GLIOSIS DEFINICION PDF

Definición de Gliosis. 01/11/ historia2. {f.} [Medicina] Proliferación patológica de la neuroglia. GLIOSIS. Fuente: Britannica. Infecciones, como encefalitis o meningitis, o antecedentes de esas infecciones ; Un proceso de cicatrización (gliosis) en una parte del lóbulo. los coágulos se produce una reacción inflamatoria y gliosis reactiva mediada por la trombina, la cual .. Grado Definición. 1. SA ≤ 5 mm. H. 2. HSA > 5 mm. 3A.

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MRI studies of older persons with disequilibrium and gait disturbances of unknown cause often show frontal atrophy and subcortical white matter T2 hyperintense foci. Kerber et al, Pathological studies, though scanty, suggest frontal atrophy shrinkageventriculomegaly i.

There are several locations for white matter lesions. Those around the center black spaces are called “periventricular white matter lesions”.

Those located between the cortex and ventricles, with some space between, are just called “white matter lesions”. There are also subtypes in the “deep white matter”, below the ventricles, some in the cerebellum, and sometimes they are seen in the brainstem.

This page is focused on the higher lesions around the ventricles. CT scans are not nearly as sensitive. The better stronger the MRI magnet, the more lesions are seen. Thus, MRI’s done on contemporary 3T units will see more and smaller white matter lesions than scans done on “open” scanners.

Cerebral white matter lesions are common, alarming, and often called “incidental” by physicians. Perhaps for this reason, the author of this page Dr. Hain has been emailed several times with vigorously phrased requests to weaken the language concerning the cognitive consequences of white matter lesions. I just report what the literature has to say, and unfortunately, “it is what it is”. Still, in response, I have adjusted the language in some places to use more “academic” terms for reduced mental function.

There is an immense body of literature about white matter lesions, and here we are just discussing a small subset of these thousands of papers. Because there are so many papers, one can generally find a paper supporting nearly any conjecture — this is good to keep in mind when reading reviews like this one.

Usually these lesions are blamed on “small vessel disease”, with the idea that a small blood vessel closes off. The term is vague, and might be applied both to blood vessels closing off as well as bleeding. Other causes of brain damage that can be spotted on MRI include bleeds, which also cause brain damage. As they contain iron from blood, they can be distinguished on MRI from other types of damage by viewing them with a “sequence” sensitive to iron, such as gradient echo GRE Greenberg et al, Cerebral microbleeds can also occur in the white matter, and can be due to trauma, hypertension, or cerebral amyloid.

Due to “blooming”, the size of the black spots on MRI can be larger than the actual area of iron deposition. GRE images with longer echo times e. Cerebral microbleeds are associated with accelerated cognitive decline.

Ding et al, The frequency of white matter lesions depends on your threshold for reporting them and population being studied.

Lin et al recently reported on hospitalized Chinese patients. They included as positive patients ranging from mild small lesions to severe large confluent lesions. Prevalence was higher in persons with hypertension, diabetes and smokers. Chowdhury et alreported on a healthier group — subjects without vascular risk factors i.

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These were subjects largely between 50 and Somewhat similar to Lin et al, they found a rather high prevalence — They found a much lower prevalence for gradewhich were defined as lesions having some confluence i.

These were subjects with no vascular risk factors, and cannot be directly compared to the subjects of Lin et al, who did have vascular risk factors. Wen et al reported on individuals aged recruited from a healthy community study. They commented that ” small punctate or focal WMHs are common in the brains of individuals in their 40s, and may represent an early stage of development of these lesions. Combining these three studies together, it is clear that small punctate white matter lesions are extremely common, they are found in roughly half of the otherwise healthy population in their 40’s, and WML increase with age.

In addition, as people age, they not only get more white matter lesions, but the WML start to merge together into bigger patches confluent white matter lesions. People who have vascular risk factors such as diabetes, smoking, hypertensionhave more of these lesions. Major causes of periventricular white matter PWM lesions include normal changes from aging then they are called UBO’s, for “unidentified bright objectssmall strokes, and disorders related to multiple sclerosis MS.

PWM are also correlated with vitamin B6 pyridoxine deficiency. The phrase “normal changes from aging” is really a synonym for “we don’t know”.

Age is certainly the single most common association of PWM. This is presumably a “wear and tear” phenomenon. You get older, and there is more water under the bridge. More fluctuations in blood pressure, more chance for small blood vessels to close, more chance of head injury, more chance for little emboli.

