Limitations of the highly abbreviated CVLT-II in screening verbal memory deficits

2014 ◽  
Author(s):  
Elizabeth S. Gromisch ◽  
Frederick W. Foley ◽  
Andrew S. Castiglione ◽  
Vance Zemon ◽  
Ralph H. Benedict ◽  
...  
Keyword(s):  
Verbal Memory ◽  
Memory Deficits

Verbal Memory Deficits in Children With Posttraumatic Stress Disorder

2008 ◽  
Author(s):  
Karen Lau ◽  
Casey Hoffman ◽  
Christiane Burnett ◽  
Kristin Samuelson
Keyword(s):  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Verbal Memory ◽  
Stress Disorder ◽  
Memory Deficits

Identification of Subtle Verbal Memory Deficits in Premanifest Huntington Disease Using the California Verbal Learning Test

2020 ◽  
Vol 33 (1) ◽  
pp. 16-22 ◽  
Author(s):  
Heather M. Holden ◽  
Savanna M. Tierney ◽  
Lisa V. Graves ◽  
Ilex Beltran-Najera ◽  
Steven Paul Woods ◽  
...  
Keyword(s):  
Huntington Disease ◽  
Verbal Memory ◽  
Verbal Learning ◽  
Memory Deficits ◽  
California Verbal Learning Test ◽  
Learning Test

scholarly journals Verbal memory and treatment response in post-traumatic stress disorder

2008 ◽  
Vol 193 (3) ◽  
pp. 254-255 ◽  
Author(s):  
Jennifer Wild ◽  
Ruben C. Gur
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Verbal Memory ◽  
Stress Disorder ◽  
Neuropsychological Functioning ◽  
Memory Deficits ◽  
Behavioural Therapy ◽  
Post Traumatic Stress ◽  
Cognitive Behavioural ◽  
Post Traumatic

SummaryPost-traumatic stress disorder (PTSD) is often associated with verbal memory deficits, which could influence treatment outcome. We assessed neuropsychological functioning in individuals with PTSD and their response to cognitive– behavioural therapy (CBT). Treatment non-responders had significantly poorer performance on measures of verbal memory compared with responders and demonstrated narrative encoding deficits. Differences were not explained by IQ, performance on tasks of attention, initial PTSD severity, depression, time since trauma, or alcohol/substance misuse. Verbal memory deficits seem to diminish the effectiveness of CBT and should be considered in its implementation.

scholarly journals The effect of white matter hyperintensities on verbal memory

Neurology ◽  
2018 ◽  
Vol 90 (8) ◽  
pp. e673-e682 ◽  
Author(s):  
Walter Swardfager ◽  
Hugo Cogo-Moreira ◽  
Mario Masellis ◽  
Joel Ramirez ◽  
Nathan Herrmann ◽  
...  
Keyword(s):  
White Matter ◽  
Alzheimer Disease ◽  
Temporal Lobe ◽  
Verbal Memory ◽  
White Matter Hyperintensities ◽  
Verbal Learning ◽  
Memory Deficits ◽  
Verbal Recall ◽  
Lobe Atrophy ◽  
Proof Of Principle

ObjectiveTo determine the relationship between white matter hyperintensities (WMH) presumed to indicate disease of the cerebral small vessels, temporal lobe atrophy, and verbal memory deficits in Alzheimer disease (AD) and other dementias.MethodsWe recruited groups of participants with and without AD, including strata with extensive WMH and minimal WMH, into a cross-sectional proof-of-principle study (n = 118). A consecutive case series from a memory clinic was used as an independent validation sample (n = 702; Sunnybrook Dementia Study; NCT01800214). We assessed WMH volume and left temporal lobe atrophy (measured as the brain parenchymal fraction) using structural MRI and verbal memory using the California Verbal Learning Test. Using path modeling with an inferential bootstrapping procedure, we tested an indirect effect of WMH on verbal recall that depends sequentially on temporal lobe atrophy and verbal learning.ResultsIn both samples, WMH predicted poorer verbal recall, specifically due to temporal lobe atrophy and poorer verbal learning (proof-of-principle −1.53, 95% bootstrap confidence interval [CI] −2.45 to −0.88; and confirmation −0.66, 95% CI [−0.95 to −0.41] words). This pathway was significant in subgroups with (−0.20, 95% CI [−0.38 to −0.07] words, n = 363) and without (−0.71, 95% CI [−1.12 to −0.37] words, n = 339) AD. Via the identical pathway, WMH contributed to deficits in recognition memory (−1.82%, 95% CI [−2.64% to −1.11%]), a sensitive and specific sign of AD.ConclusionsAcross dementia syndromes, WMH contribute indirectly to verbal memory deficits considered pathognomonic of Alzheimer disease, specifically by contributing to temporal lobe atrophy.

scholarly journals The Self-Fulfilling Prophecy of Episodic Memory Impairment in Mild Cognitive Impairment: Do Episodic Memory Deficits Identified at Classification Remain Evident When Later Examined with Different Memory Tests?

