neuroleptyk
23.06.09, 14:34
2009 Apr 30
Cortico-limbic response to personally challenging emotional
stimuli after complete recovery from depression.
Hooley JM, Gruber SA, Parker HA, Guillaumot J, Rogowska J, Yurgelun-
Todd DA.
Department of Psychology, Harvard University, Cambridge, MA 02138,
USA.
People vulnerable to depression are at increased risk of relapse if
they live in highly critical family environments. To explore this
link, we used neuroimaging methods to examine cortico-limbic
responding to personal criticisms in healthy participants and
participants with known vulnerability to major depression. Healthy
controls and fully recovered participants with a past history of
major depression were scanned while they heard praising, critical,
and neutral comments from their own mothers. Prior to scanning, the
formerly depressed and the control participants were
indistinguishable with respect to self-reported positive, negative,
or anxious mood. They also reported similar mood changes after being
praised or criticized. However, formerly depressed participants
responded to criticism with greater activation in the amygdala and
less activation in the dorsolateral prefrontal cortex (DLPFC) and
anterior cingulate cortex (ACC) than did controls. During praise and
neutral commentary, amygdala activation was comparable in both
groups, although lower levels of activation in the DLPFC and ACC
still characterized formerly depressed participants. Vulnerability
to depression may be associated with abnormalities in cortico-limbic
activation that are independent of mood state and that remain even
after full recovery. Criticism may be a risk factor for relapse
because it activates the amygdala and perturbs the affective
circuitry that underlies depression.
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Uderzające podobieństwo do najswizszego badania nt. anhedonii w
depresji.
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Predictors of nonresponse to cognitive behavioural therapy or
venlafaxine using glucose metabolism in major depressive disorder.
Konarski JZ, Kennedy SH, Segal ZV, Lau MA, Bieling PJ, McIntyre RS,
Mayberg HS.
University Health Network, Toronto General Hospital, 200 Elizabeth
St., Eaton North Wing 8-222, Toronto ON M5G2C4.
BACKGROUND: Longitudinal neuroimaging investigations of
antidepressant treatment offer the opportunity to identify potential
baseline biomarkers associated with poor outcome. METHODS: To
explore the neural correlates of nonresponse to cognitive
behavioural therapy (CBT) or venlafaxine (VEN), we compared
pretreatment (18)F-fluoro-2-deoxy-d-glucose positron emission
tomography scans of participants with major depressive disorder
responding to either 16 weeks of CBT (n = 7) or VEN treatment (n =
9) with treatment nonresponders (n = 8). RESULTS: Nonresponders to
CBT or VEN, in contrast to responders, exhibited pretreatment
hypermetabolism at the interface of the pregenual and subgenual
cingulate cortices. LIMITATIONS: Limitations of our study include
the small sample sizes and the absence of both arterial sampling to
determine absolute glucose metabolism and high-resolution structural
magnetic resonance imaging coregistration for region-of-interest
analyses. CONCLUSION: Our current findings are consistent with those
reported in previous studies of relative hyperactivity in the
ventral anterior cingulate cortex in treatment-resistant populations.
Cóż jak nie działa vanlafaksyna lub terapia cognitywno behawioralna,
to dlatego, że dolno (brzuszno) przednia zakręt obręczy jest
hiperaktywny. Chociaż autorzy zaznaczaja pewne ograniczenia tego
badania to mimo tego wyniki są zgodne z poprzednimi badaniami.
The influence of 5-HTTLPR and STin2 polymorphisms in the
serotonin transporter gene on treatment effect of selective
serotonin reuptake inhibitors in depressive patients.
Smits KM, Smits LJ, Peeters FP, Schouten JS, Janssen RG, Smeets HJ,
van Os J, Prins MH.
Department of Epidemiology, Maastricht University, Maastricht, The
Netherlands. kim.smits@epid.unimaas.nl
BACKGROUND: Serotonin transporter gene (SLC6A4) variations have been
proposed as an explanation for interindividual differences in
selective serotonin reuptake inhibitors (SSRIs) effects.
Quantitative assessment of genetic influences is necessary to
evaluate whether genetic testing before antidepressant prescription
would lead to earlier treatment effects. This study evaluates the
influence of two polymorphisms (5-HTTLPR and STin2) on SSRI
treatment outcome in depression. METHODS: We included 50 SSRI
nonresponders (cases) and 164 referents meeting Diagnostic and
Statistical Manual Of Mental Disorder-IV criteria for major
depression and using an SSRI for at least 6 weeks. Blood samples or
buccal swabs were gathered to determine 5-HTTLPR (N=48 for cases and
161 for referents) and STin2 (N=50 for cases and 162 for referents)
genotypes. The association between genotype and SSRI response was
assessed by use of logistic regression. RESULTS: Patients with the 5-
HTTLPR s-allele had a nonsignificantly increased risk of SSRI
nonresponse; odds ratio (OR) 1.60, 95% confidence interval (CI) 0.66-
3.89. 5-HTTLPR effects were strongest in female patients (OR 3.54,
95% CI 1.05-11.92), and for male patients 5-HTTLPR seemed to have no
effect (OR 0.29, 95% CI 0.04-2.34). An age-dependent effect of 5-
HTTLPR was observed; patients under 44 years of age had an increased
nonresponse risk (OR 9.34, 95% CI 1.41-61.98). STin2 genotype had no
clear influence on treatment outcome. CONCLUSION: Our findings
indicate that women with the 5-HTTLPR s-allele have a less favorable
response to SSRI treatment. To our knowledge, this is the first time
that a gender-dependent influence of 5-HTTLPR is reported. More
research is needed, particularly in subgroups of patients, before
implementation of genetic testing can be recommended.
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Czyli kobiety z wariantem genu SLC6A4 5-HTTLPR mają mniejsze szansę
na odpowiedz kliniczną przy stosowaniu leków SSRI.
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