solitary infarct dementia
Introduction
Introduction to single cerebral infarction dementia Large area infarction of the brain tissue and some important brain function sites of single infarction, clinical manifestations of dementia, large area of cerebral infarction volume of 50 ~ 60ml or more, can make one side of the frontal lobe or temporal lobe and even the brain Most of the hemisphere function is destroyed, focal localization signs and dementia occur. Dementia is related to the lesion site. The thalamus, horns, frontal and marginal systems are closely related to dementia. The bilateral thalamic and thalamic lesions can form thalamic dementia. Clinically rare. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific people Mode of infection: non-infectious Complications: depression, urinary tract infection
Cause
Cause of single cerebral infarction dementia
(1) Causes of the disease
Like multiple cerebral infarction dementia (MID), stroke is the most common cause of single cerebral infarction dementia.
(two) pathogenesis
Cerebral infarction in important functional sites causes dementia. The infarct volume may be only a few milliliters, mostly in the blood supply area of the posterior cerebral artery, including the thalamus and hippocampus. It is generally believed that the dominant hemisphere thalamus, horny back, deep frontal infarction may cause dementia, cerebral infarction. Dementia is also related to the degree of brain atrophy and the volume of white matter lesions around the ventricles.
Vascular lesions are not the only cause of dementia. Many patients have dementia 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.
Prevention
Single 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.
Complication
Complications of single cerebral infarction dementia Complications depression urinary tract infection
Patients may have autonomic dysfunction, depression, and abnormal mental behavior. In addition, secondary lung infections, urinary tract infections, and hemorrhoids should be noted.
Symptom
Symptoms of single-onset cerebral infarction dementia Common symptoms Over-extension of tongue-like dementia, expression, apathy, positioning, signs, response, dementia, dementia, sensory disturbance
1. The patient had a single cerebral infarction cerebrovascular disease with a large area of cerebral infarction or some important brain function sites. The lesions were located in the thalamus, horns, frontal lobe and marginal system, etc. Localization signs, such as hemiplegia, pyramidal tract sign, partial sensory disturbance, over-sensation, loss of reading, loss of writing, loss of recognition and miscalculation, different combinations of signs, cerebral artery occlusion caused by large area cerebral infarction, cerebral edema And even cerebral palsy; basal occlusion of the basilar artery leads to severe disturbance of consciousness and quadriplegia; fluent aphasia, loss of reading (can be associated with loss of writing), memory impairment and dyskinesia, etc.; posterior cerebral artery occlusion More common, causing damage to the upper midbrain, the central part of the thalamus (medial nucleus and most of the medial nucleus), severe memory loss and dementia, visible vertical gaze and other midbrain and pons, motor symptoms are generally not Obvious, not lasting.
2. Cognitive dysfunction is characterized by slow response, memory and computational power loss, indifferent expression, ignorance, can not continue the familiar work and normal interactions, do not recognize the family, wear the wrong pants and urinary incontinence, etc., ultimately life Can not take care of themselves, thalamic dementia is mainly based on mental symptoms, such as amnesia, mood abnormalities and lethargy.
Examine
Examination of single 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. MRI examination can detect the responsible lesions in the thalamus, temporal lobe, marginal lobe, etc. after 24 hours of onset, T1WI low signal, T2WI high signal, mild mass effect in 1 week, diseased artery stenosis, weakening of airflow effect Or disappear.
2. EEG examination in the acute phase of large-area cerebral infarction, brain tissue ischemia, necrosis and peripheral edema can be expressed as the basic rhythm of the lesion area slows down, the amplitude is reduced, diffuse irregular or wave appears; in the posterior cerebral artery In the acute phase of cerebral infarction in the blood supply area, -rhythm inhibition and pleomorphic activity in the lateral occipital region of the lesion, with spikes in the temporal region, evoked potentials and event-related potential (P300) changes can help to identify subclinical lesions.
Diagnosis
Diagnosis and diagnosis of single cerebral infarction dementia
Diagnostic criteria
1. Dementia occurs after a large area of cerebral infarction or a single infarction in some important brain functional sites.
2. Clinical manifestations of focal localized local symptoms and signs; such as hemiplegia, pyramidal tract sign, partial sensory disturbance, over-sensation, loss of reading, loss of writing, loss of recognition and miscalculation, etc. combination.
3. Imaging findings of large areas of cerebral infarction or thalamic, angular gyrus, marginal lobe and other infarct evidence.
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.
