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ANTIDEPRESSANTS
PRESENTER – Dr. Sriram.R, PG MD Psychiatry
CHAIRPERSON – Dr. RAJ KUMAR, Associate Prof of
Psychiatry
ORGANISATION
• NEUROBIOLOGY OF DEPRESSION
• GENETICS OF DEPRESSION
• RESPONSE, REMISSION, RECOVERY, RELAPSE AND RECURRENCE
• INDICATIONS OF AD
• MODE OF ACTION OF AD
• CLASSIFICATION OF AD
• ADJUNCTIVETREATMENTS
• HOW LONGTOTREAT?
• REFERENCES
NEUROBIOLOGY OF DEPRESSION
• Amine hypothesis: Depression is associated with decreased
amine-dependent synaptic transmission.
• Several brain circuits have also become dysfunctional.
• Almost all antidepressants affect metabolism or reuptake of
serotonin, norepinephrine, or both.
• Some are also selective antagonists of serotonin or
norepinephrine.
• The full clinical effects of drugs requires 4-8 weeks.
NEUROBIOLOGY OF DEPRESSION
Unipolar depression
I. Emotional processing
Increased amygdala activation to negative scenes, fearful faces
Decreased or nil amygdala activation to happy faces
Decreased VmPFC activity during sad mood.
II. Executive control
Decreased DLPFC activity during memory and attention tasks
III. Emotional regulation
Impaired top down processing.
GENETICS
BIPOLAR DISORDER
Linkage - 9p, 10q, 14q, 13q, 18, 13q, 22q, 6q, 12q
Association – 5HT Transporter, MAO-A Inhibitor, COMT, BDNF, Tyrosine
Hydroxylase, D- Amino Acid Oxidase Activator, DISC 1, DISC 2.
UNIPOLAR DEPRESSION
Linkage – 15q, 17p, 8p, 12q
Association – 5HT Transporter Linked Polymorphic Region( 5HTTLPR)
Indications of ADs
• Depression
Moderate-Severe, Atypical, SAD, Depressive episode of Bipolar disorder.
• Anxiety disorders
GAD, Panic Disorder, SocialAnxiety, Adjustment disorders, Agoraphobia,OCD,
PTSD.
• Others :
Enuresis (bedwetting), neuropathic pain, Eating disorders (Bulimia), chronic pain
etc.
Mode of Action of ADs
Mode of Action of ADs
All antidepressants function by increasing availability of
monoamines (5-HT, NA or DA) by one of the following methods:
• Presynaptic inhibition of reuptake of 5-HT, NA or DA.
• Antagonist activity at presynaptic inhibitory 5HT or NA receptors
which enhances neurotransmitter release.
• Inhibition of Monoaminase oxidase, reducing NT breakdown.
• Increasing availability of NT precursors.
Initial resolution of depressive symptoms takes minimum of 2-4 weeks.
Classification
Broadly into 2Types:
• Re-uptake Inhibitors
• Enzyme Inhibitors
Classification
Monoamine oxidase inhibitors (MAOIs)
• Irreversible
• Reversible
• Noradrenergic and specific serotonergic
antidepressant (NaSSA)
• Tetracyclic antidepressants (TeCAs)
• Selective serotonin reuptake inhibitors (SSRIs)
• Serotonin-norepinephrine reuptake inhibitors
(SNRIs)
• Norepinephrine reuptake inhibitors (NRIs)
• Tricyclic antidepressants (TCAs)
• Norepinephrine-dopamine reuptake inhibitors
(NDRIs)
• Serotonin antagonist and reuptake inhibitors
(SARIs)
SSRIs (Selective serotonin reuptake inhibitors)
Mechanism: Increases 5HT in synaptic cleft.
• Citalopram (Cipram)
• Escitalopram (Cipralex, Citanew, Neolexa)
• Paroxetine (Paroxin, Seroxat)
• Fluoxetine (Prozac, Depex)
• Fluvoxamine (Faverin)
• Sertraline (Zoloft, Sert):
Indications
• Depression
• Panic Disorder with agoraphobia
• Social Anxiety/ GAD/ OCD
• Bulimia
• PTSD
• Off-label uses of SSRIs are follows -
• The antiorgasmic effects of SSRIs make them useful as a treatment for men with
premature ejaculation. SSRIs permit intercourse for significantly longer –
fluoxetine and sertraline
• SSRIs diminish the average time per day spent in unconventional sexual fantasies,
urges, and activities
• Sertraline and fluvoxamine have been shown in controlled and open-label trials to
mitigate aggressiveness, self-injurious behavior, repetitive behaviors, some degree
of language delay, and, rarely, lack of social relatedness in adults with autistic
spectrum disorders.
