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Schizophrenia and Attention: Cognitive and Neurobiological Aspects

This  paper on schizophrenia was written during a postgraduate course in applied psychology and is more a collection of information that I have not had time to edit and refine, but the various references may be of use to some researchers. The thrust of this article is to explain that the while there are 'abnormalities' in cognition and attention in schizophrenia  the underlying  neurobiological differences are not necessarily pathological or inferior. Instead many problems occur because  the resultant differences in cognitive skills and information processing create friction between a small minority of the population and the vast majority including many clinicians. This failure to consider individual differences leads to treatment failures and behavioural psychopathology which results from either extreme arousal levels maintaining frontal-temporal control of information processing, even when hippocampal transfer is impaired resulting in delusions and hallucinations or deliberate refusal to use frontal processing as a self treatment option which results in passivity and faulty reasoning.  

COGNITIVE AND NEUROBIOLOGICAL ASPECTS

CONTENTS                  

1. Background

    Symptoms

    Neurobiological Correlates of Schizophrenia

2. Cognitive Abnormalities

    Memory

    Attention

             Selective

            Sustained

    Summary

3. Neurobiology of Attention

4. Conclusion

5. References

Schizophrenia has been described as perhaps the most devastating disorder to afflict humanity, affecting about 1% of the population. The idea that schizophrenia, with it's extreme disorders of thought and perception, could be caused only by a faulty environment is inconsistent with the neurobiological model and understanding of behaviour as demonstrated by the way in which  psychoses of the type associated with schizophrenia can be induced by the intake of drugs such as phencyclidine(PCP) and various amphetamines as well as being found in mood disorders such as bi-polar disorder(Kandel, Schwartz and Jessel, 1991, p855). 

Studies involving monozygotic twins and the occurrence of schizophrenia also confirm  that there is in fact a large genetic component(Kandel et al,1991, p993). 'Quantitative estimates of the degree of the genetic component involved in schizophrenia range as high as '70 to 80 %' (McGuffin and Murray, 1991,p99).

As noted above, about 1% of the general population will suffer from schizophrenia at some time in their life, whereas in families ie parents, siblings and children of schizophrenic patients, the occurrence is about 15%. This indicates that a genetic component or biological predisposition may be present although it does not involve a 100% penetrance rate as in some other diseases, eg Huntingdons disease, and a comparison of the rates of  occurrence of schizophrenia in dizygotic and monozygotic twins confirmed this(Kandel et al, 1991, p856). In dizygotic twins the rate of concordance was found to be about 15%, as with other siblings, whereas in monozygotic twins the concordance rate was about 50%(See figure 1).

 

 

 



 

Symptoms

 

The disease itself consists of two distinct sets of symptoms which are referred to as positive and negative symptoms. The positive symptoms reflect a psychosis or loss of touch with reality whereas the negative symptoms are the residual symptoms which are marked by the absence of normal social and interpersonal behaviour(Kandel et al, 1992, p855). This model of negative and positive symptoms has been investigated and found to have a high degree of validity(Kay,1990) Kay made the following description of the different states.

Positive	Negative
Delusions	Poor attention
Grandiosity	Emotional withdrawal
Unusual thought content	Social withdrawal
Hallucinations	Passive/apathetic
	Lack of spontaneity and conversational flow
	Poor rapport
	Blunted affect

The psychotic or positive symptoms stage would include at least one of the following:

- bizarre delusions eg being from Mars living in subjects stomach

- prominent hallucinations usually auditory in nature

or two or more of all symptoms, including those below, for at least six months

-non bizarre delusions such as being persecuted

- disordered thoughts accompanied by a loss of emotional content

-disorganised or derailed speech

-emotional flattening or avolition

The Diagnostic and Statistical Manual of Mental Disorders(DSM-IV) describes the positive symptoms as an ‘excess or distortion of normal functions’ and the negative symptoms as a ‘diminution or loss of normal functions’(p274).

 

Neurobiological Correlates

 

Magnetic resonance scanning techniques, as well as other diagnostic procedures, have shown a number of anatomical differences in the brains of some patients with schizophrenia, when compared with normal controls. The most obvious of these are the enlarged ventricles and sulci resulting from tissue loss or shrinkage in various areas, most noticeably the frontal lobes(Raz,1993) and the basal ganglia and limbic system (Bogerts, Meertz and Schonfeldt-Bausch, 1985). Later research(Gur and Gur, 1995) using more advanced scanning methods showed that frontal lobe differences between those with schizophrenia and controls was insignificant. Other anatomical abnormalities continue to be found, however not always, and this demonstrates the heterogeneity of schizophrenia. These anatomical differences appear not to be genetically based , as demonstrated by the MRI scans pictures of two monozygotic twins shown below in figure 2.



A loss of tissue in the schizophrenic twin is clearly evident but not in the unaffected twin (Kandel et al, p858). It has been suggested that this loss of tissue is not a loss of neurons as such but rather a decrease in the size of neurons although, in some subcortical areas, neuronal loss has been shown to occur(Bogerts et al, 1985). A study by Selemon et al(1995), showed that neuronal density was in fact greater in the prefrontal and occipital areas although the cortical matrix was slightly thinner. They argued it was not clear whether there were just more neurons, albeit smaller, more densely packed neurons or just an atrophy of the neuronal body as they found less synaptic connections via an analysis of the synaptosome levels in the tissue samples. This decrease in neuronal size and the paucity of synaptic connections, they argued, would cause the number of neuron detected in identical cortical slices to be higher (see figure 3). (Note: even the authors did not seemed convinced of this argument and the notion of schizophrenics having greater numbers of cortical neurons seems to be contrary to the subjective perception, even among professionals, that schizophrenics are not only abnormal but subnormal.)



 

COGNITIVE ABNORMALITIES

 

These biological abnormalities, which are clearly not all genetically based as schizophrenia does not have a 100% penetrance rate, and the absence of such biological abnormalities in some sufferers has made it difficult to precisely define accurate markers for the disease.

It has also consistently been shown that there are definite cognitive and attentional differences between both schizophrenia sufferers and their relatives when compared with normal control groups, as will be discussed below in more detail, and yet, in the case of monozygotic twins, there are cognitive differences between twins discordant for schizophrenia. This indicates that there are innate genetic cognitive differences between those disposed to schizophrenia and normals (abnormality) and there is even greater or additional cognitive differences between acute phase schizophrenics and normals (pathology).

