Drug-induced amnesia: Implications for cognitive neuropsychological investigations of memory.

Polster, Michael R.

doi:10.1037/0033-2909.114.3.477

Cited by 48 publications

(35 citation statements)

References 187 publications

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“…As predicted, triazolam produced a robust impairment in recognition memory for words presented during the encoding scans (Table 3); this finding replicates results of numerous studies demonstrating impaired memory performance with triazolam and other benzodiazepines (for reviews see Curran 1991;Duka et al 1996;Polster 1993). However, to our knowledge, this is the first study to examine the brain activity associated with triazolam-induced memory impairment.…”

Section: Triazolam-induced Changessupporting

confidence: 58%

“…In addition to their anxiolytic and sedative properties, benzodiazepines also have memory-and cognitiveimpairing effects (for reviews see Curran 1991;Duka et al 1996;Polster 1993). Acute benzodiazepine administration produces dose-related decrements in episodic memory encoding, while leaving retrieval of previously encoded material intact.…”

Section: It Is Well Documented That Acute Administration Of the Benzomentioning

confidence: 99%

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Effects of Triazolam on Brain Activity During Episodic Memory Encoding: A PET Study

Mintzer

Griffiths

Contoreggi

et al. 2001

Neuropsychopharmacology

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It is well documented that acute administration of the benzodiazepine hypnotic drug triazolam (Halcion®) impairs episodic memory encoding. We examined the neuroanatomical substrates of this effect in healthy adult volunteers using a double-blind, within-subject design. Following oral capsule administration (0.25 mg/70 kg triazolam or placebo), regional cerebral blood flow (rCBF) was measured using positron emission tomography (PET) withBenzodiazepine anxiolytic/hypnotic drugs, such as diazepam (Valium®), alprazolam (Xanax®), lorazepam (Ativan®), and triazolam (Halcion®), are among the most widely prescribed psychotropic medications. In addition to their anxiolytic and sedative properties, benzodiazepines also have memory-and cognitiveimpairing effects (for reviews see Curran 1991;Duka et al. 1996;Polster 1993). Acute benzodiazepine administration produces dose-related decrements in episodic memory encoding, while leaving retrieval of previously encoded material intact. Episodic memory refers to conscious long-term memory for a personally experienced event that is associated with a specific spatial and temporal context (Tulving 1972(Tulving , 1983. Encoding refers to the cognitive processes engaged (either intentionally or unintentionally) during the initial event that lead to the creation of a representation or trace of the event in epi- N EUROPSYCHOPHARMACOLOGY 2001 -VOL . 25 , NO . 5 Triazolam and PET 745 sodic memory. Thus, if information is presented for study while a participant is under the influence of a benzodiazepine, subsequent memory for that information is impaired, even when memory testing occurs while the drug is no longer in the system; however, if information presented before drug administration is tested under the influence of a benzodiazepine, no impairment is observed. Benzodiazepines act at specific receptor sites on the gamma-aminobutyric acid (GABA) A receptor complex by facilitating the action of GABA, the primary inhibitory neurotransmitter in the central nervous system (CNS) (Mohler and Okada 1977;Squires and Braestrup 1977). Benzodiazepine receptors are distributed widely throughout the brain, and, therefore, the initial sites of benzodiazepine action in the brain are known (Fernandez-Lopez et al. 1997;Frey et al. 1996;Millet et al. 2000;Persson et al. 1985). Nonetheless, little is known about the brain circuitry affected by benzodiazepine administration during episodic memory encoding, because the distribution of such effects likely goes beyond the sites of initial receptor interactions.Over the past decade, considerable progress has been made in identifying the brain regions involved in episodic memory encoding under nonpharmacological conditions using noninvasive functional neuroimaging techniques, such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), which enable measurement of brain activity in vivo while a human subject performs specific tasks. Encoding has been investigated most commonly by comparing brain activity associated with a cond...