• Fluoxetine has been reported to be effective for features of autism in children,
adolescents, and adults.
• Concurrent administration of an SSRI with an MAOI, L-tryptophan, or
lithium can raise plasma serotonin concentrations to toxic levels, producing
a constellation of symptoms called the serotonin syndrome
• This serious and possibly fatal syndrome of serotonin overstimulation is
composed, in order of appearance as the condition worsens, of (1) diarrhea;
(2) restlessness; (3) extreme agitation, hyperreflexia, and autonomic
instability with possible rapid fluctuations in vital signs; (4) myoclonus,
seizures, hyperthermia, uncontrollable shivering, and rigidity; and (5)
delirium, coma, status epilepticus, cardiovascular collapse, and death.
Side-effects
• GI discomfort/ nausea
• Sexual dysfunction
• Sleep disturbance
• Dry mouth
• Tremor
• Headache
• Anxiety/ restlessness.
• Fatigue
Caution:
• Be aware of interactions-inhibitory
effects on P450 & changes with
alcohol, anticoagulants, MAOIs,
TCA, smoking etc.
TCAs (Tricyclic antidepressants )
• Amitriptyline (Tryptanol)
• Clomipramine (Clomfranil)
• Desipramine (Norpramin,Pertofrane)
• Dosulepin (Prothiaden)
• Doxepin (Doxin)
• Imipramine (Tofranil, Imidol)
• Nortriptyline (Sensival)
TRICYCLICS ANDTETRACYCLICS
TCA Mechanism
Mechanism:
• Reuptake inhibition
NA, 5HT & DA.
Indications
• Depression
• Nocturnal Enuresis (Amitriptyline/ Imipramine)
• Phobic/Obsessional States
• Cataplexy with narcolepsy
• The treatment of a major depressive episode and the prophylactic
treatment of major depressive disorder are the principal indications for
usingTCAs
• Imipramine is theTCA most studied for panic disorder with agoraphobia
• Doxepin – GAD
• OCD appears to respond specifically to clomipramine, as well as the SSRIs
• Amitriptyline is theTCA most often used in pain syndromes
• Clomipramine - Premature ejaculation, movement disorders, and
compulsive behavior in children with autistic disorders
Side-effects
• Dry mouth,
• Blurred vision,
• Sedation,
• Orthostatic hypotension,
• Constipation,
• urinary incontinence.
• Disorientation or confusion
Caution:
• Arrhythmias & ECG changes. Monitor
Cardiac function, LFTs, UCEs.
• Should be used cautiously in elderly.
Overdose ofTCAs
• Are extremely dangerous in overdose (amoxapine and maprotiline
though not allTCA are as dangerous).
• More than 1 g of a tricyclic is potentially lethal
• TCAs increase suicidal risks.
• Manifestations are: mydriasis, respiratory depression, seizure, cardiac
arrhythmia and coma
TCA overdosage. Prolonged QRS interval and supraventricular
tachycardia with progressive widening of QRS complexes mimics
ventricular tachycardia.
SNRIs (Serotonin-norepinephrine reuptake inhibitors )
Mechanism: Similar to SSRI, Inhibit 5HT & NA (high doses DA)
• Venlafaxine (Effexor)
• Desvenlafaxine
• Duloxetine (Oxcym DR, Hapibar, Lyta)
• Levomilnacipran (Fetzima)
• Tramadol (Tramal, Ultram)
• Sibutramine (Meridia, Reductil)
Side-effects: Similar to SSRIs & may cause HTN.
• Venlafaxine has higher remission rates in depression than SSRIs by 6%
• The extended-release formulation of venlafaxine is approved for treatment of
GAD, SAD and panic disorder
• Venlafaxine may be beneficial in the treatment of OCD, agoraphobia, ADHD, and in
patients with a dual diagnosis of depression and cocaine dependence
• Duloxetine is formulated as a delayed-release capsule to reduce the risk of severe
nausea associated with the drug and used for depression, GAD, diabetic
neuropathy and stress urinary incontinence
• DVS - depression and for the alleviation of vasomotor symptoms (VMS) associated
with menopause
MAOIs (Monoamine oxidase inhibitors)
• Irreversible inhibition of
• MAO-A (acts on NA, DA, 5HT &Tyramine) &
• MAO-B (acts on DA,Tyramine,
Phenylethylamine, benzylamine) leading to
accumulation of monoamines in
Synaptic Cleft.
