Methamphetamine is a stimulant substance that affects the central nervous system by causing the release of dopamine, norepinephrine, and serotonin at nerve endings and preventing their reuptake, leading to an increase in their effects.
Methamphetamine can easily cross the blood-brain barrier and rapidly penetrate the brain.
It disrupts the brain’s chemistry, leading to severe depression and causing persistent anhedonia (loss of pleasure) in individuals who are addicted.
At high doses, methamphetamine induces euphoria (a feeling of well-being) by increasing alertness, motivation, and short-term brain activity. It postpones the states of sleeplessness and fatigue to create a state of euphoria. Individuals who have not slept for a long time may suddenly fall asleep at an unexpected moment.
In cases of short-term use, methamphetamine enhances an individual’s attention and self-confidence, facilitates memory functions and learning, and increases sexual desire.
Due to its enhancement of physical performance, methamphetamine can be misused as a doping agent in sports competitions.
The use of methamphetamine may increase an individual’s propensity for violence.
It may lead to reduced appetite and increased basal metabolism, resulting in weight loss for the individual.
Users may exhibit various psychotic features including paranoia, tactile and auditory hallucinations, mood swings, obsessions, and delusions.
Long-term use of methamphetamine can lead to damage to dopamine cells in the brain and a decrease in dopamine levels, resulting in serious movement disorders similar to Parkinson’s Disease.
Parkinson’s Disease: A group of cells in the substantia nigra, known as the black substance, produces a chemical substance called “dopamine.” Dopamine enables the initiation of movements and ensures their smooth and coordinated execution. In Parkinson’s disease, a decrease in the cells in the black substance leads to a deficiency of dopamine, resulting in the manifestation of the disease’s symptoms. Alongside the symptoms related to movement, patients may experience various other complaints. These may include fatigue, decreased cognitive functions, depression, anxiety, behavioral disorders, visual impairments, weight loss, sleep abnormalities, and pain.
What Are the Damages to the Brain
Long-term methamphetamine use causes both functional and structural damage to the brain.
During the addiction process, the user’s brain becomes accustomed to the substance. Therefore, the return of altered biochemical activity to normal after discontinuing drug use may take time. However, because meth damages brain cells, the extent of reversibility depends on the extent of the damage. If damage occurs in an area where other brain cells can compensate, the individual’s symptoms may improve. In areas with more specialized and fewer cells, repair might be possible but challenging.
Long-term Methamphetamine Use Harms the Brain in Three Ways:
- Inducing Acute Neurotransmitter Changes: Prolonged meth use directly alters the brain’s cellular transporters and receptors, which play a role in regulating mood. This can lead to chronic impairments and symptoms such as irritability, apathy, anger, depression, insomnia, and anxiety.
- Brain Cell Death: Heavy methamphetamine use is known to cause cell death in regions associated with self-control, including the frontal lobes, caudate nucleus, and hippocampus. Damage in these areas can manifest in various psychiatric symptoms. Cell death in these regions is irreversible and can lead to long-lasting alterations.
- Rewiring the Brain’s Reward System: Methamphetamine addiction also damages the brain’s reward center, with changes often being permanent in regions such as the ventral tegmental area (VTA), nucleus accumbens, and frontal lobes. Alterations in the reward center are responsible for the individual’s cravings when quitting the substance.
In conclusion, prolonged methamphetamine use inflicts significant harm on the brain, affecting neurotransmitter balance, causing cell death in crucial regions, and disrupting the brain’s reward system. The extent of recovery and rehabilitation depends on the severity of the damage and the brain’s capacity for compensation and repair.
The Likelihood of Reversing Brain Damage
In a study conducted by Temple University’s Department of Psychology and the Substance Abuse Research Center:
Users who abstained from methamphetamine for 6 months scored lower in motor skills, verbal abilities, and psychological tasks compared to a group that had never used the substance. However, after 12-17 months, their scores in motor and verbal skills became comparable to those who had never used. Yet, they continued to experience difficulties in performing psychological tasks, exhibiting a higher likelihood of depression, apathy, and aggression.
