See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/16394014

Stereotypy in monkeys and humans

Article in Psychological Medicine · March 1982

DOI: 10.1017/S0033291700043294 · Source: PubMed

CITATIONS READS

133 940

2 authors, including:

Rosalind Mary Ridley

University of Cambridge
218 PUBLICATIONS 8,409 CITATIONS

SEE PROFILE

All content following this page was uploaded by Rosalind Mary Ridley on 02 June 2015.

The user has requested enhancement of the downloaded file.

Psychological Medicine, 1982, 12, 61-72
Printed in Great Britain

Stereotypy in monkeys and humans

ROSALIND M.RIDLEY 1 AND HARRY F. BAKER
From the Division of Psychiatry, Clinical Research Centre, Harrow, Middlesex

SYNOPSIS Stereotyped movements are described in monkeys and humans and are classified as
arising from constraint, sensory deprivation in infancy, amphetamine treatment or psychotic states.
It is argued that, with the exception of cage stereotypies, stereotyped behaviour is evidence of
abnormality in the nervous system consequent upon distorted maturational processes, organic
defect or biochemical disturbance. Stereotypy is associated with a state of cognitive inflexibility and
social and sensory isolation in humans and monkeys. It is suggested that, while no simple biochemical
disturbance in the brain can describe these various occurrences of stereotypy, the cross-species
occurrence of a syndrome of isolation, cognitive inflexibility and stereotypy implies a related
mechanism mediating these divergent effects. If stereotypy is regarded as a consequence of failure to
use sensory input to direct behaviour, therapeutic regimes designed to stimulate responsive be-
haviours and social interactions are more likely to be effective in the long run than direct attempts
to suppress stereotypy.

