SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "L773:1601 5215 "

Sökning: L773:1601 5215

  • Resultat 1-10 av 35
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Bourke, CM, et al. (författare)
  • Neuropsychological function in bulimia with comorbid borderline personality disorder and depression
  • 2006
  • Ingår i: Acta neuropsychiatrica. - : Cambridge University Press (CUP). - 0924-2708 .- 1601-5215. ; 18:3-4, s. 162-167
  • Tidskriftsartikel (refereegranskat)abstract
    • In bulimia nervosa (BN), borderline personality disorder (BPD) and major depression (MDD) are frequently comorbid conditions. Executive function has been found to be impaired in BPD and MDD, but the impact of comorbidity on neuropsychological function has rarely been investigated.Objective:To investigate neuropsychological function in BN with a focus on comorbid BPD and MDD.Methods:One hundred forty-four medication-free female patients entering a study of psychological treatments for BN performed a brief battery of neuropsychological tests. Comorbid MDD and BPD were systematically identified using standard interviews. Neuropsychological test results were compared.Results:Forty-one subjects had comorbid BPD and 35 had comorbid MDD, while 15 had both. There was no effect of comorbid MDD, but there was a significant effect of BPD and a significant interaction between the diagnosis of MDD and BPD on executive tasks (trail making and Stroop). Thus, compared with subjects without BPD, subjects with BPD performed significantly worse on tests of executive function, while the group with both comorbidities performed even worse.Conclusions:There appears to be an additive effect of BPD and MDD resulting in impaired executive neuropsychological function. Future studies on either disorder and on BN should examine and account for the effect of comorbidity.
  •  
2.
  • Johansson, Birgitta, 1957, et al. (författare)
  • Placebo-controlled cross-over study of the monoaminergic stabiliser (-)-OSU6162 in mental fatigue following stroke or traumatic brain injury
  • 2012
  • Ingår i: Acta Neuropsychiatrica. - : Cambridge University Press (CUP). - 0924-2708 .- 1601-5215. ; 24:5, s. 266-274
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective Mental fatigue occurring after a stroke or traumatic brain injury (TBI) often results in difficulties returning to work and pursuing social activities. No effective treatment of this condition is available today. In this study, we have tested a novel pharmacological strategy using the monoaminergic stabiliser (-)-OSU6162. Methods (-)-OSU6162 was given orally for 4 weeks in doses increasing from 15 to 45 mg b.i.d. to 12 patients suffering from mental fatigue, following upon stroke (n?=?6) or TBI (n?=?6). (-)-OSU6162 was compared with placebo using a double-blind, randomised cross-over design. Patients included were well rehabilitated physically with no gross impairment in cognitive functions other than those related to the mental fatigue. Results (-)-OSU6162 caused a remarkable improvement in mental stamina, as evaluated by a self-assessment scale on mental fatigue. Statistical significance was reached on the primary endpoint (Mental Fatigue Scale). There was a trend towards improvement in the secondary endpoints processing speed and attention. Principal component analysis showed an overall positive treatment effect in 7 of 12 patients. Beneficial responses were seen already during the first few days of active drug treatment. Increasing dosage caused no further improvement. Adverse reactions consisted of short-lasting mild nausea and attenuated appetite. These side effects disappeared upon dose reduction. Conclusion The monoaminergic stabiliser (-)-OSU6162 offers promise as a candidate for treatment of mental fatigue after a stroke or TBI.
  •  
3.
