cerebral atrophy treatment in bangalore dating
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This phenomenon can occur to the entire brain or be focused on a singular part. The most troubling issue with cerebral atrophy is the potential for it to affect brain function, as the location of lost brain cells will potentially lead to neurological side effects.
What are the types of cerebral atrophy? Focal atrophy Refers to cerebral atrophy that is restricted to a localized area of the brain, often causing damage to the affected area.
Atrophy of a particular region of the brain can lead to motor, sensory, or cognitive dysfunction, depending on the region of the brain affected. Generalized atrophy Also known as complete or total cerebral atrophy, this type of cerebral atrophy is characterized by shrinkage of total brain size.
This means that the loss of brain cells is not restricted to a single region but to the entire brain as a whole. It is believed that voluntary functions and conscious thought are more likely to be affected with generalized atrophy of the brain. What are the causes and risk factors for cerebral atrophy?
Cerebral (brain) atrophy: Why your brain is shrinking and what to do about it
Normal aging It has been documented that normal aging causes the brain to shrink by an average of 1. After the age of 60, it has been reported that individuals lose about half a percent to one percent of brain volume every year.
This is believed to be the result of the number of brain cells naturally declining with age. Some areas of the brain are affected by this generalized form of brain atrophy more than others, like the hippocampus, which is involved in memory. Brain injury caused by stroke or trauma often leads to the obstruction of blood flow to the brain, starving it of vital oxygen and nutrients. This leads to brain cell death and subsequent brain atrophy.
If not treated in a timely fashion, the possibility of cognitive deficits or even death is very likely. What causes blood clots in the brain? Vitamin deficiency Not having sufficient amounts of vitamin B12 in the diet can lead to significant brain atrophy over time. A study done by the University of Oxford found that healthy volunteers with normal levels of B12 had more volume loss compared to other healthy volunteers with higher levels of the vitamins in their system.
Vitamin B12 deficiency is one of the few preventable and reversible causes of cerebral atrophy.Treatment for Cerebellar Atrophy
Excessive alcohol use Drinking more than 14 drinks per week has been linked to significant brain shrinkage, according to a study conducted by the John Hopkins Bloomberg Public School of Health.
Additionally, the more you drink, the greater brain volume loss per year.
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Women were seen to be affected by this result the most, despite drinking less per week than men. Interestingly, one study found that light to moderate amounts of alcohol may actually reduce the risk of dementia, of which cerebral atrophy is a significant contributor. In particular, wine was seen to be potentially beneficial for brain aging. However, 16 studies, in which a total of over patients were tested with various measures, did not report any association between DUP and neurocognition.
Dopaminergic catecholaminergic hyperactivity and prolonged HPA activation have been hypothesized as potential mechanisms to explain these associations.
The question that remains is whether the observed structural changes are permanent or may be reversed via antipsychotic treatment. In our paper, we will discuss the mechanisms proposed by investigators who have empirically tested the neurotoxicity hypothesis in an effort to explain an association between untreated psychosis and brain structure. To perform our review, we used a database of relevant papers that was produced for a systematic review looking at the association between untreated psychosis and brain morphology Kelly K Anderson, August 22,personal communication.
It focused on studies that included patients with treatment-naive or minimally treated psychotic disorders in an effort to reduce the confounding effects of antipsychotics and illness chronicity. We looked at studies that measured the DUP, which is the period between the onset of the active symptoms of psychosis delusions, hallucinations, or thought disorder and the initiation of adequate antipsychotic treatment.
We then extracted the hypothesized mechanisms proposed in the papers to explain the observed associations. We aimed to get a sample of the thoughts of investigators working in this line of research as to how untreated psychosis may cause damage to brain structures. Potential Underlying Mechanisms Among the 9 studies that demonstrated a positive association between DUP—DUI and outcome, 21 — 29 only 2 of the authors proposed specific biological mechanisms that could potentially underlie structural alterations occurring as a result of the neurotoxic effects of untreated psychosis.
In both cases, antipsychotics are proposed to reduce the catecholaminergic activity and HPA activation, respectively, thereby reducing the extent of neuronal damage owing to untreated psychosis.
Alternatively, both Lappin et al 25 and Malla et al 27 raise the possibility that the observed structural abnormalities may be a marker for poor premorbid functioning or an insidious onset of psychotic disorder, consequently leading to a longer delay in detection and initiation of antipsychotic treatment.
Indeed, there is evidence to suggest that people who have poor levels of premorbid functioning, especially during childhood, are more likely to show computerized tomography scan abnormalities.
Limited Evidence to Support the Neurotoxicity Hypothesis We present the hypotheses from 9 studies that have shown a link between untreated psychosis and brain morphology. Additionally, most studies that investigate the validity of the neurotoxicity hypothesis using measures of neurocognitive functioning do not find an association with DUP.
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Limitations of the Literature to Date The challenge with the discussion on potential mechanisms of neurotoxicity may, in part, reflect general issues with the literature, to date, on the association between untreated psychosis and brain structure.
Many studies have empirically examined this association, but there have been many methodological problems with this body of literature. Any rigorous investigation of the neurotoxicity hypothesis faces many complex methodological questions: Which brain structures should be considered? What types of neuroimaging techniques should be used? Does this imaging technique accurately measure the functional changes that are seen in psychosis? Are there structural changes occurring at a microscopic level that current imaging approaches may not be able to detect in vivo?
Should samples include people with psychosis generally, or people with schizophrenia specifically, given how difficult it is to make diagnoses at the first episode? How can we account for the myriad confounding factors?
In addition to these challenges, the fundamental issue that has plagued all studies in the field of early psychosis is the measurement of the DUP. Limitations in our understanding of the natural history of the illness and to our ability to accurately identify people with FEP may make it difficult not only to accurately measure DUP but also to describe its mechanisms. As previously described, the DUP is the period between the onset of the active symptoms of psychosis delusions, hallucinations, or thought disorder and the initiation of adequate antipsychotic treatment.
This is because of the variability in the onset of schizophrenia, and because a decision has to be made as to when treatment has started. Regarding the onset of active psychosis, some people with schizophrenia have a difficult-to-define onset that begins many years previously without clear psychotic symptoms, whereas others have good preservation of personality and functioning followed by an acute onset.
Morphological changes in the brain may be associated with the type of onset, such that people with an insidious onset may be more likely to show structural abnormalities.
Measuring the start date for patients with acute-onset psychosis is much easier than for those with an insidious onset.