If I Have Had Alcohol Seizures Can I Drink Again
Front Neurol. 2018; 9: 401.
Booze Use and Alcohol-Related Seizures in Patients With Epilepsy
Michael Hamerle
1Department of Cardiology, Academy Hospital Regensburg, Regensburg, Germany
2Section of Neurology, Epilepsy-Center Berlin-Brandenburg, Charité—Universitätsmedizin Berlin, Berlin, Germany
Leyli Ghaeni
2Section of Neurology, Epilepsy-Center Berlin-Brandenburg, Charité—Universitätsmedizin Berlin, Berlin, Germany
Alexander Kowski
2Section of Neurology, Epilepsy-Center Berlin-Brandenburg, Charité—Universitätsmedizin Berlin, Berlin, Germany
Florian Weissinger
2Department of Neurology, Epilepsy-Centre Berlin-Brandenburg, Charité—Universitätsmedizin Berlin, Berlin, Frg
Martin Holtkamp
twoDepartment of Neurology, Epilepsy-Eye Berlin-Brandenburg, Charité—Universitätsmedizin Berlin, Berlin, Federal republic of germany
Received 2018 Mar 13; Accepted 2018 May fifteen.
Abstruse
Purpose: This study aimed to assess booze consumption and the occurrence of alcohol-related seizures in patients with epilepsy inside the terminal 12 months.
Methods: In an epilepsy outpatient clinic, a standardized questionnaire was used to collect data retrospectively from consecutive adult epilepsy patients who had been suffering from the disease for at least ane year. Logistic regression analyses were performed to place independent predictors.
Results: A full of 310 patients with epilepsy were included. Of these, 204 subjects (65.viii%) consumed booze within the final 12 months. Independent predictors for alcohol utilize were antiepileptic drug monotherapy (OR 1.901) and physicians' advice that a light booze intake is harmless (OR four.102). Seizure worsening related to alcohol consumption was reported past 37 of the 204 patients (18.ane%) who had used alcohol. All 37 subjects had consumed large quantities of alcohol prior to the occurrence of alcohol-related seizures regardless of their usual alcohol-drinking behavior. The amount of booze intake prior to alcohol-related seizures was at least 7 standard drinks, which is equivalent to ane.4 L of beer or 0.7 L of wine. In 95% of cases, alcohol-related seizures occurred within 12 h later cessation of booze intake. Independent predictors for alcohol-related seizures were generalized genetic epilepsy (OR 5.792) and chronic heavier alcohol use (OR 8.955).
Conclusions: Two-thirds of interviewed subjects had consumed alcohol inside the concluding 12 months. This finding may exist an underestimate due to patients' self-reporting and call back error. In all cases, the occurrence of booze related-seizures was associated with timely consumption of considerably large amounts of alcohol. Thus, a responsible alcohol intake seems to be safe for most patients with epilepsy. However, subjects with epilepsy and especially those with generalized genetic epilepsy should exist made aware of an increased risk for seizures related to heavy alcohol consumption. Factors accompanying astute heavy alcohol intake such as altered sleep architecture, impaired adherence to antiepileptic medication, and metabolic disturbances may further facilitate the occurrence of seizures.
Keywords: alcohol-related seizures, booze-drinking behavior, epilepsy, generalized genetic epilepsy, alcohols
Introduction
Alcohol consumption may trigger seizures in patients with epilepsy. Yet, there is currently little knowledge on the booze-drinking behavior of epilepsy patients. In the 1940s, William G. Lennox comprehensively analyzed alcohol consumption and the occurrence of alcohol-related seizures in 1,254 subjects with epilepsy (one). However, only about 30% of patients used alcohol, thus excluding lxx% from whatever analysis of potential booze-related effects on the disease. The occurrence of booze-related seizures was reported past 21.1% of subjects who had used alcohol, and was more often stated past patients with symptomatic than with idiopathic or cryptogenic epilepsy (equally classified at that fourth dimension). Autonomously from this, there is niggling research on the occurrence of booze-related seizures in patients with epilepsy. A double-blinded, randomized, interventional report on 52 subjects with epilepsy demonstrated that a social alcohol intake over a 4-month-menstruum did not increase seizure frequencies (2). In another interventional study on xiv patients with epilepsy and x healthy controls, acute moderate alcohol consumption initially suppressed epileptiform EEG-activity. Later on however, when alcohol blood levels had declined, epileptiform EEG-activity was increased. Seizures occurred in some of those subjects and a rebound miracle was discussed (3).
Human and brute data have shown that acute alcohol intake has a biphasic effect on the primal nervous system (CNS). Initially, the inhibitory gamma-aminobutyric acid (GABA)-ergic effect of alcohol exerts CNS depressant and anticonvulsant properties (4, 5). In the postal service-alcohol state, however, when alcohol blood levels pass up, neuronal excitability is increased which may facilitate the occurrence of seizures in patients with epilepsy (half-dozen, 7).
The apply of alcohol is very mutual in western societies (eight). In Germany, 89% of all adults had consumed booze inside the last 12 months (9). This makes it necessary for neurologists and other physicians to advise patients with epilepsy adequately on how to handle alcohol consumption with their chronic affliction. The relationship between alcohol and epileptic seizures is complex. Research has mainly focused on the prevalence and pathophysiology of acute symptomatic seizures in the context of the alcohol withdrawal syndrome in alcohol-dependent subjects (ten–12) and on the risk to develop epilepsy due to regular booze consumption (thirteen, xiv). However, in that location are but a few studies that have examined the patterns of booze drinking in subjects with a known history of epilepsy, and these are limited by outdated results or small sample sizes. In particular, data on seizure worsening associated with alcohol consumption in patients with epilepsy are very sparse. Therefore, we aimed (a) to systematically analyze the booze-drinking beliefs of patients with epilepsy and (b) to identify independent predictors for alcohol use and the occurrence of alcohol-related seizures.
