Motivation and emotion/Book/2020/Methamphetamine and emotion

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Methamphetamine and emotion:
What is the effect of methamphetamine on emotion?

Overview[edit | edit source]

Methamphetamine (MA) use disorder is a major public health concern, with chronic abuse of methamphetamine associated with a myriad of problems including difficulties in emotional perception, recognition and regulation (Zhang et al., 2018). Problems with emotional processing experienced by people who use MA have been associated with neural abnormalities (London et al., 2015; Payer, Lieberman & London, 2011), deficits in emotional attention (Zhang et al., 2018), sleep disruption (Lipinska, Timol & Thomas, 2015), psychosis (Arunogiri et al.,2019) and impaired social cognitive functioning, including deficits relating to emotion recognition and theory of mind (Kim, Kwon & Chang, 2011). It is thought that these emotional deficits are implicated in the maintenance of MA addiction and risk factors for drug cravings and relapse (Zhang et al., 2018). Consequently, greater understanding of the effect of methamphetamine on emotion is important for the development of interventions that target the emotional problems experienced by those with methamphetamine use disorder (MUD).

Personal accounts of emotional deficits experienced by those who use Methamphetamine:

“I lose a sense of feeling and caring about everybody and it’s like I really don’t give a damn, I couldn’t care less if I chopped off your leg, I wouldn’t feel no remorse about it …” (Brecht & Herbeck, 2015)

“You know people weren’t important, family wasn’t important … I was out chasing my girlfriend in my brothers car somewhere and my daughter was in the car with me … I ran a red light and flipped the car upside down. My daughter went to the emergency room. And, you know, I couldn’t even think about what was going on with my daughter, all I could think about was chasing down my girlfriend …” (Brecht & Herbeck, 2015)

Figure 1. The emotional problems associated with methamphetamine use disorder are risk factors for cravings and relapse (Zhang et al., 2018).

What is methamphetamine?[edit | edit source]

Methamphetamine (MA) is a highly addictive stimulant that elevates levels of dopamine, noradrenaline and serotonin in the central nervous system (Galbraith, 2015). Dependence on MA is a global concern, with an estimated 68 million consumers worldwide (Siefried, Acheson, Lintzeris & Ezard, 2020). MA can be smoked, snorted, injected or swallowed, with the physiological effects of the drug occurring rapidly and lasting for hours (Panenka, 2012). While initially the drug increases attention, self confidence and feelings of euphoria (Uhlmann, 2016), long term use of methamphetamine has been linked to considerable adverse health conditions, including psychosis, mood and anxiety disorders, aggression and suicidality (Darke et al., 2008).

What is emotion?[edit | edit source]

The experience of emotion is universal, however it would seem that emotions are more complex than first meets the eye, with a current consensus on a scientific definition illusive (Anderson & Adolphs, 2014). In an attempt to formulate an operational definition, Izard (2010) asked 33 scientists in the field to provide their definition of emotion and although still no consensus, the following were commonly recognised as aspects of emotion:

  • neural circuits and neurobiological processes
  • phenomenal experience and feeling
  • cognitive processes

Drugs such as MA elicit powerful emotions, ranging from euphoria to devastating negative emotional states, that in the extreme can lead to a break with homeostasis (Koob, 2015).

Case study

Scarlett is a 25-year-old university student who has been using methamphetamine for 5 years. She first tried methamphetamine in the form of methamphetamine powder (‘speed’) when she was 18, developing the habit of snorting lines before going out to clubs with her university friends. This became something they did on a weekly basis and occasionally Scarlett would stay up all weekend without sleep. She would often get depressed after a big weekend, but this would usually pass. After finishing her degree, she obtained a job in a law firm and soon after tried crystal methamphetamine (‘crystal’ or ‘ice’) for the first time. Crystal is a potent form of methamphetamine that is usually smoked or injected. Smoking crystal and partying became a regular occurrence for Scarlett. When she was not intoxicated with methamphetamine her depression was impairing her functioning at work. Her work performance deteriorated noticeably as her binges on crystal necessitated days of recovery. Eventually she stopped work at the age of 23 and the next two years were spent using crystal methamphetamine for days at a time. Over this time, she became suspicious that people were following her, making her jumpy, agitated and aggressive towards others. While she no longer felt the euphoria experienced when she first started using the drug, she felt that she needed to keep using to take away the bad feelings she was having. After becoming aggressive towards shoppers at a local supermarket, Scarlett was taken into custody by police and eventually hospitalised and referred for drug treatment. (Case Study adapted from Rieger, 2017)

