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8 results

  • 15 - Tranquilizers and Sedative Use Disorders

  • from Part IV - Use Disorders with Specific Drugs
  • Perry M. Duncan, Old Dominion University, Virginia
  • Book:
    Substance Use Disorders
    Published online:
    18 September 2020
    Print publication:
    17 September 2020, pp 593-620

  • Summary

    Barbiturates and benzodiazepines (BZDs) can relieve insomnia and high levels of anxiety. Effects of barbiturates are similar to that of alcohol. Barbiturate use entails risk of addiction, and death from accidental or suicidal overdose. In the 1970s, the safer BZDs became available. Like barbiturates, BZDs facilitate the neural inhibitory action of the neurotransmitter GABA, but are unlikely to produce pleasurable intoxication and are less addictive than barbiturates. BZDs can impair driving and increase the probability of accidental falls, especially when used concurrently with alcohol. Stopping extended intake of BZDs can result in a withdrawal syndrome of anxiety, insomnia, and a general feeling of malaise. Addiction to BZDs occurs most often in individuals with an SUD of another addictive drug. As a secondary drug of abuse, BZDs can potentiate the effects of opioid drugs or alcohol, and relieve the anxiety and agitation of addictive stimulant use. Newer drugs including zolpidem (Ambien), benzodiazepine-receptor agonists with little abuse potential that produce a brief hypnotic effect with little residual sedation the following day, are now most often used to treat insomnia.

  • 5 - Disorders of Memory Capacity and Interventions

  • Walter Glannon, University of Calgary
  • Book:
    The Neuroethics of Memory
    Published online:
    18 July 2019
    Print publication:
    08 August 2019, pp 140-168

  • Summary

    This chapter focuses on chronic disorders of memory capacity and interventions to treat them. These include anterograde and retrograde amnesia and impairments in working, spatial and prospective memory. It addresses differences between therapy and enhancement in memory modification. The chapter also considers deep brain stimulation as an experimental treatment for memory impairment in early-stage Alzheimer’s disease, weighing benefits and risks. It explains why devices external to the brain could not replace it as the source of memory. The chapter then explores the potential of a hippocampal neural prosthetic to improve memory encoding and retrieval for people with damaged hippocampi. It also explores the possibility of a prosthetic that would completely replace the hippocampal complex and whether it could decode the cognitive and emotional content of episodic memories.

  • 3 - Anesthesia, Amnesia and Recall

  • Walter Glannon, University of Calgary
  • Book:
    The Neuroethics of Memory
    Published online:
    18 July 2019
    Print publication:
    08 August 2019, pp 84-111

  • Summary

    This chapter discusses whether and in what respects patients who experience intraoperative awareness with recall can be harmed by it. The chapter considers psychological and pharmacological interventions that might prevent, weaken or erase memories of intraoperative awareness. When awareness is detected during surgery, mechanisms of memory encoding and consolidation may be difficult to reverse. Intervening in the brain to erase memories already consolidated is even more difficult. If a patient recalls being aware days or weeks after surgery, then the memory may be resistant to modification. Nevertheless, memory research and actual cases indicate that these memories can be prevented by administering consolidation-blocking drugs to induce anterograde amnesia. It is also theoretically possible for reconsolidation-blocking drugs to induce retrograde amnesia and eliminate memories of awareness.

  • Retrograde Personal Semantic Memory During Post-Traumatic Amnesia and Following Emergence

  • Caroline M. Roberts, Gershon Spitz, Matthew Mundy, Jennie L. Ponsford
  • Journal:
    Journal of the International Neuropsychological Society / Volume 24 / Issue 10 / November 2018
    Published online by Cambridge University Press:
    10 September 2018, pp. 1064-1072

  • Objectives: Anecdotal reports suggest that following traumatic brain injury (TBI) retrograde memories are initially impaired and recover in order of remoteness. However, there has been limited empirical research investigating whether a negative gradient in retrograde amnesia—relative preservation of remote over recent memory—exists during post-traumatic amnesia (PTA) compared with the acute phase post-emergence. This study used a repeated-measures design to examine the pattern of personal semantic (PS) memory performance during PTA and within two weeks of emergence to improve understanding of the nature of the memory deficit during PTA and its relationship with recovery. Methods: Twenty patients with moderate-severe TBI and 20 healthy controls (HCs) were administered the Personal Semantic Schedule of the Autobiographical Memory Interview. The TBI group was assessed once during PTA and post-emergence. Analysis of variance was used to compare the gradient across lifetime periods during PTA relative to post-emergence, and between groups. Results: PS memory was significantly lower during PTA than post-emergence from PTA, with no relative preservation of remote memories. The TBI group was still impaired relative to HCs following emergence from PTA. Lower overall PS memory scores during PTA were associated with increased days to emerge from PTA post-interview. Conclusions: These results suggest a global impairment in PS memory across lifetime periods particularly during PTA, but still present within 2 weeks of emergence from PTA. PS memory performance may be sensitive to the diffuse nature of TBI and may, therefore, function as a clinically valuable indicator of the likely time to emerge from PTA. (JINS, 2018, 24, 1064–1072)

  • Dual task performance in early Alzheimer's disease, amnestic mild cognitive impairment and depression

  • J. A. Lonie, K. M. Tierney, L. L. Herrmann, C. Donaghey, R. E. O'Carroll, A. Lee, K. P. Ebmeier
  • Journal:
    Psychological Medicine / Volume 39 / Issue 1 / January 2009
    Published online by Cambridge University Press:
    15 April 2008, pp. 23-31
  • Background

    The dual task paradigm (Baddeley et al.1986; Della Sala et al.1995) has been proposed as a sensitive measure of Alzheimer's dementia, early in the disease process.

    Method

    We investigated this claim by administering the modified dual task paradigm (utilising a pencil-and-paper version of a tracking task) to 33 patients with amnestic mild cognitive impairment (aMCI) and 10 with very early Alzheimer's disease, as well as 21 healthy elderly subjects and 17 controls with depressive symptoms. All groups were closely matched for age and pre-morbid intellectual ability.

    Results

    There were no group differences in dual task performance, despite poor performance in episodic memory tests of the aMCI and early Alzheimer's disease groups. In contrast, the Alzheimer patients were specifically impaired in the trail-making test B, another commonly used test of divided attention.

    Conclusions

    The dual task paradigm lacks sensitivity for use in the early differential diagnosis of Alzheimer's disease.

  • 20 - Dementia

  • from SECTION III - SPECIFIC NEUROLOGICAL CONDITIONS
  • Edited by Sid M. Shah, Michigan State University, Kevin M. Kelly, Drexel University, Philadelphia
  • Book:
    Principles and Practice of Emergency Neurology
    Published online:
    06 August 2009
    Print publication:
    18 February 2003, pp 218-225

  • Summary

    Dementia is a syndrome, not a specific diagnosis. There are more than 70 recognized disorders that cause dementia and the ultimate responsibility of determining the precise cause of dementia lies with a multidisciplinary team or dementia clinic. Mild dementia, however, is often missed unless mental status is formally assessed. Transient global amnesia (TGA) is a rare, but dramatic entity with a benign prognosis. TGA is characterized by abrupt, temporary inability to form new memories (anterograde amnesia) and variable impairment of recent and remote memory. TGA spares nonmemory functions, such as language and visuospatial skills. The diagnostic evaluation of dementia is best done in the outpatient setting. Common complications, such as pneumonia and urinary tract infection, are considered in demented patients with a precipitous decline in cognition. Infectious precautions are required when evaluating patients with rapidly progressive dementia.

  • 8 - The amnesic syndrome

  • from Part II
  • Edited by German E. Berrios, University of Cambridge, John R. Hodges, University of Cambridge
  • Book:
    Memory Disorders in Psychiatric Practice
    Published online:
    06 January 2010
    Print publication:
    16 March 2000, pp 164-186

  • Summary

    Patients with the amnesic syndrome have an unclouded sensorium and appear alert, able to concentrate and are cooperative. Perceptual and intellectual skills are preserved. Amnesic patients do not score differently from normals on tasks that require the immediate reproduction of a sequence of stimuli not exceeding the capacity of the short-term (working) memory store (memory span). Amnesia does not affect equally memories acquired after and before the onset of disease (anterograde and retrograde amnesia, respectively). The study of amnesia has been of paramount importance to the identification of the cerebral structures that mediate memory. The amnesic syndrome, although rare in clinical practice, remains extremely important theoretically for understanding the organisation and neural basis of memory. There is still debate as to whether the amnesic syndrome represents a unitary entity, but there is clear variability in the extent of remote memory loss depending upon the site of pathology.

  • Explorations des Fonctions Mnésiques et Benzodiazepines

  • P. Boyer
  • Journal:
    Psychiatry and Psychobiology / Volume 3 / Issue S2 / 1988
    Published online by Cambridge University Press:
    28 April 2020, pp. 149s-153s
    Print publication:
    1988

  • Dans le domaine des troubles de la mémoire induits par les benzodiazépines, un des résultats le plus communément admis est que l’information acquise avant la prise du produit est conservée intacte. A l’opposé, les troubles de la mémoire antérograde ne sont pas rares. L’intensité et la durée des troubles de la mémoire antérograde semblent dépendre des facteurs suivants: nature de la benzodiazépine utilisée, dose administrée, voie d’administration, épreuve de mémoire utilisée, nombre d’heures après la prise auxquelles les informations sont présentées et les épreuves de mémoire sont employées, caractéristiques des populations testées. Les épreuves impliquant en quelques secondes une remémoration de peu d’items (jusqu’à 6) ne sont pas perturbées par les benzodiazépines. De la même façon, lorsqu’il s’agit de listes de mots le rappel des derniers mots de la liste n’est généralement pas affecté par les benzodiazépines, tandis que les mots de milieu de liste sont plus difficilement remémorés. En général quand les études ont exploré la mémoire différée, les effets amnésiogènes se sont révélés être plus importants que lorsque la mémoire est testée immédiatement après apprentissage. Deux principales explications des effets des benzodiazépines sur la mémoire ont pu être proposées. Il semble que l’hypothèse d’un défaut de consolidation recueille plus d’arguments en sa faveur que celle d'un apprentissage «état-dépendant». La sédation contribue probablement aux effets amnésiogènes mais ne les explique pas.