To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Schizoaffective disorder, bipolar type (SAD) and bipolar disorder I (BD) present a large clinical overlap. In a 1-year follow-up, we aimed to evaluate days to hospitalization (DTH) and predictors of relapse in a SAD-BD cohort of patients.
A 1–year, prospective, naturalistic cohort study considering DTH as primary outcome and incidence of direct and indirect measures of psychopathological compensation as secondary outcomes. Kaplan-Meyer survival analysis with Log-rank Mantel-Cox test compared BD/SAD subgroups as to DTH. After bivariate analyses, Cox regression was performed to assess covariates possibly associated with DTH in diagnostic subgroups.
Of 836 screened patients, 437 were finally included (SAD = 105; BD = 332). Relapse rates in the SAD sample was n = 26 (24.8%) vs. n = 41 (12.3%) in the BD sample (p = 0.002). Mean ± SD DTH were 312.16 ± 10.6 (SAD) vs. 337.62 ± 4.4 (BD) days (p = 0.002). Patients with relapses showed more frequent suicide acts, violent behaviors, and changes in pharmacological treatments (all p < 0.0005) in comparison to patients without relapse. Patients without relapses had significantly higher mean number of treatments at T0 (p = 0.010). Cox regression model relating the association between diagnosis and DTH revealed that BD had higher rates of suicide attempts (HR = 13.0, 95%CI = 4.0–42.0, p < 0.0005), whereas SAD had higher rates of violent behavior during psychotic episodes (HR = 12.0, 95%CI =.3.3-43.5, p > 0.0005).
SAD patients relapse earlier with higher hospitalization rates and violent behavior during psychotic episodes whereas bipolar patients have more suicide attempts. Psychiatric/psychological follow-up visits may delay hospitalizations by closely monitoring symptoms of self- and hetero-aggression.
Little is known about how functional imaging changes in bipolar disorder
relate to different phases of the illness.
To compare cognitive task activation in participants with bipolar
disorder examined in different phases of illness.
Participants with bipolar disorder in mania (n = 38),
depression (n = 38) and euthymia (n =
38), as well as healthy controls (n = 38), underwent
functional magnetic resonance imaging during performance of the n-back
working memory task. Activations and de-activations were compared between
the bipolar subgroups and the controls, and among the bipolar subgroups.
All participants were also entered into a linear mixed-effects model.
Compared with the controls, the mania and depression subgroups, but not
the euthymia subgroup, showed reduced activation in the dorsolateral
prefrontal cortex, the parietal cortex and other areas. Compared with the
euthymia subgroup, the mania and depression subgroups showed
hypoactivation in the parietal cortex. All three bipolar subgroups showed
failure of de-activation in the ventromedial frontal cortex. Linear
mixed-effects modelling revealed a further cluster of reduced activation
in the left dorsolateral prefrontal cortex in the patients; this was
significantly more marked in the mania than in the euthymia subgroup.
Bipolar disorder is characterised by mood state-dependent hypoactivation
in the parietal cortex. Reduced dorsolateral prefrontal activation is a
further feature of mania and depression, which may improve partially in
euthymia. Failure of de-activation in the medial frontal cortex shows