Genetic linkage studies have shown similarities between schizotypal personality and schizophrenia (Gras-Vicendon et al,1994) and it has been suggested that individuals with schizotypal personality disorder, which is an  DSM IVAxis II non-clinical condition, may have the very cognitive abnormalities which are indicators of a predisposition to schizophrenia. Examples of the personality features which are a part of the schizotypal disorder, as defined in DSM IV, would be ‘incorrect interpretations of casual incidents and external events’, ‘oddness of speech’ and ‘superstitions or preoccupations with paranormal events outside the norms of their subculture’. Two of the main areas of cognition where  abnormalities have been demonstrated  for schizophrenia sufferers are memory and attention.

The reasons for the memory impairments that are found in schizophrenia have not been clarified and there have been various explanations put forward. These include a failure to spontaneously encode information in a semantically organised way (Koh,1978 and McClain,1983), attentional capacity limitations (Neuchterlein and Dawson, 1984) and impaired executive function(Goldberg et al, 1989). Saykin et al(1991) argued that these memory impairments are selective in nature and are not totally related to attention deficits or frontal lobe impairments but to the temporal lobe-hippocampal memory system. However, almost all of the research showing memory deficits in schizophrenics has involved explicit declarative memory.

Gras-Vincendon et al(1994) found deficits in recall memory but not in recognition memory, frequency monitoring or rate of learning. They noted that long term memory is both explicit and implicit in nature. Explicit memory is assessed by recall and recognition tasks while implicit memory, which does not involve conscious memory, is assessed by noting the degree to which prior learning facilitates performance on given tasks. This can be assessed by repetition priming and procedural learning tasks.

The distinction between performance on implicit and explicit memory can also be different for normal individuals and it has been demonstrated that the role of attention plays an important part in these differences. The main distinction is that explicit memory encoding requires an effort or attention whereas implicit memory encoding requires little effort and requires only enough effort to perceive the stimulus. This was tested in five experiments in which it was shown that divided attention tasks affected both implicit conceptual tasks and explicit  recall and recognition tasks for both perceptual and conceptual encoding but had no effect on perceptual priming tasks (Mulligan, 1998). Given the similarities in attentional effects on memory and the similar deficits shown in memory function in schizophrenia it may well be that it is in fact attention that is the cause of these explicit memory deficits.

Using 24 patients with schizophrenia (all were stable and on typical antipsychotic medication such as chlorpromazine) and 24 matched controls subjects, Gras-Vincendon et al, (1994). conducted an experiment using the following assessment procedures.

1. Free recall - From two sets of 30 words one set was randomly assigned to subjects and they were required to read and then recall as many as possible.
2. Repetition Priming – 3 letter stems from both sets of 30 words were presented and then scores from the new list were subtracted from scores on the old list to give a score for priming effect.
3. Procedural Cognitive Skill Learning - This was accomplished with a version of the Tower of Hanoi test called the Tower of Toronto in which subjects are asked to move 4 disks from the left of three pegs to the right most peg. Each disk is lighter or darker than others and arranged in order of darkness with the lightest on top. They must be moved so that a darker disk is never on top of a lighter one. This requires a minimum of 15 moves. SS’s were allowed a maximum of 50 attempts and two sets of 5 trials 90 minutes apart were conducted.
4. Frequency monitoring – The Rey Auditory verbal learning test was used and SS’s were asked to listen to a list of fifteen words with five of them repeated ie a list of twenty words and then SS’s were asked whether the words were heard once or twice.

This provided two tests of implicit learning (2&3) and two of explicit learning(1&4).

They found that schizophrenics had significant deficits for explicit learning tasks but not for implicit learning tasks when comparisons between schizophrenic patients and normal controls were made. The schizophrenic group also had poorer performance for the Tower of Toronto task but their learning rate over the ten trials was the same as for the control group. This was interpreted as a deficit in problem solving ability, rather than memory or learning capacity, and the fact that explicit memory was affected but implicit memory was unaffected was thought to result from different neurobiological locations for these memories.(they note that tasks which require effort are affected but not automatic processing tasks) . This tends to support the notion that processing capacity may be diminished in schizophrenia but underlying memory systems remain intact.

Gold et al(1992) argued that if attentional capacity is reduced it would be expected that only explicit memory would be affected and the relatively automatic processes involved in implicit memory processes such as recognition memory would be unaffected. This may be the case although recognition memory may also be classified as a form of explicit memory. A further investigation of this will be discussed below. Gold et al(1992) conducted an experiment using recall, recognition and frequency monitoring paradigms, similar to those outlined above, and found that complete memory function, explicit and implicit, was affected. This also included the rate of learning. This study involved 35 schizophrenia patients and 18 control subjects. The patients were all on antipsychotic medication with the exception of one. Because all memory systems were affected similarly they argued that the memory deficits were not caused by a processing capacity deficit. If this had been the case the low capacity required for recognition memory would not have affected this type of memory to the same extent as recall memory. What was not explained was the fact that 22 of the 35 patients were using anticholinergic medication. Acetylcholine is a neurotransmitter that plays a pivotal role in memory processes and it would be expected that even normal subjects taking anticholinergic medication would show memory deficits. Enhancing acetylcholine action by injecting cholinergic agonists into the hippocampus of schizophrenics. It has been shown to reduce the sensory gating deficit, marked by the P50 wave for auditory startle response abnormalities found in schizophrenia. This is an important experimental confound that may well explain the difference between the Gras-Vincendon et al study and the Gold et al study.

Another study (La Porte, Kirkpatrick and Thakar, 1994) found that verbal recall was the same for control subjects with schizotypal personality disorder. They tested whether free recall deficits(verbal and non verbal memory) found in schizophrenic patients (Calev et al, 1983, Calev,1984 and Sengel et al, 1984) were also found in schizotypal personalities.

They used three scales from the Chapman scales originally used to assess schizotypy but now recognised as an assessment for proneness to psychosis.

Perceptual Aberration Scale	Social Anhedonia Scale	Magical Ideation Scale
eg ‘I have sometimes felt confused as to whether my body was my own.’	eg ‘I prefer hobbies and leisure activities where I am on my own.’	eg ‘At times I have felt that a lecture was meant particularly for me.

Subjects were then tested for verbal memory using two short paragraphs   psychiatric first degree relatives in comparison with nofrom theWeschler Memory scale. This has been assessed as the most sensitive test of verbal memory differences between acute schizophrenic patients and normal controls. Subjects were asked to make immediate recall then tested for recall again after 30 minutes. They found no correlation between recall and proneness to psychosis in either the immediate or the delayed recall condition and when the scores for depession and IQ, which were also scored along with ethnicity, were partialled out, it was found that there was a slight positive correlation with proneness to psychosis and better verbal memory. This was even more pronounced in African-American subjects. This tends to indicate that the verbal recall, ie explicit memory, deficits noted in schizophrenia( Neuchterlein and Dawson, 1984) are related to the disease or medication rather than an innate genetic deficit. Another study that used comprehensive statistical and subject assessment methodologies did however detect verbal memory deficits in both schizophrenics and nonrmals(Cannon et al, 1994).

