Brief Motivational Interventions Are Associated with Reductions in Alcohol-Induced Blackouts Among Heavy Drinking College Students.

BACKGROUND: Alcohol-induced blackouts, a form of anterograde amnesia that restricts the encoding of short-term memories into long-term ones, are among the most severe alcohol-related consequences. College students are at high risk of experiencing alcohol-induced blackouts, and there is a need to determine whether alcohol interventions can effectively reduce blackouts in this population. The current study uses data from 3 randomized clinical trials to examine the effect of various intervention approaches on alcohol-induced blackouts. METHODS: Four interventions were compared over 3 studies: (i) a computerized feedback intervention (electronic Check-Up To Go [e-Chug]; Study 1); (ii) a single-session brief motivational intervention (BMI; Study 1); (iii) a BMI plus behavioral economic session focused on increasing substance-free activities (BMI + Substance-Free Activity Session [SFAS]; Studies 2 and 3); and (iv) a BMI plus supplemental Relaxation Training session (BMI + Relaxation Training; Studies 2 and 3). Studies 1 and 3 also included an assessment-only control condition. For each study, participants reported whether they had experienced an alcohol-induced blackout at each time point; binary logistic regressions examined differential likelihood of experiencing an alcohol-induced blackout over time. RESULTS: Neither the single-session BMI nor e-Chug reduced alcohol-induced blackouts over assessment only; however, participants in the BMI + SFAS or BMI + Relaxation Training condition were significantly less likely to experience an alcohol-induced blackout compared to assessment only at 1-month (Wald = 4.77, odds ratio [OR] = 0.53, p = 0.03) and 6-month follow-ups (Wald = 5.72, OR = 0.52, p = 0.02). Study 2 also revealed a larger effect for the BMI + SFAS over the BMI + Relaxation Training condition at 6 months (Wald = 4.11 OR = 0.22, p = 0.043), although this was not replicated in Study 3. The effects for the 2-session BMIs lasted 6 months, at which point maturation effects diminished differences between assessment-only and intervention conditions. CONCLUSIONS: Two sessions of BMI are a substantial enough dose to result in reductions in alcohol-induced blackouts among college student heavy drinkers.

Transient epileptic and global amnesia: Real-life differential diagnosis.

OBJECTIVE: Transient epileptic amnesia (TEA) is an underestimated condition in emergency clinical setting, where most of transient amnesic episodes tend to be classified as transient global amnesia (TGA). We designed this study to evaluate the actual frequency of TEA in a real-life scenario and to highlight the features that can help clinicians distinguishing it from TGA. METHODS: We retrospectively collected clinical data of 83 patients who accessed our emergency ward for an abrupt onset of amnesic disorder, initially interpreted as TGA. All patients underwent neurological evaluation, magnetic resonance imaging (MRI) scan, and standard 21-channel scalp electroencephalography (EEG) recording (standard EEG [st-EEG]). Moreover, patients with borderline epileptiform abnormalities on st-EEG or with normal st-EEG but high clinical suspicion for TEA underwent a 16-channel 24-hour ambulatory EEG (24-h EEG). Clinical features, neurophysiological, and neuroimaging data were analyzed and compared in the two groups (TEA and TGA). RESULTS: Diagnosis of TEA, according to Zeman's criteria, was made in 15 patients (18%). From a clinical point of view recurrence (p < .001) and atypical symptoms such as confusion or language disorder (TGA plus manifestations), appear to be key elements in order to discriminate between TEA and TGA (80% of patients with TEA vs 7.8% of patients with TGA; p < .001). In our sample, duration of the episodes did not significantly differ between TGA and TEA, even though it is usually described as shorter for TEA. This result could be related with a prolonged postictal state in these patients. The analysis of st-EEG results evidenced low sensitivity for interictal epileptiform abnormalities (IEAs) detection (52.3%), with not conclusive data in distinguishing TEA from TGA. On the contrary, 24-h EEG showed IEAs in all patients with epilepsy, mostly during sleep, suggesting an essential diagnostic role of long-lasting EEG recording for TEA. Finally, structural abnormalities were more frequent in patients with TEA (26.6%). In the group with TGA, the only imaging alteration found was diffusion weighted imaging (DWI) hippocampal hyperintensity. CONCLUSION: Our findings show that in a real-life clinical scenario, TEA is frequent but often overlooked. However, simple clinical data and widely available neurophysiological examinations can truly help to effectively distinguish TEA from TGA.

Prevalence and clinical characteristics of unremembered nocturnal eating in diabetic subjects: Kurume sleep trouble in obesity and metabolic disorders (KUSTOMED) study.

Nighttime food intake is associated with weight gain and higher HbA1c levels. We experienced night eaters who have no memory of their nocturnal eating in the morning. In this study, the curious night eating behavior was designated as "unremembered nocturnal eating syndrome (UNES)". We screened 1,169 patients with diabetes for sleep quality and abnormal eating behavior at night using the Pittsburgh Sleep Quality Index questionnaire with an additional question regarding UNES. When abnormal nocturnal eating behavior was noted, detailed clinical information was extracted from interviews with the patients. We identified 9 patients who experienced UNES. They had a higher BMI compared with subjects who reported no such episodes. Among them, 6 patients who consumed food at night without memory 2-5 times per month or more had significantly higher HbA1c levels. Continuous glucose monitoring in a patient with type 1 diabetes revealed an abrupt elevation of glucose levels from midnight when some foods were consumed. Eight of the 9 patients were taking benzodiazepine and/or non-benzodiazepine hypnotic agents when they experienced the episodes. The prevalence of UNES was 0.8% in all subjects and 4% in those taking hypnotic drugs. The ratio of hypnotic drug use in subjects with UNES was significantly higher than for individuals without UNES (89% vs. 17%, p<0.0001). Although UNES seems to be etiologically heterogeneous, hypnotics-induced parasomnia and/or anterograde amnesia may be associated with the behavior. UNES is not rare in diabetic patients on hypnotic medicine and may be a hidden cause of unexpected morning hyperglycemia.

Genetic epidemiology of alcohol-induced blackouts.

BACKGROUND: Alcohol-induced blackouts (ie, periods of anterograde amnesia) have received limited recent research attention. OBJECTIVE: To examine the genetic epidemiology of lifetime blackouts and having had 3 or more blackouts in a year, including analyses controlling for the frequency of intoxication. DESIGN, SETTING, AND PARTICIPANTS: Members of the young adult Australian Twin Register, a volunteer twin panel born between January 1, 1964, and December 31, 1971, were initially registered with the panel as children by their parents between 1980 and 1982. They underwent structured psychiatric telephone interviews from February 1996 through September 2000. The current sample contains 2324 monozygotic and dizygotic twin pairs (mean [SD] age 29.9 [2.5] years) for whom both twins' responses were coded for blackout questions and for frequency of intoxication. MAIN OUTCOME MEASURE: Outcome Measure Data on lifetime blackouts and having had 3 or more blackouts in a year were collected within an examination of the genetic epidemiology of alcoholism. RESULTS: A lifetime history of blackouts was reported by 39.3% of women and 52.4% of men; 11.4% of women and 20.9% of men reported having had 3 or more blackouts in a year. The heritability of lifetime blackouts was 52.5% and that of having had 3 or more blackouts in a year was 57.8%. Models that controlled for frequency of intoxication found evidence of substantial genetic contribution unique to risk for the blackouts and a significant component of genetic risk shared with frequency of intoxication. CONCLUSIONS: The finding of a substantial genetic contribution to liability for alcohol-induced blackouts including a component of genetic loading shared with frequency of intoxication may offer important additional avenues to investigate susceptibility to alcohol-related problems.

[Primary loss of consciousness and amnesia in subarachnoid hemorrhage--a quantitative study]. / Primäre Bewusstlosigkeit und Amnesie bei Subarachnoidalblutung--eine quantifizierende Untersuchung.

