Functional Neuroanatomy of Mood Disorders Flashcards
When might you think about neuroimaging for clinical use in affective disorders?
To investigate organic cause if:
▪️ Treatment-resistant and chronic
▪️ Focal neurological symptoms
▪️ Cognitive symptoms incompatible with mood disorders (e.g., visuospatial difficulties)
E.g., slow growing frontal tumour, frontal and temporal atrophy in FTD, dopamine transporter SPECT for PD)
What organic disease may present with symptoms of affective disorder?
▪️ Frontal tumours
▪️ FTD (e.g., apathy, inappropriate affect
▪️ Parkinson’s disease
What are the two key parts of the social and emotional brain?
▪️ Limbic forebrain areas
▪️ Hypothalamus (receives most projections from the former, regulation of circadian and hormonal rhythm)
What are the main structures of the limbic forebrain?
▪️ Cortical = OFC, hippocampus
▪️ Subcortical = septal region (set of nuclei involved in emotional and memory processing), amygdaloid complex
What are the main components of the prefronto-striato-thalamic loops?
Frontal cortex (particularly DLPFC) –> striatum –> thalamus –> back to frontal cortex
(both dorsolateral and ventrolateral thalamic nucleus)
What are the main neurotransmitters involved in the prefronto-striato-thalamic loops?
▪️ Dopamine
▪️ Other monoaminergic systems (e.g., serotonin, noradrenaline)
▪️ Glutamine
particularly in ventral tegmental areas?
What are the main issues with the neuroanatomical modelling of affective disorders?
▪️ Complex interactions - oversimplifying or overcomplicating it?
▪️ Does not assign functions to brain regions
▪️ Does not explain how people become depressed or recover/relapse
What was the main conclusion of the recent meta-analysis of fMRI in MDD compared to controls?
No abnormalities in those with depression (very little difference)
What are the main limitations of cross-sectional case-controlled designs for neuroimaging studies of affective disorders?
▪️ Mood state often not properly controlled - is it just showing normal response to negative emotions and thoughts? (should we compare to someone who’s just lost their job or to other psychiatric diagnoses?)
▪️ Medication effects
▪️ Distress
▪️ Motivations to take part
▪️ Control for co-morbidity?
What is the best study design for neuroimaging research into affective disorders?
Longitudinal
▪️ Can disentangle correlates of symptoms from vulnerability
▪️ Can control for medication effects
What are the main limitations of BOLD fMRI studies?
▪️ Different subjective experience of stimuli
▪️ Whole brain illusion - signal drops out near air-filled cavities or bones which affects the limbic forebrain structures and OFC
▪️ Activation in regions not necessary for task
▪️ Reverse inference (may be active for different tasks)
How can neuroimaging more effectively be used in affective disorder research?
To find biomarkers, particularly prognostic
Subgenual cortex resting state connectivity with which three regions was found to predict treatment failure to CBT vs antidepressants?
▪️ Left frontoinsular cortex
▪️ Midbrain (including dorsal raphe area)
▪️ Ventromedial prefrontal cortex
What role does the subgenual area play in MDD?
▪️ Abnormal metabolism
▪️ Linked to how prone one is to experiencing guilt and self-blame
▪️ E.g., more active when donating to charity and in people prone to guilt and empathic concern
Blaming and self-worthlessness in depression is….
▪️ Overgeneralised
▪️ Selectively about oneself (don’t typically show an increase in negative feelings towards others)
(self-worthlessness, feeling guilty for everything)
What is non-violent irritability and anger in atypical depression associated with?
Rejection sensitivity hence low self-worth
How does access to social meaning and concept differ in those with depression and what brain areas are involved in this?
▪️ Less access (contribution to blame differentiations?)
▪️ Right superior and anterior temporal lobe
According to fMRI studies investigating people with high guilt-proneness and MDD, what might be the neuroanatomical underpinning of self-blame?
Decreased connectivity between social meaning areas (anterior temporal) and guilt related areas (subgenual)
(Even when in remission - vulnerability of reoccurrence?)
Connectivity in which brain areas may predict recurrence of depression?
Subgenual and anterior temporal lobe
(lower connectivity in those with high self-blaming irrespective or recurrence risk,
high risk of recurrence = higher levels of connection?)
MUST LOOK AT SUBDIVISIONS OF SUBGENUAL REGION
How might neurofeedback be useful for potential treatment of self-blaming MDD?
Target posterior subgenual and anterior temporal hyperconnectivity in those with insufficient remission
Superior to psychological intervention in individuals WITHOUT anxious distress
In what kind of depression was neurofeedback more useful than psychological interventions for reducing symptoms?
Those without anxious depression
(Do different subtypes respond differently to different neurofeedback targets?
