Community Outcome in Cognitively Normal Schizophrenia Patients

2014 ◽  
Vol 20 (8) ◽  
pp. 805-811 ◽  
Author(s):  
Eva Muharib ◽  
R. Walter Heinrichs ◽  
Ashley Miles ◽  
Farena Pinnock ◽  
Stephanie McDermid Vaz ◽  
...  

AbstractRecent reports suggest that cognition is relatively preserved in some schizophrenia patients. However, little is known about the functional advantage these patients may demonstrate. The purpose of this study was to identify cognitively normal patients with a recently developed test battery and to determine the functional benefit of this normality relative to cognitively impaired patients. Average-range cognitive ability was defined by the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery (MCCB) composite score (T≥40) and applied to 100 patients with schizophrenia or schizoaffective disorder and to 81 non-psychiatric research participants. With group assignment adjusted for demographic variables, this procedure yielded 14 cognitively normal patients, 21 cognitively impaired patients, and 21 healthy adults with normal-range MCCB scores. Cognitively normal patients were indistinguishable from controls across all MCCB scales. Furthermore, their performance was superior to impaired patients on all scales except Social Cognition. Cognitively normal patients were also superior to impaired patients on a summary index of simulated life skills and functional competence. Nevertheless, both patient groups were equally disadvantaged relative to controls in independent community living. These findings suggest that normal-range cognition exists in schizophrenia, but fails to translate into enhanced community outcome. (JINS, 2014, 20, 1–7)

1975 ◽  
Author(s):  
B. Boneu ◽  
J. Plante ◽  
J. Corberand ◽  
R. Biermé

Platelet volume and density distribution of three different patient groups were studied. Volumes were determined with a Coulter-Counter (Z BIC-Channelyser C 100) while the respectives densities were evaluated using a modified approach to the standard Booyse and Rafelson density assay method (ultracentrifugation on a linear sucrose gradient).In the first group of patients schowing thrombocytemia following splenectomy, platelet volumes and densities were within the normal range both before and after splenectomy in spite of sudden platelet increase.In the second group wit I.T.P. (platelets < 20,000/mm3) the gaussian distribution of log volumes was deviated towards a macrothrombocytosis; however, the dispersion of the values was significantly increased in spite of the homogeneity of platelet age. The platelet count was immediately normalised following splenectomy. The young platelets formed (age < 48 hours) presented a normal gaussian distribution of both log-volume and density.In the third group of consumption coagulopathies with mild thrombocytopenia, there was evidence of macrothrombocytosis in all eases; yet, separation of platelet populations revealed an increase in the number of light platelets (class A and B of the Booyse and Rafelson classification).Those findings strongly suggest that young platelets present normal volume and density-distributions. Only in those cases of intensive peripheral consumption do the mega-caryocytcs produce an abnormal platelet population with grater volume and dispersion as well as lower densities.


CJEM ◽  
2004 ◽  
Vol 6 (05) ◽  
pp. 313-320 ◽  
Author(s):  
Ian Colman ◽  
Niko Yiannakoulias ◽  
Don Schopflocher ◽  
Lawrence W. Svenson ◽  
Rhonda J. Rosychuk ◽  
...  

ABSTRACTObjective:Self-inflicted injury is commonly seen in emergency departments (EDs). It may be a precursor to death by suicide. The objective of this study was to examine the epidemiology of self-inflicted injury presentations to EDs in the province of Alberta.Methods:Self-inflicted injury records for the 3 fiscal years 1998/99 to 2000/01 were accessed from the Ambulatory Care Classification System, a database that captures all ED encounters in the province of Alberta. Available data for each case included demographic details, location and time of visit, diagnoses and procedures.Results:There were 22 396 self-inflicted injury presentations to Alberta EDs during the study period. Self-inflicted injury rates were higher in females, younger patients, those on social services and those with Aboriginal treaty status. There were higher rates of return visits in the year following the self-inflicted injury than in other patient groups. Data showed regional variation. Trends could be seen in the timing of self-inflicted injury presentations by hour of day, day of week, and month of year.Conclusions:Self-inflicted injury is common, with particularly high rates demonstrated among marginalized populations. This study provides comprehensive data on those who present with self-inflicted injuries, and can be used to guide further treatment, research and evaluation for this population.


Neurology ◽  
2018 ◽  
Vol 91 (4) ◽  
pp. e313-e318 ◽  
Author(s):  
Jeremy F. Strain ◽  
Robert X. Smith ◽  
Helen Beaumont ◽  
Catherine M. Roe ◽  
Brian A. Gordon ◽  
...  