  • Liberg, B., et al. (författare)
  • The neural correlates of self-paced finger tapping in bipolar depression with motor retardation
  • 2013
  • Ingår i: Acta Neuropsychiatrica. - : Cambridge University Press (CUP). - 0924-2708 .- 1601-5215. ; 25:1, s. 43-51
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Motor retardation is a characteristic feature of bipolar depression, and is also a core feature of Parkinson's disease. Within the framework of the functional deafferentiation theory in Parkinson's disease, we hypothesised that motor retardation in bipolar depression is mediated by disrupted subcortical activation, leading to decreased activation of cortical motor areas during finger tapping. Methods: We used functional magnetic resonance imaging to investigate neural activity during self-paced finger tapping to elucidate whether brain regions that mediate preparation, control and execution of movement are activated differently in subjects with bipolar depression (n = 9) compared to healthy controls (n = 12). Results: An uncorrected whole-brain analysis revealed significant group differences in dorsolateral and ventromedial prefrontal cortex. Corrected analyses showed non-significant differences in patients compared to controls: decreased and less widespread activation of the left putamen and left pallidum; increased activity in the left thalamus and supplementary motor area; decreased activation in the left lateral pre- and primary motor cortices; absence of activation in the pre-supplementary motor area; activation of the bilateral rostral cingulate motor area. Conclusion: Both movement preparation and execution may be affected in motor retardation, and the activity in the whole left-side motor circuit is altered during self-initiated motor performance in bipolar depression.
  •  
4.
  • Melkersson, K (författare)
  • Familial and sporadic schizophrenia: a comparison of somatic diseases and abuse in patients and their relatives
  • 2009
  • Ingår i: Acta neuropsychiatrica. - : Cambridge University Press (CUP). - 0924-2708 .- 1601-5215. ; 21:1, s. 4-10
  • Tidskriftsartikel (refereegranskat)abstract
    • Comparing schizophrenia patients on the basis of familial and non-familial forms of the illness provides a promising approach to the identification of genes involved in schizophrenia. The aim of this study was to search for somatic factors that discriminate between patients with and without a family history of schizophrenia and between their relatives.Methods:Ninety-five schizophrenia patients were structurally interviewed about mental and physical health and alcohol and substance use in themselves and their families. Besides this, complementary information was obtained from the patients’ case records. Patients with (41%) and without (59%) a family history were then compared.Results:The main differences were found in the patients’ relatives. Fewer patients with a family history, compared with patients without a family history, had relatives with cancer (p = 0.002). Conversely, there was a tendency towards that more patients with a family history, compared with patients without a family history, had relatives with cardiac infarction (p = 0.05).Conclusion:The genetic risk associated with schizophrenia seems to cosegregate into a factor(s) that protects against cancer and possibly also increases the risk for cardiac infarction.
  •  
5.
  • Nilsson-Todd, Linda K, et al. (författare)
  • Cerebrospinal fluid kynurenic acid in male patients with schizophrenia - Correlation with monoamine metabolites
  • 2007
  • Ingår i: Acta Neuropsychiatrica. - : Cambridge University Press (CUP). - 0924-2708 .- 1601-5215. ; 19:1, s. 45-52
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The tryptophan metabolite kynurenic acid (KYNA) is an endogenous glutamate/nicotinic receptor antagonist. Previous studies have shown that the concentration of the compound is increased in cerebrospinal fluid (CSF) of patients with schizophrenia. Furthermore, it has been found that the CSF concentration of KYNA is positively correlated to CSF concentrations of the monoamine metabolites homovanillic acid (HVA) and 5-hydroxy indoleacetic acid (5-HIAA) in healthy control subjects. Objectives: To study the correlations between KYNA and the monoamine metabolites HVA, 5-HIAA and 4-hydroxy-3- methoxyphenylglycol (HMPG) in CSF of male patients (n = 53, ranging from 20 to 48 years of age) with verified schizophrenia. Methods: CSF was obtained by lumbar puncture, and KYNA analysis was performed with an isocratic reversed-phase high-performance liquid chromatography system connected to a fluorescence detector. HVA, 5-HIAA and HMPG concentrations were measured by mass fragmentography with deuterium-labelled internal standards. Results: Positive intercorrelations were found between CSF KYNA, HVA and 5-HIAA, while CSF content of HMPG did not correlate to KYNA or any of the monoamine metabolites in CSF. Conclusion: The results of this study suggest that increased KYNA formation is associated with an increased dopamine and serotonin turnover in male patients with schizophrenia. © 2007 Blackwell Munksgaard.
  •  
6.
