COMMENTARY

CURRENT
OPINION Psychosis induced by amphetamines
Jørgen G. Bramness a and Eline B. Rognli a,b,c

Purpose of review
The study reviews publications on the use of methamphetamine and amphetamine in relation to psychotic
symptoms, substance-induced psychosis, and primary psychosis published between July 2014 and
December 2015. The databases MEDLINE, Embase, and PsycINFO were searched using the terms
‘amphetamine psychosis’ and ‘methamphetamine psychosis’ for the time period 1 July 2014 to 31
December 2015.
Recent findings
There were 37 studies published on the subject during this time period. Risk factors for psychotic symptoms,
substance-induced psychosis, and primary psychosis included patterns of drug use, but results also pointed
to the importance of nondrug-related vulnerability. Cognitive impairment is associated with both
amphetamine use and psychosis, and the impairment among those with amphetamine-induced psychosis
resembles that of schizophrenia. At the neuronal level, GABAergic mechanisms may offer some
understanding about the association between stimulant use and psychosis. Several different types of
antipsychotic medication are effective for treating agitation and psychosis, but drugs with high DRD2
blockade should be used with caution. Some novel treatments are described, but are not sufficiently
repeated to be recommended.
Summary
During the past 18 months, studies have been published that cover risk factors, neuronal mechanisms, and
treatment. These recent results do not differ from previous understandings, but the role of cognition and
GABAergic dysfunction should be further investigated, and knowledge about resilience factors is still
scarce. Also, a clearer evidence base for medical treatment of psychosis with concurrent amphetamine use
is warranted.
Video abstract
http://links.lww.com/YCO/A33
Keywords
amphetamine, drug treatment, methamphetamine, neurobiology, psychosis

INTRODUCTION unanswered. Newer studies have provided import-

Two review studies, published in 2015 as articles in
volume 120 of the International Review of Neurobiol-
ogy, summarize parts of our knowledge on psychosis
following the use of amphetamine and meth-
amphetamine (hereafter ‘amphetamines’) [1,2].
They point out that psychosis following the use
of amphetamines is characterized by persecutory
delusions and auditory hallucinations, but other
types of hallucinations and negative symptoms
occur, resembling acute schizophreniform psycho-
sis. Both studies highlight the dose–response
relationship between exposure to amphetamines
and precipitation of psychosis, as well as the
increased risk following earlier use, more use, and
more severe dependence. Even though these reviews
touch on some central features of psychosis induced
by amphetamines, they leave many questions
ant and updated knowledge about risk factors that
precipitate psychosis, the possible transition from
amphetamine-induced to primary psychosis, and
the treatment of psychosis induced by amphet-
amines. The aim of this study is to review the
literature from the past 18 months on psychosis
a
Norwegian Centre for Addiction Research (SERAF), University of Oslo,
b
Division of Mental Health and Addiction, Oslo University Hospital, Oslo
and cNorwegian National Advisory Unit on Concurrent Substance Abuse
and Mental Health Disorders, Brumunddal, Norway
Correspondence to Jørgen G. Bramness, Norwegian Centre for Addic-
tion Research (SERAF), Institute of Clinical Medicine, Box 1039 Blind-
ern, 0315 Oslo, Norway. Tel: +47 23368977; fax: +47 23368986;
e-mail: j.g.bramness@medisin.uio.no
Curr Opin Psychiatry 2016, 29:236–241
DOI:10.1097/YCO.0000000000000254

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Number 4
July 2016

Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

 Psychosis induced by amphetamines Bramness and Rognli

2015. Hits were manually reviewed by the first

KEY POINTS

Severity of the use of amphetamines is found by some,
but not all, to be associated with psychosis.

Cognitive deficits are associated with both stimulant use
and psychosis, and more research on causal
mechanisms is warranted.

Some claim primary and substance-induced psychosis
to be distinguishable disorders, but others have found
pronounced similarities and high transition rates
author to ensure relevance, and they were all
categorized as either a review or belonging to the
categories ‘attention-deficit hyperactivity disorder
(ADHD)’, ‘cognition’, ‘comorbidity’, ‘comparison
with schizophrenia’, ‘drug use as risk’, ‘GABA’,
‘prefrontal cortex’, ‘transition to schizophrenia’,
‘treatment’, or ‘use in psychosis’ (Fig. 1). Altogether
36 relevant studies were identified. One additional
review by the authors, not listed in these databases,
was added [3 ].
&&

between the two.