Materials and methods
Data drove using a standardized questionnaire, interview situations, and interview techniques
Between Oct 2008 and April 2010, sequent patients treated at the Epilepsy Outpatient Clinic, Department of Neurology, Charité—Universitätsmedizin Berlin were informed almost the study and invited to participate. The data collection on alcohol utilize was part of a research project systematically gathering data on nicotine, alcohol, and illicit drug use in epilepsy patients within the last 12 months. The data was collected by a standardized questionnaire (run into Supplementary Cloth). Nosotros have published data on epilepsy and illicit drug use earlier (15). Only subjects ≥18 years who had suffered from epilepsy for at to the lowest degree 1 year were included. Epilepsy types and seizures were classified according to the International League Confronting Epilepsy (xvi). A single unprovoked seizure was divers as epilepsy if specific EEG alterations or causal brain lesions identified by magnetic resonance imaging (MRI) indicated an increased and enduring chance for further epileptic seizures (17). Subjects were excluded from participation if they had experienced condition epilepticus or acute symptomatic seizures exclusively, if they had a history of psychogenic non-epileptic seizures, or if cerebral deficits, mental retardation or German linguistic communication barrier impeded adequate agreement and respond to the questions. Patients with legal representatives were also not enrolled.
Prior to the interview, each participant was educated on the scientific groundwork and purpose of the study. We placed smashing importance on a relaxed and informal interview atmosphere, and each subject area was thoroughly informed that all moral aspects regarding nicotine, booze, and illicit drug apply were irrelevant and that all data would be made anonymous and remain confidential. Thereby, we attempted to increase subjects' receptivity to the questions and avoid patients answering the questions in a more socially acceptable way. In several test-interviews, patients were intimidated when being asked about nicotine, alcohol, and illicit drug intake in front of their companions. Therefore, all interviews were held in a dissever written report room where just the interviewer and the patient were present. To ensure a standard and informal interview situation all patients were interviewed by the aforementioned person (MiHa) who was not one of the treating physicians at the Epilepsy Outpatient Clinic.
Alcohol consumption usually represents a taboo in the doctor-patient human relationship and questions on the smoking status are answered more than easily. Therefore, subjects were first queried about nicotine consumption and but later on asked to give details on alcohol use. Toward the end of the interview, patients were questioned on illicit drugs. Study subjects passed through the domains of the questionnaire with an increasing social stigma degree.
In the opening question on alcohol use, subjects were asked: "Practice y'all have any feel with alcohol consumption?" For this question, patients were able to respond in their own words and did not take to choose a predetermined response choice. The interviewer carefully noted the given information on the quantity and frequency of alcohol consumption in the opening question. Subjects who had consumed booze within the last 12 months stated details on alcohol intake in the opening question and afterwards by specifying the quantity and frequency of their individual booze consumption. Using that approach, the reliability of patients' responses on alcohol apply could exist evaluated regarding consistency. Data were excluded, if the patients' responses were inconsistent, if subjects were too hesitant to answer the questions, or if patients had refused to give details in simply ane of the interview's topics, that is nicotine, alcohol drinking and illicit drug use.
To ensure a comparable evaluation, alcohol consumption was translated and expressed in standard drinks containing 10 thousand of pure alcohol (18). To assistance subjects in measuring their individual boilerplate booze intake per drinking occasion, a chart illustrating dissimilar alcoholic beverages containing a single standard potable was shown to each study participant (Figure 1). Regarding the usual frequency of alcohol consumption within the concluding 12 months, subjects were able to cull one out of the post-obit unlike categories: daily, almost daily, 1–2 times a week, one–2 times a month or < ane–two times per month. According to that, patients who had consumed alcohol within the concluding 12 months were summarized in the post-obit 3 alcohol drinking categories: Patients with alcohol intake of no more than than 3–4 standard drinks daily, almost daily, 1–two times per week or less than weekly were considered equally light or occasional alcohol users. Moderate alcohol users were subjects who consumed more occasional or calorie-free users but non more 5–6 standard drinks daily, nearly daily and not more than 9–ten standard drinks ane–ii times per week. Heavier alcohol use was considered as alcohol intake of more than 5–6 standard drinks daily, nearly daily or more than 9–10 standard drinks ane–ii times per calendar week. Alcohol abstinence was divers according to the Globe Health Organization (WHO) as a menses of at least 12 months of non-consumptionone.
Amounts of dissimilar alcoholic beverages that stand for to 1 standard potable as defined past the World Health Arrangement. This illustration has been shown to the participants of this report to guide them in estimating their individual boilerplate alcohol intake per drinking occasion.
The Booze Use Disorder Identification Test (Inspect) is a ten-item core questionnaire developed by the WHO to identify hazardous and harmful booze intake (18) (Supplementary Material: questions 32–41), and was applied in all subjects who had consumed alcohol within the last 12 months. Patients are able to score upwards to a total of 40 points in domains like harmful alcohol intake and dependency symptoms. We considered patients as Audit-positive with Inspect scores ≥viii. This cut-off has been establish to provide an accurate mensurate of harmful alcohol drinking across historic period, gender, and cultures (19).