Given that the neurobiological model for memory places great emphasis on longterm potentiation in the hippocampus, a preferred site for supposed morphological abnormalities in schizophrenia, and that,

• Hippocampal LTP occurs at greater levels in schizophrenia.
• Many neuroleptic drugs have as their source of action the hippocampus and this would prevent or decrease the rate of transfer of information to a retrievable long term memory store(Best, 1990,p189)

it would be expected that storage of ‘data’ would be increased in unmedicated schizophrenics and this is consistent with subjective reports of information overload and inability to sort context from the detail. This would indicate that it is the inaccessibility of data and or the inability to encode in an easily retrievable format which is likely to be the basis of any memory deficit. In terms of motivation it may well be seen as a metamemory deficit in that a refusal to learn an effective strategy for recall processes, which are less important to everyday functioning as opposed to academic or intellectual work, results from a desire to minimise the effort that is required for explicit memory and retrieval. As a result schizophrenics tend to rely on recognition and implicit learning processes. This would be more consistent with the peculiarities of thought and ‘magical’ thinking that is often found in schizophrenics and schizotypal personality eg ‘mystical’ intuitive explanation for common occurrences and events.

In summary it appears that implicit memory processes remain unaffected by schizophrenia and that in some cases explicit memory deficits are found but this appears to be more task dependent and may well be a pathological rather than a predisposing factor.

Attention

 

The study of attention in schizophrenia has produced findings which do tend to be regularly replicated among first degree relatives and those with schizotypal personality disorders and this suggests that there is an underlying attentional abnormality not only in those with pathological schizophrenia but also those with a genetic predisposition and that these attentional differences may well be useful as markers for individuals at risk for the disease. The study of attention in schizophrenia has focussed on two areas:

• Selective attention
• Sustained attention

 

Selective Attention

 

The concept of selective attention and its dependence on the processing capacity, as a result of a combination of attention and arousal as outlined in Kahneman’s 1973 attentional model (see figure 4).

 

This is a model that is thought to have a high degree of relevance in explaining selective attentional deficits in schizophrenia(Neuchterlein,1984). Conscious processing is a function of processing capacity but automatic processing is not. The amount of capacity is affected by the level of arousal and the physiological correlates of arousal such as skin conductance response(SCR) is found to be abnormal in those suffering from schizophrenia. This is another indicator that attentional functioning is disordered in schizophrenia(Wieselgren, 1994). The study of selective attention uses approaches such as simple reaction time, choice reaction time, modality shift reaction time, dichotic listening experiments and the Stroop Colour word tests. Variations of these such as reaction time tasks with regular preparatory intervals and irregular preparatory intervals show a crossover effect which usually marks schizophrenia sufferers as while their overall reaction is slower they have an unusual pattern of response in that they, unlike normals, are initially faster with regular preparatory intervals but this crosses over and they become faster with irregular preparatory intervals unlike normals(see figure 5).

 

Examples of studies which support these paradigms are as follows

Simple Reaction Time

1. Schwartz et al(1991) used a simple reaction time test as part of an experiment to assess the relation between negative symptoms and attention. Subjects were asked to press a telegraph key when a tone was heard and at varying periods of 2.5, 3.0 or 3.5 secs a light would be shown and then subjects had to remove their finger. Reaction time was recorded for each movement and then correlations calculated with a negative symptom score taken from the Andreasen scale. The results indicated no relation between positive symptoms and RT but a significant positive relation between negative symptoms and simple reaction time.

2. Frith et al(1988) measured SCR during a forewarned reaction time task that involved a visual stimulus preceded by a warning indicator. An additional irrelevant task was presented ( a 70db tone) either during the warning period or at some other stage. An error was recorded when SS’s responded to the tone. The patients made more errors than controls and controls only made errors when the tone occurred during the warning period. This was consistent with the measurement of SCR which was higher for controls during the warning period and dropped off prior to receiving a new warning. Patients were unable to modulate their arousal level and their constant elevated arousal levels resulted in mistakes when the irrelevant tone appeared before the warning of stimulus onset.

Choice Reaction Time

1. A study by Nestor et al, 1992, investigated the effect of attentional disengagement in medicated schizophrenics. They had noted that previous work had shown that patients with posterior parietal lesions had displayed slowed rates of attentional disengagement and this was demonstrated by the costs associated with invalid cues during a reaction time task. They conducted an experiment using choice reaction time. Subjects were asked to press the left or right buttons of a mouse with the index or the middle finger of the dominant hand when a target(an asterisk) was displayed in either of two white squares five degrees to the left or right of a fixation point that was marked by a cross. On most but not all trials a red light filled one square during the interstimulus interval(ISI). This cue was considered valid if the target then appeared in the same square and invalid if the target appeared in the unlit square. The uncued trials were used as a baseline for reaction times and it had been demonstrated in normals that valid cues resulted in benefits ie faster reaction times compared to uncued trials and invalid cues resulted in costs ie slower reaction times than uncued results.

The results showed that reaction times were approximately 200ms slower in schizophrenics than controls. The benefits for a valid cue were the same for the control group and schizophrenics but the costs for the control group were greater than for the schizophrenic group( see figure 6).

 

They repeated this experiment with the same group of patients using a central cue ie a an arrow pointing to the left or right above the fixation point as this centralised position was thought to reflect controlled processing more than automatic processing when peripheral cues were involved. The results were the same with schizophrenics showing less costs for invalid cues than the normal group but stillbenefitting from valid cues even in the controlled condition. This indicated that schizophrenics did not ignore valid cues and they were still much faster in disengaging attention from a specific target.

2. Liotti et al(1993) using the same approach, but also analysing visual field differences, found that normals showed less benefit from valid cues, compared to schizophrenics, and had costs that were significantly higher than schizophrenics for invalid cues. Once again, however, overall reaction times were significantly slower for schizophrenics (see figure 7).



