Peter R. Martin: Historical Vocabulary of Addiction
The noun blackout, according to the electronic version of Oxford English Dictionary (OED), was formed within English from the phrasal verb to black out, which means “To obliterate with black, especially as form of censorship or protection.” The first use in the English language according to OED dates to 1913, when the Irish playwright, critic, polemicist and political activist George Bernard Shaw (1856-1950) referred to blackout as a theatre production technique (1956): “The more I think of that revolving business the less I see how it can be done... There will have to be a black-out.” Since this initial use, the noun has been employed in various other ways which are interesting to explore to clearly understand the use in addiction which is subtly different. All early uses of blackout related to altering the source of sensory stimulation so as to reduce sensory input: “The failure of an electricity supply (especially with respect to lighting) and the resulting darkness”; “Loss of radio reception (as a result of fading, jamming, an electrical storm, etc.)”; “The deliberate suppression of news or information and (also) a dearth of news reporting”; and “The action of extinguishing or obscuring lights, especially by covering the windows in a building, as a precaution during air raids, the resulting darkness, and the time or period of compulsory extinguishing or covering of lights.” Other uses of blackout refer to environmental changes that compromise sensory capacity. The first of these is: “Temporary loss of vision experienced when a person is subjected to strong accelerative forces, especially during flying, attributed to decreased blood flow in the central retinal artery.” Another, presumably fanciful example refers to a blackout cake: “A type of moist, rich chocolate layer cake with chocolate filling and soft chocolate icing, typically dusted with chocolate cake crumbs.” (It is recognized that any similarity in meaning of blackout cake to other uses discussed here is figurative in that ingestion of a tasty morsel might overwhelm and seemingly detract from other sensory inputs).
It is not difficult to see how blackout might be employed to describe a severe state of intoxication with a self-administered pharmacologic agent, typically alcohol. The meaning of blackout in this context is distinctly different from those discussed above, namely, sensory input and capacity are both undiminished but incorporation of the sensory experience in the nervous system as a memory trace that can be recalled is disturbed by the effects of the self-administered pharmacologic agent. Thus, the OED definition of blackout used in the field of addiction is: “A (usually temporary) loss of memory; an amnesic gap, especially for events occurring during a period of alcohol intoxication.” However, this meaning of blackout is not straightforward as the second portion of this OED definition is: “Also: a momentary or brief loss of consciousness, especially when caused by reduced blood flow to the brain; a faint.” There is a clear pathophysiological distinction between the two parts of this OED definition of blackout although they are typically used interchangeably in the vernacular of patients. Therefore, diagnosis can be challenging — it is essential to distinguish the meaning used in addiction from the term syncope (“Failure of the heart's action, resulting in loss of consciousness, and sometimes in death.”). For example, one need only look at a very early description of the vascular causes of blackout dating to Johnson (1817) to appreciate these differences: “Dr. Parr, in his London Medical Dictionary, states it as his opinion, that, ‘the cause is most probably a spasm or convulsion’ and denies that ossification of the coronary arteries is any thing but a concomitant symptom, or rather an effect of angina pectoris.” Brain electrophysiological changes have also been considered in pathogenesis of syncopal forms of blackout (Redlich 1946). Importantly, whereas impairment of memory may occur due to vascular and electrophysiological causes of syncope, the “amnesic gap” is the sine qua non of blackout associated with ingestion of alcohol or other central nervous system depressants (Goodwin, Crane and Guze 1969).
The association of cognitive disturbances with alcohol consumption, including amnesia, have been recognized by clinicians for two centuries (Sutton 1813; Courville 1955; Butters and Cermak 1980). The studies of Korsakoff between 1887 and 1900 were the first to focus attention on primarily memory disorders in alcoholism (Victor and Yakovlev 1955). Korsakoff suggested that the paucity of interest in amnesia per se was because it tended to co-occur with or complicated other diseases that were of greater concern due to their disabling global neurocognitive deficits (Levin, Peters and Hulkonen 1983). The more subtle presentation of memory deficit in isolation often requires repeated observations using focused techniques to differentiate it from global impairments of dementia and may easily be overshadowed by other clinical features (Martin, Adinoff, Weingartner et al. 1986). Formal investigations of memory functioning in alcoholism followed closely after publication in 1885 of the ground-breaking volume, Memory: A Contribution to Experimental Psychology, by German psychologist Hermann Ebbinghaus (1850-1909) who recognized that memory is a brain function subject to experimental study (Ebbinghaus 1913): “Mental states of every kind, -- sensations, feelings, ideas, -- which were at one time present in consciousness and then have disappeared from it, have not with their disappearance absolutely ceased to exist. Although the inwardly turned look may no longer be able to find them, nevertheless they have not been utterly destroyed and annulled, but in a certain manner they continue to exist, stored up, so to speak, in the memory. We cannot, of course, directly observe their present existence, but it is revealed by the effects which come to our knowledge with a certainty like that with which we infer the existence of the stars below the horizon. These effects are of different kinds.” While Ebbinghaus introduced systematic investigation of memory functioning and Korsakoff clinically identified its dysfunction in a unique clinical syndrome, the pathogenesis, psychopathology and nosology of the memory disturbances associated with alcohol ingestion and alcohol use disorder remains an active topic of investigation to the present day.
