Overview
Single cerebral infarct dementia is a large infarct of brain tissue and a single infarct of certain important functional brain areas, which can present clinically with dementia. Large infarct foci may cause a major loss of function in one side of the frontal or temporal lobe or even in the cerebral hemispheres, resulting in focal localizing signs and dementia. Dementia is related to the location of the lesion, and the thalamus, angular gyrus, frontal base and limbic system are closely related to dementia. Bilateral thalamus and thalamus base lesions may form thalamic dementia, which is rare clinically.
Etiology
It is mainly due to atherosclerosis, arterial stenosis and continuous shedding of atherosclerotic plaques, causing repeated multiple cerebral infarctions, which subsequently lead to multiple infarctive dementia (MID). Risk factors may include age, hypertension, diabetes mellitus, hyperlipidemia, history of stroke, site and size of stroke lesions, and stroke combined with aphasia. Stroke is the most common cause of dementia with single cerebral infarction.
Symptoms.
The patient has had a large cerebral infarction or a single cerebral infarctive cerebrovascular disease event in some important cerebral functional areas, and clinically presents with focal localizing signs of cerebral infarction, such as hemiparesis, pyramidal sign, hemiplegia, hyperesthesia, dyslexia, dysgraphia, dyscognition, and dyscalculia, and other symptoms and signs. Occlusion of the middle cerebral artery trunk causes large cerebral infarction, cerebral edema, and even the formation of cerebral hernia; occlusion of the basilar artery trunk leads to severe impaired consciousness and quadriplegia; angular gyrus infarction presents fluent aphasia, dyslexia (which may be accompanied by dysgraphia), memory impairment, and dyskinesia; occlusion of posterior cerebral artery thalamus-penetrating artery is more common, which leads to damage of the upper midbrain and parietal central part of the thalamus, and severe memory loss and dementia. Difficulty in vertical eye gaze is seen, etc.
Cognitive dysfunction is manifested by slow reaction, memory and computation loss, apathy, reticence, not recognizing the door of the house, wearing the wrong clothes and pants, and urinary and fecal incontinence. Thalamic dementia is characterized by psychiatric symptoms, such as amnesia, mood abnormalities and lethargy; dementia occurs after massive cerebral infarction or single infarction in some important cerebral function parts.
Examination
Routine examination of cerebrospinal fluid and determination of APOE polymorphism and quantification of Tau protein and β-amyloid fragment in cerebrospinal fluid and serum have diagnostic and differential significance.
1. Brain MRI examination
The responsible lesion can be found in thalamus, temporal lobe and limbic lobe 24 hours after the onset of the disease, showing low signal in T1WI and high signal in T2WI, and mild occupying effect can be seen within 1 week. The lesion artery is narrowed, and the flow effect is weakened or disappeared.
2. Electroencephalography
In the acute stage of large cerebral infarction, ischemia, necrosis and peripheral edema of brain tissues can be manifested as slowing down of the basic rhythm in the lesion area, decreasing of wave amplitude, and the appearance of diffuse irregular θ or δ waves; in the acute stage of cerebral infarction in the area of the posterior cerebral artery supplying cerebral artery, the α-rhythm suppression in the occipital area of the lateral side of the lesion and the polymorphic δ activity can be seen, accompanied by temporal area sharp waves. Changes in evoked potentials and event-related potentials (P300) help to identify subclinical lesions.
Diagnosis
The diagnosis of dementia is made using the National Diagnostic, Statistical Manual of Neurologic Disorders (DSM-N) criteria content as follows:
A. Evidence of short-term memory and long-term memory impairment exists:
Short-term memory impairment (inability to remember new things), e.g., first asked to memorize 3 items and cannot recall them after 5 min. Long-term memory impairment (inability to recall things known in the past), is the inability to recall things related to oneself in the past (e.g., what happened yesterday, place of birth, occupation) or general common knowledge (e.g., past presidents of the country, holidays known to anyone).
B. At least 1 of the following:
(1) Impairment in abstract thinking E.g., cannot name similarities or differences in related words, cannot name definitions or concepts of words.
(2) Impairment of judgment Inability to handle interpersonal, family, and occupational relationships correctly.
(3) Other higher cortical dysfunctions Aphasia (speech disorder), dysfunction (not only dysfunction of comprehension of true motor functions, but also inability to perform actions), dyscognition (not only perceptual disorder, but also inability to grossly recognize and differentiate between objects), and compositional disorders (e.g., molding and writing cubic shapes, stacking blocks, inability to make a picture with a matchstick).
(4) Personality changes Changes or sharpening of the lesion’s personality.
C. Disorders of A and B result in impairments in occupation, daily social life, and interpersonal relationships.
D. States of A, B, C, and D cannot be present during delirium.
E. either (1) or (2) of the following
(1) The presence of specific organic factors related to the cause of the disorder as evidenced by history, physical examination, and clinical examination.
(2) Although there is no evidence as in (1), it cannot be shown that the disorder is the result of a nonorganic mental disorder, and the presence of an organic factor that is the cause is presumed.
Treatment
Treatment includes both treatment of primary cerebrovascular disease and restoration of brain function. Treating hypertension and maintaining blood pressure at an appropriate level can stop and delay the onset of dementia.
1. Dihydroergotoxine
Eliminate vascular spasm and increase blood flow, improve neuron function, commonly used dihydroergot alkaloids as well as nicergoline.
2. Calcium antagonists
Increase cerebral blood flow, prevent calcium overload and free radical damage, dihydropyridines such as nimodipine; treatment of leukodystrophy patients with cognitive deficits, the condition of 1 year after the stabilization or improvement of dibenzylamines such as flunarizine.
3. Niacin
Can increase cerebral blood flow and improve memory.
4. Traditional Chinese medicine
Total saponin of Panax notoginseng (Thromboxane), Puerarin (Pleuromulin) and Chuanxiongxiongzine (Methylpyrazine) are chosen for their effects of activating blood circulation, removing blood stasis, improving blood viscosity and antiplatelet aggregation.
5. Antiplatelet aggregation
Aspirin is often used to inhibit platelet aggregation and prevent thrombosis; ticlopidine (against Keliad), acts on cell membrane and directly affects platelet adhesion and aggregation.
6. Brain metabolizer
Promote the utilization of amino acids, phospholipids and glucose by brain cells, enhance the patient’s reactivity and excitability, and enhance memory.
Prognosis
Closely related to the prognosis of cerebrovascular disease, at the same time, the prognosis of dementia is not consistent depending on the site and scope of the lesion, but the total cognitive function decline, an irreversible process.
Prevention
1. Early detection and avoidance of risk factors for stroke, such as hypertension, diabetes mellitus and hyperlipidemia, etc., and active treatment; high degree of carotid artery stenosis can be surgically treated, which can help reduce the occurrence of vascular dementia.
2. Quit smoking, control alcohol consumption and have a reasonable diet.
3. Those with clear genetic background should undergo genetic diagnosis and treatment.