 

Pre-attention

1. Partial report span of apprehension tasks require subjects to detect targets such as a T or an F presented tachistoscopically in arrays of varying numbers of distractor letters. Schizophrenic patients have been shown to detect fewer target stimuli than controls, including other psychiatric controls, although findings have not been consistent. A study by Granholm, Marder and Asarnow(1996) investigated this using 25 schizophrenics and 25 matched non psychiatric controls. They used 3 letter and 10 letter arrays with a target letter and varied the visual angle by moving subjects closer to the screen and moving the projector as well. They found that controls could detect significantly more targets than schizophrenics.

The analysis of attentional scan paths, which have been shown to be serial in nature, showed that the schizophrenic group used the same pathways as controls, although they both used different scanning paths for the 3 and 10 letter arrays. Schizophrenics, however, failed to reach the last targets in the serial search within the time limits of iconic memory. Schizophrenics have been shown to have normal iconic memory and it was argued that the results indicated a slower initiation of the search procedure and thus they ran out of time to reach the target if it was located at the end of the scan path.

2. Backward masking findings are taken as a measure of processing speed whereas forward masking is used to assess iconic or pre-iconic effects (Saccuzzo and Schubert, 1981). They assessed adolescent schizophrenics and adolescents with schizotypal personality on a backward masking task to investigate whether slow information processing was a trait marker for schizophrenia. They asked subjects to detect a T or an F presented tachistoscopically for 1ms with a pattern mask being presented for either 4 or 6 msec at a range of differing periods after the target had been presented. That is the mask had stimulus onset asynchronies(SOA) ranging from 20 to 360 ms. Schizophrenics made less correct responses and there was no significant difference between schizotypal personality and controls although the trend was for a continuum of performance for schizotypal and schizophrenia types. Schizophrenic performance improved as the SOA’s increased in duration and this was an indication that motivation was not the cause of what was interpreted as slowed information processing.

Facilitation and Interference

1. (Elkins and Cromwell, 1994) noted that the distractibility of schizophrenics has been thought to be the result of a failure to inhibit irrelevant stimuli and sustain focus on the relevant item. Negative priming occurs when there is increased RT to a target that was previously used as distractor but is now the target ie a sustained inhibitory effect is noticed. It has been shown that schizophrenics display less negative priming than controls indicating that schizophrenics are less capable of implementing inhibitory effects and thus screening out irrelevant data. They also noted that semantic priming effects, where word recognition tasks were facilitated by association when a word was preceded by a semantically related word had been shown to be greater in schizophrenia than normal controls. They argued that facilitation and negative priming effects may both indicate a faulty inhibitory system that is responsible for the attentional deficits found in schizophrenia.

They tested schizophrenics, depressed patients and normal controls using a paradigm for assessing inhibition. They argued that if faulty inhibition occurred in schizophrenics then associative facilitation and interference effects would be greater for schizophrenics. Schizophrenic subjects were all on antipsychotic medication except for one of twenty and eighteen of twenty depressed patients were on antidepressant medication. Subjects were asked to identify a target letter or number flanked by either numbers or letters. Sequence on of the trials was as follows:

A+A ABA or 3+3 323 Response compatible(Facilitation)

A+A A3A or 2+2 2B2 Response incompatible(Interference)

*+* *B* or *+* *3* Neutral

Overall reaction time was slower for schizophrenics but depressed patients and controls were not significantly different. It was also found that, contrary to expectations, schizophrenics showed both less interference and less facilitation than both the control and depressed groups. From this it was argued that both facilitation and interference are different processes but the paradigm itself should really be questioned as it is contrary to preattentive strategies which suggest a number is easier to detect among a field of letters, not more dificult and this may result in unintended effects.

2. Taylor et al, 1996 noted that opinion is divided on whether the attentional deficits shown in schizophrenia are a result of dysfunctional automatic processes which are fast, high capacity, parallel and difficult to modify or controlled processes which are serial, voluntary, effortful and of limited capacity. They carried out an assessment of the affects on facilitation and interference using a version of the Stroop task which is regarded as being model for assessing the effects of controlled vs automatic processing. The Stroop task involves naming the colours of colour-words presented to them and reaction time measurements are taken. Normal subjects take longer to name colour-words presented in different colours than they do to name colour words presented in the same colours ie the word ORANGE presented in blue letters will be read more slowly than ORANGE presented in orange colours. Word reading is thought to be automatic and therefore reflect automatic processes whereas controlled processing would be required if the inconsistent colour of a colour word was presented.

This is usually done by cards but is more accurate if an individual trial by trial presentation is used. An earlier study by Carter et al,1992 had found that schizophrenics had no greater interference that normal and had greater facilitation.

The experiment involved 12 patients 10 of whom were using neuroleptic medication and involved using 3 colour words in identical colour, three in contrary colour and three non colour words as a baseline. Once again overall reaction time was significantly slower in schizophrenics and the previous result was replicated in that interference was the same for patients and controls while schizophrenics showed greater facilitation.

Miscellaneous Attentional Differences

Other markers for schizophrenia are noted by Van den Bosch(1994). He notes that in modality shift selective attention paradigms, eg a light followed by a tone, schizophrenics have longer reaction times than normal controls when a light is followed by a tone compared to when a tone is followed by a another tone or vice versa.

He also notes the lack of sensory gating and habituation that occurs in schizophrenics compared to normal. He mentions the eyeblink startle response which involves measuring the eyelid response with an electromyograph to a stimulus such as a puff of air. An initial stimulus will cause a dampening of response to a subsequent stimulus of the same type within a given time frame. In schizophrenics this does not occur. A similar approach using evoked potentials specifically involving auditory tones results in a reduced amplitude P50 wave in normal controls but not schizophrenics.

 

Sustained Attention.

 

Sustained attention is widely used as a means of assessing cognitive deficits in schizophrenia and assessment is carried out using continuous performance tests(CPT)(Van den Bosch,1996) although it is not exactly clear what it is that is being measured. These tests involve continuous demands on the subject to monitor a revolving drum or tachistoscopic presentation and searching for targets appearing every 1-2 secs over an extended period of time, typically about ten minutes in duration, and measures of performance are calculated for the whole period. This can be as simple as detecting a particular letter in a string of single letters or can done so that working memory demands are made eg the target is an X only if it follows an E. The CPT is particularly good at discriminating a particular group of schizophrenics, approx 50%, and is popular for this reason. What is actually measured by this test is not however clear but it is a signal detection task and involves:

-the measure of sensitivity (d’) which reflects the % commission errors and the % of omission errors and

-response bias(b ) which measures the degree of caution or liberality used by subjects in making a decision and

-mean reaction time are the usual measures taken.

Examples of this type of study are noted below.

