Is subcortical disease associated with a poor response to antidepressants? Neurological, neuropsychological and neuroradiological findings in late-life XXXX .

@entity1 @entity308 @entity66 @entity75 @entity73 @entity16 @entity409 @entity1654 @entity21 @entity1091 @entity62
BACKGROUND: Late-life @entity308 is associated with increased subcortical @entity62 . There is some evidence that they are associated with a poorer response to acute treatment. Neurological signs and @entity409 are further evidence of @entity75 , but they have not been studied in relation to therapy resistance. METHODS: A prospective study of 24 normal controls and 75 consecutive elderly (aged 65 to 85) @entity1 with DSM-III-R major @entity308 entered a naturalistic study of treatment. Assessment of response to monotherapy and then @entity1091 augmentation or @entity1654 created three outcome groups. Investigations included magnetic resonance brain imaging, neuropsychological and neurological examination. RESULTS: Response to monotherapy within 12 weeks was shown by 42.7%, a further 37.3% responded to @entity1091 augmentation or @entity1654 within 24 weeks and 20% had responded poorly to all treatments at 24 weeks. Subcortical hyperintensities were significantly increased in the more resistant @entity1 . These included confluent deep white matter, multiple (> 5) @entity21 and pontine @entity66 . Most of the @entity73 was restricted to the resistant groups and was of a subcortico-frontal type. @entity16 characterized the resistant groups. The combination of @entity21 , pyramidal tract signs and impairment of motor hand sequencing strongly predicted resistance to 12 weeks of antidepressant monotherapy with 89% sensitivity and 95% specificity. CONCLUSION: In late-life @entity308 a poor response to antidepressant monotherapy can be expected in those @entity1 with a @entity75 , @entity21 or if MRI T2-weighted lesions are present in both the basal ganglia and the pontine reticular formation.