What to Expect After Quitting Methamphetamine Use
The possibility of restoring normal brain functions varies from individual to individual. Determining factors include the duration and frequency of substance use. Within 6-12 months after discontinuation, the following improvements in functions and/or symptoms can be anticipated:
Reduced nightmares, Improvement in depression and anxiety, Enhanced focus and attention, Normalization of brain receptors and transporters, Decreased tension and emotional anger, Restoration of neurotransmitter activity in brain regions governing personality, Stabilization of mood fluctuations.
However, one aspect that may not easily recover is an individual’s experience of drug cravings, which can persist even after years of abstinence. This particular issue often arises from damage to the brain’s reward system due to:
Diminished levels of dopamine and serotonin transporters
The depletion of dopamine and serotonin due to methamphetamine use can lead to a series of extreme mood swings, ranging from initial euphoria to subsequent periods of severe depression, apathy, and hopelessness.
Effects of Methamphetamine
Research indicates that damage to the dopamine transporter system can be significantly repaired over time with substantial abstinence. However, neural loss within the CNS cannot be fully reversed. The CNS can recover some partial functions lost to a significant degree due to a mechanism known as neural plasticity. (The ability of neurons and other structures in the brain to change and expand their functions due to severe injuries, because significant environmental cues force the remaining neurons in the brain to take on other functions). Nevertheless, this function is limited, and there is considerable individual variability in the recovery process. Individuals chronically using methamphetamine can experience a range of lasting neurological and cognitive effects.
Long-Term Cognitive Effects Associated with Methamphetamine Use
The list of cognitive and emotional effects resulting from chronic methamphetamine use continues to expand based on research. The following cognitive domains indicate significant impairment as a result of chronic methamphetamine use:
Damage to neurons in the frontal and prefrontal cortex results in chronic issues related to sustained attention, shifting focus, and concentration, often persisting even after substantial abstinence.
Judgment and Problem Solving
The damage resulting from methamphetamine use affects the individual’s ability to suppress impulses, leading to weak judgment and problem-solving abilities. The extent of this functional impairment will vary from person to person. Some individuals might be more impulsive and require initial assistance in controlling their behaviors, while others might exhibit deeper deficiencies.
Research studies have shown significant reduction in the ability to encode and recall information both in animals and humans after chronic methamphetamine use.
Damage in a series of neurons in the brain’s white matter pathways is associated with changes in motor functions, including reaction time, coordination in fine and complex skills, and even basic functions such as walking.
An individual’s ability to regulate and control their emotional states and/or genuine emotional experiences.
Individuals chronically using methamphetamine might experience emotional imbalances that can lead to mood swings, chronic depression, persistent apathy, loss of motivation, aggression issues, hostility, irritability, and even self-harm and/or suicidal behaviors.
This reflects both neurotransmitter depletion and structural damage resulting from chronic methamphetamine use.
Effects of Methamphetamine on the Brain
FOR THOSE IN NEED OF MORE DETAILED ACADEMIC INFORMATION ABOUT METHAMPHETAMINE
Pharmacology of Methamphetamine
The net result of methamphetamine is the excessive stimulation of monoaminergic pathways in the central and peripheral nervous systems, which can lead to severe dysfunction and even neuronal degeneration in many brain regions, including the striatum, prefrontal cortex, and hippocampus.
Peripheral release of monoamine neurotransmitters leads to acute effects such as euphoria, increased mental sharpness, positive mood, social and sexual disinhibition, as well as systemic sympathomimetic effects.
The effects of methamphetamine on the dopaminergic, noradrenergic, serotonergic, and opioidergic neurotransmitter systems result in behavioral and cognitive changes shortly after use.
Pharmacokinetic Properties of Methamphetamine
Inhaling methamphetamine as smoke or injecting it intravenously leads to almost instantaneous onset of a euphoric feeling that lasts for several minutes.
After intranasal and oral administration, reaching the peak euphoric state takes approximately 5 and 20 minutes, respectively, and the effect has been reported to last between 8 to 12 hours.
The substance is largely metabolized in the liver and then excreted by the kidneys.
