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4. Mood Disorders > CANMAT Guidelines: Depression Part 3 (neurostimulation etc) > Flashcards

CANMAT Guidelines: Depression Part 3 (neurostimulation etc) Flashcards

1
Q

name the first line neurostimulation treatment recommended by the guidelines for MDD?

under what conditions is this recommended?

A

tTMS

(if FAILED at least one antidepressant)

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2
Q

what level evidence is there for rTMS for MDD in the acute and maintenance phases

A

level 1 for acute and level 3 for maintenance

(has level 1 evidence for safety and tolerability)

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3
Q

what is the second line neurostimulation treatment recommended by the guidelines for MDD

A

ECT (it is first line in some situations)

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4
Q

what level evidence is there for ECT for MDD

A

level 1 for acute and maintenance, and for safety and tolerability

WE HAVE GOOD EVIDENCE ECT WORKS AND IS SAFE AND TOLERABLE

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5
Q

list two third line neurostimulation treatments for MDD

A

tDCS

VNS

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6
Q

list two investigational neurostimulation treatments for MDD

A

DBS

MST

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7
Q

what is tDCS

A

transcranial direct current stimulation

a form of brain stimulation that delivers a CONTINUOUS, LOW AMPLITUDE electrical current to a specified cortical region using SCALP electrodes

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8
Q

list some advantages of tDCS

A

ease of use

low cost

portability

potential for home based use

ability for combination with other treatments

low potential for adverse effects

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9
Q

what is the effect of ANODAL stimulation in tDCS

A

anodal stimulation over the cortex INCREASES cortical excitability through DEpolarization of neuronal membrane potential

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10
Q

what is the effect of CATHODAL stimulation in tDCS

A

cathodal stimulation DECREASES cortical excitability through HYPERpolarization of the neuronal membrane potential

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11
Q

what is the hypothesized mediator of the effects of tDCS

A

NMDA receptor-dependent mechanisms

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12
Q

are there clear parameters for the optimal delivery of tDCS

A

no cohesive summary

exact frequency and duration of stimulation have not been established

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13
Q

how is tDCS generally delivered (i.e placement of electrodes etc)

A

anodal stimulation over the left DLPFC
+
cathode used as a ground over a noncortical region

OR

anodal stimulation over the left DLPFC and cathodal stimulation over the right DLPFC

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14
Q

what is an often used parameter for frequency and intensity for tDCS treatment (to observe and antidepressant effect)

A

seems that minimum stimulation with 2 milliamperes (mA) for at least 30 min per day for 2 weeks is necessary to observe an antidepressant effect

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15
Q

is tDCS monotherapy or combo therapy with SSRI better

A

combo

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16
Q

is tDCS well tolerated

A

yes generally

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17
Q

what are the most common side effects of tDCS

A

regional effects at skin–> redness, itching, burning, heat, tingling

low rates observed of headaches, blurred vision, ear ringing, fatigue, nausea, mild euphoria, reduced concentration, disorientation, insomnia, anxiety

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18
Q

is there a risk of hypomania or mania with tDCS

A

yes–> found in study where tDCS was combined with sertraline though

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19
Q

what is rTMS

A

uses powerful (1-2.5 Tesla), focused MAGNETIC FIELD PULSES to induce electrical currents in neural tissue noninvasively via an inductor COIL placed against the SCALP

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20
Q

is anesthesia required for rTMS

A

no

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21
Q

do we have a clear understanding of the mechanism by which rTMS has antidepressant effects

A

no–> mechanisms proposed at both cell-molecular and network levels

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22
Q

what is a standard protocol for rTMS

A

once daily, 5 days per week

(there are some slower and faster schedules being investigated)

maximal effects found at about 26-28 sessions

stimulation delivered in 2-10 second trains at 10-60 sec intervals in 15-45 min sessions

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23
Q

how is stimulus intensity determined for rTMS? what is the most common stimulus intensity prarameter for rTMS?

