VOL. 15, NO.
4, 1989
Sluggish Schizophrenia in
the Modern Classification
of Mental Illness
by Anatoly B. Smulevich Abstract
The concept of latent schizophrenia
was developed by E. Bleuler (1911)
and was further promoted in the
studies of a number of research
psychiatric schools of Europe, the
United States, Japan, and other
countries. In Soviet psychiatry,
there is a long-established tradition
of studying "soft" forms of schizo-
phrenia (Kerbikov 1933; Rozen-
shtein 1933; Brukhanskii 1934). In
the systematics of schizophrenia,
developed by Snezhnevsky (1969)
and his colleagues, sluggish
schizophrenia is viewed not as an
initial (prodromal) stage of
schizophrenia, but rather an in-
dependent diagnostic category
characterized by a slowly pro-
gressive course, subclinical
manifestations in the latent period,
overt psychopathological symptoms
in the active period, and then by a
gradual reduction of positive symp-
toms, with negative symptoms
predominating the clinical picture
during patient stabilization. Studies
are reviewed examining the rela-
tionship of constitutional and
genetic factors to the clinical mani-
festation of sluggish schizophrenia.
Finally, the importance of methodo-
logical considerations and an
examination of divergent factors in
the U.S. and Soviet concepts of
schizophrenia are presented.
The study of the hidden, latent
forms of schizophrenia, which had
its origin in the research of E. Bleuler
(1911), was further developed by a
whole group of psychiatric schools
in Europe, the United States, Japan,
and other countries. Descriptions of
insidiously developing forms of the
endogenous process, which are fully
comparable to the Soviet concept of
533
sluggish schizophrenia, were cate-
gorized under various designations
for example, abortive, ambulatory,
and nonregressive schizophrenia
(Gaupp 1938; Zilboorg 1956; Nyman
1978).
In American psychiatry, especially
during the WSO's and Vi&ffs, the
problem of pseudoneurotic schizo-
phrenia was intensively investigated
(Hoch and Polatin 1949; Hoch and
Cattell 1959; Hoch et al. 1963). Dur-
ing the last decade, research atten-
tion to this problem has been in
connection with clinical genetic
studies on the disorders of the
schizophrenia spectrum (the concept
of borderline schizophrenia of
D. Rosenthal [1971], S.S. Kety [1971],
and others).
In Soviet psychiatry there is a long
tradition of the study of "soft" forms
of schizophrenia by Kerbikov (1933),
Rozenshtein (1933), Sukhareva
(1933), Brukhanskii (1934), Friedman
(1934), Melekhov (1963), and others.
In the system of schizophrenia
developed by A.V. Snezhnevsky
(1969), and his colleagues, sluggish
schizophrenia is an independent
form (Nadzharov and Smulevich
1983). In a large sample of schizo-
phrenic patients (Zharikov et al.
1973), 38.1 percent of patients in the
sample were diagnosed as suffering
from sluggish schizophrenia.
Statistics on the incidence of slug-
gish schizophrenia in the population
of the U.S.S.R. range from 1.44:1000
(Gorbatsevich and Boyarintseva
Reprint requests should be sent to Dr.
A.B. Smulevich, All Union Research
Center of Mental Health, Kashirskoye
Shosse 34, Moscow, U.S.S.R., or the
Schizophrenia Research Branch, National
Institute of Mental Health, Parklawn
Bldg., Rm. 10C-06, 5600 Fishers Lane,
Rockville, MD 20857.
534
1985) to 4.17:1000 (Zharikov et al.
1973) to 5:1000 (Dubnitskaya 1987).
Within the framework of the
schizophrenic disorders, the slug-
gish form is by no means an initial
(prodromal) stage in the manifesta-
tion of the schizophrenic psychosis,
but an independent diagnostic
category (Smulevich 1987). The
stereotypical development of the
sluggish form, in keeping with the
general nature of endogenous
diseases, is characterized by a slowly
progressive course. The course of
the disease is characterized by
subclinical manifestations in the
latent period, overt psychopatho-
logical symptoms in the active
period (a continuous course, an at-
tack, or a series of attacks), and then
a gradual reduction of positive
symptoms, with negative symptoms
predominating in the clinical picture
during the period of stabilization.
