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4 results

  • Accelerated Long-Term Forgetting: Prolonged Delayed Recognition as Sensitive Measurement for Different Profiles of Long-Term Memory and Metacognitive Confidence in Stroke Patients

  • Nikki A. Lammers, Selma Lugtmeijer, Edward H.F. de Haan, Roy P.C. Kessels
  • Journal:
    Journal of the International Neuropsychological Society / Volume 28 / Issue 4 / April 2022
    Published online by Cambridge University Press:
    06 May 2021, pp. 327-336
    • Article
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  • Objective:

    Deficits in episodic memory are frequently reported after ischemic stroke. In standard clinical care, episodic memory is assessed after a 20–30 min delay, with abnormal memory decay over this period being characterized as rapid forgetting (RF). Previous studies have shown abnormal forgetting over a prolonged interval (days to weeks) despite normal acquisition, referred to as accelerated long-term forgetting (ALF).

    Method:

    We examined whether ALF is present in stroke patients (N = 91) using immediate testing (T1), testing after a short delay (20–30 min, T2), and testing after a prolonged delay (one week, T3). Based on performance compared to matched controls (N = 85), patients were divided into (1) patients without forgetting, (2) patients with RF between T1 and T2, and (3) patients with ALF at T3. Furthermore, confidence ratings were assessed.

    Results:

    ALF was present in a moderate amount of stroke patients (17%), but ALF was even more prevalent in our stroke sample than RF after a 20–30 min delay (which was found in only 13% of our patients). Patients reported a lower confidence for their responses, independent of their actual performance.

    Conclusions:

    Adding a one-week delayed measurement may potentially assist in identifying patients with memory decrements that may otherwise go undetected.

  • Chapter 40 - Medullary infarcts and hemorrhages

  • from Section 2 - Vascular topographic syndromes
  • Edited by Louis R. Caplan, Jan van Gijn
  • Book:
    Stroke Syndromes, 3ed
    Published online:
    05 August 2012
    Print publication:
    12 July 2012, pp 461-468

  • Summary

    Anterior choroidal artery (AChA) territory infarcts represent the second most common infarct in the territory of the deep perforators of the carotid artery system. The classical pattern of clinical signs attributed to AChA territory infarction is hemiplegia, hemianesthesia, and homonymous hemianopia, often associated with neuropsychological signs. Aphasia, spatial neglect, attention disorder, executive functioning impairment, and delayed memory are reported to be less severe than when due to thalamic or cortical infarctions. The high prevalence of arterial hypertension or diabetes mellitus as an isolated risk factor of stroke in small-sized AChA infarcts suggests that small artery disease is a common etiology of AChA territory infarcts. The clinical syndromes, vascular risk factor profile, presumed etiology of stroke, and prognosis allow consideration of small and large AChA territory infarcts in the differential diagnosis of patients with brain ischemia.

  • 59 - SCLERODERMA

  • from PART V: - SYSTEMIC DISORDERS THAT ALSO INVOLVE THE CEREBROVASCULAR SYSTEM
  • Edited by Louis R. Caplan, Julien Bogousslavsky
  • Book:
    Uncommon Causes of Stroke
    Published online:
    06 January 2010
    Print publication:
    09 October 2008, pp 429-432

  • Summary

    This chapter reviews the role of calcium and magnesium in causing and ameliorating brain ischemia, respectively. Three different effects of hypercalcemia are posited to contribute to the development and severity of brain ischemia: (i) hypercalcemia stimulates vascular smooth muscle causing vasoconstriction; (ii) increased calcium concentrations enhance platelet aggregation and activate the body's intrinsic coagulation system; and (iii) calcium entry into cells, a process enhanced by an elevated extracellular-to-intracellular calcium ion gradient, causes cytotoxic effects that promote cell death and brain infarction. The rationale for the use of calcium antagonists in the prevention or treatment of secondary brain ischemia was based on the assumption that these drugs reduce the frequency of vasospasm by counteracting the influx of calcium into vascular smooth muscle cells. There is some benefit from the use of the dihydropyridine CCA nimodipine for improving outcome after aneurysmal subarachnoid hemorrhage.