Anosognosia and the very idea of psychodynamic neuroscience by Andrew Sims BA.

259 Pages·2015·2.24 MB·English

by  Andrew Sims

Anosognosia and the very idea of psychodynamic neuroscience

by

Andrew Sims
BA. (Hons.) BSc.

Submitted in fulfilment of the requirements for the degree of
Doctor of Philosophy

Deakin University
September, 2014

Acknowledgments

I couldn’t have finished this dissertation without the support of my parents, friends,
teachers, and colleagues. Professional acknowledgments are due in particular to
Russell Grigg, for his thoughtful supervision; Jim Hopkins, who introduced me to the
neuropsychoanalysis group in London and the psychoanalysis unit at UCL and who
was always very generous with his time and advice; Tamas Pataki, Matthew Sharpe,
and Geoff Boucher, who assisted with some friendly criticism and discussion of this
dissertation’s themes towards the end of writing; and Leonardo Nascimento, who is
responsible for getting me interested in the historical story that makes
psychodynamic neuroscience intelligible in the first place. Most of all though I
would like to thank my partner Ash Reynolds, without whom I would not be writing
these acknowledgments at all.
Contents

0. Introduction: why psychodynamic explanation? ................................................. 1
0.1. The poverty of cognition alone ............................................................................. 1
0.2. How does cognition interact with emotion and motivation? ................................. 5
0.3. The project of psychodynamic neuroscience ........................................................ 6
0.4. The thesis ............................................................................................................... 9
0.5. The argument ....................................................................................................... 10

1. Psychodynamic explanation and the unity of science ....................................... 15
1.1. Is psychoanalysis autonomous? ........................................................................... 15
1.2. Internal meta-theory: psychoanalysis is an extension of commonsense
psychology .................................................................................................................. 25
1.3. External meta-theory: the relationship of psychoanalysis to other disciplines ... 40
1.4. Concluding remarks ............................................................................................ 58

2. Psychodynamic explanation and its metapsychological commitments ........... 61
2.1. A classic example of psychodynamic explanation, and its philosophical
interpretation .............................................................................................................. 64
2.2. How might AHP be psychodynamically explained? ........................................... 84
2.3. Metapsychology and the role of mechanism ....................................................... 86
2.4. Metapsychological commitments of psychodynamic explanation ...................... 90
2.5. Concluding remarks ............................................................................................ 95

3. Predictive processing and the circumstances of wish-fulfilment ..................... 97
3.1. Freud and free energy: an early attempt to mechanize wish-fulfilment .............. 99
3.2. Predictive processing and the free energy principle .......................................... 106
3.3. Psychodynamic mechanisms in the free energy view of the brain .................... 124
3.4. Concluding remarks .......................................................................................... 134

4. Drives, priors, and the opacity of wish-fulfilment ........................................... 137
4.1. What are the drives, and what do they do? ........................................................ 140
4.2. Accommodating drives within the free energy framework ............................... 165
4.3. Concluding remarks .......................................................................................... 171
5. A neuropsychodynamic theory of anosognosia for hemiplegia ..................... 173
5.1. A comprehensive overview of the phenomenon to be explained ..................... 175
5.2. Cognitivist theories of anosognosia: their merits and limitations ..................... 188
5.3. Psychodynamic theories of anosognosia: their merits and limitations ............. 195
5.4. Removing objections against a neuropsychodynamic theory of anosognosia for
hemiplegia ................................................................................................................ 205
5.5. Concluding remarks .......................................................................................... 218

6. Conclusion: the very idea of psychodynamic neuroscience ........................... 220

References ............................................................................................................... 223
1

0. Introduction: why psychodynamic explanation?1

0.1. The poverty of cognition alone
0.2. How does cognition interact with emotion and motivation?
0.3. The project of psychodynamic neuroscience
0.4. The thesis
0.5. The argument