  • Angelucci, F, et al. (författare)
  • CGRP in a gene-environment interaction model for depression: effects of antidepressant treatment
  • 2019
  • Ingår i: Acta neuropsychiatrica. - : Cambridge University Press (CUP). - 1601-5215 .- 0924-2708. ; 31:2, s. 93-99
  • Tidskriftsartikel (refereegranskat)abstract
    • ObjectiveGenetic and environmental factors interact in the development of major depressive disorder (MDD). While neurobiological correlates have only partially been elucidated, altered levels of calcitonin gene-related peptide (CGRP)-like immunoreactivity (LI) in animal models and in the cerebrospinal fluid of depressed patients were reported, suggesting that CGRP may be involved in the pathophysiology and/or be a trait marker of MDD. However, changes in CGRP brain levels resulting from interactions between genetic and environmental risk factors and the response to antidepressant treatment have not been explored.MethodsWe therefore superimposed maternal separation (MS) onto a genetic rat model (Flinders-sensitive and -resistant lines, FSL/FRL) of depression, treated these rats with antidepressants (escitalopram and nortriptyline) and measured CGRP-LI in selected brain regions.ResultsCGRP was elevated in the frontal cortex, hippocampus and amygdala (but not in the hypothalamus) of FSL rats. However, MS did not significantly alter levels of this peptide. Likewise, there were no significant interactions between the genetic and environmental factors. Most importantly, neither escitalopram nor nortriptyline significantly altered brain CGRP levels.ConclusionOur data demonstrate that increased brain levels of CGRP are present in a well-established rat model of depression. Given that antidepressants have virtually no effect on the brain level of this peptide, our study indicates that further research is needed to evaluate the functional role of CGRP in the FSL model for depression.
  •  
7.
  • Baghdassarian, Eva, et al. (författare)
  • Auditory brainstem response (ABR) profiling in schizoaffective disorder
  • 2020
  • Ingår i: Acta Neuropsychiatrica. - : Cambridge University Press (CUP). - 0924-2708 .- 1601-5215. ; 32:4, s. 214-217
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: The aim of the study was to assess whether the auditory brainstem response (ABR) profiling test for schizophrenia (SZ) would recognise schizoaffective disorder (SZA) patients as SZ or not.Method: Male and female SZA patients (n = 16) from the psychosis unit at Uppsala University Hospital were investigated. Coded sets of randomised ABR recordings intermingled with patients with SZ, adult attention-deficit hyperactivity disorder (ADHD) and healthy controls were analysed by an independent party blinded to clinical diagnoses.Results: The ABR profiling test for SZ was positive in 5/16 patients (31%) and negative in 11/16 patients (69%) with SZA. A surprising finding was that 4/16 (25%) SZA patients were positive for the ABR profiling test for ADHD.Conclusion: With the ABR profiling test, a minority of patients with SZA tested positive for SZ. In contrast, a majority (85%) of patients with SZ in a previous study tested positive. These preliminary results leave us ignorant whether SZA should be regarded as a SZ-like disorder or a psychotic mood disorder and add to the questions regarding the validity of this diagnostic entity. However, the ABR profiling method is still in its infancy and its exploration in a range of psychiatric disorders is warranted.
  •  
8.
  • Baghdassarian, Eva, et al. (författare)
  • Auditory brainstem response (ABR) profiling tests as diagnostic support for schizophrenia and adult attention-deficit hyperactivity disorder (ADHD)
  • 2018
  • Ingår i: Acta Neuropsychiatrica. - : Cambridge University Press (CUP). - 0924-2708 .- 1601-5215. ; 30:3, s. 137-147
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To evaluate the performances of two auditory brainstem response (ABR) profiling tests as potential biomarkers and diagnostic support for schizophrenia and adult attention-deficit hyperactivity disorder (ADHD), respectively, in an investigator-initiated blinded study design.Method: Male and female patients with schizophrenia (n=26) and adult ADHD (n=24) meeting Diagnostic and Statistical Manual of Mental Disorders Fourth Edition (DSM IV) diagnostic criteria and healthy controls (n=58) comprised the analysis set (n=108) of the total number of study participants (n=119). Coded sets of randomized ABR recordings were analysed by an independent party blinded to clinical diagnoses before a joint code-breaking session.Results: The ABR profiling test for schizophrenia identified schizophrenia patients versus controls with a sensitivity of 84.6% and a specificity of 93.1%. The ADHD test identified patients with adult ADHD versus controls with a sensitivity of 87.5% and a specificity of 91.4%.Conclusion: The ABR profiling tests discriminated schizophrenia and ADHD versus healthy controls with high sensitivity and specificity. The methods deserve to be further explored in larger clinical studies including a broad range of psychiatric disorders to determine their utility as potential diagnostic biomarkers.
