Neuropsychiatry: Week 3- Affective Disorders (Matty's Cards)

Front 1

According to "neuropathology slide"

In affective disorders, brain anatomy is __________ ___________ and neither focal neocortical nor basal ganglia abnormalities have been consistently identified

Back 1

In affective disorders, brain anatomy is GROSSLY NORMAL and neither focal neocortical nor basal ganglia abnormalities have been consistently identified

Front 2

According to imaging data

Abnormalities in brain structure and function have
been observed in patients with affective
disorders.



CT scanning with these patients has revealed __________ ____________ in both bipolar disorders,
unipolar depression and mixed affective disorders

Back 2

According to imaging data

Abnormalities in brain structure and function have
been observed in patients with affective
disorders.



CT scanning with these patients has revealed VENTRICULAR ENLARGEMENT in both bipolar disorders, unipolar depression and mixed affective disorders.

Front 3

Ventricular enlargement is observed in what three affective disorders?

Back 3

1. Bipolar disorders
2. Unipolar depression
3. Mixed affective disorders

Front 4

Describe the neurotransmitter turnover correlates of affective disorders (3). What increases and what decreases?

Back 4

Increase turnover of noradrenaline

Decrease in serotonin and dopamine

Front 5

Imaging studies:

Numerous studies have shown that elderly depressed individuals possess values more similar to those with ___________ ___________ than to normals

Back 5

Numerous studies have shown that elderly depressed individuals possess values more similar to those with irreversible dementia than to normals.

Front 6

Resting-state functional imaging studies:

What is the best replicated finding across populations (young versus old, drug-naive and medication refractory disease and in patient sub-groups)?

Back 6

A decrease in frontal lobe activity

Involves dorso-lateral (BA 9,10,46) as well as
ventral and orbitofrontal cortex (BA 10,11,47)

Most studies report bilateral changes although
asymmetries have been reported.

Front 7

What areas of the frontal lobe show decreased activity in mood disorders?

Back 7

Dorso-lateral (BA 9,10,46)
ventral and orbitofrontal cortex (BA 10,11,47)

Most studies report bilateral changes although
asymmetries have been reported.

Front 8

In addition to decreased frontal lobe activity, what three other areas have been inconsistently identified as demonstrating decreased activity in mood disorders?

Back 8

1. Limbic (amygdala)
2. paralimbic (anterior temporal, cingulate)
3. Subcortical (basal ganglia, thalamus)

Front 9

Imaging and symptoms:

What have PET and SPECT studies demonstrated with regard to depressive symptom severity?

Back 9

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

Front 10

There is __________ ______________ in patients with
depression of varying types (unipolar, bipolar
and with OCD)

Back 10

There is COMPARABLE HYPOMETABOLISM in patients with depression of varying types (unipolar, bipolar
and with OCD)

Front 11

MRI studies: Bipolar

What is commonly seen in bipolar patients?

Back 11

White matter hyperintensities in the frontal lobes.

Majority are located in the deep white matter of the
frontal lobes or the parieto-frontal junction.

Front 12

PET studies: Bipolar

What would we expect to see during the manic phase?

Back 12

manic phase = hypermetabolic activity

Front 13

PET studies: Bipolar

What would we expect to see during the unipolar depressed phase?

Back 13

Unipolar depressed phase= hypometabolic activitiy

Front 14

How long does an untreated major depressive episode last?

Back 14

6- 13mths

Front 15

What percentage of people experience treatment resistant depression?

Back 15

Treatment resistance may be from 20-40%.

Front 16

PET:
Metabolism where predicts treatment response to antidepressant?

Back 16

rostral anterior cingulate metabolism predicts
response to antidepressant.

Front 17

Jimmy is depressed and his PET demonstrates hypermetabolic rostral anterior cingulate activity. Is he likely to benefit from antidepressants?

Back 17

Yes

Front 18

Susan is depressed and her PET demonstrates hypometabolic rostral anterior cingulate activity. Is she likely to benefit from antidepressants?