A

stimulus intensity based on individually determined resting motor threshold (RMT–> minimum intensity to elicit muscle twitches at relaxed upper and lower extremities)

most common intensity is 110%-120% RMT

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24
Q

what are the two first line rTMS stimulation protocols

A

high frequency rTMS to left DLPFC

low frequency rTMS to right DLPFC

*there are other protocols as well but i will never remember them

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25
Q

is high frequency rTMS considered excitatory or inhibitory

A

high frequency rTMS is generally considered EXCITATORY

(low frequency rTMS generally considered inhibitory)

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26
Q

does rTMS have evidence in treating treatment resistant depression

A

rTMS targeting the left DLPFC showed superior response and remission rates vs sham in this population

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27
Q

following successful rTMS is there evidence for maintenance rTMS ongoing

A

yes–> evidence for more sustained remission with maintenance rTMS

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28
Q

is rTMS as effective as ECT

A

no–> rTMS is consistently LESS EFFECTIVE than ECT (especially for psychosis)

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29
Q

are rTMS and ECT complementary or competing treatments

A

best understood as complementary

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30
Q

is rTMS effective when ECT has failed

A

no–> response rates are poor to rTMS when ECT has failed

*consider rTMS prior to pursuing ECT

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31
Q

what are common side effects of rTMS

A

scalp pain during treatment (40%)

transient headache after treatment (30%)

SEs diminish steadily over treatment

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32
Q

are there any cognitive side effects of rTMS

A

no worsening (no difference vs sham)

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33
Q

what is the most serious rTMS adverse event

A

seizure induction

*less than 25 cases worldwide

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34
Q

what is a contraindication for high frequency rTMS

A

seizure history

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35
Q

is low frequency rTMS safe in epilepsy

A

yes

*but for most practictioners a history of seizures is a contraindication for rTMS

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36
Q

what is the incidence of seizure with rTMS?

how does this compared to baseline spontaneous risk of seizures?

A

rTMS: 0.01-0.1% risk

spontaneous: 0.07-0.09% risk

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37
Q

name two absolute contraindications to rTMS

A

metallic hardware in head (except mouth)

(many consider seizure hx absolute contraindication)

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38
Q

list 4 relative contraindications to rTMS

A

cardiac pacemaker

implantable defibrillator

hx epilepsy

brain lesion (vascular, traumatic, neoplastic, infectious, metabolic)

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39
Q

what is ECT

A

a therapeutic procedure that entails induction of a seizure by applying electrical stimulus to the brain

it is an EFFECTIVE and WELL ESTABLISHED treatment method for depression and other mental disorders

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40
Q

how is ECT delivered

A

in a controlled setting under induction of general anesthesia and the application of a muscle relaxant

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41
Q

are there any ABSOLUTE contraindications to ECT

A

no

(according to CANMAT guidelines)

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42
Q

list 7 conditions that may be associated with increased safety risk in ECT

A
  1. space occupying cerebral lesion
  2. increased ICP
  3. recent MI
  4. recent cerebral hemorrhage
  5. unstable vascular aneurysm or malformation
  6. pheochromocytoma
  7. class 4 or 5 anesthesia risk
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43
Q

what is the proposed mechanism of action of ECT

A

still being investigated

main hypotheses = seizure induced changes in neurotransmitters, neuroplasticity, and functional connectivity

i.e ECT can increase levels of brain derived neurotrophic factors (BDNF) which may contribute to the antidepressant effect

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44
Q

what effect does ECT have on brain derived neurotrophic factors

A

increases levels of BDNF which may contribute to the antidepressant effect

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45
Q

why is ECT considered second line in treatment of MDD

A

because of adverse events

but can be considered first line in some situations

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46
Q

list 3 treatment parameters of ECT to consider

A

electrode position

electrical intensity

pulse width

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47
Q

that are the three most common electrode placements in ECT

A

right unilateral

bitemporal

bifrontal

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48
Q

what is the basis of the electrical intensity used in ECT treatment

A

based on the minimum intensity to produce a generalized seizure–> SEIZURE THRESHOLD

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49
Q

what electrical intensity is generally used in bitemporal and bifrontal ECT

A

1.5-2x seizure threshold

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50
Q

what electrical intensity is generally used in RUL ECT

A

5-6x (or even up to 8x) seizure threshold

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51
Q

which electrode placement is most efficacious in ECT

A

BT, BF and RUL have EQUAL efficacy but have different cognitive side effect profiles

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52
Q

which two electrode placements in ECT are recommended first line

A

BF and RUL

BT is recommended second line due to higher rates of short term cognitive adverse effects

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53
Q

what pulse width is generally used with ECT

A

brief pulse (BP)

*clinical and research interest in ultra brief pulse width treatments

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54
Q

why might ultra brief pulse width ECT be beneficial

A

may be associated with less short term cognitive impairment and specifically the loss of autobiographical memory

