Tag Archives: psychosis

Autism-a two dimensional disorder?

People with Asperger's Syndrome are often preo...
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Two main underlying deficits have been proposed in autism– one concerning an inactive or non-existent Theory of Mind module and another a tendency towards Weak Central Coherence. ToM defects reflect in the communicative, social and imaginative deficits seen in autistics; while the savant skills as well as restrictive and repetitive behavior (restricted repertoire of interests ;obsessive desire for sameness – islets of ability – idiot savant abilities – excellent rote memory – preoccupation with parts of objects ) are best explained by taking recourse to the Autism-as-a cognitive-style having weak Central Coherence argument. I’ve discussed the crucial aspects of both of these two dimensions in y series of posts on autism and psychosis and shown how they have to be seen on a continuum and more as deviation from the normal range with one end as autism and the other as psychosis. We also know that psychosis itself is two dimensional with one dimension being that of schizophrenic spectrum and the other the bipolar spectrum. Thus what I propose is that we start seeing Autism also as a two dimensional disorder with TOM defect subtype a mirror image of schizophrenia; while the Weak CC subtype a mirror image of bipolar or manic depressive phenotype. Here are autistic and psychotic features on these dimensions (from Autism, Happe, the autistic deficits and assets table):

  • ordering behavioural pictures (Baron-Cohen et al. 1986) vs ordering mentalistic pictures understanding “see” (Perner et al. 1989)
  • understanding “know” protoimperative pointing (Baron-Cohen 1989c) vs protodeclarative pointing sabotage (Sodian & Frith 1992)
  • deception false photographs (Leekam & Perner 1991, Leslie & Thaiss 1992) vs. false beliefs recognising happiness and sadness (Baron-Cohen et al. 1993a)
  • recognizing surprise object occlusion (Baron-Cohen 1992) vs. information occlusion
  • literal expression (Happé 1993) vs. metaphorical expression
  • elicited structured play (Wetherby & Prutting 1984)vs. spontaneous pretend play
  • instrumental gestures (Attwood et al. 1988) vs. expressive gestures
  • talking about desires and emotions (Tager-Flusberg 1993) vs. talking about beliefs and ideas
  • using person as tool (Phillips 1993) vs. using person as receiver of information
  • showing “active” sociability (Frith et al. 1994) vs. showing “interactive” sociability

It is also pertinent in this regard to revisit the question of co-occurrence of autism and schizophrenia. Happe maintains that psychois can only be relaibly seen in Asperge’s group who might have a late developing ToMm ability. To quote:

The higher incidence of psychiatric disorders in this group (asperger’s group) (Tantam 1991, Szatmari et al. 1989b) is well explained by this hypothesis. Depression will be more common since these people have greater insight into their own difficulties and their own feelings and thoughts. Positive symptoms of psychosis, such as hallucinations and delusions would be found only in Asperger’s syndrome cases by this account, if one takes Frith & Frith’s (1991) view of these symptoms as resulting from an “over-active” theory of mind. Asperger’s syndrome people, who gain theory of mind late and therefore abnormally, may be at high risk for having their theory of mind “go wrong”. On this hypothesis it would be impossible for a Kanner-type autistic person (who has no theory of mind) to show these psychotic or positive symptoms. In this sense (according to Frith & Frith’s theory) Asperger’s syndrome would be something of a midpoint between autism and (positive or florid) schizophrenia; while the former is due to a lack of theory of mind, and the latter due to over-active theory of mind, some people with Asperger’s syndrome may show both the scars of early lack and the florid symptoms of late acquired theory of mind working abnormally hard.

There is some preliminary evidence to support the suggestion that the term “Asperger’s syndrome” could meaningfully be restricted to those subjects with autism who have achieved some ability to think about thoughts. Ozonoff et al. (1991) found that their group labelled (perhaps arguably) as having Asperger’s syndrome did not show impairments relative to controls.

It is interesting to note the ‘over-active’ theory of mind reference to Frith and Frith. I could not locate that paper but came across another paper by Abu-akkel that propose over-active ToM as a mechanism of psychosis. There are also some full text related articles available online that may be of interest to the serious reader. As for me, it is heartening to note that others concur with the theory of autism and psychosis as opposites on a  continuum.

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The downside of cognitive enhancement

The Morris water maze task has been used to de...