INTRODUCTION STEREOTYPY IN MONKEYS

Between the repetitive movements of known Cage stereotypies (Hediger, 1955)
neurological origin (for example, tremors, myo-
When monkeys are caged singly they often
clonic jerks, choreoathetosis) and repetitive
develop repetitive behaviours which usually
movements which are skilled, learned and volun-
include to-and-fro pacing, circling, backward
tary, lies a group of abnormal movements for
somersaulting or jumping on all fours (Berkson,
which the degree of volition and neurological
1967; Draper & Bernstein, 1963). They occur at
involvement is obscure. Rituals and obsessional/
all levels of primate phylogeny from the simplest
compulsive behaviour may be accompanied by
true primate, the marmoset (Berkson et al. 1966;
varying levels of volition and insight (Janet,
and personal observation), to the great apes
1908). Repetitive movement abnormalities are
(Berkson & Mason, 1964), and are also seen in
often associated with non-focal brain damage -
many non-primate species (Meyer-Holzapfel,
for example, post-encephalitic (Slater & Roth,
1968). Cage stereotypies are usually broken very
1969), geriatric (Appenzeller & Biehl, 1967) or
easily by removing the animal from the cage
other Parkinsonian syndromes (Parkinson, 1817)
(Berkson, 1967), although this is not invariably
- or with presumed minimal brain dysfunction
the case (Meyer-Holzapfel, 1968). Occasionally
(Prechtl & Stemmer, 1962), or psychosis
cage stereotypy develops into self-mutilation
(Guirand, 1936; Jones, 1965). Those movements
(Tinklepaugh, 1928; and personal observation),
which are combined into rhythmic or complex
although the conditions necessary for this un-
sequences of obscure purpose and which have
fortunate development are obscure.
attained a level of 'functional autonomy'
(Woodworth, 1918) are usually described as
Social and sensory deprivation in infancy
stereotypies.
Social isolation and sensory monotony which
start with early separation from the mother
induce 'deprivation' stereotypies (Foley, 1934,
1
1935). Abnormal behaviour of this kind
Address for correspondence: Dr Rosalind M. Ridley, typically does not involve locomotion but may
Division of Psychiatry, Clinical Research Centre, Watford
Road, Harrow, Middlesex HA1 3UJ. include body-rocking or twirling, head rolling,
61
62 R. M. Ridley and H. F. Baker
self-clasping or digit sucking (Mason & Spon-
holz, 1963; Mason, 1968). More severe mani-
festations may include self-destructive forms of
behaviour such as head banging, self-biting and
eye-poking, with bizarre limb and body posturing
and complex hand movements (Cross & Harlow,
1965; Mitchell, 1970). Isolation reared, caged,
adult animals frequently exhibit both 'cage' and
'deprivation' stereotypies. Where deprivation
stereotypies have become well established they
are very difficult, if not impossible, to disrupt.
This difference from cage stereotypies is impor-
tant, since it implies that cage stereotypies are
the response of a normal nervous system to an
abnormal environment, while deprivation stereo-
typies are the product of an abnormal nervous
system.
Monkeys separated from other animals early
in life not only suffer from an impoverished
background but are also unable to make use of
later social situations through communicative
signals (Mason, 1968) or form normal social
attachments, including sexual (Harlow, 1962;
Rogers & Davenport, 1969) and parental ties
(Seay et al. 1964; Arling & Harlow, 1967). They
are often excessively and inappropriately aggres-
sive (Rowland, 1964; Mitchell, 1968) and in-
dulge in other grossly inappropriate behaviour,
such as coprophagy (Mitchell et al. 1966). Thus
there appears to be a strong relationship in
monkeys between movement anomalies and
disturbed social performance. Attempts at sub-
sequent social involvement (therapy) are not
completely successful (Novak & Harlow, 1975;
Suomi & Harlow, 1972; Cummins & Suomi,
1976), implying the existence of a 'sensitive
period' (Bateson, 1964; Harlow, 1965) during
which a grossly abnormal environment has
a profound effect on subsequent functioning of
the nervous system. This situation has an
obvious parallel in sensory-motor neurophysio-
logy, where a lack of sensory or motor feedback
information can permanently influence the
structure and activity of neurones in the brain
(Held & Hein, 1963; Wiesel & Hubel, 1963).
While it is not obvious whether the environ-
mental influence leading to stereotypy in this case
is the loss of social contact with other animals
per se, or loss of the sensory input of which
the social contact is comprised, or the positive
effect of the monotonous environment into
which the animal is put after separation, the
work of Harlow & Zimmermann (1959) suggests
that subsequent sensory input is particularly
important in determining future development.
Bajpai (1980) does not report the development
of stereotyped behaviour during social isolation
without physical constraint.
While parental deprivation may lead to
changes in behaviour in primates (Hinde, 1971)
and, it has been suggested, in man (Bowlby,
1953; though see Rutter, 1972), only deprivation
which is so severe as to produce a grossly im-
poverished sensory input (rather than an altered
social environment) is sufficient to produce
major changes in motor output. If deprivation
stereotypies develop under conditions of limited
sensory input, one would predict that animals
severely deprived from birth of normal sensory
input (but not socially isolated) would show
similar stereotypies. Hand stereotypies have been
observed in monkeys which were blind from
birth (Berkson & Karrer, 1968).
Drug-induced stereotypy
In monkeys, amphetamine induces stereotyped
head movements and repetitive, but idiosyn-
cratic, behavioural sequences which may include
self-grooming, staring at the hands, snatching at
the air, and covering the eyes with the hands (for
example, Randrup & Munkvad, 1970; Kjellberg
& Randrup, 1972 a; Garver et al. 1975; Ellison
et al. 1980). As treatment continues, the se-
quences become progressively more restricted
and self-destructive (Ellinwood & Kilbey, 1975).
Excoriating self-grooming, self-biting and eye-
poking may all occur (Ridley & Baker, 1981;
Ridley et al. 1979). Concomitant with this syn-
drome is a profound loss of social interaction
(Schiorring, 1979; Randrup & Munkvad, 1974;
Kjellberg & Randrup, 19726), including a dis-
ruption of mother-infant relations (Schiarring
& Hecht, 1979). Loss of interaction cannot be
ascribed simply to pre-occupation with stereo-
typed activities, since social withdrawal appears
at doses lower than that necessary to induce
severe stereotypy (Scraggs & Ridley, 1978).
STEREOTYPY IN HUMANS
Constraint
Behaviours which may be analogous to cage
stereotypies occur frequently in humans under
physical or social constraint - for example,
 Stereotypy in monkeys and humans
prisoners pacing their cells, and expectant
fathers pacing hospital waiting rooms. This form
of stereotypy is abandoned as soon as the con-
straint is removed.
Children
Stereotyped rocking and twirling, unusual hand
movements and arm flapping are seen in children
(and sometimes adults) who are congenitally
blind (Keeler, 1958), or severely mentally re-
tarded (Corbett et al. 1975; Berkson & Daven-
port, 1962). Adults stricken with blindness or
incapacitating brain damage do not develop
equivalent stereotypies (although in the latter
case there may be motor impairment), suggesting
that these stereotypies result from an abnormal
maturation process in the brain. Such stereo-
typies could be called 'isolation' stereotypies,
since the individual involved would be isolated
from a significant part of the normally available
sensory information (or the intellectual capacity
to process it) but would not be deprived in the
pejorative sense. The exceptionally long period
of development in the human, and the lack of
maturity in the neonate (an evolutionary process
known as neoteny), suggest that the human
nervous system is particularly dependent on
sensory input for normal development. Many
isolation stereotypies have been recognized as
'habit residuals' (Foley, 1934; Berkson, 1967), i.e.
they are forms of behaviour which are normal in
infancy but are usually inhibited by the develop-
ment of competing behaviours which are them-
selves responses to sensory input. It might also
be the case that a tendency to repetition is