Continuous Performance Test

1. Finkelstein et al used a continuous performance test to compare schizophrenics and groups at risk for the disorder ie first degree relatives and schizotypal personality as well with normals. They decided to test a group of patients both before the use of medication and on average about six months after they had commenced medication. Relatives of patients including those with schizotypal personality disorder and controls were only tested once.

The task involved a screen display with three adjacent locations for digit displays and all of the digit from 0-9 were randomly displayed in the three position with the relevant target to appear in the middle location. The two lateral digits displayed on any trial are distractors and a response was required whenever a 9 followed a 1 in the middle position. The task took six minutes with a trial every second and display duration was 200 msec.

Tasks like this result in errors of commission and errors of omission(selection) and in this case they used non parametric measures of attentional selectivity(A’) and response style (B") as opposed to the parametric measures of attentional selectivity or sensitivity(d’) and response style(b ).

The results of this study were lacking power due to number of available subjects in some conditions and as such the statistical reliability of some results were questioned by the authors. They found that in spite of a 46% improvement in positive symptoms after medication and a 9% improvement in negative symptoms there was no improvement in CPT results for the patient group. In terms of genetic effects, siblings, especially schizotypal siblings, were found to have similar deficits to patients when compared with controls indicating that a distractor CPT task involving a working memory component may well be an indicator of attentional deficits which are genetic in nature and independent of schizophrenic symptomatology. They also noted that only six longitudinal studies have been conducted along these lines and that only those that have used a simple vs a complex signal detection task, such as a target X, have shown any improvement along with symptom improvement. This suggests it may be a cognitive capacity problem that is the cause of deficits.

2. Another study(Mirsky et al,1995) involved the examination of schizophrenics and their relatives, from a region of west Ireland, in comparison with a normal control group. This was done in a rural region where substance abuse, apart from alcohol intake, was virtually nonexistent. This eradicated a confound that is present in many studies due to the high rate of substance abuse that occurs among schizophrenics.

They used a battery of eight tests for attentional assessment which included a number from the Weschler Adult Intelligence Scale, other neuropsychological measures and a number of versions of the CPT. These had been analysed using principal components and in a number of studies which had replicated the results found four aspects of attention - encoding, focussing-executing, sustaining and attentional shift. Relatives of schizophrenics were divided into two groups, those with other DSM-IIIR diagnoses and those without. The Weschler Vocabulary test was used as a measure of intelligence and intelligence was partialled out to gain a more accurate assessment of attentional differences.

The sustained attentional performance was assessed by using four different versions of a CPT, each increasing in difficulty. This involved a simple target X, an AX task as described above, although without distractors, a degraded target X assessed so that normal controls scored about 80% correct and auditory task involving three randomly delivered tones of differing pitch. The target was the tone with highest pitch.

The results for the four attentional measures - encoding, focussing-executing, sustaining attention and attentional shift - were significantly different(p<.001) between schizophrenics and normal controls with relatives falling between the two. Those with other diagnoses were closer to the schizophrenic performance levels than those without.

In terms of the different CPTs, which were used to measure sustained attention, the between groups results were the same for all versions of the test including the auditory test. Schizophrenics were significantly worse in terms of performance than normal controls . They not only obtained less hits or correct responses than controls they also made more errors.

The increasing effort on the three CPT tasks was associated with increasingly poor performance ie from A to AX to degraded X while about 40% of patients with schizophrenia and relatives with other diagnoses declined to perform the auditory task which was taken as indicating this was the most effortful. The relative attention deficits each category of attention, including sustained are shown below in figure 8.

 



Mirsky et al(1995) made an interesting point noting that the poor performance on the auditory test by schizophrenics relative to controls is mirrored by differences in the evoked potential P300 wave deficits often found in schizophrenics. When auditory stimuli are used as opposed to visual stimuli the deficit in the P300 wave is greater. They asked whether this relates to findings that the brain stem structure involved in auditory processing, the inferior colliculus, has higher metabolic demands than any other cerebral structure. Is this another indication of cognitive exhaustion?

The question of whether effort and motivation do in fact affect performance on the CPT was addressed in a study which referred to the concept of ‘energetics’ as the basis of motivation and related this to the negative symptoms of psychosis(Schmand et al, 1994). This was psychosis in general, not schizophrenia, but the results are enlightening. They refer to a model by Sanders where mental effort is defined as a coordinating and organizing principle that is used to coordinate the activity of arousal and activation. The study was operationalised by using elements from the Sanders model, time on task(TOT) and knowledge of results(KR) factors, and involved 73 psychotic patients and a control group of 23 psychiatric patients with no hint of psychosis at present or historically.

They presented a simple choice reaction task that lasted for 17 minutes during the course of a battery of other tests that lasted up to four hours and then dichotomised the psychotic group on the basis of "energetical" deficits. Analysis had demonstrated that in terms of reaction time, accuracy and subjective rating of effort – which was done simply by asking subjects how much effort was exerted and they quoted studies which showed objective efficacy of this approach - initially there were no significant differences between the groups but as time increased(TOT) for the psychotic group became significantly slower. This lasted until the 13^th min when a feedback bell tone was given to correct responses(KR) but although both groups increased their reaction times they did so equally. This was interpreted as meaning that there was no computational difficulty but rather an ‘energetical’ decrement.

The psychotic group was then sudivided into weak and strong TOT effect groups and using a regression analysis found the best predictor of energetical deficits were negative symptoms(R=0.13) and old age(R= 0.12) and neither medication or positive symptoms explained any of the variance.

Comparisons were then made between the three groups, non psychotic, psychotic with energetical deficit and psychotic with no deficit, on a CPT task, a verbal memory Rey’s auditory verbal memory task and an auditory distractibility task. The auditory distractibility task involved subjects repeating seven neutral series of 6 digits read by a woman interspersed with seven series of 5 digits read by the same woman but with four distractor digits read by a man in between each digit read by the woman. A correct score involved correctly repeating all the digits read by the woman. They used an AX form of CPT and subjects were asked to press a mouse button every time a 7 appeared after a 3.

In terms of sensitivity a deficit was shown by those psychotics with energetical deficits when compared with psychotics with no energetical deficits who in turn were deficient when compared with non psychiatric controls. These findings were replicated for all conditions except the neutral or no distraction segment of the auditory task and the recognition portion of the memory test. In terms of recall and distractibility those with an energetical deficit as defined in the first experiment were deficient when compared to controls and those with no deficit. These findings indicated that controlled processing is impaired but automatic processing was not it was argued.