The first issue is the clinical presentation and duration of memory deficits in relation to alcohol ingestion (Goodwin, Crane and Guze 1969; Butters and Cermak 1980). Acute amnesia (disrupted memory traces) limited to the period of intoxication, is the characteristic feature of a blackout, as discussed above. On the other hand, the classical chronic amnestic condition first described clinically by Korsakoff, now termed the Wernicke-Korsakoff syndrome since recognition that it is a complication, or the chronic phase of the acute life-threatening Gayet-Wernicke’s encephalopathy, is unrelated to acute ingestion of alcohol but rather is due to neuropathologic findings resulting from thiamine deficiency associated with malnutrition from chronic alcohol consumption (Victor, Adams and Collins 1971). This chronic syndrome is characterized by anterograde memory deficits, namely, the inability to encode/recall ongoing memories subsequent to the period when the brain insult from malnutrition was sustained (Victor, Adams and Collins 1971; Butters and Cermak 1980). The individual with Wernicke-Korsakoff syndrome, however, may have a surprising degree of knowledge of the distant past, which is often incorporated in interpretation of present experiences (confabulation) and distinguishes it from neurodegenerative disorders characterized by global neurocognitive decline (Martin, Adinoff, Weingartner et al. 1986). Therefore, a blackout represents only a short period of impaired memory functioning (encoding/recall) that resolves once alcohol leaves the bloodstream, whereas the Wernicke-Korsakoff syndrome can be an enduring deficit with neuropathologic residua that typically alter the course of a patient’s life and severely limits its quality. Ryback (1971) proposed that the acute and chronic toxic effects of alcohol consumption on memory resemble each other, specifically that short-term memory alone, rather than immediate memory or long-term memory, is disrupted in alcoholism but to varying degrees on a continuum, least in alcoholic blackout ("cocktail-party drinking") and most severely in the Wernicke-Korsakoff syndrome. This heuristically useful idea, based purely on observation of clinical phenomena rather than pathological underpinnings, has nevertheless guided researchers in the field to the present.
The next issue is when blackouts typically occur during the course of alcoholism and their clinical implications with respect to the tempo of illness progression. Goodwin, Crane and Guze (1969) and Goodwin, Othmer, Halikas and Freemon (1970) reported that more than one-third of hospitalized alcoholics had never experienced a blackout and that, among those who did report the experience, blackouts generally began relatively late in the course of alcoholism and possibly were precursors of chronic alcoholism-associated brain dysfunction. Blackouts were associated with severity and duration of alcoholism as well as the intensity of alcohol consumption in each drinking episode, capacity for drinking large amounts including “loss of control,” neglect of meals, gulping drinks and a history of head trauma. However, Tarter and Schneider (1976) concluded that alcohol-induced blackouts and memory capacity in the sober state were unrelated. Nevertheless, “blackout is tied to the history and onset of heavy drinking, and usually manifests most frequently in persons who drink until there is a loss of consciousness and exhibit a craving for alcohol.” Since early onset alcoholism is associated with precipitous acceleration of alcohol consumption with few periods of extended abstinence, once such drinking begins, it is not surprising that blackout can serve as a signal of a particularly malignant alcoholism course (Parks, Dawant, Riddle et al. 2002; Marino and Fromme 2016).