Jonah Lehrer, has an article in this week’s Nature News, (find a PDF here) , regarding 30 or so cognitively enhanced mice strains that have been bred and genetically engineered.  As Lehrer  very elaborately documents, all these have enhanced LTP as an intervening mechanism that leads to improvements in learning and memory. Most of the genes involved affcet the LTP mechanism in one way or the other to breed super mnemonist mice. However, from the time of Luria, t has been well known that those who have enhanced memory also suffer from some of its disadvantages and that the ability to forget is also very important.

Little is known about the side effects and tradeoffs
of both the current usage or the drugs in
development, but initial clues offered by smart
mice raise concerns. The Hras strain developed
in Silva’s lab might be good at learning, but its
fear response for a relatively benign stimulus
would be counterproductive for a wild mouse.
Its enhanced memory is both a blessing and a
burden. Silva cites other strains of smart mice
that excel at solving complex exercises, such as
the Morris water maze, but that struggle with
simpler mazes. “It’s as if they remember too
much,” he says — possibly taking in irrelevant
information such as the position of windows
or lights but missing the big clues.
Farah sees a parallel between these mice
and one of the few case studies of an individual
with profoundly enhanced memory.
In the early 1920s, the Russian neurologist
Alexander Luria began studying the learning
skills of a newspaper reporter called Solomon
Shereshevsky, who had been referred to the
doctor by his editor. Shereshevsky had such
a perfect memory that he often struggled to
forget irrelevant details. After a single read of
Dante’s Divine Comedy, he was able to recite
the complete poem by heart. Although this

Little is known about the side effects and tradeoffs of both the current usage or the drugs in development, but initial clues offered by smart mice raise concerns. The Hras strain developed in Silva’s lab might be good at learning, but its fear response for a relatively benign stimulus would be counterproductive for a wild mouse. Its enhanced memory is both a blessing and a burden. Silva cites other strains of smart mice that excel at solving complex exercises, such as the Morris water maze, but that struggle with simpler mazes. “It’s as if they remember too much,” he says — possibly taking in irrelevant information such as the position of windows or lights but missing the big clues.

Farah sees a parallel between these mice and one of the few case studies of an individual with profoundly enhanced memory. In the early 1920s, the Russian neurologist Alexander Luria began studying the learning skills of a newspaper reporter called Solomon Shereshevsky, who had been referred to the doctor by his editor. Shereshevsky had such a perfect memory that he often struggled to forget irrelevant details. After a single read of Dante’s Divine Comedy, he was able to recite the complete poem by heart. Although this flawless memory occasionally helped Shereshevsky at work — he never needed to take notes — Luria also documented the profound disadvantages of such a capacious memory. Shereshevsky, for instance, was almost entirely unable to grasp metaphors, as his mind was so fixated on particulars. When he tried to read poetry, for example, “the obstacles to his understanding were overwhelming”, Luria wrote in his book The Mind of a Mnemonist. “Each expression gave rise to a remembered image; this, in turn, would conflict with another image that had been evoked.”

For Luria, Shereshevsky’s struggles were a powerful reminder that the ability to forget is as important as the ability to remember. Enhancing human memory in individuals without severe cognitive defects might prove counterproductive.

It is interesting to pause here and note that many savants who have excellent memory are also autistic and that schizophrenics on the opposite end of the spectrum are characterized by too much reliance of metaphors and too much generalizations and abstractions. Further Martha Farah notes the following:

Many scientists are concerned that the animal models of enhanced cognition might obscure subtle side effects, which can’t be studied in rodents or primates. Farah is currently looking at the trade-off between enhanced attention — she gives human subjects a mild amphetamine — and performance on creative tasks. Other researchers have used computer models to show that memory is actually optimized by slight imperfections, as they allow one to see connections between different but related events9. “The brain seems to have made a compromise in that having a more accurate memory interferes with the ability to generalize,” Farah says. “You need a little noise in order to be able to think abstractly, to get beyond the concrete and literal.”

Again, one can easily see the correlations with Autism and Schizophrenia- one end marked by too narrow a focus , while the other marked by too much noise and divergent creativity. I would have been happy to incorporate the more LTP as autistic and less LTP as schizophrenics, but it flies in face of my earlier findings regarding experience dependent plasticity in autism and schizophrenia where the conclusions were just the revers. Yet, it is clear that synaptic plasticity is a majo mechanism involved in the autism/psychosis differentiation. Do let me know if you can reconcile the new findings with the older ones to come up with the right LTP and psychosis/autism relationship.

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