Multi-infarct dementia

Introduction to multiple cerebral infarction dementia Multi-infarct dementia (MID) was proposed by Canadian neurologist Hachinski (1974) and is the most common type of vascular dementia (VaD), accounting for 39.4%. Due to repeated strokes, bilateral hemisphere middle cerebral artery Or the involvement of the cortical, white matter or basal ganglia in the blood supply area of multiple branches of the posterior artery leads to intelligent and cognitive dysfunction syndrome, which is one of the common causes of senile dementia. basic knowledge The proportion of illness: 0.0003% Susceptible people: no specific people Mode of infection: non-infectious Complications: depression, urinary tract infection

Multiple causes of cerebral infarction dementia

(1) Causes of the disease

Cerebrovascular disease is the basis of multiple cerebral infarction dementia (MID). The direct cause of MID is mainly due to atherosclerosis, arterial stenosis and atherosclerotic plaque continually falling off, causing repeated multiple cerebral infarction, which in turn leads to MID. Risk factors may include age, low education, high blood pressure, diabetes, hyperlipidemia, history of stroke, location and size of stroke, and aphasia with stroke.

(two) pathogenesis

Large vessels such as the internal carotid artery or the middle cerebral artery are involved. Atherosclerosis causes stenosis of the lumen, thickening of the intima, thrombosis or emboli (multiple or multiple times), which can lead to multiple cerebral cortex and hemisphere. Large infarct lesions, multiple infarction lesions significantly reduce the volume of brain tissue, leading to brain atrophy and bilateral lateral ventricle dilatation. When the volume of infarcted brain tissue exceeds 80-150ml, clinical manifestations of dementia may occur, especially frontal lobe and temporal lobe. And vascular damage caused by specific parts such as the limbic system, often lead to dementia.

Hemorrhagic or ischemic lesions can be seen in the brain parenchyma. Ischemic is common. Common lesions are multiple lacunar lesions or large infarcts, as well as internal carotid arteries, middle cerebral artery trunks and cortical branches. Atherosclerotic lesions, diffuse lesions in the brain, multiple localized lesions or multiple lacunar lesions, mainly cortical or subcortical lesions, multiple infarct lesions, which can lead to brain atrophy, white matter atrophy Causes bilateral bilateral ventricle dilatation.

Vascular lesions are not the only cause of MID. Many patients have dementia lesions related to neurodegeneration, but the clinical manifestations are not obvious. They are in the subclinical stage. Once cerebrovascular disease occurs, the clinical manifestations of dementia syndrome can occur more rapidly. The pathology is mixed dementia.

Multiple cerebral infarction dementia prevention

1. Early detection and avoiding risk factors for stroke, such as hypertension, diabetes and hyperlipidemia, and active treatment, high carotid stenosis can be treated surgically, which helps to reduce the incidence of vascular dementia.

2. Quit smoking, control drinking and reasonable diet.

3. Those with a clear genetic background should be genetically diagnosed and treated.

Multiple complications of cerebral infarction dementia Complications depression urinary tract infection

Patients often have autonomic dysfunction, depression, and abnormal mental behavior. In addition, secondary lung infections, urinary tract infections, and hemorrhoids should be noted.

Multiple symptoms of cerebral infarction dementia Common symptoms Apathy, sensory disorder, paralysis, hypersensitivity, dementia, anxiety, localization

1. The clinical manifestations of MID are non-specific, the patient has multiple history of ischemic stroke events, focal signs of cerebral infarction, such as central facial palsy, hemiplegia, partial sensory disturbance, increased muscle tone, cone Bunch sign, pseudo-bulbar palsy, over-sensation and urinary incontinence.

2. MID can be acute onset, staged progress, and intelligent damage often has patchy defects. Mental activity disorder is directly related to vascular lesions and the location and volume of brain tissue. Cognitive dysfunction is characterized by near memory and computational power. Declining, indifferent expression, anxiety, less language, depression or euphoria, can not be qualified for the familiar work and normal interactions, go out of the way, do not recognize the family, wear the wrong pants, and ultimately live without self-care.

3. Compared with AD, vascular dementia (VaD) is oriented in time and place, short stories are immediately and delayed recall, naming and retelling are less damaging, and execution functions such as self-organizing, planning, and fine movement work are all harmful. Heavier, the clinical manifestations of different vascular lesions are different.

Examination of multiple cerebral infarction dementia

Cerebrospinal fluid routine examination and determination of cerebrospinal fluid, serum Apo E polymorphism and Tau protein quantification, amyloid fragment, have diagnostic and differential significance.