What emotion theories are relevant?[edit | edit source]

Figure #[figure renumbering needed to include this one]. MA-dependent individuals commonly display symptoms of alexithymia, which is characterised by the inability to define and explain one's emotions, as well as propensity to externalise feeling (Morie et al., 2016). In a study by Payer, Lieberman & London (2011) a correlation between the ventral inferior frontal gyrus and alexithymia suggest that low activity in this area of the brain may lead to a reduced capacity to identify feelings. These findings are thought to explain the inability of MA-dependent individuals to regulate maladaptive interpersonal behaviour, resulting in increased aggression (Payer, Lieberman & London, 2011)

Evidence suggests that the effects of methamphetamine on emotion manifest as an interplay between the biological and cognitive systems involved in emotion processing, with prolonged use causing deficits in areas of the brain implicated in several components of emotion, such as appraisal and facial emotion recognition (Kim, Kwon & Chang, 2011). Discussion around the question of what causes emotion has traditionally polarised into a biological/cognitive debate, with those in the biological camp arguing the centrality of the automatic nervous system and activation of the subcortical brain (Levenson, 2014), while those with a cognitive perspective argue different cognitive appraisals are prerequisites to emotion (Reeve, 2018). Contemporary discussion around the nature and causes of emotion tends to agree upon a two-systems view that attributes both biology and cognition as the cause of emotion (England, 2019)

Biological[edit | edit source]

The James-Lange theory of emotion proposes that physiological changes in the body cause emotional experience (i.e. stimulus > bodily reaction > emotion; Reeve, 2018). This early theory has attracted considerable criticism; however it has continued to guide and influence the contemporary biological perspective around a consensus that anger, disgust, fear, happiness and sadness qualify as basic emotions (Siegel et al., 2018) that have enduring and distinctive psychophysiological and neural correlates (Vytal & Hamann, 2010). According to Ekman and Cordaro (2011), these basic emotions originate in primal regions of the brain such as the brainstem, the limbic system and the amygdala and are not learned from culture or the environment. A meta-analysis by Vytal and Hamann (2010) found that the five basic emotions have distinctive patterns of neural activation. The results of their analysis can be seen in the following table:

Table 1.

Vytal and Hamann (2010) found that the five basic emotions have distinct patterns of neural activity.

Emotion Area of Neural Activity
Happiness Right superior temporal gyrus and rostral anterior cingulate cortex
Sadness Medial frontal gyrus and caudate anterior cingulate cortex
Anger Inferior frontal gyrus and parahippocampal gyrus
Fear Amygdala and insula
Disgust Anterior insular cortex and inferior frontal gyrus

Studies suggest that MA causes neurogenerative changes in the brain, including some regions important for emotional processing (Krasnova & Cadet, 2009).

Cognitive[edit | edit source]

Fundamental to the cognitive view of emotion is cognitive appraisal, the personal meaning attributed to a stimulus (Lazarus & Smith, 1988). According to Frijda’s (1988) Law of Situational Meaning, emotions arise in response to situations that are important to an individual, such that, events that satisfy goals produce positive emotions and those that thwart goals or threaten an individual, yield negative emotions.

MA dependent individuals commonly exhibit deficits in emotional regulation and recognition that can be attributed to problems with appraisal:

  • Emotion regulation refers to processes that influence responses to ones[grammar?] environment and can include cognitive appraisal strategies such as the reinterpretation of emotional stimuli (Okita et al., 2016)
  • Emotion recognition refers to the ability to infer the emotional state of others and is crucial for normal interpersonal relationships (Gray & Tickle-Degnen, 2010).

Two systems view[edit | edit source]

Contemporary discussion about the nature and causes of emotion bring together both the biological and cognitive perspectives into two systems view of emotion that recognises an emotional episode as involving several components, these include:

  • Appraisal
  • Motivational components
  • Physiological responses
  • Expressive and instrumental behaviour
  • Subjective experience or feeling (England, 2019)

Importantly, the emotion process is continuous, with changes in one component feeding back to cause changes in other components, for example, an altered appraisal may lead to changes in physiological responses and vice versa (Moors, Ellsworth, Scherer & Frijda, 2013).

