Creativity & Schizophrenia
Antonio Preti
THE
ALIEN MIND
Schizophrenia
is a psychosis, i. e. a mental disorder which implies a severe distortion of
reality testing: its course is greatly influenced by social and
economical factors far removed from the clinical side of its nature (Zubin and
Spring, 1977; Hirsch, 1986). Schizophrenia involves high costs for patients,
their families and society: direct costs of schizophrenia are mainly due to
hospitalization and medical services. Indirect costs are due to loss of
productivity and time spent by care-givers.
The
clinical symptomatology can be traced back to the ex novo appearence of
distortions in perception, such as illusions and hallucinations, and of thought
disorders leading to delusions (Waddington, 1993; Carpenter and Buchanan, 1994;
Andreasen, 1995). For a proper diagnosis of schizophrenia the symptomatology
should be independent of concurrent ingestion of a drug and from the presence of
a metabolic disease leading to alterations in cerebral neurochemistry (Andreasen,
1995). Generally the clinical picture of schizophrenia is associated with severe
impairment of social and occupational functioning with a negative outcome in
between 30% and 50% of cases, sometimes developing into dementia (Waddington,
1993; Carpenter and Buchanan, 1994).
“Dementia
Praecox” is in fact the name coined by the the turn-of-the-century German
psychiatrist Emil Kraepelin (1919), who was the first to isolate the disorder
now called schizophrenia from among the myriad syndromes that crowded the
treatises of the positivistic era. Kraepelin, on the basis of his observations,
distinguished the psychoses with a recurrent decourse and a conservative outcome,
which he put in the same group as cycloid psychoses (called by him
“manic-depressive illness“), from the psychoses with a progressive and
negative decourse (which he indicated with the name “Dementia Praecox“).
Kraepelin considered the outcome of this last disorder to always be negative,
biased as he was by his own position as academic psychiatrist and chairman of a
centre of excellence in which he had access to more severe cases, and living as
he did in an age without therapy for mental illness other than the containment
and shock treatment. In Kraepelin’s day, the only drugs used were laudane (opium),
belladonna (atropine, an anticholinergic) and a few other substances, generally
with a high toxicity. The impression of incurability of mental illnesses was
widespread, and most mental disorders were considered to have an unfavourable
outcome. Kraepelin was so convinced of the irreversible decourse of the disorder
now called schizophrenia, that when, during a study in Java, he observed more
favourable outcomes, sometimes even complete recovery, he was enormously
impressed (a recent replication in Leff et al, 1992).
Less
biased by the «illusion of the clinician» (as the tendency to overstimate
one’s own observations is called by epidemiologists) the Swiss Eugen Bleuler
(1911), who held the chair of “Burgholzi”
Psychiatric Hospital, where such eminent psychiatrists as Jung worked, offered a
redefinition of the concept of the psychoses coining the word
“schizophrenia“ (= broken mind) to indicate what was for him the most
relevant aspect of Dementia Praecox:
i. e. the loosening of mental
associations. For Bleuler
schizophrenia is characterized by an alteration of mental associative functions
with a concurrent, and consequent, emotional instability, resulting in
anaffectivity and autism (closure in oneself). For him hallucinations and
delusions were subsequent to the loosening of mental associations, and were
without influence on the outcome of the disorder, which was, even in his new
formulation, severe and generally bad.
The
symptomatology of schizophrenia remains manifold and includes many different
behavioural patterns, predominantly disorganized and inappropriate behaviour and
speech, loss of will and drive, and a generalized lessening of the ability to
express emotions (Andreasen, 1995;
Schultz
& Andreasen, 1999). Positive symptoms, involving excess or
distortion of normal functions, tend to fluctuate over time, whereas negative
symptoms, involving loss or diminution of normal functions, seem to be more
stable and to be less responsive to treatment (Andreasen et al, 1995; Arndt et
al, 1995;
Schultz
& Andreasen, 1999). A three dimensionsional model
(namely, positive, negative, and disorganized symtoms) now appears to be a
better description of schizophrenic symptomatology than the preceding
positive/negative dichotomy, but there is little agreement on the neural
mechanisms that generate these symptoms (Crow, 1985; Andreasen et al, 1995;
Johnstone and Frith, 1996; Schultz
& Andreasen, 1999). Studies performed with neuroimaging techniques
indicate that brain abnormalities (namely signs of cerebral atrophy) may be the
basis of schizophrenia, but the extent of such abnormalities depends on the
characteristics of the control groups (Andreasen et al, 1990). Educational and
social premorbid adjustment is often poor in schizophrenic patients, leading
precociously to defective relational abilities (Jones et al, 1994; Done et al,
1994).
Neuropathological
studies suggest that schizophrenia may result from lesions involving a
neurodevelopmental process (Weinberegr, 1995). The main support for this
assertion is the lack of gliosis in histological investigation: gliosis occurs
after many brain injuries and neurodegenerative conditions, but is not observed
after events that occur early in development. Epidemiological studies support
the genetic transmission of the risk of schizophrenia (Mc Guffin et al, 1995;
Portin and Alanen, 1997), but this genetically enhanced risk seems to consist in
a greater vulnerability to environmental factors acting in the perinatal period,
such as complications in pregnancy and at birth
or exposure to viral agents (Preti et al, 1998; Preti and Miotto, 2005).
The
final step in the pathogenesis of schizophrenia appears to be a distortion of
the systems involved in modulation or integration of information processing (Braff
and Geyer, 1990; Frith, 1992). A key role for dopaminergic pathways is suggested
by the therapeutic efficacy of dopamine blocker agents, but , as the development
of new “atypical“ neuroleptics with greater effects on serotonin indicate,
many other neurotransmitters could be implicated in the defects in information
processing.