L6+7 - Affective Disorders Flashcards
What has CT found in affective disorders?
ventricular enlargement in both bipolar disorders, unipolar depression and mixed affective disorders
What have resting state functional imaging studies found?
- decrease in frontal lobe activity - DL and Ventral and Orbitofontal cortex.
- mostly bilateral
In addition limbic (amygdala), paralimbic (anterior temporal, cingulate) and subcortical (basal ganglia, thalamus) loci have been inconsistently identified
relationship between imaging and symptoms?
Numerous PET and SPECT studies have demonstrated an inverse relationship between frontal activity and depression severity
Significant correlations demonstrated with psychomotor speed, anxiety and cognitive performance
Comparable hypometabolism in patients with depression of varying types (unipolar, bipolar and with OCD)
therefore… DRIVE is affected, EMOTION is affected.. gett up and GO affected..
What have PET studies in Bipolar Disorder shown us?
DISCONTINOUS bimodal distribution of metabolic rates with the bipolar manic phase = HYPERMETABOLIC
and depressed phase = HYPOMETABOLIC
What can predict treatment response?
hypermetabolism of rostral anterior cingulate predicts response to antidepressant
hypo = non responders
Working model of depression?
Three neuroanatomical spheres of activity
The dorsal compartment which includes both neocortical and superior limbic components and is postulated to mediate cognitive aspects; apathy, psychomotor slowing impaired attention and executive functioning
The ventral compartment including limbic, paralimbic and subcortical regions which mediate the circadian and vegetative components; sleep, appetite, libido and endocrine disturbances
The Rostral cingulate; distinct form both the dorsal and ventral components which may mediate interactions between the two (subgenual cingulate)
What can set shifting tell us?
Since set-shifting is a function of the anterior cingulate, perhaps testing this will help us identify who will and won’t respond to medicatin?
What are techniques of brain stimulation for antidepressant purposes?
- Vagal Nerve Stimulation
- TMS
- DBS
Vagal nerve stimulation?
- FDA approved for refractory depression
- most effective in patients with low to moderate, but not extreme, antidepressant resistance.
TMS?
- TMS > sham control
- degree of clinical improvement isn not large.
- not as effective as ECT
- does not penetrate far enough into the brain. ECT induces a seizure, therefore meaning it gets to the core of the brain
Deep brain stimulation?
- research technique, possible role for super refractory patients?
- DSB of the subgenual cingulate cortex can cause marked reductions in mood symptoms , and also reduced activity in subcortical areas on PET
- the antidepressant effect associated with marked reduction in local cerebral blood flow as well as changes in downstream limbic cortical sites
Neuropsych impairments in depression?
- attention and working memory - NO CONCLUSIVE EVIDENCE OF DEFICIT
- processing speed - impaired, degree of depression affects cognition more than type of depression
- learning and memory - poor encoding, organisation of material, retrieval deficit so benefit from recognition, better priming of depressive words implicating both implicit and explicit memory deficits.
some memory bias towards depressive material
Hot vs Cold cognition in depression?
depression characterised by hot cognition
mood effects the content of material retrieved from memory
HOT COG - emotionally laden, motivational
COLD COG - anhedonic, reasoned, pure imformation
How does mood effect memory in depression
- responds to negative emotional cues more quickly that positive ones.
- tend to retrieve and recognise unpleasant rather than pleasant memories
- depressed subjects always say their memory is worse, even if not objectively worse
state dependency?
Parietal lobe function in depression?
- manic patients demonstrate loss of set on language tasks
- no aphasias, gnosis or praxis.
some studies say visual memory deficits > verbal memory deficits
adaptive EF in depression?
- poor stroop - does not recover
- poor verbal fluency - recovers in remission
-
Fluency in depression?
reduced verbal and design fluency
no evidence of increased disinhibited responding
medial and dorsolateral PFC compromise
WAIS-IV performance in depression?
pretty much the norm, no cognitive impairment after controlling for motivation.
Is depression a hemispheric disorder?
no consensus
- from TBI - RIGHT FRONTAL LOBE = mood prblem
- Stroke - LEFT SIDED = mood problem
- pathological laughing - right side
- pathological crying - left side
ITS NOT HEMISPHERIC
Are cognitive deficits in depression reverisble?
- memory deficits disappear in euthymic mood
- VIQ and PIQ improved but still bad after ECT
- piq is particularly bad
If it wasn’t depression, what are some differential diagnoses?
- bereavement
- schizophrenia, schizoaffective disorder
- organic conditions: stroke, MS, hypothyroidism.. etc.
Why differentially diagnose?
If depressed (“functional”)
Better to treat actual condition if treatable; get it right!
Trajectory and outcome vastly different
If “organic”
Treatment can alleviate some cognitive impairment, even though the underlying condition may not be affected (although ECT and anti-cholinergic effects may exacerbate)
Severity of the underlying depression may have an effect on the level of cognitive impairment
Differential diagnoses in the elderly?
dementia vs. depression hard to discriminate
60% of pseudodementia go on to develop dementia 3 years later.
Stroke and mood disorder
40% stroke patients have depression
- left frontal stroke most likely have depression.
- recovery from depression is better with subcortical lesions, as opposed to cortical
what should depression in stroke be treated with?
SSRIs and TCAs… usually with recovery within one year.
Clinical features, complaints, and intellectual dysfunction in depressive dementia vs dementia?
SEE SLIDE!! PAGE 9
DCI?
Depression with cognitive impairment.. better term.
- patient variability usually means that looking at course of onset doesn’t help diagnosis
- likelihood of previous depression is also increased in DAT. doesnt help diagnosis
- not unusual for DCI to lack usual signs of depression
What kind of symptoms do we see in elderly depressed people
similar to that of subcortical dementia
lack apraxia, agnosia and aphasia.
mood disorder following TBI?
- hx of psychiatric disorder and poor social functioning = worse outcome
6-77% reported to be prevalence
more develop major deprssion, some develop minor depression
with enough motivation, study shows no differences with regard to objective neurocognitive problems. but mORE self reported depression
those with intact neuropsych functioning and normal MMPIs showed better recovery (expected recovery)
