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Graphic disorientation

Introduction
Cause
Examine
Diagnosis

Introduction

Introduction Graphical disorientation is a symptom of Alzheimer's disease. Graphical dysfunction is insidious onset, and the course of disease is irreversible. There is often no exact onset time and onset symptoms. Early stages are often difficult to detect. Once they occur, they are irreversibly slow. The onset is concealed, the course of the disease is irreversible, and there is often no exact onset time and onset symptoms. It is often difficult to be detected early, and once it occurs, it is irreversibly slow. The onset may be related to genetic, viral infection, immune dysfunction and the like.

Cause

Cause

The cause of graphic disorientation is suffering from Alzheimer's disease.

The cause of Alzheimer's disease:

(1) Genetic factors

AD has a family aggregation, and about 20% of patients have a positive family history, and their first-degree relatives have a great risk. Molecular biology studies have shown that there are abnormal gene loci on chromosomes 21, 19, 14 and 1. The genes encoded by these genes are: amyloid beta (AP-AP) and apolipoprotein E (ApoE). , Casein-1 (PS-1) and Presenilin-2 (PS-2). Mutations and polypeptide changes in these genes are associated with the pathogenesis of AD. -AP is produced by abnormal cleavage of -amyloid precursor protein (-APP) and is the main component of senile plaque formation. Apo E gene is one of the most important genetic factors affecting the aging pathway. The risk of late-onset familial AD and sporadic AD is dependent on the amount of Apo E4 allele.

(2) Neurotransmitter theory

The transmitter-related changes associated with AD are the acetylcholine system, the monoamine system, amino acids, and neuropeptide transmitters, with the reduction of choline acetyltransferase and acetylcholine transmitters being important causes of AD. Neuropharmacological studies have confirmed that AD patients have reduced acetylcholine transferase activity in the cerebral cortex and hippocampus, which directly affects the synthesis of acetylcholine and the function of the cholinergic system. In addition, no patients with AD had significantly reduced somatostatin, adrenocorticotropic factor and norepinephrine, and dopamine hydroxylase activity was significantly reduced.

(3) Viral infection

Experiments have shown that a virus that deforms sheep brain tissue can be inoculated into the brain of mice to produce typical age spots. In vitro experiments have shown that herpes virus infection can reduce the level of acetylcholine transferase in chromaffin cells PC12 cells. It suggests that viral infection may be one of the causes of this disease.

(4) Metal action

In some patients with AD, the concentration of aluminum in the brain can reach 10-30 times that of normal brain. There is aluminum deposition in the core of senile plaque (SP), and there is an increase in brain aluminum when sneak attacks cause dementia. Therefore, it is speculated that aluminum is related to dementia. But the reason why aluminum is dementia or the result is not very clear.

(5) immune dysfunction, free radical damage

Immune dysfunction, free radical damage, etc. are related to the pathogenesis of AD. The brain-reactive antibody of AD was 20% higher than that of the control group, indicating that the patient's autoantibody content increased, which may play a role in neuronal loss and aging.

Examine

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Related inspection

Brain Doppler Ultrasound (TCD) EEG

Diagnosis of graphic disorientation:

(1) The onset is concealed, and the course of the disease is irreversible. There is often no exact onset time and onset symptoms. Early stages are often difficult to detect. Once they occur, they are irreversibly slow.

(B) the core symptoms of Alzheimer's disease

1. Memory impairment: It is the first symptom of senile dementia. Both forgetting and forgetfulness. Forgetting refers to the deficiencies of remembering new knowledge, related to cortical dysfunction; forgetfulness refers to the defect of far memory, that is, the ability to recall information that has been remembered in the past is low, and is related to subcortical dysfunction. Initially there was impaired memory, and the memory was also compromised. Ultimately, memory was impaired.

2, cognitive impairment: refers to the ability to master and use knowledge. Includes linguistic and non-verbal skills, the ability to remember new knowledge, and the ability to recall knowledge from a rich knowledge base. Cognitive dysfunction is decisive for the diagnosis of dementia. Non-verbal cognitive dysfunction occurs faster and earlier than speech impairment. In the early stage of AD, miscalculation, judgment of disparity, loss of generalization ability, distraction, loss of recognition, and obvious development with the disease can occur.