It must be emphasized that one of
the cardinal signs of sluggish schizo-
phrenia is the gradual change in
symptoms from the least differen-
tiated in the sense of nosological
specificity (the latent period) to
more characteristic symptoms in the
active period and the period of
stabilization.
The pivotal symptomsobses-
sions, somatoform symptoms, and
disturbances of self-consciousness
that occur in conjunction with
symptoms of a defectdefine the
clinical picture and persist through-
out the course of the disease despite
the fact that psychopathological
complexes (syndromes) are
changing.
On this basis, within the frame-
work of sluggish schizophrenia,
clinical studies have defined several
variants in which either pseudo-
psychopathic or pseudoneurotic
symptoms predominate (asthenic,
hysteric, obsessive-phobic, deper-
sonalizing, or cenestohypochondrial),
as well as variants characterized by
paranoial or negative symptoms
(sluggish "simple" schizophrenia).
The classification of sluggish
schizophrenia presented above is
supported by the results of specially
targeted clinical-genetic research
(Dubnitskaya 1987). The endo-
genous, progressive course of slug-
gish schizophrenia reflects the basic
features of its genealogical character-
istics: in cases of sluggish schizo-
phrenia, as in other endogenous
forms, the families of probands
show an increased incidence of
schizophrenia spectrum disorders as
compared to the general population.
This statistically significant familial
association between sluggish
schizophrenia and other forms of
schizophrenic psychoses makes it
possible to consider all these forms
within the framework of the general
genetic system of which they form
a part.
Sluggish schizophrenia may be
viewed as a relatively independent
form, intermediate between the
schizophrenic psychoses and per-
sonality disturbances. The ratio of
schizophrenic psychoses is signifi-
cantly lower among the relatives of
probands with sluggish schizophre-
nia than among the relatives of pro-
bands with more floridly psychotic
forms of schizophrenia. However,
the relatives of sluggish schizophre-
nic probands show a wider range of
forms of personality disordersof
the schizoid type and all other
major types. The frequency of per-
sonality disorder among first-degree
relatives of the sluggish probands
is higher than in the general
population.
The contribution of constitutional
personality genetic factors to the
genesis of sluggish schizophrenia
can be seen in the tendency of the
SCHIZOPHRENIA BULLETIN
disorder to run symptomatically
"true to type." In the families of pro-
bands, one observes, in accordance
with the clinical variation of the
disease shown by the proband, a
differentiated inclination toward
mononomial psychopathies: schizo-
phrenia with obsessions and com-
pulsionspsychasthenia (com-
pulsive personality); "hysterical
schizophrenia'psychopathy of the
hysterical type; paranoidal schizo-
phreniaparanoidal personality
disorder; nonsymptomatic form of
schizophreniaschizoidia, etc.
Thus, the combined evidence on
the familial contribution to the ex-
pression of sluggish schizophrenia
suggests that there are two types of
genetic determinantsprocess
related and constitutional (Dubnit-
skaya et al. 1988). In agreement with
the findings of genetic-mathematic
analyses of genealogical findings,
sluggish schizophrenia is character-
ized by a specific genotypic struc-
ture, the separate components of
which appear to be common for dif-
ferent clinical forms (overt schizo-
phrenic psychoses on the one hand,
and constitutional personality
disorders on the other).
Intrinsic in its relation to the
genetically determined group of
schizophrenic variations under in-
vestigation is the nonsymptomatic
form ("simple" sluggish) of schizo-
phrenia, in which the structure of
familial incidence is confined to
disorders of the schizophrenia spec-
trum. The clinical characteristics of
each of the remaining variants of
sluggish schizophrenia are related to
the influence of constitutional
genetic factors of a nonschizoid
nature (familial psychopathological
predisposition to hysterical, psych-
asthenic, and paranoidal types).
In considering diagnostic prin-
ciples used to define sluggish
VOL. 15, NO. 4, 1989
schizophrenia, it is essential to em-
phasize that the development of
diagnostic criteria in Soviet psychi-
atry has remained on the clinically
descriptive level; quantitative
methods are much less fully
developed.
The diagnosis of sluggish schizo-
phrenia demands an integrated ap-
proach that is based not on any
distinguishing, differentiating
pathognomonic symptom or symp-
toms, but on a complex of clinical
indicators. Attempts to define the
boundaries of sluggish schizo-
phrenia that rely on models
developed for fully developed
psychotic forms of schizophrenia
and primarily based on sympto-
matology criteria alone are likely to
prove inadequate.