normal and adaptive in the infant as basic res-
ponses are acquired and the properties of the
environment are verified, but that this is norm-
ally superseded by a flexible responsiveness to
a wider functional environment (Thelen, 1979).
Stereotypies are also sometimes seen in
children deprived of normal parental or equiva-
lent care (Spitz, 1945). It has been emphasized,
however, that the environment into which
a child is placed is more important than separa-
tion from the mother herself in the development
of stereotypies (Yarrow, 1964; Casler, 1968),
since such stereotypies usually occur only in
inadequate institutions where sensory input is
impaired (for example, leaving a baby lying for
long periods staring at the ceiling), whereas they
do not occur in conditions where plentiful
63
sensory input is provided but where stable
relationships are not formed because of staff
rotation.
Severe stereotypies - including self-destructive
acts such as head banging, self-biting and eye-
poking - are an important feature of the autistic
syndrome (Kanner, 1943). These stereotypies
occur, in conjunction with profound impairments
of social interaction, communication and orien-
tation to the environment, despite only subtle
differences in parental or environmental con-
ditions and efforts at therapy and education. By
comparison with the other conditions described
it would seem that autistics are functionally de-
prived of a substantial proportion of normal
input. Since the sense organs are usually intact,
one is led to suggest a higher-order perceptual
deficit - i.e. an inability to construct meaningful
events from sensory inflow (Hermelin & Frith,
1971). Intelligence may be normal in autistics
(Wing et al. 1976), suggesting that only a specific
mechanism involved in the interpretation and
use of subtle social cues may be affected in some
cases (Eisenberg, 1956). In a detailed study of
mono- and dizygotic same-sexed twins, Folstein
& Rutter (1977) have assessed the heritability of
autism and concluded that 'there were important
hereditary influences concerning a cognitive
deficit which included but were not restricted to
autism'. The existence of, and evolutionary
pressure towards, specific mechanisms maintain-
ing social interaction and cohesion in many
species, including man, have been persuasively
argued by Ardrey (1970).
Psychosis
Stereotyped behaviour in psychosis, especially
schizophrenia (Kraepelin, 1971; Bleuler, 1950),
has been described in detail in the past but is
often overlooked in modern psychiatry, possibly
because neuroleptic treatment may sometimes
block such behaviour, or mask it with a general
motor retardation, or complicate the issue by
inducing tardive dyskinesia. Kraepelin (1971)
described stereotypies in all types of schizo-
phrenia and gave examples which range from
ritualistic obsessional behaviour with explana-
tions of 'compulsion' to movements resembling
the stereotypies of mental defectives and also
very brief stereotypies and mannerisms, some of
which resemble tics and spasms. Bleuler (1950)
considered stereotypy to be a form of catatonia.
64 R. M. Ridley and H. F. Baker
He maintained that psychotic stereotypies can be
differentiated from obsessional or neurological
movement anomalies and argued that they
originate from patients' thought processes and
attitudes. These stereotypies, however, evolve in
a manner comparable to amphetamine stereo-
typies (Ellinwood et al. 1973), such that they be-
come grossly abbreviated and can no longer be
recognized as originating in a comprehensible
idea. Thus a persistent verbal request may
degenerate into a repetitive murmur and constant
posture (personal observation).
Drug-induced stereotypy
Amphetamine-induced stereotypy in humans is
known as 'punding' and is often accompanied by
florid psychosis (Rylander, 1972). Punding may
consist of a very simple repetitive a c t - f o r
example, tapping or rotating a small object - or
may be very complex, but nonetheless repetitive -
for example, persistent dismantling and re-
assembly of mechanical equipment. Such
behaviour appears to have a compulsive quality.
Amphetamine psychosis may be indistinguishable
from schizophrenia (Connell, 1958; Janowsky &
Risch, 1979) and, although it usually occurs
after chronic drug abuse, can sometimes occur
after one large dose (Angrist et al. 1974). Para-
noid ideation has been observed after low, acute
doses in healthy volunteers (Griffiths et al. 1972).
MENTAL STATE ASSOCIATED WITH
STEREOTYPY
It is unwise to assume that forms of behaviour
which bear a superficial resemblance are, in fact,
equivalent across species. Nonetheless, where
clusters of behaviour occur together in different
species, it is not unreasonable to ask whether
a comparable mechanism is involved. It is also
important to distinguish conceptually between
the content of stereotypies which are idiosyncratic
in patients (Bleuler, 1950) and in animals
(Ridley & Baker, 1981) and the tendency
towards stereotypy which is a feature common to
withdrawn psychotic states, organisms isolated
during the process of maturation, and ampheta-
mine treatment. It is also important to distinguish
between those conditions which accentuate
a condition and those which cause it. For
example, poor environmental circumstances may
exacerbate tuberculosis, but exposure to the
tubercle bacillus is a necessary (and, on occasion,
sufficient) condition. High expressed emotion in
relatives may predispose to a relapse in schizo-
phrenia (Brown et al. 1972), but need not be the
cause of the disease. Increased arousal often
accentuates stereotypy in animals (Berkson &
Mason, 1964; and personal observation) and in
man (Hutt & Hutt, 1968), but it is not clear that
high arousal causes stereotypy. Where activity is
largely stereotyped, high arousal may lead to an
increase in stereotypy, but in a normal individual
increased activity may take on any manner of
forms. Although it has often been assumed in
the past (McDougall, 1923; Tinbergen, 1951), it
is not necessary to propose an energy model of
motivation in order to explain the appearance of,
or increase in, certain behaviours (Hinde, 1960;
Bindra, 1959). By analogy with 'displacement
activities' (Zeigler, 1964) it would seem that
stereotypies are not motivated by 'energy spilling
over' from other frustrated desires, but rather
that the non-occurrence of more appropriate
behaviour permits other activities to fill the
behavioural vacuum.
It has been suggested that stereotypy is a form
of self-stimulation designed to increase sensory
input under conditions of deprivation. While
this may be true in some cases (for example,
cage stereotypies) it does not explain why such
behaviour should be performed in conjunction
with social withdrawal and lack of responsive-
ness to a normal environment in psychotic or
autistic states.
In this section it is our intention to describe
various behavioural and cognitive states associ-
ated with stereotypy in monkeys and to attempt
to relate these to certain human conditions. Our
own work with amphetamine and other studies
using monkeys suggest that three conditions are
associated with stereotypy: sensory isolation,
social isolation and cognitive inflexibility. In so
far as evidence is available, stereotypy in humans
appears to be associated with a comparable
syndrome.
Chronic amphetamine treatment in the vervet
monkey
It has been suggested (Ellinwood, 1971) that
amphetamine induces stereotypy by a process of
'accidental conditioning': i.e. that pre-potent
responses are reinforced by amphetamine action
on neural reward pathways (Stein, 1964), and
 Stereotypy in monkeys and humans
that the evolution of stereotypy consists of
a positive feedback whereby an increasing re-
petition of a diminishing behavioural repertoire
is seen. We were recently in a position (Ridley &
Baker, 1981) to administer amphetamine to
a small group of vervet monkeys (Cercopithecus
aethiops) who already exhibited marked cage
stereotypy consisting mainly of pivoting from
side to side about a posterior axis. Rather
surprisingly, this cage stereotypy was blocked by
amphetamine, although other stereotyped be-
haviour - including staring at the hands, staring
at the cage walls, self-grooming and snatching
at the air - emerged over the course of some days
of treatment. This change from cage- to isolation-
type stereotypy after psychopharmacological
treatment argues against the theory of accidental