EFFECTS OF METHAMPHETAMINE
Repeated monoamine release in the central nervous system (CNS) is responsible for various neurological and psychiatric issues observed in methamphetamine users.
Excessive dopaminergic function leads to psychotic symptoms, while disruptions in glutamatergic, GABAergic, cholinergic, and opioidergic transmission result in other symptoms such as aggression, depression, motor disorders, and sleep disturbances.
Short-term effects of methamphetamine include euphoria, alertness, wakefulness, increased confidence, hyperactivity, and loss of appetite.
Dopamine release is responsible for the euphoric effects of methamphetamine, but prolonged use of the drug induces molecular changes in the dopamine system and contributes to terminal nerve damage in the brain. This leads to impaired motor skills, rapid cognitive decline, increased anxiety, psychotic disorders, violent behavior, hallucinations, delusions, and depression.
At higher doses, methamphetamine induces aggression, restlessness, repetitive behaviors, agitation, confusion, anxiety, irritability, dysphoria, violent behavior, psychomotor disturbances, stereotypes, auditory hallucinations, panic, and paranoia.
In the late stages of high-dose methamphetamine use, euphoria is replaced by negative symptoms such as anxiety and feelings of emptiness, along with many of the previously described symptoms.
Withdrawal from Methamphetamine
The withdrawal period from methamphetamine is subjectively uncomfortable but not life-threatening.
The intensity and duration of withdrawal syndrome vary. Common symptoms include depression, fatigue, hypersomnia, increased appetite, irritability, anxiety, aggression, and intense cravings for methamphetamine.
Depressive symptoms are the most prominent feature of methamphetamine withdrawal and can persist even after a 2-week abstinence period.
During this time, depression and anxiety can lead to suicidal thoughts. Aversion to the drug can last at least 5 weeks, with users being particularly vulnerable to relapse between days 7 to 14 of abstinence.
Psychosis that occurs during single-use or withdrawal is usually temporary, but chronic methamphetamine use increases susceptibility to psychotic disorders.
An observational study in Thailand showed that a quarter of patients with methamphetamine psychosis were diagnosed with schizophrenia within 5 years of their initial hospitalization.
Depression, suicidal behavior, violence, psychosis, poor physical health, and extreme weight loss are highlighted problems in methamphetamine users.
Depressive symptoms and suicidal thoughts can occur during active drug use, withdrawal, and even abstinence periods.
Mood shifts and impulsive behavior are components of methamphetamine-related psychiatric syndromes; their most serious consequence is an increased tendency toward suicide.
High-risk methamphetamine users have been reported to exhibit elevated levels of accidents and suicide compared to the normal population.
Pharmacotherapy for Methamphetamine Use Disorder
There is no approved medication to treat methamphetamine use disorder, and pharmacotherapy is recommended as an adjunct to psychosocial interventions rather than a primary component of treatment. Investigated medications for methamphetamine use disorder include acetylcysteine, antidepressants, antiepileptic drugs, atypical antipsychotics, calcium antagonists, muscle relaxants, opioid antagonists, psychostimulants, and varenicline. Methamphetamine-associated psychosis, depressive syndromes, anxiety, and sleep disorders, as well as persistent or co-occurring syndromes related to methamphetamine, are generally treated symptomatically.
Medication administration should be done with caution, considering the possibility of concurrent substance use. If the patient requires treatment for evident agitation, aggression, or psychotic symptoms, benzodiazepines should be the preferred initial agents.
If benzodiazepines are insufficient to calm the patient, especially if they have delusions or hallucinations, the addition of an antipsychotic medication could be considered. Patients with methamphetamine use disorder should be recommended for qualified withdrawal treatment for a minimum of three weeks, and acute treatment should be combined with other psychotherapeutic methods such as behavioral therapy or contingency-based therapy (reward-focused therapy) as soon as possible.
Dusunen Adam The Journal of Psychiatry and Neurological Sciences 2018;31:1-10 Editoryal / Editorial DOI: 10.5350/DAJPN20183101001 makalesinden alıntılanmıştır.Devamı