Playing with mobile phone is easy to cause brain atrophy?

Main factors:

Brain atrophy is caused by multiple factors. Heredity, brain trauma, stroke, encephalitis, meningitis, cerebrovascular malformations, brain tumors, long-term seizures, excessive smoking and alcohol, malnutrition, thyroid dysfunction, gas poisoning, Alcoholism, cerebral arteriosclerosis, cerebral ischemia, hypoxia, etc. can cause brain parenchyma destruction and atrophy, deformation, and disappearance of nerve cells. Clinically, hypertension, dyslipidemia, and cerebral arteriolar sclerosis are important risk factors for senile cerebral atrophy.

Image source: www.pixabay.com

The most important causative factor of cerebral atrophy is long-term chronic ischemia of cerebral blood vessels, resulting in a decrease in the deformation ability of red blood cells, insufficient effective blood perfusion of micro vessels, brain tissue in a state of chronic ischemia and hypoxia, and brain cell morphology and function are affected, that is, the formation of brain atrophy. Its pathological changes can be seen in flattened cerebral gyrus, widening of cerebral sulcus, enlargement of ventricle cisterns, and loss of brain weight. Mostly cerebral cortical atrophy. Due to the different location and scope of atrophy, it can be divided into localized and diffuse brain atrophy, cerebellum, olive body, pontine atrophy, cortical and central atrophy.

Clinical manifestations

The clinical manifestations of brain atrophy are divided into two categories: brain function decline and cognitive function decline, which are mainly related to the location and degree of brain atrophy. Diffuse cerebral cortical atrophy is mainly dementia, mental decline, memory impairment, personality changes, and behavioral disorders. Some are accompanied by hemiplegia and seizures. Focal brain atrophy is dominated by personality behavior changes; Cerebellar atrophy is predominantly due to speech disorders, limb ataxia, and intention tremor.

1. Systemic symptoms

In the early stage of the lesion, patients often have dizziness and headache, insomnia and dreams, soreness of waist and knees, numbness of hands and feet, tinnitus and deafness, and gradually slow response, slow movements, muttering, and answering non-questions. In the somatic aspect, it is often manifested as senile dragon bell, white teeth, dry skin, pigmentation, or hemiplegia, epilepsy, ataxia, tremor, etc., and neurological symptoms may or may be missing.

2. Memory impairment

Recent memory deficits occur earlier, such as often losing items and forgetting things that have been promised. As the disease progresses, memory is completely lost.

3. Changes in personality behavior

Personality changes are often an early symptom of the disease, and patients become depressed and do not like to interact with others; or manifested as lack of ideals, desires, and lack of feelings for children and relatives; or stereotypical and weird living habits, impatient personality, increased speech or verbosity, suspicious and selfish; or pay special attention to their own health and safety, often entangled by some minor discomfort; or manifested as amnesia or mania, with hallucinations, visual hallucinations, auditory hallucinations, aphasia, and agnosia. Patients have varying degrees of decline in all advanced emotional activities, such as shame, responsibility, honor and morality, and may also have changes in sleep rhythm.

4. Decreased intelligence, dementia

It is manifested as an overall decline in intellectual activities such as understanding, judgment, and calculation ability, unable to adapt to social life, and difficult to be competent for work and housework; Gradually unable to answer his name, age, and food, he did not know how to go home, and he collected waste paper and debris as a treasure. In the later stage of the disease, he was bedridden all day long, could not take care of himself, did not care for himself, was incontinent, slurred speech, slurred speech, and finally complete dementia.

Examine 

1. Clinical examination

In addition to taking the history and observing symptoms, patients with cerebral atrophy can find that their various nerve reflexes are dull or reduced to varying degrees. Superficial reflexes such as abdominal wall reflex, cremasteric reflex, reflex are dull, biceps and triceps reflex, radial periosteum reflex, knee tendon reflex, Achilles tendon reflex can also be reduced, and occasionally pathological reflexes may appear. In patients with cerebellar atrophy, through clinical examination, it can be found that the gait is faltering, the stride is wide, the inability to walk in a straight line, the drunken gait, and it is difficult to close the eyes: the eyes are unstable, especially after closing the eyes. Slow, abrupt speech, intention tremor, positive pathological signs, unstable finger-nose test, and inaccurate heel and tibial test.

2. Neuroimaging examination

Neuroimaging tests such as CT and MR (magnetic resonance) may reveal a decrease in the volume of brain tissue and enlargement of the ventricles. If the brain is atrophied, the space between the cerebral cortex and the skull plate is enlarged, the cerebral sulcus is widened and deepened, the gyrus is flattened and reduced, the lateral ventricle and the third ventricle are enlarged, and the density around the anterior and posterior corners of the lateral ventricle is reduced. When the cerebellar is atrophied, it can show that the cerebellar sulcus is widened and deepened, the volume is reduced, the image is branched and leafy, the space around the cerebellum is enlarged, and the fourth ventricle is enlarged. If there is pontine olive body atrophy, neuroimaging may show narrowing and narrowing of the brainstem, enlarged surrounding space, and flattened or narrowed olive body.

3. Cerebral angiography

Cerebral artery vessels may be seen with thinning and narrowing or occlusion. Transcranial Doppler ultrasound (TCD) can reveal slowed blood flow and increased vascular resistance.

Diagnosis 

Diagnosis of cerebral atrophy is not difficult based on history, symptoms, clinical examination, and neuroimaging.

Treat 

The principle of treatment is to remove the cause; Activates brain metabolic functions, indirectly inhibits the progression of diseases; Activates brain cells in an inhibited, sleeping state; Reduce the occurrence of various symptoms and complications with brain atrophy; Maintain residual brain function and improve quality of life.

1. Symptomatic treatment

Cerebral atrophy is mainly treated symptomatically, and related drugs are used symptomatically according to different symptoms of cerebral atrophy.

2. Rehabilitation

Rehabilitation is meaningful for patients with cerebral atrophy, especially after cognitive and motor dysfunction, and rehabilitation is of great value for functional recovery.

Post a Comment

0 Comments