• RIMAs: Reversible inhibition of
MAO-A.
MAOIs (Monoamine oxidase inhibitors)
Irreversible
• Isocarboxazid (Marplan)
• Phenelzine (Nardil)
• Selegiline (Selgin, Eklin)
Reversible
• Moclobemide (Aurorix, Manerix)
• Pirlindole (Pirazidol)
Indications
• Depression (atypical)
• Parkinson's Disease,
• Migraine prophylaxis
• Other disorders: panic disorder with agoraphobia, social phobia, bulimia,
PTSD, borderline personality disorder, and bipolar depression.
Side-Effects
Caution:
• Dietary restriction (Tyramine) e.g:
cheese, chocolate, wine, beans &
soy products.
• Serotonin Syndrome: Life-
threatening condition with
somatic, autonomic & cognitive
effects-Tachycardia, myoclonus,
tremors, altered Mental status,
hyperthermia, DIC, metabolic
disturbances.
• Hypertensive crisis
• Dizziness/ Headaches
• Hepatotoxicity
• Sleep disturbance
• Weight gain
• Sexual dysfunction
• Drug Interactions
Tetracyclic antidepressants (TeCAs)
Mode: Similar toTCA without anticholinergic SE
Indications: TCA with sedation.
S/E- Cardiotoxicity
• Mirtazapine (Remeron) - NaSSA
• Mianserin (Bolvidon, Norval,Tolvon)
• Amoxapine (Asendin)
• Maprotiline (Ludiomil)
Noradrenergic and specific serotonergic antidepressant (NaSSA)
Mode: α2 inhibitor (^NA/5HT), 5HT1, 5HT2 antagonist.
Indications: Depression (+anxiety,wt loss) adjunct SSRI/venlafaxine to improve SxD, GI discomfort.
Advantages: LowToxicity, less sexual dysfunction & GI upset.
• Mirtazapine (Remeron) is unique among drugs used to treat major
depression in that it increases both norepinephrine and serotonin through a
mechanism other than reuptake blockade
• Mirtazapine is effective for the treatment of depression.
• It is highly sedating, making it a reasonable choice for use in depressed
patients with severe or long-standing insomnia
• Mirtazapine is often combined with SSRIs or venlafaxine (Effexor) to
augment antidepressant response or counteract serotonergic side effects of
those drugs
MIRTAZAPINE
(SARIs)
Serotonin antagonist and reuptake inhibitors
Mode: 5HT reuptake inhibitor & antagonist.
(sedation/ antihistamine)
Indication: Depression (+insomnia) /Anxiety
Advantage: Less antimuscranic/ cardiotoxic thanTCA.
• Trazodone (Deprel)
• Etoperidone (Axiomin, Etonin)
• Nefazodone (Serzone, Nefadar)
• Trazodone is structurally related to nefazodone (Serzone)
• The main indication for the use of trazodone is major depressive disorder
• Trazodone is a first-line agent for the treatment of insomnia because of
its marked sedative qualities and favorable effects on sleep architecture
• Trazodone is associated with an increased risk of priapism
TRAZODONE
• Structurally related to trazodone, not routinely used
• Used for treating major depression, panic disorder and panic with comorbid
depression or depressive symptoms, of generalized anxiety disorder, and of
premenstrual dysphoric disorder, and for the management of chronic pain
• increases sleep continuity
• Also of use in patients with PTSD and chronic fatigue syndrome
NEFAZODONE
• Norepinephrine-dopamine reuptake inhibitor (NDRI) - Bupropion (Wellbutrin, Zyban)
Mode: NA/DA reuptake inhibition
Indications: Depression (with marked psychomotor retardation or hypersomnia),
Nicotine/stimulants dependence, ADHD.
Advantage: Unusual mode of action-alerting effects, controls impulse disorders & secondary
benefits as AD.
S/E: Seizures & hypersensitivity.
