Cerebral atrophy

Some degree of cerebral shrinkage occurs naturally with the dynamic process of aging. Structural changes continue during adulthood as brain shrinkage commences after the age of 35, at a rate of 0.2% per year. The rate of decline is accelerated when individuals reach 70 years old. By the age of 90, the human brain will have experienced a 15% loss of its initial peak weight. Besides brain atrophy, aging has also been associated with cerebral microbleeds.

Causes

Cerebral atrophy is not a disease, but rather a sign of one or more disease or biological processes. Many diseases that cause cerebral atrophy are associated with dementia, seizures, and a group of language disorders called the aphasias. Dementia is characterized by a progressive impairment of memory and intellectual function that is severe enough to interfere with social and work skills. Memory, orientation, abstraction, ability to learn, visual-spatial perception, and higher executive functions such as planning, organizing and sequencing may also be impaired. Seizures can take different forms, appearing as disorientation, strange repetitive movements, loss of consciousness, or convulsions. Aphasias are a group of disorders characterized by disturbances in speaking and understanding language. Receptive aphasia causes impaired comprehension. Expressive aphasia is reflected in odd choices of words, the use of partial phrases, disjointed clauses, and incomplete sentences. The pattern and rate of progression of cerebral atrophy depends on the disease involved.

Injury

• Stroke, loss of brain function due to a sudden interruption of blood supply in the brain
• Moderate-to-severe traumatic brain injury

Diseases and disorders

• Alzheimer's disease; high resolution MRI scans have shown the progression of cerebral atrophy in Alzheimer's disease
• Cerebral palsy, in which lesions (damaged areas) may impair motor coordination
• Senile dementia, fronto-temporal dementia, and vascular dementia
• Pick's disease, causes progressive destruction of nerve cells in the brain
• Huntington's disease, and other genetic disorders that cause build-up of toxic levels of proteins in neurons
• Leukodystrophies, such as Krabbe disease, which destroy the myelin sheath that protects axons
• Multiple sclerosis, which causes inflammation, myelin damage, and lesions in cerebral tissue
• Epilepsy, in which lesions cause abnormal electrochemical discharges that result in seizures
• GLUT1 deficiency syndrome
• Anorexia nervosa, bulimia nervosa, and other eating disorders
• Malnutrition, caused by lack or excess of nutrition from foods
• Type II diabetes, where the body does not use insulin properly resulting in high blood sugar
• Bipolar disorder, significant loss of brain tissue during manic episodes; however it's not verified whether the episodes cause brain tissue loss or vice versa
• Schizophrenia is associated with brain tissue volume loss.
• Mitochondrial encephalomyopathies, such as Kearns–Sayre syndrome, which interfere with the basic functions of neurons
• Posterior cortical atrophy: in the most posterior area of the brain lies the visual cortex, the area of the brain where visual information is received and processed. When cortical atrophy occurs in this brain area due to neurodegeneration, the first symptom is impairment in vision. A common vision impairment seen in patients with posterior cortical atrophy is simultanagnosia, where a person is unable to see multiple locations at once or to quickly shift attention between these locations. When looking at images of a brain with posterior cortical atrophy, one can see a loss in volume of the dorsal and ventral visual pathways, where visual stimuli is brought to the visual cortex and integrated information is sent back out to other areas of the brain. Because this disorder results in visual impairments, there is often a missed or delayed diagnosis, as the assumption is that there is a problem is in the eyes when the reality is that the problem is all the way in the back of the brain.
• Prion diseases, a group of invariably fatal encephalopathies that cause the progressive death of neurons.

Infections

An infectious agent or the inflammatory reaction to it can destroy neurons and their axons. These include:

• Encephalitis, acute inflammation in the brain
• Neurosyphilis, an infection in the brain or spinal cord
• AIDS, disease of the immune system

Drug-induced

• Alcohol (partially reversible): Standardized MRI evidence suggest chronic alcoholism (alcohol use disorder) is associated with widespread cortical atrophy and major brain changes. In contrast to healthy controls, macrostructural findings indicate alcoholic brains are smaller in mass and volume. Neuroimaging studies also show that cortical shrinkage in "uncomplicated alcoholism" is most severe in the frontal lobe in comparison to the other divisions of the cerebral cortex. In addition, neurological diseases that co-occur with excessive alcohol consumption—such as Wernicke–Korsakoff syndrome (WKS)—are characterized by substantial volume deficits of the diencephalon structures. In comparison to unaffected, non-alcoholic participants, tissue degeneration in WKS patients is found in specific white matter structures including the corpus callosum, the hippocampus, the subcortical basal ganglia (hypothalamus, thalamus, putamen), and the mammillary bodies.
• Antipsychotic use. However, untreated psychosis is associated with decreases in brain volume also.
• Corticosteroid use (There appears to be correlations between degree of dosing with corticosteroids and cerebral atrophy)