CASE REPORT Open Access

Acute alcohol intoxication may cause delayin stroke treatment – case reportsTamas Arokszallasi1*, Eszter Balogh1, Laszlo Csiba1,2, Istvan Fekete1, Klara Fekete1 and Laszlo Olah1

Abstract

Background: The signs and symptoms of acute alcohol intoxication resemble those of vertebrobasilar stroke. Dueto their shared symptoms including double vision, nystagmus, dysarthria, and ataxia, the differential diagnosis ofalcohol intoxication and vertebrobasilar stroke may pose a challenge. Moreover, if alcohol intoxication and strokeoccur simultaneously, the signs and symptoms of stroke may be attributed to the effects of alcohol, leading todelayed stroke diagnosis and failure to perform reperfusion therapy.

Case presentations: Three cases of alcohol intoxication and stroke are presented. The first patient (female, 50 yearsold) had dysarthria, nystagmus and trunk ataxia on admission. Her blood alcohol level was 2.3‰. The symptomsimproved after forced diuresis, but 5.5 h later progression was observed, and the patient developed diplopia anddysphagia in addition to her initial symptoms. Angiography showed occlusion of the basilar artery. Intraarterialthrombolysis was performed. The second patient (male, 62 years old) developed diplopia, dysarthria and trunkataxia after consuming 4-units of alcohol, and his symptoms were attributed to alcohol intoxication. Two hourslater, neurological examination revealed dysphagia and mild right-sided hemiparesis, which questioned the causalrelationship between the symptoms and alcohol consumption. Cerebral CT was negative, and intravenousthrombolysis was administered. The third patient (male, 55 years old) consumed 10 units of alcohol before fallingasleep. Three hours later, his relatives tried to wake him up. He was unresponsive, which was attributed to alcoholintoxication. When he woke up 8 h later, right-sided hemiparesis and aphasia were observed, and cerebral CTalready revealed irreversible ischemic changes.

Conclusions: Our cases show that alcohol consumption may interfere with stroke diagnosis by mimicking the signsand symptoms of vertebrobasilar stroke. Moreover, attributing the symptoms of stroke to alcohol intoxication maydelay stroke diagnosis resulting in failure of reperfusion therapy. Based on our observations we conclude that strokeshould be considered in the case of worsening symptoms, dysphagia, hemiparesis and disproportionately severesigns that cannot be attributed to the amount of alcohol consumed. In the case of ambiguity, ambulance shouldbe called, and if stroke cannot be excluded, specific therapy should be administered.

Keywords: Alcohol intoxication, Stroke, Thrombolytic therapy, Diagnostic errors

BackgroundAmong patients presenting with acute neurologicalsymptoms, it is crucial to decide in time whether theysuffer from ischemic stroke and whether they are eligiblefor intravenous tissue plasminogen activator (IV tPA)treatment [1]. The short time window, however, may notalways allow neurologists to establish a correct diagno-sis, therefore it may be difficult to determine whether

acute neurological signs are due to stroke or to othercauses. Conditions with stroke-like symptoms but withother etiology than stroke are called stroke mimics [2–6].One of the conditions that may mimic stroke is acutealcohol intoxication. Specifically, alcohol intoxication re-sults in symptoms very similar to vertebrobasilar ischemia[7, 8], therefore the simultaneous occurrence of vertebro-basilar stroke and alcohol intoxication may result in themisdiagnosis of stroke. The common overlapping signs ofvertebrobasilar stroke and alcohol intoxication includingdizziness, dysarthria, nystagmus, ataxia with or withoutdouble vision and somnolence can easily be attributed to

* Correspondence: aroksztamas@gmail.com1Department of Neurology, Faculty of Medicine, University of Debrecen,Moricz Zs. krt 22, Debrecen 4032, HungaryFull list of author information is available at the end of the article

© The Author(s). 2019 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, andreproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link tothe Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Arokszallasi et al. BMC Neurology (2019) 19:14 https://doi.org/10.1186/s12883-019-1241-6

the acute effects of alcohol, and the misdiagnosis may leadto delayed stroke recognition and failure to administerappropriate therapy [9]. Moreover, as acute alcohol intakemay be associated with inability to walk, hemisphericsymptoms may also be overlooked by lay people with poorstroke awareness. Although there was one article whichmentioned alcohol intoxication as a stroke mimic [5], tothe best of our knowledge, no detailed description of thistopic has been published in the scientific literature. Duringthe past years, the acute effects of alcohol caused diagnos-tic challenges in some patients who presented with strokesymptoms at our department.

