Abstract
A recent trend in the availability of amphetamine-related stimulants in Australia and New Zealand is the emergence of different forms of methamphetamine, 1 – 4 with the most readily available form being methamphetamine powder (‘speed’). Since around 1998, there has been increased availability of more potent forms of methamphetamine, 1 – 4 namely base methamphetamine (‘base’) and crystalline methamphetamine (‘ice’). ‘Base’ is a sticky, gluggy, waxy or oily form of damp powder, paste or crystal. ‘Ice’ is a high-purity crystalline form of methamphetamine, also known as ‘crystal’, ‘crystal meth’, ‘P’, ‘Pure’ and ‘shabu’.
Reports indicate that base and crystalline methamphetamine have a higher potential to cause dependence than powdered methamphetamine, and are associated with higher rates of psychiatric harm 3 and an increase in psychotic symptoms in methamphetamine users in Australia and New Zealand. 2 , 3 , 5
Methamphetamine psychosis usually occurs during a phase of chronic, high-dose use, but can be seen with one or several large doses. The clinical picture resembles paranoid schizophrenia, and sometimes mimics mania. 6
Clinical features 6 , 7 include high levels of suspiciousness, with delusions of reference and persecution in a state of clear consciousness. The individual has no insight and is usually very frightened, leading to panicky or aggressive behaviour. ‘Defensive violence’ can occur in the presence of persecutory beliefs, such as a fear that others are plotting against one. 2 Hallucinations may or may not be present. They may be auditory, tactile, visual, gustatory or olfactory.
Once stimulant use ceases, the psychosis usually clears within days to a month. 6 However, protracted symptoms have been reported in some patients and may represent the emergence of schizophrenia or a form of protracted drug-induced psychosis. 1 , 8 Individuals with previous methamphetamine psychosis appear to have an ongoing vulnerability to further episodes of psychosis with further exposure to methamphetamine or stress. Neuroleptics appear to prevent such a recur-rence. 9 There are also reports of patients with persistent methamphetamine psychosis developing longlasting residual symptoms resembling the negative symptoms of schizophrenia, including emotional blunting and volitional disturbances. 9
CASE DESCRIPTION
JH (not her real initials) is a 44-year-old mother of three who lived with her violent defacto partner. She had a 27 year history of opioid dependence, which had been successfully managed for 18 years on methadone until she stopped the methadone abruptly. She presented in opioid withdrawal requesting further methadone treatment and was stabilized on 60 mg daily. She was hepatitis C positive.
JH had been a shy, anxious child who developed problems with conduct disorder in adolescence after her father's death when she was 12 years old. She associated with an older peer group who introduced her to drug use. She had behavioural difficulties at school and left in Year 9, subsequently working as a waitress and prostitute to support an addiction to heroin. She had a number of relationships with abusive, antisocial male partners and had three children to different fathers. She maintained a supportive relationship with her mother. There was no family history of mental health or substance-use problems.
Psychiatric history included a suicide attempt at 23 after a relationship breakup, during benzodiazepine intoxication. She responded to antidepressant medication and counselling. There was no history of psychosis prior to the onset of regular methamphetamine use.
Other psychiatric history included the development of psychotic symptoms 4 years previously after chronic high-dose use of powdered methamphetamine (injecting 2 g or more daily for 12 months) followed by crystalline methamphetamine (injecting 1 g or more daily for 12 months). She was not abusing other drugs or alcohol during this time. She was aware of some problems with misperceiving things around her on powdered methamphetamine and developed frank hallucinations and persecutory delusions with regular crystalline methamphetamine use. She believed her partner was injecting her with drugs, and she saw persecutory messages written on objects around her. At times, she worried that cameras and bugs were planted in the ceiling. She had good insight into these symptoms; they did not interfere with her life and she sought no treatment for them. They gradually subsided during 2 years of minimal stimulant use, at a time when she was on methadone and not abusing other drugs or alcohol.
JH reported resumption in daily crystalline methamphetamine use in the 12 months prior to assessment, injecting up to 2 g daily with her partner and more recently 0.125 g three times daily. During this time, she was on methadone and not abusing other drugs or alcohol. After 4–6 months of daily methamphetamine use, she experienced persecutory delusions and vivid visual hallucinations. She again believed her partner was injecting her with drugs. She could see unpleasant messages directed at her and written all around her. Over the 12 months, she had four brief admissions to psychiatric units with a diagnosis of Delusional Disorder. Her methamphetamine use was overlooked as she minimized her drug use and had no urine drug screens. She was treated with risperidone and later olanzapine, but ceased them as an outpatient.
At assessment, she reported ongoing psychotic phenomena. She saw persecutory writing all around her, being on her skin, the clouds and the walls. The writing said she was a ‘crazy bad woman’ and her children would be sexually harmed or burned. She believed her partner was responsible. She tried to scrape the writing off her skin with a knife. Her skin was covered in skin picking marks from stimulant abuse, but she wondered if her partner had secretly injected her.
She went to a motel to escape. She hallucinated her partner talking to his sister, and spent all night looking under doors to make sure he had not followed her. She thought she had been raped, injected with poisons and had a microchip implanted in her body. She felt it was part of an elaborate plan by her partner to drive her mad. She slept with a screwdriver and switchblade knife under her bed.
