Overview
Multiple infarct dementia is a dementia syndrome caused by multiple cerebral infarcts involving the cerebral cortex or subcortical regions, and is the most common type of vascular dementia. The main pathologic changes are cerebral atrophy and widening of the sulcus, and multiple infarcts of varying sizes and ages in different parts of the brain can be seen on cross-sectional examination, each of which is often centered around one or more small penetrating arteries with atherosclerotic changes. Due to the varying degree of newness of the lesions, some of them have formed small cystic cavities surrounded by glial cell proliferation.
Etiology
Cerebrovascular lesions are the direct cause of vascular dementia, mainly due to atherosclerosis, arterial stenosis, and continuous shedding of atherosclerotic plaques, which cause recurrent multiple cerebral infarctions followed by vascular dementia. Risk factors may include age, hypertension, diabetes mellitus, hyperlipidemia, and history of stroke.
Symptoms
1. Progressive dementia/memory loss, poor orientation to time, place, and people, lack of self-awareness and judgment, cognitive dysfunction with stepwise exacerbation and fluctuating course.
2. Focal neurologic signs such as tremor paralysis syndrome and pseudomyelitis.
3. Systemic atherosclerotic changes such as fundus arteriosclerosis, coronary arteriosclerosis and renal arteriosclerosis.
4. Psychiatric symptoms: some patients may exhibit psychiatric symptoms such as apathy, anxiety, dysphoria, hallucinations, delusions, depression, etc. at a certain stage of the disease.
Examination
1. Cerebrospinal fluid routine examination
Measurement of APOE polymorphisms, Tau protein quantification and β-amyloid fragments in cerebrospinal fluid and serum.
2. Psychological examination
Neuropsychological tests, such as daily life and social ability assessment, are commonly used: Simple Mental State Examination Scale, Wechsler’s Adult Intelligence Scale, Clinical Dementia Rating Scale and Blessed Behavioral Scale, etc. Hachinski Ischemia Score Scale can be used to identify with degenerative disease dementia.
3. Neuroimaging examination
(1) CT scan of the brain: it can show multiple low-density infarct foci of varying sizes in the cerebral cortex and white matter of the brain, halo-shaped low-density area next to the lateral ventricles, cerebral leukoencephalopathy and brain atrophy.
(2) MRI: multiple T1WI low signal and T2WI high signal can be seen in bilateral basal nuclei, brain cortex and white matter; old foci have clear boundaries and low signals without obvious occupying effect; fresh foci have unclear boundaries and inconspicuous signal intensity; early T1WI changes can be inconspicuous, and T2WI can show the foci; the brain tissues around the foci have limited cerebral atrophy or total cerebral atrophy.
4. Electrophysiologic examination
(1) Electroencephalogram (EEG) examination: EEG of normal old people mainly shows slowing down of α-rhythm, which slows down from 10-11Hz in young adults to 9.5Hz in old age, and there are slow waves of 3-8Hz in temporal region; diffuse θ or δ activities appear in bilateral frontal and central regions, which is especially significant in the state of drowsiness and suggests cerebral aging; α-rhythm further slows down to 8-9Hz in multiple cerebral infarcts, and α-rhythm further slows down to 8-9Hz in multiple cerebral infarcts; α-rhythm is also significantly reduced in multiple cerebral infarcts. further slowed down to below 8-9 Hz, and diffuse theta waves with focal paroxysmal high-amplitude δ rhythms appeared in bilateral frontal, temporal, and central regions.
(2) Evoked potentials: MEP and SEP both show prolonged latency and decreased wave amplitude, with a positivity rate of 80% to 90% or more in large cerebral infarcts and 30% to 50% in small focal infarcts; in about 40% of patients with occipital infarcts leading to cortical blindness, the VEP may show abnormal waveforms and prolonged latency time limits, and the VEP (visual evoked potential) waveforms improve significantly after visual recovery; in ischemic stroke The detection rate of BAEP abnormality is 20% to 70%, which is characterized by delayed inter-peak latency (IPL) from Ⅰ to Ⅴ. In patients with brainstem infarction, BAEP is abnormal bilaterally, with disappearance of waveforms from Ⅳ to Ⅴ and prolonged absolute latency (PL).
Diagnosis
This disease has a history of hypertension or cerebral arteriosclerosis with stroke; relatively acute onset, fluctuating course, mostly stepwise progression; early clinical manifestations are mainly memory impairment of recent events, emotional instability, and relatively intact personality; positive neurological signs due to cerebrovascular lesions can often be found; and there are special manifestations in brain imaging examination.
Differential diagnosis
This disease is mainly differentiated from Alzheimer’s disease: the latter has a slow onset and persistent progression, with personality changes and loss of self-awareness at an early stage; CT and MRI examinations mostly show brain atrophy, with fewer signs of neurological focal damage, and a Hachinski ischemia score of ≤4.
Treatment
1. Etiologic treatment
Control blood pressure and other risk factors such as hyperlipidemia, smoking, alcoholism, diabetes, obesity, atrial fibrillation and carotid artery stenosis.
2. Improve cognitive function
Cholinesterase inhibitor donepezil and non-competitive NMDA receptor blocker memantine may have an ameliorating effect on their cognitive deficits. Vitamin E, ginkgo biloba preparation, nicergoline, piracetam, etc., may have a certain auxiliary effect.
3. Control of psychiatric symptoms
Many patients in a certain stage of the disease will appear some psychiatric symptoms, such as: hallucinations, delusions, anxiety, depression, etc., may be appropriate to give antidepressants and antipsychotics, antidepressants can be used 5-HT reuptake inhibitors, such as: fluoxetine, paroxetine, sertraline and so on. Antipsychotic drugs can be used: risperidone, olanzapine and so on.
4.Rehabilitation treatment
As the intellectual impairment of vascular dementia is often patchy or non-comprehensive, with focal neurological signs, rehabilitation therapy can often receive better results. Rehabilitation should be targeted, including daily life ability training, muscle and joint mobility training and speech disorder rehabilitation. Patients should be allowed to have more contact with the outside world and participate in certain social activities. Improve the quality of life of patients through comprehensive treatment with Chinese and Western medicines, rehabilitation and nursing care.
5. Chinese medicine treatment
Multiple infarct dementia belongs to the category of “dullness”, “forgetfulness” and “dullness” in Chinese medicine. Chinese medicine believes that the main pathogenesis of vascular dementia includes kidney essence deficiency, phlegm and blood stasis, and treatment is mostly based on tonifying the kidney, resolving phlegm and eliminating stagnation. Most of the treatment is based on tonifying the kidney, transforming phlegm and activating blood, and the more common types of Chinese medicine include kidney essence deficiency, phlegm obstruction, blood stasis obstruction and so on, and the more commonly used formulas are: Dihuang Drink, Tongkou Xiexue Tang, Qifu Drink, and Tonic Yang Huiwu Tang, etc. Acupuncture and moxibustion treatment of vascular dementia is based on the principle of diagnosis and treatment and the main use of meridian meridian acupuncture points that have the main effects of relaxing tendons and pains, waking up the brain to open up the mind and activating qi and blood, and the more commonly used acupoints are: Baihui, Ashansanli, Fengchi, Sishincong, and Sishincong, etc, The more commonly used points are: Baihui, Fengchi, Si Shencong, Taixi, Sanyinjiao and so on.