*BUT ultra brief pulse width may have slower speed of improvement and require more treatments that brief pulse

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55
Q

what is the typical index course of ECT

A

6-15 treatments

*usually delivered 2-3x per week in the index course

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56
Q

are more than 3 ECT treatments per week recommended

A

no–> associated with more cognitive side effects

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57
Q

list 9 clinical indications for ECT as a FIRST LINE treatment for MDD

A
  1. acute suicidal ideation
    –level 1
  2. psychotic features
    –level 1
  3. treatment resistant depression
    –level 1
  4. repeated medication intolerance
  5. catatonic features
  6. prior favorable response to ECT
  7. rapidly deteriorating physical status
  8. during pregnancy, for any of the above indications
  9. patient preference
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58
Q

is ECT effective in treating MDD? what is the response rate?

A

it is one of the MOST effective treatments for MDD

response rates can reach 70-80% with remission rates 40-50% or higher depending on patient population and type of stimulus

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59
Q

what is the strongest predictor of non response to ECT

A

the degree of resistance to previous treatments

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60
Q

what is the response rate to ECT in patients with a previous treatment failure to psychological or pharmacolgical treatment

A

50%

(compared to 65% response for those who had not failed another treatment)

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61
Q

list clinical factors associated with higher response rates to ECT

A

older patients

psychotic features

shorter episode duration

?lesser depressive severity

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62
Q

what are the relapse/recurrence rates associated with ECT

A

also high

highest in first 6 months post ECT

relapse rates of about 50% have been observed within 1-2 years

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63
Q

how does maintenance ECT compared to pharmacotherapy post ECT

A

maintenance ECT is as effective as pharmacotherapy (in preventing relapse and recurrence)

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64
Q

what pharmacotherapy should be used post ECT for maintenance

A

an untried antidepressant
OR
nortriptyline + lithium
OR
venlafaxine + lithium

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65
Q

how does pharmacotherapy post ECT compare to continuation/maintenance ECT with regard to preventing relapse/recurrence

A

about equally effective

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66
Q

what is a typical schedule for continuation/maintenance ECT

A

weekly x 4 weeks
then
biweekly x 8 weeks
then monthly

if deteriorates, increase frequency

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67
Q

what is the impact of antidepressants post ECT on relapse rates

A

decreases relapse rates by half

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68
Q

have any studies demonstrated damage to brain structures related to administration of ECT

A

no

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69
Q

what is the mortality rate associated with ECT

A

less than 1 in 73440 treatments (0.0014%)

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70
Q

list the 3 most common side effects of ECT

A

headache (about half)

muscle soreness (20%)

nausea (up to 25%)

*most are associated with treatment, are transient and can be treated symptomatically

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71
Q

what is the rate of manic switch with ECT

A

7%

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72
Q

list possible cognitive side effects of ECT

A
  1. transient disorientation when recovering from ECT (post ictal + effects of general anesthesia)
  2. retrograde amnesia
  3. anterograde amnesia
  4. there is mild, short term impairment in memory and other cognitive domains during and immediately following a course of ECT
    –> impairments are usually TRANSIENT with recovery of cognitive functioning occurring within weeks to months after an acute course of ECT–> no eventual cognitive differences between ECT parameters including electrode placement or pulse width
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73
Q

list 3 factors associated with greater risk of cognitive impairment related to ECT

A

pre-existing cognitive impairment

older age

use of bitemporal placement

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74
Q

is the retrograde amnesia sometimes seen in ECT also transient?

A

some studies suggest PERSISTING DEFICITS

others suggest objective tests of autobiographical memory did not persist beyond 6 months post ECT

patient self reports indicate some persistent cognitive dysfunction, especially retrograde amnesia, but self reports of cognitive dysfunction are usually highly correlated with PERSISTENT DEPRESSIVE SYMPTOMS and are NOT correlated with objective testing

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75
Q

is there a benefit to treating with ADs during the ECT course (rather than sequentially after)

A

yes–> lower relapse rates

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76
Q

why might you reconsider lithium treatment in a patient undergoing ECT

A

may increase risk of side effects

higher risk of cognitive symptoms

risk of encephalopathy

risk of spontaneous seizures

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77
Q

why might you reconsider benzodiazapine or anticonvulsant treatment during a course of ECT

A

likely to raise the seizure threshold and decrease seizure efficacy

*lamotrigine may be less problematic

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78
Q

what is magnetic seizure therapy (MST)