Apart from that, all interviewed subjects were asked what their trusted neurologist or physician had told them regarding alcohol consumption in the context of their epilepsy. Patients were able to choose one out of four response options: (a) booze should be avoided completely, (b) booze can be consumed without whatsoever restriction, (c) light booze intake is harmless, or (d) no advice given past the physician.
Alcohol-related seizures
In this study, an alcohol-related seizure was defined as a seizure in the context of epilepsy that occurred within short temporal relation to alcohol utilize (<24 h). Alcohol users were asked "Practise you lot have experienced an alcohol-related seizure within the last 12 months?" If patients had experienced an alcohol-related seizure in the last 12 months, they were requested to recall details on the quantity of alcohol intake prior to the seizure and on the time between cessation of alcohol intake and seizure manifestation (<6 h/≥6–<12 h/≥12–<24h). The quantity of alcohol intake over again was calculated and expressed in standard drinks to ensure a comparable evaluation (Figure i). If patients had experienced more than one seizure related to booze use inside the last 12 months, they were asked to land details on the seizure occurrence they remembered the best.
Statistical analysis
Continuous data are presented as mean ± standard deviation (SD) or median where appropriate. Logistic regression analyses were used to calculate odds ratios with 95% confidence intervals as estimates for variables independently predicting booze employ and the occurrence of booze-related seizures within the terminal 12 months.
In the logistic regression models, clinical data on patients' sex, age at interview, duration of epilepsy, epilepsy type, antiepileptic drug therapy, seizure frequency, alcohol drinking beliefs over the concluding 12 months, and physicians' advice on alcohol utilize were included equally possible confounding variables. In the results department of logistic regression analyses, findings were just noted if 95% CIs of the confounding variable did not include i; if the 95% CI included i, the corresponding variable was not meaning and therefore was not pointed out. Statistical analyses were calculated using IBM SPSS statistics 24.0.
Results
Written report population
The study population consisted of 310 patients with epilepsy (Table 1). Of these, 7 subjects had suffered from simply 1 unmarried unprovoked seizure: In iv of these patients remote structural brain lesions were demonstrated past neuroimaging indicating focal epilepsy. In one patient, interictal EEG findings were consistent with generalized genetic epilepsy, and in ii subjects, EEG showed regional spikes and sharp waves without MRI structural brain lesions indicating focal epilepsy of unknown origin.
Table 1
Characteristics of the study population (n = 310).
| Variable | No. (%)/mean ±SD a | |
|---|---|---|
| Sex | Female | 171 (55.2) |
| Male | 139 (44.eight) | |
| Age (in years) | 44.vii ± 16.2 | |
| Elapsing of epilepsy (in years) | 20.1 ± xvi.eight | |
| Epilepsy type | Focal | 213 (68.7) |
| GGEb | 67 (21.half-dozen) | |
| Unknown | thirty (9.seven) | |
| AEDc | Monotherapy | 184 (59.iv) |
| Polytherapy | 121 (39.0) | |
| No treatment | five (1.6) | |
| Seizure frequency | ≥1/calendar month | 130 (41.nine) |
| <ane/month | 180 (58.1) | |
| Alcohol use in the last 12 months | Alcohol forbearance | 106 (34.ii) |
| Occasional or low-cal employ | 147 (47.4) | |
| Moderate use | 43 (13.ix) | |
| Heavier apply | fourteen (4.5) | |
| Physicians' communication on the use of alcohol | Alcohol should be avoided completely | 127 (41.0) |
| No advice given | 94 (thirty.3) | |
| Alcohol can be consumed without brake | ii (0.vi) | |
| Low-cal alcohol intake is harmless | 87 (28.1) |
Booze consumption
Out of 310 interviewed subjects, 204 (65.viii%) had used alcohol within the last 12 months, 158 (51%) within the concluding 30 days, and 108 (34.8%) within the last 7 days. Antiepileptic drug monotherapy (OR 1.901) and physicians' advice that a low-cal alcohol intake is harmless (OR 4.102) were independent predictors for alcohol use within the last 12 months (Tables 2, three). Out of the 204 patients who used alcohol, 147 (72%) were occasional or low-cal booze users, 43 (21.1%) were moderate users and 14 subjects (6.9%) skillful heavier alcohol utilise. 9 subjects of the report population (2.9%) were Inspect positive indicating hazardous and harmful alcohol use. All Inspect positive subjects were heavier alcohol users.
Tabular array 2
Possible confounding variables that were included in the logistic regression model regarding alcohol consumption inside the terminal 12 months.
| Variable | Alcohol use within the last 12 months (n = 204) | Booze-abstinence (n = 106) | |
|---|---|---|---|
| No. (%)/hateful ±SD a | No. (%)/mean ±SD | ||
| Sexual practice | Female | 108 (52.9) | 63 (59.iv) |
| Male | 96 (47.1) | 43(xl.6) | |
| Age (in years) | 43.8 ± xv.nine | 46.three ± sixteen.7 | |
| Duration of epilepsy (in years) | 18.9 ± 15.8 | 22.five ± 18.four | |
| Epilepsy type | Focal | 135 (66.ii) | 78 (73.6) |
| GGEb | 45 (22.ane) | 22 (twenty.8) | |
| Unknown | 24 (eleven.seven) | 6 (5.6) | |
| AEDc | Monotherapy | 130 (63.seven) | 54 (50.9) |
| Polytherapy | 69 (33.viii) | 52 (49.ane) | |
| No treatment | 5 (2.5) | 0 | |
| Seizure frequency | ≥i/month | 76 (37.3) | 54 (l.9) |
| <1/calendar month | 128 (62.7) | 52 (49.1) | |
| Physicians' advice | Booze should be avoided completely | 73 (35.viii) | 54 (51) |
| No communication | 56 (27.4) | 38 (35.eight) | |
| Alcohol can be consumed without restriction | 2 (1) | 0 | |
| Low-cal alcohol intake is harmless | 73 (35.viii) | xiv (thirteen.2) |
Table 3
Independent predictors for alcohol consumption inside the last 12 months.