conditioning; however, it is consistent with our
suggestion that cage stereotypies represent
normal reactions to an abnormal environment,
whereas isolation and deprivation stereotypies
are the results of a malfunctioning nervous
system. Unfortunately, it was not possible to
observe social interaction in these monkeys,
since they were housed individually. However,
after eight days on amphetamine treatment it was
noticed that these animals were remarkably un-
responsive to external events and could even be
poked in the face without retaliating or changing
position.
Amphetamine treatment in the marmoset
We have also studied the effects of acute and
chronic amphetamine treatment on a group of
small South American monkeys - common mar-
mosets (Callithrix jacchus). When given acutely,
amphetamine (Scraggs & Ridley, 1978) induces
very rapid stereotyped head movements (check-
ing), while during chronic treatment checking
gives way to destructive self-grooming (Ridley
et al. 1979). Social isolation occurs during both
acute and chronic amphetamine treatment.
Orientation to the environment was measured
(Ridley et al. 1980 a) by placing the animals in-
dividually in an enclosed circular box with four
small windows which could be open or closed.
Saline injected (control) marmosets spent a con-
siderable proportion (~ 50 %) of the time look-
ing out of the windows at other marmosets in
the room, whereas they spent only ~ 5 % of the
time adjacent to the windows when they were
closed. After amphetamine treatment animals
65
spent only ~ 15 % of the time at open windows
(~ 5 % when windows were closed), suggesting
that the drug reduces external control over
behaviour. Although checking has been ascribed
to hypervigilance, our experiment suggests that
it is more likely that checking is an internally
driven motor stereotypy than a response to
external visual stimulation.
Cognitive flexibility after amphetamine in the
marmoset
We have also carried out a series of experiments
which have attempted to assess changes in cog-
nitive states brought about by acute, low doses
of amphetamine in marmosets. Some of the
changes which we have observed resemble the
effects of frontal lobe dysfunction in monkeys;
for example, impaired performance on delayed
response tasks (Jacobsen et al. 1935; Rosvold &
Szwarcbart, 1964) and successive visual dis-
crimination tasks (Brutkowski et al. 1963) has
been observed after frontal lesions and after
amphetamine treatment! (Weight et al. 1980;
Ridley et al. 19806). A similar impairment of
reversal learning (but not new learning) is seen
after frontal lesions (Butter, 1969) and after
amphetamine (Ridley et al. 19816). In the
reversal learning task the monkey was required
to choose one of two objects presented simul-
taneously in a series of trials in a Wisconsin
General Test Apparatus (Harlow, 1958) until
a pre-determined criterion of so many correct
(food rewarded) responses in a number of con-
secutive trials was reached (for example, five
consecutive correct responses). The reward con-
tingency was then reversed so that the originally
rewarded object became unrewarded, and the
animal was required to choose the other object
in order to obtain reward. After amphetamine,
many perseverative errors were made: i.e. the
animal continued to choose the originally re-
warded object so that it received less than 50 %
rewards (chance performance) over the initial
trials. When this perseverative tendency was
broken and the animal had achieved chance per-
formance, it then learnt the new discrimination
at a rate comparable to the original learning.
This perseveration could occur either because
the animal cannot break the 'habit' of responding
to the first rewarded object (a response-
organizing dysfunction) or because it cannot
break the association between the first object and
66 R. M. Ridley and H. F. Baker
the reward (an associative dysfunction). In a
further experiment (Ridley et al. 1981a) we
observed that, like frontal lesioned animals
(Brush et al. 1961), amphetamine-treated animals
also had difficulty in relinquishing an object
preference. On the first trial animals were allowed
to indicate their preference for either object in a
'free' two-choice trial. On subsequent trials the
preferred object was used as either the rewarded
or non-rewarded stimulus in a series of discrimi-
nation trials. Under amphetamine, animals con-
tinued to choose their preferred object, whether
it was rewarded or not.
RELATION OF ANIMAL STUDIES TO
HUMAN CONDITIONS
There are many problems associated with
attempting to infer a mental state from be-
havioural manifestations in animals. The
example of 'hypervigilance' after amphetamine
has already been described. The amphetamine
syndrome in monkeys has been described as
paranoid (Haber et al. 1977), autistic (Schi0rring,
1979), hallucinatory (Ellison et al. 1980) and
psychotic (Ellinwood et al. 1973). Of these, the
term autistic is perhaps the most descriptive of
behaviour and therefore the least difficult to use.
In addition to profound social isolation and
stereotypies, the autistic syndrome in humans
often involves an apparent insensitivity to
external stimulation (including painful stimuli)
(Stengel et al. 1958) and a cognitive inflexibility
or 'insistence on sameness' (Kanner, 1943).
Amphetamine-treated animals, under different
test situations, may exhibit all of these symptoms.
We would suggest that, under normal con-
ditions, the nervous system is designed to change
behaviour via changes in cognitive state in
response to stimulation. Where sensory input is
restricted or meaningless, cognitive flexibility
and hence changes in behaviour will be restricted,
leading to a tendency to stereotypy. The various
conditions which lead to stereotypy in animals
and man differ greatly. The common feature,
however, appears to be a lack of control of be-
haviour by external events. This may occur
because of sensory incapacity, impaired learning
following insufficient sensory stimulation, or
a gross defect of higher-order perceptual pro-
cessing. In psychosis, disorders of higher-order
processing mechanisms may be manifest as
thought disorder and delusions, while the exist-
ence of perceptual processing defects is implied
by the occurrence of hallucinations. In the case of
amphetamine treatment we would suggest that
this drug alters the balance between the external
control of behaviour and internal generation of
behaviour without reference to external events.
There is considerable evidence to suggest that
autistic children suffer from an abnormal
balance between the internal and external deter-
mination of behaviour. Thus, Frith (1970 a, b,
1972) has shown in experiments concerning the
production and recall of patterned sequences
that autistic children are impaired on feature
extraction from sensory input but show an ab-
normal tendency to impose pattern or structure
on unstructured material. Thus, internally
generated rules are imposed on sensory input,
while patterns or rules inherent in the sensory
stimuli are ignored.
The relevance of amphetamine-induced be-
haviour to psychosis is particularly interesting
with respect to social isolation. We believe that
isolation in monkeys treated with amphetamine
results from an active state of social avoidance.
Since it occurs at doses lower than those neces-
sary to induce severe stereotypy (Scraggs &
Ridley, 1978) and since social interaction is not
reinstated when stereotyped behaviour is blocked
by neuroleptics (Ridley et al. 1979; Scraggs &
Ridley, 1979), it does not arise as an inevitable
consequence of performance of other behaviours.
In their study of the effects of amphetamine and
neuroleptics in schizophrenics, Angrist et al.
(1980) found that amphetamine exacerbated not
only positive 'florid' symptoms but also increased
emotional withdrawal. This emotional with-
drawal consisted of incongruity rather than
flattening of affect. This suggests that severe
social isolation might be more closely related to
positive symptoms which have been attributed
to dopaminergic dysfunction than to true nega-
tive or 'type II' symptoms (Crow, 1980), despite
the marginal effect of neuroleptics on emotional
withdrawal found by Angrist et al. (1980).
BIOCHEMICAL CORRELATES OF
STEREOTYPY
The relevance of the biochemical effects of
amphetamine to the biological mechanism of
psychosis and behavioural disturbance is diffi-
 Stereotypy in monkeys and humans
