cognitive deficit

teratomatastic  asked:

What kind of physical therapy or recovery is needed for someone coming out of a coma of a few months' duration?

Heads up: this answer may not be what you want it to be. I’m sorry about that.

In my experience, most writers look to coma as sort of an ultimate plot device, a way to remove a character from the world of interaction. They try to turn characters on and off like lightswitches, which simply isn’t the case in the real world.

Let me tell you, friend, if your character has been in a coma for months they are permanently brain damaged. Healthy brains might take short breaks; anything from a few seconds to a minute or so (fainting) to a few hours (sleeping), but brains that cannot be conscious for months at a time are damaged brains. Your character may have speech impairments, severe cognitive deficits, the inability to remember basic skills like brushing their teeth and using the bathroom. They may have damage to areas of the brain that control speech, or language, or motor function. They may have severe personality changes due to damage in the frontal lobes.

This is a brain that has just barely survived some terrible tragedy. Your character won’t just wake up like a lightswitch one day. It will be slow, and take weeks.  They’ll have to relearn almost everything again, but this time with an older, less plastic brain that might have serious wiring problems.

As for the physical rehab, as you asked… That’s going to depend a lot on the patient. How much they can move, how their fine motor skills are. Depending on what caused their coma, walking may be possible, or it may not. Being still for so long causes issues. Expect them to likely have diaper rash, potential bedsores. They might or might not actually lose weight, because their feeding will be very careful—no munching on Big Macs in the neuro ICU!—but the muscles will atrophy significantly from lack of use. Physical therapy will be done to start getting strength back, very slowly. They’ll start off with very short distances on a walker (if they’re able), then further and further, typically with a nurse or a PT. Eventually they’ll be able to walk 20 feet, then 50, then 100, and more.All of this is also going to be modified based around what their brain is capable of, and whatever injuries their body took when they got into the coma in the first place.

I am not a physical therapist, so beyond that I’m not really sure. I’ve heard a lot of good things about working in warm baths with patients, because the water helps with buoyancy and increases resistance a little bit while people are walking, but I don’t know what the inclusion/exclusion criteria are, how much/how often it might be done, etc.  

I realize all this is probably not what you were hoping for as a writer. I don’t mean to make this all sound crazy bleak, but the outcome for patients with prolonged coma IS bleak. I hope you, and other writers, have the courage to convey it that way.

xoxo, Aunt Scripty


anonymous asked:

It would be improper to claim that George Washington was an evil man because he owned slaves simply because during his life, the majority opinion was that owning slaves was not evil. As a better example, let’s say that in 100 years, we discover that plants have advanced consciousness. It would be ignorant for people of that time to say that everyone alive today is evil for eating plants, because in todays standards, eating plants is not only acceptable, but encouraged.

Man I needed a laugh today, either your are suffering from some type of empathetic cognitive deficit disorder or you are serious about your scary premise. Never in the discussion of ponerology, do I hear anyone say, oh can’t call Mussolini, Hitler and Franco evil, because the majority of their people thought they were right. Only Black people have to suffer that indignity when talking about slavery. You should feel ashamed but the schools have so programmed you that its normal to be self-deceiving.

Behavioral deficits induced by myelin disruption

Myelin is required for proper nerve conduction and has an important role in normal axonal function. Indeed, myelin alterations are observed in various neurological diseases. Furthermore, although polymorphism in myelin genes is associated with conditions including depression, schizophrenia, and bipolar disorder, little is known about the neuronal and behavioral consequences of myelin disruption alone and the role of myelin genes in pathology. To address the contribution of myelin function to behavioral and cognitive deficits, Gould et. al used a mouse line lacking the myelin proteolipid protein (PLP), as these mice generate myelin but exhibit progressive myelin dysfunction and eventual axonal degeneration. 

The group tested 3 and 8 month-old PLP knockout PLP(-/Y) male mice in a battery of behavioral tests. 

Rotarod: No motor deficits were observed in 3 and 8 month old PLP(-/Y) mice on the Rotarod, a classical test of motor function. 