| Variable | ORa | 95% CIb | P-value | |
|---|---|---|---|---|
| AEDc | Polytherapy | i.0 (ref.) | ||
| Monotherapy | 1.901 | 1.152–3.138 | p = 0.012 | |
| None | Northward/Ad | N/A | N/A | |
| Physicians' advice | Alcohol should be avoided completely | ane.0 (ref.) | ||
| Alcohol can exist consumed without restriction | N/A | N/A | Due north/A | |
| No advice | ane.043 | 0.599–1.814 | p = 0.883 | |
| Low-cal alcohol intake is harmless | 4.102 | ii.078–eight.097 | p <0.0001 |
Ninety-five patients (thirty.7%) were alcohol-experienced but had been abstinent in the final year. Eleven subjects xi (3.5%) had never tried booze in their lifetime.
In alcohol-experienced subjects, who abstained from alcohol inside the last 12 months (n = 95), epilepsy was reported to be the most common reason for no longer drinking alcohol (due north = fifty; 52.6%). Of those 50 patients, 49 subjects stated that they would eat booze if epilepsy had not been diagnosed and 16 patients stated that alcohol abstinence due to epilepsy is a claiming.
Alcohol-related seizures
30-vii out of 204 booze users (18.1%) had experienced booze-related seizures within the last 12 months (Table 4). In 95% (n = 35) of cases, these seizures had occurred within 12 h after cessation of alcohol intake.
Table four
Clinical variables of patients with epilepsy who had experienced alcohol-related seizures inside the last 12 months (n = 37).
| Patient-ID | Booze intake prior to booze-related seizures (standard drinks) | Time between abeyance of booze intake and seizure occurrence (range in hours) | Usual alcohol-drinking behavior within the last 12 months | Epilepsy type |
|---|---|---|---|---|
| #17 | fifteen | ≥12– <24 | Occasional or light apply | Unknown |
| #25 | 8.75 | <vi | Occasional or light employ | GGE a |
| #31 | fifteen | ≥6– <12 | Occasional or low-cal use | Focal |
| #32 | 10 | ≥vi– <12 | Occasional or low-cal employ | Focal |
| #38 | 34 | <6 | Heavier use | Focal |
| #forty | vii | ≥6– <12 | Moderate use | GGE |
| #53 | 12 | <6 | Occasional or calorie-free utilize | Focal |
| #54 | 17.5 | <6 | Occasional or light use | Focal |
| #63 | xv | ≥6– <12 | Occasional or light use | GGE |
| #65 | 12.5 | ≥vi– <12 | Moderate use | GGE |
| #77 | 7.5 | <6 | Occasional or light use | GGE |
| #81 | 20 | <6 | Heavier use | GGE |
| #83 | 7.v | ≥half-dozen– <12 | Heavier apply | GGE |
| #87 | 12 | <half dozen | Moderate use | GGE |
| #116 | vii.5 | <6 | Occasional or light apply | Focal |
| #133 | Not remembered | <vi | Heavier use | Focal |
| #140 | 12.5 | <half dozen | Moderate utilize | GGE |
| #141 | Not remembered | ≥6– <12 | Heavier utilise | Focal |
| #144 | 12.v | ≥6– <12 | Occasional or light use | Focal |
| #147 | 15 | <6 | Occasional or low-cal utilise | Focal |
| #154 | ten | ≥12– <24 | Moderate use | Focal |
| #178 | 15 | <6 | Occasional or light utilize | Unknown |
| #185 | 15 | <half dozen | Heavier employ | Unknown |
| #188 | xiv.v | <vi | Occasional or light use | Focal |
| #199 | 11.five | <half dozen | Occasional or calorie-free utilize | Focal |
| #223 | Non remembered | <six | Heavier employ | GGE |
| #258 | fifteen | <vi | Moderate utilise | GGE |
| #264 | vii.5 | <6 | Occasional or lite use | GGE |
| #272 | xv | <6 | Occasional or light use | Unknown |
| #274 | xxx | <6 | Occasional or lite use | GGE |
| #276 | 10.5 | ≥6– <12 | Occasional or light use | GGE |
| #278 | 12.v | <six | Occasional or light employ | GGE |
| #280 | xiii | ≥half dozen– <12 | Occasional or light use | Focal |
| #282 | 7.5 | ≥6– <12 | Occasional or light use | Unknown |
| #283 | x | <6 | Occasional or low-cal use | GGE |
| #291 | 8.75 | <six | Moderate use | GGE |
| #308 | 15 | ≥6– <12 | Heavier use | Focal |
In multivariate analysis, subjects with heavier alcohol use in the final 12 months were more likely to experience alcohol-related seizures (OR viii.955), whereas occasional or light and moderate alcohol apply was non associated with increased risk for alcohol-related seizures (Tables 5, 6). However, virtually of the patients (78.4%) who reported alcohol-related seizures were occasional, lite or moderate alcohol users who had changed their usual alcohol intake toward college consumption on the drinking occasion prior to the seizures (Tabular array 4). The amount of booze intake before the occurrence of alcohol-related seizures was very high in all of the cases with a mean of 13.3 ± 5.8 standard drinks (median 12.v, range 7–34), which is equivalent to 2.v L of beer or 1.25 L of vino. The minimum was 7 standard drinks, equivalent to ~ane.4 L of beer or 0.vii 50 of wine.