As part of the diagnostic process,
information on the premorbid per-
sonality development in childhood,
puberty, and adolescence must be
taken into account. The appearance
in the premorbid periods of atypical
or bizarre interests (Lichko 1985),
but also sharp characterological
changes of limited duration, accom-
panied by a "breakdown of the pro-
fessional standard" (Mundt 1983)
and transformations in all aspects of
the "life curve," acquires great
significance for the establishment of
the endogenous nature of the subse-
quently appearing symptoms.
Information on family incidence
(cases of familial schizophrenia) and
on impaired social adaptation is also
significant. In contrast to borderline
conditions, a gradual reduction of
the ability to work, linked with a
decline of intellectual activity and
initiative, is noted in cases of
schizophrenia.
Pathological manifestations that
are used as clinical criteria in the
diagnosis of sluggish schizophrenia
are grouped into two basic categor-
ies: pathologically productive symp-
toms (positive psychopathological
symptoms) and negative symptoms
(the appearance of a defect state).
From our point of view, for the
recognition of sluggish schizophre-
nia, the latter is not merely obliga-
tory, but also verifies the diagnostic
verdict: The diagnosis of sluggish
schizophrenia may be established
only in the presence of definite
symptoms of a defect state.
In this manner, provision is made
for the exclusion of conditions
which are defined not so much by
the influence of the endogenic
process (latent, residual) as by the
"interaction" of personality and en-
vironment (Magnusson and Ohman
1987).
An integrated model of the schizo-
phrenic defect state (Smulevich and
Vorob'yov 1988) forms the basis for
the reliability of the diagnosis of
sluggish schizophrenia. As part of
this model, negative symptoms are
not restricted to any isolated sphere
of mental functions (e.g., affective,
cognitive, volitional, or personality),
but to one degree or another encom-
pass all the levels of mental activity.
This approach can be distinguish-
ed in principle from several other
concepts of the defect state, which
confine the defect to relatively
isolated spheres of mental activity.
The first of these can be traced back
to the study by J.H. Jackson (1958)
and has been developed on the
clinical level by H. Ey (1954), J.
Mazurkiewicz (1980), and A.V.
Snezhnevsky (1969). This concept
implies the development of a defect
in the initial stages or during the
slow evolution of the process which
affects the higher spheres of mental
activity and is expressed by symp-
toms of personality disharmony,
which are represented first of all by
schizoidia.
535
The second concept, first ex-
pounded by K. Conrad (1958) with
regard to the reduction of energetic
potential on the clinical level, was
more fully developed by G. Huber
(1966). Huber proposed that in
schizophrenia, the first or even the
only areas to be affected involve
elements of the highest level of
neural activity, which are responsi-
ble for psychological activity (e.g.,
spontaneity, alertness, initiative,
vitality, and concentration).
The concept of a multilevel system,
analogous to the organization of
highest neural activity (Bernstein
1947; Luria 1970; Pribram 1971;
Polyakov 1976; Bekhtereva 1980;
Bratus' 1988), provides the
theoretical basis for the integrated
model of the schizophrenic defect.
As in the close mutual bonds of
separate substructures that form a
"functional organ" (Leont'ev 1975),
changes that occur as part of a
disease process cannot exist in isola-
tion and inevitably will affect other
psychological functions. A change in
one area will be reflected to one
degree or another in the activity of
all areas of the system.
On the psychopathological level,
the integrated model of defect is
represented by the combining of
changes similar to pseudo-
psychopathic and pseudo-organic
(Vnukov 1937) changes.1
In sluggish schizophrenia, disease-
related changes, being inseparably
linked, correlate among themselves
'Asthenic defect and manifestations of
a reduction of energetic potential are also
related to the clinical appearance of the
pseudo-organic defect together with in-
tellectual decline.
536
within the framework of two varia-
tions of the defect, which may also
be regarded as diagnostic criteria. In
one of these variations the defect is
accompanied by hypertypical dis-
integration of personality, and in the
other by hypotypical disintegration
of personality2 (Luk'yanova, in
press).
In cases of a defect with hyper-
typical disintegration of personality,
one finds crude changes similar to
psychopathy, which are revealed as
a result of the decline in the level of
personality (pseudo-organic defect).