A

noninvasive convulsive neurostimulation therapy that relies on the principle of ELECTROMAGNETIC INDUCTION to induce an electric field in the brain strong enough to elicit a generalized tonic clonic seizure

being investigated as alternative to ECT

seizure is elicited under GA with assisted ventilation and EEG monitoring

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79
Q

why might you opt for MST over ECT

A

MST has potential for fewer side effects such as cognitive dysfunction

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80
Q

how is MST performed

A

uses a neurostimulator and coil that is placed in direct contact with the skull

when electrical current passes through the coil, a strong FOCAL MAGNETIC FIELD is generated (around 2 Tesla)

magnetic field crosses the skull and soft tissue unimpeded to reach brain tissue–> induces electrical current that causes neuronal depolarization and eventually triggering seizure

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81
Q

what are the delivery parameters of MST

A

The optimal delivery parameters for MST are still being investigated.

Most studies have used a coil placement at the vertex
(i.e., Cz in 10-20 electroencephalogram [EEG] system) with a
frequency of stimulation of 100 Hz, pulse width of 0.2to 0.4 ms,
and stimulation duration of 10 seconds.

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82
Q

how often is MST given? how long is an index course?

A

usually similar to ECT

index around 12 treatments, 2-3 x per week

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83
Q

are there any studies comparing MST to sham?

A

no

84
Q

how does efficacy compare between MST and ECT

A

MST vs RUL ECT showed no significant differences in response/remission rates

but there are no studies of MST in relapse or relapse prevention

*recommended as investigational treatment alternative to ECT

85
Q

how do side effects comapre between MST and ECT

A

MST showed (compared to ECT):

lower rates of headache and muscle ache

no significant impact on retrograde and anterograde amnesia

shorter reorientation time

in MST vs RUL ECT there was no difference in neuropsych testing after 12 treatments

86
Q

what is vagus nerve stimulation (VNS)

A

an IMPLANTABLE neurostimulation technology originally approved i 1997 for treatment of drug resistant epilepsy

comprises an implantable pulse generator (IPG) which is SURGICALLY inserted underneath the skin of the chest, connected to an electrode placed in one of the VAGUS NERVES in the neck

electrical stimulation of the vagus nerve provides stimulation to the NUCLEUS TRACTUS SOLITARIUS–> in turn able to modulate multiple regions of brain via its neuronal connections to anatomically distributed subcortical and cortical regions of the brain

87
Q

what specific brain area is stimulated via the vagus nerve during VNS

A

the nucleus tractus solitarius

(which in turn is able to modulate
multiple regions of the brain via its neuronal connections to
anatomically distributed subcortical and cortical regions of
the brain)

88
Q

what are the optimal treatment parameters for VNS

A

under investigation

89
Q

is VNS approved by the US FDA

A

yes–> as adjunctive treatment for chronic/recurrent depression in those who have failed to response to 4 or more adequate antidepressant trials

90
Q

are there studies comparing VNS to sham?

A

yes–> showed NO significant differences at 12 weeks

BUT open label studies have shown response rate of about 30%

*therefore is 3rd line

91
Q

does VNS seem to be more effective in short term or longer term treatment

A

longer term–> ?antidepressant effects ACCRUE over time

median time to response seems to be between 3-9 months

effects may be sustained at 12-24 months

92
Q

what are the most common side effects of VNS

A

VOICE ALTERATION (69%)

dyspnea (30%)

pain (28%)

increased cough (26%)

*voice + cough SEs are direct effects and improve by turning VNS off

93
Q

name two possible serious adverse psychiatric events that have been associated with VNS

A

suicide + attempted suicide –> 4.6%

treatment emergent hypomania/mania –> 2.7%

94
Q

how does all cause mortality differ between treatment for MDD with VNS vs treatment as usual

A

LOWER all cause mortality (including suicide) with VNS than treatment as usual

95
Q

what is deep brain stimulation (DBS)

A

INVASIVE neurosurgical procedure involving implantation of electrodes under MRI guidance into discrete brain targets

electrodes internalized and connected to an IPG (implantable pulse generator) that is typically implanted in the chest below right clavicle

96
Q

what is currently the most common indication for DBS

A

movement disorders (more specifically Parkinsons)

–> DBS for difficult to treat psychiatric disorders including treatment resistant depression is growing research field

