are still wrapped in slender arteries or veins. They contain lipids and iron-containing blood depending on the old and new infarcts. The number of phagocytic cells of flavin is also different. Sometimes the deep perforating artery or its branches are visible. The diseased arteries often have a transparent change. The muscle layer, the elastic fiber layer and the outer membrane are replaced by uniform eosinophils, and the lumen is narrowed. Or enlargement, arteries other than lesions are accompanied by atherosclerotic changes such as elastic fiber rupture, endothelial proliferation, or collagen deposition.
Prevention
Elderly lacunar infarction prevention
The main measures to prevent this disease are to actively control various risk factors of stroke, especially those with high risk factors, such as transient ischemic attack, and more active treatment to prevent the development of cerebral infarction.
Complication
Complications of lacunar infarction in the elderly Complications
Can be complicated, aphasia, mental disorders and so on.
Symptom
Symptoms of lacunar infarction in the elderly Common symptoms Responsive conscious dysfunction cerebral ischemic loss of dementia Dizziness dysphonia Drowsiness gait instability dysphagia
Lacunar infarction is the most common cerebrovascular disease in the elderly, accounting for 20% of ischemic stroke. The peak age of onset is 60-69 years old, more men than women, 2-6 times more than women, and most of them are affected during the day. Most of them have no obvious incentives. They are common in subacute and chronic onset. Symptoms usually peak at 12h to 3 days. About 20% of patients have temporary ischemic attack before the disease.
The diversity of the location, number, size, etc. of lacunar infarction leads to a variety of clinical manifestations. In addition to the 21 types of lacunar syndrome and lacunar state reported by Fisher, it has been suggested that reversible ischemia should be Attacks (such as TLAs, RIND) and other clinical syndromes such as pseudobulbaric palsy, lacunar dementia, or subcortical arteriosclerotic encephalopathy (Binswanger's disease) that may be due to lacunar damage are included. Non-existent or rare performances are continually seen in the literature.
1. Clinical features
Common symptoms include dizziness, headache, limb numbness, dizziness, memory loss, unresponsiveness, convulsions, dementia, unconsciousness, and psychiatric symptoms. The main clinical signs are tongue stiffness, slow speech, varying tone of speech, mild central facial paralysis. Lateral limbs are paralyzed or sensory, some pyramidal tract signs are positive, and ataxia is rare.
2. Clinical type
(1) simple exercise hemiparesis (PMH): the most common, accounting for 40% to 60%, the main features are objective examination without sensory disturbance, visual field defect, aphasia, misuse or loss of recognition; and only one side of the face and upper and lower limbs Inability or incomplete paralysis, lesions can occur in the internal capsule, pons, cerebral peduncle, basal ganglia, cerebral cortex, radiation crown, etc., often recover within 2 weeks, but easy to relapse.
(2) pure sensory stroke (PSS): no muscle disorder, dizziness, diplopia, aphasia and visual field defects, but only one side of the face and upper and lower limbs of the sensory disturbance, the lesion is located in the posterior nucleus of the thalamus, usually the brain The posterior arterial thalamic perforating branch is caused by infarction. A few cases can be caused by the spinal thalamus bundle and the lesion of the thalamic cortex. It can also be caused by the lesion invading the outer thalamus and the posterior limb of the internal capsule. It is often within a few weeks. restore.
(3) Sensorimotor stroke (SMS): manifested as one side of the face, trunk and upper and lower limbs, sensory and facial, lingual and upper and lower extremity, unconsciousness, memory impairment, aphasia, loss of recognition and misuse, In the past, this type was considered to be rare. In recent years, domestic and foreign literature reports are second only to PMH. The lesions are located in the posterior lateral nucleus of the thalamus and the posterior limb of the internal capsule. It is usually caused by the occlusion of the posterior cerebral artery or the posterior choroidal artery. Prognosis good.
(4) Ataxia-induced hemiparesis (HAH): manifested as hemiparesis and cerebellar ataxia on the contralateral side of the lesion, and the lower extremity is heavier than the upper limb, sometimes accompanied by sensory disturbance, nystagmus, poor resolution, dysarthria , dumped to one side, the lesion occurs in the base or inner capsule of the pons, radiation crown, cerebellum, etc. can also occur, often recover within a few weeks.