3. Aphasia: Language change is a sensitive indicator of cortical dysfunction. Aphasia is a common characteristic symptom of AD and is not common in other causes of dementia. Spoken language comprehension is impaired, and the retelling function is relatively preserved until it is damaged in the late stage. The syntax and pronunciation of the language are relatively retained to the late stage and the semantic aspect is progressively damaged. It can be expressed as difficulty in finding words, verbose spontaneous language, naming not, glare aphasia, and gradually becoming erroneous. In the middle and late stages of the disease, there are various obvious repetitive speech disorders, such as: imitating the language, repeating the words and phrases spoken by the examiner for the patient. Heavier speech, repeating the words and words that he or she said for the patient; the end of the word repeats, repeating the last part of the word for the patient. To the late stage, there are dysarthria (incomprehensible sounds) and even silence (dumbless speech).

4. Visual space skills, loss of recognition and misuse: In the early stage of AD, visual space skills were impaired, which was more serious than other types of dementia. If you can't copy graphics, you can't do structural work, connect tests, and build blocks, puzzles, and so on. Nearly one-third of AD patients have visual dissonance, facial disappearance, body image disorder, visual spatial agnosia, geographic misorientation, etc., and are aggravated as the disease progresses. AD patients can have a variety of disuse: structural disuse, dressing disuse, intentional sports disability, intentional disability, walking disability, misuse of loss of writing and so on.

(3) Accompanying symptoms of Alzheimer's disease

Psychotic symptoms: that is, the accompanying symptoms of AD. Expressed as reduced initiative, apathy or loss of control, depression, restlessness, excitement or euphoria, insomnia, hallucinations (listening, visual), delusions (victimization, theft, delusion, etc.), jealousy, meaningless hyperactivity, self-speaking Self-speaking or talking loudly, restless, unclean behavior, attack tendency, etc. These symptoms are often the purpose of seeking treatment in patients with AD and should not be overlooked when diagnosing dementia.

(D) Symptoms: The core symptoms gradually increase with the course of the disease, and the accompanying mental symptoms do not significantly increase with time.

(5) The characteristics are not obvious: AD generally has no signs of nervous system. In the early stage, about 7% of patients have myoclonic seizures, and in the advanced stage, there may be episodes of positive pyramidal tract disease or epilepsy (systemic tonic sputum).

(VI) Clinical evolution process: The sequential loss of advanced cognitive function in AD patients and the time sequence of behavioral and nervous system dysfunction are important line speeds for clinical diagnosis of AD. Cummings et al. divided the clinical course of AD into three phases. The first stage: the disease period is 1-3 years. Memory - learning new knowledge has obstacles, long-term memory damage; visual space skills - graphic orientation obstacles, structural obstacles; language - list a class of nouns poor ability, naming can not; personality - emotional apathy, accidental irritability Or sadness; exercise system - normal; EEG - normal; CT - normal. The second stage: the disease period is 2-10 years. Memory - near and far memory is obviously damaged; depending on spatial skills - poor composition, spatial orientation disorder; language - fluent aphasia; computational power - miscalculation; personality - indifference, apathy; exercise system - restlessness; EEG Background EEG is a slow rhythm; CT - normal or ventricular enlargement and sulcal widening. The third stage: the disease period is 8-10 years. Intelligence - severe decline; exercise - limb rigidity, flexion posture; sphincter control - urine, incontinence; EEG - diffuse slow wave; CT - ventricle enlargement and sulcal widening.

Diagnosis

Differential diagnosis

Graphical dysfunction differential diagnosis:

1. Mild cognitive impairment: only memory impairment, no other cognitive impairment; some patients may be early manifestations of AD.

2. Depression: Early AD can be similar to depression, such as depression, lack of interest in various things, memory impairment, insomnia, fatigue or weakness.