Neurological/neuropsychiatric
disorders are often poorly described and poorly treated, but adult-onset
conditions have historically been taken much more seriously and so the research
is more advanced . I find myself quite
often looking at research on schizophrenia and bipolar; many of the same genes
and metabolic dysfunctions common in autism show up in those conditions.
Many people
really dislike the term Mental Retardation (MR), which is actually a very
accurate descriptive term, meaning that someone is cognitively behind
their peers. Most lay people have no
idea what Intellectual Disability (ID) means.
It is interesting
that about 90% of people with schizophrenia and 50% of people with bipolar are
cognitively behind their peers. I
suspect the figure for autism would also be about 90%, if someone measured it. Most people with Asperger’s are not top of
the class.
Only in
extreme cases of being cognitively behind their peers, when their IQ is less
than 70, does a person get diagnosed with MR/ID.
So the
clinical diagnosis of MR/ID is just an arbitrary cut-off point. The idea that if IQ is greater than 70 there
is no cognitive deficit is entirely flawed.
It seems
than in autism, as in schizophrenia and bipolar we should assume that cognitive
dysfunction is present; the only question is how much and what to do about it.
Having
treated the cognitive dysfunction(s), the person is then in a better place to
compensate for the other dysfunctions they might have.
Even though
the psychiatrists and psychologists will tell you that autism is all about the
triad of impairments, I think they are missing the most important element,
which is cognitive dysfunction.
As people with autism age, many find their symptoms
associated with the above “triad of impairments” mellow. The substantial minority who experience untreated flare-ups
driven by inflammation caused by things like allergy, GI problems and even
juvenile arthritis may not be so lucky.
I imagine that cognitive function in adulthood remains at
the level it reached as a teenager.
Cognitive
Function as the Therapeutic Target
Since many children with autism do eventually overcome many
of their challenges in childhood, perhaps cognitive function really should be
given a higher priority in treatment and research.
Many caregivers and educators are mainly focused on
minimizing bad/disruptive behaviors (and bruises) rather than the emergence of
good behaviors and learning. This is sad
but true.
As the child matures, in many cases these bad/disruptive
behaviors may fade without any clever interventions.
So an intervention that stops stereotypy in a toddler, which
was blocking learning, may have very much less impact in an adolescent. Or at least the impact may be much less
obvious.
I remember reading about a parent with two children with
Fragile-X who was very upset when the Arbaclofen trials were halted, since her
kids had responded well. But two years
later in another article it was clear that things were going fine without
Arbaclofen. The son whose violence towards
his mother had been controlled by Arbaclofen, was no longer aggressive. He continued to suffer cognitively, being a
male with Fragile-X, the sister was much less affected (females with fragile X syndrome have two X
chromosomes and only one of the chromosomes usually have an abnormal gene, so
usually females are less affected).
The advantage of using cognitive function as a target is
that it is much easier to measure than subjective behavioral deficits. For the majority of people it is likely to be
the most important factor in their future success and well-being.
In the substantial minority of cases where there are seizures
and/or factors causing autism flare-ups, the behavioral deficits may remain undiminished into
adulthood. These people would also benefit
from maximized cognitive function.
Cognitive
Deficit in Schizophrenia & Bipolar (BPD)
To most lay people
schizophrenia is characterized by abnormal social behavior and failure to recognize what is real. Common symptoms include false beliefs, unclear or confused thinking, hearing voices, reduced social
engagement and emotional expression, and a lack
of motivation. People often have
additional mental health problems such as major
depression, anxiety disorders, or substance use disorder. Symptoms typically come on gradually,
begin in early adulthood, and last a long time.
Cognitive impairments and psychopathological parameters in patients of the schizophrenic spectrum.
Abstract
Cognitive impairment is a core feature of schizophrenia and it is
considered by many researchers as one of the dimensional components of the
disorder. Cognitive
dysfunction occurs in 85% of schizophrenic patients and it is negatively
associated with the outcome of the disorder, the psychosocial
functioning of the patients, and non-compliance with treatment. Many different
cognitive domains are impaired in schizophrenia, such as attention, memory,
executive functions and speech. Nowadays, it is argued that apart from clinical
heterogeneity of schizophrenia, there is probable heterogeneity in the
accompanying neurocognitive dysfunction. Recent studies for cognitive
dysfunction in schizophrenia employ computerized assessment batteries of
cognitive tests, designed to assess specific cognitive impairments.
Computerized cognitive testing permits for more detailed data collection (e.g.
precise timing scores of responses), eliminates researcher's measurement errors
and bias, assists the manipulation of data collected, and improves reliability
of measurements through standardized data collection methods. The aims of the
present study are: the comparison of cognitive performance of our sample of
patients and that of healthy controls, on different specific cognitive tests,
and the testing for possible association between patients' psychopathological
symptoms and specific cognitive impairments, using the Cogtest computerized
cognitive assessment battery. 71 male inpatients diagnosed with schizophrenia
or other psychotic spectrum disorders (mean = 30.23 ± 7.71 years of age),
admitted in a psychiatric unit of the First Department of Psychiatry, Athens
University Medical School, Eginition Hospital (continuous admissions) were
studied. Patients were excluded from the study if they suffered from severe
neurological conditions, severe visual or hearing impairment, mental
retardation, or if they abused alcohol or drugs.
Bipolar disorder, also known as bipolar affective disorder or manic depression, is a mental disorder characterized by periods of depression and periods of elevated mood. The
elevated mood is significant and is known as mania or hypomania depending
on the severity or whether symptoms of psychosis are present. During mania an individual feels or acts
abnormally happy, energetic, or irritable. They
often make poorly thought out decisions with little regard to the consequences.
The need for sleep is usually reduced. During
periods of depression there may be crying, poor eye contact with others, and a
negative outlook on life
It also
turns out that cognitive deficit is generally present in bipolar disorder (BPD).
“One area that Dr. Burdick is exploring is the frequency of
neurocognitive impairment in BPD. Research shows that approximately 90 percent
of schizophrenic patients suffer from cognitive deficits compared to only 40 to
60 percent of BPD patients. Understanding
why certain patients develop significant cognitive difficulties while others do
not is critical in optimizing patients’ quality of life, she says.”
Bipolar is probably not something you would connect with
autism. Being an observational diagnosis
you would not tend to look at the biological underpinnings. The
biological basis of both bipolar and schizophrenia are far better studied than
autism and do significantly overlap with it.
In a recent post I looked at epigenetics and autism, when
it comes to schizophrenia and bipolar the role of epigenetics is far more in
the mainstream.
There is an approved epigenetic therapy (the HDAC
inhibitor Valproate) for Bipolar mania and there is a clinical trial to improve
cognitive function in schizophrenia using ather epigenetic therapy (the HDAC
inhibitor Sodium Butyrate.)
Butyrate is also
showed promise in a mouse model (D-AMPH) of Bipolar.
Epigenetic mechanisms in schizophrenia
Effects of sodium butyrate on oxidative stress and behavioral changes induced by administration of D-AMPH
Conclusion
I think
people should be more open to discuss cognitive deficits and not hide behind
politically correct terminology.
It seems
that in both bipolar and schizophrenia cognitive deficits are recognized to be
at the core of the disorder, even though 99% will not have an IQ<70 and so
not be labelled with MR/ID.
Autism therapies
which clearly improve cognitive function, like Bumetanide and low-dose
Clonazepam, should be promoted as such.
Clinical trials should measure the cognitive improvement separately from
autism measures. As the person ages I think
the benefit will often be more noticeable/measurable cognitively than
behaviorally.