(5) poor articulation - hand awkward syndrome (DHS): manifested as obvious dysarthria, sputum eating, difficulty swallowing, mild hand weakness and fine motor disorders such as ataxia, and can be accompanied by ipsilateral Central facial, tongue, hyperreflexia and pathological signs positive, gait instability during walking, but no sensory disturbance, no TLA before this type of disease, acute onset, rapid symptoms, the lesion is located at the base of the pons /3 and 2/3 junction or the uppermost part of the inner pocket of the knee.
(6) Variant PMH: There are 7 variants of PMH.
1 PMH combined with motor aphasia, the lesion is located in the knee and forefoot of the internal capsule, and the lower part of the radiograph is caused by the occlusion of the bean-like artery supplying the area.
2 PMH without facial paralysis, caused by vertebral artery and its penetrating occlusion, may have mild vertigo and nystagmus during onset, may be accompanied by abnormal numbness and weakness of the lingual muscles, and may affect the contralateral cone in the late stage, causing four sputum .
3 PMH with ipsilateral gaze palsy, the lesion is located in the center of the lower part of the pons, showing facial paralysis and upper and lower extremity paralysis, with transient gaze gaze and cross-core interocular muscle paralysis (ie one-and-a-half Syndrome), while abductor nerves function normally.
4 PMH combined with Weber syndrome is caused by infarction in the middle of the cerebral peduncle involving the oculomotor nerve fibers.
5 PMH combined with nerve paralysis, the lesion located in the middle of the lowermost part of the pons, involving the ipsilateral nerve.
6 combined with mental disorder of PMH, lesions occur in the anterior and posterior limbs of the hindlimb of the internal capsule, affecting the frontal lobe associated with the fibers of the thalamus, manifested as acute insanity, attention and memory impairment with PMH.
7 PMH manifested as atresia syndrome: caused by bilateral PMH caused by bilateral corticospinal infarction, can be seen in bilateral internal capsule, pons, pyramidal or cerebral infarction.
(7) Midbrain thalamic syndrome: usually the posterior anterior and posterior cerebral arteries of the posterior cerebral artery, one or more of the four arteries, including the median superior and inferior median and middle arteries. As a result, the typical infarct is butterfly-shaped, involving the bilateral median midbrain, the thalamus and thalamus, clinical manifestations of one or bilateral oculomotor nerve paralysis, Parinaud syndrome, or vertical gaze numbness with drowsiness, Loss of consciousness and memory impairment.
(8) Basal artery lower branch syndrome: due to small branch occlusion of the lower part of the basilar artery or the upper part of the vertebral artery, resulting in hypothalamus, brainstem invagination of the cover, manifested as dizziness, nystagmus, diplopia, side vision paralysis, nucleus Interocular eye muscle paralysis, difficulty swallowing, cerebellar ataxia, gait instability, facial muscle weakness, burning sensation in the eyes and numbness in the trigeminal nerve distribution area.
(9) Various other types of syndromes:
1Claud syndrome: cerebellar ataxia with oculomotor paralysis.
2 half body twitching, medullary lateral syndrome.
3 bridge extension lateral syndrome.
4 amnesia.
5 one side of the lower limbs unable to fall.
6 dysarthria, acute thalamic dystonia.
7 partial dance chorea.
8 thalamic dementia.
9 pseudo-brain paralysis.
10 pseudo Parkinson's disease.
Due to the complexity of the structure and function of the human brain, the location, size, and uncertainty of the lacunar infarction have led to an increase in the number of reports of clinical syndromes. It seems that there is an inexhaustible trend, so it is still necessary to continuously learn and understand. ,to sum up.
(10) Cavity state: It is believed that the lacunar state is not only caused by multiple infarction of basal ganglia or pons, but the main lesion is the cavity of white matter of frontal lobe and its diffuse incomplete softening. The clinical manifestation is dementia. Pronunciation disorder, difficulty in swallowing, difficulty in stretching the tongue, hyperthyroidism, quadriplegia, bilateral pathological signs, strong crying and laughing, and other symptoms of pseudobulbaric palsy and muscle stiffness, slow movement, short gait and other symptoms of Parkinson's disease , urinary incontinence.