The complication of disharmony
of personality is evidenced by
polymorphic psychopathological
symptoms along with an increase of
discordant psychological processes,
eccentricity, pathological autistic
activity, and many inadequately
motivated actions that are linked
closely to emotional blunting and a
decline of insight. Cognitive disturb-
ances take place as well as unex-
pected outpourings of ideas and a
tendency toward paradoxical think-
ing and overvalued bizarre ideas.
In cases of a defect with hypo-
typical disintegration of personality,
pseudo-organic changes are accom-
panied by impoverishment in all the
spheres of mental function, and
reflected in the structure of schizoid
manifestations (withdrawal from
social contacts, emotional impover-
ishment, flattening and toning down
of individual personality traits).
The deepening of pseudo-organic
defect features occurs due to ergic
and cognitive manifestations-
marked decline in intellectual ac-
tivity, loss of initiative, apathy,
2
The term was adopted by them from
the research of W. von Baeyer (1947),
which focused on organic diseases of the
central nervous system.
reduction of intellectual functions
and ability to think abstractly, dif-
ficulty in comprehension, and
increased rigidity.
In diagnosing sluggish schizo-
phrenia, the two following types of
productive psychopathological
manifestations are simultaneously
noted: Type 1symptoms predomi-
nantly typical for the endogenous
process from the moment of its for-
mation; Type 2symptoms which
display an endogenic process-related
transformation during further stages
of the disease.
The first group contains mild
manifestations appearing as
episodically occurring exacerbations:
Verbal hallucinations of a commen-
tative, imperative character; "calling
out," "sounding of ideas"; somatic
hallucinations, tactile hallucinations;
rudimentary ideas of being influ-
enced, persecution, special mean-
ing, etc.
The group of positive symptoms
which display a transformation
typical for endogenic process in later
stages of the disease consists of the
following:
Hysterical conditions with a
transformation of conversion and
disassociative manifestations to the
cenestohypochondrial, subcatatonic,
pseudohallucinatory ones;
Obsessive-phobic conditions
with subsequent change of ap-
pearance from simple phobias to
generalized ideo-obsessive condi-
tions ("madness of doubts," con-
trasting phobias) through ideo-
obsessive delusion with ambiten-
dentious ritual conduct and abstract
composition of symptoms;
Hypochondrial conditions with
progression from neurotic and
overvalued-type hypochondria to
cenestohypochondrial, due to the
appearance of somatoform symp-
SCHIZOPHRENIA BULLETIN
toms and cenesthesias, essential
cenestopathies, and of possession
symptoms;
Depersonalizations which
change their appearance due to the
development of persistent distur-
bances of id, manifestations of
autopsychological depersonalization
(alienation of higher emotions,
awareness of personal psychological
changes, of the inadequacy of the
entire psychological life);
Overvalued ideas with the
changes of the clinical picture in
stages: Overvalued ideasover-
valued delusionssystematic
paranoidal delusion lacking
coherent composition with paradox-
ical, unrealistic content.
The breakdown in facial expres-
sion, which gives the features of the
sick individuals the appearance of
strangeness, oddness, and eccen-
tricity has an auxiliary, though, in
the opinion of modern European
psychiatrists (Glatzel 1978, 1981;
Weitbrecht and Glatzel 1978),
extremely vital importance for
diagnosis.
A disregard for the rules of per-
sonal hygiene, "neglectfulness," in-
attention to grooming of one's hair
or clothes; characteristic avoidance
of eye contact; awkwardness, jerki-
ness, "twitchiness" of body move-
ments; and bombastic speech with
exaggerated meanings but lacking in
adequate intonation. The totality of
these characteristics of the expres-
sive sphere which gives a sense of
unusualness or alienness was defin-
ed by H.C. Rumke (1958) as
"Praecoxgefiih" ("praecox feeling" in
English).
From materials presented above,
the conflict between the clinical
diagnostic criteria used to define
sluggish schizophrenia in the
U.S.S.R. edition and those of DSM-
IH-R (American Psychiatric Associa-
VOL. 15, NO. 4, 1989
tion 1987) becomes obvious. If the
diagnosis of schizophrenia according
to DSM-III-R presumes the obli-
gatory presence of typical psychotic
symptoms (delusions of an outlan-
dish nature, predominantly verbal
hallucinations of a commentative
character, incoherent thoughts,
catatonic behavior, flattened or
clearly inadequate affect), then in
the U.S.S.R. system these symptoms
are certainly not always necessary
for the diagnosis of sluggish
schizophrenia.