Back 18

No

Front 19

Normal sadness and depression:

Shifts in ________ ________ involve an identical set
a ventral limbic/para-limbic (sub-genual
cingulate, anterior insula, cerebellum) and
dorsal neocortical (prefrontal, parietal post-
cingulate) regions (Mayberg et al, 1999)

Back 19

Shifts in MOOD STATE an identical set
a ventral limbic/para-limbic (sub-genual
cingulate, anterior insula, cerebellum) and
dorsal neocortical (prefrontal, parietal post-
cingulate) regions.

Front 20

Recovery from depression is associated with decreases in __________ ____________ areas and increases in __________ ____________ regions

Back 20

Recovery is associated with decreases in
ventral paralimbic areas and increases in
dorsal neocortical regions.

Induction of sadness in healthy volunteers
shows the reverse pattern

Front 21

Mayberg's working model of depression argues that
depression comes about as a consequence of
three neuroanatomical spheres of activity. What are the three spheres?

Back 21

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 disturbance

The ROSTRAL CINGULATE: distinct form both the
dorsal and ventral components which may mediate
interactions between the two

Front 22

Mayberg's working model of depression:

Describe and elaborate upon the DORSAL compartment. What are the components and what does it mediate?

Back 22

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

Front 23

Mayberg's working model of depression:

Describe and elaborate upon the VENTRAL compartment. What are the components and what does it mediate?

Back 23

The ventral compartment including limbic,
paralimbic and subcortical regions which mediate
the circadian and vegetative components; sleep,
appetite, libido and endocrine disturbances

Front 24

Mayberg's working model of depression:

Describe and elaborate upon the Rostral cingulate compartment.

Back 24

The Rostral cingulate; distinct form both the
dorsal and ventral components which may mediate
interactions between the two

Front 25

Label the three areas of Mayberg's model for depression

Back 25

1. DORSAL COMPARTMENT
2. VENTRAL COMPARTMENT
3. SUB-GENUAL CINGULATE

Front 26

Brain stimulation antidepressant strategies:

________ nerve stimulation. When is it indicated? Which patients is it most effective in?

Back 26

Vagal Nerve Stimulation


FDA approved for treatment refractory depression

NS appears to be most effective in patients with low to moderate, but not extreme, antidepressant resistance

Front 27

Transcranial Magnetic Stimulation:

Does it work? Is the treatment effect large?

Back 27

There is a fairly consistent statistical evidence for the
superiority of TMS over a sham control, though the degree of clinical improvement is not large

Front 28

Is TMS more effective than ECT?

Back 28

No.

TMS is not as effective as ECT, and ECT was substantially more effective for the short-term treatment of depression.

Front 29

Which patients might be considered candidates for deep brain stimulation?

Back 29

Super refractory patients

Front 30

What area of the brain is targeted with DBS?

Back 30

Subgenual cingulate cortex

reduced activity in cortical and subcortical
areas, as measured by PET (Mayberg et al,
2005)

Front 31

DBS in depression causes reduced activity in _______ and ____________ areas as measured by PET.

Back 31

Causes reduced activity in cortical and subcortical
areas, as measured by PET (Mayberg et al,
2005)

Front 32

IN DBS, antidepressant effects are associated with a marked reduction in local __________ _________ _______ as
well as changes in downstream limbic and cortical
sites, measured using positron emission
tomography.

Back 32

Antidepressant effects were associated with a
marked reduction in local CEREBRAL BLOOD FLOW as
well as changes in downstream limbic and cortical
sites, measured using positron emission
tomography.

Front 33

Location of the electrode contact points from nine
patients successfully treated with DBS lies
within the ____ _________ ________ region. The anatomical connectivityto this region supports the suggestion that treatment efficacy is mediated by effects on a distributed network of frontal, limbic and visceromotor brain regions:

Back 33

Location of the electrode contact points from nine
patients successfully treated with DBS lies within the SUB GENUAL REGION. The anatomical connectivity to this region supports the suggestion
that treatment efficacy is mediated by effects on
a distributed network of frontal, limbic and
visceromotor brain regions.

Front 34

Neuropsychological features of depression.

The data tends to be ______ _________ and it seems the principle focus has been on dissociating _________ from ___________.

Back 34

The data tends to be PIECE MEAL and it seems the principle focus has been on dissociating DEPRESSION from DEMENTIA.

Front 35

What are some of the methodological issues in assessing the neuropsycholoigcal sequela of mood disorders?