Table 5
Possible confounding variables that were included in the logistic regression model regarding the occurrence of alcohol-related seizures in patients with epilepsy within the last 12 months.
| Variable | Alcohol-related seizure occurrence within the final 12 months (northward = 37) | No alcohol-related seizures within the concluding 12 months (n = 167) | |
|---|---|---|---|
| No. (%)/mean ±SD a | No. (%)/hateful ±SD | ||
| Sexual practice | Female | 17 (45.9) | 91 (54.v) |
| Male person | xx (54.1) | 76 (45.5) | |
| Age (in years) | 40.7 ± 14.7 | 44.5 ± xvi.1 | |
| Duration of epilepsy (in years) | xx.iii ± 15.1 | 18.6 ± xvi | |
| Epilepsy type | Focal | 15 (twoscore.6) | 120 (71.9) |
| GGEb | 17 (45.9) | 28 (sixteen.eight) | |
| Unknown | 5 (xiii.5) | xix (11.three) | |
| AEDc | Monotherapy | 22 (59.5) | 108 (64.7) |
| Polytherapy | xiv (37.8) | 55 (32.nine) | |
| No handling | i (two.7) | 4 (2.4) | |
| Seizure frequency | ≥one/calendar month | xiii (35.1) | 63 (37.7) |
| <1/calendar month | 24 (64.9) | 104 (62.3) | |
| Booze utilise within the last 12 months | Occasional or light use | 22 (59.5) | 125 (74.8) |
| Moderate utilise | 7 (18.9) | 36 (21.half dozen) | |
| Heavier use | 8 (21.6) | 6 (iii.half dozen) |
Table 6
Independent predictors for the occurrence of alcohol-related seizures within the last 12 months in patients with epilepsy.
| Variable | ORa | 95% CIb | P-value | |
|---|---|---|---|---|
| Epilepsy type | Focal | one.0 (ref.) | ||
| GGEc | v.792 | 2.427–13.823 | p <0.0001 | |
| Unknown | two.185 | 0.664–7.189 | p = 0.198 | |
| Alcohol utilize within the last 12 months | Occasional or low-cal utilize | 1.0 (ref.) | ||
| Moderate use | 0.819 | 0.306–ii.194 | p = 0.691 | |
| Heavier use | 8.955 | two.625–thirty.545 | p <0.0001 |
Patients with generalized genetic epilepsy (OR 5.792) were more likely to experience booze-related seizures compared to patients with focal epilepsy (Tables 5, 6). In patients with focal epilepsy, the hateful amount of alcohol intake prior to alcohol-related seizures was 14.4 ± 6.5 (median thirteen, range 7.5–34) standard drinks, and in subjects with generalized genetic epilepsy 12.3 ± 5.9 (median xi.3, range seven–xxx). No meaning difference was detected (p = 0.366).
In female patients, the mean corporeality of alcohol intake before booze-related seizures was 10.nine ± 3.1 standard drinks (median eleven.3, range seven–xv), and in male subjects, 15.four ± six.8 (median 15, range 7.5–34; p = 0.02).
Fifteen out of 95 (15.eight%) booze-experienced but now abstinent subjects had experienced alcohol-related seizures in the past. In that grouping, the mean amount of alcohol intake prior to the seizures was 10.ix standard drinks. All of these patients stated that they had stopped alcohol consumption because of the experience of alcohol-related seizures.
Discussion
In this study, we aimed to systematically clarify alcohol drinking and the occurrence of booze-related seizures in 310 epilepsy patients. Even though alcohol use may trigger seizures, 65% of interviewed subjects had consumed alcohol within the concluding 12 months and every third patient had consumed alcohol inside the last vii days. Our results are in line with previous population-based study findings from Canada reporting a 12-month prevalence of alcohol use in patients with epilepsy of 57.vi% (twenty). In our study, well-nigh subjects were occasional or light alcohol users. Regarding chronic heavy alcohol consumption, our cohort of patients had used booze far more responsibly than the general adult High german population. Just two.ix% of our interviewed study subjects were AUDIT positive indicating chancy and harmful alcohol intake. By contrast, data from the general developed German population showed that a proportion of 19.7% is Inspect positive (9).
In multivariate analysis, booze consumption inside the last 12 months was independently related to AED monotherapy. It is highly likely that subjects with well-controlled epilepsies on monotherapy are more probable to swallow alcoholic beverages than those with difficult-to-treat variants. Physicians' communication that "a light alcohol intake is harmless" was identified as an additional predictor for booze employ. Patients with epilepsy may experience unsure most alcohol consumption on chronic medication and therefore may exist willing to follow physicians' advices more frequently.
Thirty-seven out of 204 epilepsy patients who had consumed booze remembered that they had experienced an booze-related seizure within the terminal 12 months. These seizures occurred in the timely context of acute heavy alcohol consumption. The occurrence of seizures in short temporal relation to alcohol consumption may not testify that these seizures were necessarily causally related to alcohol use. The post-obit arguments however back up this hypothesis: Most subjects with alcohol-related seizures were occasional, light or moderate alcohol users only a noticeable alter in their usual alcohol-drinking beliefs toward college consumption prior to the seizures could be documented. This taken together with the fact that virtually all alcohol-related seizures (95%) had occurred inside the commencement 12 h after cessation of alcohol intake support a causal relationship between alcohol employ and temporally close seizure manifestation in these cases.