  •  
9.
  • Cleland, N, et al. (författare)
  • A 16-year-old girl with anti-NMDA-receptor encephalitis and family history of psychotic disorders
  • 2015
  • Ingår i: Acta neuropsychiatrica. - : Cambridge University Press (CUP). - 1601-5215 .- 0924-2708. ; 27:6, s. 375-379
  • Tidskriftsartikel (refereegranskat)abstract
    • Autoimmune NMDA-R encephalitis (ANRE) shares clinical features with schizophrenia. Recent research also indicates that both disorders are associated with dysfunction of the N-Methyl-D-Aspartate glutamate receptors (NMDA-R) subunit 1.MethodsWe present the case of Ms A, 16 years old. Ms A presented with acute personality change, bizarre behaviour, delusional ideas and atypical seizures. She had a family history of psychotic disorders, and autistic traits diagnosed in childhood. She was initially diagnosed with a psychotic disorder. Delayed testing of CSF indicated ANRE. As the patient was a Jehovah's witness the treating team was unable to use gammaglobulin therapy; they instead relied on combined plasmapheresis and rituximab. To exclude the possibility that the affected members of this family shared a gene coding for an abnormal configuration of the NMDA receptor subunit 1 we sequenced the region of the GRIN1 gene in DNA extracted from blood in both Ms A and her grandmother.ResultsMs A’s condition improved dramatically, though her long-term memory is still demonstrably impaired. No genetic abnormality was detected.ConclusionsThis case emphasizes how important it is, for a first episode psychosis, to exclude ANRE and other autoimmune synaptic encephalitides, even in the face of significant family history, and if seronegative, the importance of testing for CSF autoantibodies.
  •  
10.
  • Edvinsson, Dan, et al. (författare)
  • Gender differences of axis I and II comorbidity in subjects diagnosed with attention-deficit hyperactivity disorder as adults
  • 2013
  • Ingår i: Acta Neuropsychiatrica. - 0924-2708 .- 1601-5215. ; 25:3, s. 165-174
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To investigate gender differences in psychiatric comorbidity patients diagnosed with attention-deficit hyperactivity disorder (ADHD) as adults. Methods: Interviews about current ADHD symptoms and psychiatric comorbidity on axis I and II (Structured Clinical Interview for DSM-IV axis I and axis II) were conducted in a clinical cohort of 168 patients (78 women, 90 men). Independent information on childhood and current symptoms was collected from parents, partners and patient files. Results: The lifetime prevalence of psychiatric comorbidity on axis I reached 92%, and current comorbidity, including autism spectrum disorders and Tourette's syndrome, was 47%. Women had a higher lifetime prevalence of mood and eating disorders compared with men, where substance-use disorders were more frequent. Ten per cent of patients fulfilled diagnostic criteria for a personality disorder. When excluding the general diagnostic criteria, 46% of the patients endorsed the specific criteria for at least one personality disorder. Gender differences were identified with predominance of histrionic personality traits in women and conduct disorder in men. Conclusion: Patients diagnosed with ADHD as adults display an extremely high lifetime axis I comorbidity with a gender-specific pattern similar to the general population. No gender differences were identified with regard to personality disorders; however, an increased prevalence of deviant personality traits was confirmed. This study stresses the importance of evaluating comorbidity among patients diagnosed with ADHD as adults to secure optimal treatment.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 35

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy