bubble_chart Overview

This disease is caused by cerebral arteriosclerosis affecting the blood supply to the brain, particularly a dementia syndrome resulting from recurrent cerebrovascular accidents. External cerebral arteries (carotid or vertebrobasilar arteries) hardening and microemboli or ischemia from dissipating ecchymosis lead to scattered multiple small infarcts in the central white matter of the brain, hence termed multi-infarct dementia. The onset of this disease mostly occurs in middle-aged and elderly individuals. According to data from Shanghai, it accounts for about 1% of hospitalized psychiatric patients, with males slightly outnumbering females. The course of the disease often progresses in a stepwise manner and is frequently accompanied by localized neurological signs.

bubble_chart Etiology

The root cause of this disease is organic changes in brain tissue caused by cerebral arteriosclerosis.

bubble_chart Pathological Changes

The degree of sclerosis in cerebral blood vessels can vary depending on the location. The middle cerebral artery and basal arteries are more prone to hardening, while the walls of small arteries and precapillary arterioles thicken, with more breaks in the elastic layer. The basal ganglia may also show hyaline degeneration and fibrosis of capillaries. The brain exhibits diffuse and localized atrophy, with enlarged ventricles. Microscopic examination reveals infarcted softening lesions of varying sizes in the frontal lobe and white matter center, surrounded by glial cell proliferation, forming small cysts, scars, and sparse areas of epilepsy. Neuronal degeneration and glial cell proliferation are most pronounced around blood vessels. Sclerosis of blood vessels can also be observed in organs such as the heart and kidneys, with retinal artery sclerosis being more common.

bubble_chart Clinical Manifestations

Most patients have a history of hypertension and hyperlipidemia, and some may also have experienced cerebrovascular accidents. Early-stage patients complain of headache, dizziness, insomnia or drowsiness, easy fatigue, and reduced concentration. Their pre-existing personality traits become more pronounced, making them prone to agitation or hypersensitivity. Gradually, they develop short-term memory impairment, while long-term memory remains relatively intact. Cognitive impairments may sometimes only affect specific, localized functions, such as difficulty with calculations or naming. However, general reasoning and judgment may remain intact for a considerable period. Patients are often aware of these deficits and actively seek medical help or attempt to compensate, earning the condition the nickname "lacunar dementia." Emotional instability and increased irritability are common, with patients prone to crying or laughing over trivial triggers, a phenomenon known as emotional incontinence. Occasionally, symptoms like depression, anxiety, suspicion, and delusions may appear.

In the advanced stage, self-control is lost, and patients become unable to care for themselves, sometimes making it difficult to distinguish from Alzheimer's disease. Acute onset often occurs after a cerebrovascular accident, presenting as confusion accompanied by behavioral disturbances, hallucinations, and delusions. After the episode, personality and cognitive impairments emerge. Depending on the location of vascular occlusion, various neurological signs may appear, such as hemiplegia, nystagmus, agnosia, blindness, ataxia, and positive pyramidal signs.

The disease progresses in a stepwise manner, characterized by alternating periods of sudden worsening and incomplete remission. It can last for years or even over a decade, with heart or kidney failure being the most common causes of death.

Electroencephalography often shows significant abnormalities, while cerebrospinal fluid tests may reveal grade I protein elevation. Rheoencephalography indicates reduced vascular elasticity, increased resistance, and decreased, sluggish blood flow. CT scans may show low-density areas and localized ventricular enlargement, while magnetic resonance imaging can reveal lacunar infarcts.

bubble_chart Diagnosis

The diagnosis of this disease is mainly based on a history of hypertension or cerebral arteriosclerosis accompanied by apoplexy or cerebral ischemia, manifestations of recent memory impairment and emotional instability, relatively intact personality; the course is characterized by stepwise progression and may also be accompanied by focal neurological positive signs.

To differentiate this disease from Alzheimer's disease, the ischemic score scale proposed by Hachinski can be used as a reference:

A total score of 7 or above can diagnose arteriosclerotic dementia, while a score of 4 or below can diagnose Alzheimer's disease.

bubble_chart Treatment Measures

Patients with hypertension and arteriosclerosis should receive symptomatic treatment in internal medicine. For acute ischemic episodes, injections such as Salvia and Sichuan Lovage Rhizome can be administered. Surgical treatment may be considered for eligible cases. To improve cognitive function, medications like piracetam, pyritinol, and ribonucleic acid can be taken. Hyperbaric oxygen therapy and ultraviolet blood irradiation and oxygenation may provide some efficacy for certain early-stage patients. When psychiatric symptoms are prominent, small doses of antipsychotic drugs such as thioridazine can be used in combination. Medication can be discontinued once symptoms are under control.