0.1. The poverty of cognition alone

In some patients who suffer damage to a particular region of their right
cerebral hemisphere, they suffer a peculiar malady that seems to have two
components. The first component is a paralysis on the left side of the body,
which often co-occurs with a neglect on that side – an inability to attend to and
engage with objects in the affected part of the visual field.2 The second
component is an inability to recognize these impairments, as well as a tendency
to go to great lengths in order to deny them – sometimes to the point of
denying ownership of the affected part of the body, or trying again and again to
walk unassisted when their paralysis makes this impossible. This inability to
recognize one’s symptoms does tend to subside after the acute phase of this
condition, and is often replaced by a curious emotional attitude towards the
affected part of the body which ranges from benign disinterest to intense
hatred. The condition is sometimes called right parietal lobe syndrome, but
most often all of these symptoms are assimilated to the label of “anosognosia
for hemiplegia.” (AHP)3

1 I will be using both “psychoanalytic” and “psychodynamic” to denote the style of explanation
which is at issue in this dissertation. The difference between these has been thought to come
down to the specificity of the former in comparison to the latter; psychoanalysis involves
clinical treatment five days a week along lines close to what Freud originally practiced, but
psychodynamic therapies cover a wider range of different theories and methods (Cf., Shedler
2006: 9-10). The relatively small differences between psychodynamic treatments will not be
relevant here, since I establish a specific view on the general structure of psychodynamic
explanation in chapter two (and I am not primarily concerned with the clinical efficacy of
psychodynamic treatment).
2 However, there is no necessary connection between anosognosia and neglect, and there are
cases in the literature for which these are dissociated (Jekhonen et al. 2000).
3 The nosology is in fact slightly more complicated than this, since the condition is comprised
of a number of symptoms that do not always occur together. The denial of paralysis itself is
anosognosia for hemiplegia, the delusion that the damaged limb does not belong to the patient
is somatoparaphrenia, and the existence of distorted emotional attitudes towards the deficit is
2

The impetus behind this thesis is a related set of questions about how to
explain conditions like these. For example, what roles are emotion and
cognition each playing in this illness, and how can we distinguish between
them? In order to elucidate this query a provisional definition is in order. I am
referring to the emotions both in their neuropsychological and
phenomenological aspects. That means I am referring to the way that the
emotion feels as well as to the physical structure (in the brain, at least) that is a
necessary condition for its existence. I will, however, sometimes explicitly
distinguish between these physical and phenomenological aspects.
Furthermore, I include the behavioural, perceptual, and cognitive aspects that
are often also taken to be constitutive of the emotion. By cognition, I mean all
thought that is evaluable in terms of truth-conditions; what that means is that
cognitive tokens have conceptual content – they represent the world in the
same way that language represents the world.4 These initial definitions are not
perfect and will become clearer over the course of the thesis, but they will do at
this point.

Back to the initial question: what roles are affect and cognition playing
in AHP, and can we make them conceptually distinct in explanations of that
illness? For example, can we eschew emotion entirely in the aetiology of the
illness by understanding it as being solely caused by cognitive deficit? That
kind of explanation would seek to elucidate the illness in terms of mechanisms
that can no longer perform their proper function and so produce the
pathological phenomena though their breakdown. One example of this
explanatory strategy is that of Cutting (1978), who suggests that for many
anosognosics it is in virtue of a failure to integrate information about the body
into judgments about impairment – this failure being caused by the neglect –
that the patient cannot recognize their deficit.

anosodiaphoria if the attitude is indifference and misoplegia if the attitude is hatred. See Orfei
et al. (2007) for a relatively recent review that elucidates this clinical variability in more detail.
4 This might seem like a non-standard definition of what cognition is, whereas what might
seem more appropriate is mental activity that can be understood in terms of information-
processing. The reason I opt for this one is that I wish to include personal-level states like
delusional beliefs attributed by the clinician that may be the result of information processing
but which are not themselves information-processing states in the sense meant by cognitive
scientists.
3