97
Q

what are the treatment parameters to consider in DBS

A

pulse width

frequency

amplitude

98
Q

list the four anatomical targets for DBS in the treatment of treatment resistant depression

A
  1. subcallosal cingulate white patter (SCC) (majority of reports focus on this)
  2. ventral capsule, ventral striatum (VC/VS)
  3. nucleus accumbens (NA)
  4. medial forebrain bundle (MFB)
99
Q

what are the response and remission rates currently seen in DBS

A

response between 30-60%

remission between 20-40%

at 3 or 6 months

*note that these studies done in highly treatment refractory patients

one small study (n=7) showed response rate of 85.7% and remission rate above 50%

HOWEVER–> two sham controlled RCTs of DBS were stopped early due to LACK of an efficacy signal for acute treatment resistant depression

100
Q

how effective is DBS over extended treatment

A

antidepressant effects seem to accrue over months and years of chronic stimulation with improved rates of functional and clinical outcomes observed beyond 1 year post surgery

but data does not yet demonstrate efficacy for acute treatment of TRD

likely ongoing DBS required to maintain remission

101
Q

is there evidence of negative impact of performance on neuropsych testing due to DBS

A

no–> may actually improve it

102
Q

list psychiatric adverse events associated with DBS

A

psychosis, hypomania–> transient, reversible

reports of suicidality, completed suicide–> unclear association

103
Q

list some possible non-psych adverse events associated with DBS

A

oculomotor adverse event–> blurred vision, strabismus

risks of surgical procedure itself, perioperative risks

104
Q

list 5 CAM treatments for MDD in the “physical and meditative treatments” section

A

exercise

light therapy

yoga

acupuncture

sleep deprivation

105
Q

is exercise a first or second line treatment for MDD

A

both!

first line as monotherapy for mind-moderate MDD

second line as adjunctive treatment for mod-severe MDD

106
Q

is light therapy first or second line for MDD

A

both!

first line monotherapy for seasonal (winter) MDD

second line as either mono or adjunctive treatment for mold to moderate non-seasonal MDD

107
Q

list two first line physical/meditative treatments for MDD

A

exercise and light therapy

108
Q

list 3 second line physical/meditative treatments for MDD

A

exercise

light therapy

yoga

109
Q

list 2 third line physical/meditative treatments for MDD

A

acupuncture (for mild to mod MDD)

sleep deprivation (for mod-severe MDD)

110
Q

what is the standard protocol for light therapy for MDD

A

10 000 lux during the early morning

30 min per day for 6 weeks

see response within 1-3 weeks

111
Q

what are the proposed mechanisms of light therapy for MDD

A

alteration of circadian rhythm

modulation of serotonin and catecholamine systems

112
Q

name common side effects of light therapy for MDD

A

eye strain

headache

agitation

nausea

sedation

*generally well tolerated

113
Q

what is/are the protocols for sleep deprivation in treating MDD

A

keep patients awake for an extended period of time

2-4 times over 1 week

total SD–> up to 40 hours

partial SD–> 3-4 hours of sleep per night

total SD often interspersed with partial SD or normal/recovery sleep

114
Q

is sleep deprivation effective at treating symptoms of depression

A

“continues to demonstrate rapid antidepressant effects in recent publications”

*relapse after discontinuation is often rapid

115
Q

what are the proposed mechanisms for the antidepressant effects of sleep deprivation in MDD treatment

A

increased activity of all neurotransmitter systems

increased synaptic potentiation + glial signalling

116
Q

what are the practical limitations of sleep deprivation as treatment for MDD

A

difficult to maintain use for more than a few weeks

often rapid relapse after discontinuation

117
Q

sleep deprivation in combination with what other therapy may be more practically useful than sleep deprivation alone

A

combined SD + chronotherapy (sleep phase advance)

rapid onset of efficacy, greater clinical utility + sustained response

118
Q

what is the most common side effect of sleep deprivation for MDD treatment

A

may have recurrence of panic attacks

low rates of SD-induced mania

119
Q

what is a contraindication to sleep deprivation therapy

A

epilepsy

*high risk of seizure induction

120
Q

which is more effective for exercise therapy for MDD, aerobic or anaerobic exercise

A

same–neither is superior

121
Q

how often should you work out in exercise therapy for MDD

A

30 min 3x/week for 9 weeks

122
Q

what are proposed potential mechanisms that explain the efficacy of exercise therapy for MDD