The longtime observation, using Kahneman’s terminology, that it is not an overall lack of resources ie computational capacity, but rather a quick exhaustion of the resources or capacity that occurs in psychosis and that this is supported by this study. It was suggested that because the KR effect was the same for control and psychotic groups and because initially they performed identically then it must have been actual mental effort that was deficient and there were three possible explanations for this deficit. These are "deficits in arousal, activation or in evaluation".

They argued that they demonstrated arousal cannot be the cause of the deficit because time on task(TOT) deficits in sensitivity(d’) are not demonstrated in most of the CPTs used for schizophrenia research. Exceptions occur for those that have greater demands on capacity such as rapid presentation of target, working memory or degraded target. Activation was also dismissed because it would have led to stereotypy in response and as a result, increasing error rates. This did not happen. If these are not the causes of the deficits it must be the subjective assessments, of subjects with energetical deficits, that they exerted similar effort as the others must be incorrect. This is therefore a deficit in self evaluation which is a fault in meta cognition. They then relate this to Frith’s lack of willed action or willed intention. This would have to be questioned however as it is clear that there are abnormalities of arousal in schizophrenia and that low arousal levels are related to negative symptoms(Van denBosch, 1994) and ‘energetical’ deficts are also related to negative symptoms. This leaves the possibility that arousal levels are deliberately are down regulated in the light of a longer term perspective and performance as such is unrelated to to task demands.

 

Summary of Findings on Attention.

 

The literature on attention and information processing in schizophrenia has consistently found arguments in favour of deficits in either controlled or automatic processing as noted by Taylor et al(1996). The work on schizophrenia is clouded by the confounding factors of substance abuse, medication, genetics and diagnosis but, despite this, a general picture can be drawn.

In terms of the selective attention studies outlined all studies show that overall reaction time is slower for schizophrenics. The studies where facilitation and interference were assessed found no difference in interference between schizophrenics and controls and indeed greater facilitation for schizophrenics in the Stroop tests. Less interference but also less facilitation was found in the Elkins study contrary to expectations. This may have resulted from a bad design in using numbers and letters in combinations that have the opposite preattentive effects from those expected in this study. In terms of disengagement of attention, studies indicated that schizophrenics were faster than normals and that invalid cues had less cost. This would indicate that automatic processing in some form is actually faster in schizophrenics despite the results from the backward masking study. The study by Nestor et al(1992) noted that faster disengagement of attention is indicates faster posterior parietal lobe performance. They also noted that parietal lesions caused slower disengagement of attention. This was confirmed by a study of psychopaths(Raine and Venables, 1988) which showed that faster reaction times are consistent with above average parietal lobe performance. A finding of faster automatic processing in schizophrenics would allow rapid switches of attention, if required, but if not rerquired then greater facilitation would occur as more processing per unit time would be occurring. In terms of the interference and valid cue performance, which it is argued is more dependent on controlled processing, the findings were similar.

This does not explain why the overall reaction time is still much slower in schizophrenics. If we consider that deficient controlled processing is more consistent with negative symptoms and enhanced controlled processing is associated with positive symptoms – this is consistent with the DSM-IV definitions given earlier - then the study by Schwartz et al(1991), which showed that negative symptoms were related to slowed reaction times but not related to positive symptoms, would indicate that the slowed reaction times are the result of a ‘deficit’ in controlled processing.

As had been noted earlier, controlled processes have a limited capacity and are dependent to some extent on arousal ie too much or too little arousal limits capacity in a manner consistent with the Yerkes-Dodson law(Metcalf et al, 1996). It is also noted that faster automatic processing is likely to result in more mistakes. This would result in a psychological impetus to engage in strategies for greater control as a means of limiting mistakes ie consistent and persistent efforts to manage all input in a controlled manner, especially if controlled processing is activated by constant arousal, as has been shown to occur . This would result in a loss of capacity from either over arousal or cognitive ‘exhaustion’ as arousal is a physiological process. This ‘ignoring’ of automatic processing would result in slowed reaction time, but once the focus of attention is directed to the automatic processing occurring in the parietal lobe, functions such as disengagement would still be faster for schizophrenics. This finding is consistent with the interpretation of the span of attention preattentive study where schizophrenics were at least as fast as normals but they took longer to initiate the searching process and the resulting performance in target detection was deficient compared to normals(Granholm et al, 1996).

The relatively consistent findings in the studies which used sustained attention paradigms largely confirm that loads on processing capacity affect signal detection performance. These studies all showed CPT deficits for relatives and schizotypal personality individuals. This was indicative of an underlying cognitive capacity deficit of either a physiological or motivational type that would appear to be a trait marker rather than a result of symptoms. Given that there is a significant genetic component and the deficit is found in those who are not ill, it must have at least some biological basis. The Finkelstein study shows that even when there was a dramatic improvement in positive symptoms and a smaller improvement in negative symptoms following treatment with medication there was no improvement in CPT performance. This indicates CPT deficits observed in tests of a more complicated kind are genetic in nature.

The study by Mirsky et al showed clearly that in terms of sustained attention, distraction and verbal memory, controlled processing but not automatic processing was affected. They also noted that the finding on distractibility, which was not a reaction time task, was thought to relate to positive symptoms. The findings of Schmand et al, were that a rapid decline in processing capacity occurs, but that it is not attributed to an actual physiological decline in resource level. They attributed the decrease in capacity to a misreading of the amount of effort required to carry out the task ie an error of metacognition. This is consistent with the earlier interpretation that I have made. That is, the effort required to remain in a continuous mode of controlled processing must result in decreased capacity and slowed reaction times. This is independent of the reasons, be they physiological or motivational, and there is conflicting experimental evidence as to the motivational status of schizophrenics – backward masking vs CPT. The increased level of error measured by d’ and found in schizophrenics would be expected in a time based target detection task, such as the CPTs used, because schizophrenics are focussed on the slower controlled processes in order to prevent ‘excessive’ speed and the resultant mistakes in automatic processing. The number of ‘mistakes’ are only greater when compared to the general population but this creates a social interaction problem.

The motivational deficits or metacognitive errors that occur in judging the effort to perform a task may result because controlled processing to perform an identical task is actually more difficult in schizophrenics than normals and yet they persist because the results of automatic processing are more prone to unexplained error or perhaps just abnormality. A genetic impact on either automatic or controlled processing such that a loss of confidence in automatic processing as a way of dealing with social situations and context in general would result in an over emphasis on controlled processing. This would cause attentional deficits as measured by reaction time and CPTs and be consistent with the above findings.

 

THE NEUROBIOLOGY OF ATTENTION

 

The basic anatomical structure of the central nervous system, including those structures involved in attention and information processing, are shown below in figure 9.

