Binswanger disease

Introduction to Binswanger disease Binswanger disease (Binswangerdisease), also known as subcortical arteriosclerotic encephalopathy, is a relatively common small vascular dementia. Binswanger (1894) first reported a 54-year-old female patient with sexual intelligence disorder, speech disorder, weakness of both lower extremities with tremors of the hands, description of cerebral arteriosclerosis, bilateral enlarged ventricles, white matter atrophy, and multiple ependymal enlargements. Thick pathological changes, Alzheimer officially proposed the disease in 1902, and named after his teacher Binswanger. basic knowledge The proportion of sickness: 0.00001% Susceptible people: more than 55 to 65 years old men and women Mode of infection: non-infectious Complications: high blood pressure, urinary tract infection, hemorrhoids

The cause of Binswanger's disease

(1) Causes of the disease

The cause of the disease is unclear. Fisher (1989) found in 72 patients with pathologically confirmed Binswanger's disease, 94% of patients had a history of hypertension, suggesting that the disease may be associated with hypertension and white matter in the white matter. Related to degeneration.

(two) pathogenesis

The pathogenesis of Binswanger's disease is unknown. Schmidt conducted a 3-year follow-up study of 273 elderly patients. MRI was used to observe abnormal white matter changes. 49 patients (17.9%) had white matter changes, suggesting the genetic role of the disease. About 73% of the genes that cause changes in white matter may be associated with hypertension genes. Apo E and superoxide gene may be risk factors for white matter lesions.

Pathological changes: cerebral sulcus and cerebral gyrus are generally normal, visible middle and severe atherosclerosis, brain slice lesions mainly involve white matter, white matter atrophy, bilateral ventricle enlargement, ventricular septal white matter multiple lacunar infarction, sometimes visible corpus callosum Thinning, microscopic examination of the brain, pons, basal ganglia and other small arteries rich in white matter vacuolization, accompanied by a decrease in the number of myelin fibers, deep hemispherical white matter and small arteries, especially the perforating arterioles, glassy degeneration, deep white matter Myelin loss is mainly located in the occipital lobe, temporal lobe and fiber associated with the frontal lobe. The cortical and subcortical U-shaped fibers remain intact and the corpus callosum is often unaffected.

Binswanger disease prevention

1. Smoking cessation, control of drinking and reasonable diet, genetic diagnosis and treatment should be carried out in a clear genetic background.

Binswanger disease complications Complications, hypertension, urinary tract infection, acne

May be associated with autonomic dysfunction, hypertension, in addition, should pay attention to secondary lung infections, urinary tract infections and hemorrhoids.

Symptoms of Binswanger's disease Common symptoms Local signs Urinary incontinence Cognitive dysfunction Dementia Ataxia Disorders

1. More than 55 to 65 years old, the incidence of men and women is equal, most cases have a history of hypertension for many years, the incidence is concealed, showing a subacute or chronic course.

2. Chronic progressive dementia, focal neurological signs and psychiatric symptoms; long-term stability or rapid exacerbation after stroke, mostly cognitive impairment as the first symptom, memory loss, depression, disorientation, development into life Can not be completely self-care, limb movement disorders are mild, there may be ataxia, urinary incontinence and other symptoms, is the result of the gradual superposition of most small focal signs, rarely complete hemiplegia signs, can appear pseudobulbar paralysis.

3. EEG rhythm slowed down to 8 ~ 9Hz, may be associated with focal amplitude high amplitude rhythm; 40% of patients can not induce significant P300 waveform, suggesting severe impairment of cognitive function, CT, MRI examination can be seen in the brain The atrophy is mainly white matter, the cerebral cortex is mildly atrophied, and there are varying degrees of ventricular dilatation, which may be associated with multiple lacunar infarction.

According to long-term hypertension, middle-aged and elderly patients with cognitive dysfunction, mild limb dyskinesia, ataxia and urinary incontinence, neuroimaging showed white matter atrophy, ventricular leukopenia with multiple lacunar infarction.

Binswanger's disease check

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. EEG rhythm slows down to 8 ~ 9Hz, bilateral diffuse waves appear in the frontal area, temporal region and central region, can be associated with focal high-amplitude rhythm, visual evoked potential (VEP), brain The latency of dry auditory evoked potential (BAEP) and event-related potential (ERP) P300 was significantly longer than that of the same age control group, and 40% of patients could not induce significant P300 waveform, suggesting severe impairment of cognitive function.

2. Imaging examination showed mild atrophy of the cerebral cortex, varying degrees of ventricular dilatation, bilateral ventricle anterior horn, posterior horn and bilateral blurred lenticular low-density shadows on both sides of the body, which may be associated with basal ganglia, thalamus and There are multiple lacunar infarctions in the periosteal arterioles such as pons. The MRI examination shows that the brain atrophy is mainly white matter, the cortex is light, and the T1WI low signal and the T2WI high signal are scattered around the bilateral ventricles and semi-oval centers. In patients with multiple lacunar infarction, PET examination showed diffuse reduction of white matter cerebral blood flow around the bilateral ventricles and a significant decrease in glucose and oxygen metabolism.

Diagnosis and identification of Binswanger disease

1. Normal intracranial pressure hydrocephalus also shows progressive gait abnormalities of the disease, urinary incontinence, dementia triad, ventricular enlargement, cerebrospinal fluid secretion or resorption disorder and CSF circulation pathway blocked, onset occult, disease There is a history of brain trauma, subarachnoid hemorrhage or meningitis, no history of stroke, mild age of onset, normal intracranial pressure, and bilateral ventricular symmetry enlargement in CT, third, fourth ventricle and midbrain guidance The water tube was significantly expanded, and there was no evidence of cerebral infarction in imaging.

2. Multiple sclerosis (MS) MRI showed that the lateral ventricle paraventricular white matter scattered multiple T1WI low signal, T2WI high signal, lesions and blood vessel distribution, MS onset age is mild, spinal cord, brain stem, cerebellum and optic nerve symptoms, signs , course of disease relief - recurrence, increased CSF lymphocytes, increased IgG index and oligoclonal bands, etc., clinically difficult to identify.

3. Alzheimer's disease gradually develops memory impairment, cognitive dysfunction, daily life needs help from others, severe cases are bedridden, CT shows obvious cerebral cortex atrophy and ventricular dilatation, diagnosis requires brain tissue biopsy, sometimes AD can coexist with vascular dementia At this time, AD is often accompanied by amyloid cerebrovascular disease, combined with cerebral hemorrhage.

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