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Section: Triazolam-induced Changessupporting

confidence: 58%

Section: It Is Well Documented That Acute Administration Of the Benzomentioning

confidence: 99%

Effects of Triazolam on Brain Activity During Episodic Memory Encoding: A PET Study

Mintzer

Griffiths

Contoreggi

et al. 2001

Neuropsychopharmacology

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“…Curran, 1991;in press;Polster, 1993). As Nyberg and Tulving (1996) point out, pharmacological dissociations between memory systems can compliment more traditional dissociations made functionally, developmentally, or neuropsychologically.…”

Section: Introductionmentioning

confidence: 93%

Dissociative Effects of Alcohol on Recollective Experience

Curran

Hildebrandt

1999

Consciousness and Cognition

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“…Particularly exciting is the prospect of using amnestic individuals as their own controls to examine both the loss and the subsequent recovery of various memory functions. A similar line of research involves the pharmacological induction of a temporary amnestic state by the use of drugs in the benzodiazepine family (Danion, Zimmerman, WillardSchroeder, Grange, & Singer, 1989;Fang, Hinrichs, & Ghoneim, 1987;Polster, 1993;Polster, McCarthy, O'Sullivan, Gray, & Park, 1993). However, participants in such a drugged state are encumbered by a general diminution of cognitive skills, whereas patients experiencing TGA appear to be fully functional with the exception of the mnemonic deficit.…”

Section: Looking Forwardmentioning

confidence: 99%

Transient global amnesia

Brown

1998

Psychonomic Bulletin & Review

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Transient global amnesia (TGA) is a memory dysfunction characterized by a sudden onset of dense anterograde amnesia (AA)that gradually resolves across several hours. TGAis typically accompanied by repeated questions (concerning present circumstances) with retrograde amnesia for events preceding the attack, and it usually strikes individuals in their late 50s and early 60s. The etiology of TGA remains unclear, although it probably reflects a temporary disruption of the blood supply to the temporallobe. The physical and psychological events preceding the attack are diverse, but they often include acute emotional and physical stressors. TGA appears to be benign, with low risk for recurrence or residual complications. While systematic memory research on TGApatients is rare, these individuals present a unique opportunity to study amnestic behaviors in otherwise normal individuals. A guide to conducting future research is provided. 401Over the last 4 decades, a considerable literature has accumulated concerning transient global amnesia (TGA). Originally described by Hague (1954; see Haas, 1983), the term TGA was coined by Fisher and Adams (1958) to describe a reversible, short-term (several hour) inability to store and/or retrieve new information most commonly observed in older adults (50-70 years old). Its onset is sudden, and its resolution is gradual. A period of retrograde amnesia (RA) is usually observed, the duration of which is highly variable (hours to years) across individuals and shrinks during the recovery period. TGA victims often ask the same question(s) repeatedly and are generally confused regarding time, place, and circumstances. Despite the inability to retain new information, general intellectual function (reading, writing, speaking, calculation) and selfidentity are preserved, and obvious neurological abnormalities are absent. Oddly, most TGA victims experience only one episode in a lifetime. TGA appears to be unassociated with any obvious physical or psychological disease process or residual disability, contrasting with other memory maladies, such as Alzheimer's dementia, Korsakoff's disease, drug addiction, or hysterical fugue states (Markowitsch, 1995).The primary purpose ofthe present review is to acquaint behavioral researchers with a common malady that is relatively unknown among psychology professionals. Despite a large literature on TGA, the phenomenon is poorly understood, and no consensus has emerged on its psychological or physiological cause. The present literature summary will hopefully allow cognitive, clinical, and healthThe author wishes to extend special thanks to Billie Stovall in the Interlibrary Loan Office of Southern Methodist University for her herculean efforts in procuring hundreds of articles from medical journals at other universities.

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Drug-induced amnesia: Implications for cognitive neuropsychological investigations of memory.

Cited by 48 publications

References 187 publications

Effects of Triazolam on Brain Activity During Episodic Memory Encoding: A PET Study

Effects of Triazolam on Brain Activity During Episodic Memory Encoding: A PET Study

Dissociative Effects of Alcohol on Recollective Experience

Transient global amnesia

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