Back 35

Severity of depression or mania

Florid psychosis

Medication status

Previous ECT

Other state-dependent variables

Cooperation issues

Control of general intelligence

Self-reported versus DSM-IV diagnosis

Front 36

What are some of the methodological issues in neuroimaging for mood disorders? (4)

Back 36

1.
Many steps of data processing increasing the risk
of inaccuracy and error

2. Statistical evidence often disregards important
evidence from exceptional images

3. Situational levels of anxiety, gender, age, arousal
and ultradian rhythm may affect baseline and
results

4. Reliability, construct validity, and difficulty of
task used during activation studies not always
considered and may seriously affect result

Front 37

Attention and Working memory in mood disorders. Deficits?

Back 37

No conclusive evidence of deficit.

Channon et al (1993) neither articulatory
loop nor visual sketch pad were affected in
clinically depressed patients

Patients with affective psychoses (mania and
depression) demonstrate deficits in digit and
block span with block span worse than
patients with schizophrenia

Front 38

Processing Speed and mood disorders?

Back 38

Tracking speed and set shifting on the TMT correlated with depressive symptoms.

Front 39

Is there any difference between processing speed in neurotic depression and endogenous depression?

Back 39

No difference between endogenous and
neurotic depression.

Front 40

The _________ ____ __________affects cognition more than type of depression.

Back 40

Degree of depression affects cognition
more than type of depression.

Front 41

Learning and memory:
Effects of depression?

Back 41

Memory consistently compromised in
depressive disorders (including SAD & CFS)

Front 42

The memory deficits in depression include:

Back 42

1. Poor encoding, attention and concentration
2. Difficulty with organzizing materal for recall


-Depressed patients show better recognition than recall even when tasks have comparable discriminating power

-Depressed patients show less benefit from increased semantic structure than do controls

-Not due to inability to generate retrieval cues but to
an inability to exert effort to use retrieval cues

Front 43

Depressed individuals have both ________ and _________ memory deficits.

Back 43

both implicit and explicit memory deficits

Front 44

Is recognition or recall better in depressed patients?

Back 44

Recognition is better

Front 45

What is the difference between "hot" and "cold" cognition?

Back 45

Distinction between the “hot” (affectively, motivationally and emotionally laden) and “cold” (anhedonic/reasoned/purely informational) cognition

Front 46

Is depression characterized by hot or cold cognition?

Back 46

Depression characterized by “hot” cognition.

Mood affects the content of material retrieved from memory (? state dependency)

Front 47

Depressed patients respond to _______ ________ cues more quickly than positive ones.

Back 47

Respond to negative emotional cues more quickly than positive ones.

Front 48

Depressed patients tend to retrieve _____________ rather than _________ memories.

Back 48

Tend to retrieve unpleasant rather than pleasant
memories.

They tend also to recognize unpleasant material more easily and pleasant material less easily.

Front 49

Depressed patients perform more poorly on measures sensitive to _________ __________ and had a higher negative emotional bias.

Back 49

Perform more poorly on measures sensitive to happiness discrimination and had a higher negative emotional bias.

Front 50

We can say that __________ _________ does affect the retrieval of information during depression.

Back 50

We can say that emotional bias does affect the retrieval of information during depression.

Front 51

How will depressed patients describe their memory?

Back 51

Depressed subjects consistently report their memory to be worse when depressed even if there is no evidence of memory deficit.

Front 52

What are the FOUR key points regarding depression and memory?

Back 52

1. Encoding difficulties which may be improved by
training
2.
A retrieval deficit producing a disparity between
recall and recognition and difficulty benefiting
from organizational structure
3. Working memory largely intact but perhaps
problems with the executive memory
4.
Some evidence of bias towards recall of
depressive material

Front 53

Parietal lobe functions in mood disorders.

Research findings into mood and aphasia?

Back 53

No formal aphasias, but manic patients
demonstrate frequent loss of set on language tasks (e.g., which letter / category)

Front 54

Depression and gnosis / praxis findings:

Back 54

No clear evidence reported of disruption of
gnosis or praxis

Front 55

Findings regarding depression and visuospatial/constructional abilities (including memory)?

