Blackouts vs. Passing Out: Distinguishing Loss of Memory from Loss of Consciousness
It’s important to distinguish between blackouts and passing out (loss of consciousness). Blackouts are memory impairment with consciousness maintained; you can do complex things but have no memory of those events. Passing out is complete loss of consciousness due to alcohol’s depressant effects on the central nervous system, particularly its suppression of brainstem activity that is responsible for wakefulness.
The physiology is different. Blackouts affect hippocampal function, interrupting memory consolidation whereas passing out involves global suppression of brain activity, affecting areas responsible for arousal and awareness. Both are consequences of excessive drinking but understanding the difference helps us understand the specific risks of each state.
Defining Alcohol-Related Blackouts: A Neuroscience Perspective

Blackouts are periods of anterograde amnesia that occur during alcohol intoxication, which describes a period of lost time, or a lack of memory of the events that took place while intoxicated . It’s important to distinguish between en bloc and fragmentary blackouts. En bloc blackouts are a complete and permanent memory loss for a specific period where there is no recall even when prompted. Fragmentary blackouts, also known as greyouts, are patchy memory loss where some details can be recalled with effort or context.
Alcohol affects memory through its effects on neurotransmitters, GABA and glutamate. GABA is the brain’s relaxation and sedation neurotransmitter, reducing neural activity. Glutamate is the brain’s learning and memory formation neurotransmitter. Alcohol boosts GABA and suppresses glutamate, disrupting hippocampal communication and memory consolidation. This is why we black out and the brain can’t encode new memories even though we’re conscious.
The Neurochemistry of Blackouts: Impact on Memory Encoding
The neurochemical disruption caused by alcohol is the main driver of blackouts. Alcohol interferes with two key neurotransmitters essential for synaptic plasticity and memory formation: glutamate and GABA. Glutamate , the brain’s main excitatory neurotransmitter, is critical necessary for long-term potentiation (LTP), the process of strengthening synaptic connections and consolidating new memories. Alcohol inhibits glutamate activity by blocking NMDA receptors, which are critical for LTP. This disrupts hippocampal signalling, preventing new information from being stored.

At the same time, alcohol enhances GABA activity, the brain’s primary inhibitory neurotransmitter. Increased GABAergic activity leads to generalised neural inhibition, further preventing the hippocampus to encode new memories . This imbalance between glutamate and GABA signalling creates a neurochemical state of reduced excitatory signalling, that severely inhibits memory formation.
Research indicates that even moderate drinking can severely impair glutamate-mediated LTP in the hippocampus
A combination of altered glutamate, GABA and dopamine signalling underpin alcohol-induced amnesia or blackouts, when high quantities of alcohol are consumed. Although dopamine signalling is not directly responsible for memory impairment, dopamine dysfunction within the mesolimbic system may exacerbate blackouts since motivation, reward and salience are impaired, contributing to weakened memory formation.
Risk Factors and Predisposing Conditions
Several things can increase the chances of blacking out. The rate and amount of alcohol consumed is key; rapid consumption to high BACs is a big one. An empty stomach accelerates alcohol absorption leading to higher and faster BAC spikes.
Moreover, women are known to have less alcohol dehydrogenase, the enzyme that breaks down alcohol and a higher fat-to-water ratio,leading to higher BACs than men who consume the same amount. Genetic predispositions can affect alcohol metabolism and neurotransmitter function making you more susceptible to blackouts. Co-occurring mental health conditions like anxiety disorders or a history of trauma can increase the risk as you may use alcohol as a coping mechanism and consume more. Stress increases the risk too as it affects alcohol consumption patterns and neurobiological responses.
Cognitive and Behavioural Consequences of Repeated Blackouts

Repeated blackouts can have long term effects on cognitive function. Chronic alcohol use and repeated blackouts are associated with impaired executive function (planning, decision making, impulse control), attention deficits and reduced working memory capacity in people who have had frequent blackouts.
There’s a big link between blackouts and alcohol use disorder (AUD). Research shows that people who blackout are at higher risk of developing AUD because of impaired decision making and reinforcement of drinking behaviour. Not being able to remember past drinking episodes can give you a false sense of control and make you underestimate your drinking. Over time this cycle of impaired judgement and memory loss can lead to increased tolerance, more drinking and higher risk of addiction.
Neuropathology: Structural and Functional Brain Changes
Chronic alcohol use and repeated blackouts can lead to structural and functional changes in the brain over time. Neuroimaging studies (MRI and fMRI) have shown reduction in brain volume, particularly in the prefrontal cortex and hippocampus, in heavy drinkers. These changes are associated with cognitive impairment, including memory deficits and executive dysfunction.
Functional changes are changes in brain activity patterns, reduced connectivity between brain regions. These disruptions affect information processing and cognitive performance. Long term alcohol consumption can also cause white matter degradation, likely due to myelin damage, impairing neural signalling and further impeding cognitive function.
The Role of Trauma and Stress in Alcohol-Induced Blackouts
There’s a complicated dance between trauma, stress and the vulnerability to blackouts. People with a history of trauma may use alcohol as a coping mechanism for distressing emotions or memories, which can increase the risk of heavy drinking and blackouts, however, not all trauma survivors become reliant on alcohol or experience blackouts.
Stress can also impact drinking patterns and neurobiological responses. High levels of stress can impair executive function and decision making, making people more likely to engage in risky behaviour such as heavy drinking. Stress can also alter the brain’s reward system, making alcohol more reinforcing and encouraging more drinking.
Assessment and Diagnosis of Blackout-Related Memory Impairment

Accurate assessment and diagnosis is key to addressing blackout-related memory impairment. This includes cognitive tests to assess memory function such as recall tasks and recognition tests. Clinical interviews gather information on drinking history, blackout experiences, and associated cognitive and behavioural changes. Since individuals may have impaired memories of blackout events, collateral reports from friends and family can help to provide additional context. Self report measures such as questionnaires to get more information about the individual’s subjective experiences and perceived cognitive deficits. A full assessment helps to determine the extent of memory impairment and informs treatment.
Prevention Strategies and Harm Reduction Techniques
Blackouts occur when BAC rises to high levels often due to high consumption rates, drinking on an empty stomach, or individual differences in metabolism. Key guidelines include pacing, drinking, not drinking on an empty stomach, staying hydrated and knowing your limits. Don’t mix alcohol with drugs or medications as this can increase the risk of adverse effects. Education and awareness campaigns play an important role in promoting responsible drinking habits and minimising blackout risk. These are essential for brain health as per the Behavioural Medicine approach.
Highlands Recovery is located in the hills of Sydney Australia and we adopt the behavioural medicine approach which recognises the interconnectedness of biological, psychological and social factors in recovery. Our intensive residential program gets to the root of addiction and trauma and aims for lasting change. While we do not provide medical detoxification on site, we can arrange prior to admission, ensuring you are medically stabilised before beginning our program.
Reviewed by: Dr. Emma Bardsley

Dr Emma Bardsley is a neuroscientist with a PhD from Oxford and a post doctorate from Auckland University, along with an undergraduate degree in Pharmacology from King’s College London. She has lectured extensively on neuroscience, physiology, and pharmacological interventions, bridging foundational research and its clinical applications. With a strong record of publications in high-impact journals and extensive experience in scientific writing, editing, and peer review, she excels at translating complex research into practical insights. Based in New Zealand and collaborating internationally, Emma is dedicated to advancing understanding and treatment in the fields of trauma, addiction, and recovery.
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