How does methamphetamine interact with the brain?[edit | edit source]

MA increases concentrations of dopamine, serotonin and noradrenaline in the central nervous system by blocking their presynaptic reuptake (Homer et al., 2008). Chronic use of MA causes damage to dopaminergic and serotonergic transmitter systems (Homer et al., 2008) interfering with the brains[grammar?] natural ability to produce these neurotransmitters, ultimately leading to problems with mood and behaviour.

Dopamine[edit | edit source]

Dopamine is associated with reward seeking behaviour. MA causes an increase in dopamine, resulting in a feeling of euphoria. Long-term use of MA results in dopamine decline, leading to feelings of losing control and compulsive drug taking.

Serotonin[edit | edit source]

Serotonin is responsible for learning and memory. MA causes an increase in serotonin, resulting in elevated feelings of well-being. Chronic use of MA causes a decline in serotonin and problems with mood.

Noradrenaline[edit | edit source]

Noradrenaline is responsible for arousal and motivation. MA causes an increase in noradrenaline which is associated with an increase in alertness and attention, however chronic MA use leads to deficits in these areas.

(Australian Government Department of Health, 2018).

Neurotransmitter links[edit | edit source]
Figure 2. The mesolimbic dopamine pathway, often referred to as the pleasure centre of the brain, mediates our experience of reward, whether that be a natural high or a drug-induced high (Arias-Carrión et al., 2014)
Limbic system[edit | edit source]

What effect does methamphetamine have on emotion?[edit | edit source]

Figure 3. The Amygdala - Research has implicated the amygdala in emotional processes, with amygdala damage reported to cause problems in the interpretation of facial expressions, with this most apparent for fear expressions (Phelps & LeDoux, 2005). Interestingly, studies have shown that MA-dependent individuals have problems with emotion recognition, in particular a decreased arousal to fear emotion stimuli, which is thought to account for problems with emotion regulation (Chen, Wang, Li & Sui, 2018). However, there have been mixed results from studies around the effect of methamphetamine on amygdala function, with some finding abnormalities linked to emotional deficits (Okita et al., 2017) and others linking problems with emotion processes to deficits in other areas of the brain, such as the inferior frontal gyrus and insula (Payer, Lieberman & London, 2011; Kim et al., 2010).

Deficits in serotonin and dopamine systems and cortical/sub-cortical brain circuits suggest a biological basis for emotional problems experienced by those who use MA, leading to problems with emotion processes. Studies that have used positron emission tomography (PET) have shown damage to dopaminergic and serotonergic transmitter systems in MA-dependent individuals (Homer et al., 2008). Dopamine and serotonin play crucial roles in a range of physiological systems that can affect emotion processing, including the regulation of the reward system, emotional responses, circadian rhythm and sleep/wake cycles (Homer et al., 2008). Other studies have identified difficulties with emotion regulation and recognition, particularly attentional biases toward threatening facial expressions, thought to be caused by MA induced deficits in cortical and sub-cortical brain circuits (Okita et al., 2017; Payer, Lieberman & London, 2011; Kim et al., 2010; Zhang et al., 2018).

Emotion recognition[edit | edit source]

Chronic use of MA has been linked to interpersonal problems and antisocial behaviours (Hanegraaf et al., 2020). This is partly explained by studies that have shown that individuals with MA dependence have difficulties with emotion recognition (Hanegraaf et al., 2020). In a study by Hanegraaf et al. (2020) examining dysfunctional personality beliefs amongst MA users, it was proposed that maladaptive personality schemas underlie interpersonal problems and difficulties with emotion recognition. In another study by Chen, Wang, Li & Sui (2018) self-reports, skin conductance and startle reflex were used to investigate the responses of those with MA dependence to positive and negative emotional stimuli compared to normal controls. Results of the study found a deceased response to joy and decreased arousal to fear emotion stimuli.  Based on their findings, Chen, Wang, Li & Sui (2018) hypothesised that MA-dependent individuals may have difficulty avoiding negative stimuli, leading to interpersonal problems and the risk of relapse. Also worth noting is that many MA-dependent individuals experience psychotic symptoms and according to a study by Arunogiri et al. (2019), this population exhibits poorer emotion recognition, particularly for anger and sadness. Arunogiri et al. (2019) believe that these deficits in emotion recognition lead to the misinterpretation of threat, explaining the often-aggressive response to benign stimuli displayed by those who use MA. Yet another study by Kim, Kwon and Chang (2011) that assessed the emotion recognition and Theory of Mind (ToM) of MA users, found they performed poorly on a Facial Emotion Recognition Task and Wisconsin Card Sorting Test. The results of this study suggest impairments in social cognition, originating from abnormalities in the prefrontal cortex, that in turn leads to the inability to identify facial emotions and infer the mental state of others (Kim, Kwon & Chang, 2011).