Back 55

1. Deficits in copying of the RCFT have been
noted (Rossi et al, 1990; Calev et al, 1991)
2. A number of studies reporting greater visual than verbal memory deficits

Front 56

What we expected in terms of stroop and verbal fluency in a depressed person?

Back 56

Poor stroop and verbal fluency performance during depression when compared to verbal intelligence.

Front 57

What happens to stroop and verbal fluency performance one's someone's depression resolves?

Back 57

Verbal fluency reverses with recovery from
depression, Stroop does not totally resolve.

Front 58

What would we expect in terms of WCST test performance in depression?

Back 58

Impaired WCST in line with symptom severity regardless of whether the diagnosis was dysthymic
disorder or major depression.

Front 59

Fluency in depression:
Performance for visual and verbal fluency?

Back 59

Clear that the depressed subjects produce fewer items for both the verbal and design fluency

Front 60

Fluency in depression:

Do depressed patients demonstrate higher
tendency towards disinhibited responding?

Back 60

No

Front 61

The impairments in fluency in depression and most likely attributable to compromise where?

Back 61

Medial and dorsolateral pre-frontal compromise.

Front 62

Veiel's meta-analysis of cognition in depression found three levels of effect in terms of impairment. What cognitive domains were

Low:
Medium:
High:

?

Back 62

Three levels of effect


Low: attention and concentration


Moderate: visuo-motor tracking, visual/spatial
functions and verbal fluency


High: mental flexibility and control and composite
indicators of brain impairment

Front 63

___% of patients with major depression will score two or more SDs below normals on the TMT(B) or the Colour-word from of the Stroop as well as on composite indicators (e.g. pathognomonic indicator of LNRB)

Back 63

50%

15% will score in this range on tests of
memory, visuomotor tracking/scanning, visual
spatial functions and verbal fluency

Front 64

Simple attention in depression compared to normals?

Back 64

Same.

Front 65

Both the severity and the profile of cognitive deficiencies in depression are postulated to be similar to those seen in _________ ___________ ___________ ___________ _________.

Back 65

Both the severity and the profile of cognitive deficiencies in depression are postulated to be similar to those seen in moderately severe traumatic brain injury.

Front 66

Is depression a hemispheric disorder?

Back 66

No clear consensus.

- Traumatic frontal lobe injuries indicate a high
correlation between affective disturbances and
right frontal lobe

-
Stroke studies indicate that left-sided lesions are
more likely to result in depressive symptoms


- In states of pathological laughing and crying:
crying is more common with left-sided lesions
while laughter more common in right-sided lesions


- Temporal lobe epilepsy, no consensus


-Cutting (1990) no conclusive results; newer PET
evidence goes both ways

Front 67

Reasons to deferentially diagnose depression.

If depressed "functional"?

Back 67

- Better to treat actual condition if treatable; get
it right!

- Trajectory and outcome vastly different

Front 68

Reasons to deferentially diagnose depression.

If depressed "organic"?

Back 68

- 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

Front 69

Reversibility of the deficits in depression:

What happens when depressed person becomes euthymic in terms of memory function?

Back 69

Memory deficits in depression appear to disappear.

Front 70

Following ECT

IQ =
Disparity between VIQ and PIQ?

Back 70

Sackheim et al (1992) 100 depressed and 50
controls; matched for VIQ, but depressed had
significant deficits in PIQ. After ECT IQ
improved but the disparity between VIQ and PIQ
remained

Front 71

What happens to Stroop, PIQ and visual/constructional abilities following depression treatment?

Back 71

Trichard et al (1995) deficits in Stroop, PIQ and
visual/constructional tasks PERSIST after treatment.

?Two types of depression; one irreversible one
not?

Front 72

DDx for depression.

Psycho-social factor? (1)

Back 72

Bereavement

Front 73

DDx for depression.

Psychiatric factors? (3)

Back 73

Schizophrenia: frequent co-morbidity
Schizoaffective disorder: involves episodes of
depression
Bipolar disorder

Front 74

DDx for depression.

Organic factors? (8)

Back 74

1. stroke
2. hypothyroidism
3. MS
4. seasonal affective states
5. TBI
6. infectious disease
7. drug use (particularly alcohol)
8. dementia in the elderly

Front 75

Depression and Dementia

What percentage of elderly with dementia have depression?

