The first thing to clarify is that not all brain atrophy requires treatment and not all brain atrophy is pathologically significant. Nowadays, there is a phenomenon that artificially exaggerates the pathological consequences of brain atrophy, which creates fear in many people, and this is something that should be clarified. In the following we will talk about those brain atrophy that do not require treatment and do not need to generate fear.
Cerebral atrophy is the atrophy of the brain tissue itself due to organic changes caused by different reasons. Cerebral atrophy includes microcephaly and macrocephaly. It can occur at any age, with a high incidence above the age of 50, and can last for several years to decades, with more men than women. There are diffuse brain atrophy (including cortical atrophy, cerebellar atrophy, cortical, cerebellar and brainstem atrophy) and limited brain atrophy (mostly seen after limited organic brain lesions such as trauma, vascular disease, intracranial limited infection, etc.). Because of its complex etiology, slow onset, not easily detected, long course, slow progress, and may atrophy gradually aggravated, some affect the patient’s normal life and work before being discovered, most of them are found during physical examination.
Another large proportion of patients, found during physical examination or CT or MRI examination of the head, are mostly brain atrophy, mainly manifesting as bilateral frontal and parietal lobe mild atrophy, and these atrophy patients have no obvious clinical symptoms, but are easily told of brain atrophy, and patients have a heavy psychological burden.
Etiology
There are many causes of cerebral atrophy, the most common factor is caused by long-term chronic ischemia of cerebral blood vessels. Brain tissue is in a state of chronic ischemia and hypoxia, and the morphology and function of brain cells will be affected, i.e., brain atrophy is formed. The pathology can be seen as flattening of the brain gyrus, widening of the brain sulcus, enlargement of the ventricles and brain pools, and reduction of brain weight. Cortical atrophy is mostly seen, and can be divided into limited and diffuse brain atrophy depending on the location and extent of involvement. Trauma is also a common cause, mostly seen in severe occipital trauma, where patients develop atrophy after bilateral or unilateral frontal lobe injury.
Clinical manifestations
The clinical manifestations of cerebral atrophy can be divided into two categories: brain function decline and dementia and other intelligence loss, mainly related to the location and degree of cerebral atrophy.
Symptoms of cerebral atrophy, including diffuse cortical atrophy with dementia, diminished intelligence, memory loss, personality changes, and behavioral disorders. Cerebellar atrophy is dominated by language impairment and poor coordination of limbs and trunk form and tremor.
1.Systemic symptoms
In the early stage of the disease, patients often have dizziness and headache, weakness of the waist and knees, numbness of the hands and feet, tinnitus and deafness; gradually become unresponsive, slow movement, mumbling and answering questions. In the physical aspect, they often show old age, white hair and teeth, dry skin, hyperpigmentation, or even hemiplegia, epilepsy, or ataxia, tremor, etc. Neurological symptoms may be present or absent.
2.Memory impairment
In particular, the recent memory deficit occurs earlier and more obvious, patients have a significant lack of memory of today, yesterday and other things, such as often lost items, forgetting what has been promised, etc.. With the development of the disease, gradually to the distant memory is also impaired.
3.Change of personality and behavior
Personality change is often the early symptom of the disease. Patients become lonesome, do not like to interact with others, or show no ideal, desire, lack of affection for children and relatives; life habits are stereotypical and strange, impatient personality, increased speech.
4. Decreased intelligence, dementia
It is manifested as an overall decline in understanding, judgment, calculation ability and other intellectual activities, unable to adapt to social life, difficult to perform work and household chores; gradually unable to correctly answer their names, age, eat without knowing hunger, do not know the way back after going out, collect waste paper and miscellaneous objects as treasures. In the late stage of the disease, the patient is bedridden, cannot take care of himself, does not distinguish between relatives and relatives, is incontinent, has vague speech, slurred speech, and miscellaneous words, and eventually becomes completely demented.
Imaging
CT and MR imaging tests can reveal a decrease in brain tissue volume and enlarged ventricles. If the brain is atrophied, the gap 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 ventricles and the third ventricle are enlarged, and the density around the anterior and posterior corners of the lateral ventricles is reduced. Cerebellar atrophy may show coarse texture of the cerebellum, reduced volume of the image showing a branched dendritic shape, increased low density of the pericerebellar space, and enlarged fourth ventricle. If there is pontocerebellar olivary atrophy, the brainstem may become thin and narrow on the image, the surrounding cavities may widen, and the olivary may become flattened or narrow.
Treatment
As we mentioned above, some of the brain atrophy is non-pathological, which does not produce behavioral abnormalities such as memory loss and clumsy movements clinically.
For pathological cerebral atrophy, in other words, those who produce symptoms clinically, and to treat is important, in addition to functional training and other rehabilitation treatments. This type of approach is also different and more characteristic of each place, and will not be described here.