cult to assess. Amphetamine releases dopamine
and noradrenaline from nerve terminals (Groves
& Rebec, 1976; Baker & Ridley, 1979), produc-
ing, initially, increased activity and eventually
depletion of these stores of monoamines (Owen
et al. 1981). Despite the longevity of the 'dopa-
mine hypothesis' of schizophrenia (Randrup &
Munkvad, 1965; Meltzer & Stahl, 1976), altera-
tions in dopamine systems in post-mortem
brains of schizophrenics (Owen et al. 1978; Lee
& Seeman, 1980) cannot be unequivocally attri-
buted to the disease process, but may be due to
drug treatment (MacKay et al. 1980). Neurolep-
tics which block dopamine receptors remain,
nevertheless, the preferred drug treatment for
schizophrenia, amphetamine psychosis and cer-
tain unmanageable behaviour disorders. Al-
though these drugs are most useful for suppress-
ing florid symptoms, they do not appear to be
able to reinstate social competence in with-
drawn patients (Johnstone et al. 1978; Crow,
1980; though see Goldberg et al. 1965). Similarly,
in animal studies neuroleptics block the 'positive
symptoms' induced by amphetamine but are
unable to counteract the loss of social interaction
(Scraggs & Ridley, 1979; Ridley et al. 1979).
Although this might suggest that social inter-
action is mediated by a non-dopaminergic
system, a state of social isolation can be induced
in primates by the use of the direct dopamine
receptor agonist, apomorphine (Schlemmer et al.
1980; Scraggs et al. 1979). Manipulation of the
serotonergic systems in primates alters, but does
not abolish, social interaction (Raleigh et al.
1979). There is some evidence that serotonin
mechanisms may be involved in schizophrenia
(Bennett et al. 1979; but see Whitaker et al.
1981) and autism (Cohen et al. 1974), and they
are known to be disturbed by large, acute (Fuxe
& Ungerstedt, 1970), or chronic (Trulson &
Jacobs, 1979) doses of amphetamine. Failure to
find a gross defect in the levels of monoamines
in brains from psychotic patients implies that the
relevance of amphetamine effects in animals and
man to psychosis cannot be regarded as one of
simple biochemical equivalence. Further ad-
vances in the study of biochemical changes in
psychosis and after amphetamine treatment may
eventually elucidate the relationship but, for the
present, a comparison of amphetamine effects
and psychosis at the psychological level may be
illuminating.
67
It is clear that dopamine is intimately involved
in many motor disorders. Thus, the Parkinsonian
disorders can be alleviated by L-dopa (Birk-
mayer & Hornykiewicz, 1961) and exacerbated
by neuroleptics; Huntington's Chorea(Oliphant
et al. 1960), other choreoathetoses and Tourette's
Syndrome (Shapiro & Shapiro, 1968) can be
contained by neuroleptics. The hyperkinetic-
minimal brain dysfunctions and the tardive
dyskinesias pose special problems of interpreta-
tion. The former may be helped by amphetamine
(Knights, 1974) or neuroleptics (Ounsted, 1955),
whereas the tardive dyskinesias are both caused
by and blocked by neuroleptic treatment (Crane
& Smeets, 1974). There is also some evidence
that spontaneous dyskinesias can occur in some
non-neuroleptic-treated patients (Jeste & Wyatt,
1981). The relation between motor disorders and
psychosis in terms of our limited understanding
of biochemical mechanisms should not be
ignored. If dyskinesia, like amphetamine effects,
is an instance of internally generated behaviour
without reference to external events, then
a psychotic state might also be understood as
a case where the balance of external and internal
control of behaviour has been tipped in favour of
internally generated behaviour.
THERAPEUTIC IMPLICATIONS
We have tried to suggest in this review that
stereotypy arises as a consequence of insufficient
meaningful sensory input, especially in infancy.
From this it follows that treatment designed to
decrease stereotypy without increasing sensory
input, or stimulating alternative behaviours is
unlikely to be successful in the long term.
Stereotypy might be used to assess the success
of attempts at integration into the environment.
A well established stereotypic routine, however,
is likely to interfere with attempts at social inter-
action, making rehabilitation of neglected cases
particularly difficult. Any behaviour which may
be considered to be a response to the environment
(even eating proferred food) will compete at the
behavioural level with the performance of stereo-
typy and can be used as the basis for establishing
and developing sensory and social input and
appropriate responses. This method of be-
havioural competition has already been used to
good effect in profoundly disturbed children
3-2
68 R. M. Ridley and H. F. Baker
(Azrin et al. 1973). It has also been reported that
socially unsophisticated infant monkeys which
disrupt stereotypies in disturbed animals by
physically demanding cuddling make better
'therapists' than more socially developed older
monkeys (Suomi & Harlow, 1972; Harlow et al.
1965).
If stereotypy in children represents a distorted
maturational process, it follows that intensive
intervention at the first signs of stereotypy should
be more efficacious than subsequent attempts at
rehabilitation. Since sustained social interaction
is greatly facilitated by the use of language, any
success in the area of language use and compre-
hension is likely to have the additional bonus of
weakening stereotypy. A strong relationship
between the development of language and other
behavioural improvements has often been
emphasized (Brown, 1960). Ellinwood (1980) has
pointed out that psychosis in humans and
stereotypy in animals after amphetamine treat-
ment can be postponed by engaging the indivi-
dual in responsive behaviour. In view of the
relationship between isolation and stereotypy
and the development of inappropriate aggressive
and self-destructive behaviour, it would seem
that confinement, and particularly solitary con-
finement, would have a deleterious effect on in-
dividuals who are prone to stereotypy or to
outbursts of ill-directed aggression and self-
destructive behaviour (including parasuicide).
This exacerbation might be expected to out-
weigh the behaviour suppressing and deterrent
effects of punishment by imprisonment, resulting
ultimately in the production of chronic be-
havioural disturbance with criminal complica-
tions.
The use of amphetamines and related stimu-
lants in the treatment of childhood hyper-
kinesis has been the subject of much controversy.
In a careful review of amphetamine effects,
Robbins & Sahakian (1979) conclude that im-
provement on certain tasks may be accompanied
by impairment on others. Low doses of stimu-
lants may reduce distractibility and hyper-
activity, but careful observation may reveal
cognitive inflexibility, 'over-focusing' of atten-
tion, and perseveration of thought (Sahakian &
Robbins, 1977; Robbins & Sahakian, 1979),
stereotyped movements and exacerbation of tics
(Robbins & Sahakian, 1979; Denckla et al.
1976), irritability (Epstein et al. 1968), reduced
social interaction (Barkley & Cunningham,
1979), and occasional psychotic episodes (Wins-
berg et al. 1972). It would seem that almost all of
the improvements in performance in humans
after amphetamine result from a release from
extinction decrements produced by habituation
and fatigue (Weiss & Laties, 1971) and that
little improvement is found on complex tasks, or
intellectual functioning (Knights, 1974; Mohs
et al. 1978), or long-term levels of achievement
(Rie et al. 1976; Weiss & Minde, 1974). Thus, it
would seem that stimulants should only be used
with extreme care, since apparently decreased
distractibility and improved attention to details
could equally well be described as perseveration
and a decrease in the overall impact of the en-
vironment on behaviour. In the long term such
treatment may result in a state of social isolation.
The use of neuroleptics and benzodiazepines
also requires care. Although such treatment may
be considered necessary for behavioural manage-
ment, any treatment which sedates to the extent
of decreasing responses to the environment is
unlikely to be of therapeutic value. Apart from
the dangers of long-term treatment with either
neuroleptics (Crane & Smeets, 1974) or minor
tranquillizers (Kaplan, 1980), the use of these
drugs merely to suppress stereotypy without
stimulating other responsive behaviours would
