Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there. Did your doctor somehow miss the recovery protocol that Pedro Bach-y-Rita used to recover fully back in 1958 with only a partial brain?

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label Psychosis. Show all posts
Showing posts with label Psychosis. Show all posts

Tuesday, July 23, 2024

Growing Evidence Supports the Link Between Cannabis Use and Psychosis Risk

 Really? Because you haven't considered that these people are self-medicating with marijuana? I'm going to be doing plenty of marijuana after my next stroke.

My 13 reasons for marijuana use post-stroke.  

Don't follow me, I'm not medically trained and I don't have a Dr. in front of my name.

Growing Evidence Supports the Link Between Cannabis Use and Psychosis Risk

Cannabis use was associated with a more than 11 times greater risk for psychotic disorder among adolescents, compared to no cannabis use.

There is a significant, age-dependent association between cannabis use and psychotic disorder risk – as adolescence appears to be a particularly susceptible period for cannabis-related psychosis. These study results were recently published in Psychological Medicine.

Cannabis use has been previously associated with an increased risk for psychotic disorders. However, the debate over causality persists due to methodological limitations and the rising prevalence of cannabis over time.

To this aim, investigators conducted an observational longitudinal study to understand the relationship between cannabis use and subsequent risk for psychotic disorders among adolescents and young adults residing in Ontario, Canada. The investigators used population-based survey data from the Canadian Community Health Survey to identify Ontario residents who completed the survey between 2009 and 2012 and were aged 12 to 24 years at the time of survey completion. Additionally, the investigators linked the survey data with health data from the Institute for Clinical Evaluative Sciences to investigate outcomes up to 2018. Cannabis consumption was assessed based on self-reported use over the past year. The primary outcomes of interest included the number of days until the first outpatient physician visit, emergency department visit, or hospital discharge related to a psychotic disorder.

A total of 11,363 participants were included in the final analysis. The mean (interquartile range [IQR]) age of participants was 18.3 (15.2-21.3) years, 51.0% were boys/men, 67.1% were White, and 86.4% lived in an urban area. Among the respondents, 23.4% (n=2,659) reported using cannabis in the past year. During the follow-up period, 1.2% of respondents utilized health services for psychotic disorders, while 4% were censored due to loss of health insurance registration or death.

Based on the precautionary principle, as more jurisdictions move to liberalize cannabis use and perception of harm declines among youth, this study suggests that evidence- based cannabis prevention strategies for adolescents are warranted.

The investigators found that cannabis use was significantly associated with psychotic disorders during adolescence (adjusted hazard ratio [aHR], 11.2; 95% CI, 4.6 to 27.3), but not during young adulthood (aHR, 1.3; 95% CI, 0.6 to 2.6). Adolescents who used cannabis also had a substantially higher risk for hospitalizations and emergency department visits (aHR, 26.7; 95% CI, 7.7 to 92.8), while there was no substantial risk observed in young adulthood (aHR, 1.8; 95% CI, 0.6 to 5.4).

The investigators found that across all incident psychotic disorder hospitalizations and emergency department visits among adolescents, 77.8% (95% CI, 56.4%-99.3%) of adolescents had reported past-year cannabis use and 82.3% (95% CI, 64.7%-100.0%) had reported lifetime use.

“Based on the precautionary principle, as more jurisdictions move to liberalize cannabis use and perception of harm declines among youth, this study suggests that evidence-based cannabis prevention strategies for adolescents are warranted,” the investigators concluded.

These study findings may be limited, given the reliance on self-reported data during a period of cannabis prohibition – which may have led to underreporting – and the inability to establish causality due to the observational study design.


Thursday, February 22, 2024

Poststroke psychosis: a systematic review

Did your doctor and hospital initiate research studies on antipsychotics in the last 7 years? We should have results by now. Or were they incompetent in not doing anything with this research?

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

The latest here:

 Poststroke psychosis: a systematic review


  1. Helle Stangeland1,2,
  2. Vasiliki Orgeta2,
  3. Vaughan Bell2
  1. Correspondence to Dr Vaughan Bell, Division of Psychiatry, Faculty of Brain Sciences, London W1T 7NF, UK; Vaughan.Bell@ucl.ac.uk

Abstract

A preregistered systematic review of poststroke psychosis examining clinical characteristics, prevalence, diagnostic procedures, lesion location, treatments, risk factors and outcome. Neuropsychiatric outcomes following stroke are common and severely impact quality of life. No previous reviews have focused on poststroke psychosis despite clear clinical need. CINAHL, MEDLINE and PsychINFO were searched for studies on poststroke psychosis published between 1975 and 2016. Reviewers independently selected studies for inclusion, extracted data and rated study quality. Out of 2442 references, 76 met inclusion criteria. Average age for poststroke psychosis was 66.6 years with slightly more males than females affected. Delayed onset was common. Neurological presentation was typical for stroke, but a significant minority had otherwise ‘silent strokes’. The most common psychosis was delusional disorder, followed by schizophrenia-like psychosis and mood disorder with psychotic features. Estimated delusion prevalence was 4.67% (95% CI 2.30% to 7.79%) and hallucinations 5.05% (95% CI 1.84% to 9.65%). Twelve-year incidence was 6.7%. No systematic treatment studies were found. Case studies frequently report symptom remission after antipsychotics, but serious concerns about under-representation of poor outcome remain. Lesions were typically right hemisphere, particularly frontal, temporal and parietal regions, and the right caudate nucleus. In general, poststroke psychosis was associated with poor functional outcomes and high mortality. Poor methodological quality of studies was a significant limitation. Psychosis considerably adds to illness burden of stroke. Delayed onset suggests a window for early intervention. Studies on the safety and efficacy of antipsychotics in this population are urgently needed.

This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 4.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properly cited. See: http://creativecommons.org/licenses/by/4.0/

Thursday, July 16, 2020

Does cannabis really affect memory? Here's what research currently says

At least they acknowledge that it doesn't cause psychosis as compared to this bad research:

Marijuana Chokes Alzheimer's-Related Brain Regions - Really? April 2020 

Now we just need our survivor led stroke associations to conduct the research necessary on amounts of CBD and THC needed for stroke recovery. 

My 13 reasons for marijuana use post-stroke.  

Don't follow me, I'm not medically trained and I don't have a Dr. in front of my name.

The latest here:

Does cannabis really affect memory? Here's what research currently says

Ian Hamilton, Associate Professor, Addiction and Mental Health, University of York and Elizabeth Hughes, Professor of Mental Health, University of Leeds



Does cannabis really affect memory? Here's what research currently says
Does cannabis really affect memory? Here's what research currently says

Cannabis use has long been associated with memory loss. But until now, this notion was largely anecdotal. As researchers begin to look into cannabis and the effect that it has on human health, they’re beginning to better understand the effect it has on the human brain – and whether cannabis really does impair memory.
Memory is divided into both short-term and long-term memory. Short-term memory is where immediate events are temporarily stored, whereas long-term memory is where information is stored indefinitely.
Current evidence shows that cannabis intoxication may temporarily alter or distort short-term memory processing. This seems to be caused by compounds in cannabis that disrupt neural signalling when binding to receptors responsible for memory in the brain. Interrupted short-term memory can indeed impact on learning, and may also cause loss of interest or problems with concentration.

However, early research also shows that cannabis could have a positive impact on neurodegenerative diseases that affect memory, such as Alzheimer’s, Huntington Chorea, and epilepsy. In mainly animal studies, when researchers used components found in cannabis, they found it could slow or even prevent the advance of these diseases – essentially through the creation of neurons.
These apparently paradoxical effects from the same drug are best explained by two chemicals found in cannabis. Namely delta 9-tetrahydrocannabinol (THC) and cannabinoids (CBD). We all have naturally occurring cannabinoid receptors in our brains. THC is able to effectively bind to these receptors, creating euphoric effects. However CBD can interfere with this binding process, which dampens the feeling of euphoria.
Different ratios of these two chemicals are found in various types of cannabis. Consuming a cannabis product with THC but no CBD increases the risk of developing mental health problems, such as psychosis. However, CBD could actually be used to treat psychosis.
Cannabis with higher levels of THC and lower, or negligible, amounts of CBD appear to have a detrimental effect on short-term memory, particularly in adolescents. The main problem is their ability to retain and recall information. Fortunately this is not permanent.
But these recent discoveries about the role of THC and CBD in cannabis show that we can no longer simply say cannabis itself causes psychosis, or is detrimental to memory. Rather, it might be the type of cannabis, and the compounds it contains, that may have specific risks or benefits.
And while there’s little doubt that some people who use cannabis do experience impaired memory, establishing that cannabis is the cause is tricky. One reason for this is because it’s difficult to rule out the impact of other drugs that people may have used – and whether these drugs contributed to this memory impairment. For example, alcohol misuse can also cause brain damage and memory loss. Another obvious problem when researching this is when asking people with impaired memory to recall their past drug use and any associated problems. Their ability to recall these details could be compromised.
Recent research even suggests that any memory impairment associated with using cannabis can be reversed when people stop using cannabis. This effect was seen mainly in those who used cannabis at least once a week.
Just as higher doses of alcohol can potentially cause brain damage, higher doses or more frequent use of cannabis may also cause long-term memory problems – the ability to learn effectively and the ability to concentrate on a task for example. Some people will use both alcohol and cannabis, often at the same time, which may both worsen the potential impact on memory.
New research also suggests that it’s cannabis, rather than alcohol, that’s responsible for damage to developing teen brains. Though alcohol can destroy or severely damage brain neurons and their signalling functions, this study showed cannabis actually changes the neural brain tissue responsible for memory. But this change can be reversed within a matter of weeks if a person abstains. Though surveys suggest fewer young people are using both cannabis and alcohol, those teenagers that do use cannabis use it twice as frequently.

Frequent cannabis by teens may impact their memory and ability to concentrate. mooremedia/ Shutterstock
Research shows that young, frequent users of cannabis have thinner temporal and frontal cortices, which are both areas that help process memory functioning. Memory is a critical aid to learning and study – but cannabis doesn’t just effect memory, it can also reduce motivation to learn. This dual influence reduces a young person’s engagement in education and their ability to perform.
However, using cannabis later in life (age 50 and over) appears to have only a moderate impact on cognitive functioning, including on memory. These modest declines are not fully understood, and there is a lack of high quality research in this area. That will need to change as it’s not just young people that use cannabis. As more countries legalise cannabis, older people might also want to try it.
While there is likely to be no great harm to a person’s memory if they experiment with cannabis, current research seems to agree that the more frequent the use, the greater the risk. Though there is still a lot that researchers don’t yet know about cannabis use on memory, current evidence suggests that any memory impairment can be reversed if a person abstains from use.

Monday, May 27, 2019

Daily Marijuana Use And Highly Potent Weed Linked To Psychosis

I think you have this completely backwards, psychotic people are using marijuana to self treat themselves. Learn about cause and effect, please.

Daily Marijuana Use And Highly Potent Weed Linked To Psychosis

Wednesday, November 9, 2016

Cannabis abuse possible cause of psychosis

It is crappy titles and invalid research like this that is preventing us from getting legalized marijuana. It is far more likely that the cannabis user is trying to self treat psychosis. I wish people would learn about cause and effect.
I am going to do marijuana after my next stroke. I'll have to drive across the country to get it legally.

My 13 reasons for marijuana use post-stroke. 

Cannabis abuse possible cause of psychosis


The risk of developing psychosis is more than tripled for those who abuse cannabis, according to results from a new twin study.
Researchers from the Norwegian Institute of Public Health (NIPH), together with colleagues from Virginia Commonwealth University, examined the relationship between cannabis and psychosis using psychiatric interviews of Norwegian twins. The interviews reveal whether the twins had symptoms of psychosis and cannabis abuse.
“Previous research has shown that patients with psychotic disorders use cannabis more often than the general population. However research has been divided over whether cannabis use was the cause of the psychotic disorders,” says Ragnar Nesvåg, senior researcher at NIPH and the main author of the study.
Genetic factors influence both cannabis abuse and psychosis and the same genes may lead to an increased risk for both problems.
“The relative importance of genes in the causes of a disease is known as heritability, and we know from previous studies at the NIPH that cannabis abuse is very heritable, explains Eivind Ystrom, senior researcher at NIPH.
“In order to determine whether cannabis abuse can lead to psychosis, it is important to account for genetic risk,” he adds.
The researchers therefore tested both the hypotheses that cannabis use causes psychotic symptoms and that psychotic symptoms lead to cannabis abuse.
Abuse increased the risk by 3.5
The hypothesis best suited to the data was that cannabis abuse caused symptoms of psychosis. Within a twin pair, the twin with symptoms of cannabis abuse had a 3.5 times higher risk of developing symptoms of psychosis compared with the twin who did not have symptoms of cannabis abuse.
“Our analyses showed a significant association between cannabis abuse and symptoms of psychosis in the general population. We also tested the hypothesis that symptoms of psychosis caused cannabis abuse, but the hypothesis was less suited to the data. Therefore, it appears that cannabis abuse can be a cause of psychosis,” says Ystrom.
Confirmed high heritability
Previous studies have shown that cannabis abuse is very heritable, which was also confirmed in this study. As much as 88 per cent of the causes of why some people abused cannabis, yet others did not, could be attributed to some people having risk genes.
Despite this, the researchers found that a common genetic risk could not explain the entire association with symptoms of psychosis. Even after genetic risk and risk of childhood environment were taken into account, people with cannabis abuse still had a multiplied risk of developing symptoms of psychosis.
Nesvåg says that psychosis is associated with huge costs to society. These findings should be considered when evaluating the cost of policies for increased cannabis availability, such as decriminalisation or legalisation.
About twin studies
Investigating whether a particular risk factor causes disease requires studies where you look at two people who are otherwise identical, where one is exposed to a risk factor and the other is not. The effects on their health can be investigated. For obvious reasons, these experiments are neither practical, ethical or legally feasible.
Studying twins is a viable option because they have genetic similarity, they have grown up in the same family, and they have the same socioeconomic background.
https://www.fhi.no/en/news/2016/cannabis-abuse-psychosis/

Saturday, November 28, 2015

Smoking high-strength cannabis may damage nerve fibres in brain

But is it the smoking that does this or the marijuana? Easy to find out, just injest the same strength and test what happens. This result will not change my use after my next stroke.
My 13 reasons for marijuana use post-stroke. Don't follow me but I will figure out some way to get some after my next stroke.
 Treating brain diseases with marijuana 


 Smoking high-strength cannabis may damage nerve fibres in brain
High-strength cannabis may damage nerve fibres that handle the flow of messages across the two halves of the brain, scientists claim. Brain scans of people who regularly smoked strong skunk-like cannabis revealed subtle differences in the white matter that connects the left and right hemispheres and carries signals from one side of the brain to the other.
The changes were not seen in those who never used cannabis or smoked only the less potent forms of the drug, the researchers found.

The study is thought to be the first to look at the effects of cannabis potency on brain structure, and suggests that greater use of skunk may cause more damage to the corpus callosum, making communications across the brain’s hemispheres less efficient.
Paola Dazzan, a neurobiologist at the Institute of Psychiatry at King’s College London, said the effects appeared to be linked to the level of active ingredient, tetrahydrocannabinol (THC), in cannabis. While traditional forms of cannabis contain 2 to 4 % THC, the more potent varieties (of which there are about 100), can contain 10 to 14% THC, according to the DrugScope charity.
“If you look at the corpus callosum, what we’re seeing is a significant difference in the white matter between those who use high potency cannabis and those who never use the drug, or use the low-potency drug,” said Dazzan. The corpus callosum is rich in cannabinoid receptors, on which the THC chemical acts.

“The difference is there whether you have psychosis or not, and we think this is strictly related to the potency of the cannabis,” she added. Details of the study are reported in the journal Psychological Medicine.
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The researchers used two scanning techniques, magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI), to examine the corpus callosum, the largest region of white matter, in the brains of 56 patients who had reported a first episode of psychosis, and 43 healthy volunteers from the local community.
The scans found that daily users of high-potency cannabis had a slightly greater – by about 2% – “mean diffusivity” in the corpus callosum. “That reflects a problem in the white matter that ultimately makes it less efficient,” Dazzan told the Guardian. “We don’t know exactly what it means for the person, but it suggests there is less efficient transfer of information.”
The study cannot confirm that high levels of THC in cannabis cause changes to white matter. As Dazzan notes, it is may be that people with damaged white matter are more likely to smoke skunk in the first place.
“It is possible that these people already have a different brain and they are more likely to use cannabis. But what we can say is if it’s high potency, and if you smoke frequently, your brain is different from the brain of someone who smokes normal cannabis, and from someone who doesn’t smoke cannabis at all,” she said.

But even with the uncertainty over cause and effect, she urged users and public health workers to change how they think about cannabis use. “When it comes to alcohol, we are used to thinking about how much people drink, and whether they are drinking wine, beer, or whisky. We should think of cannabis in a similar way, in terms of THC and the different contents cannabis can have, and potentially the effects on health will be different,” she said.
“As we have suggested previously, when assessing cannabis use, it is extremely important to gather information on how often and what type of cannabis is being used. These details can help quantify the risk of mental health problems and increase awareness of the type of damage these substances can do to the brain,” she added.
In February, Dazzan and others at the Institute of Psychiatry reported that the ready availability of skunk in south London might be behind a rise in the proportion of new cases of psychosis being attributed to cannabis.

Monday, February 16, 2015

Psychosis five times more likely for cannabis users: study

My god, the stupidity of not knowing what cause and effect is. I would say it is vastly more likely that those with psychosis are self medicating with marijuana. But don't listen to me, I'm stupidly stroke-addled. It is obvious they had a conclusion already in mind that they had to support even if it meant not following scientific principles.
You will have to make the decision if the benefits of helping stroke recovery outweigh any possible harm.  But first you will need to pound into your representatives and senators stupid little heads that marijuana does not belong on the Schedule I drug list.
My 13 reasons to use it post-stroke.

http://news.yahoo.com/psychosis-five-times-more-likely-cannabis-users-study-005717669.html