At interview, she was well dressed and had normal social skills, speech and language. She was very distressed, but had no suicidal thoughts.
She was started on quetiapine and admitted as a voluntary patient for 2 weeks, as her symptoms were slow to settle and she reported thoughts of wanting to harm her partner. Because of concerns for his safety, he was notified with her permission. The option of taking out an AVO against him was not pursued because of fears of violent reprisal. The Department of Community Services was already involved and was notified. Quetiapine was increased to 800 mg daily and within a week her psychotic symptoms abated. Monthly reviews over 18 months revealed a stable mental state with no evidence of psychotic, affective, negative or abnormal cognitive symptoms. She had full insight into her symptoms. Because of chronic insomnia, quetiapine was slowly reduced to 150 mg at night with no recurrence of symptoms. She remained on 70 mg of methadone daily. Drug and alcohol abuse were not evident apart from use of powdered methamphetamine every 2 months. During this time, she separated from her partner, cared for her children part-time and sought specialist review of her Hepatitis C.
She experienced a brief but rapid recurrence of symptoms after 12 months when she injected less than 1 g of powdered methamphetamine during a week when she ran out of quetiapine and was robbed by a male friend. While it was likely that she had been victimized by this man, her interpretation of events escalated to a delusional level. She believed that he had sabotaged her phones, painted inside her house, defrauded her using her credit cards and physically violated her. She was afraid that he would shoot her and barricaded herself inside her house, frequently calling the police. She had no plan to harm him, and acute admission was not required. She restarted quetiapine 400 mg, stopped methamphetamine and avoided the man concerned. The psychotic symptoms rapidly resolved and were no longer evident 2 weeks later. She has remained on quetiapine 200 mg at night with a normal mental state and minimal methamphetamine use.
CONCLUSIONS
JH was an emotionally vulnerable child who developed features of Cluster B personality traits after the loss of her father in early adolescence. These traits included emotional instability, impulsivity with severe drug dependence and intense, unstable interpersonal relationships (particularly with abusive, antisocial male partners).
JH presented with a chronic and recurrent metham-phetamine-induced psychosis characterized by vivid visual hallucinations, delusions of persecution and fleeting auditory hallucinations. A diagnosis of schizophrenia appeared unlikely because of the close time relationship of symptoms to methamphetamine use, the absence of psychosocial decline, eventual resolution of symptoms with abstinence, absence of formal thought disorder with retention of insight and lack of a family history. 6 , 10 While the presence of negative and cognitive symptoms are not required to make the diagnosis of schizophrenia, these features are commonly part of the disorder and were notably absent in JH's case. A diagnosis of schizoaffective disorder appeared unlikely in the absence of manic or depressive symptoms. 10 The chronological relationship of methamphetamine use to the onset and remission of psychotic symptoms, as well as the presence of prominent visual hallucinations, indicates that a diagnosis of delusional disorder is unlikely. 10
The diagnosis of brief psychotic disorder 10 in a patient with borderline personality structure needs to be considered. While reality testing appears intact for most borderline patients on a day-to-day basis, ego function can regress under stress and in close interpersonal situations, sometimes resulting in transient psychotic episodes. Such episodes usually resolve within a month, are spontaneously reversible and always triggered by obvious psychosocial stressors. 10 – 13 In JH's case, the temporal relationship of methamphetamine use to the onset and abatement of psychosis suggests a physiological trigger.
While psychostimulants can exacerbate psychosis in individuals with pre-existing psychotic disorders, they can also trigger psychotic symptoms in healthy or vulnerable individuals with no past history of psychosis. 14 While JH had no family or past history of psychosis, her borderline personality organization and psychosocial situation provided a background of vulnerability factors for psychosis, particularly in the context of methamphetamine abuse.
For most individuals with methamphetamineinduced psychosis, the psychotic symptoms resolve rapidly. However, for some the symptoms are protracted and persist despite being abstinent from the drug for over a month. In some individuals, this may represent the emergence of schizophrenia triggered by psychostimulants. For others the psychostimulants may have triggered a chronic psychotic disorder, which looks similar to schizophrenia but is a form of protracted drug-induced psychosis. 8
Stimulant-induced psychosis generally occurs after high-dose binge use, particularly with escalating doses. The exceptions are those with schizophrenia whose psychotic symptoms may be triggered or exacerbated with relatively low doses. 15 While a possible causal association between cannabis and psychosis in vulnerable youth has been described, the link between psychostimulants and psychotic disorders is less clear. 1 , 16
Once stimulant-induced psychosis has occurred, the individual may experience ‘behavioural sensitization’ or ‘reverse tolerance’ so that a recurrence of psychosis may occur after using a lower dose of a stimulant than that which previously triggered psychosis 8 , 17 or after non-specific psychological stressors. 18 There appears to be individual vulnerability to the process of sensitization that may be genetically influenced. The evidence that psychostimulants cause neurotoxicity resulting in neurodegenerative changes, which might mediate this increased vulnerability to psychosis with time, is currently inconclusive. 1 JH demonstrated sensitization, and regular quetiapine appears to have had a protective effect, reducing the risk of further psychotic symptoms with low-level methamphetamine use.