not seem to be indicated in the long term.
CONCLUSION
In conclusion, while some stereotyped be-
haviour (cage stereotypies and their human
equivalents) may be regarded as the attempt of
a normal individual to cope with an abnormal
environment, most stereotyped behaviour may
be considered as the product of an abnormal
nervous system. This abnormality may reflect
a disturbed maturational process resulting from
a variety of congenital defects which impair
sensory input or the meaningful analysis of that
input. Concomitant with stereotypy is a state of
social isolation and cognitive inflexibility. A syn-
drome of abnormal movements, social isolation
and a cognitive state which includes a loss of
flexibility is observed after amphetamine.
Despite the lack of simple biochemical equiva-
lence between amphetamine treatment and
psychotic states, the similarity of amphetamine
psychosis to schizophrenia suggests that further
 Stereotypy in monkeys and humans
comparisons may be illuminating. Motor ab-
normalities in schizophrenia may have been
under-emphasized. Social isolation might be
regarded as a cardinal symptom rather than as
a consequence of pre-occupation with delusions
or of rejection by other people. The isolated
states of psychosis and infantile autism may be
related in mechanism without the diseases being
equivalent. The normal nervous system develops
in such a manner as to be primarily responsive in
its behaviour. Where this responsive behaviour is
disrupted, other motor patterns including stereo-
typies will be uncovered.
REFERENCES
Angrist, B., Sathananthan, G., Wilk, S. & Gershon, S. (1974).
Amphetamine psychosis: behavioural and biochemical
aspects. In Catecholamines and Schizophrenia (ed. S. W.
Matthysse and S. S. Kety), pp. 13-23. Pergamon Press:
Oxford.
Angrist, B., Rotrosen, J. & Gershon, S. (1980). Differential
effects of amphetamine and neuroleptics on negative vs.
positive symptoms in schizophrenia. Psychopharmacology
72, 17-19.
Appenzeller, O. & Biehl, J. P. (1967). Mouthingin the elderly.
Neurology 17, 290.
Ardrey, R. (1970). The Social Contract. Collins: London.
Arling, G. L. & Harlow, H. F. (1967). Effects of social
deprivation on maternal behaviour of rhesus monkeys.
Journal of Comparative and Physiological Psychology 64,
371-378.
Azrin, N. H., Kaplan, S. J. & Foxx, R. M. (1973). Autism
reversal: eliminating stereotyped self-stimulation of re-
tarded individuals. American Journal of Mental Deficiency
78, 241-248.
Bajpai, R. K. (1980). The effects of early social deprivation
on rhesus monkeys: social responsiveness. Primates 21,
510-514.
Baker, H. F. & Ridley, R. M. (1979). Increased HVA levels
in primate ventricular CSF following amphetamine ad-
ministration. Brain Research 167, 206-209.
Barkley, R. A. & Cunningham, C. E. (1979). The effects of
methylphenidate on the mother-child interaction of hyper-
active children. Archives of General Psychiatry 36, 201-208.
Bateson, P. P. G. (1964). An effect of imprinting on the per-
ceptual development of domestic chicks. Nature (London)
202, 421-422.
Bennett, J. P., Enna, S. J., Bylund, D. B., Gillin, J. C , Wyatt,
R. J. & Snyder, S. H. (1979). Neurotransmitter receptors
in frontal cortex of schizophrenics. Archives of General
Psychiatry 36, 927-934.
Berkson, G. (1967). Abnormal stereotyped motor acts. In
Comparative Psychopathology (ed. J. Zubin and H. F.
Hunt), pp. 76-94. Grune & Stratton: New York.
Berkson, G. & Davenport, R. K. (1962). Stereotyped move-
ments of mental defectives I. Initial survey. American
Journal of Mental Deficiency 66, 849-852.
Berkson, G. & Karrer, R. (1968). Travel vision in infant
monkeys: maturation rate and abnormal stereotyped be-
haviours. Developmental Psychobiology 1, 170-174.
Berkson, G. & Mason, W. A. (1964)- Stereotyped behaviours
of chimpanzees: relation to general arousal and alternative
activities. Perceptual and Motor Skills 19, 635-652.
69
Berkson, G., Goodrich, J. & Kraft, I. (1966). Abnormal
stereotyped movements of marmosets. Perceptual and
Motor Skills 23, 491-498.
Bindra, D. (1959). Motivation: a Systematic Reinterpretation.
Ronald Press: New York.
Birkmayer, W. & Hornykiewicz, D. (1961). Der L-3, 4-
dioxyphenylalanin (Dopa) - Effekt bei der Parkinson-
Akinese. Wiener Klinischer Wochenschrift 73, 787-
788.
Bleuler, E. (1950). Dementia Praecox or the Group of Schizo-
phrenias (transl. J. Zinkin). International Universities
Press: New York.
Bowlby, J. (1953). Some pathological processes set in train by
early mother-child separation. Journal of Mental Science
99, 265-272.
Brown, G. W., Birley, J. L. T. & Wing, J. K. (1972). Influence
of family life on the course of schizophrenic disorders:
a replication. British Journal of Psychiatry 121, 241-
258.
Brown, J. L. (1960). Prognosis from presenting symptoms of
pre-school children with atypical development. American
Journal of Orthopsychiatry 30, 382-390.
Brush, E. S., Mishkin, M. & Rosvold, H. E. (1961). Effects of
object preferences and aversions on discrimination learning
in monkeys with frontal lesions. Journal of Comparative
and Physiological Psychology 54, 319-325.
Brutkowski, S., Mishkin, M. & Rosvold, H. E. (1963). Posi-
tive and inhibitory motor CR's in monkeys after ablation
of orbital or dorsolateral surface of the frontal cortex. In
Central and Peripheral Mechanisms of Motor Functions (ed.
E. Gutman). Academy of Sciences: Czechoslovakia.
Butter, C. M. (1969). Perseveration in extinction and in dis-
crimination reversal tasks following selective frontal abla-
tions in Macaca mulatta. Physiology and Behaviour 4,
163-171.
Casler, L. (1968). Perceptual deprivation in an institutional
setting. In Early Experience and Behaviour: Psychological
and Physiological Effects of Early Environmental Variation
(ed. S. Newton and S. Levine), pp. 573-626. C. C. Thomas:
Springfield, III.
Cohen, D. J., Shaywitz, B. A., Johnson, W. T. & Bowers, M.
(1974). Biogenic amines in autistic and atypical children.
Archives of General Psychiatry 31, 845-853.
Connell, P. H. (1958). Amphetamine Psychosis. Maudsley
Monograph No. 5. Chapman and Hall: London.
Corbett, J. A., Harris, E. & Robinson, R. (1975). Epilepsy.
In Mental Retardation and Developmental Disabilities
Vol. 7. An Annual Review (ed. J. Wortis), pp. 79-111.
Brunner/Mazel: New York.
Crane, G. E. & Smeets, R. A. (1974). Tardive dyskinesia and
drug therapy in geriatric patients. Archives of General
Psychiatry 30, 341-343.
Cross, H. A. & Harlow, H. F. (1965). Prolonged and pro-
gressive effects of partial isolation on the behaviour of
macaque monkeys. Journal of Experimental Research in
Personality 1, 39—49.
Crow, T. J. (1980). Molecular pathology of schizophrenia:
more than one disease process? British Medical Journal 280,
66-68.
Cummins, M. S. & Suomi, S. J. (1976). Long term effects of
social rehabilitation in rhesus monkeys. Primates 17,
43-51.
Denckla, M. B., Bemporad, J. R. E. & Mackey, M. D.
(1976). Tics following methylphenidate administration,
a report of 20 cases. Journal of the American Medical
Association 235, 1349-1350.
Draper, W. A. & Bernstein, I. S. (1963). Stereotyped be-
haviour and cage size. Perceptual and Motor Skills 16,
231-234.
Eisenberg, L. (1956). The autistic child in adolescence.
American Journal of Psychiatry 112, 607-612.
70 R. M. Ridley and H. F. Baker
Ellinwood, E. H. (1971). 'Accidental conditioning' with
chronic methamphetamine intoxication: implications for
the theory of drug habituation. Psychopharmacologia 21,
131-138.
Ellinwood, E. H. (1980). Neuropharmacology of ampheta-
mines and related stimulants. In Amphetamines and
Related Stimulants: Chemical, Biological, Clinical and
Sociological Aspects (ed. J. Caldwell), pp. 69-84. CRC
Press: Florida.
Ellinwood, E. H. & Kilbey, M. M. (1975). Amphetamine
stereotypy: the influence of environmental factors and
prepotent behavioural patterns on its topography and
development. Biological Psychiatry 10, 3-16.
Ellinwood, E. H., Sudilovsky, A. & Nelson, L. M. (1973).
Evolving behaviour in the clinical and experimental
amphetamine (model) psychosis. American Journal of
Psychiatry 130, 1088-1093.
Ellison, C , Nielsen, E. B. & Lyon, M. (1980). Animal model
of psychosis; hallucinatory behaviours in monkeys during
the late stage of continuous amphetamine intoxication.
Journal of Psychiatric Research 16, 13-22.
Epstein, L. C , Lasagna, L., Conners, C. K. & Rodriguez, A.
(1968). Correlation of dextroamphetamine excretion and