Hartzler and Fromme (2003) found two forms of blackouts in young adult volunteers: fragmentary blackouts (episodes for which retrieval of experiences is facilitated by provision of memory cues) and en bloc blackouts (occurrence of full and permanent memory loss for events during intoxication). They found that the less severe, fragmentary form, was threefold more prevalent than full blackouts. However, blood alcohol concentrations were not correlated with the most severe blackout type, suggesting interindividual differences in susceptibility. One explanation for this finding may have been that most en bloc blackouts in these young drinkers involved concurrent use of illicit substances, which may have had an additive or synergistic effect with alcohol in compromising neuronal circuits that subserve memory functioning. Nelson, Heath, Bucholz et al. (2004) examined the genetic epidemiology of lifetime blackouts among young adults in the Australian Twin Register and reported substantial genetic contributions to liability for alcohol-induced blackouts as well as for frequency of intoxication experienced. Wetherill, Castro, Squeglia and Tapert (2013) prospectively demonstrated that substance-naïve adolescents who subsequently experience alcohol-induced blackouts required greater neural activation, or effort, for inhibitory processing determined by fMRI with a go/no-go task compared to adolescents who go on to drink at similar levels without experiencing blackouts and nondrinking controls. These findings suggest mechanisms underlying blackout and susceptibility to alcohol use disorder and its complications. For example, worse performance on a response inhibition task, a demonstrated risk factor for development of alcohol use disorder, and in particular, early-onset alcoholism, may also represent neurobiological vulnerability to development of alcohol-induced blackout (Begleiter, Porjesz, Bihari and Kissin 1984; Tarter, Hegedus, Goldstein et al. 1984; Cloninger 1987). These observations complement those of Schuckit (1980) who reported that young men with a family history positive for alcoholism rated themselves less intoxicated than did controls without family histories of alcoholism, despite comparable blood alcohol levels. Hence, young individuals with genetic loading for alcoholism may feel they can drink more and thus be more likely to develop both blackouts and alcoholism. When Hingson, Zha, Simons-Morton and White (2016) examined the incidence, predictors and behavioral correlates of blackouts, they concluded that blackouts were phenomenologically important in alcoholism, as having blackouts was the strongest independent predictor of most other alcohol problems.
The final issue is our understanding of the neurobiological substrate of a blackout. The alcoholic blackout provides insights about alcoholism as indicated above, but also offers mechanistic understanding of the phenomena that constitute memory functioning (Berglund, Prohovnik and Risberg 1989). The memory impairment in a blackout occurs concurrently with a rapid rise in brain alcohol levels, which diminishes alertness and attention to the surrounding environment (arousal) by its effects on the major inhibitory (GABAA receptors) and excitatory (NMDA receptors) neurotransmitter systems in the brain (Goodwin, Crane and Guze 1969; Martin and Patel 2017). (This resetting of the balance in inhibitory/excitatory neurotransmission also explains why other central nervous system depressants such as barbiturates, nonbarbiturate hypnosedatives and benzodiazepines can also cause blackouts [Bixler, Scharf, Soldatos et al. 1979] and act synergistically with alcohol). While not related to memory functioning in the sober state (Tarter and Schneider 1976), memory disturbances during blackout are demonstrably anterograde in nature and state-dependent (Goodwin, Powell, Bremer et al. 1969). These observations are consistent with the hypothesis proposed by Hebb (1949) that the relationship between the efficiency of learning and the level of alertness, namely, the arousal of the nervous system at the moment learning occurs, is fundamentally important. Thus, learning can be inefficient during intoxication and, consequently, recall of material that was learned may be disturbed. Therefore, the conditions at the moment of learning and testing recall are critical — memory performance is enhanced if the condition of the nervous system at the time of learning (intoxication) is identical to that during testing for recall.
Clinical and neuropsychological characterization of alcohol-associated amnesia eventually advanced to neuroimaging studies in order to investigate the brain mechanisms involved. In patients with Wernicke-Korsakoff syndrome, regional cerebral blood flow (rCBF) was unexpectedly elevated above levels observed in comparison groups with neurocognitive compromise, i.e., dementia (Simard, Olesen, Paulson et al. 1971) or alcoholics (Berglund and Ingvar 1976). Additionally, Berglund, Prohovnik and Risberg (1989) reported a large increase in mean rCBF during blackout in an alcoholic patient compared with values during abstinence, not unexpected based on the effects of alcohol on rCBF (Battey, Heyman and Patterson 1953). Thus, rCBF similarities in acute blackout and in the chronic state of Wernicke-Korsakoff syndrome are compatible with the proposal of Ryback (1971). Techniques permitting more granular neuroanatomic brain mapping (positron emission tomography, PET) or during performance of memory-related tasks (functional magnetic resonance imaging, fMRI) identified disruptions of related brain circuits in Wernicke-Korsakoff syndrome and in alcoholic blackout (Martin, Rio, Adinoff et al. 1992). As discussed above, atypical brain responses during inhibitory processing may be a neural risk factor for the occurrence of alcohol-induced blackouts. Wetherill, Schnyer and Fromme (2012) examined whether neural activation during a contextual memory task differed between individuals who experienced fragmentary blackouts with drinking and those who did not. While contextual memory was not different in the two groups, acute alcohol consumption affected dorsolateral prefrontal cortex and posterior parietal cortex neural activation differentially, suggesting that frontoparietal abnormalities are a potential biomarker for vulnerability to alcohol‐induced memory impairments. Interestingly, related, though perhaps not identical circuits can be compromised in neurocognitive disorders that resemble Wernicke-Korsakoff syndrome (Welch, Nimmerrichter, Kessler et al. 1996). As research in learning and memory progresses, these findings may advance to the cellular level in the relevant neuronal circuits (Josselyn and Tonegawa 2020).
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May 7, 2020