This article was written by our trainer Maria Vittoria Zulli
Part 2: Stimulants, cannabis and Opioids
Stimulants (cocaine, methamphetamine)
Stimulant drugs are known to induce heightened feelings of well-being, euphoria and increased arousal by accelerating the central nervous system (CNS). They increase heart rate, body temperature, and blood pressure while also enhancing energy levels, focus, attention, alertness and wakefulness.
Stimulants such as cocaine and methamphetamine (MA) directly or indirectly affect the reward system in the brain by disrupting the dopamine neurotransmitter system and increasing the amount of dopamine in the brain (Ashok et al., 2017, Volkow et al., 2018, Paulus & Stewart 2020). Dopamine regulates the sensation of pleasure and satisfaction and is also a vital component in cognition, motor control, motivation and reward (Bromberg et al., 2010). However, excess dopamine in the brain can trigger psychotic symptoms, including delusions, hallucinations and paranoia (Kesby et al., 2018; Klein et al., 2019). Long-term and high-dose use of stimulants can lead to changes in mood, behavioural deficits, cognitive impairments, depression, anxiety, insomnia, psychosis and suicidal thoughts (Jan et al., 2012; Wood et al., 2013; Ashok et al., 2017). The overstimulation of the CNS by these drugs can make it difficult for the brain to function properly, interfering with normal activities. The way these drugs affect dopamine levels and the limbic reward system makes them highly addictive.
Methamphetamine and EEG changes
Prolonged use of methamphetamine induces changes in the brain’s dopamine system that are linked to a decline in coordination, impaired verbal learning, emotional disturbances, memory loss, hallucinations, and paranoia (Volkow et al., 2001). In fact, a study suggests that former methamphetamine users have an elevated risk of developing Parkinson’s disease, a disorder of the nerves that affect movement (Curtin et al., 2015). Although some of these methamphetamine-induced alterations in brain function may revert after abstaining from the drug for over a year or more, others can persist even after a prolonged period (Wang et al., 2004).
EEG brain mapping has revealed a reduction in the alpha frequency band and increased theta power (Ceplova et al., 2014). These changes persisted for about a month after the discontinuation of methamphetamine and were associated with considerable cognitive decline. Further neurocognitive testing revealed mild cognitive impairments that were most pronounced in working memory.
Another study involving methamphetamine-dependent individuals with four days of abstinence found increased EEG power in the delta and theta bands, indicative of generalised encephalopathy (Newton et al., 2003). When analysing the EEG and neurocognition in methamphetamine users, theta QEEG power was associated with impaired cognitive performance (Newton et al., 2004).
Cocaine-induced EEG changes
Drugs like cocaine and methamphetamine are known to induce a powerful sense of euphoria by rapidly flooding the brain with dopamine. This excessive dopamine transmission can have detrimental effects on the central nervous system, leading to various negative consequences. Cocaine has been associated with a range of psychiatric symptoms, such as agitation, paranoia, psychosis (including visual, verbal and tactile hallucinations), and violent behaviour (Morton, 1999; Brady et al., 1991).
Prolonged use of cocaine is associated with EEG changes, including decreases in delta and theta and/or increases in alpha and beta frequencies ( Liu et al., 2022). For instance, individuals with severe cocaine dependence who abstained from using the drug showed increased absolute and relative alpha power (Alper et al., 1990) and reduced absolute and relative delta and theta power in anterior and posterior regions (Prichep et al., 1996). Increased alpha power has also been reported on the EEG of depressed patients (Jaworska et al., 2012). There is a high comorbidity between cocaine users and depression, and symptoms of depression can worsen with cocaine use (Morton, 1999)
In a study of individuals recovering from polysubstance abuse who primarily used cocaine, they observed reduced absolute and relative delta and theta power and increased relative alpha and beta power (Roemer et al., 1995). They also found asymmetry in frontal delta, theta, and alpha power, with right power being greater than left, and reduced interhemispheric coherence in delta and theta bands, as well as frontally in the beta band.
The available literature on cocaine use and its impact on EEG power in the beta frequency range presents some discrepancies. While some studies suggest an increase in the beta range (Costa & Bauer, 1997; Herning et al., 1997; Roemer et al., 1995), others indicate a decrease in absolute EEG power in individuals who use cocaine (Noldy et al., 1994; Copersino et al., 2009). These inconsistencies may stem from various factors, such as variations in analysis methods, EEG recording protocols, duration of abstinence, concurrent use of other substances and the presence of other disorders.
Marijuana, also known as cannabis, is a substance that can have both stimulant and depressant effects on the body. The main psychoactive component in marijuana is known as tetrahydrocannabinol (THC), which interacts with cannabinoid receptors in the brain. Cannabinoid receptors are highly concentrated in the CNS and play a crucial role in regulating physiological processes such as mood, appetite, pain sensation, memory and immune function (Scott et al., 2017). When marijuana overstimulates these receptors, it can cause a range of effects, including altered sensory perception, changes in mood, impaired motor function, altered thinking, memory impairment, and increased appetite (Koob et al., 2014). These effects are commonly referred to as the ‘high’ associated with marijuana use.