Figure 4. Kim, Kwon & Chang (2011) found that MA-dependent individuals performed poorly in the Facial Emotion Recognition Task.

Emotion regulation[edit | edit source]

Individuals who use MA have been found to lack empathy, exhibit anxiety, depression, aggression, alexithymia and irritability, thought to be due to deficits in emotion regulation (Kim et al., 2011; Okita et al., 2017; Payer, Lieberman & London, 2011). Amygdala hyperactivity has been associated with emotion dysregulation and in a study by Okita et al. (2017) it was found that methamphetamine use increases dopaminergic transmission in the amygdala, which in turn leads to greater emotional responses in individuals who use MA. Contrary to Okita et al. (2017), a study by Payer, Lieberman and London (2011), found no deficits in amygdala function in MA users, instead they observed decreased activity in the bilateral ventral inferior frontal gyrus (IFG), a region of the brain implicated in recognising the emotional states of oneself and others. As a result, Payer, Lieberman and London (2011) concluded that MA-related aggression, problems with emotion regulation and alexithymia could be attributed to poor emotional insight and the misinterpretation of the environment as a threatening place. In another study, Kim et al. (2011) used functional magnetic resonance imaging (fMRI) to examine the emotional experience of threatening or fearful images in MA users compared to healthy controls. Like Payer, Lieberman and London (2011), they found no abnormality with amygdala function, however, they observed functional deficits in several brain regions, most notably the insula, a region associated with emotional awareness and subjective feeling. Kim et al. (2011) concluded that the functional impairment of the insula may explain the lack of emotional awareness and empathy that leads to the interpersonal problems experienced by MA users  

Sleep loss[edit | edit source]

It is well known that the heightened arousal and alertness caused by MA leads to insomnia and extended periods, sometimes days, without sleep (Lipinska, Timol & Thomas, 2015). Studies have shown that sleep loss increases emotional reactivity and negative mood states, while also impairing the ability to recognise and express emotions (Simon, Vallat, Barnes & Walker, 2020). Furthermore, sleep loss has been found to cause deficits in amygdala, insula and cingulate cortex function, impairing the ability to discern threatening from non-threatening stimuli (Simon, Vallat, Barnes & Walker, 2020). Given the link between sleep loss and problems with emotional processing, it is hypothesised that the sleep loss experienced by those who use MA could explain, in part, the emotional problems observed in this population (Lipinska, Timol & Thomas, 2015).

Interventions[edit | edit source]

There is currently no broadly effective pharmacotherapy for the treatment of methamphetamine induced psychological distress and there is very little research that examines the effectiveness of psychological interventions (Stuart et al., 2020). In a systematic review carried out by Stuart et al. (2020) there was some suggestion that motivational interviewing, cognitive behavioural therapy (CBT), acceptance and commitment therapy (ACT) and a recovery model called the Matrix Program are effective treatments among people who use methamphetamine. Given the evidence suggesting neurogenerative changes in the brain caused by MA, interventions using neuromodulation techniques such as transcranial direct current stimulation (tDCS) and transcranial magnetic stimulation (TMS) are thought to be promising approaches to treating the emotional problems caused by MA use (Lapenta et al., 2018; Zhang et al., 2018). To date, preliminary applications of tDCS and TMS have seen it used to reduce cravings and improve emotional attention in MA-dependent individuals, with anodal stimulation applied over the left dorsolateral prefrontal cortex producing some positive results, although further investigations are needed before it can be used in clinical settings (Lapenta et al., 2018; Zhang et al., 2018).