Case presentationsCase 1 - A 50-year-old woman celebrated her birthdayand consumed an unknown amount of alcohol. Herfamily was unable to wake her up the following morning(7 a.m.), therefore the patient was transferred to our de-partment (Fig. 1). On admission, somnolence, moderatedysarthria, horizontal gaze-directed nystagmus, moder-ate trunk ataxia, and in-coordination were found. Herlaboratory values showed moderate alcohol intoxication(Table 1). The symptoms were attributed to the effects ofalcohol, therefore, after a negative CT and CT-angiography,forced diuresis was started (8:30 a.m.), and her clinicalstatus was checked every hour. Initially, consciousnessimproved, the patient became alert, and dysarthria andataxia ameliorated. However, early in the afternoon (2 p.m.),

the control examination revealed worsening symptoms, shebecame somnolent again and developed severe horizontalnystagmus, double vision, dysarthria and dysphagia. Due torapid progression, cerebral CT was repeated, which wasnegative again. Similarly, duplex ultrasound showed nostenosis of the carotid or vertebral arteries, however, trans-cranial Doppler (TCD) revealed high pulsatility index andlow flow velocity in the basilar artery. Due to rapid progres-sion and the sound suspicion of basilar artery occlusion,

Fig. 1 Timeline of the 3 cases. The delay of treatment due to alcohol intoxication is indicated by diagonal lines. Bold text highlights thesymptoms which helped differentiate between stroke and alcohol intoxication. TCD: transcranial Doppler; DSA: digital subtraction angiography;CT: computer tomography; CTA: CT angiography; MCA: middle cerebral artery

Table 1 Laboratory values of the patients

Laboratory values Case 1 Case 2 Case 3

Glucose (mmol/L) 9,2 7,2 17,6

Creatinine (μmol/L) 78 65 58

CK (U/L) 47 78 133

AST (U/L) 15 18 14

ALT (U/L) 7 14 18

GGT (U/L) 10 21 38

CRP (mg/L) UK 3,83 4,99

Ethanol (‰) 2,3 UK < 0,1a

Ethanol (mg/dL) 230 UK < 10a

White Blood Cell (G/L) 8,58 10,21 14,74

Hemoglobin (g/L) 135 150 161

Platelet (G/L) 294 277 281

INR 0,97 1 0,9a measured about 12 h after alcohol intake, UK unknown

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digital subtraction angiography (DSA) was performed. DSAshowed basilar artery occlusion, therefore intraarterialthrombolysis was performed. After the administration of25mg rt-PA, the basilar artery was successfully recanalised(Fig. 2) and the symptoms rapidly improved. The controlCT 24 h after the treatment showed no abnormalities. Atdischarge, the patient was symptom-free.Case 2 - A 62-year-old man consumed about 32 g

ethanol (4 units) in the evening (Fig. 1). Before going tobed, his wife noticed his slurred speech, and the patientcomplained of double vision and trunk ataxia that wasdisproportionate to the amount of alcohol he hadconsumed. His wife attributed the symptoms to alcoholconsumption; however, the patient disagreed. Therefore,paramedics were called who found mild right-sidedhemiparesis and severe dysphagia in addition to doublevision, dysarthria, and trunk ataxia. On admission to ourdepartment, the clinical examination confirmed thesefindings (NIHSS: 6 points). Cerebral CT showed no cere-bral hemorrhage or infarction, therefore thrombolysiswas performed within 3 h of the onset of symptoms. Thecontrol examination showed significant improvement,and the NIHSS evaluated 24 h after thrombolysis de-creased to 1 point.Case 3 - A 55-year-old man consumed approximately

80 g etanol (10 units) during the night at a wedding cere-mony and fell asleep at about 2 a.m. (Fig. 1). His relativestried to wake him up early in the morning (5 a.m.), thepatient opened his eyes, but could not speak. He seemedto be drunk, therefore the relatives attributed the signsto alcohol consumption and let him sleep back. Uponawakening in the early afternoon (1 p.m.), his relativesrealized that he had facial asymmetry, mild right-sidedweakness and speech disturbance. On admission,right-sided homonymous hemianopsia, paresis of thelower half of right side of the face, mild right-sidedhemiparesis, and severe receptive and expressive aphasiawere found. Urgent CT scan (1:30 p.m.) revealed a hugeinfarction in the left middle cerebral artery (MCA)

territory (Fig. 3). Aspirin was administered and the riskfactors were controlled. The neurological status did notchange significantly.