drug response in hyperkinetic children. Journal of Nervous
and Mental Disease 146, 136-146.
Foley, J. P. (1934). First year development of a rhesus
monkey (M. mulatto) reared in isolation. Journal of Genetic
Psychology 45, 39-105.
Foley, J. P. (1935). Second year development of a rhesus
monkey reared in isolation. Journal of Genetic Psychology
47, 39-105.
Folstein, S. & Rutter, M. (1977). Infantile autism: a genetic
study of 21 twin pairs. Journal of Child Psychology and
Psychiatry 18, 297-321.
Frith, U. (1970a). Studies in pattern detection in normal and
autistic children. I. Immediate recall of auditory sequences.
Journal of Abnormal Psychology 76, 413-420.
Frith, U. (19706). Studies in pattern detection in normal and
autistic children: II. Reproduction and production of
colour sequences. Journal of Experimental and Child
Psychology 10, 120-135.
Frith, U. (1972). Cognitive mechanisms in autism: experi-
ments with colour and tone sequence production. Journal
of Autism and Childhood Schizophrenia 2, 160-173.
Fuxe, K. & Ungerstedt, U. (1970). Histochemical, bio-
chemical and functional studies on central monoamine
neurons after acute and chronic amphetamine administra-
tion. In Amphetamines and Related Compounds (ed. E.
Costa and S. Garattini), pp. 257-288. Raven Press: New
York.
Garver, D. L., Schlemmer, R. F., Maas, J. W. & Davis, J. M.
(1975). A schizophreniform behavioural psychosis medi-
ated by dopamine. American Journal of Psychiatry 132,
33-38.
Goldberg, S. C , Klerman, G. L. & Cole, J. O. (1965).
Changes in schizophrenic psychopathology and normal
behaviour as a function of phenothiazine treatment.
British Journal of Psychiatry 111, 120-133.
Griffiths, J. D., Cavanaugh, J., Held, J. & Oates, J. A.
(1972). Dextramphetamine - evaluation of psychomimetic
properties in man. Archives of General Psychiatry 26,
97-100.
Groves, P. M. & Rebec, G. V. (1976). Biochemistry and
behaviour: some central actions of amphetamine and
antipsychotic drugs. Annual Review of Psychology 27,
91-127.
Guirand, P. (1936). Analyse de symptome stereotypie.
VEncephale 31, 229-270.
Haber, S., Barchas, P. & Barchas, J. (1977). Effects of
amphetamine on social behaviour of rhesus macaques: an
animal model of paranoia. In Animal Models in Psychiatry
and Neurology (ed. I. Hanin and E. Usdin), pp. 107-114.
Pergamon Press: Oxford.
Harlow, H. F. (1958). Behavioural contributions to inter-
disciplinary research. In Biological and Biochemical Bases
of Behaviour (ed. H. F. Harlow and C. N. Woolsey), pp.
3-23. University of Wisconsin Press: Madison.
Harlow, H. F. (1962). The heterosexual affectional system in
monkeys. American Psychologist 17, 1-9.
Harlow, H. F. (1965). The affectional systems. In Behaviour
of Non-human Primates, Vol. 2 (ed. A. M. Schrier, H. F.
Harlow and F. Stollnitz), pp. 287-333. Academic Press:
New York.
Harlow, H. F. & Zimmermann, R. P. (1959). Affectional
responses in the infant monkey. Science 130, 421-432.
Harlow, H. F., Dodsworth, R. O. & Harlow, M. K. (1965).
Total social isolation in monkeys. Proceedings of the
National Academy of Sciences 54, 90-96.
Hediger, H. (1955). Studies of the Psychology and Behaviour of
Captive Animals in Zoos and Circuses. Criterion Press: New
York.
Held, R. & Hein, A. (1963). Movement-produced stimulation
in the development of visually guided behaviour. Journal of
Comparative and Physiological Psychology 56, 872-876.
Hermelin, B. & Frith, U. (1971)- Psychological studies of
childhood autism. Can autistic children make sense of what
they hear? Journal of Special Education 5, 1107-1117.
Hinde, R. A. (1960). Energy models of motivation. Symposia
of the Society for Experimental Biology 14, 199-213.
Hinde, R. A. (1971). Social development. In Behaviour of
Non-human Primates, Vol. 3 (ed. A. M. Schrier, H. F.
Harlow and F. Stollnitz), pp. 1-60. Academic Press: New
York.
Hutt, S. J. & Hutt, C. (1968). Stereotypy, arousal and autism.
Human Development 11, 277-286.
Jacobsen, C. F., Wolfe, J. B. & Jackson, T. A. (1935). An
experimental analysis of the functions of the frontal
association area in primates. Journal of Nervous and Mental
Disease 83, 1-4.
Janet, P. (1908). Obsessions and Psychasthenia, pp. 130-132.
Alcan: Paris.
Janowsky, D. S. & Risch, C. (1979). Amphetamine psychosis
and psychotic symptoms. Psychopharmacology 65, 73-77.
Jeste, D. V. & Wyatt, R. J. (1981). Changing epidemiology of
tardive dyskinesia: an overview. American Journal of
Psychiatry 138, 297-309.
Johnstone, E. C , Crow, T. J., Frith, C. D., Carney, M. W. P.
& Price, J. S. (1978). Mechanism of the antipsychotic effect
in the treatment of acute schizophrenia. Lancet i, 848-851.
Jones, I. H. (1965). Observations on schizophrenic stereo-
typies. Comprehensive Psychiatry 6, 323-335.
Kanner, L. (1943). Autistic disturbance of affective contact.
Nervous Child 2, 217-250.
Kaplan, S. R. (1980). Benzodiazepine withdrawal symptoms.
American Journal of Psychiatry 137, 750-751.
Keeler, W. R. (1958). Autistic patterns and defective com-
munication in blind children with retrolental fibroplasia.
In Psychopathology of Communication (ed. P. H. Hoch and
J. Zubin), pp. 64-83. Grune & Stratton: New York.
Kjellberg, B. & Randrup, A. (1972a). Changes in social be-
haviour in pairs of vervet monkeys (Cercopithecus) pro-
duced by single, low doses of amphetamine. Psycho-
pharmacologia (Berlin) 26, 117.
Kjellberg, B. & Randrup, A. (19726). Stereotypy with selec-
tive stimulation of certain items of behaviour observed in
amphetamine-treated primate monkeys. Cercopithecus spp.
Pharmakopsychiatrie und Neuropsychopharmakologie 5,
1-12.
Knights, R. M. (1974). Psychometric assessment of stimulant-
induced behaviour change. In Clinical Use of Stimulant
Drugs in Children (ed. C. K. Conners), pp. 221-231.
Excerpta Medica: Amsterdam.
 Stereotypy in monkeys and humans
Kraepelin, E. (1971). Dementia Praecox and Paraphrenia
(transl. R. M. Barclay). Robert E. Krieger: New York.
Lee, T. & Seeman, P. (1980). Elevation of brain neuroleptic/
dopamine receptors in schizophrenia. American Journal of
Psychiatry 137, 191-197.
MacKay, A. V. P., Bird, E. D., Spokes, E. G., Rossor, M.,
Iversen, L. L., Creese, r. & Snyder, S. H. (1980). Dopamine
receptors and schizophrenia: drug effect or illness? Lancet
ii, 915-916.
Mason, W. A. (1968). Early social deprivation in the non-
human primates. Implications for human behaviour. In
Environmental Influences (ed. D. C. Glass), pp. 70-100.
Rockefeller University and Russell Stage Foundation:
New York.
Mason, W. A. & Sponholz, R. R. (1963). Behaviour of
rhesus monkeys raised in isolation. Journal of Psychiatric
Research 1, 299-306.
McDougall, W. (1923). An Outline of Psychology. Methuen:
London.
Meltzer, H. Y. & Stahl, S. M. (1976). The dopamine hypo-
thesis of schizophrenia: a review. Schizophrenia Bulletin 2,
19-76.
Meyer-Holzapfel, M. (1968). Abnormal behaviour in zoo
animals. In Abnormal Behaviour in Animals (ed. M. W.
Fox), pp. 476-503. W. B. Saunders: Philadelphia.
Mitchell, G. (1968). Persistent behaviour pathology in rhesus
monkeys following early social isolation. Folia primato-
logicaS, 132-147.
Mitchell, G. (1970). Abnormal behaviour in primates. In
Primate Behaviour: Developments in Field and Laboratory
Research, Vol. 1 (ed. L. A. Rosenblum), pp. 195-249.
Academic Press: New York.
Mitchell, G., Raymond, E. J., Ruppenthal, G. C. & Harlow,
H. F. (1966). Long term effects of total social isolation
upon behaviour of rhesus monkeys. Psychological Reports
18, 567-580.
Mohs, R. C , Tinklenberg, J. R., Roth, W. T. & Ropell, B. S.
(1978). Methamphetamine and diphenhydramine effects on
the rate of cognitive processing. Psychopharmacology 58,
13-19.
Novak, M. A. & Harlow, H. F. (1975). Social recovery of
monkeys isolated in the first year of life. Developmental
Psychology 11, 453-455.
Oliphant, J., Evans, J. I. & Forrest, A. D. (1960). Hunting-
ton's Chorea — some biochemical and therapeutic aspects.
Journal of Mental Science 106, 718-725.
Ounsted, C. (1955). The hyperkinetic syndrome in epileptic
children. Lancet ii, 303-311.
Owen, F., Cross, A. J., Crow, T. J., Longden, A., Poulter, M.
& Riley, G. J. (1978). Increased dopamine-receptor sensi-
tivity in schizophrenia. Lancet ii, 223-226.
Owen, F., Baker, H. F., Ridley, R. M., Cross, A. J. & Crow,
T. J. (1981). Effect of chronic amphetamine administration
on central dopaminergic mechanisms in the vervet. Psycho-
pharmacology 74, 213-216.
Parkinson, J. (1817). An Essay on the Shaking Palsy. Whit-