A

biological–> increased turnover of neurotransmitters, endorphins, BDNF; decreased cortisol levels

psychological–> increased self efficacy

long term benefits in MDD less clear

123
Q

what are the proposed mechanisms behind yoga therapy for MDD

A

increased turnover of dopamine and GABA

regulation of HPA axis

normalization of HR variability

124
Q

are there any side effects to yoga for MDD

A

rarely

case reports of meditation induced mania/psychosis

excessive/incorrect practice can lead to artery occlusion, neuropathy

125
Q

how often is it recommended to practice yoga for treatment of MDD

A

2-4 sessions per week for 2-3 months

126
Q

are there any first line natural health products for the treatment of MDD

A

yes–> St. John’s Wort

monotherapy for mild to moderate MDD

127
Q

list the second line natural health product treatments for MDD

A

St. Johns Wort

Omega 3

SAME-e

128
Q

list the third line natural health products for treatment of MDD

A

acetyl-L-carnitine

saffron

DHEA

folate

lavender

129
Q

are there any natural health products NOT recommended for treatment of MDD

A

inositol

tryptophan

roseroot

130
Q

what are the proposed mechanisms for how st johns wort works

A

direct effect of serotonin receptors

MAOi

neuroendorine and ion channel modulation

131
Q

what are the side effects of st johns wort

A

GI upset
headaches
skin irritation
photosensitivity
dry mouth

*risks of P450 drug interactions

*better tolerated than many SSRIs

132
Q

what are risks of st johns wort

A

reports of serotonin syndrome, hypomania if using concurrent ADs

133
Q

how is st johns wort recommended to be used for MDD treatment

A

first line monotherapy for mild-moderate MDD

second line adjunct for mod-severe MDD

134
Q

how do the guidelines recommend omega-3s be used

A

second line monotherapy for mild-mod MDD

second line adjunct for mod-severe MDD

135
Q

what is SAM-e

A

a natural substrate found in the body, including in the brain, that is thought to function as a methyl donor in various physiological processes

prescribed in europe for MDD (is OTC in canada)–> 800-1600mg po/day for 4-12 weeks

136
Q

– what is the proposed mechanism for SAM-e in the treatment of MDD

A

modulation of monoaminergic neurotransmission

137
Q

what are possible side effects of SAM-e

A

GI upset

tachycardia

sweating

headache

irritability

restlessness

anxiety

insomnia

fatigue

138
Q

what is the guidelines recommendation for use of SAM-e

A

second line adjunct for mild-mod MDD

139
Q

how do MDD symptoms tend to differ in adolescents

A

more HYPERsomnia

fewer appetite/weight changes

fewer psychotic symptoms

140
Q

what is a semi-structure interview approach for kids and teens who screen positive for MDD

A

K-SADS (kiddie schedule for affective disorders)

141
Q

what psychotherapeutic interventions are recommended in the C&A population for MDD

A

CBT + IPT

142
Q

are there clear advantages of pharmacotherapy vs psychotherapy in treating MDD in C&A populations?

A

no clear advantage for either

*combining them showed no significant differences in achieving remission or preventing relapse but combo DID reduce FUNCTIONAL IMPAIRMENT in the short term

143
Q

what approach to treatment showed greatest improvements in depressed youth who had recently attempted suicide

A

CBT for suicide prevention + pharmacotherapy

144
Q

is psychotherapy first line for MDD in depressed youth

A

yes–for mild - mod depression

145
Q

does paroxetine have evidence for efficacy in C&A population

A

no efficacy shown

146
Q

does citalopram have evidence in C&A populations

A

little evidence–> does have higher remission rates compared to placebo

147
Q

what is the first choice SSRI for depressed youth

A

FLUOXETINE

–> superior to placebo (we have the best evidence for fluoxetine)

148
Q

list 3 SSRIs that do have evidence for efficacy in treating depressed youth

A

fluoxetine

escitalopram
–> superiority on function and depression scores compared to placebo

sertraline
–> some evidence superior to placebo but small effects

149
Q

what SSRI should be avoided in patients with congenital longQT syndrome

A

citalopram

150
Q

are TCAs useful in children?