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Shannon Zofia Klekociuk ◽  
Mathew James Summers
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Episodic Memory ◽  
Verbal Memory ◽  
Memory Function ◽  
Memory Deficits ◽  
Memory Tests ◽  
Amnestic Mci ◽  
Screening Assessment ◽  
Multiple Domain

Previous studies of mild cognitive impairment (MCI) have been criticised for using the same battery of neuropsychological tests during classification and longitudinal followup. The key concern is that there is a potential circularity when the same tests are used to identify MCI and then subsequently monitor change in function over time. The aim of the present study was to examine the evidence of this potential circularity problem. The present study assessed the memory function of 72 MCI participants and 50 healthy controls using an alternate battery of visual and verbal episodic memory tests 9 months following initial comprehensive screening assessment and MCI classification. Individuals who were classified as multiple-domain amnestic MCI (a-MCI+) at screening show a significantly reduced performance in visual and verbal memory function at followup using a completely different battery of valid and reliable tests. Consistent with their initial classification, those identified as nonamnestic MCI (na-MCI) or control at screening demonstrated the highest performance across the memory tasks. The results of the present study indicate that persistent memory deficits remain evident in amnestic MCI subgroups using alternate memory tests, suggesting that the concerns regarding potential circularity of logic may be overstated in MCI research.

Dissociable mechanisms for memory impairment in bipolar disorder and schizophrenia

2006 ◽  
Vol 36 (8) ◽  
pp. 1085-1095 ◽  
Author(s):  
DAVID C. GLAHN ◽  
JENNIFER BARRETT ◽  
CARRIE E. BEARDEN ◽  
JIM MINTZ ◽  
MICHAEL F. GREEN ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Verbal Memory ◽  
Memory Task ◽  
Cognitive Remediation ◽  
Memory Deficits ◽  
Absolute Level ◽  
Memory Impairments ◽  
Remediation Strategies ◽  
Organizational Dysfunction ◽  
Bipolar Patients

Background. Although memory deficits are consistently reported in schizophrenia and bipolar disorder, the mechanisms underlying these impairments are poorly understood. Clarifying the nature and degree of overlap in memory deficits between the two illnesses could help to distinguish brain systems disrupted in these illnesses, and indicate cognitive remediation strategies to improve patient outcomes.Method. We examined performance on a non-verbal memory task in clinically stable out-patients with bipolar disorder (n=40), schizophrenia (n=40), and healthy comparison subjects (n=40). This task includes conditions in which distinct mnemonic strategies – namely, using context to organize familiar stimuli or using holistic representation of novel stimuli – facilitate performance.Result. When compared to a reference condition, bipolar patients had deficits consistent with organizational dysfunction and poor detection of novel information. Although patients with schizophrenia performed worse than the other groups, they were only differentially impaired when organizational demands were significant. Task performance was not correlated with severity of clinical symptomatology.Conclusions. This pattern of distinct memory impairments implies disturbances in partially overlapping neural systems in bipolar disorder and schizophrenia. Evidence of impairment in detection of novel stimuli that is unique to bipolar disorder suggests that, while the absolute level of cognitive dysfunction is less severe in bipolar disorder as compared to schizophrenia, subtle disruptions in memory are present. These findings can be used to plan targeted cognitive remediation programs by helping patients to capitalize on intact functions and to learn new strategies that they do not employ without training.

scholarly journals Addictiveness as a risk factor for verbal memory deficit in schizophrenia: a case-control study

2021 ◽  
Vol 46 (3) ◽  
pp. 48-59
Author(s):  
Sonia López-Lorenzo ◽  
Natalia Jimeno-Bulnes ◽  
Martín L. Vargas-Aragón
Keyword(s):  
Verbal Memory ◽  
Cognitive Deficit ◽  
Memory Deficits ◽  
Relevant Information ◽  
Actual State ◽  
Control Group ◽  
Global Mode ◽  
State Evolution ◽  
With Memory ◽  
Control Study