Subarachnoid hemorrhages (SAH) being sudden events affecting the brain in a rather wide-spread fashion are apt to induce loss of consciousness (LOC) and amnesia. The aim of the present study was to collect data on their frequency and extent. To this end we examined 48 patients at a mean of one year post-onset. Two thirds of them reported anterograde and an additional 17% retrograde amnesia; in 40% LOC (median 6 minutes) was observed. The durations were extremely skewed towards shorter times with a median of 2.7 days for anterograde and 1.3 days for retrograde amnesia who--with a single exception--were markedly shorter than anterograde amnesia. Summing up, a significant proportion of all SAH suffered LOC and amnesia occurred in the majority of cases. SAH therefore are events which with respect to LOC and amnesia bear some resemblance with closed head injuries. Exact observation and history taking may disclose important data on their severity and possible sequelae.

[Post-traumatic Korsakoff's syndrome: clinical and anatomical report]. / Syndrome de Korsakoff post-traumatique: étude anatomo-clinique.

Clinical and anatomical report of a post traumatic amnestic syndrome (Korsakoff's syndrome), associating anterograde amnesia persisting for fifteen years, with temporal disorientation, false recognitions, initially intense transitory confabulation and secondarily bursts of confabulation, intact remote memory and persistence of old learnings. Death after twelve years from mesenteric infarction. Anatomically, post-traumatic sequellae are limited to both cingulate gyri in their anterior part. This cingula involvement is easy to understand if one knows that post-traumatic Korsakoff's syndrome appears after severe cranial traumatisms, with at least three days of coma, and develops constantly, even if transitory, after long duration comas with 20 to 30 days of loss of consciousness. Anatomical explanation depends on the fact that Korsakoff's syndromes from various etiologies need, to be produced, a bilateral damage of the limbic circuit and that severe head traumatisms, when dying early in the evolution without possibility of a neuro-psychological investigation, have always a destruction of corpus callosum or cingulate gyri or both, resulting from crushing of these structures by the edge of the faulx cerebri. Consistent with these constatations, it is logical that a Korsakoff's syndrome develops after severe head traumas with bilateral lesions of the limbic circuit and especially of the cingulate gyri. But anatomical evidence remains rare, because early fatal evolution does not permit psychological evaluation and, reversely, long survivals who may die from another pathology would not have brain examination. We prefer the name of "Korsakoff's syndrome" rather than that of "amnesic syndrome" to denominate the anterograd amnesia (amnésie des faits récents) encountered in nutritional disorders due to B1 deficiency in true Korsakoff's disease, but also with other etiologies such as cerebral tumours, vascular cerebral disorders, post-commital anoxia, herpetic encephalopathy, head traumas, all of them developing amnesia for recent events, formerly classified under the title of "korsakowian syndrome" or "mental syndrome of Korsakoff" and more recently under the denomination of "amnesic syndrome". But whatever is the etiology of the memory disorder, the amnesic syndrome remains identical and the advanced small differences, such as euphoria in alcoholics or mood depression in tumours, are often fallacious, so that the only way of differentiation deals with accessory symptoms such as intracranial hypertension in tumours, sudden onset in vascular etiologies or polyneuritis in B1 deficiency. Post-traumatic Korsakoff's syndrome joins with this scheme, for its clinical aspect is so similar to that of nutritional disorders that it might be difficult to reach the exact diagnosis when an alcohol addict develops, after a head trauma, an amnesia which could be the consequence of the trauma but also of a nutritional disorder developed after the accident with inadequate parenteral treatment. Our case, which is the first well documented observation of this disease reported with long clinical survey and final pathological examination, was presented in 1981 at a joint meeting of the French and Dutch neurological societies. It gives the proof of the importance, in limbic circuit, of the cingulate gyri. A comparison is made with four other clinical cases of post traumatic amnestic syndrome with MNR procedures which show, for two of them, cingula lesions explaining the clinical features, for one of them a bilateral lesion of Ammon's homs and for the last one extra-limbic lesions, with destruction of the inferior part of both frontal lobes, associated with a possible deafferentation of the right cingula cortex.