***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND The hippocampus , amygdala and related functional circuits have been implicated in the regulation of emotional expression and memory processes , which are affected in major depression . Several recent investigations have reported abnormalities in these structures in adult and elderly depressives . METHODS Elderly DSM-III-R unipolar depressives ( N = 40 ) and normal controls ( N = 46 ) participated in a magnetic resonance imaging study ( 1.0 T ) . Brain images were obtained in the coronal plane . Using established anatomical guidelines for structure delineation , volumetric measurements of left and right hippocampus and anterior hippocampus/amygdala complex were completed under blinded conditions using a semi-automated computer mensuration system , with patients and controls in r and om order . RESULTS Medial temporal volumes did not significantly distinguish either elderly depressed and age-similar normal control subjects , or late onset and early onset depressed patients ( ANCOVA ) . Major overlap of measured volumes existed between patient and control groups . In depressives , hippocampal volumes significantly correlated with age , and cognitive and depression ratings , but not with number of prior depressive episodes or age-at-onset of first depression . CONCLUSIONS Hippocampal volumes do not discriminate a typical clinical population of elderly depressed patients from age-similar normal control subjects . If hippocampal dysfunction contributes to a diagnosis of syndromal depression in the elderly , such dysfunction does not appear to be regularly reflected in structural abnormalities captured by volumetric measurement as conducted . On the other h and , relationships between hippocampal volumes and clinical phenomena in depressives , but not controls , suggest potentially meaningful interactions between hippocampal structure and the expression of major depression in the elderly Subjects at their first psychotic episode show an enlarged volume of the pituitary gl and , but whether this is due to hypothalamic – pituitary – adrenal ( HPA ) axis hyperactivity , or to stimulation of the prolactin-secreting cells by antipsychotic treatment , is unclear . We measured pituitary volume , using 1.5-mm , coronal , 1.5 T , high-resolution MRI images , in 78 patients at the first psychotic episode and 78 age- and gender-matched healthy controls . In all , 18 patients were antipsychotic-free ( 12 of these were antipsychotic-naïve ) , 26 were receiving atypical antipsychotics , and 33 were receiving typical antipsychotics .  As hypothesized , patients had a larger pituitary volume than controls ( + 22 % , p<0.001 ) . When divided by antipsychotic treatment , and compared to controls , the pituitary volume was 15 % larger in antipsychotic-free patients ( p=0.028 ) , 17 % larger in patients receiving atypicals ( p=0.01 ) , and 30 % larger in patients receiving typicals ( p<0.001 ) . Patients receiving typicals not only had the largest pituitary volume compared to controls but also showed a trend for a larger pituitary volume compared to the other patients grouped together ( + 11 % , p=0.08 ) . When divided by diagnosis , and compared to controls , the pituitary volume was 24 % larger in patients with schizophrenia/schizophreniform disorder ( n=40 , p<0.001 ) , 19 % larger in depressed patients ( n=13 , p=0.022 ) , 16 % larger in bipolar patients ( n=16 , p=0.037 ) , and 12 % larger in those with other psychoses ( n=9 , p=0.2 ) . In conclusion , the first-episode of a psychotic disorder is associated with a larger pituitary independently of the presence of antipsychotic treatment , and this could be due to activation of the HPA axis . Typical antipsychotics exert an additional enlarging effect on pituitary volume , likely to be related to activation of prolactin-secreting cells . This activation of the hormonal stress response could participate to the important metabolic abnormalities observed in patients with psychosis BACKGROUND Previous studies have shown that major depression is frequently accompanied by hypercortisolemia . There is some evidence suggesting that an increase in the glucocorticoid levels may make hippocampal cells more vulnerable to insults caused by hypoxia , hypoglycemia , or excitatory neurotransmitters . Using magnetic resonance imaging ( MRI ) , the hippocampi of patients with major depression were measured and compared with values observed in control subjects . METHODS Thirty-eight patients with primary unipolar major depression were recruited . Twenty control subjects were matched for age , gender , and years of education . The hippocampal volume was measured from coronal MRI scans in all of the subjects . Patients were also grouped and compared as responders and nonresponders to treatment with fluoxetine of 20 mg/day , for 8 weeks .  