 

The biological basis of attention has not been clarified definitively but a picture can be derived from the work discussed in Kandel et al (1991) and Mesulam(1990). The locus ceruleus, a brainstem area which sends noradrenergic fibres to most cortical areas, is activated by novel stimuli(p681). These fibres have differing effects in that when they activate b -adrenergic receptors on nerve cells, such as in the hippocampus, they result in increased excitability and activation but in other areas, where they activate a -adrenergic receptors, activation results in a reduction in the firing rate of the nerve cells(p696). In terms of cortical involvement the posterior parietal cortex is identified as the association cortex which responds in terms of visual attention even before the eyes are directed to the object via the frontal eyefields and the superior colliculus. Treisman and others note that the posterior parietal cortex is polymodal association cortex and that attention is dependent on what they identify as the ‘binding problem’.

This is the need to temporarily activate differing groups of neurons at the same time(p459-61) and this includes ‘recruiting’ neurons to focus on the object of interest. Activation of the posterior parietal cortex in relation to a particular object in the visual field may then result in increased activation of cells in the primary visual cortex and subcortical cells involved in directing the eyes to focus on the object. This is described as a ‘winner take all’ strategy. The posterior parietal cortex also has auditory and somatic input and it would be expected that this is the site for initiating all attention, not just visual attention which has been much more widely studied. A typical functional map which demonstrates the involvement of the various areas and role of the posterior parietal cortex is shown below in figure 10.

 



 

There are extensive reciprocal connections between the posterior parietal cortex and the prefrontal asscociation areas and the prefrontal areas are thought to be involved in planning and organisation. The posterior parietal cortex is thought to be involved in working memory however as l large frontal lesions having little effect on intelligence(Kandel et al, p829). While functionality in the brain is widely distributed localisation is also easily demonstrated. Electrical stimulation of the pre frontal cortex(Cai, 1990) and posterior association cortex appear to have no motor or sensory effects whereas stimulation of the temporal lobe areas can create auditory and visual halluccinations(Kandel et al, p829). Lesions of the left temporal lobes result in verbal and auditory learning deficits and lesions of the right temporal lobe result in visual learning deficits(Kandel et al, p830). It is thought that the prefrontal association cortex actually contains a map of the contralateral visual field(Kandel et al, p828) but the failure to stimulate visual hallucinations, as occurs in the temporal lobes, through electrical stimulation may indicate that it is only a map of the connections which can instigate memory retrieval from the temporal lobes.

To understand how controlled processing can interfere with the effects of automatic processing it is necessary to have a better understanding of what is referred to as the ‘perception and action’ or the ‘what and where’ streams of visual processing.

Goodale and Milner(1992) compiled results of electrophysiological, behavioural and anatomical studies and proposed that are were two streams of visual processing:

-the dorsal stream: from the occipital cortex to the posterior parietal cortex.

-the ventral stream: from the occiptal cortex to the inferotemporal cortex.

A diagram setting out both systems is shown below in figure 11

 



Behavioural studies involving lesions to both of these cortical areas indicated that they were involved in spatial cues and pattern recognition respectively. These are related to:

- automatic tasks requiring vision(dorsal stream)

- tasks of visual perception or object and pattern recognition(ventral stream)

Damage to the inferotemporal cortex results in an inability for people to recognise common objects or even faces even though they can navigate through the world seemingly unimpaired. Damage to the posterior parietal areas results in an inability to reach accurately for visually recognised targets which implies more than just an impairment of spatial ability(polymodal association cortex).

They then referred to monkey studies and, while noting that findings from monkey studies can't necessarily be related to humans, the case for relative similarities is understood. Recording from neurons in the posterior parietal cortex showed neurones that were responsive to, not only to space, but visual fixation, pursuit and saccadic eye movements, eye hand coordination and visually guided reaching movements. Neurons in the inferotemporal area however are extremely sensitive to form, pattern and colour. It was noted that these cells could maintain object recognition in the face of changing visual perspectives whereas lesions to the inferotemporal area caused deficits in visual recognition but not in catching flies for example.

They also considered the notion of attention. They thought that it was physically non unitary and applied to both systems, which is more likely than Posner’s view(Posner and Petersen,1990), because attention is not the same as consciousness. They suggest that direct awareness may not be connected with the dorsal system but ratehr a prehension as differentiated from apprehension. They suggested that this lack of direct awareness is a mechanism for preventing interference with the perceptual tasks of the ventral system where access to conscious object recognition and thus apprehension would appear to be located.

To demonstrate this they referred to a study where subjects were required to track a moving light target within a brief time window. They monitored saccadic eye movements and found that if the target moved twice the subjects were unable to acknowledge both movements although eye movements associated with the posterior parietal cortex demonstrated that the attentional system had monitored both movements.

They concluded that it was feasible for conscious awareness to involve the participation of the ventral stream of processing although suggesting that the prefrontal association area is probably the major component in conscious processing. Posner and Petersen(1990) noted that it takes about 80 msecs longer to activate the ventral stream of processing than it does for the dorsal stream to be activated. The dorsal stream makes more mistakes but is faster they also note.

This would seem to provide a possible explanation for some of the attentional deficits or differences found in schizophrenia. The posterior parietal cortex, the superior colliculus and the anterior frontal eyefields are involved predominantly in automatic processing while the inferotemporal, hippocampal and prefrontal areas are predominantly involved in controlled processing. It would appear from experience that a similar process also occurs in auditory processing and auditory pathways travel into the superior temporal cortex as well as to the posterior parietal cortex.

A neurobiological approach to the role of attention and automaticity was outlined by Schneider et al(1994). This also emphasises the different processing areas in the brain involved in effortful controlled processing and the automatic processing which have been shown to be at the centre of the argument’s concerning the basis of schizophrenia. They also argue that the emphasis is on anterior prefrontal cortical activation in deliberate controlled attention relative to posterior parietal functioning when tasks become automatised. The functional areas are shown below in figure 12.

 



This resultant automatisation is explained as the resulting from posterior parietal synaptic connections being strengthened or primed, as a result of task performance, in acordance with Hebb’s synaptic strengthening rule. They note that in schizophrenia, over time, processing continues to be maintained, predominantly, in the controlled mode. This factor, maintenance of controlled processing, would appear to be consistent with some of the reaction time deficits found in schizophrenics’ attentional task performance.

It has been shown that schizophrenics cannot modulate attention and they maintain consistently high levels of arousal during selective attentional tasks(Frith et al,1988) It has also been noted that functionality in the hippocampus increases with arousal but when arousal reaches a critical level, hippocampal processing of information is reduced.

