What are the neurological side effects of marijuana smoking?

Neurological Side Effects of Marijuana Smoking

Marijuana smoking causes significant neurological impairment affecting multiple cognitive domains, with the most consistent and severe effects on verbal learning and memory, attention, and executive function—particularly when use begins during adolescence when the developing brain is most vulnerable to long-term structural and functional damage. 1

Acute Neurological Effects (During Intoxication)

Immediate cognitive impairment occurs during active intoxication, affecting:

• Memory and learning: Verbal learning and memory are most consistently impaired during acute cannabis use 2
• Psychomotor function: Significantly affected during acute intoxication, impairing coordination and performance 3, 2
• Attention and concentration: Acute deficits in attentional processing occur with use 2
• Anxiety and psychotic symptoms: High doses of THC may trigger acute anxiety, psychotic symptoms, and suicidal ideations in vulnerable individuals 4, 3

Chronic Neurological Effects (Long-Term Users)

Persistent cognitive deficits develop with regular use, even when not acutely intoxicated:

Cognitive Impairments

• Memory dysfunction: Verbal learning and memory remain impaired in chronic users, with deficits persisting for days, weeks, or longer after last use 5, 2
• Attention deficits: Sustained attention problems persist beyond acute intoxication 5, 2
• Executive function impairment: Deficits in inhibitory control, decision-making, and executive functions occur with chronic use 1, 5
• Processing speed: Reduced processing speed is documented in long-term users 1

Structural Brain Changes

Cannabis causes measurable brain alterations, particularly in adolescents:

• Gray matter volume changes: Altered gray matter volume in key brain regions 1
• Cortical thickness alterations: Changes in cortical thickness, especially in developing brains 1
• Prefrontal cortex connectivity: Disrupted connectivity in the prefrontal cortex, affecting decision-making and impulse control 1
• Orbitofrontal cortex damage: Specific effects on the orbitofrontal cortex, essential for adolescent decision-making 1

Neurochemical Mechanisms of Damage

The neurological harm occurs through specific pathways:

• Glutamate excitotoxicity: Cannabis inhibits GABAergic inhibitory action on glutaminergic neurons, increasing susceptibility to excitotoxic damage 1
• Dopamine signaling alterations: Changes in glutamate and dopamine signaling contribute to cognitive deficits and psychosis risk 1
• Endocannabinoid system disruption: Long-term use causes neuroadaptations and altered functioning of the endogenous cannabinoid system, which normally regulates cognitive processes 5

Psychiatric and Neuropsychiatric Complications

Serious mental health consequences emerge with cannabis use:

• Psychosis and schizophrenia: Heightened risk for transition to schizophrenia and psychosis, with cannabis worsening positive psychotic symptoms (odds ratio 5.21) and total psychiatric symptoms (odds ratio 7.49) 1, 4, 6
• Depression: Increased risk for developing depressive disorders and exacerbation of existing psychiatric conditions 4, 3
• Suicidal behavior: Association with suicidal ideation and attempts 4, 3
• Cannabis use disorder: Approximately 10% of chronic adult users develop cannabis use disorder; risk nearly doubles with medical cannabis card access 4

Central Nervous System Adverse Events

Direct CNS toxicity manifests as:

• Sedation and obtundation: Particularly in older adults, acute cannabis toxicity can cause significant sedation 4
• Impaired coordination: Persistent coordination deficits increase motor vehicle crash risk (odds ratio 1.27) 6
• Cannabinoid hyperemesis syndrome: Long-standing use can cause cyclical vomiting episodes with neurological components 4

Age-Specific Vulnerabilities

Adolescents (Highest Risk Population)

Early initiation causes the most severe and lasting neurological damage:

• Rapid brain changes: Neural changes occur more rapidly in adolescents than adults, with many structural changes unique to this age group 1
• Enhanced vulnerability: The developing adolescent brain shows increased susceptibility to cannabis-induced excitotoxicity and structural damage 1
• Long-term consequences: Early onset (especially before age 13) strongly predicts future dependence, neuropsychological decline, and elevated risk for psychotic disorders in adulthood 1, 4
• Irreversible effects: Cannabis use during adolescence may have deleterious effects on brain development that persist into adulthood 4

Older Adults

• Behavioral health issues: Higher risk for anxiety and depression 4
• Emergency presentations: Increased cannabis-related emergency visits with acute toxicity causing sedation and obtundation 4

Persistence and Recovery

Critical caveat: While some cognitive deficits may improve with abstinence, evidence shows:

• Prolonged impairment: Verbal memory, attention, and executive function deficits may persist after prolonged abstinence 2
• Incomplete recovery: Recovery across all cognitive domains remains underresearched, and complete reversal is not guaranteed 2
• Withdrawal symptoms: Non-life-threatening withdrawal symptoms (sleep disturbances, appetite changes, abdominal pain) occur within 3 days of cessation and may last up to 14 days 4

Dose-Response Relationships

Higher potency increases all neurological risks:

• THC concentration: Average THC content nearly doubled from 9% (2008) to 17% (2017), with concentrates reaching 70% THC 4
• Dose-dependent effects: Higher doses of THC are associated with more severe acute effects, including psychosis 4
• Cumulative exposure: Chronic psychiatric risks correlate with cumulative exposure and age of first use 4

Clinical Bottom Line

Convincing evidence from multiple high-quality guidelines supports complete avoidance of cannabis during adolescence and early adulthood, in individuals prone to or with mental health disorders, and in anyone concerned about cognitive function. 6 The neurological side effects are not benign—they include measurable brain damage, persistent cognitive impairment, and serious psychiatric complications that can fundamentally alter quality of life and functional capacity.