The association between use of amphetamines and
psychosis may involve GABAergic cortical dysfunction RESULTS AND DISCUSSION
or damage.
Risk factors for psychosis induced by

A wide spectrum of antipsychotics can be used to treat amphetamines
agitation and psychosis, but drugs with high DRD2
blockade should be used with caution.
Substance use as risk factor
Several studies explore pattern of substance use as a
risk factor for precipitation of psychotic symptoms,
following amphetamine use and to highlight substance-induced psychosis, and primary psycho-
novel findings. sis in users of amphetamines.

MATERIALS AND METHODS Psychotic symptoms

The databases MEDLINE, Embase, and PsycINFO In young offenders (14–18 years), dependence on
were searched using the search terms ‘amphet- amphetamines or sedatives, as well as daily use of
amine psychosis’ and ‘methamphetamine psycho- cannabis and sedatives, is associated with psychotic
sis’ for the time period 1 July 2014 to 31 December symptoms [4].

ADHD, 2
Drug use in
psychosis, 3

Cognition, 4
Treatment, 4

Comparison with
Prefrontal cortex, 3 schizophrenia, 5

Transition, 1

Comorbidity, 1

Review, 7 Drug as risk, 6

GABA, 2

FIGURE 1. Studies on psychosis following use of amphetamines from 1 July 2014 to 31 December 2015 by theme (N ¼ 37).
Broad categories are chosen, but one study may belong to more than one category. Review studies are only belonging to
review category as they often contain information on several points of interest.

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Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

Addictive disorders
Drug-induced psychosis
The intensity of stimulant use, as measured by high
number of years with daily use of stimulants or a
diagnosis of stimulant dependence, is associated
with increased risk of substance-induced psychosis
[5]. In contrast to this, a study by our group in a
sample of amphetamine users from the Swedish
criminal justice system found that sociodemo-
graphic and psychiatric risk factors were related to
later hospitalization because of substance-induced
psychosis but pattern of substance use (age of onset
and years of use) was not [6]. There also seems to be
an interaction between frequency of use of meth-
amphetamine and adverse childhood experiences.
High use of methamphetamine seems to be a greater
risk factor for psychosis among those with more
adverse childhood experiences [7], playing into
the notion of a stress vulnerability model as
suggested previously by our group [8]. However, this
could be because of competing risks for psychosis.
Primary psychosis
Polysubstance use, including the use of amphet-
amines, lowers the age of onset of schizophrenia
spectrum disorders [9]. However, a study from
the Swedish criminal justice system found that
sociodemographic and psychiatric risk factors were
related to primary psychosis, but pattern of amphet-
amine use was not [6]. This discrepancy could be
because of the age differences between the groups
studied, and drug use may have a greater effect on
psychosis in the young than in the old [9].
Attention-deficit hyperactivity disorder
The link between ADHD and amphetamine-induced
psychosis has been noted from early on [8]. Patients
with ADHD have an increased tendency to abuse
stimulant drugs [5]. Central stimulants used for
treatment of ADHD may also precipitate psychosis
[10]. However, it has been suggested that the link
between ADHD and psychosis is not mediated by
drug use, but rather through a common dysphoric
&&
mood [11 ].
Cognition
Cognitive impairment may follow the use of
amphetamines, and seem to precede psychosis in
users [8], suggesting cognitive impairment as a
possible mediator between use of amphetamines
and psychosis. Among psychotic patients who have
used stimulants, recent and frequent use of stimu-
lants increase the risk of cognitive impairment
&&
[12 ]. Cognitive stability is also reduced among
users of stimulants, indicated by the fact that
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intraindividual variability in cognitive performance
is greater among users of methamphetamine
compared with nonabusing controls, but the esti-
mates only reached statistical significance among
those who have experienced methamphetamine
psychosis [13]. When individuals with different
duration of methamphetamine-induced psychosis
are compared, the cognitive impairment in those
with persistent methamphetamine-induced psy-
chosis resembles that seen in patients with schizo-
phrenia, whereas those with transient psychosis are
less impaired [14]. Also here, nonpsychotic patients
with methamphetamine use showed less cognitive
impairment. Yet another recent study shows that
the cognitive impairment of psychosis following use
of amphetamines resembles that found in schizo-
phrenia, although functions related to the frontal
lobes seem to be somewhat different [15].
Complex relationship between primary
psychosis and amphetamine-induced
psychosis
Use in patients with primary psychosis
People with primary psychosis use more substances
and are more often substance-dependent than
individuals without psychosis. Approximately half
of those with primary psychosis also have a sub-
stance use disorder, and approximately one-third of
these have stimulant use disorders [16,17]. Use is
more common in young people in urban areas, and
is related to negative outcomes like mental health
admissions, increased self-harm, and more home-
lessness [16,17]. An interesting study from the
Middle East among first-episode psychosis patients
shows a somewhat lower rate of substance use
disorders in general, but a similar rate of stimulant
use [18]. Here, use was higher in single nonimmi-
grant men with higher education.
Comparison between substance-induced
and primary psychosis
Several earlier studies have shown considerable sim-
ilarities between symptoms of acute schizophrenia
and psychosis induced by amphetamines [8]. Glas-
&
ner-Edwards and Mooney [19 ], however, claim that
with thorough diagnostics and observing how long
the psychosis lasts, it is possible to distinguish the
two. A qualitative study found the clinical manifes-
tation of psychosis induced by amphetamines to be
different from that induced by schizophrenia, with
more rare symptoms such as vivid visual hallucina-
tions [20]. A review of methamphetamine use in Iran
provided information that such vivid visual halluci-
nations are a known clinical phenomenon [21].
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July 2016