The theory proposed by Cutting is what philosophers call a “one-factor
theory” of the anosognosia. The distinction between one-factor theories and
two-factor theories is one that originates in the study of delusions (e.g., Davies
et al. 2001). A one-factor theory of delusion is one that explains it to be a
normal cognitive response to an unusual experience brought on by some kind
of sensory or cognitive deficit. In the case of AHP, a simple one-factor theory
of the condition would posit that the denial of paralysis is a normal cognitive
response for somebody who lacks proprioceptive information about or who
cannot attend to the paralysed limb. The deficit causes an unusual experience,
which causes the agent to form a false belief about the state of the body. It is,
on the theory, a reasonable belief to form under the circumstances of the
deficit. The only pathogenic cause that is present according to this one-factor
theory of anosognosia is the deficit (for example, in the mechanisms of
attention), and it is thought that this deficit alone is enough to explain the
subsequent delusion in conjunction with ordinary processes of belief fixation.

The flaw in single factor theories of the condition is that the
neuropsychological deficit is not a sufficient condition for the illness, either
descriptively or normatively. It is not descriptively sufficient because there are
people who have the same cognitive deficit that do not have the anosognosia.
For example, and with reference to Cutting, it has been found that neglect and
anosognosia for paralysis “double-dissociate”; we can find each symptom in a
patient along with an absence of the other. (e.g., Jehkonen et al. 2000) The
single factor is not normatively sufficient for the delusion either. What that
means is that although an unusual experience caused by deficit might give rise
to a candidate belief that seems particularly salient or plausible due to that
experience, it does not explain why this belief is accepted despite other
evidence to the contrary; some examples of contrary evidence might be
testimony from the examining doctor or nurses, or visual evidence that one’s
paralysed arm is not moving. And it does not explain why the delusional belief
persists as this evidence accumulates.

By contrast, the “two-factor theory” of anosognosia posits a second
pathological factor in the genesis and persistence of the condition. One theory
4

of this type is that of Davies, Aimola Davies and Coltheart (2005). The first
factor in their theory is the neuropsychological deficit that leads to an unusual
experience eliciting a false belief about the state of the body. They suggest that
the second factor in the right theory of anosognosia will be a deficit in belief-
evaluation processes, and that this will account for the persistence of the
anosognosia. This is a theory of anosognosia that continues to explain it in
terms of cognitive deficit, but that explains it in terms of two cognitive deficits
(or maybe two types of deficit, since each factor may well include more than
one functional deficit) that together produce the anosognosia.

Now, there is a further debate about the nature of the second factor in
anosognosia. More specifically, it is a debate over the nature of the second
factor with respect to the distinctions between cognitive, affective, and
motivational states. For example, is the anosognosic patient’s failure to update
his delusional beliefs in response to contrary evidence the result of a deficit in
the cognitive mechanisms that govern evaluation of belief, or does he maintain
these beliefs because (say) the motivation to hold these beliefs is
overpowering? Early theories of anosognosia gave a central explanatory role to
motivational factors. Weinstein and Kahn (1950), for instance, hypothesized
that denial of illness was a generalized defensive reaction against the negative
emotion that acknowledgment of illness would cause. But theories of this kind
have seriously fallen out of favour since the uptake of theories that purport to
fully explain the illness in terms of cognitive deficit.

One-factor or two-factor, a theory of anosognosia that relies exclusively
on cognitive deficit for its explanation will just not do.5 This view will be
defended more substantially against various objections in chapter five of the
thesis, and I introduce it only in order to discuss the problems that
motivationally-based explanations of pathology must face. But here are some

5 My claim here is not, however, that all cases of anosognosia for hemiplegia must be
explained in terms of motivation and emotion. That seems pretty clearly untrue, and I suspect
that there are many subsets of the clinical population with anosognosia whose illness could be
explained without drawing on these factors (e.g., along lines suggested by Aimola Davies &
Davies (2009)). The claim is rather that these factors (emotion and motivation) are needed to
explain some cases, and therefore that we need a more general account of how it is that these
factors could come to play a role in such illnesses. I am claiming that cognitive deficit accounts
are insufficient to account for all cases of anosognosia on their own.