ObjectiveWhite matter (WM) projections were assessed from Alzheimer disease (AD) gray matter regions associated with β-amyloid (Aβ), tau, or neurodegeneration to ascertain relationship between WM structural integrity with Aβ and/or tau deposition.MethodsParticipants underwent diffusion tensor imaging (DTI), PET Aβ ([18F]AV-45 [florbetapir]), and PET tau ([18F]AV-1451 [flortaucipir]) imaging. Probabilistic WM summary and individual tracts were created from either a composite or individual gray matter seed regions derived from Aβ, tau, and neurodegeneration. Linear regressions were performed for Aβ, age, tau and WM hyperintensities (WMH) to predict mean diffusivity (MD) or fractional anisotropy (FA) from the corresponding WM summaries or tracts.ResultsOur cohort was composed of 59 cognitively normal participants and 10 cognitively impaired individuals. Aβ was not associated with DTI metrics in WM summary or individual tracts. Age and WMH strongly predicted MD and FA in several WM regions, with tau a significant predictor of MD only in the anterior temporal WM.ConclusionTau, not Aβ, was associated with changes in anterior temporal WM integrity. WMH, a proxy for vascular damage, was strongly associated with axonal damage, but tau independently contributed to the model, suggesting an additional degenerative mechanism within tracts projecting from regions vulnerable to AD pathology. WM decline was associated with early tau accumulation, and further decline may reflect tau propagation in more advanced stages of AD.


Geriatrics ◽  
2022 ◽  
Vol 7 (1) ◽  
pp. 12
Author(s):  
Fatimah Maria Tadjoedin ◽  
Sri Lelyati C. Masulili ◽  
Muhammad Ihsan Rizal ◽  
Lindawati S. Kusdhany ◽  
Yuda Turana ◽  
...  

Increasing evidence has shown an association between periodontitis and cognitive impairment. Subgingival microbiota play a great role in periodontitis pathogenesis. However, the correlation between the subgingival microbiome and cognitive impairment remains unclear. This study aimed to evaluate the red and orange complex subgingival microbiome of cognitively impaired and cognitively normal elderly Indonesian subjects with periodontitis. Twenty-eight elderly subjects diagnosed with periodontitis underwent two cognitive examinations using the Hopkins Verbal Learning Test and the Mini-Mental State Examination. Gingival crevicular fluid taken from the periodontal pocket, at a depth between 5 and 7 mm, using a paper point was used as the subgingival samples. The subgingival microbiome in the cognitive impairment group (n = 14) and cognitively normal group (n = 14) was compared using the 16S rRNA Metagenomic iSeq™ 100 Sequencing System. There was β-diversity in the subgingival microbiota between the cognitively impaired and cognitively normal subjects. The metagenomic analysis showed a higher abundance of Porphyromonas and Treponema bacteria in the cognitive impairment group than in the normal cognitive group (p < 0.05). The abundance of Porphyromonas gingivalis and Treponema denticola was higher in the cognitively impaired elderly subjects. The role of P. gingivalis and T. denticola in the pathogenesis of cognitive impairment needs further investigation.


2021 ◽  
Vol 12 ◽  
Author(s):  
Gavin Giovannoni ◽  
Patricia K. Coyle ◽  
Patrick Vermersch ◽  
Bryan Walker ◽  
Julie Aldridge ◽  
...  

Cladribine tablets (CladT) preferentially reduce B and T lymphocyte levels. As aging is associated with a decline in immune function, the effect of CladT on lymphocyte levels may differ by age. This post hoc analysis combined data from the Phase 3 CLARITY, CLARITY Extension, and ORACLE-MS studies to examine the effect of age (≤50 or &gt;50 years) on lymphopenia following CladT 3.5 mg/kg (CladT3.5; cumulative dose over 2 years) treatment over 96 weeks. Both CladT3.5 and placebo were given over Weeks 1 and 5 (Year 1 treatment) and Weeks 48 and 52 (Year 2 treatment) from the start of the studies. Absolute lymphocyte count (ALC) and levels of lymphocyte subsets were examined in 1564 patients (Age ≤50 [placebo: N=566; CladT3.5: N=813]; Age &gt;50 [placebo: N=75; CladT3.5: N=110]). In both age groups, following CladT3.5 treatment, nadir for ALC occurred at Week 9 (8 weeks following start of Year 1 treatment) and Week 55 (7 weeks following start of Year 2 treatment) of the 96-week period; for CD19+ B lymphocytes, nadir occurred at Week 9 (Year 1) and Week 52 (Year 2). For CD4+ T lymphocytes, nadir occurred at Week 16 (Year 1) in both age groups, and at Weeks 60 and 72 (Year 2) in the Age ≤50 and &gt;50 groups, respectively. Nadir for CD8+ T lymphocytes occurred at Week 16 (Year 1) and Week 72 (Year 2) in the Age ≤50 group and levels remained in the normal range; nadir occurred at Week 9 (Year 1) and Week 96 (Year 2) in the Age &gt;50 group. Lymphocyte recovery began soon after nadir following CladT3.5 treatment and median levels reached normal range by end of the treatment year in both age groups. By Week 96, ~25% of patients treated with CladT3.5 reported ≥1 episode of Grade ≥3 lymphopenia (Gr≥3L). The rate of certain infections was numerically higher in older versus younger patients who experienced Gr≥3L. In conclusion, CladT3.5 had a similar effect on ALC and lymphocyte subsets in both younger and older patient groups.