Two studies show similar cognitive impairment
in those with psychosis induced either by amphet-
amines or by schizophrenia [14,15]. A study
using inhibition tasks found great similarities
in the ventrolateral prefrontal cortex, suggesting
similarities in the underlying pathophysiology of
psychosis induced by amphetamines and by schizo-
phrenia [22]. However, both this and another study
found that, despite great similarities, there are also
subtle differences in the prefrontal cortex [23].
Those with methamphetamine-induced psychosis
show a similar age of onset of methamphetamine
use and the same frequency of current substance use
&
as those with primary psychosis [24 ], but the former
have fewer hospital admissions and lower use of
antipsychotics despite similar severity of psychotic
symptoms. In all other respects, the two groups
looked quite similar.
Transition to primary psychosis
A study by our group showed that approximately
one-third of the patients diagnosed with amphet-
amine-induced psychosis over time ended up with a
diagnosis of primary psychosis, indicating that there
is a substantial transition in diagnosis over time
&
[25 ]. Our group also published a review of seven
studies investigating transition rates, and found a
range from 13 to 64% for substance-induced
psychosis in general, and from 22 to 33% for
amphetamine-induced psychosis [3 ].
&&
Neurobiology
As pointed out earlier, cognitive impairment is both
a risk factor for amphetamine-induced psychosis and
a possible consequence both of use and of psychosis.
It may be that all neurobiological factors should
be viewed as both risk ‘and’ consequence of use of
amphetamines and of psychosis following use.
Repeated administration of methamphetamine
to rats can produce changes in the prefrontal cortex,
which could elucidate the cognitive and behavioural
dysfunctions seen in psychosis precipitated by
amphetamines and which could also explain
increased vulnerability and transition to primary
&
psychosis [26 ]. Interestingly, a dysfunctional GABA-
ergic system could play a role both in use of amphet-
amines and proneness to psychosis [27]. Use of a
benzodiazepine antagonist increases the likelihood
of positive psychotic symptoms after the use of
amphetamines in healthy volunteers [28]. These find-
ings are interesting because GABAergic cortical dys-
&
function seems to be related to schizophrenia [29 ].
A theory-driven study by Hsieh and coworkers
& &
[29 ] sums up much of the knowledge on the neuro-
biology of psychosis induced by amphetamines and
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Psychosis induced by amphetamines Bramness and Rognli
partially compares this with schizophrenia, offering
a description of the potential neuronal mechanisms
involved in the transition from drug-induced psy-
chosis to schizophrenia. Earlier theories have
suggested that the presence of free monoamines
in axonal terminals because of amphetamines’ inhi-
bition of the vesicular monoamine transporter of
the monoaminergic cells could result in neuronal
apoptosis [30]. This could elucidate sensitization to
the psychotic effects of amphetamines and ulti-
mately the transition to primary psychosis or
chronic amphetamine-induced psychosis as is the
preferred terminology and understanding in Asia
[8]. Hsieh and coworkers suggest an alternative
model where the excessive enhancement of dopa-
minergic pathways leads to glutamate overflow
in the cerebral cortex, damaging GABAergic inter-
neurons in the cerebral cortex. The loss of GABA-
ergic interneurons in the cerebral cortex leads
to dysregulation of glutamate in the cortex precip-
&
itating psychosis [29 ].
Drug treatment
Early studies showed that psychosis following intake
of amphetamines in healthy study participants
could be inhibited by the use of antipsychotic drugs
[31,32]. Furthermore, psychosis precipitated by
amphetamines can be treated with antipsychotics.
However, a Cochrane review from 2009 identified
only one randomized controlled trial of treatment
for psychosis induced by amphetamines, which met
high-quality criteria [33]. The study, and thus the
