The recognition and management of protracted alcohol withdrawal may improve and modulate the pharmacological treatment of alcohol use disorder

2020 ◽  
Vol 34 (11) ◽  
pp. 1171-1175
Author(s):  
Fabio Caputo ◽  
Mauro Cibin ◽  
Antonella Loche ◽  
Roberto De Giorgio ◽  
Giorgio Zoli

About 50% of persons with an alcohol use disorder may have symptoms of alcohol withdrawal syndrome (AWS) when they reduce or discontinue their alcohol consumption. Protracted alcohol withdrawal (PAW), an underestimated and not yet clearly defined clinical condition that follows the acute stage of AWS, is characterized by the presence of substance-specific signs and symptoms (i.e. anxiety, irritability, mood instability, insomnia, craving) common to acute AWS, but persisting beyond the generally expected acute AWS time frames. Considering that PAW symptoms are mainly related to the neuro-adaptive changes of gamma-aminobutyric acid (GABA) and N-methyl-d-aspartate (NMDA) systems, naltrexone, nalmefene, and disulfiram may not be able to suppress the symptoms of PAW. After treatment of the acute phase of AWS, a more specifically pharmacological therapy able to suppress PAW symptoms could perhaps be used earlier and may be more helpful in preventing the risk of alcohol relapse, which remains higher during the first months of treatment. In light of this, medications acting on GABA and NMDA neurotransmitter systems to counterbalance the up-regulation of NMDA and the down-regulation of GABA could be employed in combination and started as soon as possible.

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Alice Laniepce ◽  
Nicolas Cabé ◽  
Claire André ◽  
Françoise Bertran ◽  
Céline Boudehent ◽  
...  

Abstract In alcohol use disorder, drinking cessation is frequently associated with an alcohol withdrawal syndrome. Early in abstinence (within the first 2 months after drinking cessation), when patients do not exhibit physical signs of alcohol withdrawal syndrome anymore (such as nausea, tremor or anxiety), studies report various brain, sleep and cognitive alterations, highly heterogeneous from one patient to another. While the acute neurotoxicity of alcohol withdrawal syndrome is well-known, its contribution to structural brain alterations, sleep disturbances and neuropsychological deficits observed early in abstinence has never been investigated and is addressed in this study. We included 54 alcohol use disorder patients early in abstinence (from 4 to 21 days of sobriety) and 50 healthy controls. When acute physical signs of alcohol withdrawal syndrome were no longer present, patients performed a detailed neuropsychological assessment, a T1-weighted MRI and a polysomnography for a subgroup of patients. According to the severity of the clinical symptoms collected during the acute withdrawal period, patients were subsequently classified as mild alcohol withdrawal syndrome (mild-AWS) patients (Cushman score ≤ 4, no benzodiazepine prescription, N = 17) or moderate alcohol withdrawal syndrome (moderate-AWS) patients (Cushman score > 4, benzodiazepine prescription, N = 37). Patients with severe withdrawal complications (delirium tremens or seizures) were not included. Mild-AWS patients presented similar grey matter volume and sleep quality as healthy controls, but lower processing speed and episodic memory performance. Compared to healthy controls, moderate-AWS patients presented non-rapid eye movement sleep alterations, widespread grey matter shrinkage and lower performance for all the cognitive domains assessed (processing speed, short-term memory, executive functions and episodic memory). Moderate-AWS patients presented a lower percentage of slow-wave sleep, grey matter atrophy in fronto-insular and thalamus/hypothalamus regions, and lower short-term memory and executive performance than mild-AWS patients. Mediation analyses revealed both direct and indirect (via fronto-insular and thalamus/hypothalamus atrophy) relationships between poor sleep quality and cognitive performance. Alcohol withdrawal syndrome severity, which reflects neurotoxic hyperglutamatergic activity, should be considered as a critical factor for the development of non-rapid eye movement sleep alterations, fronto-insular atrophy and executive impairments in recently detoxified alcohol use disorder patients. The glutamatergic activity is involved in sleep-wake circuits and may thus contribute to molecular mechanisms underlying alcohol-related brain damage, resulting in cognitive deficits. Alcohol withdrawal syndrome severity and sleep quality deserve special attention for a better understanding and treatment of brain and cognitive alterations observed early in abstinence, and ultimately for more efficient relapse prevention strategies.


Author(s):  
Carol S. North ◽  
Sean H. Yutzy

Alcohol use disorder involves use of alcohol in quantities sufficient to produce intoxication over long periods and use continuing despite significant alcohol-related problems, resulting in a cluster of cognitive, behavioral, and physiological symptoms. Indicators of alcohol use problems include consumption of more alcohol than intended, inability to cut down on use, alcohol craving, excessive involvement in obtaining and using alcohol, continued use despite negative psychosocial and medical consequences, and physiological tolerance to the effects of alcohol and alcohol withdrawal. Complications of alcohol use disorders include social problems, such as legal and marital problems, and medical problems including metabolic and hepatic disease and cancers. Approximately half of people with an alcohol use disorder will experience an alcohol withdrawal syndrome, typically manifesting within several hours or days of reduction or cessation of heavy and prolonged alcohol consumption and typically lasting 4–5 days.


