STAHL'S ESSENTIAL PSYCHOPHARMACOLOGY
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission
Stem
A 34-year-old woman with major depressive disorder has partial
response to an SSRI (sertraline 100 mg daily) after 8 weeks:
mood improved but she reports persistent anergia and
psychomotor slowing. She has no cardiac disease and desires
treatment that may increase dopaminergic tone without
worsening anxiety. Which mechanism-based pharmacologic
change best fits Stahl’s neurotransmission framework?
Options
A. Add bupropion (norepinephrine–dopamine reuptake
,inhibitor).
B. Switch to venlafaxine (SNRI) at equivalent serotonergic
potency.
C. Add low-dose amisulpride (selective D2/D3 antagonist).
D. Augment with low-dose mirtazapine (α2 antagonist; 5-HT2/3
blockade).
Correct answer
A
Rationales
Correct (A): Bupropion blocks DAT and NET, increasing synaptic
dopamine and norepinephrine in projection areas tied to
motivation and psychomotor drive. Stahl’s discussion of
transporter blockade predicts improved anergia without
significant direct serotonergic stimulation that can worsen
sexual dysfunction or activation-related anxiety. Its
dopaminergic enhancement aligns with the symptom cluster.
Incorrect (B): Venlafaxine increases norepinephrine at higher
doses but has less direct DAT blockade; it may modestly
improve energy via NE but is less dopaminergic than bupropion
per transporter profiles.
Incorrect (C): Amisulpride is a D2/D3 antagonist in clinical
doses—antagonism would worsen, not improve, dopaminergic
anergia.
Incorrect (D): Mirtazapine’s α2 antagonism increases NE/5-HT
release but predominantly increases
,noradrenergic/serotonergic tone and sedation via H1; it does
not selectively boost dopamine in circuits mediating motivation.
Teaching Point
Target DAT/NET blockade to address antidepressant-resistant
anergia.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission
Stem
A 62-year-old man with Parkinson disease is treated with
levodopa/carbidopa but develops troublesome dyskinesias. His
psychiatrist considers adding an agent to reduce peak-dose
dyskinesia by modulating glutamatergic synaptic plasticity
rather than further altering dopaminergic synaptic availability.
Which mechanism aligns with this goal?
Options
A. Add amantadine (NMDA receptor antagonist).
B. Add entacapone (COMT inhibitor).
C. Add pramipexole (D2/D3 agonist).
D. Increase carbidopa to enhance peripheral decarboxylation
blockade.
, Correct answer
A
Rationales
Correct (A): Amantadine is an NMDA receptor antagonist that
reduces glutamate-mediated excitatory transmission implicated
in the pathophysiology of levodopa-induced dyskinesia; Stahl
emphasizes NMDA modulation of synaptic plasticity and motor
output, making amantadine mechanismally appropriate.
Incorrect (B): Entacapone increases CNS levodopa availability
via COMT inhibition and may worsen dyskinesia by increasing
dopaminergic peaks rather than correcting glutamatergic
hyperactivity.
Incorrect (C): Pramipexole is a dopaminergic agonist that can
alter motor response and possibly exacerbate dyskinesia; it
doesn’t directly modulate NMDA-mediated plasticity.
Incorrect (D): Increasing carbidopa increases peripheral
inhibition of decarboxylation but does not reduce central
glutamatergic contributions to dyskinesia; it alters levodopa
dosing effects peripherally.
Teaching Point
NMDA antagonism can reduce levodopa-induced dyskinesia by
modulating glutamatergic plasticity.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission
Stem
A 34-year-old woman with major depressive disorder has partial
response to an SSRI (sertraline 100 mg daily) after 8 weeks:
mood improved but she reports persistent anergia and
psychomotor slowing. She has no cardiac disease and desires
treatment that may increase dopaminergic tone without
worsening anxiety. Which mechanism-based pharmacologic
change best fits Stahl’s neurotransmission framework?
Options
A. Add bupropion (norepinephrine–dopamine reuptake
,inhibitor).
B. Switch to venlafaxine (SNRI) at equivalent serotonergic
potency.
C. Add low-dose amisulpride (selective D2/D3 antagonist).
D. Augment with low-dose mirtazapine (α2 antagonist; 5-HT2/3
blockade).
Correct answer
A
Rationales
Correct (A): Bupropion blocks DAT and NET, increasing synaptic
dopamine and norepinephrine in projection areas tied to
motivation and psychomotor drive. Stahl’s discussion of
transporter blockade predicts improved anergia without
significant direct serotonergic stimulation that can worsen
sexual dysfunction or activation-related anxiety. Its
dopaminergic enhancement aligns with the symptom cluster.
Incorrect (B): Venlafaxine increases norepinephrine at higher
doses but has less direct DAT blockade; it may modestly
improve energy via NE but is less dopaminergic than bupropion
per transporter profiles.
Incorrect (C): Amisulpride is a D2/D3 antagonist in clinical
doses—antagonism would worsen, not improve, dopaminergic
anergia.
Incorrect (D): Mirtazapine’s α2 antagonism increases NE/5-HT
release but predominantly increases
,noradrenergic/serotonergic tone and sedation via H1; it does
not selectively boost dopamine in circuits mediating motivation.
Teaching Point
Target DAT/NET blockade to address antidepressant-resistant
anergia.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission
Stem
A 62-year-old man with Parkinson disease is treated with
levodopa/carbidopa but develops troublesome dyskinesias. His
psychiatrist considers adding an agent to reduce peak-dose
dyskinesia by modulating glutamatergic synaptic plasticity
rather than further altering dopaminergic synaptic availability.
Which mechanism aligns with this goal?
Options
A. Add amantadine (NMDA receptor antagonist).
B. Add entacapone (COMT inhibitor).
C. Add pramipexole (D2/D3 agonist).
D. Increase carbidopa to enhance peripheral decarboxylation
blockade.
, Correct answer
A
Rationales
Correct (A): Amantadine is an NMDA receptor antagonist that
reduces glutamate-mediated excitatory transmission implicated
in the pathophysiology of levodopa-induced dyskinesia; Stahl
emphasizes NMDA modulation of synaptic plasticity and motor
output, making amantadine mechanismally appropriate.
Incorrect (B): Entacapone increases CNS levodopa availability
via COMT inhibition and may worsen dyskinesia by increasing
dopaminergic peaks rather than correcting glutamatergic
hyperactivity.
Incorrect (C): Pramipexole is a dopaminergic agonist that can
alter motor response and possibly exacerbate dyskinesia; it
doesn’t directly modulate NMDA-mediated plasticity.
Incorrect (D): Increasing carbidopa increases peripheral
inhibition of decarboxylation but does not reduce central
glutamatergic contributions to dyskinesia; it alters levodopa
dosing effects peripherally.
Teaching Point
NMDA antagonism can reduce levodopa-induced dyskinesia by
modulating glutamatergic plasticity.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