The earlier discussion, that had electrical stimulation of the temporal lobes causing ‘real’ experiences that did not occur in the other association areas, infers that retrievable long term memories are stored in the temporal lobes. The role of the hippocampus in storage of longterm memories has been demonstrated with amnesics, such as HM, where bilateral hippocampal removal was carried out. They have lost the capacity to encode retrievable memories for events that occurred after the damage but not for those that occurred beforehand (Best, 1990, p189).

In terms of the priming which also results from automatic processing it is often thought schizophrenics have excessive priming although many studies show that priming levels are normal. It was suggested that priming might increase above normal when neuroleptics were administered because this slowed down processing. Another interesting possibility is the generator effect (Best, p159). When subjects are asked to generate a word instead of just viewing it, their explicit memory in the form of recognition is enhanced compared to priming effects. However when they do not generate words, but just view them, priming effects are greater relative to recognition effects. If greater priming does occur in schizophrenics as a result of a genetic characteristic it may well result in the continuous processing of information through the non automatic ventral stream. This process would be closer to generation than automatic processing and could be used as a means of diminishing priming effects. This decrease in priming would create social perceptions closer to that of normals but at the cost of the cognitive exhaustion that would result from continuous controlled processing.

Another distinguishing feature of schizophrenia is the age of onset, typically around the age of 20 in males and a little later in females. Is this consistent with the above theory regarding an emphasis on controlled processing? One area of anatomical abnormality that is often found in schizophrenics is decrease in size of the hippocampus(Bogerts et al,1985). It would seem that, as discussed, the hippocampus is involved in controlled processing or at least involved in encoding the information used in controlled processing, longterm memories. It has been noted on a number of occasions that schizophrenics show elevated arousal levels and that this causes increased excitability of hippocampal neurons(Zahn, 1985). Myelination of the hippocampus is not completed until the late twenties(Bencs et al, 1994) and the onset of increased retrievable longterm processing may well be the cause of psychological problems which result in an over emphasis on controlled processing resulting in a pathological outcome. This could be the result of vaso constriction which seems to be associated with hippocampal activation(Sergent,1994).

Metcalfe et al, (1996) notes that the memories related to hippocampal processing are ‘cool’ memories devoid of emotional contamination but automatic processing, which also involves the amygda, results in emotional memories or ‘hot’ memories that can be repressed by the frontal lobes in conjunction with hippocampal memories but this takes effort. This is a biological framework for repression. This appears to be exactly what is happening in schizophrenia except that it is totality of automatic processing outcome that is being suppressed rather than a specific incident.

The genetic predisposition causes high natural arousal levels which activate the hippocampus resulting in unusual controlled processing outcomes such as greater associative learning, as well as a less fluent interaction with the posterior parietal system of automatic processing (see figure 13). This would create the peculiarities observed in schizotypal personality such as difficulties in social context, magical thinking etc. but they still maintain their psychological integrity because they do not try to suppress this abnormality.



 

CONCLUSION

 

Given that thought disorder has been shown to have no genetic basis it would seem that the onset of pathology in schizophrenia is therefore the result of faulty strategies to cope with either developmental factors or social factors facilitated by high arousal levels or other genetic influences resulting in increased neural excitability such as abnormal glutamate receptor expression (Akbaran et al,1995). As arousal levels increase, emotional salience and emotional memories, encoded into the automatic system via the amygdala, create further psychological pressure to ‘flee’ into the controlled mode of processing.

Attempts to ‘generate’ memories or safer realities through the organizational capacities of the prefrontal cortex result in ‘hallucinations’ and ‘delusions’ with a detached over activation of ‘inforamtion’ encoded in the temporal cortex ie positive symptoms. The delusions come from the higher levels of valid spatial and temporal associations that would occur as a result of heightened hippocampal function. It is the interpretation of these associations, especially the erroneous attribution of causality that lead to delusions although it works both ways in that often valid associations in regard to social interaction are denied by others ie there have often been clinical reports where patients say even their own relatives say one thing when they mean another. The distractibility that occurs on attentional tasks would be generated by this focus on internal stimuli.

Negative symptoms result from a downregulation of arousal and this may result from a learned vaso constriction capacity, which often happens after traumatic evnts, and a passive interaction with the ventral stream of processing. This may eventually result in cortical atrophy in the parietal areas(Zahn,1985). The lack of activation of prefrontal areas then allows a slower more deliberate approach to task performance.

This would explain the schizophrenic dependence on concrete, object centred cognition as opposed to the automatic, abstract and socially relevant processing that occurs in the automatic processing mode that is associated with the dorsal posterior parietal lobe. Van den Bosch(1994) quotes a number of patients who talk about cognitive fragmentation.

‘everything is in bits.’ and ‘the picture you had is still there but in bits. You have to put everything back to together again’ and ‘different kinds of sensory input are separated’

This tends to indicate that the binding capacity of the parietal cortex is playing a secondary role to the object perception in the temporal lobe.

If the noradrenergic fibres that activated the parietal lobe neurons did so via the b -adrenergic receptors, which are widely distributed in parietal and prefrontal cortex, we would have a situation that enabled faster performance once focus had returned to the posterior parietal system. This would be consistent with the faster disengagement of attention noted in schizophrenics but the slower activation of this system results from the constant engagement of the ventral of processing. This results in deficits in reality monitoring, central monitoring of action and social contextual judgements, all of which rely on automatic processing.

This biological view is consistent with the attentional data presented and the anatomical data on atrophy does not indicate irretrievable damage from cell death and probably results from vaso constricion either self induced as a slowing mechanism or resulting from uncontrolled excesses of noradrenalin. Acute treatment with drugs should only be short term. A cognitive-behavioural therapy approach which explains the faulty interactions with others as well as activities which stimulate the posterior parietal cortex and nutritional support would seem to be the desired approach. However it may well be that a continuum in terms of the genetic effects means that arousal level is so high that hippocampal activity and processing will create extreme examples and this seems to be the case with autistics.

A final note in that an interesting comparison has emerged between the schizophrenic and the psychopath. While both have poor frontal lobe performance at certain stages, the schizophrenic appears to be deficient in automatic processing(parietal lobe) and the psychopath in controlled processing(temporal lobe). The schizophrenic places spiritual and mystical interpretations on events, has a pathological lack of self awareness and a lack of social ‘grace’. The psychopath is just the opposite and is regarded as materialistic, selfish and socially adroit and manipulative.

 

 

 

 

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                                                        ©Philip Pocock 1998