A

NO

only marginal evidence in teens, but not useful in children

151
Q

are MAOIs recommended in the C&A population

A

NO

(limited data + safety concerns)

152
Q

what is first line for mild depression in youth

A

Psychotherapy (CBT, IPT first)

153
Q

what should be the treatment approach for moderate MDD in youth

A

consider medication if psychotherapy not accessible

154
Q

what should be the treatment approach for severe MDD in youth

A

pharmacotherapy is first line

fluoxetine = first choice

escitalopram, sertraline, citalopram = second choice

155
Q

how often should you monitor youth when starting an antidepressant

A

WEEKLY for the first MONTH (both USFDA and CPA recommend this)

q2weeks for 2nd month

then after 12 weeks

(second two are only recommended by the USFDA)

*especially for more depressed patients, high SI and family conflict

156
Q

how should you titrate SSRIs in youth with MDD

A

initial LOW dose for FOUR WEEKS at least before considering increase

if only partial response after 12 weeks, CHANGE TREATMENT

157
Q

how long should you treat a youth with antidepressants after presenting with MDD

A

very little data and this is based on adult research

if no MDD hx–> 6-12 months

if hx 2 or more MDEs or 1 severe/chronic MDE–> tx for 1 year or longer

*if want to d/c, d/c with slow taper during stress free time

158
Q

according to the TORDIA trial, what should you do if less than 20% response after initial SSRI trial in depressed youth

A

switch to another SSRI

159
Q

why is venlafaxine less preferable in treatment of MDD in depressed youth

A

venlafaxine is LESS preferable as has equal response but leads to more self harm events

160
Q

is ECT recommended in kids younger than 12

A

no

use with extreme caution in tens (i.e severe MDD, TRD)

161
Q

fluoxetine can work for what other often comorbid conditions in youth with depression

A

for mild-mod AUD

oppositional symptoms

162
Q

are there ANY health canada approved antidepressants for C&A population

A

NO

163
Q

are there ANY FDA approved antidepressants for C&A populations

A

fluoxetine for ages 8+

escitalopram for ages 12+

164
Q

what is the black box warning associated with antidepressants

A

SSRI use in people under 24–> risk of increased suicidal ideation and behaviour

4% risk vs baseline 2.5% risk (1.5-2x risk)

165
Q

what is first, second and third line for mild-moderate perinatal depression

A

first line–> CBT, ITP

second line–> citalopram, escitalopram, sertraline

third line–> combo SSRI + CBT/IPT

166
Q

what three SSRIs are considered “best” in pregnancy/lactation

A

citalopram

escitalopram

sertraline

167
Q

name two antidepressants that have risks of fetal cardiac defects

A

paroxetine

clomipramine

168
Q

why aren’t MAOIs recommended for treating perinatal depression

A

interactions with anesthetics, analgesics

169
Q

what is recommended first, second and third line for severe perinatal depression

A

first line–> citalopram, sertraline, escitalopram
or combo of one of those SSRIs with CBT/IPT

second line–> other SSRIs (except paroxetine), newer ADs, TCAs

third line–> consider ECT

170
Q

list antidepressants with risk of major congenital malformations if used during pregnancy

A

paroxetine–> cardiac defects

fluoxetine (early in pregnancy)–> small increase in congenital malformations

clomipramine–> cardiac defects

171
Q

should you use fluoxetine in pregnancy

A

no–> small increase in congenital malformations

172
Q

are there risks in pregnancy of other (non-fluoxetine, paroxetine) SSRIs, buproprion, mirtazapine, SNRIs, TCAs?

A

no significant risk

173
Q

what are the risks of SSRI use generally in pregnancy

A

very modest link with SPONTANEOUS ABORTION

SHORTENED gestational duration (by 4 days)

DECREASED birth weight (by 74 grams)

174
Q

what are the symptoms of neonatal adaptation syndrome

A

jitteriness

irritability

tremor

respiratory distress

excessive crying

**NO association with increased mortality or long term neurodevelopmental problems)*

175
Q

what is the etiology of neonatal adaptation syndrome

A

SSRI exposure during THIRD trimester

15-30% of exposed infants will develop

176
Q

what antidepressants (3) have the highest risk of causing neonatal adaptation syndrome if taken by women in pregnancy

A

paroxetine

fluoxetine

venlafaxine

177
Q

how long does neonatal adaptation syndrome usually last

A

time limited–> 2-14 days

178
Q

other than neonatal adaptation syndrome, what is another risk of taking SSRIs late in pregnancy

