A blackout is a phenomenon caused by the intake of alcohol or other substance in which long term memory creation is impaired or there is a complete inability to recall the past. Blackouts are frequently described as having effects similar to that of anterograde amnesia, in which the subject cannot create memories after the event that caused amnesia.
The term blackout is often confused with passing out or losing consciousness from drinking, blackouts do not involve the loss of consciousness but instead consist of the disrupting effect of alcohol informing memories for events occurring during a drinking episode.
Blackouts are caused by breakdown in the transfer of short-term memory into long-term storage and subsequent retrieval primarily through dose-dependent disruption of hippocampal CA1 pyramidal cell activity.
TYPE OF BLACKOUT
An alcoholic blackout may be complete (en-bloc) or partial.
An en bloc blackout is complete amnesia for significant events otherwise memorable under usual circumstances.
En bloc blackouts are classified by the inability to later recall any memories from the intoxication period, even when prompted. These blackouts are characterized also by the ability to easily recall things that have occurred within the last 2 minutes, yet inability to recall anything prior to this period. As such, a person experiencing an en bloc blackout may not appear to be doing so, as they can carry on conversations or even manage to accomplish difficult feats. It is difficult to determine the end of this type of blackout as sleep typically occurs before they end.
Fragmentary blackouts occur more frequently. They are characterized by the ability to recall certain events from an intoxicated period, yet be unaware that other memories are missing until reminded of the existence of these 'gaps' in memory. Although initially the subject may be unaware that memory is missing, reminders usually help the subject remember forgotten events.
Alcohol is a threat to global health, accounting for 4% of the global health burden, a proportion that is comparable to tobacco and hypertension. Nevertheless, alcohol continues to be a part of human culture. Several aspects related to interpersonal environment, behaviour, and emotional experience have been found to increase blackout susceptibility in a drinker.
Because of a high prevalence of alcohol use and ease of accessibility, recent blackout research has focused primarily on college students. An estimated 70% of college students consume alcohol at least once a month, and prevalence rates of alcohol-induced memory impairment as high as 40% to
50% have been reported among young adults.
Among 772 undergraduates who had consumed alcohol at least once, 51% reported at least 1 lifetime blackout, 40% reported a blackout in the previous year, and 9.4% of those who had drank in the past 2 weeks reported a blackout. The male-female incidence of blackout was similar despite more frequent and heavier drinking among the male respondents.
Life transitional changes such as assuming adult roles appear to be a strong influence on the process of disengagement from problem drinking. Those who continued to experience blackouts after four years were male, comparatively young, unmarried, and with a lower socioeconomic status.
In addition to the background characteristics discussed earlier that place groups of persons at heightened risk of experiencing alcohol-induced blackouts, variations in the genetic makeup and gender differences have also been found to increase the vulnerability to blackouts. Potential genetically transmitted mechanisms of blackout vulnerability include neurotransmitter gene expression and genes that mediate alcohol pharmacokinetics (PK).
About gender differences women are at greater risk of experiencing blackouts at lower levels of alcohol consumption than men.
HOW DOES MEMORY WORK?
- encoding or initial registration and interpretation of stimuli
- storage or consolidation and maintenance of encoded stimuli
- retrieval or search and recovery of stored stimuli.
Alcohol has its greatest effects on encoding.
The phases of memory include:
- immediate or acquisition memory;
- short-term or retention memory;
- recent or consolidation memory;
- remote, retrieval, or long-term memory.
Long-term memory can be divided into declarative (explicit memory [EM]) and procedural (implicit memory [IM]) memories, with declarative memory involving direct recall from previous learning such as memorization and verbatim repetition of speciﬁc facts, whereas procedural memory involves behavioural responses that do not involve the direct recall of previous learning, such as motor tasks.
Figure 1. A general model of memory formation, storage, and retrieval based on the modal model of memory originally proposed by Atkinson and Shiffrin (1968). Alcohol seems to influence most stages of the process to some degree, but its primary effect appears to be on the transfer of information from short–term to long–term storage. Intoxicated subjects are typically able to recall information immediately after it is presented and even keep it active in short–term memory for 1 minute or more if they are not distracted. Subjects also are normally able to recall long–term memories formed before they became intoxicated; however, beginning with just one or two drinks, subjects begin to show impairments in the ability to transfer information into long–term storage. Under some circumstances, alcohol can impact this process so severely that, once sober again, subjects are unable to recall critical elements of events, or even entire events, that occurred while they were intoxicated. These impairments are known as blackouts.
