Rosemary Fama1, Anne-Pascale Le Berre2, Stephanie A Sassoon3, Natalie M Zahr4, Kilian M Pohl4, Adolf Pfefferbaum4, Edith V Sullivan2. 1. Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Rd, Stanford, CA 94305, USA; Center for Health Sciences, Bioscience Division, SRI International, 333 Ravenswood Ave, Menlo Park, CA 94025, USA. Electronic address: rfama@stanford.edu. 2. Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Rd, Stanford, CA 94305, USA. 3. Center for Health Sciences, Bioscience Division, SRI International, 333 Ravenswood Ave, Menlo Park, CA 94025, USA. 4. Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Rd, Stanford, CA 94305, USA; Center for Health Sciences, Bioscience Division, SRI International, 333 Ravenswood Ave, Menlo Park, CA 94025, USA.
Abstract
BACKGROUND: Episodic memory deficits occur in alcohol use disorder (AUD), but their anatomical substrates remain in question. Although persistent memory impairment is classically associated with limbic circuitry disruption, learning and retrieval of new information also relies on frontal systems. Despite AUD vulnerability of frontal lobe integrity, relations between frontal regions and memory processes have been under-appreciated. METHODS: Participants included 91 AUD (49 with a drug diagnosis history) and 36 controls. Verbal and visual episodic memory scores were age- and education-corrected. Structural magnetic resonance imaging (MRI) data yielded regional frontal lobe (precentral, superior, orbital, middle, inferior, supplemental motor, and medial) and total hippocampal volumes. RESULTS: AUD were impaired on all memory scores and had smaller precentral frontal and hippocampal volumes than controls. Orbital, superior, and inferior frontal volumes and lifetime alcohol consumption were independent predictors of episodic memory in AUD. Selectivity was established with a double dissociation, where orbital frontal volume predicted verbal but not visual memory, whereas inferior frontal volumes predicted visual but not verbal memory. Further, superior frontal volumes predicted verbal memory in AUD alone, whereas orbital frontal volumes predicted verbal memory in AUD+drug abuse history. CONCLUSIONS: Selective relations among frontal subregions and episodic memory processes highlight the relevance of extra-limbic regions in mnemonic processes in AUD. Memory deficits resulting from frontal dysfunction, unlike the episodic memory impairment associated with limbic dysfunction, may be more amenable to recovery with cessation or reduction of alcohol misuse and may partially explain the heterogeneity in episodic memory abilities in AUD.
BACKGROUND: Episodic memory deficits occur in alcohol use disorder (AUD), but their anatomical substrates remain in question. Although persistent memory impairment is classically associated with limbic circuitry disruption, learning and retrieval of new information also relies on frontal systems. Despite AUD vulnerability of frontal lobe integrity, relations between frontal regions and memory processes have been under-appreciated. METHODS: Participants included 91 AUD (49 with a drug diagnosis history) and 36 controls. Verbal and visual episodic memory scores were age- and education-corrected. Structural magnetic resonance imaging (MRI) data yielded regional frontal lobe (precentral, superior, orbital, middle, inferior, supplemental motor, and medial) and total hippocampal volumes. RESULTS: AUD were impaired on all memory scores and had smaller precentral frontal and hippocampal volumes than controls. Orbital, superior, and inferior frontal volumes and lifetime alcohol consumption were independent predictors of episodic memory in AUD. Selectivity was established with a double dissociation, where orbital frontal volume predicted verbal but not visual memory, whereas inferior frontal volumes predicted visual but not verbal memory. Further, superior frontal volumes predicted verbal memory in AUD alone, whereas orbital frontal volumes predicted verbal memory in AUD+drug abuse history. CONCLUSIONS: Selective relations among frontal subregions and episodic memory processes highlight the relevance of extra-limbic regions in mnemonic processes in AUD. Memory deficits resulting from frontal dysfunction, unlike the episodic memory impairment associated with limbic dysfunction, may be more amenable to recovery with cessation or reduction of alcohol misuse and may partially explain the heterogeneity in episodic memory abilities in AUD.
Authors: Bridget F Grant; Risë B Goldstein; Tulshi D Saha; S Patricia Chou; Jeesun Jung; Haitao Zhang; Roger P Pickering; W June Ruan; Sharon M Smith; Boji Huang; Deborah S Hasin Journal: JAMA Psychiatry Date: 2015-08 Impact factor: 21.596
Authors: Adolf Pfefferbaum; Natalie M Zahr; Stephanie A Sassoon; Dongjin Kwon; Kilian M Pohl; Edith V Sullivan Journal: Biol Psychiatry Cogn Neurosci Neuroimaging Date: 2018-07-04
Authors: Rosemary Fama; Margaret J Rosenbloom; Stephanie A Sassoon; Megan A Thompson; Adolf Pfefferbaum; Edith V Sullivan Journal: Alcohol Clin Exp Res Date: 2010-12-01 Impact factor: 3.455
Authors: B Guillery-Girard; B Desgranges; C Urban; P Piolino; V de la Sayette; F Eustache Journal: J Neurol Neurosurg Psychiatry Date: 2004-11 Impact factor: 10.154