• Bupropion is a monocyclic aminoketone
• A side-effect profile characterized by little risk of sexual dysfunction or
sedation, and with modest weight loss during acute and long-term
treatmentComparable to SSRIs in treating depression, even though SSRI
are first line
• Bupropion - prevents seasonal major depressive episodes in patients with a
history of SAD
BUPROPION
• Norepinephrine reuptake inhibitors (NRIs)-
Indication:Atypical Depression
Reboxetine (Edronax)
MELATONIN AGONISTS
• Ramelteon essentially mimics melatonin's sleep-promoting properties. It has high
affinity for melatonin MT1 and MT2 receptors in the brain
• Ramelteon mainly shortens latency to sleep onset and, to a lesser extent, increases
total duration of sleep.
• Melatonin (N-acetyl-5 methoxytryptamine) is a hormone mainly produced at night
in the pineal gland. Its secretion is stimulated by the dark and inhibited by light
• It is hypothesized that the antidepressant-like activity of Agomelatine most
probably involves a combination of both its melatonin agonist and 5-HT2C
receptor antagonist properties
Adjunctive treatments
Itself doesn’t possess antidepressant quality but works in combination.
Atypical antipsychotics
• Aripiprazole (Aripip)
• Olanzapine (Olanzia,Amprexa)
• Quetiapine (Qusel)
• Risperidone (Risperdal,Persch, Neoris)
Others
• Carbamazepine
• Lamotrigine (Lamictal)
• Lithium salts
• Triiodothyronine (T3; a thyroid hormone)
• SSRIs are not sedative, safe in overdose and have mild adverse
effects so they are widely prescribed.
• Finding the right drug and the right dose must be accomplished
empirically.
• If it is the first depressive episode and if the treatment was
satisfactory, withdraw treatment after 6-9 months.
• A patient who has had previous episodes of depression is a
candidate for maintenance therapy.
• The duration of maintenance treatment varies and may
continue indefinitely.
REFERENCES
• KAPLAN AND SADOCK’S COMPREHENSIVETEXTBOOK OF PSYCHIATRY,
9TH EDITION
• STAHL’S ESSENTIAL PSYCHOPHARMACOLOGY – 4th EDITION
• MAUDSLEY’S PRESCRIBING GUIDELINES – 10TH EDITION
THANKYOU

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Antidepressants

  • 1. ANTIDEPRESSANTS PRESENTER – Dr. Sriram.R, PG MD Psychiatry CHAIRPERSON – Dr. RAJ KUMAR, Associate Prof of Psychiatry
  • 2. ORGANISATION • NEUROBIOLOGY OF DEPRESSION • GENETICS OF DEPRESSION • RESPONSE, REMISSION, RECOVERY, RELAPSE AND RECURRENCE • INDICATIONS OF AD • MODE OF ACTION OF AD • CLASSIFICATION OF AD • ADJUNCTIVETREATMENTS • HOW LONGTOTREAT? • REFERENCES
  • 3. NEUROBIOLOGY OF DEPRESSION • Amine hypothesis: Depression is associated with decreased amine-dependent synaptic transmission. • Several brain circuits have also become dysfunctional. • Almost all antidepressants affect metabolism or reuptake of serotonin, norepinephrine, or both. • Some are also selective antagonists of serotonin or norepinephrine. • The full clinical effects of drugs requires 4-8 weeks.
  • 4.
  • 5. NEUROBIOLOGY OF DEPRESSION Unipolar depression I. Emotional processing Increased amygdala activation to negative scenes, fearful faces Decreased or nil amygdala activation to happy faces Decreased VmPFC activity during sad mood. II. Executive control Decreased DLPFC activity during memory and attention tasks III. Emotional regulation Impaired top down processing.
  • 6. GENETICS BIPOLAR DISORDER Linkage - 9p, 10q, 14q, 13q, 18, 13q, 22q, 6q, 12q Association – 5HT Transporter, MAO-A Inhibitor, COMT, BDNF, Tyrosine Hydroxylase, D- Amino Acid Oxidase Activator, DISC 1, DISC 2. UNIPOLAR DEPRESSION Linkage – 15q, 17p, 8p, 12q Association – 5HT Transporter Linked Polymorphic Region( 5HTTLPR)
  • 7.
  • 8.
  • 9.