(11) Vascular dementia: Multiple infarction dementia (MID) caused by multiple lacunar infarction is a common type of vascular dementia. It is confirmed by autopsy in elderly people that the more infarction, the higher the incidence of dementia. Clinical features include:
1 has a history of hypertension, diabetes, cerebral arteriosclerosis;
2 Most have a history of stroke;
3 can detect signs of focal and diffuse neurological damage;
4 There are different levels of mental retardation, memory, computational power, orientation disorder, most patients are apathetic, lack of agility, but the personality is relatively preserved;
5CT or MRI showed multiple deep luminal stalks in the brain.
(12) Asymptomatic lacunar infarction: CT or MRI scan of the head indicates lacunar infarction, but there are no obvious localized signs and symptoms in the clinic. The infarction site is more common in the basal ganglia, the inner capsule area, the radioactive crown, and the lesion. Smaller, less than 1.5cm in diameter, some of the lesions are classified as such because the symptoms and signs of impaired neurological function are easily overlooked or lack of recognition (eg, right frontal infarction leading to body image disorder, disease) Loss of sensation or unilateral neglect, occipital infarction leads to hemianopia or quadrant blindness, etc.).
Examine
Examination of lacunar infarction in the elderly
General examinations should include blood glucose, blood lipids, hemorheology, plasma prothrombin time, and thromboplastin time.
1. ECG, blood pressure monitoring.
2. EEG: The electroencephalogram of patients with vascular dementia is basically diffuse low-wavelength slow wave, that is, with a wide range of or waves as background, showing obvious focal or asymmetrical slow waves, a few cases have cycles Sexually sharp wave fusion, EEG changes can not distinguish the type of vascular dementia.
The size of lacunar infarction lesions is related to the abnormal rate of EEG. For example, 45% of patients with lesions of 1.5 to 3 mm have abnormalities. If less than 1.5 mm, 65% of EEG is normal.
3. Cerebral blood flow map and Doppler ultrasonography: cerebral blood flow map changes mainly due to the elasticity of blood vessel wall and blood flow, and the abnormal rate is very high. Transcranial Doppler ultrasonography can not only accurately determine the degree of vascular stenosis, but also The size, number and flow status of the thrombus can be dynamically explored.
Evoked potential
(1) Somatosensory evoked potential (SEP): The abnormality of SEP is related to the location of the lesion. For example, most of the cystic lesions have a decrease or disappearance of N20 amplitude, and P22, N30 amplitude is reduced, and late component N63 is abnormal. P27 can be seen in parietal lesion. P25 amplitude decreased; thalamic lesions P15, N20, P25 amplitude loss and N20 peak latency (PL) prolonged; medullary lesion N13, P14 amplitude decreased, SEP of vascular dementia mainly caused by peak-to-peak latency (IPL) extension, equivalent to central conduction Time (CT) prolonged, when white matter lesions are extensive, more significant, which can be differentiated from senile dementia, the latter SEP measurement is mostly normal.
(2) Brainstem Auditory Evoked Potential (BAEP): Since the potential activity of BAEP is recorded in the brainstem, the BAEP of cerebrovascular disease focuses on the detection of vertebral basilar artery system. The relationship between BAEP abnormality and lesion site is affected. VIII cranial nerve and cochlear circulation, BAEP waves can not be elicited; the lower part of the pons in the bilateral cochlear nucleus lesions only see I wave; the lower part of the pons is covered with lesions, BAEPIII wave and subsequent wave abnormalities; upper pons lesions, IV, V wave abnormalities; On one side of the pons and the midbrain junction, the ipsilateral V wave disappeared and the contralateral BAEP was normal.
(3) Event-ralated potentials (ERPs): The P300 latency of patients with multiple lacunar infarction was significantly longer than that of the control group. However, the change of P300 latency was not significantly different from that of the normal control group. The conclusions of the report are not yet uniform.