Conclusion[edit | edit source]

Evidence suggests that methamphetamine affects emotion processes considerably, with associated problems with emotion regulation and recognition particularly debilitating for those who chronically use the drug. To date, there appears to be no definitive explanation for the cause of the emotional deficits experienced by those who use MA, with some studies implicating damage to the amygdala (Okita et al., 2017), while others argue deficits to other areas of the brain are the cause, namely the inferior frontal gyrus (Payer, Lieberman & London, 2011) and insula (Kim et al., 2010). That there is damage to the dopaminergic and serotonergic systems does seem to be universally agreed upon, along with the subsequent reduction in neurotransmitter production thought to be implicated in the various mood disorders reported by those who use MA (Homer et al., 2008). Another common finding relates to problems with emotion recognition, in particular the misinterpretation of threat in the environment that can lead to inappropriate, often aggressive, responses to otherwise benign stimuli (Arunogiri et al., 2019; Kim, Kwon & Chang, 2011; Payer, Lieberman & London, 2011). Other studies link the heightened arousal and extended periods without sleep experienced by MA users to the deficits in emotion processing, with sleep loss causing damage to areas of the brain responsible for emotion regulation and recognition (Lipinska, Timol & Thomas, 2015; Simon, Vallat, Barnes & Walker, 2020). Taken together, it appears that the effect of methamphetamine on emotion is complex, with evidence to suggest that numerous interconnected biological and cognitive systems are impacted by the drug. Although there is no broadly effective treatment, interventions incorporating cognitive behavioural therapy (CBT), acceptance and commitment therapy (ACT) and neuromodulation techniques are considered promising new approaches to treating the emotional deficits experienced by those who use MA (Stuart et al., 2020; Lapenta et al., 2018; Zhang et al., 2018).  

See also[edit | edit source]

References[edit | edit source]

Anderson, D. J., & Adolphs, R. (2014). A framework for studying emotions across species. Cell, 157(1), 187-200.

Arias-Carrión, O., Caraza-Santiago, X., Salgado-Licona, S., Salama, M., Machado, S., Nardi, A. E., Menendez-Gonzalez, M., & Murillo-Rodriguez, E. (2014). Orquestic regulation of neurotransmitters on reward-seeking behavior. International archives of medicine, 7(1), 1-15.

Arunogiri, S., Verdejo-Garcia, A., McKetin, R., Rubenis, A. J., Fitzpatrick, R. E., & Lubman, D. I. (2019). Emotion recognition and impulsive choice in relation to methamphetamine use and psychosis symptoms. Frontiers of Psychiatry, 10, 1-7.

Australian Government Department of Health (2018). The effects of crystal methamphetamine on the brain.

Brecht, M. L., & Herbeck, D. (2013). Methamphetamine use and violent behaviour: User perceptions and predictors. Journal of Drug Issues, 43 (4), 468-482.

Chen, X. J., Wang, C. G., Li, Y. H., & Sui, N. (2018). Psychophysiological and self-reported responses in individuals with methamphetamine use disorder exposed to emotional video stimuli. International Journal of Psychophysiology, 133, 50-54.

Darke, S., Kaye, S., McKetin, R., & Duflou, J. (2008). Major physical and psychological harms of methamphetamine use. Drug and Alcohol Review, 27, 253-262.

Ekman, P., & Cordaro, D. (2011). What is meant by calling emotions basic. Emotion review, 3(4), 364-370.

England, R. (2019). The cognitive/noncognitive debate in emotion theory: A corrective from Spinoza. Emotion Review, 11(2), 102-112.

Frijda, N. H. (1988). The laws of emotion. American psychologist, 43(5), 349.

Galbraith, N. (2015). The methamphetamine problem. BJPsych Bulletin, 39(5), 218-220.

Gross, J. J. (2002). Emotion regulation: Affective, cognitive, and social consequences. Psychophysiology, 39, 281-291.

Hanegraaf, L., Arunogiri, S., Hohwy, J., & Verdejo-Garcia, A. (2020). Dysfunctional personality beliefs and emotion recognition in individuals with methamphetamine dependence. Addictive Behaviours, 105, 1-6.

Homer, B. D., Solomon, T. M., Moeller, R. W., Mascia, A., DeRaleau, L., & Halkitis, P. N. (2008). Methamphetamine abuse and impairment of social functioning: A review of the underlying neurophysiology causes and behavioural implications. Psychological Bulletin, 134(2), 301-310.

Izard, C. E. (2010). The many meanings/aspects of emotion: Definitions, functions, activation, and regulation. Emotion Review, 2(4), 363-370.

Khakbaz, H., Farhoudian, A., Azkhosh, M., Dolatshahi, B., Karami, H., & Massah, O. (2016). The effectiveness of group acceptance and commitment therapy on emotion regulation in methamphetamine-dependant individuals undergoing rehabilitation. International Journal of High Risk Behaviours and Addiction, 5(4), 1-9.