Zero maze: Altered emotionality was observed in 3 and 8 month PLP(-/Y) mice. 3 month PLP(-/Y) mice spent more time in open arms of the zero maze (apparently increasing in popularity as a test of anxiety?) while no change was observed at 8 months. 8 month PLP(-/Y) mice spent less time in the center of an open field, while exploration of the walls was increased. PLP(-/Y) mice demonstrated a decrease in the motivation to bury marbles in the marble burying task. 

Y maze: Performance on the Y maze, a test of spatial memory and hippocampal function, was normal in 3 and 8 month old PLP(-/Y) mice. 

Puzzle Box: In the Puzzle Box, a test of problem-solving and executive function, 3 and 8 month PLP(-/Y) mice displayed longer latency to reach the goal box when presented with a new challenge, indicating deficits in higher cognition. 

Taken together, these findings suggest that myelin dysfunction results in targeted behavioral deficits and cognitive dysfunction even long before significant axonal degeneration can be observed. Furthermore, these data raise the possibility that there could be a myelin-specific dimension to certain neurological disorders, which may warrant specific therapeutic interventions. 


E. A. GOULD, N. BUSQUET, D. RESTREPO, W. MACKLIN. Myelin disruption leads to targeted behavioral deficits. Program No. 224.29/G31. Neuroscience Meeting Planner. Chicago, IL: Society for Neuroscience, 2015. Online.

Old Drug Offers New Hope to Treat Alzheimer’s Disease

Scientists from the Gladstone Institutes have discovered that salsalate, a drug used to treat rheumatoid arthritis, effectively reversed tau-related dysfunction in an animal model of frontotemporal dementia (FTD). Salsalate prevented the accumulation of tau in the brain and protected against cognitive impairments resembling impairments seen in Alzheimer’s disease and FTD.

Salsalate inhibits tau acetylation, a chemical process that can change the function and properties of a protein. Published in Nature Medicine, the researchers revealed that acetylated tau is a particularly toxic form of the protein, driving neurodegeneration and cognitive deficits. Salsalate successfully reversed these effects in a mouse model of FTD, lowering tau levels in the brain, rescuing memory impairments, and protecting against atrophy of the hippocampus—a brain region essential for memory formation that is impacted by dementia.

“We identified for the first time a pharmacological approach that reverses all aspects of tau toxicity,” says co-senior author Li Gan, PhD, an associate investigator at the Gladstone Institutes. “Remarkably, the profound protective effects of salsalate were achieved even though it was administered after disease onset, indicating that it may be an effective treatment option.”

Although tau has been a target in dementia research for some time, there are no tau-targeted drugs available for patients. Additionally, how the protein builds up in the brain, causing toxicity and contributing to disease, still remains largely a mystery.

By investigating post-mortem brains with Alzheimer’s disease, Dr. Gan’s team found that tau acetylation is one of the first signs of pathology, even before tau tangles are detectable. The acetylated form of tau not only marked disease progression, it also served as a driver for tau accumulation and toxicity. What’s more, in an animal model of FTD, when tau was acetylated, neurons had reduced ability to degrade the protein, causing it to build up in the brain. This in turn led to atrophy in the region and cognitive impairment in the mice on several different memory tests.

The Gladstone scientists discovered that salsalate can inhibit the enzyme p300 in the brain, which is elevated in Alzheimer’s disease and triggers acetylation. Blocking tau acetylation in this way enhanced tau turnover and effectively reduced tau levels in the brain. This reversed the tau-induced memory deficits and prevented loss of brain cells.

“Targeting tau acetylation could be a new therapeutic strategy against human tauopathies, like Alzheimer’s disease and FTD,” says co-senior author Eric Verdin, MD, a senior investigator at the Gladstone Institutes. “Given that salsalate is a prescription drug with a long-history of a reasonable safety profile, we believe it can have immediate clinical implications.”

The scientists say a clinical trial using salsalate to reduce tau levels in progressive supranuclear palsy, another tau-mediated neurological condition, has already been initiated.