IJSP-2010(3-4) - Indian Association For Social Psychiatry

Multidimensional Assessment of Psychotic Prodrome (MAPP)
(Yung & McGorry,1996).
Duration of the schizophrenia prodrome
Virtually all patients experience a prodromal phase, which
varies in duration from a very brief period to several years.
Varsamis and Adamson (1971) found a tendency for the
duration of the prodromal phase to be bimodal in distribution:
For some patients it was less than 1 year and for others more
than 4 years. Beiser et al (1993) reported that the prodromal
period was highly variable in length, from none at all to 20
years duration. Loebel et al (1992) found that the time interval
from the onset of prodromal symptoms to the onset of psychotic
symptoms lasts a mean of 98.5 weeks. This time interval was
not significantly different for the schizophrenia and
schizoaffective subjects, and there was no significant gender
difference.
Progression to schizophrenia
Conversion rates depend not only on the inclusion criteria but
also on the population sampled and the treatments applied.
Although conversion to psychosis is considered to be the main
criterion, transitions to other severe mental disorders are also
common but receive less attention. Conversion rates to
psychosis vary across various studies even though the
samples were recruited through comparable criteria. The most
widely used criteria for inclusion for pharmacological pre onset
prevention programmes, the Australian Criteria (Yung et al,
1998), predict conversion to psychosis with approximately 50
percent probability within 1 year under naturalistic treatment
conditions, as shown in the table 3.
Table 3
Neurodevelopmental issues
Siddiqui et al
Pantelis et al (2003) reported striking baseline differences in
regional gray matter volume between those who subsequently
developed a psychotic illness and those who did not;
specifically, those who developed psychosis had less gray
matter in the right medial temporal, lateral temporal inferior
frontal cortex and in the cingulate cortex bilaterally. In the
longitudinal comparison, when rescanned, individuals who
had developed psychosis showed a reduction in gray matter
in the left parahippocampal, fusiform, orbitofrontal cerebellar
cortices and the cingulate gyri, whereas longitudinal changes
were restricted to the cerebellum in those who did not become
psychotic. Such a progressive developmental pathophysiology
of the illness during adolescence may result from several
factors working singly or in combination.
First, genetic factors may predispose to an excess synaptic
elimination, increased neuronal apoptosis, decreased cell
somal size, or a combination of these processes during
adolescence. Such changes might result from altered
expression of genes that are critical for neurodevelopmental
processes such as glutamatergic NMDA receptor expression
(Olney & Farber, 1995), brain-derived neurotrophic factor levels
(Nawa et al, 2000), or altered dynamics of dopaminergic and
GABAergic neurotrans-mitter systems .
Second, hormonal changes, especially of the reproductive
steroids, could modulate brain maturational processes such
as synaptic pruning and/or myelination (Amateau & McCarthy,
2002). This possibility is supported by observations that agerelated
gray matter volume reductions during adolescence in
Study Inclusion criteria Conversion rate
Yung & McGorry, 1996 1) Psychosocial decline with positive family,
or 2) two DSM-III-R prodromal symptoms,
or 3) schizotypal or schizoid personality
21% in 20 months
Yung et al, 1998 1) BLIPS, 41% in 12 months,
or 2) subthreshold psychiatric symptoms,
or 3) psychosocial decline with positive family history
50% in 24 months
Cornblatt & Malhotra, 2001 Identical with Yung et al, 1998 14% after 6 months
McGlashan et al, 2001 Identical with Yung et al, 1998 54% in 12 months
Klosterkotter et al,2001 Two cognitive "basic symptoms" in subjects with mental state at risk 59% in 6-9 years, 97% with variable length
of state at risk follow-up period (mean 9.6 yrs)
© 2010 Indian Association for Social Psychiatry 105