Cognitive deficit is one of the main prognostic predictors in schizophrenia, mainly the deficit in verbal memory. The causal relationship between substances use, substance use disorders and psychotic syndrome is probably multidirectional and still is under the possible effect of confusion factors. The Addictiveness in the Psychotic Syndrome Assessment Scale (APSAS) evaluates in a global mode the dimension of adictivity taking in account all these factors: beginning, frequency, length, and intensity. The objective of the study is to know if the dimension of adictivity is associated to memory disorders. A group of psychotic subjects with memory deficits (n = 47) and a control group of psychotic subjects without memory deficits (n = 58) are compared obtaining a major adictivity in the first group. According to our results, the score of APSAS > 55 indicates possible memory deficits. This measuring can provide relevant information on the actual state, evolution and prognose of patients with comorbidity of psychosis and addiction.

Lack of Insight and Concomitant Neuro- psychological Deficits in Schizophrenia

2001 ◽  
Vol 12 (1) ◽  
pp. 54-60 ◽  
Author(s):  
Gudrun Sartory ◽  
Anja Thom ◽  
Judith Griese ◽  
Donald Young ◽  
Mario Butorac ◽  
...  
Keyword(s):  
Verbal Memory ◽  
Neuropsychological Tests ◽  
Clinical Symptoms ◽  
Verbal Learning ◽  
Executive Dysfunction ◽  
Memory Deficits ◽  
Pathological Feature ◽  
Schizophrenic Patients ◽  
Healthy Control ◽  
The Uk

Abstract: Lack of insight is a core pathological feature of schizophrenia. It has been assumed to be part of the dysregulation of executive dysfunction evident in this disorder. Lack of insight has also been found to be associated with amnestic disorders. As schizophrenia is additionally characterized by memory deficits, we investigated which of the two cognitive impairments - executive dysfunction or memory deficits - accounted better for lack of insight in this disorder. Eighty-one chronic schizophrenic patients and 38 healthy control probands took part in the study. The patients were recruited in Canada, the UK, Germany and Croatia. Patients were assessed with regard to clinical symptoms and the awareness of mental illness; both groups were administered neuropsychological tests of verbal memory, verbal learning, and executive function. Schizophrenic patients performed less well than healthy controls in all areas of cognitive function. Multiple regression analyses revealed that lack of awareness of schizophrenic disorder is best accounted for by poor verbal memory and disorganization.

Verbal memory deficits after left temporal lobectomy for epilepsy

1985 ◽  
Vol 62 (1) ◽  
pp. 101-107 ◽  
Author(s):  
George A. Ojemann ◽  
Carl B. Dodrill
Keyword(s):  
Electrical Stimulation ◽  
Verbal Memory ◽  
Memory Loss ◽  
Major Complication ◽  
Memory Deficits ◽  
Memory Deficit ◽  
Temporal Lobectomy ◽  
Dominant Hemisphere ◽  
Content Type ◽  
Intraoperative Localization

✓ Verbal memory deficits remain a major complication of dominant hemisphere temporal lobectomy for epilepsy. The extent of this deficit was assessed preoperatively and 1 month and 1 year postoperatively with the Wechsler Verbal Memory Scale (WMSV) in 14 adults undergoing left temporal lobectomy. Intraoperative localization of language and verbal memory was also performed by electrical stimulation mapping. The WMSV score decreased an average of 22% at 1 month (13 cases), and 11% at 1 year (10 cases), even though in the majority of cases the medial extent of the resections had been significantly modified as a result of preoperative memory changes in response to intracarotid amobarbital perfusion testing. Memory decline was greater in patients who were not seizure-free, and correlated with the lateral (but not the medial) extent of the resection. The memory deficit could be predicted intraoperatively with 80% accuracy from the relationship of the resection to sites identified by electrical stimulation mapping as essential to naming or input or storage aspects of memory. This technique was applied prospectively in two additional cases with left temporal epileptic foci and complete verbal memory loss with left hemisphere amobarbital inactivation. These resections were tailored to avoid the essential naming and memory sites; the WMSV score increased 1 month postoperatively in both cases. This study identifies a lateral cortical component for verbal memory. Sites essential for that component can be localized intraoperatively with stimulation mapping; when they are spared in a resection, verbal memory deficit following dominant hemisphere temporal lobectomy can be prevented even in high-risk cases.

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