1997 ◽  
Vol 3 (4) ◽  
pp. 348-358 ◽  
Author(s):  
LYNN NIELSEN-BOHLMAN ◽  
DEVON BOYLE ◽  
CHRISTIE BIGGINS ◽  
FRANK EZEKIEL ◽  
GEORGE FEIN

HIV+ subjects have shown impairment on tests of executive function including automatic attention and verbal tasks. Impairment of semantic priming in HIV patients would suggest a disruption of automatic semantic activation. We examined semantic priming in HIV+ individuals and HIV− control participants with no history of substance abuse, neurologic or psychiatric disorder unrelated to HIV. HIV+ participants were divided into cognitively normal and cognitively impaired subgroups on the basis of a neuropsychological battery of 15 tests. Participants were presented with English words and nonword letter strings and indicated if the stimulus was a word or nonword. The nonwords were orthographically and phonologically correct and were created by rearranging the letter sequence of words (“ulpit”). All words had an obvious antonym (“deep”); two-thirds were presented as sequential antonym pairs (“enter”–“exit”). There were no group differences in speed of response to nonwords, indicating no generalized reaction time deficit. While control and cognitively normal HIV+ participants showed an effect of priming on reaction time to correctly detected words, cognitively impaired HIV+ participants did not. The lack of semantic priming demonstrated by cognitively impaired HIV+ participants suggests that they have lessened activation of automatic semantic networks. (JINS, 1997, 3, 348–358.)


2021 ◽  
Author(s):  
Joana B. Pereira ◽  
Shorena Janelidze ◽  
Ruben Smith ◽  
Niklas Mattsson-Carlgren ◽  
Sebastian Palmqvist ◽  
...  

AbstractAlthough recent clinical trials targeting amyloid-β (Aβ) in Alzheimer’s disease (AD) have shown promising results, there is increasing evidence suggesting that understanding alternative disease pathways that interact with Aβ metabolism and amyloid pathology might be important to halt the clinical deterioration. In particular, there is evidence supporting a critical role of astroglial activation and astrocytosis in AD. However, to this date, no studies have assessed whether astrocytosis is independently related to Aβ or tau pathology, respectively, in vivo. To address this question, we determined the levels of the astrocytic marker glial fibrillary acidic protein (GFAP) in plasma and cerebrospinal fluid (CSF) of 217 Aβ-negative cognitively unimpaired individuals, 71 Aβ-positive cognitively unimpaired individuals, 78 Aβ-positive cognitively impaired individuals, 63 Aβ-negative cognitively impaired individuals and 75 patients with a non-AD neurodegenerative disorder from the Swedish BioFINDER-2 study. Subjects underwent longitudinal Aβ (18F-flutemetamol) and tau (18F-RO948) positron emission tomography (PET) as well as cognitive testing. We found that plasma GFAP concentration was significantly increased in all Aβ-positive groups compared with subjects without Aβ pathology (p<0.01). In addition, there were significant associations between plasma GFAP with higher Aβ-PET signal in all Aβ-positive groups, but also in cognitively normal individuals with normal Aβ values (p<0.001), which remained significant after controlling for tau-PET signal. Furthermore, plasma GFAP could predict Aβ-PET positivity with an area under the curve of 0.76, which was greater than the performance achieved by CSF GFAP (0.69) and other glial markers (CSF YKL-40: 0.64, sTREM2: 0.71). Although correlations were also observed between tau-PET and plasma GFAP, these were no longer significant after controlling for Aβ-PET. In contrast to plasma GFAP, CSF GFAP concentration was significantly increased in non-AD patients compared to other groups (p<0.05) and correlated with Aβ-PET only in Aβ-positive cognitively impaired individuals (p=0.005). Finally, plasma GFAP was associated with both longitudinal Aβ-PET and cognitive decline, and mediated the effect of Aβ-PET on tau-PET burden, suggesting that astrocytosis secondary to Aβ aggregation might promote tau accumulation. Altogether, these findings indicate that plasma GFAP is an early marker associated with brain Aβ pathology but not tau aggregation, even in cognitively normal individuals with a normal Aβ status. This suggests that plasma GFAP should be incorporated in current hypothetical models of AD pathogenesis and be used as a non-invasive and accessible tool to detect early astrocytosis secondary to Aβ pathology.


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