In the study population, generalized genetic epilepsy was an independent predictor for the occurrence of booze-related seizures. The hateful alcohol intake prior to booze-related seizures was not college in patients with generalized genetic epilepsy than in subjects with focal epilepsy. Lennox stated that booze-related seizures had occurred more than ofttimes in patients with symptomatic than in cryptogenic or idiopathic epilepsies (1). The then applied syndromatic allocation, even so, may not be in exact conformance with the present classifications (16, 17). Janz (21) later observed that alcohol-related seizures were more probable to occur in subjects with generalized genetic epilepsy than in those with focal epilepsy, which is consistent with our findings (21).
Astute alcohol consumption suppresses primal nervous excitability by activating the inhibitory GABA-system (22). GABA is the major inhibitory neurotransmitter in the encephalon. Furthermore, booze inhibits glutamate activeness, which is the major excitatory neurotransmitter of the CNS. Thus in subjects with epilepsy, alcohol intake initially reduces CNS epileptiform EEG-activity. Later however, when alcohol blood levels decline, epileptiform EEG-action has been shown to be increased which is associated with a college gamble for seizures (4–6, 23). In an experimental study on mice with chronic epilepsy, seizure thresholds were measured later on the assistants of ethanol. Initially, anticonvulsant properties of ethanol were observed, but after a transient lowering of seizure thresholds and hyper-susceptibility to seizures were reported (7).
In patients with generalized genetic epilepsy, seizures ordinarily manifest within xxx min later on awakening. A transcranial magnetic stimulation written report on patients with genetic generalized epilepsy demonstrated that motor cortex excitability was significantly increased in the early morning (24). In subjects with generalized genetic epilepsy, this increased neuronal excitability in the early morning time may be potentiated by the hyper-excitable post-alcohol state, and this effect may be responsible for the increased susceptibility to alcohol-related seizures compared to focal epilepsy.
Clinical perspective
Most of our interviewed subjects (>fourscore%) that consumed booze within the last 12 months did non experience alcohol-related seizures. Current data on the quantity of alcohol intake prior to the occurrence of booze-related seizures in patients with epilepsy highly suggest that these situations are related to the acute consumption of considerably large amounts of alcohol. Subjects who reported alcohol-related seizures had consumed at least 7 standard drinks before seizures occurred which is equivalent to 1.4 L of beer or 0.vii Fifty of wine. Occasional or light and moderate alcohol-drinking behavior was not associated with alcohol-related seizure occurrences. In the general German population, 89% of all adults had used alcohol inside the last 12 months, only 8% were alcohol-experienced simply abstinent, and 3% had never used booze in their lifetime (9). In the present written report, 30.7% of patients were alcohol-experienced merely abstemious and iii.5% had never consumed alcohol in their lifetime. Therefore, the proportion of alcohol-experienced only abstinent subjects with epilepsy was almost four times higher than in the full general population. Epilepsy was oftentimes stated to be the only reason for booze-forbearance, which felt challenging to many subjects. Alcohol abstinence may not exist necessary every bit long as epilepsy patients practice a responsible alcohol intake. Subjects with generalized genetic epilepsy still should be made aware of their increased susceptibility to booze-related seizures.
Limitations
Our systematic data drove based on personal interviews immune us to provide updated knowledge on the patterns of booze drinking and the occurrence of alcohol-related seizures in a big cohort of 310 epilepsy patients.
Several limitations have to be discussed. First, our data on alcohol use depended on patients' self-reporting and may be affected by recall bias. Information technology has been demonstrated that assessing alcohol consumption is biased by call up fifty-fifty when the call back period is but 1 week (25). In our study population, booze consumption is probably underestimated. However, this does not bear upon our main findings. Moreover, patients were seen at our institution at scheduled outpatient visits and did not attend the clinic after acute manifestations of booze-related seizures. Only a minority of patients documented details on booze-related seizures in seizure diaries. Our retrospective information collection on alcohol-related seizures also depended on subjects' recall adequacy, and may reflect bias due to recall errors. We addressed this by focusing only on alcohol-related seizures that had occurred within the last 12 months. Details were simply recorded on those alcohol-related seizures that subjects were able to recollect the best. As a consequence however, alcohol-related seizures may have also occurred after smaller amounts of alcohol intake or in other circumstances that were not taken into business relationship in the present study.
Second, every bit patients were interviewed retrospectively on the occurrence of booze-related seizures, nosotros were not able to provide information on AED drug levels afterwards the acute manifestation of these seizures. Nosotros cannot exclude that subjects might take been more than decumbent to seizure occurrences due to AED not-adherence. Furthermore, we cannot exclude hypoglycemic episodes caused by acute heavy alcohol consumption (26), which may have contributed to the manifestation of epileptic seizures (27).
Third, other studies have shown that booze consumption and particularly the consumption of considerable large amounts of booze may reduce slumber quality by increasing lite slumber and wake-upwards periods during the second half of the night fourth dimension slumber period (28, 29). In add-on to that, booze intake significantly suppresses REM sleep periods (30). Reduced sleep quality and consecutive sleep impecuniousness accept long been discussed to facilitate the occurrence of seizures in patients with epilepsy (31), and peculiarly in those with generalized genetic epilepsy (32–34). Altered sleep compages due to acute alcohol consumption constitutes a non-negligible and important co-factor for seizure chance in patients with epilepsy. Due to the retrospective design of the present study, we were not able to appraise sleep quality prior to booze-related seizure occurrences. Time to come prospective research, e.g., using polysomnography, will exist needed to provide insight into the complex relationship between alcohol consumption, altered sleep architecture and timely manifestation of seizures.