While marijuana can produce a temporary feeling of relaxation, chronic use can have negative effects on brain development and the formation of connections between areas necessary for learning and memory. It can also lead to neurocognitive impairments, such as executive dysfunction, attentional deficits, and poor performance, as well as social dysfunction, demotivation, lack of enjoyment in activities, and sensitivity to sound (Murray 1986). Regular use of marijuana has been linked to an increased risk of anxiety, depression, paranoia, dysphoria, depersonalisation and psychotic symptoms (Nutt, 2012). While it is known that marijuana use can be a risk factor for schizophrenia and may contribute to around 50% of psychosis and schizophrenia cases, the exact neurobiological processes underlying these effects are not well understood (Iversen, 2003, Shrivastava et al., 2014). The National Institute on Drugs Abuse (NIDA, 2021) has suggested a possible link between marijuana use and the onset of psychosis and psychiatric disorders such as schizophrenia, particularly in individuals who are genetically susceptible. Additionally, the repeated use of synthetic cannabis substances has been shown to cause hallucinogen-persisting perception disorder (HPPD) and significant anxiety in some individuals (G Lerner et al., 2014).
Marijuana-induced EEG alterations
The earlier scientific literature contains numerous reports on the effects of acute and chronic cannabis use on EEG activity. One study conducted in 1989 by Struve and colleagues found that long-term daily marijuana psychiatric users (1 to 12 years of THC exposure) displayed significant elevations in absolute and relative power of alpha and interhemispheric coherence of alpha activity over the bilateral frontal cortex (also known as alpha hyperfrontality). Additionally, they observed a decrease in relative power of delta (1.5-3.5 Hz), Theta (3.5-7.5 Hz) and Beta (12.5-20 Hz) activity and elevated absolute power of all frequencies over all cortical areas. To control for the variable of psychiatric inpatient populations, further studies were conducted with psychiatrically and medially normal daily THC users and non-user controls. These studies replicated the findings from the first study, including hyperfrontality of alpha, a generalised increase of absolute power of non-alpha frequencies over widespread cortical regions, decreased relative power of delta and beta activity over the frontal cortex, and increased interhemispheric coherence of theta and delta activity over the frontal cortex (Struve et al., 1998; Struve et al., 1994; Struve et al., 1999; Allsop et al., 2012) An increase in theta can be interpreted as a sign of slowed cognitive processing, and alpha hyperfrontality may indicate early withdrawal effects.
Recent studies on cannabis users have observed patterns of reduced delta with increased theta, beta and gamma power compared to controls (Prashad et al., 2018). They also showed less efficient communication between cortical regions compared to controls, which may contribute to cognitive impairments. Another recent study examining EEG functional connectivity in cannabis users found increased delta connectivity between several networks, such as the salience network and central executive network. They concluded that individuals with problematic cannabis use could be characterised by a specific dysfunctional interaction between these networks, which may reflect the neurophysiological basis of attentional and emotional processes related to cannabis thoughts, memories and cravings (Imperatori et al., 2020).
Opioids like heroin bind to opioid receptors in the brain, mimicking the effects of natural endorphins and generating potent analgesic (pain-relieving) and euphoric effects. Opioids trigger the release of dopamine in specific brain regions, giving rise to temporary feelings of pleasure (Kosten & George, 2002). This hijacks the limbic system, inducing an intense high that individuals frequently seek to replicate, resulting in compulsive drug-seeking behaviour and addiction.
Opioid drugs have a critical role in medicine for managing physical pain, commonly prescribed to individuals with traumatic injuries or those recovering from surgery. They function as central nervous system depressants and interrupt the natural production of norepinephrine, which contributes to their sedative effects. They block pain sensations, induce drowsiness, reduce body temperature, and slow heart rate, blood pressure and respiration function (Benyamin et al., 2008). Additionally, opioids can have negative effects on cognitive function. They can impair memory formation and attention and reduce the ability to make decisions (Motlagh et al., 2018). Chronic opioid use can also lead to changes in brain structure and function, which may have long-term consequences on cognitive and emotional processing (Upadhyay et al., 2010).
Heroin and EEG changes
The chronic use of heroin is associated with mild changes in cognitive function and brain electrical activity, which progressively intensify with prolonged daily heroin abuse (Briun et al., 2001). Heroin addicts are likely to exhibit deficits in several areas of cognitive performance, including long-term memory, working memory, short-term memory, problem-solving, and psychomotor speed. These deficits are believed to be linked to various frequency bands, such as alpha, beta, theta and delta (Polunina & Davydov 2006).
Heroin use has been shown to have significant effects on brain EEG activity. For example, Motlagh and colleagues (2016) found that heroin users had elevated beta power and reduced delta, theta and alpha waves compared to healthy individuals. In addition, heroin users showed a decline in brain-evoked potential amplitude, indicating impaired preattentive and attentional processing, which could lead to attentional deficits and reduced discrimination abilities.
Other studies have revealed that heroin-dependent patients had reduced power in fast theta and slow and fast alpha frequency bands while exhibiting increased power in the slow and fast beta frequency bands (Polunina et al., 2004). Enhanced beta power, as well as increased interhemispheric gamma coherence, have also been observed in other studies (Franken et al., 2004; Wang et al., 2016).
However, there has been some inconsistency in studies investigating the impact of heroin administration and delta activity specifically. Stoermer and colleagues (2003) reported an increase in delta waves (1- 3.5 Hz) following heroin administration, while Motlah and colleagues (2016) found a decrease. These results highlight the complex nature of heroin’s effects on brain activity and the need for further research in this area.
Hu and colleagues (2017) investigated functional connectivity changes induced by heroin addiction using EEG. Their findings revealed that heroin addicts exhibit abnormalities in functional connectivity, with weaker network alterations in the parietal region and stronger functional connectivity in the left occipital regions. Furthermore, chronic heroin use may lead to deterioration in the brain’s white matter, potentially affecting a person’s response to stress, emotion regulation and decision-making abilities (Li et al., 2013).
Full list of references for this article can be found here