Hamilton Depression Rating Scale ( HDRS ) was used to determine the severity of depression . RESULTS No significant differences were observed between the hippocampal volumes of patients with major depression and control subjects ; however , a significant correlation was observed between the left hippocampal volume of men and their HDRS baseline values . In addition , female responders had a statistically significant higher mean right hippocampal volume than nonresponders . CONCLUSIONS The results of our study indicate no reduction in the volume of the hippocampus in patients with major depression . Nonetheless , the results do suggest that the effects of disease severity , gender , and treatment response may influence hippocampal volume THE amygdala is a key structure in the brain 's integration of emotional meaning with perception and experience.1 Patients with depression have impaired functioning in emotional tasks involving the amygdala,2 and have abnormal resting amygdala blood flow.3 To better underst and the anatomical basis for these functional changes we measured the volumes of the total amygdala and of the core amygdala nuclei  in 20 patients with a history of depression and 20 pair-wise matched controls .  Depressed subjects had bilaterally reduced amygdala core nuclei volumes and no significant differences in total amygdala volumes or in whole brain volumes . Since patients with a depression history have bilateral hippocampal volume reduction4 the volume loss in this closely related structure suggests a shared effect on both structures , potentially glucocorticoid-induced neurotoxicity5 mediated by the extensive reciprocal glutamatergic connections BACKGROUND The amygdala has a central role in processing emotions , particularly fear . During functional magnetic resonance imaging ( fMRI ) amygdala activation has been demonstrated outside of conscious awareness using masked emotional faces . METHODS We applied the masked faces paradigm to patients with major depression ( n = 11 ) and matched control subjects ( n = 11 ) during  fMRI to compare amygdala activation in response to masked emotional faces before and after antidepressant treatment . Data were analyzed using left and right amygdala a priori regions of interest , in an analysis of variance block analysis and r and om effects model . RESULTS Depressed patients had exaggerated left amygdala activation to all faces , greater for fearful faces . Right amygdala did not differ from control subjects . Following treatment , patients had bilateral reduced amygdala activation to masked fearful faces and bilateral reduced amygdala activation to all faces . Control subjects had no differences between the two scanning sessions . CONCLUSIONS Depressed patients have left amygdala hyperarousal , even when processing stimuli outside conscious awareness . Increased amygdala activation normalizes with antidepressant treatment The purpose of our study was to examine the neuroanatomical correlates of late-onset minor and major depression and to compare them with similar measures obtained from nondepressed controls . Our study groups were comprised of 18 patients with late-onset minor depression , 35 patients diagnosed with late-onset major depression , and 30 nondepressed controls . All subjects were scanned by using a 1 . 5-tesla MRI scanner . Absolute whole brain volume and normalized measures of prefrontal and temporal lobe volumes were obtained and used for comparison among groups . Our findings indicate that patients with minor depression present with specific neuroanatomical abnormalities that are comparable with the major depression group but significantly different from the controls . Normalized prefrontal lobe volumes show a significant linear trend with severity of depression , with volumes decreasing with illness severity . Whole brain volumes did not differ significantly among groups . These findings have broad implication s for the biology of late-life depression and suggest that there may be common neurobiological substrates that underlie all clinical ly significant forms of late-onset mood disturbances Behavioral studies suggest that emotional reactivity in depressed persons predicts subsequent symptom reduction . Using functional magnetic resonance imaging in a prospect i ve study , we show that greater amygdala activation to emotional facial expressions among depressed patients predicts symptom reduction 8 months later , controlling for initial depression severity and medication status . Functional magnetic resonance imaging may thus be used as a method to identify neural markers in depressed patients at risk for poor outcome BACKGROUND Previous magnetic resonance imaging ( MRI ) studies of patients with major depressive disorder ( MDD ) have consistently shown bilateral and unilateral reductions in hippocampal volume relative to healthy controls . Recent structural MRI studies have addressed the question of whether changes in the volume of hippocampal subregions may be associated with MDD . METHODS We used a comprehensive and reliable 3-dimensional tracing protocol that enables delineation of hippocampal subregions ( head , body , tail ) to study changes in the hippocampus of patients with MDD . We recruited 39 MDD patients ( 16 medicated , 23 unmedicated ) and 34 healthy age- and sex-matched controls . We acquired images using a magnetization-prepared rapid acquisition gradient echo sequence on a 1.5-T scanner with a spatial resolution of 1.5 mm x 0.5 mm x 0.5 mm . We performed volumetric analyses , blinded to diagnosis , using the interactive software package Display . All volumes were adjusted for intracranial volume . RESULTS We found a significant reduction in the volume of the hippocampal tail bilaterally , right hippocampal head and right total hippocampus in MDD patients . Medicated MDD patients showed increased hippocampal body volume compared with both healthy controls and unmedicated patients . LIMITATIONS This study was cross-sectional . Further prospect i ve studies are needed to determine the direct effect of antidepressant treatment . CONCLUSION Our results suggest that decreased hippocampal tail and hippocampal head volumes could be trait changes , whereas hippocampal body changes may be dependent on treatment . We showed that long-term antidepressant treatment may affect hippocampal volume in patients with MDD It has been hypothesized that one of the effects of antidepressants is to increase functional connectivity between the cortical mood-regulating and the limbic mood-generating regions . One consequence of this antidepressant effect is thought to be decreased limbic activation in response to negative emotional stimuli . Twelve unmedicated unipolar depressed patients and 11 closely matched healthy comparison subjects completed two magnetic resonance imaging ( MRI ) scanning sessions at baseline and after 6 weeks . Depressed patients received treatment with sertraline between the two sessions . During each MRI session , subjects completed a resting state functional connectivity scan and a conventional block- design negative vs. neutral pictures regional brain activation scan . After 6 weeks of sertraline treatment resting state , functional connectivity between the ACC and limbic regions increased while limbic activation in response to negative versus neutral pictures decreased . The results of this study are consistent with the hypothesis that antidepressant treatment has reciprocal effects on corticolimbic functional connectivity and limbic activation in response to emotional stimuli Abstract Resting state activity in the ventral cingulate may be an important neural marker of symptomatic improvement in depression . The number of task related functional magnetic resonance imaging ( fMRI ) studies correlating blood oxygenation level dependent ( BOLD ) response with symptomatic improvement is limited and method ologies are still evolving . We measured BOLD responses to sad and happy facial stimuli in 12 severely depressed individuals in the early stages of antidepressant treatment ( Time 1 ) and 12 weeks later ( Time 2 ) using event-related fMRI . We calculated correlations between temporal changes in BOLD response and changes in symptom scores . Most subjects improved markedly by Time 2 . At Time 1 , depression severity correlated positively with responses to sad stimuli in the right visual cortex , subgenual cingulate , anterior temporal pole and hippocampus and correlated negatively with responses to happy stimuli in left visual cortex and right cau date . Decreases in individual effect sizes of right subgenual cingulate and right visual cortical responses to sad , but not happy , facial stimuli were correlated with decreases in symptom scores . There are contrasting cortical and subcortical responses to sad and happy stimuli in severe depression . Responses to sad stimuli show the strongest correlates of clinical improvement , particularly in the subgenual cingulate BACKGROUND Hippocampal volumes obtained from a group of medication-free , remitted subjects with recurrent major depressive disorder ( MDD ) were compared against corresponding measures from healthy controls . METHODS Thirty-one subjects with recurrent MDD in full remission , and 57 healthy controls underwent high resolution magnetic resonance imaging ( MRI ) on a GE 3 T scanner .  Eight patients with MDD were medication-naive , and twenty-three MDD patients were off antidepressant medications for a mean of 30 months at the time of the MRI study . RESULTS Patients showed smaller total and posterior hippocampal volume relative to controls . Anterior hippocampal volume did not differ between patients and controls . CONCLUSIONS Recurrent depression is associated with smaller hippocampal volume which is most prominent in the posterior hippocampus . 
    Output:
    
Unipolar depression was characterised by reduced brain volume in areas involved in emotional processing , including the frontal cortex , orbitofrontal cortex , cingulate cortex , hippocampus and striatum .
There was also evidence of pituitary enlargement and an excess of white matter hyperintensity volume in unipolar depression .