Psychotic symptoms cause crises and are very dramatic and disruptive but once controled with medication cognitive and negative symptoms are what people are disabled by. Cognitive function in particular has been getting a lot of attention. Some people would say that it is the essence of schizophrenia, and that it determines functional outcome in schizophrenia. Functional outcome is a pretty simple concept. Does the individual do well in school, do they work full time, did they get married, do they own a house, a car? I recently attended a presentation by Dr. Susan McGurk, a NARSAD grant recipient, who has been doing research on cognition. She showed a graph of functional outcome studies that have been done since 1890. There has been very little change in this measure since 1890 in any population with schizophrenia. The new atypical medications will change that, but they are so recent the studies haven't been done yet. Dr. McGurk and other psychiatrists believe it is cognitive function that is driving functional outcomes.
Cognitive abilities are much like intelligence but quite distinct from IQ Much of the research on human cognition has been done on Alzheimer's patients who have a steady deterioration of cognitive function over time. It has different causes than cognitive deterioration in schizophrenia though. Measuring these symptoms involves an eight hour battery of tests, which are believed to measure fairly specific abilities of the prefrontal cortex: attention or vigilance, abstraction, verbal memory, spatial memory, language skills, and sensory motor function. Different researchers favor different tests to measure related but slightly different abilities which makes the comparison of different studies problematic and the whole field of cognitive studies in schizophrenia is just beginning. Some tests are increasingly associated with schizophrenia, like the Wisconsin Card Sorting test, one which people with schizophrenia typically have great difficulty with. The considerable variability of schizophrenia also complicates comparison of research results. Disability varies from individual to individual. Cogentin and other anticholinergic medication has a negative impact on cogntive function and test scores improve just with the elimination of that medication. Anticholinergics were commonly used with conventional antipsychotics to control side effects. I don't know whether their use or nonuse is factored into cognitive studies comparing conventional and atypical medications. Nicotine from cigarettes and caffeine from coffee also affect cognitive scores and are difficult to control for. There has been a lot of recent research but I find the results rather confusing.
The cognitive researchers say these deficits predate the first psychotic episode and are fairly stable for most people with schizophrenia thereafter, unaffected by psychotic episodes. In some studies cognitive scores improve after the first psychotic episode with treatment. In some people there is a steady deterioration over the years, slower than in Alzheimer's but with a similar end result. That is in contrast to researchers saying they can prevent cognitive deterioration with early intervention and relapse prevention. How cognitive function would behave with people who are treated in the first six months of their first psychotic episode is unclear. If psychotic episodes are "toxic" and cause brain damage, what is being damaged if it isn't a cognitive function? the cognitive researchers are finding that first degree relatives also show some cognitive disability even though they don't develop schizophrenia. The studies of cognitive symptoms treated with atypicals are still underway, and from what I've heard cognitive function improves in some domains with the atypicals now available. McGurk mentioned a study showing a 30% improvement in verbal memory with Risperidone.How much improvement in what domains by which subgroup of people taking which medication is beginning to become clearer as research is reported in the academic journals. There is definitely some improvement.
Serotonin blockade, an effect of all atypicals so far, appears to improve cognitive ability by stimulating D1 dopamine transmission, even though some atypicals also block D1 receptors to some degree. Atypicals have an affinity for up to 10 different receptors. They all have an affinity for Serotonin and Dopamine 2 receptors. There are at least a half dozen Serotonin receptor sub types with different functions in the different areas of the brain. It is not uncommon for an individual to be taking an antidepressant, which increases the amount of Serotonin, and a Serotonin blocking atypical. Somehow they are both effective in spite of each other.
The D1 dopamine receptor, of which there are a lot in the prefrontal cortex is believed to be critical to cognitive function. The cognitive researchers think a good D1 agonist that would increase D1 activity would theoretically improve cognitive function.
Almost all the conferences and dinner presentations I attend now have presentations on cognitive function, and it is generally accepted that they have a major impact on functional outcome.
What is schizophrenia? | | My story | | Condensed story | | Recovery | | Prodrome | | Medication | | Compliance Early Intervention | | Relapse prevention | | Cognition | | Housing and benefits | | Meaningful activity | | Family and social support | | ACT Teams | | Movies, books | | Web sites | | Poster | | Origins of this site | | Persistent delusions | | Photo of me | | My addictions | | First graph | | Guest book 2004 | |