A statistical analysis showed that there was no significant correlation between the P300 latency and the number of patients with infarcted lesions; it was closely related to the extent of ventricular enlargement or decreased peripheral tissue density (luminance) in CT images; and was measured with the Hasegawa Dementia Scale. The intelligence scores are clearly negatively correlated.
(4) Visual evoked potential (VEP): The lacunar infarct of the occipital lobe does not produce a P100 latency change in VEP.
5. CT scan of the head (CT): patients with clinical manifestations of lacunar infarction, 66% to 76% of patients with lacunar infarction on CT, CT is easy to find on the lesions with >5mm on the surface. For lesions <5mm or located in the brainstem, it is often difficult to detect. Rascal et al reported that the simple exercise hemiplegic syndrome has a positive rate of 97% at 36h after the disease, and is more likely to change positively after about 10 days.
(1) Non-enhanced scanning: the lesion is mainly located in the basal ganglia, the thalamus, the internal capsule, the brainstem or the radioactive crown, and the lateral ventricle, with a circular or elliptical low-density foci with clear boundaries, diameter 2-20 mm, mass effect Light, generally only the adjacent ventricle is compressed, and there is no midline structure displacement. The infarct density is close to the cerebrospinal fluid density after about 4 weeks, and shows atrophic changes, ie ipsilateral ventricle and/or adjacent cerebral pool, brain The limitation of the ditch is expanded, and the midline structure may have a slight ipsilateral displacement.
(2) Enhanced scan: 3 days to 1 month after infarction, the lesions may be uniform or patchy, and this effect is most obvious at 2 to 3 weeks. When the lesion density is equal to the density of cerebrospinal fluid, it is no longer strengthened.
(3) CT scan signs of multiple infarction dementia:
1 cerebral cortex or subcortical multiple low-density infarcts of different sizes, mainly distributed in the basal ganglia and the frontal, temporal, and occipital cortex.
2 Most cases can show brain atrophy changes, that is, the ventricle or sulci enlargement, cerebral cortex, medulla atrophy.
3 may be associated with Binswanger's disease (subcortical arteriosclerotic leukoencephalopathy, SAE) CT features: roughly symmetrical low-density shadows in the white matter around the ventricles and semi-oval centers, with a halo or umbrella shape, blurred edges, and more Located in front of or behind the lateral ventricle, the gray/white matter density ratio increases.
6. Magnetic resonance (MRI)
The detection rate of lacunar infarction by MRI is significantly better than that of skull CT scan, especially for brain stem and cerebellar cerebral infarction. At 72h after surgery, MRI of 75% of patients can show lacunar lesions 15mm,5 Within a day, the positive rate was 92%. In the acute phase, the MRI image was characterized by a decrease in T1 signal and an increase in T2 signal, and the change in T2 signal was more sensitive.
7. Magnetic resonance angiography (MRA)
MRA can provide clear image of carotid artery and vertebral artery, and quickly detect vascular occlusion. However, it is not widely used in the diagnosis of acute cerebral infarction. If conditions permit, this should be considered for people at high risk of cerebrovascular disease.
8. Single photon emission tomography (SPECT)
Using this technique, the cerebral blood flow (rCBF) changes in the detectable area according to the radioactive material uptake gradient of different parts of the brain tissue. After the stroke, the rCBF perfusion occurs seriously, so SPECT can be found within 24 hours after the infarction.
SPECT-rCBF imaging is a good method to identify Alzheimer's disease and MID. Alzheimer's disease is characterized by reduced symmetry of radioactivity distribution in sputum, apex, occipital and frontal areas, especially in sputum, top and frontal areas; MID is cerebral cortex. Internally distributed or patchy multiple perfusion area.
9. Positron emission tomography (PET)
This test can reflect changes in blood flow, glucose metabolism and oxygen metabolism (CMRO2) in brain tissue. The patients with lacunar infarction were detected by PET. The above indicators did not change significantly, but the tissues and lesions located in the small infarct of 25 mm small infarct were found. Contralateral cerebellar hemisphere CBF and CMRO2 were significantly reduced, the latter suggesting that PET abnormalities in the infarct of the cavity are not only related to the size of the lesion but also to the location of the lesion. The improved PET examination technique can distinguish 12mm and pathophysiological changes of the subcortical structure. .