  • 10. Indications of ADs • Depression Moderate-Severe, Atypical, SAD, Depressive episode of Bipolar disorder. • Anxiety disorders GAD, Panic Disorder, SocialAnxiety, Adjustment disorders, Agoraphobia,OCD, PTSD. • Others : Enuresis (bedwetting), neuropathic pain, Eating disorders (Bulimia), chronic pain etc.
  • 11. Mode of Action of ADs
  • 12. Mode of Action of ADs All antidepressants function by increasing availability of monoamines (5-HT, NA or DA) by one of the following methods: • Presynaptic inhibition of reuptake of 5-HT, NA or DA. • Antagonist activity at presynaptic inhibitory 5HT or NA receptors which enhances neurotransmitter release. • Inhibition of Monoaminase oxidase, reducing NT breakdown. • Increasing availability of NT precursors. Initial resolution of depressive symptoms takes minimum of 2-4 weeks.
  • 13. Classification Broadly into 2Types: • Re-uptake Inhibitors • Enzyme Inhibitors
  • 14. Classification Monoamine oxidase inhibitors (MAOIs) • Irreversible • Reversible • Noradrenergic and specific serotonergic antidepressant (NaSSA) • Tetracyclic antidepressants (TeCAs) • Selective serotonin reuptake inhibitors (SSRIs) • Serotonin-norepinephrine reuptake inhibitors (SNRIs) • Norepinephrine reuptake inhibitors (NRIs) • Tricyclic antidepressants (TCAs) • Norepinephrine-dopamine reuptake inhibitors (NDRIs) • Serotonin antagonist and reuptake inhibitors (SARIs)
  • 15. SSRIs (Selective serotonin reuptake inhibitors) Mechanism: Increases 5HT in synaptic cleft. • Citalopram (Cipram) • Escitalopram (Cipralex, Citanew, Neolexa) • Paroxetine (Paroxin, Seroxat) • Fluoxetine (Prozac, Depex) • Fluvoxamine (Faverin) • Sertraline (Zoloft, Sert):
  • 16. Indications • Depression • Panic Disorder with agoraphobia • Social Anxiety/ GAD/ OCD • Bulimia • PTSD
  • 17.
  • 18.
  • 19.
  • 20.
  • 21.
  • 22. • Off-label uses of SSRIs are follows - • The antiorgasmic effects of SSRIs make them useful as a treatment for men with premature ejaculation. SSRIs permit intercourse for significantly longer – fluoxetine and sertraline • SSRIs diminish the average time per day spent in unconventional sexual fantasies, urges, and activities • Sertraline and fluvoxamine have been shown in controlled and open-label trials to mitigate aggressiveness, self-injurious behavior, repetitive behaviors, some degree of language delay, and, rarely, lack of social relatedness in adults with autistic spectrum disorders. • Fluoxetine has been reported to be effective for features of autism in children, adolescents, and adults.
  • 23. • Concurrent administration of an SSRI with an MAOI, L-tryptophan, or lithium can raise plasma serotonin concentrations to toxic levels, producing a constellation of symptoms called the serotonin syndrome • This serious and possibly fatal syndrome of serotonin overstimulation is composed, in order of appearance as the condition worsens, of (1) diarrhea; (2) restlessness; (3) extreme agitation, hyperreflexia, and autonomic instability with possible rapid fluctuations in vital signs; (4) myoclonus, seizures, hyperthermia, uncontrollable shivering, and rigidity; and (5) delirium, coma, status epilepticus, cardiovascular collapse, and death.
  • 24. Side-effects • GI discomfort/ nausea • Sexual dysfunction • Sleep disturbance • Dry mouth • Tremor • Headache • Anxiety/ restlessness. • Fatigue Caution: • Be aware of interactions-inhibitory effects on P450 & changes with alcohol, anticoagulants, MAOIs, TCA, smoking etc.
  • 25. TCAs (Tricyclic antidepressants ) • Amitriptyline (Tryptanol) • Clomipramine (Clomfranil) • Desipramine (Norpramin,Pertofrane) • Dosulepin (Prothiaden) • Doxepin (Doxin) • Imipramine (Tofranil, Imidol) • Nortriptyline (Sensival)
  • 27.
  • 28.
  • 29. TCA Mechanism Mechanism: • Reuptake inhibition NA, 5HT & DA.