Cochrane review, showed that both olanzapine and
haloperidol in clinically relevant doses were effec-
tive in treating psychotic symptoms. A new review
identified five randomized controlled trials, two
prospective controlled studies, four case series,
and 10 case reports on the use of antipsychotics
for the treatment of psychosis following use of
amphetamines [34]. One of the studies included
in this updated review was also picked up by the
&
literature search for this study [35 ]. In addition, we
identified two cases on the use of clozapine in treat-
ment of resistant methamphetamine psychosis
showing favourable results [36]. All these studies
taken together suggest that olanzapine, haloperidol,
aripiprazole, risperidone, and quetiapine, and
possibly also droperidol and clozapine, can be used
in the treatment of amphetamine-induced psycho-
sis and in psychosis with concurrent amphetamine
use. Haloperidol may be less recommended owing to
higher levels of extrapyramidal side-effects, dysto-
nia, and prolonged QT interval, and also because of
the possibility of GABAergic cell death [19 ]. In
summary, the literature suggests that risperidone
www.co-psychiatry.com 239
Addictive disorders
is more effective in treating positive symptoms
than aripiprazole, but may be less tolerated because
of its purer DRD2 profile [34].
As atypical antipsychotics may interfere with
QTc time, it could be that their use should
be restricted in the acute phase, while the heart is
still affected by amphetamines, to prevent increased
risk of cardiovascular events [37,38]. In the immedi-
ate acute phase, the use of benzodiazepines will be
a good alternative [39] and is recommended in
guidelines [40,41]. However, the updated review
identified only one case series and one case report
using benzodiazepines, leading to the conclusion
that benzodiazepines may be adequate for control-
ling agitation, but less evidence is available for their
use in treating psychosis [34].
The review also identified one case report using
a a2-adrenergic agonist [34] and we found one study
from Iran that used ECT on treatment resistant
methamphetamine psychosis [42]. None of these
treatments can be recommended as evidence-based
treatments for amphetamine-induced psychosis
or psychosis with concurrent amphetamine use,
but should inspire further research to provide
more evidence.
CONCLUSION
Much of the new research on psychosis following
the use of amphetamines tries to differentiate
between primary psychosis and psychosis following
use of amphetamines. Although some studies
find small differences in clinical expression or neu-
rocognitive function, the similarities between the
two conditions seem more and more evident.
The association with ADHD and similarities with
schizophrenia, both in neurobiology and cognitive
deficits, points to vulnerability being a central
part of the risk for developing psychosis after use
of amphetamine. New information has emerged
on the possible mechanism for the sensitization
to amphetamines and ultimately the transition
to primary psychosis. Several new trials have shown
that the use of a wide spectrum of antipsychotics
is effective in treating both agitation and psychosis,
but one should be careful in the use of drugs with
high DRD2 blockade and drugs that might increase
QTc time.
Research in the future should not so much focus
on the differences between substance-induced and
primary psychosis, but rather on factors linked
to resilience toward the development of both types
of psychosis. Some people seem to be able to use
central stimulants in abundance without precipitat-
ing such adverse events, and research on resilience
or protective factors could be as useful as research on
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risk factors. Also, further research on prefrontal
cortex and possible GABAergic deficits would be
of interest in identifying vulnerable individuals.
Acknowledgements
All the work included in this study was performed by the
two coauthors.
Financial support and sponsorship
None.
Conflicts of interest
There are no conflicts of interest.
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