560 SEC TION III Neurology and Special Senses   

neurology—OPHTHALMOLOGY

Internuclear Medial longitudinal fasciculus (MLF): pair of MLF in MS.

ophthalmoplegia tracts that interconnect CN VI and CN III When looking left, the left nucleus of CN VI
nuclei. Coordinates both eyes to move in same fires, which contracts the left lateral rectus and
horizontal direction. Highly myelinated (must stimulates the contralateral (right) nucleus of
communicate quickly so eyes move at same CN III via the right MLF to contract the right
time). Lesions may be unilateral or bilateral medial rectus.
(latter classically seen in multiple sclerosis, Directional term (eg, right INO, left INO) refers
stroke). to the eye that is unable to adduct.
Lesion in MLF = internuclear ophthalmoplegia INO = Ipsilateral adduction failure, Nystagmus
(INO), a conjugate horizontal gaze palsy. Opposite.
Lack of communication such that when
CN VI nucleus activates ipsilateral lateral
rectus, contralateral CN III nucleus does not
stimulate medial rectus to contract. Abducting
Right frontal
eye field
eye displays nystagmus (CN VI overfires to
Voluntary gaze
stimulate CN III). Convergence normal.
to left
L R Right frontal Right INO (right MLF lesion)
Lateral Medial eye field
rectus rectus
Voluntary gaze
to left
L R
Lateral CN VI Medial CN III
rectus rectus

Oculomotor
CN VI CN III (CN III) nucleus
Midbrain
Right gaze
Oculomotor
Midbrain (CNRight
III) nucleus
MLF

Paramedian pontine
reticular formation (PPRF)
Pons Right MLF
Abducens Impaired adduction Nystagmus
(CN VI) nucleus
Paramedian pontine (convergence normal)
reticular formation (PPRF)
Pons Abducens Left gaze
(CN VI) nucleus

Medulla

Medulla

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 Neurology and Special Senses   
neurology—Pharmacology SEC TION III 561

NEUROLOGY—PHARMACOLOGY
` 

Anticonvulsants
MECHANISM COMMON ADVERSE EFFECTS RARE BUT SERIOUS ADVERSE EFFECTS
Narrow spectrum (focal seizures)
Phenytoin Sedation, dizziness, diplopia, SJS, DRESS, hepatotoxicity,
gingival hypertrophy, rash, neuropathy, osteoporosis,
hirsutism, drug interactions folate depletion, teratogenicity
(CYP450 induction)
Block Na+ channel
Carbamazepine Sedation, dizziness, diplopia, SJS, DRESS, hepatotoxicity,
vomiting, diarrhea, SIADH, agranulocytosis, aplastic
rash, drug interactions anemia, folate depletion,
(CYP450 induction) teratogenicity
Gabapentinoids Block Ca2+ channel Sedation, dizziness, ataxia,
Gabapentin, weight gain
pregabalin
Narrow spectrum (absence seizures only)
Ethosuximide Blocks Ca2+ channel Sedation, dizziness, vomiting
Broad spectrum (focal and generalized seizures)
Valproate Blocks Na+ channel Sedation, dizziness, vomiting, Hepatotoxicity, pancreatitis,
Blocks Ca2+ channel weight gain, hair loss, easy teratogenicity
Blocks GABA transaminase bruising, drug interactions
(CYP450 inhibition)
Lamotrigine Blocks Na+ channel Sedation, dizziness, rash SJS, DRESS
Levetiracetam Blocks Synaptic Vesicle protein Sedation, dizziness, fatigue Neuropsychiatric (eg,
2A (SV2A) psychosis)
Topiramate Blocks Na+ channel Sedation, dizziness, mood Kidney stones, angle-closure
Potentiates GABA A receptor disturbance (eg, depression), glaucoma
weight loss, paresthesia

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 562 SEC TION III Neurology and Special Senses   
neurology—Pharmacology

Anticonvulsants (continued)

EXCITATORY
NEURON

Action
+
potential Ca² CHANNEL BLOCKERS
Na+ CHANNEL BLOCKERS
Voltage-gated
Phenytoin Na+ channel Gabapentinoids
Carbamazepine Ethosuximide
Na+
Valproate Valproate
Lamotrigine
Topiramate Depolarization
Voltage-gated
Ca2+ channel
Glutamate vesicle Ca2+
release
SV2A RECEPTOR BLOCKER SV2A
receptor
Levetiracetam

Ca2+
Na+
NMDA
receptor
AMPA
receptor
GABAA AGONISTS Depolarization

Benzodiazepines GABAA Cl_

Phenobarbital receptor
Topiramate
Action
Cl
_ potential

GABA GABA POST-SYNAPTIC

reuptake NEURON
GAD receptor
Glutamate
GABA
INHIBITORY Succinic semi- GABA
NEURON aldehyde (SSA) transaminase

GABA TRANSAMINASE
BLOCKER

Valproate

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 Neurology and Special Senses   
neurology—Pharmacology SEC TION III 563

Barbiturates Phenobarbital, pentobarbital.

MECHANISM Facilitate GABA A action by  duration of Cl− channel opening, thus  neuron firing (barbidurates
 duration).
CLINICAL USE Sedative for anxiety, seizures, insomnia.
ADVERSE EFFECTS Respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by
alcohol use); dependence; drug interactions (induces cytochrome P-450).
Overdose treatment is supportive (assist respiration and maintain BP).
Contraindicated in porphyria.

Benzodiazepines Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide,

alprazolam.
MECHANISM Facilitate GABA A action by  frequency of Cl– channel opening (“frenzodiazepines”  frequency).
 REM sleep. Most have long half-lives and active metabolites (exceptions [ATOM]: Alprazolam,
Triazolam, Oxazepam, and Midazolam are short acting Ž higher addictive potential).
CLINICAL USE Anxiety, panic disorder, spasticity, status epilepticus (lorazepam, diazepam, midazolam), eclampsia,
medically supervised withdrawal (eg, alcohol/DTs; long-acting chlordiazepoxide and diazepam
are preferred), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation),
hypnotic (insomnia). Lorazepam, Oxazepam, and Temazepam can be used for those with liver
disease who drink a LOT due to minimal first-pass metabolism.
ADVERSE EFFECTS Dependence, additive CNS depression effects with alcohol and barbiturates (all bind the GABA A
receptor). Less risk of respiratory depression and coma than with barbiturates. Treat overdose with
flumazenil (competitive antagonist at GABA benzodiazepine receptor). Can precipitate seizures
by causing acute benzodiazepine withdrawal.

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 564 SEC TION III Neurology and Special Senses   
neurology—Pharmacology

Insomnia therapy
AGENT MECHANISM ADVERSE EFFECTS NOTES
Nonbenzodiazepine Examples: Zolpidem, Ataxia, headaches, confusion These ZZZs put you to sleep
hypnotics Zaleplon, esZopiclone Cause only modest day-after Short duration due to rapid
Act via the BZ1 subtype of psychomotor depression and metabolism by liver enzymes;
GABA receptor few amnestic effects (vs older effects reversed by flumazenil
sedative-hypnotics)  dependency risk and
 sleep cycle disturbance (vs
benzodiazepine hypnotics)
Suvorexant Orexin (hypocretin) receptor CNS depression (somnolence), Contraindications: narcolepsy,
antagonist headache, abnormal sleep- combination with strong
related activities CYP3A4 inhibitors
Not recommended in patients
with liver disease
Limited risk of dependency
Ramelteon Melatonin receptor agonist: Dizziness, nausea, fatigue, No known risk of dependency
binds MT1 and MT2 in headache
suprachiasmatic nucleus

Triptans Sumatriptan
MECHANISM 5-HT1B/1D agonists. Inhibit trigeminal nerve activation, prevent vasoactive peptide release, induce
vasoconstriction.
CLINICAL USE Acute migraine, cluster headache attacks. A sumo wrestler trips and falls on their head.
ADVERSE EFFECTS Coronary vasospasm (contraindicated in patients with CAD or vasospastic angina), mild
paresthesia, serotonin syndrome (in combination with other 5-HT agonists).

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 Neurology and Special Senses   
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Parkinson disease The most effective treatments are non-ergot dopamine agonists which are usually started in
therapy younger patients, and levodopa (with carbidopa) which is usually started in older patients. Deep
brain stimulation of the STN or GPi may be helpful in advanced disease.
STRATEGY AGENTS
Dopamine agonists Non-ergot (preferred)—pramipexole, ropinirole; toxicity includes nausea, impulse control disorder
(eg, gambling), postural hypotension, hallucinations, confusion, sleepiness, edema.
Ergot—bromocriptine; rarely used due to toxicity.
 dopamine availability Amantadine ( dopamine release and  dopamine reuptake); mainly used to reduce levodopa-
induced dyskinesias; toxicity = peripheral edema, livedo reticularis, ataxia.
 l-DOPA availability Agents prevent peripheral (pre-BBB) l-DOPA degradation Ž  l-DOPA entering CNS Ž  central
l-DOPA available for conversion to dopamine.
ƒ Levodopa (l-DOPA)/carbidopa—carbidopa blocks peripheral conversion of l-DOPA to
dopamine by inhibiting DOPA decarboxylase. Also reduces adverse effects of peripheral
l-DOPA conversion into dopamine (eg, nausea, vomiting).
ƒ Entacapone and tolcapone prevent peripheral l-DOPA degradation to 3-O-methyldopa
(3‑OMD) by inhibiting COMT. Used in conjunction with levodopa.
Prevent dopamine Agents act centrally (post-BBB) to inhibit breakdown of dopamine.
breakdown ƒ Selegiline, rasagiline—block conversion of dopamine into DOPAC by selectively inhibiting
MAO-B, which is more commonly found in the Brain than in the periphery.
ƒ Tolcapone—crosses BBB and blocks conversion of dopamine to 3-methoxytyramine (3-MT) in
the brain by inhibiting central COMT.
Curb excess Benztropine, trihexyphenidyl (Antimuscarinic; improves tremor and rigidity but has little effect on
cholinergic activity bradykinesia in Parkinson disease). Tri Parking my Mercedes-Benz.
  DOPA
CIRCULATION
DECARBOXYLASE Dopamine 3-OMD
INHIBITOR
– L-DOPA
COMT INHIBITORS
Carbidopa DDC COMT – (peripheral)

BLOOD-
BRAIN Entacapone
BARRIER Tolcapone

L-DOPA

DDC COMT INHIBITOR

(central)
PRESYNAPTIC
Dopamine –
TERMINAL FROM THE COMT Tolcapone
SUBSTANTIA NIGRA
3-MT
DOPAC

–
Autoregulatory MAO TYPE B
receptor INHIBITORS
Reuptake
Selegiline
Rasagiline

DOPAMINE +
AVAILABILITY

Amantadine

Dopamine receptors + DOPAMINE AGONISTS

POSTSYNAPTIC
TERMINAL IN
THE STRIATUM Pramipexole (non-ergot)
Ropinirole (non-ergot)
Bromocriptine (ergot)

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 566 SEC TION III Neurology and Special Senses   
neurology—Pharmacology

Carbidopa/levodopa
MECHANISM  dopamine in brain. Unlike dopamine, l-DOPA can cross BBB and is converted by DOPA
decarboxylase in the CNS to dopamine. Carbidopa, a peripheral DOPA decarboxylase inhibitor
that cannot cross BBB, is given with l-DOPA to  bioavailability of l-DOPA in the brain and to
limit peripheral adverse effects.
CLINICAL USE Parkinson disease.
ADVERSE EFFECTS Nausea, hallucinations, postural hypotension. With progressive disease, l-DOPA can lead to “on-
off” phenomenon with improved mobility during “on” periods, then impaired motor function
during “off” periods when patient responds poorly to l-DOPA or medication wears off.

Neurodegenerative disease therapy

DISEASE
Alzheimer disease
Amyotrophic lateral
sclerosis
Huntington disease
AGENT MECHANISM NOTES
Donepezil, rivastigmine, AChE inhibitor 1st-line treatment
galantamine Adverse effects: nausea, dizziness,
insomnia; contraindicated
in patients with cardiac
conduction abnormalities
Dona Riva dances at the gala
Memantine NMDA receptor antagonist; helps Used for moderate to advanced
prevent excitotoxicity (mediated by dementia
Ca2+) Adverse effects: dizziness,
confusion, hallucinations
Riluzole  neuron glutamate excitotoxicity  survival
Treat Lou Gehrig disease with
riLouzole
Deutetrabenazine, Inhibit vesicular monoamine May be used for Huntington
tetrabenazine transporter (VMAT) Ž  dopamine chorea and tardive dyskinesia
vesicle packaging and release

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 Neurology and Special Senses   
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Local anesthetics Esters—benzocaine, chloroprocaine, cocaine, Local anesthetic Sodium

tetracaine. channel
Amides—bupivacaine, lidocaine, mepivacaine, Axonal membrane
prilocaine, ropivacaine (amides have 2 i’s in
name).

Cell interior

MECHANISM Block neurotransmission via binding to voltage-gated Na+ channels on inner portion of the channel
along nerve fibers. Most effective in rapidly firing neurons. 3° amine local anesthetics penetrate
membrane in uncharged form, then bind to ion channels as charged form.
Can be given with vasoconstrictors (usually epinephrine) to enhance block duration of action by
 systemic absorption.
In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane
effectively Ž need more anesthetic.
Order of loss: (1) pain, (2) temperature, (3) touch, (4) pressure.
CLINICAL USE Minor surgical procedures, spinal anesthesia. If allergic to esters, give amides.
ADVERSE EFFECTS CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension,
arrhythmias (cocaine), methemoglobinemia (benzocaine, prilocaine).

General anesthetics CNS drugs must be lipid soluble (cross the BBB) or be actively transported.
Drugs with  solubility in blood (eg, nitrous oxide [N2O]) = rapid induction and recovery times.
Drugs with  solubility in lipids (eg, isoflurane) =  potency.
MAC = Minimum Alveolar Concentration (of inhaled anesthetic) required to prevent 50% of
subjects from moving in response to noxious stimulus (eg, skin incision). Potency = 1/MAC.
MECHANISM ADVERSE EFFECTS/NOTES
Inhaled anesthetics
Sevoflurane Respiratory depression,  cough reflex
Desflurane Myocardial depression,  BP
 cerebral blood flow ( ICP),  metabolic rate
Isoflurane
 skeletal and smooth muscle tone
Mechanism unknown Postoperative nausea and vomiting
Malignant hyperthermia
N2O Diffusion into and expansion (N2O) of gas-filled
cavities (eg, pneumothorax); very low potency
Intravenous anesthetics
Propofol Potentiates GABA A receptor Respiratory depression,  BP; most commonly
Inhibits NMDA receptor used IV agent for induction of anesthesia
Etomidate Potentiates GABA A receptor Acute adrenal insufficiency, postoperative
nausea and vomiting; hemodynamically
neutral
Ketamine Inhibits NMDA receptor Sympathomimetic:  BP,  HR,  cerebral blood
flow ( ICP), bronchodilation
Psychotomimetic: hallucinations, vivid dreams

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 568 SEC TION III Neurology and Special Senses   
neurology—Pharmacology

Neuromuscular Muscle paralysis in surgery or mechanical ventilation. Selective for Nm nicotinic receptors at
blocking drugs neuromuscular junction but not autonomic Nn receptors.
Depolarizing Succinylcholine—strong Nm nicotinic receptor agonist; produces sustained depolarization and
neuromuscular prevents muscle contraction.
blocking drugs Reversal of blockade:
ƒ Phase I (prolonged depolarization)—no antidote. Block potentiated by cholinesterase inhibitors.
ƒ Phase II (repolarized but blocked; Nm nicotinic receptors are available, but desensitized)—may
be reversed with cholinesterase inhibitors.
Complications include hypercalcemia, hyperkalemia, malignant hyperthermia.  risk of prolonged
muscle paralysis in patients with pseudocholinesterase deficiency.
Nondepolarizing Atracurium, cisatracurium, pancuronium, rocuronium, vecuronium—competitive Nm nicotinic
neuromuscular receptor antagonist.
blocking drugs Reversal of blockade—sugammadex or cholinesterase inhibitors (eg, neostigmine). Anticholinergics
(eg, atropine, glycopyrrolate) are given with cholinesterase inhibitors to prevent muscarinic effects
(eg, bradycardia).

Malignant Rare, life-threatening, hypermetabolic condition caused by the administration of potent inhaled
hyperthermia anesthetics (sevoflurane, desflurane, isoflurane) or succinylcholine in susceptible individuals.
Susceptibility to malignant hyperthermia is caused by de novo or inherited (autosomal dominant)
mutations to ryanodine (RYR1) or dihydropyridine receptors (DHPR).
  Ca2+ release from sarcoplasmic reticulum Ž sustained muscle contraction Ž hypercapnia,
tachycardia, masseter/generalized muscle rigidity, rhabdomyolysis, hyperthermia.
Treatment: dantrolene (ryanodine receptor antagonist).

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 Neurology and Special Senses   
neurology—Pharmacology SEC TION III 569

Skeletal muscle relaxants

DRUG MECHANISM CLINICAL USE NOTES
Baclofen GABA B receptor agonist in Muscle spasticity, dystonia, Acts on the back (spinal cord)
spinal cord multiple sclerosis May cause sedation
Cyclobenzaprine Acts within CNS, mainly at the Muscle spasms Centrally acting
brainstem Structurally related to TCAs
May cause anticholinergic
adverse effects, sedation
Dantrolene Prevents release of Ca2+ from Malignant hyperthermia Acts directly on muscle
sarcoplasmic reticulum of (toxicity of inhaled anesthetics
skeletal muscle by inhibiting and succinylcholine) and
the ryanodine receptor neuroleptic malignant
syndrome (toxicity of
antipsychotics)
Tizanidine α2 agonist, acts centrally Muscle spasticity, multiple
sclerosis, ALS, cerebral palsy

Opioid analgesics
MECHANISM Act as agonists at opioid receptors (μ = β-endorphin, δ = enkephalin, κ = dynorphin) to modulate
synaptic transmission—close presynaptic Ca2+ channels, open postsynaptic K+ channels
Ž  synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.
EFFICACY Full agonist: morphine, meperidine (long acting), methadone, codeine (prodrug; activated by
CYP2D6), fentanyl.
Partial agonist: buprenorphine.
Mixed agonist/antagonist: butorphanol, nalbuphine.
Antagonist: naloxone, naltrexone, methylnaltrexone.
CLINICAL USE Moderate to severe or refractory pain, diarrhea (loperamide, diphenoxylate), acute pulmonary
edema, maintenance programs for opiate use disorder (methadone, buprenorphine + naloxone),
neonatal abstinence syndrome (methadone, morphine).
ADVERSE EFFECTS Nausea, vomiting, pruritus (histamine release), opiate use disorder, respiratory depression,
constipation, sphincter of Oddi spasm, miosis (except meperidine Ž mydriasis), additive CNS
depression with other drugs. Tolerance does not develop to miosis and constipation. Treat toxicity
with naloxone and prevent relapse with naltrexone once detoxified.

Tramadol
MECHANISM Very weak opioid agonist; also inhibits the reuptake of norepinephrine and serotonin.
CLINICAL USE Chronic pain.
ADVERSE EFFECTS Similar to opioids; decreases seizure threshold; serotonin syndrome.

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 570 SEC TION III Neurology and Special Senses   
neurology—Pharmacology

Butorphanol, nalbuphine
MECHANISM μ-opioid receptor partial agonists and κ-opioid receptor full agonists.
CLINICAL USE Analgesia for severe pain (eg, labor).
NOTES Mixed opioid agonists/antagonists cause less respiratory depression than full opioid agonists. Can
cause opioid withdrawal symptoms if patient is also taking full opioid agonist (due to competition
for opioid receptors). Not easily reversed with naloxone.

Capsaicin Naturally found in hot peppers.

MECHANISM Excessive stimulation and desensitization of nociceptive fibers Ž  substance P release Ž  pain.
CLINICAL USE Musculoskeletal and neuropathic pain.

Glaucoma therapy  IOP via  amount of aqueous humor (inhibit synthesis/secretion or  drainage).
“βαD humor may not be politically correct.”
DRUG CLASS EXAMPLES MECHANISM ADVERSE EFFECTS
β-blockers Timolol, betaxolol, carteolol  aqueous humor synthesis No pupillary or vision changes
α-agonists Epinephrine (α1),  aqueous humor synthesis via Mydriasis (α1); do not use in
apraclonidine, vasoconstriction (epinephrine) closed-angle glaucoma
brimonidine (α2)  aqueous humor synthesis Blurry vision, ocular
(apraclonidine, brimonidine) hyperemia, foreign body
 outflow of aqueous humor via sensation, ocular allergic
uveoscleral pathway reactions, ocular pruritus
Diuretics Acetazolamide  aqueous humor synthesis No pupillary or vision changes
via inhibition of carbonic
anhydrase
Prostaglandins Bimatoprost, latanoprost  outflow of aqueous humor via Darkens color of iris
(PGF2α)  resistance of flow through (browning), eyelash growth
uveoscleral pathway
Cholinomimetics (M3) Direct: pilocarpine, carbachol  outflow of aqueous humor via Miosis (contraction of pupillary
Indirect: physostigmine, contraction of ciliary muscle sphincter muscles) and
echothiophate and opening of trabecular cyclospasm (contraction of
meshwork ciliary muscle)
Use pilocarpine in acute angle
closure glaucoma—very
effective at opening meshwork
into canal of Schlemm

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 HIGH-YIELD PRINCIPLES IN

Psychiatry

“Words of comfort, skillfully administered, are the oldest therapy known to ` Psychology 572
man.”
—Louis Nizer ` Pathology 575

“Psychiatry at its best is what all medicine needs more of—humanity, art, ` Pharmacology 592
listening, and sympathy.”
—Susannah Cahalan

“It’s time to tell everyone who’s dealing with a mental health issue that
they’re not alone, and that getting support and treatment isn’t a sign of
weakness, it’s a sign of strength.”
—Michelle Obama

“I have schizophrenia. I am not schizophrenia. I am not my mental

illness. My illness is a part of me.”
—Jonathan Harnisch

This chapter encompasses overlapping areas in psychiatry, psychology,

sociology, and psychopharmacology. High-yield topics include schizo­
phrenia, mood disorders, eating disorders, personality disorders, somatic
symptom disorders, substance use disorders, and antipsychotics. Know
the DSM-5 criteria for diagnosing common psychiatric disorders.

571

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 572 SECTION III Psychiatry   
Psychiatry—PSYCHology

PSYCHIATRY—PSYCHOLOGY
` 

Classical conditioning Learning in which a natural response
(salivation) is elicited by a conditioned,
or learned, stimulus (bell) that previously
was presented in conjunction with an
unconditioned stimulus (food).
Usually elicits involuntary responses.
Pavlov’s classical experiments with dogs—
ringing the bell provoked salivation.

Operant conditioning Learning in which a particular action is elicited because it produces a punishment or reward.
Usually elicits voluntary responses.
Reinforcement Target behavior (response) is followed by desired Skinner operant conditioning quadrants:
reward (positive reinforcement) or removal of
Increase behavior Decrease behavior
aversive stimulus (negative reinforcement).
Punishment Repeated application of aversive stimulus

stimulus stimulus
Positive Positive

Remove a Add a
(positive punishment) or removal of desired reinforcement punishment
reward (negative punishment) to extinguish
unwanted behavior. Negative Negative
reinforcement punishment
Extinction Discontinuation of reinforcement (positive or
negative) eventually eliminates behavior. Can
occur in operant or classical conditioning.

Transference and countertransference

Transference Patient projects feelings about formative or other important persons onto physician (eg, psychiatrist
is seen as parent).
Countertransference Physician projects feelings about formative or other important persons onto patient (eg, patient
reminds physician of younger sibling).

Ego defenses Thoughts and behaviors (voluntary or involuntary) used to resolve conflict and prevent undesirable
feelings (eg, anxiety, depression).
IMMATURE DEFENSES DESCRIPTION
Acting out Subconsciously coping with stressors or
emotional conflict using actions rather than
reflections or feelings.
Denial Avoiding the awareness of some painful reality.
Displacement Redirection of emotions or impulses to a neutral
person or object (vs projection).
Dissociation Temporary, drastic change in personality,
memory, consciousness, or motor behavior to
avoid emotional stress. Patient has incomplete
or no memory of traumatic event.
EXAMPLE
A patient skips therapy appointments after deep
discomfort from dealing with his past.
A patient with cancer plans a full-time work
schedule despite being warned of significant
fatigue during chemotherapy.
After being reprimanded by her principal, a
frustrated teacher returns home and criticizes
her wife’s cooking instead of confronting the
principal directly.
A survivor of sexual abuse sees the abuser and
suddenly becomes numb and detached.

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 Psychiatry   
Psychiatry—PSYCHology
Ego defenses (continued)
IMMATURE DEFENSES DESCRIPTION
Fixation Partially remaining at a more childish level of
development (vs regression).
Idealization Expressing extremely positive thoughts of self
and others while ignoring negative thoughts.
Identification Largely unconscious assumption of the
characteristics, qualities, or traits of another
person or group.
Intellectualization Using facts and logic to emotionally distance
oneself from a stressful situation.
Isolation (of affect) Separating feelings from ideas and events.
Passive aggression Demonstrating hostile feelings in a
nonconfrontational manner; showing indirect
opposition.
Projection Attributing an unacceptable internal impulse to
an external source (vs displacement).
Rationalization Asserting plausible explanations for events that
actually occurred for other reasons, usually to
avoid self-blame.
Reaction formation Replacing a warded-off idea or feeling with an
emphasis on its opposite (vs sublimation).
Regression Involuntarily turning back the maturational
clock to behaviors previously demonstrated
under stress (vs fixation).
Repression Involuntarily withholding an idea or feeling
from conscious awareness (vs suppression).
Splitting Believing that people are either all good or all
bad at different times due to intolerance of
ambiguity. Common in borderline personality
disorder. Borders split countries.
MATURE DEFENSES
Sublimation Replacing an unacceptable wish with a course
of action that is similar to the wish but socially
acceptable (vs reaction formation).
Altruism Alleviating negative feelings via unsolicited
generosity, which provides gratification (vs
reaction formation).
Suppression Intentionally withholding an idea or feeling from
conscious awareness (vs repression); temporary.
Humor Lightheartedly expressing uncomfortable feelings
to shift the internal focus away from the distress.
Mature adults wear a SASH.
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SECTION III 573
EXAMPLE
A college student studying for a stressful exam
begins sucking her thumb.
A patient boasts about his physician and his
accomplishments while ignoring any flaws.
A resident starts putting her stethoscope in her
pocket like her favorite attending, instead of
wearing it around her neck like before.
A patient diagnosed with cancer discusses the
pathophysiology of the disease.
Describing murder in graphic detail with no
emotional response.
A disgruntled employee is repeatedly late to
work, but won’t admit it is a way to get back at
the manager.
A man who wants to cheat on his wife accuses
his wife of being unfaithful.
An employee who was recently fired claims that
the job was not important anyway.
A stepfather treats a child he resents with
excessive nurturing and overprotection.
A previously toilet-trained child begins
bedwetting again following the birth of a
sibling.
A 20-year-old does not remember going to
counseling during his parents’ divorce 10 years
earlier.
A patient says that all the nurses are cold and
insensitive, but the physicians are warm and
friendly.
A teenager’s aggression toward her parents
because of their high expectations is channeled
into excelling in sports.
A mafia boss makes a large donation to charity.
An athlete focuses on other tasks to prevent
worrying about an important upcoming match.
A nervous medical student jokes about the
boards.
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 574 SECTION III Psychiatry   
Psychiatry—PSYCHology

Grief Natural feeling that occurs in response to the death of a loved one. Symptoms and trajectory vary
for each individual, are specific to each loss, and do not follow a fixed series of stages. In addition
to guilt, sadness, and yearning, patients may experience somatic symptoms, hallucinations of the
deceased, and/or transient episodes of wishing they had died with or instead of their loved one.
Typical acute grief is time limited (adaptations within 6 months) and is not a disorder.
Prolonged grief disorder—diagnosed if thoughts are persistent and prolonged, significantly impair
functioning, and do not meet criteria for another disorder (eg, major depressive disorder [MDD]).

Normal infant and Milestone dates are ranges that have been approximated and vary by source. Children not meeting
child development milestones may need assessment for potential developmental delay.
AGE MOTOR
Infant Parents
0–12 mo Primitive reflexes disappear—
Moro, rooting, palmar,
Babinski (Mr. Peanut Butter) Separation anxiety (by 9 mo)
Posture—lifts head up prone (by
1 mo), rolls and sits (by 6 mo),
crawls (by 8 mo), stands (by
10 mo), walks (by 12–18 mo)
Picks—passes toys hand to
hand (by 6 mo), Pincer grasp
(by 10 mo)
Points to objects (by 12 mo)
Toddler Child
12–36 mo Cruises, takes first steps (by
12 mo)
Climbs stairs (by 18 mo)
Cubes stacked (number)
= age (yr) × 3
Cutlery—feeds self with fork
and spoon (by 20 mo)
Kicks ball (by 24 mo)
Preschool Don’t
3–5 yr Drive—tricycle (3 wheels at
3 yr)
Drawings—copies line or
circle, stick figure (by 4 yr)
Dexterity—hops on one foot
by 4 yr (“4 on one foot”), uses
buttons or zippers, grooms
self (by 5 yr)
SOCIAL
Start
Social smile (by 2 mo)
Stranger anxiety (by 6 mo)
Rearing
Recreation—parallel play (by
24–36 mo)
Rapprochement—moves away
from and returns to parent (by
24 mo)
Realization—core gender
identity formed (by 36 mo)
Forget, they’re still
Freedom—comfortably spends
part of day away from parent
(by 3 yr)
Friends—cooperative play, has
imaginary friends (by 4 yr)
VERBAL/COGNITIVE
Observing,
Orients—first to voice (by
4 mo), then to name and
gestures (by 9 mo)
Object permanence (by 9 mo)
Oratory—says “mama” and
“dada” (by 10 mo)
Working,
Words—uses 50-200 words (by
2 yr), uses 300+ words (by 3 yr)
Learning!
Language—understands 1000
(3 zeros) words (by 3 yr),
uses complete sentences and
prepositions (by 4 yr)
Legends—can tell detailed
stories (by 4 yr)

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PSYCHIATRY—PATHOLOGY
` 

Child abuse
Physical abuse
SIGNS Nonaccidental trauma (eg,
fractures, bruises, burns).
Injuries often in different
stages of healing or in
patterns resembling possible
implements of injury.
Includes abusive head trauma
(shaken baby syndrome),
characterized by subdural
hematomas or retinal
hemorrhages.
Caregivers may delay seeking
medical attention for the
child or provide explanations
inconsistent with the child's
developmental stage or
pattern of injury.
EPIDEMIOLOGY 40% of deaths related to child
abuse or neglect occur in
children < 1 year old.
Sexual abuse
STIs, UTIs, and genital, anal,
or oral trauma. Most often,
there are no physical signs;
sexual abuse should not be
excluded from a differential
diagnosis in the absence of
physical trauma.
Children often exhibit sexual
knowledge or behavior
incongruent with their age.
Peak incidence 9–12 years old.
Emotional abuse
Babies or young children may
lack a bond with the caregiver
but are overly affectionate
with less familiar adults.
They may be aggressive
toward children and animals
or unusually anxious.
Older children are often
emotionally labile and prone
to angry outbursts. They may
distance themselves from
caregivers and other children.
They can experience vague
somatic symptoms for which
a medical cause cannot be
found.
~80% of young adult victims of
child emotional abuse meet
the criteria for ≥ 1 psychiatric
illness by age 21.

Child neglect Failure to provide a child with adequate food, shelter, supervision, education, and/or affection.
Most common form of child maltreatment. Signs: poor hygiene, malnutrition, withdrawal,
impaired social/emotional development, failure to thrive.
As with other types of child abuse, suspected child neglect must be reported to local child
protective services.

Vulnerable child Parents perceive the child as especially susceptible to illness or injury (vs factitious disorder
syndrome imposed on another). Usually follows a serious illness or life-threatening event. Can result in
missed school or overuse of medical services.

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 576 SECTION III Psychiatry   
Psychiatry—Pathology

Childhood and early-onset disorders

Attention-deficit Onset before age 12, but diagnosis can only be established after age 4. Characterized by
hyperactivity hyperactivity, impulsivity, and/or inattention in ≥ 2 settings (eg, school, home, places of worship).
disorder Normal intelligence, but commonly coexists with difficulties in school. Often persists into
adulthood. Commonly coexists with other behavioral, cognitive, or developmental disorders.
Treatment: stimulants (eg, methylphenidate) +/– behavioral therapy; alternatives include
atomoxetine and α2-agonists (eg, clonidine, guanfacine).
Autism spectrum Onset in early childhood. Social and communication deficits, repetitive/ritualized behaviors,
disorder restricted interests. May be accompanied by intellectual disability and/or above average abilities in
specific skills (eg, music). More common in males. Associated with  head and/or brain size.
Conduct disorder Repetitive, pervasive behavior violating societal norms or the basic rights of others (eg, aggression
toward people and animals, destruction of property, theft). After age 18, often reclassified as
antisocial personality disorder. Conduct = children, antisocial = adults. Treatment: psychotherapy
(eg, cognitive behavioral therapy [CBT]).
Disruptive mood Onset before age 10. Severe, recurrent temper outbursts out of proportion to situation. Child is
dysregulation constantly angry and irritable between outbursts. Treatment: CBT, stimulants, antipsychotics.
disorder
Intellectual disability Global cognitive deficits (vs specific learning disorder) that affect reasoning, memory, abstract
thinking, judgment, language, learning. Adaptive functioning is impaired, leading to major
difficulties with education, employment, communication, socialization, independence.
Treatment: psychotherapy, occupational therapy, special education.
Intermittent explosive Onset after age 6. Recurrent verbal or physical outbursts representing a failure to control aggressive
disorder impulses. Outbursts last < 30 minutes and are out of proportion to provocation and may lead
to legal, financial, or social consequences. Episodes are not premeditated and may provide an
immediate sense of relief, followed by remorse. Treatment: psychotherapy, SSRIs.
Oppositional defiant Pattern of anger and irritability with argumentative, vindictive, and defiant behavior toward
disorder authority figures lasting ≥ 6 months. Treatment: psychotherapy (eg, CBT).
Selective mutism Onset before age 5. Anxiety disorder lasting ≥ 1 month involving refraining from speech in certain
situations despite speaking in other, usually more comfortable situations. Development (eg, speech and
language) not typically impaired. Interferes with social, academic, and occupational tasks. Commonly
coexists with social anxiety disorder. Treatment: behavioral, family, and play therapy; SSRIs.
Separation anxiety Overwhelming fear of separation from home or attachment figure lasting ≥ 4 weeks. Can be
disorder normal behavior up to age 3–4. May lead to factitious physical complaints to avoid school.
Treatment: CBT, play therapy, family therapy.
Specific learning Onset during school-age years. Inability to acquire or use information from a specific subject
disorder (eg, math, reading, writing) near age-expected proficiency for ≥ 6 months despite focused
intervention. General functioning and intelligence are normal (vs intellectual disability).
Treatment: academic support, counseling, extracurricular activities.
Tourette syndrome Onset before age 18. Sudden, recurrent, nonrhythmic, stereotyped motor (eg, grimacing,
shrugging) and vocal (eg, grunting, throat clearing) tics that persist for > 1 year. Coprolalia
(involuntary obscene speech) found in some patients. Associated with OCD and ADHD.
Treatment: psychoeducation, behavioral therapy. For intractable and distressing tics:
tetrabenazine, antipsychotics, α2-agonists.

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Orientation Patients’ ability to know the date and time, where they are, and who they are (order of loss: time
Ž place Ž person). Common causes of loss of orientation: alcohol, drugs, fluid/electrolyte
imbalance, head trauma, hypoglycemia, infection, nutritional deficiencies, hypoxia.

Amnesias
Retrograde amnesia Inability to remember things that occurred before a CNS insult.
Anterograde amnesia Inability to remember things that occurred after a CNS insult ( acquisition of new memory).
Korsakoff syndrome Amnesia (anterograde > retrograde) and disorientation caused by vitamin B1 deficiency. Associated
with disruption and destruction of the limbic system, especially mammillary bodies and anterior
thalamus. Seen in chronic alcohol use as a late neuropsychiatric manifestation of Wernicke
encephalopathy. Confabulations are characteristic.

Dissociative disorders
Depersonalization/ Persistent feelings of detachment or estrangement from one’s own body, thoughts, perceptions,
derealization and actions (depersonalization) or one’s environment (derealization). Intact reality testing (vs
disorder psychosis).
Dissociative amnesia Inability to recall important personal information, usually following severe trauma or stress.
May be accompanied by dissociative fugue (abrupt, unexpected travelling away from home).
Dissociative identity Formerly called multiple personality disorder. Presence of ≥ 2 distinct identities or personality
disorder states, typically with distinct memories and patterns of behavior. More common in females.
Associated with history of sexual abuse, PTSD, depression, substance use, borderline personality
disorder, somatic symptom disorders.

Delirium “Waxing and waning” level of consciousness Delirium = changes in sensorium.

with acute onset,  attention span,  level
of arousal. Characterized by disorganized
thinking, hallucinations (often visual),
misperceptions (eg, illusions), disturbance
in sleep-wake cycle, cognitive dysfunction,
agitation. Reversible.
Usually 2° to other identifiable illness (eg, CNS
disease, infection, trauma, substance use/
withdrawal, metabolic/electrolyte disturbances,
hemorrhage, urinary/fecal retention), or
medications (eg, anticholinergics), especially
in older adults.
Most common presentation of altered mental
status in inpatient setting, especially in the
ICU or during prolonged hospital stays.
EEG may show diffuse background rhythm
slowing.
Treatment: identification and management of
underlying condition. Orientation protocols
(eg, keeping a clock or calendar nearby),
 sleep disturbances, and  cognitive
stimulation to manage symptoms.
Antipsychotics (eg, haloperidol) as needed.
Avoid unnecessary restraints and drugs that
may worsen delirium (eg, anticholinergics,
benzodiazepines, opioids).