Discussion and conclusionsBased on worldwide data, the average alcohol consump-tion in 2010 amounted to 6.2 l of pure alcohol perperson among people aged 15 years or older [10]. Thehighest alcohol consumption and the highest prevalenceof heavy episodic drinking were shown in high-incomecountries.In a systematic review and meta-analysis, acute alcohol

ingestion was reported to cause an approximatelytwo-fold increase in stroke as early as 1 h subsequent toalcohol consumption [11]. These results suggest that thesimultaneous occurrence of alcohol intoxication andstroke is not a coincidence, because even moderatealcohol consumption is associated with an immediateincrease in the risk of stroke. As the signs and symptomsof moderate-severe alcohol intoxication resemble thoseof vertebrobasilar stroke, stroke symptoms may be at-tributed to the effects of alcohol if the two conditionsdevelop simultaneously. Moreover, heavy episodic drink-ing may also mask the signs of hemispheric stroke forpeople with poor knowledge of cerebrovascular diseases.According to heteroanamnesis, all of our 3 patients

undoubtedly drank significant amounts of alcohol beforeadmission to our clinic. However, the time between alco-hol consumption and blood alcohol level measurementsvaried (about 6 h in the first patient, and at least 12 h inthe third patient), therefore the blood alcohol levelmeasured after admission did not reflect the amount ofethanol consumed. Since the symptoms of alcoholintoxication and stroke overlapped and in the first andthird patients the symptoms were only noticed after awak-ening, it was impossible to determine the precise onset ofstroke. Based on our assessment, symptoms developedwithin 2 and 3 h of alcohol consumption in the secondand third patients, respectively. The onset-to-door time

Fig. 2 Case 1: Non-enhanced cranial CT showed no acute ischemic signs or hemorrhage. Digital subtraction angiography revealed basilar arteryocclusion (A) and successful recanalisation after intra-arterial thrombolysis with 25 mg rtPA

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was about 2 h in the second patient, but due to the delayin the recognition of stroke it was more than 8 h in thethird patient. In the first patient, neurological symptomswere noticed within 5 h of alcohol consumption, however,these symptoms were most likely to be caused by alcoholintoxication, and obvious stroke symptoms developedlater, already in the hospital.Our observations show that acute alcohol intoxication

may cause difficulties in differential diagnosis of stroke,especially if ischemia develops in the vertebrobasilar ter-ritory. Our cases suggest that thorough examination andobservation are necessary to recognise stroke in the caseof simultaneous occurrence of alcohol intoxication.Therefore, patients with alcohol intoxication requireincreased attention during emergency medical care. Thefirst presented case underlines the importance of strictobservation after alcohol consumption. Although cere-bral CT and angio-CT were negative and the patient’ssymptoms improved during forced diuresis, the cause ofinitial symptoms cannot be clearly determined. Theycould be due solely to alcohol intoxication or to alcoholintoxication with concomitant vertebrobasilar strokewith improving symptoms. Certainly, the worsening ofclinical symptoms several hours after the initial improve-ment could not be explained by alcohol ingestion, butsupported the diagnosis of stroke in this period of thecondition. It remains unclear whether vertebrobasilarstroke was induced by alcohol and dehydration due toforced diuresis, or was independent of these conditions.This case underlines that patients with alcohol intoxication

require increased medical attention, and emphasizes theneed for repeated controls. Certainly, if MRI is available,diffusion-weighted imaging may help differentiate betweenalcohol intoxication and stroke [12, 13].Our second case demonstrates that symptoms dispropor-