The indicated divergence
represents, in the opinion of a
number of Western psychiatrists,
proof of the existence in the U.S.S.R.
of an expanded concept of schizo-
phrenia. However, in reality this
divergence does not lead to dis-
agreement about the limits of slug-
gish schizophrenia, but rather
reflects the principal differences of
approach to the qualification of
groups of patients who are defined
by this concept.
In DSM-III-R, wherein Axis I the
criteria of syndromal diagnosis are
introduced, the conditions that cor-
respond in the understanding of
Soviet psychiatrists to the different
variations of sluggish schizophrenia
are separated from the category of
endogenous diseases and are in-
cluded in the category of "personal-
ity disorders." It follows therefore
that the cause of divergences
between Soviet and American
psychiatric schools (if one is to judge
by DSM-III-R) lies not in the differ-
ences of approach to the nosological
definition of conditions which are
defined by the concept of "sluggish
schizophrenia," but by the principal
differences of approach to these con-
ditions of formal classification. An
analysis of DSM-III-R criteria for
personality disorders demonstrates
this. First of all, the category of
schizotypal personality disorders in-
cludes conditions that in aggregate
are unilaterally defined in Soviet
psychiatry by the concept "sluggish
schizophrenia." It is not by chance
that in the previous edition (DSM-
III; American Psychiatric Association
1980), latent, simple, borderline, and
residual schizophrenia were listed as
synonyms for schizotypal personali-
ty disorders.
Another category is that of
borderline personality disorders.
The insufficient preciseness of initial
diagnostic criteria (and, above all, of
the possibility of a diagnostic
overlap between borderline per-
sonality disorders and schizotypal
personality disorders as indicated in
DSM-III-R as well) allows a range of
intense, impulsive, unstable
manifestations that belong to certain
variants, from our point of view, of
sluggish schizophrenia to fit within
the boundaries of personality
disorders.
Attempts to define the boundaries
of sluggish schizophrenia using
DSM-III-R diagnostic criteria do not
appear to be correct. The model of
schizophrenia as defined in
DSM-III-R applies to manifest psy-
chotic forms of this illness, which
cannot be used in the identification
of sluggish schizophrenia.
In conclusion, it must be empha-
sized that the grouping of non-
manifested mental disorders of an
endogenic-process nature with
neurotic personality manifestations
and deviations and transitory reac-
tive conditions on a syndromal basis
has been widely criticized, even by
American psychiatrists (cf. Kendler
1985). The conditionality of this
unification is reflected in DSM-III-R.
This is shown in part by a large
degree of overlap between sets of
diagnostic criteria for the prodromal
and residual phases of schizophrenia
537
and for schizotypal personality
disorders (Axis I of DSM-III-R). Axis
II of DSM-III-R corresponds to the
breakdown of ontogenesis and per-
sonality. In the section on "Differen-
tial diagnosis of schizophrenia,"
DSM-III-R points out the difficulties
of distinguishing borderline and
schizotypal personality disorders
from the prodromal phase of
schizophrenia.
It is evident that the problem of
the relationship of slowly progress-
ing endogenic diseases and the
borderline mental conditions cannot
be resolved by a "transfer" of
psychopathologies from one of the
nosological groups to another. Fur-
ther study, with an objective com-
parison of the results of the studies
of different national schools of
psychiatric thought, of the role of
factors which unite different forms
of psychopathology (inheritance,
similarity of psychopathological
manifestations, level of social adap-
tation, treatment strategy, etc.) is
essential, as well as a more accurate
definition of the factors which reflect
the heterogeneity of those forms
(difference of the course, terminal
conditions, and particular reactions
to psychogenic, somatogenic, and
other stresses).
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The Author
Anatoly B. Smulevich, M.D., is
Chief, Clinical Department of
Slowly Progressive Endogenous
Diseases and Borderline Mental
Disorders, Research Institute of
Clinical Psychiatry, All Union
Research Center of Mental Health,
U.S.S.R. Academy of Medical
Sciences, Moscow, U.S.S.R.