What happens to dementia vs. depression Dx over time with elderly?

Back 75

20% of elderly with dementia feature depression


- 5-15% of initial diagnoses of dementia later
changed to depression (Feinberg & Goodman,
1984)

-
Reverse less frequent: 2.6-3% of major depression later amended to dementia

Front 76

What do families of individuals with DAT tend to do in terms of their other-report of depressive symptoms?

Back 76

Families tend to over pathologize: DATs 13.9%
DSM-III depression, families give rate of 50%.

Front 77

10-20% of the depressed elderly experience ________ ____________in addition to depressive symptoms.

Back 77

10-20% of the depressed elderly experience
cognitive impairment in addition to depressive
symptoms

Front 78

Differential diagnosis: Elderly

Are somatic symptoms more or less useful in term of making a DDx in the elderly vs the young?

Back 78

Somatic symptoms useful in young but less so in
elderly (less sleep, energy, sex etc)

Front 79

Traditionally thought that “Pseudodementia”
quickly reverses with aggressive psychiatric
treatment (eg ECT).

Why is it not so clearly the case now? (2 points)

Back 79

- Not so clear now; e.g. Alexopolous (1991) 60% of
depressive pseudodementia group went on to
develop primary dementia three years later

- Most investigators now believe that depression
and dementia co-exist (Jones & Reifler, 1994)

Front 80

Affective illness and stroke:

What percentage of stroke survivors subsequently develop depression?

Back 80

40% of patients.

Mania rarely seen.

Front 81

What type of stroke (which area? is most likely to result in depression?

Back 81

Left frontal stroke most likely to result in depression, the closer to the left frontal pole the more likely.

Front 82

Depression and stroke

Is recovery from depression faster with subcortical
or cortical lesions?

Back 82

Recovery from depression faster with subcortical
as opposed to cortical lesions

Front 83

Depression and stroke:

Is anxious depression more common in cortical
or subcortical stroke?

Back 83

Anxious depression more common in cortical
versus subcortical stroke

Front 84

Depression in stroke responds to which two antidepressants?

By which time will most people recover?

Back 84

Depression in stroke responds to SSRIs and
TCAs, usually with recovery within one year.

Front 85

Telling the difference (depression vs dementia):

Read.

Back 85

Beliauskas (1993)…”depressive-like symptoms have
little or no impact on cognitive functions….these
are more likely disease-based rather than the
result of emotional factors such as depression” (p.
119).

However may occur in cases with a psychiatric
history of primary depression together with a
sufficient loss of self-esteem.

Front 86

Elderly depressed show deficits similar to what type of dementia?

Back 86

Elderly depressed show deficits similar to sub-
cortical dementia i.e. lack apraxia, agnosia, and
aphasia.

Front 87

Back 87

Front 88

Depression following TBI


Prevalence?

Back 88

varies from 6-77%

42% developed major depression and 9% minor
at some time during 12mths follow-up

Front 89

Risk factors for depression following TBI? (2)

Back 89

1. Previous Hx of psychiatric disorder (particularly mood)
2. Poorer social funcitoning

Front 90

What percentage of TBIs feature depression?

Back 90

42%. (beware self-report)

Front 91

Stroop and TMT B performance will be impaired in what % of adult onset major depression?

Back 91

50%.

Front 92

What % of depressed elderly will feature
cognitive deficits?

Back 92

10-20%.

Front 93

How does depression affect cognition:

What is the cognitive interference hypothesis?

Back 93

the cognitive interference hypothesis according to which depressive thoughts and worries interfere and disrupt performance

Front 94

How does depression affect cognition:

What is the reduced motivation hypothesis?

Back 94

the reduced motivation hypothesis which suggests that depressed people are insufficiently motivated to perform normally.

Front 95

How does depression affect cognition:

What is the learned helplessness hypothesis?

Back 95

the learned helplessness hypothesis, which states that depressed people expect that their responses will make no difference and so they give up trying

Front 96

What is the alternate view to the above hypotheses?

Back 96

Alternate view is that the physical effects per se disrupt cognition (e.g. neuranatomical/transmitter)

Front 97

Is the cognitive interference hypothesis likely?