Kim, Y. T., Kwon, D. H., & Chang, Y. (2011). Impairments of facial emotion recognition and theory of mind on methamphetamine abusers. Psychiatry Research, 186, 80-84.

Kim, Y. T., Song, H. J., Seo, J. H., Lee, J. J., Lee, J., Kwon, D. H., Yoo, D. S., Lee, H. J., Suh, K. J., & Chang, Y. (2011). The differences in neural network activity between methamphetamine abusers and healthy subjects performing an emotion‐matching task: functional MRI study. NMR in Biomedicine, 24(10), 1392-1400.

Koob, G. F. (2015). The dark side of emotion: The addiction perspective. European Journal of Pharmacology, 753, 73-87.

Krasnova, I. N., & Cadet, J. L. (2009). Methamphetamine toxicity and messengers of death. Brain Research Reviews, 60(2), 379-407.

Lapenta, O. M., Marques, L. M., Rego, G. G., Comfort, W. E., & Boggio, P. S. (2018). tDCS in addiction and impulse control disorders. The journal of ECT, 34(3), 182-192.

Lazarus, R. S., & Smith, C. A. (1988). Knowledge and appraisal in the cognition—emotion relationship. Cognition & Emotion, 2(4), 281-300.

Levenson, R. W. (2014). The autonomic nervous system and emotion. Emotion Review, 6(2), 100-112.

Lipinska, G., Timol, R., & Thomas, K. G. F. (2015). The implications of sleep disruption for cognitive and affective processing in methamphetamine abuse. Medical Hypotheses, 85, 914-921.

London, E. D., Kohno, M., Morales, A. M., & Ballard, M. E. (2015). Chronic methamphetamine abuse and corticostriatal deficits revealed by neuroimaging. Brain research, 1628, 174-185.

Moors, A., Ellsworth, P. C., Scherer, K. R., & Frijda, N. H. (2013). Appraisal theories of emotion: State of the art and future development. Emotion Review, 5(2), 119-124.

Okita, K., Ghahremani, D. G., Payer, D. E., Robertson, C. L., Dean, A. C., Mandelkern, M. A., & London, E. D. (2017). Emotion dysregulation and amygdala dopamine D2-type receptor availability in methamphetamine users. Drug and Alcohol Dependence, 161, 163 – 170.

Panenka, W. J., Procyshyn, R. M., Lecomte, T., MacEwan, G. W., Flynn, W., Honer, W. G., & Barr, A. M. (2012). Methamphetamine use: A comprehensive review of molecular, preclinical and clinical findings. Drug and Alcohol Dependence, 129, 167-179.

Payer, D. E, Lieberman, M. D., & London, E. D. (2011). Neural correlates of Affect and Aggression in methamphetamine dependence. Archives of General Psychiatry, 68 (3), 271-282.

Phelps, E. A., & LeDoux, J. E. (2005). Contributions of the amygdala to emotion processing: from animal models to human behavior. Neuron, 48(2), 175-187.

Reeve, J. (2018). Understanding motivation and emotion (7th ed.). John Wiley & Sons.

Rieger, E. (2017). Abnormal psychology: Leading researcher perspectives (4th ed.). McGraw-Hill Education Australia.

Siefried, K. J., Acheson, L. S., Lintzeris, N., & Ezard, N. (2020). Pharmacological treatment of methamphetamine/amphetamine dependence: A systematic review. CNS Drugs, 34, 337-365.

Simon, E. B., Vallat, R., Barnes, C. M., & Walker, M. P. (2020). Sleep loss and the socio-emotional brain. Trends in Cognitive Sciences, 24 (6), 435 – 450.

Stuart, A. M., Baker, A. L., Denham, A. M., Lee, N. K., Hall, A., Oldmeadow, C., Dunlop, A., Bowman, J., McCarter, K. (2020). Psychological treatment for methamphetamine use and associated psychiatric symptom outcomes: A systematic review. Journal of Substance Abuse Treatment, 109, 61-79.

Vytal, K., & Hamann, S. (2010). Neuroimaging support for discrete neural correlates to basic emotions; A voxel-based meta-analysis. Journal of Cognitive Neuroscience, 22, 2864-2885.

Zhang, L., Cao, X., Liang, Q., Li, X., Yang, J., & Yuan, J. (2018). High-frequency repetitive transcranial magnetic stimulation of the left dorsolateral prefrontal cortex restores attention bias to negative information in methamphetamine addicts. Psychiatry Research, 265, 151-160.

External links[edit | edit source]