  • 30. Indications • Depression • Nocturnal Enuresis (Amitriptyline/ Imipramine) • Phobic/Obsessional States • Cataplexy with narcolepsy
  • 31. • The treatment of a major depressive episode and the prophylactic treatment of major depressive disorder are the principal indications for usingTCAs • Imipramine is theTCA most studied for panic disorder with agoraphobia • Doxepin – GAD • OCD appears to respond specifically to clomipramine, as well as the SSRIs • Amitriptyline is theTCA most often used in pain syndromes • Clomipramine - Premature ejaculation, movement disorders, and compulsive behavior in children with autistic disorders
  • 32. Side-effects • Dry mouth, • Blurred vision, • Sedation, • Orthostatic hypotension, • Constipation, • urinary incontinence. • Disorientation or confusion Caution: • Arrhythmias & ECG changes. Monitor Cardiac function, LFTs, UCEs. • Should be used cautiously in elderly.
  • 33. Overdose ofTCAs • Are extremely dangerous in overdose (amoxapine and maprotiline though not allTCA are as dangerous). • More than 1 g of a tricyclic is potentially lethal • TCAs increase suicidal risks. • Manifestations are: mydriasis, respiratory depression, seizure, cardiac arrhythmia and coma
  • 34. TCA overdosage. Prolonged QRS interval and supraventricular tachycardia with progressive widening of QRS complexes mimics ventricular tachycardia.
  • 35. SNRIs (Serotonin-norepinephrine reuptake inhibitors ) Mechanism: Similar to SSRI, Inhibit 5HT & NA (high doses DA) • Venlafaxine (Effexor) • Desvenlafaxine • Duloxetine (Oxcym DR, Hapibar, Lyta) • Levomilnacipran (Fetzima) • Tramadol (Tramal, Ultram) • Sibutramine (Meridia, Reductil) Side-effects: Similar to SSRIs & may cause HTN.
  • 36.
  • 37.
  • 38. • Venlafaxine has higher remission rates in depression than SSRIs by 6% • The extended-release formulation of venlafaxine is approved for treatment of GAD, SAD and panic disorder • Venlafaxine may be beneficial in the treatment of OCD, agoraphobia, ADHD, and in patients with a dual diagnosis of depression and cocaine dependence • Duloxetine is formulated as a delayed-release capsule to reduce the risk of severe nausea associated with the drug and used for depression, GAD, diabetic neuropathy and stress urinary incontinence • DVS - depression and for the alleviation of vasomotor symptoms (VMS) associated with menopause
  • 39. MAOIs (Monoamine oxidase inhibitors) • Irreversible inhibition of • MAO-A (acts on NA, DA, 5HT &Tyramine) & • MAO-B (acts on DA,Tyramine, Phenylethylamine, benzylamine) leading to accumulation of monoamines in Synaptic Cleft. • RIMAs: Reversible inhibition of MAO-A.
  • 40. MAOIs (Monoamine oxidase inhibitors) Irreversible • Isocarboxazid (Marplan) • Phenelzine (Nardil) • Selegiline (Selgin, Eklin) Reversible • Moclobemide (Aurorix, Manerix) • Pirlindole (Pirazidol)
  • 41. Indications • Depression (atypical) • Parkinson's Disease, • Migraine prophylaxis • Other disorders: panic disorder with agoraphobia, social phobia, bulimia, PTSD, borderline personality disorder, and bipolar depression.
  • 42.
  • 43.
  • 44. Side-Effects Caution: • Dietary restriction (Tyramine) e.g: cheese, chocolate, wine, beans & soy products. • Serotonin Syndrome: Life- threatening condition with somatic, autonomic & cognitive effects-Tachycardia, myoclonus, tremors, altered Mental status, hyperthermia, DIC, metabolic disturbances. • Hypertensive crisis • Dizziness/ Headaches • Hepatotoxicity • Sleep disturbance • Weight gain • Sexual dysfunction • Drug Interactions
  • 45. Tetracyclic antidepressants (TeCAs) Mode: Similar toTCA without anticholinergic SE Indications: TCA with sedation. S/E- Cardiotoxicity • Mirtazapine (Remeron) - NaSSA • Mianserin (Bolvidon, Norval,Tolvon) • Amoxapine (Asendin) • Maprotiline (Ludiomil) Noradrenergic and specific serotonergic antidepressant (NaSSA) Mode: α2 inhibitor (^NA/5HT), 5HT1, 5HT2 antagonist. Indications: Depression (+anxiety,wt loss) adjunct SSRI/venlafaxine to improve SxD, GI discomfort. Advantages: LowToxicity, less sexual dysfunction & GI upset.