tingham and Rowland, London. Reprinted in Archives of
Neurology and Psychiatry 7, 681-710; Medical Classics,
Vol. 2. No. 10 (1938). Williams and Wilkins: Baltimore.
Prechtl, H. F. R. & Stemmer, C. J. (1962). The choreiform
syndrome in children. Developmental Medicine and Child
Neurology 4, 119-127.
Raleigh, M. J., Brammer, G. L., Yuwiler, A., Flannery, J. W.,
McGuire, M. T. & Geller, E. (1979). Serotonergic in-
fluences on the social behaviour of vervet monkeys (Cerco-
pithecus aethiops sabaeus). Experimental Neurology 68,
322-334.
Randrup, A. & Munkvad, I. (1965). Special antagonism of
amphetamine-induced abnormal behaviour. Inhibition of
stereotyped activity with increase of some normal activities.
Psychopharmacologia (Berlin) 7, 416-422.
71
Randrup, A. & Munkvad, 1. (1970). Biochemical, anatomical
and psychological investigations of stereotyped behaviour
induced by amphetamines. In Amphetamines and Related
Compounds (ed. E. Costa and S. Garattini), pp. 695-714.
Raven Press: New York.
Randrup, A. & Munkvad, I. (1974). Pharmacology and
physiology of stereotyped behaviour. Journal of Psychiatric
Research 11, 1-10.
Ridley, R. M. & Baker, H. F. (1981). Amphetamine psy-
chosis in the New World and Old World monkeys (Calli-
thrix jacchus and Cercopithecus aethiops). Proceedings of
the 1th Congress of the International Primatology Society,
1979. Bangalore, India (in the press).
Ridley, R. M., Baker, H. F. & Scraggs, P. R. (1979). The
time course of the behavioural effects of amphetamine and
their reversal by haloperidol in a primate species. Biological
Psychiatry 14, 753-765.
Ridley, R. M., Baker, H. F. & Crow, T. J. (1980a). Be-
havioural effects of amphetamines and related stimulants;
the importance of species differences as demonstrated by
a study in the marmoset. In Amphetamines and Related
Stimulants: Chemical, Biological, Clinical and Sociological
Aspects (ed. J. Caldwell), pp. 97-116. CRC Press: Florida.
Ridley, R. M., Baker, H. F. & Weight, M. L. (19806).
Amphetamine disrupts successive but not simultaneous
visual discrimination in the monkey. Psychopharmacology
67, 241-244.
Ridley, R. M., Haystead, T. A. J. & Baker, H. F. (1981a).
An involvement of dopamine in higher order choice
mechanisms in the monkey. Psychopharmacology 72,
173-177.
Ridley, R. M., Haystead, T. A. J. & Baker, H. F. (1981 b).
An analysis of visual object reversal learning in the
marmoset after amphetamine and haloperidol. Pharma-
cology, Biochemistry and Behaviour 14, 345-351.
Rie, H. E., Rie, E. D. & Stewart, S. (1976). Effects of methyl-
phenidate on underachieving children. Journal of Consult-
ing and Clinical Psychology 4, 250-260.
Robbins, T. W. & Sahakian, B. J. (1979). 'Paradoxical' effects
of psychomotor stimulant drugs in hyperactive children
from the standpoint of behavioural pharmacology. Neuro-
pharmacology 18, 931-950.
Rogers, C. M. & Davenport, R. K. (1969). Effects of res-
tricted rearing on sexual behaviour of chimpanzees.
Developmental Psychology 1, 200-204.
Rosvold, H. E. & Szwarcbart, H. K. (1964). Neural structures
involved in delayed response performance. In The Frontal
Granular Cortex and Behaviour (ed. J. M. Warren and
K. A. Akert), pp. 1-15. McGraw-Hill: New York.
Rowland, G. L. (1964). The effects of total social isolation
upon learning and social behaviour in rhesus monkeys.
Doctoral Dissertation: University of Wisconsin.
Rutter, M. (1972). Maternal Deprivation Reassessed. Penguin
Books: Harmondsworth.
Rylander, G. (1972). Psychoses and the punding and chorei-
form syndromes in addiction to central stimulant drugs.
Folia psychiatrica, neurologica et neurochirurgica 75,
203-212.
Sahakian, B. J. & Robbins, T. W. (1977). Are the effects of
psychomotor stimulant drugs on hyperactive children
really paradoxical? Medical Hypotheses 3, 154-158.
Schierring, E. (1979). Social isolation and other behavioural
changes in groups of adult vervet monkeys (Cercopithecus
aethiops) produced by low, non-chronic doses of d-
amphetamine. Psychopharmacology 64, 297-302.
Schiorring, E. & Hecht, A. (1979). Behavioural effects of low,
acute doses of rf-amphetamine on the dyadic interaction
between mother and infant vervet monkeys (Cercopithecus
aethiops) during the first six post-natal months. Psycho-
pharmacology 64, 219-224.
Schlemmer, R. F., Narasimhachari, N. & Davis, J. M.
72 R. M. Ridley and H. F. Baker
(1980). Dose-dependent behavioural changes induced by
apomorphine in selected members of a primate social
colony. Journal of Pharmacy and Pharmacology 32,
285-289.
Scraggs, P. R. & Ridley, R. M. (1978). Behavioural effects of
amphetamine in a small primate: relative potencies of the
d- and /-isomers. Psychopharmacology 59, 243-245.
Scraggs, P. R. & Ridley, R. M. (1979). The effect of dopamine
and noradrenaline blockade on amphetamine-induced
behaviour in the marmoset. Psychopharmacology 62,41 -45.
Scraggs, P. R., Baker, H. F. & Ridley, R. M. (1979). Inter-
action of apomorphine and haloperidol: effects on loco-
motion and other behaviour in the marmoset. Psycho-
pharmacology 66, 41—43.
Seay, B. M., Alexander, B. K. & Harlow, H. F. (1964).
Maternal behaviour of socially deprived rhesus monkeys.
Journal of Abnormal and Social Psychology 69, 345-354.
Shapiro, A. K. & Shapiro, E. (1968). Treatment of Gilles de
la Tourette's Syndrome with haloperidol. British Journal of
Psychiatry 114, 345-350.
Slater, E. & Roth, M. (1969). Postencephalitic Parkinsonism.
In Clinical Psychiatry (3rd edn), pp. 514-516. Bailliere,
Tindall and Cassell: London.
Spitz, R. A. (1945). Hospitalism. An inquiry into the genesis
of psychiatric conditions in early childhood. Psychoanalytic
Study of the Child 1, 53-74.
Stein, L. (1964). Amphetamine and neural reward mech-
anisms. In Animal Behaviour and Drug Action (ed. H.
Steinberg), pp. 91-113. Little, Brown and Co.: Boston.
Stengel, E., Oldham, A. J. & Ehrenberg, A. S. C. (1958).
Reactions of low-grade mental defectives to pain. Journal
of Mental Science 104, 434-438.
Suomi, S. J. & Harlow, H. F. (1972). Social rehabilitation of
isolate-reared monkeys. Developmental Psychology 6,
487-496.
Thelen, E. (1979). Rhythmical stereotypies in normal human
infants. Animal Behaviour 27, 699-715.
Tinbergen, N. (1951). The Study of Instinct. Clarendon Press:
Oxford.
Tinklepaugh, O. L. (1928). The self-mutilation of a male
Macacus rhesus monkey. Journal of Mammology 9,
293-300.
View publication stats
Trulson, M. E. & Jacobs, B. L. (1979). Long-term ampheta-
mine treatment decreases brain serotonin metabolism:
implications for theories of schizophrenia. Science 205,
1295-1297.
Weight, M. L., Ridley, R. M. & Baker, H. F. (1980). The
effects of amphetamine on delayed response performance
in the monkey. Pharmacology, Biochemistry and Behaviour
12, 861-864.
Weiss, B. & Laties, V. G. (1971). Reconciling the effects of
amphetamine on human and animal behaviour. In The
Correlation of Adverse Effects in Man with Observations in
Animals (ed. S. D. de Baker), pp. 32-36. International
Congress Series no. 220. Excerpta Medica: Amsterdam.
Weiss, G. & Minde, K. K. (1974). Follow-up studies of
children who present with symptoms of hyperactivity. In
Clinical Use of Stimulant Drugs in Children (ed. C. K.
Conners), pp. 67-78. Excerpta Medica: Amsterdam.
Whitaker, P. M., Crow, T. J. & Ferrier, I. N. (1981). Tritiated
LSD binding in frontal cortex in schizophrenia. Archives
of General Psychiatry 38, 278-280.
Wiesel, T. N. & Hubel, D. H. (1963). Effects of visual
deprivation on morphology and physiology of cells in the
cat's lateral geniculate body. Journal of Neurophysiology
26, 978-993.
Wing, L., Yeates, S. R., Brierley, L. M. & Gould, J. (1976).
The prevalence of early childhood autism: comparison of
administrative and epidemiological studies. Psychological
Medicine 6, 89-100.
Winsberg, B. G., Bialer, L., Kupietz, S. & Tobias, J. (1972).
Effects of imipramine and dextroamphetamine in be-
haviour of neuropsychiatrically impaired children.
American Journal of Psychiatry 128, 1425-1431.
Woodworth, R. S. (1918). Dynamic Psychology. Columbia
University Press: New York.
Yarrow, J. L. (1964). Separation from parents during early
childhood. In Review of Child Development Research (ed.
M. L. Hoffman and L. N. W. Hoffman), pp. 89-136.
Russell Sage Foundation: New York.
Zeigler, H. P. (1964). Displacement activity and motivational
theory. A case study in the history of ethology. Psycho-
logical Bulletin 61, 362-376.