1. Mainly through the patient's daily life and social ability assessment and neuropsychological test, commonly used Simple Mental State Examination Scale (MMSE), Webster's Adult Intelligence Scale (WAIS-RC), Clinical Dementia Rating Scale (CDR) and The Blessed Behavioral Scale (BBBS), etc., the Hachinski Ischemic Score (HIS) scale can be distinguished from degenerative dementia.

2. Neuroimaging

(1) CT scan: It can show multiple irradiance infarcts of different sizes in the cerebral cortex and white matter, leukoaraeosis and brain atrophy in the low-density area of the lateral ventricle.

(2) MRI examination: bilateral basal ganglia, multiple T1WI low signal in cerebral cortex and white matter, high signal on T2WI, clear boundary of old lesions, low signal, no obvious space-occupying effect, unclear boundary of fresh lesions, signal intensity Not obvious, early T1WI changes can not be obvious, T2WI can show lesions; local brain atrophy or global brain atrophy around the brain.

Electrophysiological examination

(1) EEG examination: EEG in normal elderly is mainly characterized by slowing of rhythm, rhythm is slowed from 10-11 Hz in young adults to 9.5 Hz in old age, 3-8 Hz slow wave appears in sputum area; bilateral frontal area and central area Diffuse or activity, especially in the state of drowsiness, significantly indicates brain aging; on the basis of multiple cerebral infarction lesions leading to EEG changes, the alpha rhythm is further slowed down to 8-9 Hz, bilateral frontal, temporal and central Diffuse waves appeared in the area, with focal volatility and high amplitude rhythm.

(2) Evoked potentials: Both MEP and SEP showed prolonged latency and decreased amplitude. The positive rate of large-area cerebral infarction was 80%-90% or more, and the positive rate of small-scale infarction was 30%-50%; about 40% of occipital infarction In patients with cortical blindness, VEP can show abnormal waveform and prolonged latency, and VEP waveform is improved after visual recovery. The abnormal detection rate of BAEP in ischemic stroke is 20%-70%, showing I-V peak-to-peak latency (IPL) Delayed, bilateral BAEP abnormalities in patients with brain stem infarction, IV ~ V waveform disappeared, absolute latency (PL) prolonged.

Diagnosis and diagnosis of multiple cerebral infarction dementia

Diagnostic criteria

According to recurrent stroke events, associated neurological signs and cognitive dysfunction, the diagnosis depends on pathological examination, the clinical diagnostic criteria of MID:

1. Dementia with sudden or slow cerebrovascular events, manifested as emotional changes such as cognitive dysfunction and depression.

2. The condition progressed step by step, with signs of cortical and subcortical dysfunction such as aphasia, hemiplegia, sensory disturbance, hemianopia and pyramidal tract sign. The signs of focal neurological deficits were scattered and the symptoms were aggravated after each stroke.

3. CT or MRI examination showed multiple infarct lesions.

Differential diagnosis

1.Binswanger's disease, or subcortical atherosclerotic encephalopathy, is a chronic progressive cognitive decline caused by leukocytic ischemic damage in the anterior cortex of the brain, gait instability and urinary incontinence. Similar to the clinical manifestations of normal intracranial hydrocephalus, no apraxia or agnosia caused by cortical damage.

2. Progressive multifocal leukoencephalopathy (PML) is a rare multi-system disease with unknown etiology, which may be related to viral infection and immune dysfunction. The lesion is a bilateral hemispherical white matter asymmetric multiple demyelinating lesion, under the microscope Brain tissue necrosis, inflammatory cell infiltration and gliosis, may have inclusion bodies, imaging changes similar to MID, but the cortex is not tired, according to the history and clinical manifestations can usually be identified.

3. The cognitive impairment of AD with stroke AD is slowly progressing, and there may be risk factors such as hypertension and diabetes. Imaging studies show cerebral infarction and brain atrophy, and cortical atrophy is obvious.

4. Autosomal dominant cerebral arterial disease with subcortical infarction and leukoencephalopathy (CADASIL) is more common in 35 to 45 years old, often with a family history, manifested as recurrent TIA, subcortical ischemic infarction and lacunar Infarction, may have migraine, dementia, pseudobulbar paralysis, depression and urinary incontinence, no history of hypertension, MRI can be seen in the subcortical or pons infarction, brain or skin biopsy visible characteristic vascular wall thickening, vascular smooth muscle middle layer Cellular eosinophilic deposition.

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