Secondary Schizophrenia (51 page)

chotic syndrome. They provided additional evidence
Charles-Nicolas
[28]
studied the histories and clin-implicating a premorbid vulnerability to psychosis as
ical pictures of 25 amphetamine-abusing chronic psy-well as to early and heavy amphetamine use in individ-chotic patients. He found seven of them to have had
uals developing chronic or prolonged postabstinence
no psychotic tendencies before the addiction. These
psychotic syndromes
[35].
Additionally, Chen and col-patients were followed in his center for several years
leagues
[35]
showed that family members of patients
prior to the onset of psychosis.

with MAP had a five times greater morbid risk for
The clinical characteristics of MAP have been
schizophrenia than users without psychosis.

well described in the Japanese population
[29].
MAP

Disturbance of consciousness due to MA abuse was
involves paranoid-hallucinatory states indistinguish-reported in two patients by Nakatani and Hara
[16].

able from paranoid schizophrenia, with residual voli-These authors noted that in both cases mental status
tional disturbances (e.g., loss of spontaneity and idle-changed, passing through three distinct stages: rest-ness). Paranoid-hallucinatory states persist after the
lessness and insomnia, hallucinatory paranoid state,
pharmacological effects of MA have worn off and
and disturbance of consciousness following a period
readily reappear upon re-injection of MA. Addition-of amphetamine use. In addition to delirium dur-ally, individuals with a history of MAP were also
ing intoxication, Askevold
[36]
described abstinence
observed to experience spontaneous recurrence of
delirium in amphetamine abusers, reporting a latency
their paranoid-hallucinatory states in response to
period between the beginning of abstinence and the
stress
[29].

onset of delirium of between 3 and 10 days, followed
Goto
[30]
described 23 patients with persisting
by a period of delirium of between 4 and 18 days. Fatal
MAP who suffered from residual symptoms such as
delirium has also been reported in association with
emotional blunting or manic-depressive states follow-cocaine intoxication
[37].

ing a drug-free period of 4.6–9.7 years. Utena and col-In a sample of 19 subjects who met DSM-IV cri-leagues
[31]
reported that 5% of patients with MAP

teria for amphetamine or cocaine-induced psychosis,
were hospitalized for years after the cessation of MA
Harris and Batki
[7]
showed that all had persecu-use because of their volitional disturbances (as noted
tory delusions; 95% had bizarre delusions, 53% had
earlier).

grandiose delusions, and 32% had somatic delusions.

Sato and colleagues
[10]
observed that MAP

Of the entire sample, 95% experienced auditory hal-

130

patients may develop acute paranoid psychotic exac-lucinations, with 32% describing voices of running
Chapter 9 – Stimulants and psychosis

commentary and 58% hearing more than one voice
a common clinical scenario that presents the clinician
conversing with each other. Additionally, 68% had
with a diagnostic dilemma:

visual, 26%, tactile, and 26%, olfactory hallucinations. Although negative symptoms were less than
In summary, a teenage male with no evidence of increased risk for
what would be expected in a group of schizophrenia
schizophrenia (i.e. no abnormal behaviour, good school performance,
patients, they were detectable (particularly anergia)
good social skills, and lack of family history of psychiatric disorders
and correlated significantly with length of stay in the
except drug use) began abusing amphetamine and marijuana on a
emergency room or subsequent hospitalization.

regular basis with occasional use of hallucinogens and cocaine for a
Yui and colleagues
[29]
observed that paranoid-period of about 10 years. Family pressure was applied and he stopped
hallucinatory states gradually disappear, although
drug use. In a few weeks, he began to develop paranoid ideations
idleness and emotional flattening tend to increase 1

that became delusions. Delusions were nonbizarre at the beginning
month after the cessation of MA use. Although at
but progressively became more bizarre and hallucinations eventually
odds with Connell’s
[25]
original observations that
also occurred. There was no evidence of continued amphetamine use
amphetamine psychosis is never prolonged after excre-but marijuana was used occasionally. The patient also exhibited nega-tion of MA in the urine, suggesting that continued
tive symptoms (withdrawal and alogia). The patient’s positive symp-use of MA is essential to maintain the psychosis syn-toms responded well to haloperidol but without effect on negative
drome, some have suggested that the development
symptoms.

of MAP may be etiologically related to persisting
brain damage or changes in brain metabolism induced
Flaum and Schultz
[41]
proposed that this case
by MA
[32].
Yui and colleagues concluded that the
suggested an etiologic role for amphetamine and
Japanese experience of MAP, in which psychotic symp-polysubstance use in the development of a chronic
toms can develop with the progression of MA-induced
schizophrenia-like psychotic disorder. Whether some
brain damage in the course of chronic MA use, there-form of genetic liability to developing a psychotic dis-fore differs from Connell’s experience. However, the
order existed in this case could not be positively ruled
authors note that, in Japan, MA is injected without any
out, and brings to focus the chicken and egg nature of
other substance, with most users re-injecting before
the question raised here. Early work by Angrist and
the effects of the previous MA injection have dimin-Gershon
[5]
suggested that a predilection to the psy-ished. They conclude that such exclusive and repeti-chogenic effects of stimulants is an important factor
tive use of MA may engender enduring vulnerability to
contributing to the emergence of these symptoms with
paranoid-hallucinatory states, leading to spontaneous
stimulant use.

recurrences of MAP
[2].