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 578 SECTION III Psychiatry   
Psychiatry—Pathology

Psychosis Distorted perception of reality characterized by delusions, hallucinations, and/or disorganized

thought/speech. Can occur in patients with psychiatric illness or another medical condition, or
secondary to substance or medication use.
Delusions False, fixed, idiosyncratic beliefs that persist despite evidence to the contrary and are not typical
of a patient’s culture or religion (eg, a patient who believes that others are reading his thoughts).
Types include erotomanic, grandiose, jealous, persecutory, somatic, mixed, and unspecified.
Disorganized thought Speech may be incoherent (“word salad”), tangential, or derailed (“loose associations”).
Hallucinations Perceptions in the absence of external stimuli (eg, seeing a light that is not actually present).
Contrast with misperceptions (eg, illusions) of real external stimuli. Types include:
ƒ Auditory—more commonly due to psychiatric illness (eg, schizophrenia) than neurologic
disease.
ƒ Visual—more commonly due to neurologic disease (eg, dementia), delirium, or drug
intoxication than psychiatric illness.
ƒ Tactile—common in alcohol withdrawal and stimulant use (eg, “cocaine crawlies,” a type of
delusional parasitosis).
ƒ Olfactory—often occur as an aura of temporal lobe epilepsy (eg, burning rubber) and in brain
tumors.
ƒ Gustatory—rare, but seen in epilepsy.
ƒ Hypnagogic—occurs while going to sleep. Sometimes seen in narcolepsy.
ƒ Hypnopompic—occurs while waking from sleep (“get pomped up in the morning”).
Sometimes seen in narcolepsy.
Contrast with illusions, which are misperceptions of real external stimuli (eg, mistaking a shadow
for a black cat).

Mood disorder Characterized by an abnormal range of moods or internal emotional states and loss of control over
them. Severity of moods causes distress and impairment in social and occupational functioning.
Includes major depressive, bipolar, dysthymic, and cyclothymic disorders. Episodic superimposed
psychotic features (delusions, hallucinations, disorganized speech/behavior) may be present at any
time during mood episodes (other than hypomania).
MDE MDE with psychotic Bipolar I Bipolar II Schizoaffective disorder
features
Mania

Hypomania

Euthymia

Dysthymia

Depression
Psychosis only occurs Requires 1 episode of mania. Requires 1 episode of Psychosis overlaps with mood episodes
with mood episodes Psychotic features possible hypomania and 1 MDE. but must occur by itself for > 2 weeks
Psychotic features
during manic or depressive Psychotic features possible
Mania/hypomania episodes. during MDE, but does not
Euthymia occur with hypomania
Major depressive episode (MDE)

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Schizophrenia spectrum disorders

Schizophrenia Chronic illness causing profound functional Associated with altered dopaminergic activity,
impairment. Symptom categories include:  serotonergic activity, and  dendritic
ƒ Positive—excessive or distorted functioning branching. Ventriculomegaly on brain
(eg, hallucinations, delusions, unusual imaging. Lifetime prevalence—1.5% (males
thought processes, disorganized speech, > females). Presents earlier in males (late teens
bizarre behavior) to early 20s) than in females (late 20s to early
ƒ Negative—diminished functioning (eg, flat 30s).  suicide risk.
or blunted affect, apathy, anhedonia, alogia, Heavy cannabis use in adolescence is associated
social withdrawal) with  incidence and worsened course of
ƒ Cognitive—reduced ability to understand or psychotic, mood, and anxiety disorders.
make plans, diminished working memory, Treatment: atypical antipsychotics (eg,
inattention risperidone) are first line.
Diagnosis requires ≥ 2 of the following active Negative symptoms often persist after treatment,
symptoms, including ≥ 1 from symptoms #1–3: despite resolution of positive symptoms.
1. Delusions
2. Hallucinations, often auditory
3. Disorganized speech
4. Disorganized or catatonic behavior
5. Negative symptoms
Symptom onset ≥ 6 months prior to diagnosis;
requires ≥ 1 month of active symptoms over
the past 6 months.
Brief psychotic disorder—≥ 1 positive symptom(s) lasting between 1 day and 1 month, usually
stress-related.
Schizophreniform disorder—≥ 2 symptoms lasting 1–6 months.
Schizoaffective Shares symptoms with both schizophrenia and mood disorders (MDD or bipolar disorder). To
disorder differentiate from a mood disorder with psychotic features, patient must have ≥ 2 weeks of
psychotic symptoms without a manic or depressive episode.
Delusional disorder ≥ 1 delusion(s) lasting > 1 month, but without a mood disorder or other psychotic symptoms. Daily
functioning, including socialization, may be impacted by the pathological, fixed belief but is otherwise
unaffected. Can be shared by individuals in close relationships (folie à deux).
Schizotypal Cluster A personality disorder that also falls on the schizophrenia spectrum. May include brief
personality disorder psychotic episodes (eg, delusions) that are less frequent and severe than in schizophrenia.

Manic episode Distinct period of abnormally and persistently elevated, expansive, or irritable mood and  activity
or energy. Diagnosis requires marked functional impairment with ≥ 3 of the following for ≥ 1
week, or any duration if hospitalization is required (people with mania DIG FAST):
ƒ Distractibility ƒ Flight of ideas—racing thoughts
ƒ Impulsivity/Indiscretion—seeks pleasure ƒ  goal-directed Activity/psychomotor
without regard to consequences (hedonistic) Agitation
ƒ Grandiosity—inflated self-esteem ƒ  need for Sleep
ƒ Talkativeness or pressured speech

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