cognitive deficit

anonymous asked:

Hey Aunty! First of all, I wanted to say thanks for how helpful this blog is :3 Second, I have a question that has been bothering me for some time: because of reasons, MC is knocked out and she remains 4 hours inconscious. What I wanted to know is: is that realistic? Would that fall into the coma label? Thanks in advance!

Hey there anon!

Yes, your main character could be unconscious for 4 hours from a head injury. Yes, it would be considered a coma.

But if you choose to have your character unconscious for that long – for longer than a minute or two, generally – there need to be significant neurological consequences in order to maintain realism. is a great site for traumatic brain injuries, but here’s a quick and nasty run-down on what your character may have to deal with once they wake up:

  • Headaches
  • Nausea
  • Cognitive deficits
  • Memory loss (being wholly or partly unable to store short-term memory after the event is very common)
  • Possibly behavioral changes / personality changes 
  • Difficulty walking / ataxia

For more info, check the TBI tag and the head injury tag!

Best of luck.

xoxo, Aunt Scripty


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fawn-tails  asked:

Hello! I was wondering if low empathy and/or low sympathy are related to schizo spectrum disorders.

yes. Schizophrenia and other spectrum disorders often include cognitive deficits in areas that help people understand one another, recognize emotions in themselves and other people, feel empathy, and respond in socially appropriate ways to emotional cues. 

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


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.

DNA Repair Protein BRCA1 Implicated in Cognitive Function and Dementia

Researchers from the Gladstone Institutes have shown for the first time that the protein BRCA1 is required for normal learning and memory and is depleted by Alzheimer’s disease.

BRCA1 is a key protein involved in DNA repair, and mutations that impair its function increase the risk for breast and ovarian cancer. The new study, published in Nature Communications, demonstrates that Alzheimer’s disease is associated with a depletion of BRCA1 in neurons and that BRCA1 depletion can cause cognitive deficits.

“BRCA1 has so far been studied primarily in dividing (multiplying) cells and in cancer, which is characterized by abnormal increases in cell numbers,” says first author Elsa Suberbielle, PhD, a research scientist at the Gladstone Institutes. “We were therefore surprised to find that it also plays important roles in neurons, which don’t divide, and in a neurodegenerative disorder that is characterized by a loss of these brain cells.”

(Image caption: Reduced levels of BRCA1 (red) in neurons (blue). Amyloid-beta plaques in the brain can deplete neurons of BRCA1, contributing to cognitive deficits in Alzheimer’s disease. Credit: Elsa Suberbielle)

In dividing cells, BRCA1 helps repair a type of DNA damage known as double-strand breaks that can occur when cells are injured. In neurons, though, such breaks can occur even under normal circumstances, for example, after increased brain activity, as shown by the team of Gladstone scientists in an earlier study. The researchers speculated that in brain cells, cycles of DNA damage and repair facilitate learning and memory, whereas an imbalance between damage and repair disrupts these functions.

To test this idea, the scientists experimentally reduced BRCA1 levels in the neurons of mice. Reduction of the DNA repair factor led to an accumulation of DNA damage and to neuronal shrinkage. It also caused learning and memory deficits. Because Alzheimer’s disease is associated with similar neuronal and cognitive problems, the scientists wondered whether the problems might be mediated by depletion of BRCA1. They therefore analyzed neuronal BRCA1 levels in post-mortem brains of Alzheimer’s patients.

Compared with non-demented controls, neuronal BRCA1 levels in the patients were reduced by 65-75%. To determine the causes of this depletion, the investigators treated neurons grown in cell culture with amyloid-beta proteins, which accumulate in Alzheimer brains. These proteins depleted BRCA1 in the cultured neurons, suggesting that they may be an important cause of the faulty DNA repair seen in Alzheimer brains. Further supporting this conclusion, the researchers demonstrated that accumulation of amyloid-beta in the brains of mice also reduced neuronal BRCA1 levels. They are now testing whether increasing BRCA1 levels in these mouse models can prevent or reverse neurodegeneration and memory problems.

“Therapeutic manipulation of repair factors such as BRCA1 may ultimately be used to prevent neuronal damage and cognitive decline in patients with Alzheimer’s disease or in people at risk for the disease,” says senior author Lennart Mucke, MD, director of the Gladstone Institute of Neurological Disease. “By normalizing the levels or function of BRCA1, it may be possible to protect neurons from excessive DNA damage and prevent the many detrimental processes it can set in motion.”

Brain Boost: Research to Improve Memory through Electricity

In a breakthrough study that could improve how people learn and retain information, researchers at the Catholic University Medical School in Rome significantly boosted the memory and mental performance of laboratory mice through electrical stimulation.

The study, sponsored by the Office of Naval Research (ONR) Global, involved the use of Transcranial Direct Current Stimulation, or tDCS, on the mice. A noninvasive technique for brain stimulation, tDCS is applied using two small electrodes placed on the scalp, delivering short bursts of extremely low-intensity electrical currents.

“In addition to potentially enhancing task performance for Sailors and Marines,” said ONR Global Commanding Officer Capt. Clark Troyer, “understanding how this technique works biochemically may lead to advances in the treatment of conditions like post-traumatic stress disorder, depression and anxiety—which affect learning and memory in otherwise healthy individuals.”

The implications of this research also have great potential to strengthen learning and memory in both healthy people and those with cognitive deficits such as Alzheimer’s.

“We already have promising results in animal models of Alzheimer’s disease,” said Dr. Claudio Grassi, who leads the research team. “In the near future, we will continue this research and extend analyses of tDCS to other brain areas and functions.”

After exposing the mice to single 20-minute tDCS sessions, the researchers saw signs of improved memory and brain plasticity (the ability to form new connections between neurons when learning new information), which lasted at least a week. This intellectual boost was demonstrated by the enhanced performance of the mice during tests requiring them to navigate a water maze and distinguish between known and unknown objects.

Using data gathered from the sessions, Grassi’s team discovered increased synaptic plasticity in the hippocampus, a region of the brain critical to memory processing and storage.

Although tDCS has been used for years to treat patients suffering from conditions such as stroke, depression and bipolar disorder, there are few studies supporting a direct link between tDCS and improved plasticity—making Grassi’s work unique.

More important, the researchers identified the actual molecular trigger behind the bolstered memory and plasticity—increased production of BDNF, a protein essential to brain growth. BDNF, which stands for “brain-derived neurotrophic factor,” is synthesized naturally by neurons and is crucial to neuronal development and specialization.

“While the technique and behavioral effects of tDCS are not new,” said ONR Global Associate Director Dr. Monique Beaudoin, “Dr. Grassi’s work is the first to describe BDNF as a mechanism for the behavioral changes that occur after tDCS treatment. This is an exciting and growing research area of great interest to ONR.”

Beaudoin said tDCS treatment could one day benefit Sailors and Marines, from helping them learn faster and more effectively to easing the effects of post-traumatic stress disorder.

“Our warfighters face tremendous challenges that are both physically and cognitively taxing,” she said. “They perform their duties in stressful environments where there are often suddenly and randomly varying levels of environmental stimulation, disrupted sleep cycles and a constant need to stay alert and vigilant.

“We want to explore all interventions that could help them stay healthy and perform optimally in these environments—especially when treatments are potentially noninvasive, effective and lead to long-lasting changes.”

Learn more about the work of Grassi and his team, which was published in Scientific Reports.