Nevertheless, while clinicians often suggest that changes in the brain that are similar to others of the same age are not important, and call them “incidental”, data suggests that even a few of these PWM reduce cognitive performance see below. A period of hypertension is a common cause.

Brain Gliosis & Homoeopathy

In the authors experience, just a few days of extreme hypertension may be enough. This is the “stress is not good for you” connection.

Progression of these lesions is associated with variability as well Liu et al, This might suggest that small bleeds are the cause in some. There is a related disorder called ” superficial siderosis ” due to cerebral bleeds as well as cerebral microbleeds briefly discussed above.

Clinical studies of PWM also show association with diabetes, but not consistently with atherosclerosis. PWM are often reported in persons with migraineand occur especially in women with migraine and aura.

PWM are also more common in persons with frequent syncope and orthostatic intolerance Kruit et al, WM lesions are associated with retinal microvascular abnormalities. MS and related conditions: Demyelinating disorders such as multiple sclerosis and relatives can cause PWM.

These generally have a different look on MRI, definicoin they often resemble “fingers” pointing towards the ventricles. Rarer causes of white matter disease include “Autoimmune processes include multiple sclerosis and related diseases: Infectious processes include Lyme disease neuroborreliosisprogressive multifocal leukoencephalopathy, and human immunodeficiency virus HIV encephalopathy.

Vascular processes include different types of small-vessel disease: Toxic-metabolic processes include osmotic myelinolysis, methotrexate leukoencephalopathy, and posterior reversible encephalopathy syndrome. Definicioj et al, This is basically a laundry list of mostly rare conditions that has little practical consequences, but lets one know that there are many possibilities.

As is the case with most genetic testing, this test is prohibitively expensive and the result generally has no clinical implications.

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PRES reversible posterior leukoencephalopathy syndromecan cause similar white matter lesions, but this condition is acute, and has some possibility of reversal. There is strong evidence that cerebral white matter lesions impair brain function, and in particular impair thinking ability and walking. White matter lesions correlate strongly with reduced gait speed as well as reduced mental ability Starr et al, ; Guttman et al, ; Glilsis et al, ; Bazner gliosiis al, Periventricular location of white matter lesions seem to cause the most serious consequences.

Here we are mainly talking about the larger white matter lesions – -the ones that are “confluent”, or grades on the graph above. Persons with one or two “punctate” white matter lesions are not thought to have these problems. There are also patient groups that don’t really fall that well into the grades — perhaps they have 40 or so punctate lesions.

They probably belong with the grade 2 partially confluent group.

Individuals with PVM lesions perform nearly 1 standard deviation below average on tasks involving psychomotor speed. Persons with severe periventricular WVL perform about 1 standard deviation lower than average subjects on tasks involving psychomotor speed, and about 0.

To put this into more familiar terms, on the IQ test, 1 SD is 15 points. Even “silent” white matter lesions in middle-aged hypertensive patients predict reduced attention Sierra et al, Severe white matter lesions predict poor activities of daily definicoon Yamashita et al, Deep white matter lesions are reportedly even more burdensome than periventricular white matter lesions to cognition Soriano-Raya et al, Fortunately these are drfinicion uncommon.

According to Degroot et al”After adjusting for age, gender, educational level, measures of depression, and brain atrophy and infarcts, subjects with severe periventricular white matter lesions experienced cognitive decline nearly three times as fast” as the average. Acceleration definiciion white matter hyperintensity burden, is a pathologic change that occurs early in the presymptomatic phase leading to mild cognitive impairment.

In fact, on average, acceleration occurs 10 years prior to onset of mild definicuon impairment.

Silbert et al, If we consider gait and balance, more white matter lesions predicts decreased mobility Onen et al, It would seem to us that people may simply be more cautious and walk more slowly when they are more prone to fall. Pathologically, PWM correspond to areas of myelin thinning and gliosis, and are often accompanied by lacunar small holes infarctions and small vessel atherosclerotic disease.

Lacunes are also associated with cognitive disturbances Jokinen et al, Practically, PVM seem to be associated with severe consequences. As once you have them, they are there for life, prevention is the main goal of treatment. We advocate attention to reducing vascular risk factors, and especially controlling labile i. Thus if definiciln blood pressure is “only up at the doctor’s gloosis, this does not mean that you are safe from PVM.

A beta blocker might help. Reducing elevated cholesterol, and strict control of diabetes is probably helpful too. As diabetes is often correlated with being overweight, reducing calorie intake until the BMI becomes normal is prudent.