Compared with PET in patients with multiple infarction and non-dementia, the oxygen metabolism rate of the left and right cerebral hemispheres decreased, and the upper, middle, lower and basal ganglia decreased.
The PET of Binswanger disease showed that the cerebral cortex, white matter cerebral blood flow, and cerebral oxygen metabolism rate were all reduced, especially the white matter of the brain was more obvious, and the white matter area around the anterior horn of the lateral ventricle was especially decreased.
Unlike multiple infarction dementia, PET images of patients with Alzhenmer disease often show normal glucose metabolism in the frontal lobe, and glucose metabolism and cerebral blood flow in the parietal lobe to temporal lobe are characteristically decreased; or in different parts of the cerebral cortex Based on the decrease in the rate of glucose metabolism, the decline in the parietal and temporal lobe is more pronounced.
10. Examination of cognitive function of dementia
Simple clinical examinations include conversations and gauges, which are commonly used in the following ways:
1 Intelligence status check: including Simple Intelligence State Check (MMSE), Blessed Dementia (BDS) and Hasegawa Dementia Scale (HDS).
2 Daily life and social ability assessment: including the Activity of Daily Activity Scale (ADL) and Pfeffer's Functional Activity Questionnaire (POD).
3 Neuropsychological tests: including the Fuld Object Memory Test (FOM), which examines memory and learning ability, the Fast Vocabulary Test (RVR) for speech function, the Digital Breadth Test (DS) for assessing attention/immediate memory, and the examination structure and The WISC Building Block Test (BD) for graphic recognition functions.
(HDS was compiled by Japanese scholar Hasegawa in 1974. It is mainly used to screen subjects of dementia for further examination and diagnosis. This method is easy to use and widely used in China).
Diagnosis
Diagnosis and diagnosis of lacunar infarction in the elderly
Diagnostic criteria
1. Diagnostic criteria for lacunar infarction The diagnostic criteria for each report are different, but the combination of clinical, pathological and CT scans is basically used.
Diagnostic criteria for the Fourth National Cerebrovascular Disease Conference of the Chinese Medical Association:
(1) The onset is caused by hypertensive arteriosclerosis, which is acute or subacute.
(2) Many unconscious obstacles.
(3) There is no red blood cell in the cerebrospinal fluid.
(4) clinical manifestations are not serious, more often manifested as pure sensory stroke, pure motor hemiparesis, ataxia hemiparesis, dysplasia - hand clumsy syndrome or sensorimotor stroke.
(5) If necessary, perform a CT examination to confirm the diagnosis.
Vascular dementia
Multi-infarct dementia is a type of vascular dementia. Lacunar infarction is an important pathological change. The clinical manifestations are: sudden onset, stepwise deterioration, volatility course, nighttime confusion, relative preservation of personality, emotional vulnerability Strong crying and laughing, often with high blood pressure, history of heart disease and stroke, combined with signs of atherosclerosis, signs and signs of focal neurological damage, CT or MRI showed multiple infarcts in the brain and (or) brain atrophy.
The diagnostic criteria of the Fourth National Conference on Cerebrovascular Diseases of the Chinese Medical Association (in Chengdu in 1995) were:
(1) Comply with the fourth edition of the Diagnostic and Statistical Manual of Psychiatry to diagnose dementia standards.
(2) Neurological symptoms and signs of acute or subacute onset.
(3) There is a history of stroke in the past.
(4) The course of disease fluctuates in a stepwise progression.
(5) often combined with hypertension, diabetes, coronary heart disease, hyperlipidemia and so on.
(6) Hachinski ischemic scale score 7 points.
(7) CT and MRI confirmed multifocal cortical or subcortical ischemic changes in the brain.
Differential diagnosis
Clinical should be differentiated from cerebral hemorrhage, cerebral embolism, and intracranial space-occupying lesions.