Back 97

Cognitive interference hypothesis is unlikely as generally working memory is spared and should be
most susceptible.

Front 98

Is the reduced motivation/learned helplessness hypothesis likely?

Back 98

Reduced motivation/learned helplessness:
probable; (e.g. Rohling et al, 2002) ; but why
do only some feature the cognitive deficits?

Front 99

Heritability of depression?

Back 99

~37%

- This is much lower than the heritability of SZ (~75%)

- Partly due to heritable depressive personality traits (neuroticism)

Front 100

Is MDD a single gene disease?

Back 100

No.

Some chromosomal loci of linkage have been replicated,
But none has been replicated in every family study.

Front 101

Possible Contributions of Neural Circuits to depression:

Orbitofrontal cortex? (3)

Back 101

Depressed patients respond faster to sad words, more to negative feedback, and have smaller volumes

Front 102

Possible Contributions of Neural Circuits to depression:

Anterior cingulate gyrus (3)

Back 102

Show decreased metabolism, have smaller volumes, and respond faster to sad words

Front 103

Possible Contributions of Neural Circuits to depression:

Dorsolateral prefrontal cortex (2)

Back 103

Show increased activation by emotional Stroop, but reduced metabolism overall

Front 104

Possible Contributions of Neural Circuits to depression:

Hippocampus

Back 104

Depressed elderly adults shown reduced volume;
findings are mixed in younger adults, but more consistent in those with recurrent depression

Front 105

Major Depressive Disorder is a mood disorder, but it involves ___________ __________.

Back 105

Major Depressive Disorder is a mood disorder, but it involves cognitive dysfunction

Front 106

Cognitive deficits in depression are _______ ________
depression than mania or schizophrenia.

Back 106

Deficits are more severe during depression
than mania or schizophrenia

Front 107

Cognitive deficits tend to be __________ ________ and
________ when the symptoms reverse (but can
persist in a sub-group of patients)

Back 107

Deficits tend to be mood dependent and
reverse when the symptoms reverse (but can
persist in a sub-group of patients).

Front 108

Hemispheric localization data re: depression is __________.

Back 108

Hemispheric localization data is equivocal.

Front 109

Which major part of the the brain is clearly implicated in the cognitive impairments in mood disorders?

Back 109

Clear the frontal lobes are implicated.

Front 110

Evidence for lack of effortful processing is
___________?

Back 110

Evidence for lack of effortful processing
equivocal.

Front 111

MDD prevalence in men vs women?

Back 111

MDD is very prevalent, afflicts more women than men,
and can emerge at almost any age.

Front 112

Depression is ___________ __________ or accompanied by other conditions.

Back 112

Depression is frequently preceded or accompanied by other conditions.

Front 113

The pathophysiology of depression _________ __________ __________.

Back 113

Likely caused by both genetic and non-genetic factors,
but its pathophysiology remains poorly understood

Front 114

A deficiency in what neurtransmitter and or abnormalities in what seem to be important in depression?

Back 114

More evidence points to monoamine deficiency and/or HPA abnormalities than other putative mechanisms.

Front 115

Neuroimaging studies suggest that abnormalities in several _________ _________ might play a role in MDD

Back 115

Neuroimaging studies suggest that abnormalities in several neural structures might play a role in MDD.

Front 116

Combined treatment for depression is better than _________.

Back 116

Combined treatment better than monotherapy

Front 117

Studies show state- and trait-like ________ _____________of mild to moderate severity in depression.

Back 117

Studies show state- and trait-like cognitive
impairments of mild to moderate severity

Front 118

Cognitive deficits are __________ __________in elderly patients with depression

Back 118

Deficits more severe in elderly patients with depression.

Front 119

Executive deficits might be more specific to which EARLY/LATE onset depression?

Back 119

Executive deficits might be more specific to LOD.

Front 120

Decreased speed and memory are common to EOD/LOD?

Back 120

Decreased speed and memory are common to both EOD and LOD.

Front 121

Psychotherapy leads to remission of symptoms in up to __% of individuals with mild-moderate MDD

Back 121

However, psychotherapy leads to remission of
symptoms in up to 50% of individuals with mild-
moderate MDD.