  • 46.
  • 47. • Mirtazapine (Remeron) is unique among drugs used to treat major depression in that it increases both norepinephrine and serotonin through a mechanism other than reuptake blockade • Mirtazapine is effective for the treatment of depression. • It is highly sedating, making it a reasonable choice for use in depressed patients with severe or long-standing insomnia • Mirtazapine is often combined with SSRIs or venlafaxine (Effexor) to augment antidepressant response or counteract serotonergic side effects of those drugs MIRTAZAPINE
  • 48. (SARIs) Serotonin antagonist and reuptake inhibitors Mode: 5HT reuptake inhibitor & antagonist. (sedation/ antihistamine) Indication: Depression (+insomnia) /Anxiety Advantage: Less antimuscranic/ cardiotoxic thanTCA. • Trazodone (Deprel) • Etoperidone (Axiomin, Etonin) • Nefazodone (Serzone, Nefadar)
  • 49. • Trazodone is structurally related to nefazodone (Serzone) • The main indication for the use of trazodone is major depressive disorder • Trazodone is a first-line agent for the treatment of insomnia because of its marked sedative qualities and favorable effects on sleep architecture • Trazodone is associated with an increased risk of priapism TRAZODONE
  • 50. • Structurally related to trazodone, not routinely used • Used for treating major depression, panic disorder and panic with comorbid depression or depressive symptoms, of generalized anxiety disorder, and of premenstrual dysphoric disorder, and for the management of chronic pain • increases sleep continuity • Also of use in patients with PTSD and chronic fatigue syndrome NEFAZODONE
  • 51. • Norepinephrine-dopamine reuptake inhibitor (NDRI) - Bupropion (Wellbutrin, Zyban) Mode: NA/DA reuptake inhibition Indications: Depression (with marked psychomotor retardation or hypersomnia), Nicotine/stimulants dependence, ADHD. Advantage: Unusual mode of action-alerting effects, controls impulse disorders & secondary benefits as AD. S/E: Seizures & hypersensitivity.
  • 52. • Bupropion is a monocyclic aminoketone • A side-effect profile characterized by little risk of sexual dysfunction or sedation, and with modest weight loss during acute and long-term treatmentComparable to SSRIs in treating depression, even though SSRI are first line • Bupropion - prevents seasonal major depressive episodes in patients with a history of SAD BUPROPION
  • 53. • Norepinephrine reuptake inhibitors (NRIs)- Indication:Atypical Depression Reboxetine (Edronax)
  • 54.
  • 55. MELATONIN AGONISTS • Ramelteon essentially mimics melatonin's sleep-promoting properties. It has high affinity for melatonin MT1 and MT2 receptors in the brain • Ramelteon mainly shortens latency to sleep onset and, to a lesser extent, increases total duration of sleep. • Melatonin (N-acetyl-5 methoxytryptamine) is a hormone mainly produced at night in the pineal gland. Its secretion is stimulated by the dark and inhibited by light • It is hypothesized that the antidepressant-like activity of Agomelatine most probably involves a combination of both its melatonin agonist and 5-HT2C receptor antagonist properties
  • 56. Adjunctive treatments Itself doesn’t possess antidepressant quality but works in combination. Atypical antipsychotics • Aripiprazole (Aripip) • Olanzapine (Olanzia,Amprexa) • Quetiapine (Qusel) • Risperidone (Risperdal,Persch, Neoris) Others • Carbamazepine • Lamotrigine (Lamictal) • Lithium salts • Triiodothyronine (T3; a thyroid hormone)
  • 57. • SSRIs are not sedative, safe in overdose and have mild adverse effects so they are widely prescribed. • Finding the right drug and the right dose must be accomplished empirically. • If it is the first depressive episode and if the treatment was satisfactory, withdraw treatment after 6-9 months. • A patient who has had previous episodes of depression is a candidate for maintenance therapy. • The duration of maintenance treatment varies and may continue indefinitely.
  • 58. REFERENCES • KAPLAN AND SADOCK’S COMPREHENSIVETEXTBOOK OF PSYCHIATRY, 9TH EDITION • STAHL’S ESSENTIAL PSYCHOPHARMACOLOGY – 4th EDITION • MAUDSLEY’S PRESCRIBING GUIDELINES – 10TH EDITION