Finally, the present written report population was exclusively recruited at a tertiary intendance epilepsy heart where usually patients with more astringent variants of the disease are treated. This indicates a potential pick bias and our results may not be generalized to all epilepsy patients without restrictions.
Ethics statement
The written report was approved by the local Institutional Review Board (EA 1/146/08), and signed informed consent was obtained from all participants.
Author contributions
MiH: information drove, statistical, analysis, wrote manuscript. LG, AK, and FW helped recruiting patients, helped to improve manuscript. MaH: statistical assay, wrote manuscript.
Conflict of involvement argument
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Acknowledgments
MaH holds the Friedrich-von-Bodelschwingh endowed Professorship for Clinical and Experimental Epileptology at the Charité—Universitätsmedizin Berlin funded by von Bodelschwingh Foundation. Statistical analyses were conducted with the assistance of Martin Donhauser, Ph.D., Department of Statistics, University of Regensburg. We thank David Richard Urry for helpful comments in editing the manuscript.
Footnotes
References
i. Lennox WG. Booze and epilepsy. Q J Stud Alcohol. (1941) 2:1–xi. [Google Scholar]
2. Höppener RJ. The effect of social alcohol use on seizures in patients with epilepsy. In: Porter RJ, Mattson RH, Cramer JA, Diamond I. editors. Alcohol and Seizures: Basic Mechanisms and Clinical Concepts. Philadelphia, PA: FA Davis; (1990). p. 222–32. [Google Scholar]
3. Mattson RH, Fay ML, Sturman JK, Cramer JA, Wallace JD, Mattson EM. The furnishings of various patterns of alcohol apply on seizures in patients with epilepsy. In: Porter RJ, Mattson RH, Cramer JA, Diamond I. editors. Alcohol and Seizures: Basic Mechanisms and Clinical Concepts. Philadelphia, PA: FA Davis; (1990). p. 233–twoscore. [Google Scholar]
4. Vossler DG, Browne TR. The electroencephalogram in patients with booze-related seizures. In: Porter RJ, Mattson RH, Cramer JA, Diamond I. editors. Alcohol and Seizures: Basic Mechanisms and Clinical Concepts. Philadelphia, PA: FA Davis; (1990). p. 179–96. [Google Scholar]
5. Ticku MK. The effects of acute and chronic ethanol administration and its withdrawal on gamma-aminobutyric acrid receptor binding in rat brain. Br J Pharmacol. (1980) lxx:403–10. 10.1111/j.1476-5381.1980.tb08716.x [PMC costless commodity] [PubMed] [CrossRef] [Google Scholar]
6. Nagy Fifty, Zsadanyi O, Nagy J, Zsigmond K. Cerebral electric phenomena elicited by alcohol. Z Rechtsmed. (1973) 73:185–xc. 10.1007/BF02116822 [PubMed] [CrossRef] [Google Scholar]
7. McQuarrie DG, Fingl E. Effects of unmarried doses and chronic assistants of ethanol on experimental seizures in mice. J Pharmacol Exp Ther. (1958) 124:264–71. [PubMed] [Google Scholar]
8. WHO Global Status Study on Booze and Health 2011. Geneva: Globe Wellness Organization; (2011). [Google Scholar]
9. Papst A, Kraus Fifty. Alkoholkonsum, alkoholbezogene Störungen und Trends. Ergebnisse des Epidemiologischen Suchtsurveys 2006. Sucht (2008) 54:36–46. 10.1024/2008.07.05 [CrossRef] [Google Scholar]
10. Victor M, Adams RD. The consequence of booze on the nervous arrangement. Res Publ AssocRes Nerv Ment Dis. (1953) 32:526–73. [PubMed] [Google Scholar]
11. Victor M, Brausch C. The role of forbearance in the genesis of alcoholic epilepsy. Epilepsia (1967) viii:1–20. x.1111/j.1528-1157.1967.tb03815.x [PubMed] [CrossRef] [Google Scholar]
12. McKeon A, Frye MA, Delanty Due north. The alcohol withdrawal syndrome. JNNP (2008) 79:854–62. ten.1136/jnnp.2007.128322 [PubMed] [CrossRef] [Google Scholar]
13. Samokhalov AV, Irving H, Mohapatra Due south, Rehm J. Alcohol consumption, unprovoked seizures, and epilepsy: a systematic review and meta-analysis. Epilepsia (2010) 51:1177–84. 10.1111/j.1528-1167.2009.02426.x [PubMed] [CrossRef] [Google Scholar]
fourteen. Dworetzky BA, Bromfield EB, Townsend MK, Kang JH. A prospective study of smoking, caffeine, and alcohol equally gamble factors for seizures or epilepsy in immature adult women: data from the Nursus' Health Written report 2. Epilepsia (2010) 51:198–205. ten.1111/j.1528-1167.2009.02268.ten [PMC free article] [PubMed] [CrossRef] [Google Scholar]
15. Hamerle M, Ghaeni L, Kowski A, Weissinger F, Holtkamp M. Cannabis and other illicit drug use in epilepsy patients. Eur J Neurol. (2014) 21:167–lxx. 10.1111/ene.12081 [PubMed] [CrossRef] [Google Scholar]