A

persistent pulmonary hypertension of the newborn –> limited data

179
Q

is breastfeeding contraindicated in post partum depression

A

no

180
Q

what antidepressant must you absolutely avoid in breastfeeding mothers

A

doxepin

significant adverse effects in breastfeeding infants

181
Q

what is first line in mild to moderate post partum depression

A

similar to perinatal depression (CBT/IPT first, then citalopram/escitalopram/ sertraline)

182
Q

what is first line treatment for severe post partum depression

A

pharmacotherapy–> citalopram, escitalopram, sertraline

ECT can be first line, especially if psychosis is present

183
Q

can you continue breastfeeding during ECT

A

yes

184
Q

how does breastfeeding exposure compared to in utero exposure to antidepressants

A

5-10x lower exposure during breastfeeding compared to in utero

185
Q

what 3 antidepressants have the lowest relative infant dose during breastfeeding

A

sertraline

paroxetine

fluvoxamine

(minor reactions with sertraline, paroxetine)

186
Q

what 2 antidepressants have the highest rate of infant reactions when taking by breastfeeding mothers

A

citalopram

fluoxetine

187
Q

what symptoms may be seen in infants whose mothers are breastfeeding while taking an antidepressant

A

irritability

restlessness

sedation

insomnia

188
Q

how does menopause affect the risk of depression

A

increased risk of depression

increased depressive symptoms

increased risk of recurrence + new MDE

189
Q

what is the only antidepressant specifically studied via RCT for perimenopausal depression

A

desvenlafaxine

was superior to placebo

190
Q

what are the recommendations for treatment for perimenopausal depression

A

same as general adult population due to lack of data

191
Q

is HRT considered effective augmentation treatment for perimenopausal depression

A

perimenopause–> estrogen superior to placebo

post menopause–> transdermal estradiol NOT superior to placebo

post menopause–> methyltestosterone superior to placebo

192
Q

are hormonal agents first line for treating depression around menopause

A

no–> second line

for women who understand the risks and have no contraindications

193
Q

what is different about late life depression (above age 60)

A

worse prognosis

more chronic course

higher relapse rates

more medical comorbidity, cognitive impairment, mortality

may be DEMENTIA PRODROME

194
Q

what is the vascular depression hypothesis

A

considers cerebrovascular disease as predisposing/precipitating/perpetuating factor for depression

affects FRONTOSTRIATAL circuitry–> depression and cognitive impairment

195
Q

which psychotherapy has the strongest evidence in late life depression

A

(vs supportive therapy)

Problem Solving Therapy

showed significant decrease in depression scores and decreased disability

196
Q

what age is considered “young-old”? what about “old-old”

A

young-old = under 75

old old is 75 and above

197
Q

how do you titrate antidepressants in older people

A

start low and go slow (and keep going)

suggest longer AD trials up to 10-12 weeks

198
Q

list 3 changes in pharmacokinetics that occur with aging

A
  1. decrease absorption rate and bioavailability
  2. increased half life for lipid soluble drugs
  3. increased concentration for water-soluble drugs/metabolites
199
Q

what antidepressant side effects are more common in the elderly

A

bone loss

serotonin syndrome

NMS

EPS

falls, hyponatremia, GI bleeding (with SSRIs)

QTc prolongation (citalopram)

200
Q

what medication has evidence for treating severe MDD in old-old people

A

citalopram

(also better tolerability and fewer drug interactions)

201
Q

what SSRIs are often avoided in the elderly

A

paroxetine–> anticholinergic

fluoxetine–> drug interactions

(in RCTs there is positive evidence for efficacy though in late life depression)

202
Q

what SSRI is often clinically considered first line for late life depression

A

citalopram/escitalopram

due to better tolerability and fewer drug interactions but a RCT showed no superiority over placebo in the elderly

203
Q

is there evidence for vortioxetine, duloxetine and agomelatine in treating late life depression

A

yes–> improved depression scores

vortioxetine and duloxetine also improved verbal learning and vortioxetine improved processing speed

204
Q

what two atypical antipsychotics have evidence as treatment for late life depression

A

aripiprazole adjunctive + AD = EFFECTIVE (more common side effects)

quetiapine XR monotherapy = EFFECTIVE (higher dropout rates, less effective over age 75)

205
Q

is there evidence that using a sedating AD for sleep improves overall outcomes in the treatment of late life depression

A

no

206
Q

how do you approach treatment of treatment resistant depression in populations above age 55

A

50% respond to switch or augmentation

lithium augmentation has the most consistent data

sequential treatment strategy has the highest response rates

4. Mood Disorders (17 decks)

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