Schuckit
[24]
conducted a systematic review of
manuscripts published in the English language since
Recent studies of amphetamine

approximately 1970 in order to investigate the comorbidity between substance-use disorders and psychi-

psychosis

atric conditions. Results of this review generally
In a recent systematic review, Curran and colleagues
supported the conclusion that substance-use men-

[38]
concluded that there was clear evidence that “irre-tal disorders exist, especially regarding stimulant-or
spective of the individual’s mental state, a large enough
cannabinoid-induced psychoses, substance-induced
dose of a stimulant drug can produce a brief psychotic
mood disorders, and substance-induced anxiety con-reaction, usually lasting only hours and being self-ditions. Schuckit
[24]
concluded that “temporary
limiting in the majority of individuals.” The pattern
schizophrenia-like conditions of hallucinations (pre-of stimulant abuse most commonly associated with
dominantly auditory) and/or delusions (usually para-the induction of psychosis is the initial use of lower
noid) developing without insight and observed in a
doses, typically administered in an escalating manner
clear sensorium can be induced by stimulants.” How-and ultimately leading to multiple binges or runs
[39,

ever, Schuckit cautioned that these conditions should
40].
Emergence of psychotic syndromes usually occurs
be distinguished from the life-long schizophrenic
during a binge.

disorders, as they are likely to require only short-Chronic psychosis, on the other hand, may emerge
term antipsychotic medications, whereas schizophre-during a period of abstinence. Flaum and Schultz
[41]

nia often requires treatment with medications for
131

presented a demonstrative case in detail exemplifying
many years.

Organic Syndromes of Schizophrenia – Section 3

Cocaine-induced psychosis

observation that although cocaine-induced psychosis
shows sensitization (i.e., psychosis becomes more
Post
[42]
reviewed the evidence for cocaine-induced
severe and occurs earlier with repeated cocaine use),
psychosis and its predeterminants. He reported that
this occurs only with psychosis and not with other
with chronic cocaine use, a syndrome of insomnia,
effects of cocaine
[49]
. Moreover, cocaine abusers
painful delusions, and apathy can develop. This phase
who exhibit sensitization to the psychogenic effects of
occurs during the transition from initial euphoria to
cocaine seem to have less naturally occurring crav-paranoid psychosis. When the cocaine-induced para-ing and are likely to reduce their cocaine and other
noid psychosis is fully developed, it is almost indis-substance use
[50].
Some researchers found cocaine-tinguishable from paranoid schizophrenia. Post stated
induced psychosis and schizophrenia to be distinct
that with cessation of cocaine use, hallucinations usu-enough as to question the concept of cocaine psy-ally stop, but delusions may persist.

chosis as a model for schizophrenia
[51].
These inves-Satel and Edell
[43]
showed that heavy cocaine
tigators highlighted that increased intensity of col-users who experience transient paranoia while intox-ors, change of light intensity, objects appearing more
icated may be at higher risk for development of psy-vivid, and macropsia and micropsia were reported by
chosis than cocaine users who do not experience para-the cocaine-intoxicated individuals. They also stated
noia. However, the development of a cocaine-induced
that even if paranoia is present, it tends to be rather
chronic psychosis seems to be rare
[44].
Rounsaville
transitory.

and colleagues
[45]
found that only 4 (all male) of 298

chronic cocaine users had received the diagnosis of
schizophrenia or schizoaffective disorders.

Biological studies

Given the dearth of well-defined cohorts of stimulant-

Follow-up studies

induced psychosis patients, it is not surprising
Although essential to clarify differences between
that genetic, pharmacological, neuropsychological,
drug-induced and idiopathic psychotic syndromes,
electrophysiological, or imaging studies specifically
follow-up studies are rare in this literature. A 6-year
addressing this population are few.

follow-up study provided evidence that chronic use
In one study, patients with a history of MAP exhib-of stimulants, but not depressants or narcotics, can
ited impairment of selective attention, although with
lead to the development of a psychotic disorder that is
less cognitive deficit than schizophrenic patients
[29].

not secondary to acute intoxication
[46]
. On the other
Similarly, in mild to moderate drug use in humans, no
hand, a significant number of patients who used seda-differences were found between the effects of cocaine
tives developed serious depression. Typically, cocaine
and amphetamine on cognition
[52].

abusers develop delusions and hallucinations that tend
Information processing studies utilized the event-to be related to their drug use behavior (e.g., ideas
related potential (ERP) technique to assess deficits in
of being watched). Furthermore, first-rank Schneide-these populations. Iwanami and colleagues
[53]
found
rian symptoms (e.g., thought withdrawal and thought
that methamphetamine dependence correlated with a
broadcast), tend to be absent in cocaine-intoxicated
reduction in P3a amplitude, a marker of detection of
patients who are experiencing psychotic symptoms
novelty. Methamphetamine psychosis was associated
[47].
Retrospectively, formal thought disorder and
with reduced mismatch negativity (MMN), an indica-bizarre delusions significantly predicted a diagnosis
tor of preattentive ability to detect change in ongoing
of schizophrenia, with odds ratios (OR) of 3.55:1 and
sensory input, and not P300. Earlier, the same group
6.09:1, respectively. Suicidal ideation (OR
=
0.32:1),
reported MAP subjects to have reduced P300 ante-intravenous cocaine abuse (OR
=
0.18:1), and a history
riorly, whereas schizophrenia patients reduced more
of drug detoxification (OR
=
0.26:1) or methadone
posteriorly, suggesting differences in the orientation
maintenance (OR
=
0.18:1) demonstrate inverse rela-of the cerebral sources of the activity
[54].
The same
tionships with a schizophrenia diagnosis
[48].