2017 ◽  
Vol 41 (S1) ◽  
pp. s866-s866
Author(s):  
M. Juncal Ruiz ◽  
O. Porta Olivares ◽  
L. Sánchez Blanco ◽  
R. Landera Rodríguez ◽  
M. Gómez Revuelta ◽  
...  

IntroductionAlcohol consumption represents a significant factor for mortality in the world: 6.3% in men and 1.1% in women. Alcohol use disorder is also very common: 5.4% in men and 1.5% in women. Despite its high frequency and the seriousness of this disorder, only 8% of all alcohol-dependents are ever treated. One potentially interesting treatment option is oriented toward reducing alcohol intake.AimsTo describe one case who has improved his alcohol consumption after starting treatment with nalmefene, an opioid receptor antagonist related to naltrexone.MethodsA 35-year-old male with alcohol use disorder since 2001 came to our consult in November 2015. He was in trouble with his family and he had a liver failure. We offer a new treatment option with nalmefene 18 mg to reduce alcohol consumption.ResultsBefore to start nalmefene he drank 21 drinks/week. Six-month later, he decreased alcohol intake until 5 drinks/week with better family relationship and liver function. After starting nalmefene he complained of nausea, so we recommend to take the middle of the pill for next 7 days. After this time he returned to take one pill with good tolerance and no more side effects or withdrawal syndrome.ConclusionsNalmefene appears to be effective and safe in reducing heavy drinking and in preventing alcohol withdrawal syndrome due to its opioid receptor antagonism. This case suggests nalmefene is a potential option to help patients, who do not want or cannot get the abstinence, in reducing their alcohol consumption.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2020 ◽  
Author(s):  
Régis Alarcon ◽  
Margaux Tiberghien ◽  
Raphael Trouillet ◽  
Stéphanie Pelletier ◽  
Amandine Luquiens ◽  
...  

CNS Drugs ◽  
2015 ◽  
Vol 29 (4) ◽  
pp. 293-311 ◽  
Author(s):  
Christopher J. Hammond ◽  
Mark J. Niciu ◽  
Shannon Drew ◽  
Albert J. Arias

2020 ◽  
Vol 12 (1) ◽  
pp. 23-25 ◽  
Author(s):  
Andrew Chunkil Park ◽  
Leigh Goodrich ◽  
Bobak Hedayati ◽  
Ralph Albert ◽  
Kyle Dornhofer ◽  
...  

Purpose The purpose of this paper is to illustrate delirium as a possible consequence of the application of symptom-triggered therapy for alcohol withdrawal and to explore alternative treatment modalities. In the management of alcohol withdrawal syndrome, symptom-triggered therapy directs nursing staff to regularly assess patients using standardized instruments, such as the Clinical Institute for Withdrawal Assessment of Alcohol, Revised (CIWA-Ar), and administer benzodiazepines at symptom severity thresholds. Symptom-triggered therapy has been shown to lower total benzodiazepine dosage and treatment duration relative to fixed dosage tapers (Daeppen et al., 2002). However, CIWA-Ar has important limitations. Because of its reliance on patient reporting, it is inappropriate for nonverbal patients, non-English speakers (in the absence of readily available translators) and patients in confusional states including delirium and psychosis. Importantly, it also relies on the appropriate selection of patients and considering alternate etiologies for signs and symptoms also associated with alcohol withdrawal. Design/methodology/approach The authors report a case of a 47-year-old male admitted for cardiac arrest because of benzodiazepine and alcohol overdose who developed worsening delirium on CIWA-Ar protocol. Findings While symptom-triggered therapy through instruments such as the CIWA-Ar protocol has shown to lower total benzodiazepine dosage and treatment duration in patients in alcohol withdrawal, over-reliance on such tools may also lead providers to overlook other causes of delirium. Originality/value This case illustrates the necessity for providers to consider using other available assessment and treatment options including objective alcohol withdrawal scales, fixed benzodiazepine dosage tapers and even antiepileptic medications in select patients.


2019 ◽  
Vol 54 (5) ◽  
pp. 503-509 ◽  
Author(s):  
Andrzej Silczuk ◽  
Bogusław Habrat ◽  
Michał Lew-Starowicz

The association of thrombocytopenia (TP) and alcohol use has been demonstrated. Also TP as possible risk factor for alcohol withdrawal complications (cAWS) have been reported. In this study, the relationship between the presence of TP and cAWS was clearly established and assessed below what platelets count (<119k/mL) this risk increases.


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