So, first up Schizophrenia is a syndrome of psychosis.
Psychosis is a very broad term which covers a range of phenomenon which result
as a problem with ‘reality testing’. As said previously the symptoms of
this disorder are broadly lumped into ‘positive’ (things that are added in;
perceptual abnormalities, delusions) and ‘negative’ (things that are taken
away; poor motivation, blunting of affect). When people are ‘unwell’ they tend
to be experiencing predominantly positive symptoms. These can be highly
distressing and disruptive for the individual and may lead to hospitalisation.
When people are ‘well’ they experience less positive symptoms but may be very
disabled by negative symptoms. They may require a great deal of support as, for
example, they may not take care their food, finances or personal care.
The term paranoia in the psychiatric sense is used to describe
interpreting things around you as being related to yourself, i.e. having delusions
of self-reference. It may include thoughts of persecution but it does not refer
to them exclusively. So delusional thoughts of being monitored and tracked by a
shady government organisation which is bent on ruining you by framing you for
some heinous crime is a ‘paranoid’, but so too is holding the delusional belief
that you are on a special mission to stop terrorism and the strangers on the
bus are really fellow agents sending you subtle secret messages by holding
their telephones a certain way or glancing at you from time to time.
Delusions in general can either be primary or secondary.
Secondary delusions follow on from abnormal experiences. If you hear people
muttering through the walls, have an uncanny sense of being watched all the
time and feel threatened you may conclude that you are being spied on by people
who mean you harm. In these cases I find it striking how delusions are really
just a rational mind trying to make sense of highly abnormal experiences. These
delusions can become highly detailed and complex. They also tend to be very
representative of people’s social context. I’m lucky enough to own a copy of a
book called ‘Presumed Curable’ which is a set of case studies, accompanied by
photographic portraits, of patients admitted to Bethlem Hospital in the late 19th
century. Spies of the Kaiser, nobles and religious miracles abound. During the
latter half of the 20th century aliens and spacemen hounded our
psychotic patients. Now they are increasingly tormented on social media. It’s
fascinating how the content of delusional thought shifts over time and across
cultures whilst the underlying cognitive errors remain static. Primary
delusions are those which appear to just appear de novo without any other
apparent psychotic phenomenon driving them.
As to why. I’ve got no choice but to be even more
reductionist here that I already have been. First up: chemicals. Brain
chemicals, neurotransmitters. The neurochemical theories of Schizophrenia are
essentially exercises in reverse engineering. This has important implications
for proclamations about the aetiology of psychiatric illnesses but also should
not led us, in my view, to dismiss the utility of such drugs. The drugs used to
treat the positive symptoms of Schizophrenia are essentially dopamine blocking
agents. Dopamine is the primary inhibitory neurotransmitter in mammals. The
first ‘antipsychotic’ developed was Chlorpromazine. This was synthesised in the
first half of the 20th century on the back of another drug,
Promethazine, which had been developed as an antihistamine (I used to love to take this drug for sedation and its antihistamine properties, doubling or even tripleing the recommended dose unitl it gave me akathsia prompting me to be kicked out of bed - not good for morale) The sedative
effects quickly became apparent and these drugs were initially utilised for surgical
procedures. Soon they were given to psychotic patients and the effects appeared
dramatic to those using them. Remember that up until this point patients were
commonly treated (or rather ‘brought under proper control’) with ECT (a safe
and effective treatment to this day!), psychosurgery (neither safe nor
effective, barbarism), insulin coma therapy (utter madness), seclusion and
physical restraint. The dopamine hypothesis was born. Too much Dopamine made
you psychotic, blocking dopamine made Schizophrenics better, right?
The
evidence for this hypothesis is really shaky. People really do get better when
given antipsychotics (in terms of psychosis anyway) and we know these drugs
primarily block dopamine. We know that if you pump someone full of cocaine their dopamine levels increase and they can become psychotic. We know that if we
treat Parkinson’s patients with Levodopa (a dopamine precursor which is able to
cross the blood-brain barrier) they can become psychotic. Cerebro-spinal fluid
examination of psychotic patients shows homovanillic acid (a dopamine
metabolite) levels correlate with the severity
of psychosis but not with the psychosis
itself.
Ropey stuff indeed. Is it likely that the most complex know object
in the universe can malfunction? Yes. Is it likely that this is due to one
single chemical imbalance? I very much doubt it. Do antipsychotic drugs have
utility in the treatment of psychosis? Absolutely, but let us not kid ourselves
that we know why that might be. Other neurotransmitters, such as Glutamate,
have been the target of antipsychotic drug development but these avenues have
not born fruit. How might all this help us unlock paranoia? I personally don’t know enough to join the
dots other than to say that positive symptoms in Schizophrenia have been
related in functional MRI studies to disorders of the medial prefrontal cortex
(executive functioning, attention and theory of mind), amygdala (fear) and hippocampus/para-hippocampal
region (memory and spatial awareness) and that signalling problems in these
areas probably leads to changes in cognitive processes which end up looking,
phenotypically, like psychosis. I’m not trying to be a smart arse, throwing
around neuroanatomical jargon here, as my view is that this sort of stuff lends
us precious little understanding of what is happening and why.
The second way to approach this issue is to look at psychological
or cognitive errors. Liddle (1987) proposed three clinical syndromes of
Schizophrenia, one of which was that of ‘reality disturbance’. Liddle et al
found regional cerebral blood-flow correlates in the left medial temporal lobe
and cingulate cortex which led to impairments in an individual’s ability to
‘self-monitor’ and experience delusions and hallucinations. Think of it as the
system which ‘tells you’ that your internal monologue is just that, breaks.
Random intrusive thoughts become critical ‘third person’ auditory
hallucinations (he’s so stupid), thoughts about what you are doing become a
‘running commentary’ (he’s buttering his toast again), intrusive thoughts or
thoughts about genuine desires may become ‘command hallucinations’. This may
seem more related to the first point about chemicals at first but it is a
really important concept. The ability to appropriately self-monitor one’s own
thoughts, emotions and bodily sensations is vital if one is to properly make
sense of this information. The concepts of ‘self’ and ‘other’ break down in
psychosis. Some people speak of their minds becoming porous during psychotic
episodes. Humans are already seriously prone to magical thinking, attribution
errors and biases. If the areas of the brain which regulate an individual’s
ability to monitor their own internal experiences malfunctions and the ability
to accurately determine other people’s thoughts, emotions and intent go awry,
it seems logical to me that correlates are increasingly perceived as
causatives.
People tend to be a bit mad in any case,,
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