tionate to the amount of alcohol consumed and the asym-metry of symptoms are warning signs for stroke. It must behighlighted, however, that the patient’s relative would haveattributed the severe stroke symptoms to the effect ofsmall-moderate amount of alcohol. In the third case, thepatient’s status was attributed to alcohol intoxication andtherefore the stroke was not noticed in due time. The delayin stroke diagnosis resulted in late arrival at hospital beyondthe thrombolysis time window, which eventually resulted inan unfavourable outcome. It is well-known that thrombo-lytic therapy helps dissolve blood clots and restore cerebralblood flow, and thus improves the outcome in acute ische-mic stroke [14]. Based on our cases, it can be concludedthat in the case of simultanoeus occurrence of stroke andalcohol intoxication, unusal alcohol-related clinical symp-toms, such as dysphagia or hemiparesis, and disproportionbetween the symptoms and the amount of alcoholconsumed may help the recognition of stroke in thebackground of symptoms. One of the lessons of this reportis that in case of ambiguity, paramedics should be calledand the patient should be transferred to a stroke unit. Aspatients with alcohol intoxication and stroke within thethrombolytic time window require increased medicalattention, CT examination, angiography, and IV tPA treat-ment, these patients should be observed at a neurologicalICU or in a well-equipped stroke unit. If the diagnosis ofstroke cannot be excluded, diffusion-weighted MRI, if avail-able, can be useful to determine the etiology of symptoms[13, 15]. However, it has to be emphasized that despitebeing the most sensitive technique for cerebral ischemia,even diffusion-weighted MRI may result in a false negativefinding in stroke patients, especially in brain-stem strokes[13, 15]. If MRI is not available or negative, but clinicalevaluation strongly suggests stroke, the worst should be as-sumed. In the case of dysphagia, asymmetry in symptomsincluding hemiparesis, or symptoms disproportionatelysevere to the amount of alcohol, ischemic stroke and rtPAtreatment should be considered. In our patients, whoarrived at the hospital in time and stroke diagnosis couldbe established within the therapeutic time window, thromb-olysis resulted in a significant improvement of clinicalsymptoms. On the contrary, when stroke was not recog-nised, and therefore reperfusion therapy could not beinitiated, no improvement was achieved. As thrombolysisin the case of stroke mimics is associated with no or only aminimal risk of hemorrhagic complications [16, 17], rtPAtreatment can be suggested for patients with potentialischemic stroke and simultaneous alcohol intoxication,provided that the patient is eligible for rtPA therapy.

Fig. 3 Case3: Non-enhanced cranial CT showed subacute ischemiclesion in the area of the left middle cerebral artery

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AbbreviationsALT: Alanine aminotransferase; AST: Aspartate aminotransferase; CK: Creatinekinase; CRP: C-reactive protein; CT: Computer tomography; DSA: Digitalsubtraction angiography; GGT: Gamma-glutamyl transpeptidase;INR: International Normalized Ratio; IV tPA: Intravenous tissue plasminogenactivator (IV tPA); MCA: Middle cerebral artery; MRI: Magnetic resonanceimaging; NIHSS: National Institutes of Health Stroke Scale; rtPA: Recombinanttissue plasminogen activator; TCD: Transcranial Doppler

AcknowledgmentsThe authors wish to express their sincere thanks to the co-workers of theIntensive Care Unit of the Department of Neurology, University of Debrecen,and Affidea Ltd.

FundingThe study was supported by the Hungarian National Brain Research Program,NAP_13-1-2013-0001, 2017–1.2.1-NKP-2017-00002 and by the NationalResearch, Development and Innovation Office, NKFH- K 120042 and K109712. The funders had no role in study design, data collection, analysisand interpretation of data, or preparation of the manuscript.

Availability of data and materialsThe datasets supporting the conclusions of this case report are includedwithin the article.

Authors’ contributionsLO, EB and TA were involved in clinical work-up, manuscript preparation,editing and submission. IF and KF were directly involved in the diagnosisand treatment of the patients. IF, KF and LCs revised the manuscript criticallyfor important content. All authors have read and approved the finalmanuscript.

Ethics approval and consent to participateNot applicable.

Consent for publicationInformed written consent was obtained directly from patients who wereable to fully understand and answer our questions and were oriented intime, place and their personal data (Case 1 and 2). However, in the case ofthe patient with severe expressive and receptive aphasia (Case 3), informedwritten consent was given by a family member (wife).

Competing interestsThe authors declare that they have no conflict of interest.

Publisher’s NoteSpringer Nature remains neutral with regard to jurisdictional claims inpublished maps and institutional affiliations.

Author details1Department of Neurology, Faculty of Medicine, University of Debrecen,Moricz Zs. krt 22, Debrecen 4032, Hungary. 2Cerebrovascular andNeurodegenerative Research Group of the Hungarian Academy of Sciences,Moricz Zs. krt 22, Debrecen 4032, Hungary.

Received: 30 August 2018 Accepted: 16 January 2019

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