sixteen. Scheffer IE, Berkovic S, Capovilla Thou, Connolly MB, French J, Guilhoto L, et al. . ILAE classification of the epilepsies: Position newspaper of the ILAE Commission for Classification and Terminology. Epilepsia (2017) 58:512–21. 10.1111/epi.13709 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
17. Fisher RS, Acevedo C, Arzimanoglou A, Bogacz A, Cantankerous JH, Elger CE, et al. . ILAE official report: a practical clinical definition of epilepsy. Epilepsia (2014) 55:475–82. 10.1111/epi.12550 [PubMed] [CrossRef] [Google Scholar]
18. Saunders JB, Aasland OG, Babor TF, De la Fuente JR, Grant M. Evolution of the Booze Apply Disorder Indentification Test (Audit): WHO collaborative project on early detection of persons with harmful alcohol consumption—II. Addiction (1993) 88:791–804. 10.1111/j.1360-0443.1993.tb02093.ten [PubMed] [CrossRef] [Google Scholar]
nineteen. Allen JP, Litten RZ, Fertig JB, Babor T. A review of research on the Alcohol Apply Disorders Identification Examination (AUDIT). Alcohol Clin Exp Res. (1997) 21:613–19. 10.1111/j.1530-0277.1997.tb03811.x [PubMed] [CrossRef] [Google Scholar]
20. Hinnell C, Williams J, Metcalfe A, Patten SB, Parker R, Wiebe S, et al. . Health status and wellness-related behaviors in epilepsy compared to other chronic conditions—a national population-based study. Epilepsia (2010) 51:853–61. 10.1111/j.1528-1167.2009.02477.x [PubMed] [CrossRef] [Google Scholar]
21. Janz D. Die Epilepsien: Spezielle Pathologie und Therapie. 1st ed Stuttgart; New York, NY: Georg Thieme Verlag; (1969). [Google Scholar]
22. Mehta AK, Ticku MK. Ethanol potentiation of GABAergic transmission in cultured spinal cord neurons involves gamma-aminobutyric acidA-gated chloride channels. J Pharmacol Exp Ther. (1988) 246:558–64. [PubMed] [Google Scholar]
23. Rodin EA, Frohman CE, Gottlieb JS. Effect of acute alcohol intoxication on epileptic patients. Arch Neurol. (1961) 4:103–6. 10.1001/archneur.1961.00450070105012 [PubMed] [CrossRef] [Google Scholar]
24. Badawy RAB, MacDonell RAL, Jackson GD, Berkovic SF. Why practice seizures in generalized epilepsy ofttimes occur in the morning? Neurology (2009) 73:218–22. 10.1212/WNL.0b013e3181ae7ca6 [PubMed] [CrossRef] [Google Scholar]
25. Ekholm O, Strandberg-Larsen K, Gronbaek M. Influence of the recollect menstruation on a beverage-specific weekly drinking measure for booze intake. Eur J Clin Nutr. (2011) 65:520–v. 10.1038/ejcn.2011.1 [PubMed] [CrossRef] [Google Scholar]
26. Field JB, Williams HE, Mortimore GE. Studies on the mechanism of ethanol-induced hypoglycaemia. J Clin Invest. (1963) 42:497–506. 10.1172/JCI104738 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
27. Beghi Eastward, Carpio A, Forsgren L, Hesdorffer DC, Malmgren One thousand, Sander JW, et al. Recommendation for a distinction of astute symptomatic seizures. Epilepsia (2010) 54:671–75. 10.1111/j.1528-1167.2009.02285.x [PubMed] [CrossRef] [Google Scholar]
28. Williams DL, MacLean AW, Cairns J. Dose-response effects of ethanol on the sleep of young women. J Stud Alcohol. (1983) 44:515–23. 10.15288/jsa.1983.44.515 [PubMed] [CrossRef] [Google Scholar]
29. Roehrs T, Yoon J, Roth T. Nocturnal and next-mean solar day effects of ethanol and basal level of sleepiness. Human Psychopharmacol Clin Exp. (1991) six:307–11. ten.1002/hup.470060407 [CrossRef] [Google Scholar]
30. Williams H, Salamy A. Alcohol and sleep. In: Kissin B, Begleiter H. editors. The Biology of Alcoholism. New York, NY: Plenum Printing; (1972). p.435–83. [Google Scholar]
31. Chihorek AM, Abou-Khalil B, Malow BA. Obstructive sleep apnea is associated with seizure occurrence in older adults with epilepsy. Neurology (2007) 69:1823–seven. ten.1212/01.wnl.0000279334.78298.d5 [PubMed] [CrossRef] [Google Scholar]
32. Janz D. The grand mal epilepsies and the slumber-waking bicycle. Epilepsia (1962) iii:69–109. 10.1111/j.1528-1157.1962.tb05235.x [PubMed] [CrossRef] [Google Scholar]
33. Pedersen SB, Petersen KA. Juvenile myoclonic epilepsy: clinical and EEG feaures. Acta Neurol Scand. (1998) 97:160–3. ten.1111/j.1600-0404.1998.tb00630.x [PubMed] [CrossRef] [Google Scholar]
34. Bråthen G, Ben-Menachem E, Brodtkorb E, Galvin R, Garcia-Monco JC, Halasz P, et al. . EFNS guideline on the diagnosis and direction of alcohol-related seizures: study of an EFNS job forcefulness. Eur J Neurol. (2005) 12:575–81. 10.1111/j.1468-1331.2005.01247.ten [PubMed] [CrossRef] [Google Scholar]
Articles from Frontiers in Neurology are provided hither courtesy of Frontiers Media SA
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5996121/
Belum ada Komentar untuk "If I Have Had Alcohol Seizures Can I Drink Again"
Posting Komentar