NEUROPHYSIOLOGICAL AND CHEMICAL MECHANISM
Alcohol interferes with the transfer of information from short-term to long-term storage, whereas immediate memory and long-term retrieval memory remain intact .
Memory impairment due to alcohol has been linked to disruption of hippocampal function -- in particular affecting gamma-Aminobutyric acid (GABA) and N-methyl-D-aspartate (NMDA) neurotransmission which negatively impacts long-term potentiation(LTP) .
The molecular mechanisms of the effects of alcohol on the hippocampus are not clear.
However, one leading candidate for a cellular substrate of memory formation is long-term potentiation (LTP), which is the establishment of long lasting heightened responsiveness to signals from other cells.
The hippocampus incorporates information from other brain regions to form new autobiographical memories, and CA1 pyramidal cells send the results of this processing from the hippocampus to the neocortex.
Ethanol’s effect on LTP in area CA1 of the hippocampus is thought to involve both inhibition of the NMDA receptor and potentiation of the γ-aminobutyric acid A (GABA-A) receptor transmission, which leads indirectly to further NMDA receptor inhibition. So ethanol may disrupt hippocampal function through potentiation of GABA-mediated inhibition in hippocampal microcircuits .
Speciﬁc GABA A receptor subtypes are sensitive to low-dose alcohol ingestion, whereas other subtypes are activated only through intoxication-level alcohol ingestion.
Alcohol increases GABAergic neurotransmission directly and indirectly through elevation of endogenous GABAergic neuroactive steroids ( allopregnanolone), presynaptic release of
GABA, and dephosphorylation of GABA A receptors, which promote increases in GABA sensitivity.
Upon activation, these GABA receptors conduct Cl-, resulting in neuronal hyperpolarization. This hyperpolarization decreases the chance of an action potential occurring and, thus, has an inhibitory effect on neurotransmission in the central nervous system.
Glutamate is the primary excitatory neurotransmitter used by synapses among principal cells in the hippocampus. In addition to antagonizing hippocampal NDMA receptor activity, ethanol reduces overall hippocampal glutamate release. The site of alcohol-induced NMDA inhibition
likely involves the NMDA receptor protein accessible from the extracellular environment, and this decreased hippocampal synaptic NMDA neurotransmission is likely to reﬂect, and subsequently contribute to, reduced hippocampal pyramidal and granule cell activity.
A critical requirement for establishing LTP in the hippocampus is NMDA2 receptor activation, which facilitates the entrance of calcium into the cell resulting in a sequence of events leading
to long lasting changes in the structure and function of the cell or both. So the primary mechanism underlying the effects of alcohol on LTP is believed to be the interference of hippocampal NMDA2 receptor activation, which prevents the inﬂux of calcium and the changes that follow.
Disruption of neurochemical pathways involved in hippocampal CA1 pyramidal cell activity is believed to be the underlying mechanism of alcohol-induced cognitive impairment, but the catalyst of alcohol-induced blackouts seems to be the rate of BAC (Blood Alcohol concentration) elevation. The rate at which BAC rises is perhaps the strongest predictor of blackout occurrence.
ALCOHOL AFFECTS NOT ONLY HYPPOCAMPUS
Alcohol-induced disruption of other brain structures involved in memory formation, storage, and retrieval may contribute to blackout . The frontal lobe region mediates STM and the formation and retrieval of long-term explicit memories. Frontal lobe function is impaired by acute alcohol ingestion, including performance on tasks requiring planning, decision making, and impulse control, and memory processes in the frontal lobes and hippocampus are coordinated by reciprocal connections ( dentate gyrus and ventral tegmetal area are also involved) .
Alcohol can have a dramatic impact on memory.
Alcohol primarily disrupts the ability to form new long–term memories; it causes less disruption of recall of previously established long–term memories or of the ability to keep new information active in short–term memory for a few seconds or more.
At low doses, the impairments produced by alcohol are often subtle, though they are detectable in controlled conditions. As the amount of alcohol consumed increases, so does the magnitude of the memory impairments. Large quantities of alcohol, particularly if consumed rapidly, can produce a blackout, an interval of time for which the intoxicated person cannot recall key details of events, or even entire events.
En bloc blackouts are stretches of time for which the person has no memory whatsoever. Fragmentary blackouts are episodes for which the drinker’s memory is spotty, with “islands” of memory providing some insight into what transpired, and for which more recall usually is possible if the drinker is cued by others.
Alcohol disrupts activity in the hippocampus via several routes—directly, through effects on hippocampal circuitry, and indirectly, by interfering with interactions between the hippocampus and other brain regions.