Curso temporal del síndrome de abstinencia alcohólica en un hospital general

Secades, Rafael Monte; Rey, Ramón Rabuñal; Fuentes, F Paz; Ferro, Ana; Pértega-Díaz, Sonia; Alvaredo, Mercedes Bal; Vales, Emilio Casariego

doi:10.20882/adicciones.203

Cited by 4 publications

(2 citation statements)

References 13 publications

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“…16 In general, the evolutionary clinical course of alcohol withdrawal syndrome follows a clearly recognizable temporal pattern that enables clinicians to predict and assess the onset of complications during its evolution. 18 Several characteristic aspects of the temporal course of withdrawal symptoms (early and late) and their intensity (less and more) have been differentiated in the literature, 19 already recognizable in the classical description by Victor and Adams. 16 Thus, early or minor syndrome refers to symptoms that manifest in the first 24---48 h after the cessation of the interruption or the reduction in alcohol consumption.…”

Section: Clinical Manifestationsmentioning

confidence: 95%

Inpatient alcohol withdrawal syndrome

Monte-Secades

Rey

Guerrero-Sande

2015

Revista Clínica Española (English Edition)

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Section: Clinical Manifestationsmentioning

confidence: 95%

Inpatient alcohol withdrawal syndrome

Monte-Secades

Rey

Guerrero-Sande

2015

Revista Clínica Española (English Edition)

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“…El episodio de delirio no dura más de 72 horas en el 80% de los casos, aunque un pequeño porcentaje de enfermos puede ser más prolongado 16 . En general, el curso clínico evolutivo de un síndrome de abstinencia alcohólica sigue una pauta temporal claramente reconocible que permite predecir y valorar la aparición de complicaciones durante su evolución 18 .…”

Section: Manifestaciones Clínicasunclassified

Síndrome de abstinencia alcohólica en pacientes hospitalizados

Monte-Secades

Rey

Guerrero-Sande

2015

Revista Clínica Española

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Intermittent hypoxia training: Powerful, non-invasive cerebroprotection against ethanol withdrawal excitotoxicity

Jung

Mallet

2018

Respiratory Physiology & Neurobiology

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Ethanol intoxication and withdrawal exact a devastating toll on the central nervous system. Abrupt ethanol withdrawal provokes massive release of the excitatory neurotransmitter glutamate, which over-activates its postsynaptic receptors, causing intense Ca loading, p38 mitogen activated protein kinase activation and oxidative stress, culminating in ATP depletion, mitochondrial injury, amyloid β deposition and neuronal death. Collectively, these mechanisms produce neurocognitive and sensorimotor dysfunction that discourages continued abstinence. Although the brain is heavily dependent on blood-borne O to sustain its aerobic ATP production, brief, cyclic episodes of moderate hypoxia and reoxygenation, when judiciously applied over the course of days or weeks, evoke adaptations that protect the brain from ethanol withdrawal-induced glutamate excitotoxicity, mitochondrial damage, oxidative stress and amyloid β accumulation. This review summarizes evidence from ongoing preclinical research that demonstrates intermittent hypoxia training to be a potentially powerful yet non-invasive intervention capable of affording robust, sustained neuroprotection during ethanol withdrawal.

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Curso temporal del síndrome de abstinencia alcohólica en un hospital general

Cited by 4 publications

References 13 publications

Inpatient alcohol withdrawal syndrome

Inpatient alcohol withdrawal syndrome

Síndrome de abstinencia alcohólica en pacientes hospitalizados

Intermittent hypoxia training: Powerful, non-invasive cerebroprotection against ethanol withdrawal excitotoxicity

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